ICL #1 - ISAKOS

ICL #1 

BASIC SCIENCE AND CLINICAL USE OF CELL THERAPY IN ARTICULAR CARTILAGE REPAIR 

Tuesday, March 11, 2003 • Location: Carlton Hotel, Room: Carlton I 

Chairman: Lars Peterson, MD, PhD, Sweden 

Faculty: Scott Gillogly, MD, USA, Bert Mandelbaum, MD, USA, Anders Lindahl, MD, PhD, Sweden, Wayne Gersoff, USA 

and Carl Winalski, MD, USA 

Introduction. Indications for cell therapy in cartilage repair 

Lars Peterson 

Basic Scientific background for cell therapy 

Anders Lindahl 

Different treatments for cartilage repair and results of autologous chondrocyte transplantation (ACT) and 

Report from Cartilage Repair Registry Data 

Bert Mandelbaum 

ICLs 

ACT, surgical technique and pearls and pitfalls 

Scott Gillogly 

ACT and meniscus transplantation 

Wayne Gersoff 

ACT and long-term results 

Lars Peterson 

Magnetic resonance imaging in diagnosing cartilage lesions and evaluation of cartilage repair 

Carl Winalski 

Discussion 

3.1

ICL #2 

COMPUTERS IN CLINICAL PRACTICE 

Tuesday, March 11, 2003 • Location: Carlton Hotel, Room: Carlton II 

Chairman: Don Johnson, MD, Canada 

Faculty: Vladimir Bobic, MD, United Kingdom, Nicola Maffulli, MD, MS, PhD, FRCS, United Kingdom and Ronald Selby, 

MD, USA 

NOTES: 


3.2


ISSUES IN ACL SURGERY 

Tuesday, March 11, 2003 • Aotea Centre, Kupe/Hauraki Room 

Chairman: Peter J. Fowler, MD, FRCS, Canada 

Faculty: Charles Brown, Jr., MD, USA, Burt Klos, Netherlands and Philippe Neyret, MD, France 

INDICATIONS FOR ANCILLARY SURGERY IN ACL DEFICIENT KNEE 

Ph. NEYRET, T. LOOTENS, T. AIT SI SELMI, E. SERVIEN 

, , , 

A 

C 

L 

I 

N 

J 

U 

R 

Y 

“Isolated” 

Complete 

Partial 

Posterolateral < 5% 

Evolved 

ACLaxity 

with 

Pre-OA 

OA 

due to 

Acl Laxity 


25-35y 

1/ Isolated Chronic Anterior Insufficiency 

To better understand the place and the indication of this ancillary surgery let introduce this diagram. An ACL 

deficient knee can be seen in different circumstances. The so called "complete isolated" anterior chronic laxity 

is where the end point of the Trillat-Lachman test is soft, the pivot shift is positive and the differential 

anterior tibial translation is under 6 mm measured with telos and under 4 mm measured with the differential 

lateral X-Rays on monopodal stance. 

The anterior chronic insufficiency is partial and isolated if the end point is hard and delayed and a slip is 

found. 

In such an isolated laxity we can propose an ACL graft, but one may add an extraarticular reconstruction particularly 

if the patient practices strenuous activities. Sometimes intraarticular gestures can be associated, as 

osteochondral grafting. 

Over time, the anterior chronic laxity become evolved . 

2/ Evolved chronic Anterior laxity. 

Following ACL rupture, secondary lesions occur as a result of recurrent instability causing medial lesions: 

postero-medial capsular detachment, medial meniscus , or menisco-tibial tears. The end point of the Trillat- 

Lachman test is obvious as the pivot shift.Often one can find an anterior drawer or a medial meniscus tear. 

The differential anterior tibial translation is superior to 6 mm measured with telos and superior to 4 mm 

measured with the differential lateral X-Rays on monopodal stance. 

In evolved anterior laxity we can discuss ancillary or complementary gestures. Particularly, one may discuss 

postero-medial gestures medial meniscus repair or proximal postero-medial reefing. 

In 1995, we analyzed a series of 34 proximal posteromedial reefing at 5 years follow-up. We concluded this 

gesture permits to better control the recurvatum and the anterior tibial translation on monopodal stance. 

3.3

Nevertheless the postero-medial structures are stretched and the quality of the capsule not good.We continue 

to perform this gesture only in case of severe asymmetrical recurvatum or very large amount of anterior 

tibial translation. 

3/ Chronic Anterior laxity with Preosteoarthritis 

In the absence of treatment progressively, due to the repeated episodes of instability, secondary intraarticular 

lesions happen. The patient complains mainly instability, rarely swelling or pain. 

X-Rays permit to detect an incomplete narrowing of the medio femorotibial compartment. 

We called this stage chronic Anterior Laxity with Preosteoarthritis. 

3a/ Frontal Imbalance 

The frontal imbalance can be due to medial femoro-tibial narrowing. This situation is very different of a 

frontal imbalance due to lateral opening without medial narrowing. 

Anterior chronic laxity with pre-osteoarhritis is frequent when the delay injury-operation is superior to five 

years or when an isolated previous medial meniscectomy had been performed in this unstable knee. 


Let me give a short overview of the publication we did in 1994 (Dejour, Neyret, Boileau Corr 1994) :It was a 

series of 50 patients with symptoms of ACL insufficiency and varus malalignment. 44 were available at follow-up. 

At 3.5 years follow-up we noted improved clinical symptoms, particularly objective and subjective 

stability. Moreover Osteoarthritis seemed to be stabilized. Nevertheless only one patient was able to return 

to competitive sport activities. 

We recently evaluate the results of the combined operation at ten years follow-up. The inclusion criteria were 

very strict. Only 47 knees with mild or moderate radiological preoperative changes, it means grade B or C in 

the IKDC classification, were operated on between 1983 and 1999. At follow-up, 35 knees were avalaible.The 

mean delay Injury-Operation was 8 years with a large standard deviation. In 66% of cases a previous medial 

meniscectomy had been performed. 

A closing wedge Osteotomy was performed at the beginning of our experience and progressively we preferred 

to combine an opening wedge Osteotomy. 

The IKDC subjective score depends on symptoms, functional evaluation and sport activities. The average 

score is 79 at more than 10 years follow-up. Considering the index of satisfaction, 96% considered their knee 

as normal or almost normal 

At follow up 42% of patients practiced recreational sports and only 6% continue competitive sports. The final 

evaluation allows to underline that 60% of patients belong to the grade A or B, 34% to the grade C and only 

6% to the grade D. 

Radiologically we noticed a tendancy to decrease the tibial slope in case of closing wedge osteotomy and a 

tendancy to increase the tibial slope in case of opening wedge osteotomy, but the difference was not statistically 

significative, in this short series. 

Sometimes In ACL Insufficiency with pre-osteoarthritis we do not find frontal imbalance. In fact the imbalance 

in saggital 

3b/ Saggital Imbalance 

This imbalance is observed when there is long history of instability, a previous medial meniscetomy or a tibial 

slope superior to 15 degrees. 

3.4

Deflexion High Tibial Osteotomy combined with ACL Reconstruction. This option must be discussed when 

there is a grade B or C radiological changes without frontal malalignment. 

You see the tibial slope was decreased by the anterior closing wedge osteotomy and the anterior tibial translation 

was controlled. 

Technically a Bone-Patellar tendon Bone graft is harvested, if necessary on the contralateral knee, the tunnels 

are drilled. Then the deflexion osteotomy is performed, the tibial tunnel is calibrated and the graft fixed. 

To control the recurvatum a posterior medial reefing is neccessary, once the ACL graft fixed. Two sagittal pins 

allow to fluoroscopically control the direction of the osteotomy.The osteotomy starts above the ATT and go 

to the tibial insertion of the PCL. Remember that 1 mm is about 2 degrees of correction of the tibial slope. 

The osteotomy is fixed with two staples. 

4/ Postero lateral chronic Anterior Insufficiency. 

In a very few percentage of cases, less than 5 %, there is postero-lateral lesions.It’s a different entity. Lateral 

Collateral Ligament and postero-lateral corner can be torn. 

The Trillat-Lachman test is soft and the pivot shift is present. One must detect a varus laxity, a thrust when 

walking, a Hughston’Recurvatum test or a lateral hypermobility as described by Bousquet. 

The differential anterior tibial translation is most often from 2 to 6 mm measured with telos and inferior to 4 

mm measured on monopodal stance.An asymmetrical lateral opening on weight-bearing X-Rays confirms the 

diagnosis. 


One needs to obtain a complete preoperative check-up to detect an asymmetrical lateral opening. 

These postero-lateral lesions lead to an frontal imbalance. But the problem is very different in case of asymmetrical 

lateral opening without medial narrowing. 

In case of asymmetrical lateral opening due to an intersticial rupture of the lateral collateral ligament we 

recommand to perform, during the same surgery, The ACL Reconstruction, The opening wedge HTO and a 

Lateral Collateral Ligament graft, using a 6mm Bone-Patellar tendon-Bone graft harvested on the contralateral 

knee. The role of the Osteotomy is to protect the grafts and a small amount of valgus, 2 or 3 degrees is 

enough. In the absence of LCL graft an obvious hypercorrection would be required. 

5/ Place of the extra articular tenodesis. 

The most controversy ancillary surgery is an additional extra-articular tenodesis or " Lemaire plasty". In the 

past we used a 10mm large strip of fascia lata. To reduce the approach and the scar we proposed a new technique 

using the semi-tendinosus or the gracilis to perform the extra articular tenodesis. We shall give you 

some details about the technique before to present our results. 

5a/ Technique 

We perform a 6 cm long skin incision and then we open the fascia lata, in direction of the Gerdy’ tubercle. 

The ACL graft is prepared with the gracilis passed through the bone block. We prepare a tunnel under the 

Gerdy’s tubercle with an awl. Once the femoral tunnel drilled just behind the femoral attachment of the LCL, 

we insert the ACL graft and impact the bone block with Gracilis tendon in the femoral tunnel. The Gracilis is 

passed and crossed under-neath the LCL. The two bundles are passed through the Gerdy’tunnel in an opposite 

way. During fixation of extraarticular tenodesis (sutures) the knee is in neutral rotation. Excessive bundles 

are removed and fascia is closed without tension. 

3.5

5b/ Results will be presented (1) 

5c /Discussion 

Even if Draganish (8) demonstrated that isolated extra-articular tenodesis can control some amount of laxity 

at 30° flexion we know that after isolated extra-articular tenodesis without ACL Reconstruction, clinical 

failures are frequent. The anterior tibial translation is not controlled. At long term the arthrosis is frequent. 

O’ Brien [14], Holmes [9], Buss [4], in different retrospective studies found no superiority to add an extra 

articular tenodesis. 

At the contrary Frank Noyes [13] underlined the benefits to add an extraarticular tenodesis when an allograft 

is performed. Failure rate decreased from 16% to 3% and the control of anterior laxity is better. 

Very recently during the FRENCH SOCIETY, Hulet from Caen in a retrospective study did not find statistical 

difference between two groups with and without extraarticular tenodesis but the factor ß was unknown and 

the number of patients in the two groups not large enough. 


Recently, F Cladiere ( Lerat-Moyen) [5] compared in a prospective randomised study two groups with and 

without extraarticular tenodesis and recommanded a lateral complementary procedure when there is a preoperative 

differential anterior tibial translation measured on the lateral compartment, called "TACE" of more 

than 8 mm. 

Conclusions 

The place of extraarticular is still discussed. We need prospective study with larger groups and longer Followup. 

Personally I continue to discuss and perform extraarticular tenodesis combined to ACL reconstruction in 

case of sport at risks like soccer, basket, volley..; in case of evolved anterior chronic laxity, and in revision surgery. 

The take-home message is to consider that the treatment of all the types of ACL insufficiencies cannot be the 

Isolated ACL graft under Arthroscopy. The next step will be considered each element, variable or component 

of the ligament evaluation IKDC form pre and post-operatively to try to distinguish the different situations. 

This is the key to improve our results and to avoid unnecessary gesture. 

Bibliography 

1- AIT SI SELMI T, FABIE F, MASSOUH T, POURCHER G, ADELEINE P, NEYRET Ph. Greffe du LCA au tendon 

rotulien avec ou sans plastie antero externe : Etude prospective randomisée à propos de 120 cas in « le genou 

du sportif » Sauramps Medical, Montpellier 2002 : 221-224. 

2- BONIN N, AIT SI SELMI T, DEJOUR H, NEYRET Ph, Association Reconstruction du LCA et ostéotomie tibiale 

de valgisation. A 11 ans de Recul in « Le Genou du sportif », Sauramps Medical, Montpellier 2002 : 225-235. 

3- BOSS A, STUTZ G, OURSIN C, GACHTER A. Anterior cruciate ligament reconstruction combined with valgus 

tibial osteotomy (combined procedure). Knee Surg. Sports Traumatol Arthrosc 1995: 3: 187-91. 

4- BUSS D, WARREN RF, WICKIWICZ TL & COL. Arthroscopically assisted reconstruction of the anterior cruciate 

ligament with use of autogenous patellar ligament grafts. J. Bone Joint Surg., 75A : 1346-1355,1993. 

5- CLADIERE F, Etude comparative de la reconstruction du ligament croisé antérieur isolée ou associée à une 

plastie extra articulaire externe. Thèse Médecine Lyon 2000. 

6- DEJOUR H, DEJOUR D, AIT SI SELMI T, Chronic anterior laxity of the knee treated with free patellar graft 

and extra-articular lateral plasty : 10 year follow-up of 148 cases, Rev. Chir. Orthop. 1999: 85: 777-89. 

7- DEJOUR H, NEYRET P, BOILEAU P, DONELL ST. Anterior cruciate reconstruction combined with valgus tibial 

osteotomy. Clin Orthop 1994: 220-8. 

8- DRAGANISH LF, REIDER B, MILLER PR. An in vitro study of the Muller anterolateral femorotibial ligament 

tenodesis in the anterior cruciate ligament deficient knee. Am.J. Sports Med. 17: 357-362, 1989. 

9- HOLMES PF, JAMES SL., JAMES SL., LARSON RL & COL. Retrospective direct comparaison of three 

intraaticular anterior cruciate ligament reconstructions. Am.J. Sports Med. 19: 596-600, 1991. 

3.6

10- LATTERMANN C, JAKOB RP. High Tibial osteotomy alone or combined with ligament reconstruction in 

anterior cruciate ligament-deficient knees. Knee Surg. Sports Traumatol Arthrosc 1996: 4: 32-8. 

11- LEMAIRE M, COMBELLES F. Technique actuelle de plastie ligamentaire pour rupture ancienne du ligament 

croisé antérieur. Rev. Chir. Orthop. 1980: 66: 523. 

12- NEYRET P., PALOMO JR, DONELL ST, DEJOUR H. Extra articular tenodesis for anterior cruciate ligament 

rupture in amateur skiers. Br. J. Sports Med. 28: 31-34, 1994. 

13- NOYES FR, BARBER SD. The effect of an extra-articular procedure on allograft reconstructions for chronic 

ruptures of the anterior cruciate ligament. J. Bone Joint Surg., 73A : 882-892, 1991. 

14- O’BRIEN WR, WARREN RF, WICKEWICZ TL & COL. The iliotibial band lateral sling procedure and its effect 

on the results of anterior cruciate ligament reconstruction Am.Sports Med. 19:21-25, 1991. 

15- SHELBOURNE KD, GRAY T. Results of anterior cruciate ligament reconstruction based on meniscus and 

articular cartilage status at the time of surgery : five to Fifteen-year evaluations. Am.J. Sports Med. 2000 vol 

28 (4): 446-452. 

16- VAIL TP, MALONE TR, BASSET FH. Long term functional results in patients with anterolateral rotatory 

instability treated by iliotibial band transfer. Am.J.Sports Med.20: 274-282, 1992 

17- WU WM, HACKETT T, RICHMOND JC. Effects of meniscal and Articular Surface Status on knee Stability, 

Function and Symptoms after anterior cruciate ligament reconstruction. A long term Prospective Study. 

Am.J.Sports Med. 2002 vol 30(6): 845-850. 


3.7


CURRENT CONCEPTS IN POSTEROLATERAL INSTABILITY OF THE KNEE 

Tuesday, March 11, 2003 • Aotea Centre, ASB Theatre 

Chairman: Robert F. LaPrade, MD, USA 

Faculty: Fred A. Wentorf, MS, USA, Lars Engebretsen, MD, PhD, Norway and Steinar Johansen, MD, Norway 


I. Introduction/Incidence 

A. Mechanism 

1. Hyperextension 

2. Varus blow 

3. Noncontact twisting 

B. Incidence 

1. 6-11% MRI studies 

2. Previous underestimated 

C. Importance 

1. Do not heal 

2. Lead to residual instability/DJD 

3. Compromise cruciate ligament reconstructions 

II. Applied Anatomy of the Posterolateral Knee (LaPrade) 

A. Fibular Collateral Ligament (FCL) 

1. Primary stabilizer to varus opening 

2. Femoral attachment - proximal/posterior to lateral epicondyle 

3. Fibular attachment - midway along lateral fibular head 

B. Popliteus Complex (Stäubli, 1990) 

1. Important stabilizer to posterolateral rotation of the knee 

2. Popliteus attachment on femur 

• 2 cm from FCL attachment on femur 

• attaches on anterior fifth of popliteal sulcus 

• anterior to FCL attachment 

3. Popliteofibular Ligament (PFL) 

• originates at popliteus musculo-tendinous junction 

• attaches to medial aspect of posterior 

• fibular styloid (posterior division) and anterior medial downslope of styloid 

(anterior division) 

• important static stabilizer of external rotation 

C. Mid-Third Lateral Capsular Ligament 

1. Secondary stabilizer to varus opening 

2. Thickening of lateral midline capsule - equivalent to "deep MCL" 

3. Meniscotibial portion - frequently injured. Site of Segond fracture and soft-tissue 

Segond injuries. 

D. Biceps Femoris Complex 

1. Two heads - through attachments to capsule, FCL, tibia, and fibula - help to dynamically 

stabilize the lateral com-partment of the knee 

2. Short Head Biceps Femoris 

• 5 components at the knee 

• main attachments are to fibular styloid, posterolateral capsule, and an anterior 

tibial arm 

3. Long Head Biceps Femoris 

• 5 components at the knee 

• main attachments are to fibular styloid 

3.8

III. 

Diagnosis of Posterolateral Knee Complex (PLC) Injuries (LaPrade) 

A. History 

1. Usually due to varus or hyperextension injuries 

2. Fifteen percent have a common peroneal nerve injury 

3. Majority (but not all) occur as combined ligamentous injuries (ACL/PLC, PCL/PLC most 

common) 

B. External Rotation Recurvation Test (Hughston, 1980) 

1. Lift up the big toe 

2. Observe for increased recurvation and relative varus 

3. Usually indicative of a combined PLC/cruciate ligament injury 

C. Varus Stress Test at 30º (Hughston, 1966) 

1. Fingers over joint line to assess amount of opening 

2. Apply varus stress through foot/ankle 

3. Compare opening to contralateral (normal) knee 

D. Posterolateral Drawer Test (Hughston, 1980) 

1. Knee flexed to 90º, foot external rotation to 15º 

(I sit on the foot) 

2. Apply a gentle posterolateral rotation force and assess amount of posterolateral rotation 

(compare to normal contralateral knee) 

E. Dial Test (Gollehon, 1987; Grood, 1988) 

1. Assesses ER component of posterolateral knee injury (Grood, 1988; Veltri, 1995) 

2. Perform with knee flexed over side of examining bed, apply an external rotation force 

through the foot and look for external rotation of the tibial tubercle 

3. Increased amount of external rotation at 30º indicates a posterolateral knee injury (arc 13º) 

4. Dial test at 90º 

• isolated posterolateral knee injury – slightly decreased external rotation 

compared to 30º (may not be visually detectable difference) (usually 5º ER) 

C an increased amount of external rotation is indication of a combined PCL/ 

posterolateral knee injury (Gollehon, 1987; Grood, 1988) or a combined ACL/ 

posterolateral knee injury (Wroble, 1993) 

F. Reverse Pivot Shift Test (Jakob, 1981) 

1. Largest variability among all motion tests - 35% in normal knees (Cooper, 1991) 

2. Knee flexed to 45º, foot externally rotated 

3. Knee is then extended. If subluxed in flexion, the knee is reduced by the iliotibial band 

as it changes function from a flexor to an extender of the knee 

G. Varus Thrust Gait 

1. Usually (but not always) have underlying varus alignment 

2. Patients learn to adapt with flexed knee gait 

H. Radiographs 

• AP varus thrust or stress x-ray 

• AP (Segond, arcuate fractures) 

• Long leg alignment x-ray 

I. MRI (LaPrade, 2000) 

a. Thin slice (2mm), include entire fibular head/styloid, add coronal obliques 

b. Iliotibial band 

• superficial layer 

• deep layer 

c. Long head biceps femoris 

• direct arm 

• anterior arm 

d. Short head biceps femoris 

• direct arm 

• anterior arm 

e. Fibular collateral ligament 

f. Popliteus complex 

• femoral attachment 

• popliteomeniscal fascicles 

3.9 

ICLs

• popliteofibular ligament 

g. Fabellofibular ligament 

J. Arthroscopic Evaluation (LaPrade, 1997) 

a. "Drive-through" sign – > 1 cm lateral joint line opening 

b. Popliteus attachment 

c. Mid-third lateral capsular ligament 

• meniscofemoral 

• meniscotibial 

d. Popliteomeniscal fascicles 

e. Coronary ligament 


IV. Biomechanics of the Posterolateral Knee (Wentorf) 

A. Varus instability 

• FCL is major restraint to varus at all knee flexion angles. The popliteus complex, postero 

lateral capsule (including FFL, PFL), and cruciates also play an important role in preventing 

varus 

1. Grood, et al, 1988 

• Additional sectioning of popliteus tendon and other structures (PFL, capsule, etc) 

increases varus 

2. Gollehon, et al, 1987 

• Additional sectioning of popliteus tendon increases varus 

3. Cruciate ligaments and varus 

• Recruited with deficient posterolateral complex (PLC) to resist varus 

a. Markolf, et al, 1993 

• section of PLC increases mean force on ACL at all flexion angles 

• section of PLC increases force on PCL at >45º 

b. Gollehon, et al, 1987 

• section of PCL after PLC resulted in large increase in varus rotation 

B. Rotational instabilities 

1. External rotation 

• Sectioning of PLC structures increases ER (Grood, et al, 1988) 

a. 30º of flexion = 13º increase ER 

b. 90º of flexion = 5.3º increase ER 

• Additional sectioning of PLC/PCL increases ER at 90º Flexion (Gollehon, 1987; 

Grood, 1988; Kaneda, 1997) 

• Additional sectioning of ACL/PLC also increases ER at 90º (Wroble, 1993) 

2. Internal rotation 

• Isolated/combined cutting of FCL, popliteus, PLC joint structures increases IR 

(Grood, et al, 1988; Noyes, et al, 1993, LaPrade, 1999) 

• Variable differences across knees 

C. Anterior/posterior translation 

1. Sectioning PLC results in no primary increase in anterior translation (Gollehon, et al, 

1987; Grood, et al, 1988) 

a. PLC is important 2º restraint to ATT with combined ACL/PLC injury (Nielsen, 1986; 

Wroble, 1993; Veltri, 1995) 

b. Clinically detectable as increased ATT on Lachman test 

c. Force on PLC with ACL intact is minimal; significant forces present on PLC with 

ACLD (Kanamori, 2000) – suggests need for combined ACLR with PLC repair/ 

reconstruction 

2. Posterior tibial translation 

a. Between 0º and 30º of flexion no difference in posterior translation between 

isolated PLC versus isolated PCL sectioning (Gollehon, et al, 1987) 

b. Combined PCL/PLC cutting significantly increases posterior translation compared 

to isolated section of either (Gollehon, et al, 1987; Grood, et al, 1988) 

c. Effect of popliteus on posterior translation (Harner, et al., 1998) 

d. Simulated popliteus contraction decreases in situ forces on the PCL at 30º and 

90º (Harner, et al, 1998) 

3.10

D. Does the PLC heal? 

1. In vivo model-rabbits 

2. FCL/popliteus do not heal 

E. Forces in the intact PLC 

1. FCL loaded at all flexion angles – varus 

2. FCL loaded near extension in ER 

3. Popliteus/PFL complementary to FCL – loaded in flexion to ER 

F. Effect of PLC injuries on ACL reconstructions 

1. Effect of grade III PLC injuries on an ACL reconstruction graft (LaPrade, 1999) 

a. Significant increase in graft force seen for varus and combined varus-IR at 0º and 30º 

b. Recommend to repair/reconstruct PLC injuries at time of ACLR to reduce risk of 

ACLR failure 

2. Effects of tensioning on an ACL graft and integrity of the PLC on tibiofemoral orientation 

(Wentorf, AJSM, 2002) 

a. Significant increase in ER seen with increasing ACL graft tension 

b. Recommended to repair/reconstruct PLC injuries first, prior to ACL graft fixation, 

to reduce risk of ER deformity 

G. Effect of PLC injuries on PCL reconstructions 

1. Effect of grade III posterolateral knee injuries on a PCL reconstruction graft (LaPrade, 1999) 

a. Significant increase in graft force at 0º, 60º, and 90º with FCL, PFL, and popliteus 

tendon cut 

b. Significant increase in graft force at 30º, 60º, and 90º with FCL, PFL, and popliteus 

tendon cut 

2. No significant increase in PCL graft force for an isolated posterior drawer or external 

rotation torque when the posterolateral structures were sectioned 

a. Recommend to repair/reconstruct posterolateral structures in knees with varus 

and/or coupled posterior drawer-external rotation instability at time of PCL 

reconstruction to decrease chance of post-reconstruction PCL graft failure 

b. Important – assess for posterolateral knee injury prior to PCL graft fixation. 

Once the PCL graft is fixed, possible pathologic amounts of posterolateral instability 

– which may cause graft failure – will not be detectable on the operating table 

3. Effect of tensioning on the PCL graft and the integrity of posterolateral structures on 

tibiofemoral orientation (Wentorf, unpublished data, 1999) 

• No significant increase in external rotation seen before/after PLC sectioning. 

Therefore, if the PCL graft is fixed at 90º, it makes no difference if the PCL graft or 

the PLC structures are secured/repaired first 

4. Effect of deficient PLS on PCLR (Harner, 2000) 

a. Forces on PCL graft significantly increased for PLS deficiency 

b. PCL graft is ineffective and overloaded with PLS deficiency if PLC not repaired 

H. Summary of key points of PLC biomechanics 

1. FCL is key structure for preventing abnormal varus motion 

2. FCL and popliteus complex prevent abnormal ER 

3. Understanding PLC applied anatomy, abnormal motion with injuries, and biomechanics 

assists in treatment of combined ACL and/or PCL injuries 

4. It is important to recognize PLC injury prior to cruciate ligament(s) reconstruction; 

performance of an isolated cruciate ligament reconstruction with a PLC injury places 

the cruciate ligament graft at risk for failure 


V. Surgical Treatment Options for Acute Posterolateral Knee Injuries (Engebretsen) 

A. Acute grade III PLC injuries 

1. Repair/reconstruct < 2 weeks after injury 

a. Attempt anatomic repair 

b. Prior to scar tissue planes developing 

2. Surgical incision 

• Lateral hockey stick 

• Center over Gerdy’s tubercle 

• Align along posterior border iliotibial band 

3.11


3. Fascial incisions (Terry and LaPrade, 1997) 

a. Split iliotibial band in line with its fibers (Gerdy’s tubercle and proximal) 

b. Posterior to LH biceps concurrent with peroneal neurolysis 

c. Posterior border of iliotibial band (optional) 

d. In acute injuries, may need to follow injury plane 

4. Diagnostic arthroscopy after surgical approach completed (LaPrade, 1997) 

a. Assist in surgical approach 

b. Accurate to diagnose popliteus tendon, popliteomeniscal fascicle, coronary 

ligament, and mid-third lateral capsular ligament injuries 

5. Avulsions off femur 

a. Popliteus avulsion-recess procedure (Stäubli) 

b. FCL avulsion – recess procedure 

c. Lateral gastrocnemius tendon – direct repair (suture anchor) 

6. Avulsions off tibia 

a. Lateral capsule – direct repair to bone 

b. Anterior arm of short biceps – direct repair to bone 

c. Coronary ligament of posterior horn of lateral meniscus - direct repair to bone 

d. Popliteomeniscal fascicle tears – direct repair if lateral meniscus unstable 

7. Avulsion off fibular head/styloid 

a. Popliteofibular ligament – suture anchor 

b. Direct arms of long-short heads of biceps femoris – suture anchors 

c. FCL – suture anchor 

d. Arcuate avulsion fracture – cerclage suture fixation 

8. Midsubstance tears 

a. Consider augmentation (biceps femoris, ITB, hamstrings) 

b. Anatomic reconstruction (Johansen) 

B. Rehabilitation for Acute PLC Repairs (Engebretsen) 

1. Nonweight bearing – 6 weeks crutches 

2. Range of motion 

1. "Safe zone" at time of PLC repair 

2. Strive for full extension initially 

3. Goal of 0-120º by 6 weeks postop 

3. Exercises 

1. Quads sets/straight leg raises in immobilizer only 

2. Exercise bike POW #7 (based on ROM) 

3. Rehab like ACLR POW #10-12 

VI. Surgical Treatment Options for Chronic Grade III Posterolateral Knee Injuries 

1. Assess for varus alignment first 

a. Long leg standing x-ray 

b. Correct for varus alignment or soft tissue reconstruction will stretch out 

c. Proximal tibial opening wedge osteotomy (to tighten up structures) 

d. Reassess at 6 months postop osteotomy for need for soft tissue reconstruction 

2. Posterolateral corner reconstructions - historical 

a. Most previous reconstructions 

• Sling procedures 

• Nonanatomic 

• Few biomechanical studies 

b. Biceps tenodesis – Sling procedure 

• Redirect LH biceps tendon over a screw and washer 

• Requires intact biceps attachments to posterior capsule (capsular arm) and FCL 

• If fails, difficult to reconstruct due to loss of biceps dynamic function 

c. FCL reconstruction (Tibone) 

• Patellar tendon graft 

• Reconstructs FCL attachments to femur and fibula 

d. Popliteus complex reconstruction 

• Muller, popliteus bypass 

3.12

• Stabilize against ER 

3. Anatomic reconstruction of FCL/popliteofibular ligament/popliteus tendon 

• Cooperative biomechanics project between Universities of Minnesota and Oslo 

• Two tailed reconstruction of FCL/PFL and popliteus tendon 

• Biomechanically restores function of native ligaments 

a. Tunnel placement 

• Fibular head (7 mm) 

• Tibia (9 mm) 

• Femur (7 mm x 20 mm x 2) 

b. Split achilles graft 

• Bone blocks in femur 

• Fix in fibular head (FCL) and on tibia (PLT/PFL) 

• Bone plugs (7 mm x 20 mm) in femur 

• Fix in fibula (bioscrew – FCL) 

• Fix PLT/PFL on tibia (staple) 

A. Rehabilitation of Chronic PLC Surgery 

A. Weight bearing status 

1. Nonweight bearing for 6 weeks 

2. Crutches/protected weight bearing POW #7-10 

3. Wean off crutches 

B. Range of motion 

1. Full ROM immediately 

2. Gentle ROM out of immobilizer Q/D on CPM 

C. Exercises 

1. Quad sets/straight leg raises in immobilizer only for 6 weeks 

2. Exercise bike/leg presses (20 kg to 70º) at POW #7 

3. Rehab "slow track" ACLR at POW #12 


References: 

1. Cooper DE: Tests for posterolateral instability of the knee in normal subjects. J Bone Joint Surg, 73- 

A:30-36, 1991. 

2. Gollehon DL, Torzilli PA, Warren RF: The role of the posterolateral and cruciate ligaments in the stability 

of the human knee: A biomechanical study. J Bone Joint Surg, 69-A:233-242, 1987. 

3. Grood ES, Stowers SF, Noyes FR: Limits of movement in the human knee: Effect of sectioning the posterior 

cruciate ligament and posterolateral structures. J Bone Joint Surg, 70-A:88-97, 1988. 

4. Harner CD, H—her J, Vogrin TM, et al: The effects of a popliteus muscle load on in situ forces in the 

posterior cruciate ligament and on knee kinematics. Am J Sports Med, 26:669-673, 1998. 

5. Harner CD, Vogrin TM, H—her J, et al: Biomechanical analysis of a posterior cruciate ligament reconstruction. 

Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med, 

28:32-39, 2000. 

6. Hughston JL, Norwood LA: The posterolateral drawer test and external rotation recurvation test for posterolateral 

rotatory instability of the knee. Clin Orthop Rel Res, 147:82-87, 1980. 

7. Jakob RP, Hassler H, Stäubli H-U: Observations on rotatory instability of the lateral compartment of the 

knee: Experimental studies on the functional anatomy and pathomechanism of the true and reverse 

pivot shift sign. Acta Orthop Scand, 52(Suppl):1-32, 1981. 

8. Kanamori A, Sakane M, Zeminski J, et al: In situ force in the medial and lateral structures of intact and 

ACL-deficient knees. J Orthop Sci, 5:567-571, 2000. 

9. LaPrade RF, Terry GC: Injuries to the posterolateral aspect of the knee. Association of Injuries with 

Clinical Instability. Am J Sports Med, 25(4):433-438, 1997. 

10. LaPrade RF: Arthroscopic evaluation of the lateral comparison of knees with grade 3 posterolateral 

complex knee injuries. Am J Sports Med, 25(5):596-602, 1997. 

11. LaPrade RF, Hamilton CD: The fibular collateral ligament-biceps femoris bursa. Am J Sports Med, 

25:439-443, 1997. 

12. LaPrade RF, Resig S, Wentorf FA, Lewis JL: The effects of grade 3 posterolateral knee injuries on force 

in an ACL reconstruction graft: A biomechanical analysis. Am J Sports Med, 27:469-475, 1999. 

13. LaPrade RF, Bollom TS, Gilbert TJ, Wentorf FA, Chaljub G: The MRI appearance of individual structures 

of the posterolateral knee: A prospective study of normal and surgically verified grade 3 injuries. Am J 

3.13


Sports Med, 28:191-199, 2000. 

14. LaPrade RF, Muench CW, Wentorf FA, Lewis JL: The effect of injury to the posterolateral structures of 

the knee on force in a posterior cruciate ligament graft. A biomechanical study. Am J Sports Med, 

30(2):233-238, 2002. 

15. LaPrade RF: The medial collateral ligament complex and the posterolateral aspect of the knee. Sports 

Medicine Orthopaedic Knowledge Update - 2nd ed., AAOS, 1999. 

16. LaPrade RF, Hamilton CD, Engebretsen L: Treatment of acute and chronic combined anterior cruciate 

ligament and posterolateral knee ligament injuries. Sports Med and Arth Rev, 5:91-99, 1997. 

17. Markolf KL, Slauterbeck JL, Armstrong KL, et al.: A biomechanical study of replacement of the posterior 

cruciate ligament with a graft. Part II: Forces in the graft compared with forces in the intact ligament. J 

Bone Joint Surg, 79-A:381-386, 1997. 

18. Maynard MJ, Deng X-H, Wickiewicz TL, et al.: The popliteofibular ligament: Rediscovery of a key element 

in posterolateral stability. Am J Sports Med, 24:311-316, 1996. 

19. Noyes FR, Barber-Westin SD: Surgical reconstruction of severe chronic posterolateral complex injuries 

of the knee using allograft tissues. Am J Sports Med, 23(1):2-12, 1995. 

20. Noyes FR, Barber-Westin SD, Hewett TE: High tibial osteotomy and ligament reconstruction for varus 

angulated anterior cruciate ligament-deficient knees. Am J Sports Med, 28(3):282-296, 2000. 

21. Simonian PT, Sussman PS, van Trommel M, Wickiewicz TL, Warren RF: Popliteomeniscal fasciculi and 

lateral meniscal stability. Am J Sports Med, 25:849-853, 1997. 

22. Stäubli H-U, Birrer S: The popliteus tendon and its fascicles at the popliteus hiatus: gross anatomy and 

functional arthroscopic evaluation with and without anterior cruciate ligament deficiency. Arthroscopy, 

6:209-220, 1990. 

23. Terry GC, LaPrade RF: The biceps femoris complex at the knee: Its anatomy and injury patterns associated 

with acute anterolateral-anteromedial rotatory instability. Am J Sports Med, 24:2-8, 1996. 

24. Terry GC, LaPrade RF: The posterolateral aspect of the knee. Anatomy and surgical approach. Am J 

Sports Med, 24(6):732-739, 1996. 

25. Veltri DM, Deng X-H, Torzilli PA, et al.: The role of the cruciate and posterolateral ligaments in stability 

of the knee: A biomechanical study. Am J Sports Med, 23:436-443, 1995. 

26. Wascher DC, Grauer DJ, Markolf KL: Biceps tenodesis for posterolateral instability of the knee: An in 

vitro study. Am J Sports Med, 21:400-406, 1993. 

27. Wentorf FA, LaPrade RF, Lewis JL, Resig S: The effect of ACL graft force on the tibiofemoral orientation 

in knees with posterolateral corner injuries. Am J Sports Med, 2002. 

3.14


CLAVICLE FRACTURES AND DISLOCATIONS 

Tuesday, March 11, 2003 • Aotea Centre, Kaikoura Room 

Chairman: Ulrich Bosch MD, Germany 

Faculty: Reinhard Fremerey, MD, PhD, Germany, Stephen J. Snyder, MD, USA and Eugene Wolf, MD, USA 

Outline 

Acute and Chronic AC Joint Dislocation 

Classification and Diagnosis R. Fremerey 8’ 

Treatment: When and How? 

Nonoperative R. Fremerey 10’ 

Mini-Open Technique S. Snyder 15’ 

Arthroscopic Technique E. Wolf 15’ 


Degenerative Disorders of the AC Joint 

How to treat? S. Snyder 10’ 

SC Joint Dislocation 

Diagnosis and Management R. Fremerey 10’ 

Clavicular Fractures 

Classification and Treatment Options U. Bosch 12’ 

Discussion 10’ 

Acute and Chronic AC Joint Dislocation 

Classification and Diagnosis 

Treatment: When and How? – Nonoperative Treatment 

R. Fremerey, MD, Phd. 

Trauma Department 

Krankenhaus Hildesheim GmbH 

Weinberg 1 

D-31141 Hildesheim 

ReinhardFremerey@t-online.de 

Epidemiology 

- about 12% of all dislocations of the shoulder girdle 

- caused by direct or indirect trauma 

Anatomy and Biomechanics 

Anatomy: 

- the AC-joint is a diarthrodial joint involving the medial facet of the acromion and the distal clavicle 

- the articular surfaces are covered with hyaline cartilage 

- a fibrocartilaginous disk of varying size and shape is present in the joint 

- along with the SC-joint, it provides a bony link of the shoulder to the axial skeleton 

- in children, the clavicle is surrounded by a thick periosteal tube that extends all the way to the acromioclavicular 

joint, so that children are more prone to fracture and pseudodislocations than true dislocation of 

the acromioclavicular joint 

3.15

Biomechanics: 

- enhances overhead activity 

- there is only little motion between the acromion and clavicle in rotating and lifting of the arm, hence, 

most scapulothoracic motion occurs at the SC-joint. 

- the anteroposterior (horizontal) stability is provided by the acromioclavicular ligament 

- the superoinferior stability (vertical) is provided by the coracoclavicular ligaments (conoid and trapezoid) 


Classification 

ROCKWOOD: 

Type I: 

Type II: 

Type III: 

Type IV: 

Type V: 

Type VI: 

Sprain of the acromioclavicular ligaments only 

Acromioclavicular ligament and joint capsule disrupted 

Coracoclavicular ligaments intact 

Up to 50% vertical subluxation of the clavicle 

Acromioclavicular ligament and capsule disrupted 

Coracoclavicular ligaments disrupted 

Dislocation of acromioclavicular joint 



Acromioclavicular joint dislocation with clavicle displaced posteriorly into or through the 

trapezius muscle 



Complete detachment of deltoid and trapezius fascia from the distal clavicle 

Acromioclavicular joint dislocated with extreme superior elevation of the clavicle (100% to 

300% of normal) 



Acromioclavicular joint disrupted with the clavicle displaced inferior to the acromion or 

coracoid process 

Diagnosis 

- swelling, deformity, distal clavicle superior, dropping of the shoulder girdle 

X-ray: 

- ap acromioclavicualar joint radiograph, 15-degree-cephalic tilt view (Zanca), stress or weighted radiographs 

of both AC-joints 

Treatment – Acute Injury 

Nonoperative: 

Type I: 

- conservative treatment, analgesic medications, sling, physiotherapy 

Type II: 

- conservative treatment, analgesic medications, sling, physiotherapy 

Type III: 

- the trend in the treatment of these injuries is toward a more conservative approach 

- a distinct advantage of surgical treatment over conservative care has never been clearly demonstrated 

- for the throwing athlete’s dominant extremity, the stabilization remains controversial because the results 

of nonoperative treatment are similar as compared to the operative procedure even in those patients 

- nonoperative treatment includes analgesia, icing and a sling 

- acceppting the deformity and skillfull neglection" is the trend because correction of the deformity by 

external stabilizers (e.g. braces, taping) is rarely possible 

Operative 

Type IV: 

- the goal is to reduce the deformity, either by closed reduction or open reduction and stabilization 

Type V: 

- operative reduction because of the significant stripping of deltotrapezial fascia 

- reconstruction of the coracoclavicular and of the acromioclavicular ligaments 

3.16

- conservative treatment remains controversial 

Type VI: 

-open reduction and stabilization 

Injuries in Children 

Type I, II, III: 

- conservative treatment with a sling, ice, and mild analgesics 

Type IV,V,VI: 

- open reduction and stabilization 

Complications 

- posttraumatic arthritis of the AC-joint: if symptomatic, resection of the distal end of the clavicle 

- very rarely slight loss of power in overhead activities in both conservative and operative treatment 

Literature 

1. Fremerey RW, Lobenhoffer P, Bosch U, Freudenberg E, Tscherne H (1996) Die operative Behandlung der 

akuten, kompletten AC-Gelenksprengung. Indikation, Technik und Ergebnisse. Unfallchirurg 99: 341-345 

2. Phillips AM, Smart C, Groom AFG (1998) Acromioclavicular dislocation. Conservative or surgical therapy. 

Clin Orthop 353: 10-17 

3. Rockwood CA Jr. (1985) Disorders of the acromioclavicular joint. In: Rockwood CA Jr, Matson FA III, eds. 

The shoulder. Philadelphia: WB Saunders: 413–476. 


SC-Joint Dislocation 

Diagnosis and Management 

R. Fremerey, MD, Phd. 

Trauma Department 

Krankenhaus Hildesheim GmbH 

Weinberg 1 

D-31141 Hildesheim 

ReinhardFremerey@t-online.de 

Epidemiology 

- about 3% of all dislocations of the shoulder girdle 

- most commonly caused by indirect trauma 

- ratio of anterior:posterior dislocation: 4:1 – 20:1 

Anatomy and Biomechanics 

- the SC-joint is a diarthrodial joint and is the only true articulation between the clavicle of the upper 

extremity and the axial skeleton 

- it creates a saddle-type joint with the clavicular notch of the sternum 

- the joint has only few bony stabilization so that it is stabilized by the Intraarticular Disk Ligament, the 

Costoclavicular Ligament, the Interclavicular Ligament and by the Capsular Ligament 

- the joint is freely movable and has motion in almost all planes 

- it is most likely the most frequently moved joint of the long bones in the body because almost any 

motion of the upper extremity is transferred proximally to the sternoclavicular joint. 


Anatomic Classification: 

- Anterior Dislocation: most common. 

- Posterior Dislocation: uncommon. 

Etiologic Classification: 

- Traumatic Injuries: Sprain or Subluxation, Acute Dislocation, Recurrent Dislocation (rare), unreduced Dislocation 

3.17

Diagnosis 

- swelling, deformity, pain 

X-ray: 

routine x-ray, CT scan to distinguish between anterior and posterior dislocation 

Signs Common to Anterior and Posterior Dislocations: 

Anterior Dislocation: 

- medial end of the clavicle is visibly prominent anterior to the sternum and can be palpated anterior to 

the sternum, either being fixed or mobile 


Posterior Dislocation: 

- usually more painful than anterior dislocation 

- the usually palpable medial end of the clavicle is displaced posteriorly 

- venous congestion may be present in the neck or in the upper extremity 

- breathing difficulties, shortness of breath, or a choking sensation, circulation to the ipsilateral arm may 

be decreased 

- complete shock due to injury of the great vessels or pneumothorax 

- CAVE: the distinction between anterior and posterior dislocation may be difficult by clinical findings or 

routine x-ray alone! 

- CT-Scan should be performed to make a clear diagnosis! 

Treatment 

Traumatic Injuries 

Anterior Dislocation: 

- mild sprain: analgesics, ice, sling for 3 to 4 days 

- moderate sprain (Subluxation): analgesics, ice, figure-of-eight dressing 

- anterior dislocation: nonoperatively, closed reduction, but most acute anterior dislocations are unstable 

following reduction: “skillfull neglect” 

After reduction: 

- joint stable: figure-of-eight dressing for 6 weeks 

- joint unstable: figure-of-eight dressing for 4-7 days 

- in patients up to 25 years of age, usually there are no dislocations of the sternoclavicular joint but type I 

or II physeal injuries, which heal and remodel without operative treatment 

Posterior Dislocation: 

- rule out damage to the pulmonary and vascular system 

- closed reduction under general anaesthesia, the joint is almost always stable 

- figure-of-eight dressing for 4 to 6 weeks 

Recurrent or unreduced posterior Dislocation: 

- open reduction and stabilization, figure-of-eight dressing for 4 to 6 weeks 

Atraumatic Problems 

Spontaneous Subluxation or Dislocation: 

- spontaneous anterior subluxations and dislocations of the SC-joint are seen most often in patients under 

20 years of age, and more often in females 

- associated with laxity in other joints of the extremities 

- self-limiting condition which should not be treated with attempted surgical reconstruction 

- spontaneous posterior dislocations are not reported in the literature 

Complications 

Anterior dislocation 

- cosmetic "bump" or late degenerative changes 

3.18 

Posterior dislocation 

- pneumothorax and laceration of the superior vena cava, respiratory distress, venous congestion in the 

neck; rupture of the esophagus, pressure on the subclavian artery,,myocardial conduction abnormalities, 

compression of the right common carotid artery, brachial plexus compression, hoarseness of the voice

- migration of pins in operative procedures, cardiac tamponade, damage to the vessels 

Literature 

Gangahar DM and Flogaites T. (1978) Retrosternal Dislocation of the Clavicle Producing Thoracic Outlet 

Syndrome. J Trauma, 18: 369–372. 

Kanoksikarin S and Wearne WM (1978) Fracture and Retrosternal Dislocation of the Clavicle. Aust. NZ J 

Surg, 48: 95–96. 

Rockwood CA, Jr. Injuries to the Sternoclavicular Joint (1984). In: Rockwood, CA, Jr., and Green, DP (eds.): 

Fractures, 2nd ed. vol. 1, pp. 910–948. Philadelphia, J.B. Lippincott 

Rockwood CA, Jr and Odor JM (1988). Spontaneous Atraumatic Anterior Subluxation of the Sternoclavicular 

Joint in Young Adults: Report of 37 Cases (abstract). Orthop Trans, 12: 557. 

Clavicular Fractures 

Ulrich Bosch, MD 

Professor of Orthopaedic Traumatology 

Hannover Medical School 

Center of Orthopaedic Surgery, Sports Traumatology 

International Neuroscience Institute 

Hannover, Germany 


Epidemiology 

- about 4% of all fractures, 35% of all fractures in the shoulder region 

- distribution of clavicular fx: 

76% middle third 

21% distal clavicle 

3% medial clavicle 

Anatomy and Function 

anatomy: 

- first bone to ossify in the embryo 

- ossification proceeds from two separate centers 

- "s"-shaped curvature with an apex anteromedially and an apex posterolaterally 

- made up of very dense trabecular bone, no well defined medullary canal, 

- the midportion is the thinnest and narrowest portion of the clavicle, mechanically weak area, most 

common site of fracture 

- stabilization of clavicular articulation: 

medial - costoclavicular and sternoclavicular ligaments 

lateral - coracoclavicular and acromiocalvicular ligaments, trapezius 

muscle and deltoid origin (deltotrapezoid fascia) 

-close relation to the brachial plexus, subclavian vessels, and apex of lung 

function: 

- enhances overhead activity 

- serves as framework for muscular attachment, 

- provides protection for underlying neurovascular structures 

- transmits forces of accessory muscles of respiration 


Allman: 

Neer: 

Craig: 

middle, distal, proximal third 

fx distal to the trapezoid ligament 

type I lateral to the cc-ligamants, cc-ligaments intact 

type II medial fragment displaced, conoid ligament ruptured 

type III similar to type I, with extension into AC-joint 

medial fx 

type I - minimally displaced 

3.19

type II - displaced 

type III - intraarticular 

type IV - physeal separation 

type V – comminuted 

- pseudodislocation of AC-joint in children: 

distal physeal injuries with displacement of the proximal fragment separated from the surrounding 

periosteum, cc-and ac-ligaments remain attached to the periosteal sleeve. 

Mechanism of Injury 

- birth injury 

- indirect: fall on outstretched arm 

- direct: fall, direct blow on tip of shoulder 

- violent trauma 


Clinical Evaluation 

swelling, deformity (apex typically superior, shortening), ecchymosis over fracture site, adduction and 

dropping of the shoulder girdle, arm is held against trunk, tenderness at fracture site, assessment of 

neurovascular status, 

associated injuries: vascular, brachial plexus, pneumothorax 

Radiographic Evaluation 

- middle third: AP view, 45°-(20° to 60°)-cephalad tilted view 

- distal third: 15° cephalad tilted view, axillary view, stress/wighted views 

- medial third: AP view, 40°-cephalad tilted view, CT scan often necessary 

Treatment 

- midclavicular fx 

nondisplaced, minimally displaced fx - nonoperative 

• figure of eight bandage or sling for 4 wks 

• good functional results despite residual deformity in most of the fractures 

displaced fx – best treatment still disputed 

• closed reduction, figure of eight bandage 

• plate fixation (ORIF) according to the AO/ASIF technique – more extensive exposure 

• Prevot-Nail (intramedullary fixation of the clavicle with elastic pin) – limited exposure 

- distal clavicular fx 

little or no displacement: sling 

displaced fx: Kirschner wires in combination with tension 

band wire or small T-plate 

- medial clavicular fx 

nonoperative for most of the fx, sling until discomfort subsides 

operative only in specific situations 

resection of the medial clavicle if symptoms persist 

Complications 

- nonunion (1-4%) 

asymptomatic: no treatment 

symptomatic: (deformity, dysfunction, neurovascular compromise) restoration of alignment and 

continuity of the clavicle is recommended (ORIF, autogenous bone graft in atrophic nonunions), 

resection only for distal and medial nonunions with small fragments 

- malunion 

if associated with ipsilateral shoulder dysfunction osteotomy through the plane of deformity, 

realignment of the calvicle, and plate fixation is recommended. Interposition of a tricortical iliac 

crest bone graft may be useful to restore length and alignment an to promote healing 

3.20

- neurovascular complications 

are rare, can occur delayed as result of compression by malunited fracture or hypertrophic callus/ 

non-union 

correction of cause of compression, removal of callus, reshaping of malunion 

References: 

1. Bosch U, Skutek M, Peters G, Tscherne H (1998) Extension osteotomy in malunited clavicular fractures. J 

Shoulder Elbow Surg 7: 402-405 

2. Brunner U (2002) Claviculafrakturen. In: Habermeyer P (ed) Schulterchirurgie. Urban & Fischer, München, 

Jena, p. 437-451 

3. Jupiter JB, Ring D (1999) Fracture of the clavicle In: Iannotti IP, Williams GR (eds) Disorders of the shoulder: 

diagnosis and management. Lipincott Williams & Wilkins, Philadelphia, p.709-736 

4. Miller ME, Ada JR (1992) Injuries to the shoulder girdle. In: Browner BD, Jupiter JB, Levine AM, Trafton PG 

(eds) Skeletal Trauma Vol II. WB Saunders, Philadelphia, London, Toronto, p.1291-1310 

S & M (Scope and Mini-Open) Technique for Acromioclavicular Joint Reconstruction 

Stephen J. Snyder, MD 


This outline presents a technique for logical repair of a symptomatic dislocated AC joint. 

This technique requires special equipment, including the following: (1) arthroscopic electro 

surgical “Subacromial Electrode TM “ from Linvatec, Inc.; (2) plastic CuffLink TM from 

Innovasive, Inc.; (3) SecureStrand TM 1mm surgical cable from Surgical Dynamics; (4) a 

medium sized rotator cuff suture retriever from Linvatec, Inc.; (5) a Nitenol Wire Suture 

Passer TM from Arthrex, Inc. 

Technique: 

Scope Portion 

1. (A) Release the entire coraco-acromial (CAL) 

ligament from the undersurface of the 

acromion and dissect it off the deltoid to the 

coracoid process using a Linvatec 

Subacromial Electrode (Figure 1). 

(B) Tether the end of the CAL using #1 PDS 

suture. Insert a spinal needle through the 

ligament, pass the PDS, and retrieve it out 

the lateral cannula. Insert the needle again 

and pass a Shuttle Relay TM through the 

CAL, out the lateral cannula and carry the 

PDS back through the CAL. Pass the 

Shuttle and retrieve the PDS a third time to 

complete the tethering (Figure 2). 

(C) Pull the CAL inside the lateral operating 

cannula and clamp the sutures to store it 

until it is passed to the open surgical site. 

Mini Open Portion 

2. (A) Make a 5 cm mini-open incision from 

anterior to posterior one cm medial to and 

parallel to the distal clavicle and excise 1 

cm of clavicle. 

(B) Prepare the distal clavicle (3 steps) 

a. burr a 1mm deep trough from anterior 

to posterior 3 mm from the end of the 

bone (a); 

b. drill 2 parallel suture holes from 

Figure 

1 

Figure 

2 

3.21

anterior to posterior on either side of 

the through (b); 

c. drill 2 additional holes for the 

SecureStrand® holes from superior to 

inferior through the center of the 

clavicle 2 cm and 5 cm from the 

end.(c) (Figure 3-A) 

Figure 3-B 


(C) 

Delivery of the CAL to the surgical site, 

passing the lateral cannula under the 

acromion and retrieving the lead sutures. 

b 

a 

c 

(D) Fixate the end of the CAL with a doublewhip 

stitch of #2 Ethibond. (Figure 3-A) (d) 

3. (A) Pass suture leaders through all four drill 

holes in the clavicle. 

Figure 

3 A&B 

d 

Figure 3-A 

(B) 

Pass doubled over suture as a leader 

around coracoid using medium-sized 

Linvatec suture retriever loaded with an 

Arthrex nitenol suture passer. (Figure 3-B). 

4. (A) Using the suture passer, carry both 

doubled-over SecureStrands (4 strands 

total) around the coracoid insuring that the 

looped end is on the posterior side of the 

coracoid. (Figure 4) 

(B) 

Carry the loop-end of one of the doubled 

SecureStrands through the medial and one 

through the lateral drill holes in the clavicle 

from inferior to superior using the passing 

sutures. 

Figure 4 

5. Thread the SecureStrand loop through the Cuff 

Link device using a lead suture and seat the 

Cuff Links in the bone holes on the superior 

aspect of the clavicle (Figure 5-a). 

a 

6. (A) Reduce the AC joint and cinch and lock the 

medial SecureStrand using a “racking 

hitch” knot (Figure 5-b). 

(B) Cinch and lock the lateral SecureStrand 

with a racking hitch knot. 

b 

7. (A) Carry the lead sutures for the CAL graft 

Figure 5 

3.22

through the posterior aspect of the clavicle 

and out anteriorly to pull the CAL into the 

trough on the top of the clavicle. (a) 

(B) 

Tie the two sutures together, locking the 

CAL into the trough on top of the clavicle 

(Figure 7). 

8. (A) Repair the deltoid and trapezius with sideto-side 

sutures above the clavicle. 

(B) 

Imbricate the capsular remnant over the AC 

joint. 

Figure 


9. Meticulously stop all bleeding and close the 

skin with subcuticular closure. 

10. Protect the arm postop in an UltraSling® from 

d.j. Orthopedics for 4-6 weeks, allowing biceps, 

elbow, wrist and hand and gentle pendulum 

exercises. Active shoulder motion as tolerated 

at 6 weeks progressing to full activities at 4 

months. 

Figure 7 

The S&M AC joint reconstruction was developed in response to the myriad of problems 

encountered when using the traditional techniques employing screws, wires and circlage cables. 

The steps of this operation are exacting but the final result is a stable AC joint with a small incision 

and no need for reoperation for hardware removal. Harvesting the CAL using arthroscopy insures 

that there is no injury to the deltoid tendon and the length of the CAL is maximized. The clavicle is 

protected by making the drill holes in the center of the bone (AP) and by using the Cuff Links to 

stress shield the Secure Strand passing through them. The Secure Strand is extremely strong, 

flexible and easy to tie using the “racking hitch” knot. The initial security of the clavicle is insured 

by using two drill holes for the Secure Strand located in the position of the two torn ligaments. 

Finally, the CAL is anchored over the top of the clavicle in a trough giving it a biomechanically 

sound easily adjustable fixation. To date there have been no failures. 

3.23

A New Technique All 

Arthroscopic Treatment of AC 

Joint Disruption 

Eugene M. Wolf, M. D. 

Acromioclavicular Dislocations 

(Rockwoood) 

• Types I through VI 

• Types I and II: non-operative 

• Types IV, V, and VI: operative 

• Type III: controversial 

• Fracture dislocations of ACJ 


Non-operative Treatment 

• Glick: 35 Type III. None disabled 

• Dias et al: 52 of 53: Good results 

• Sleeswijk et al: 90 to 100% satisfactory 

• Schwartz and Leixnering: 90 to 100% 

satisfactory 

Operative Vs Non-operative 

Studies 

• Indrekvam et al: less pain, greater function when 

operated 

• Park et al: higher rating when operated 

• Larsen et al: high complication rate in operated 

• Taft et al: slightly better results in operated 

• Bakalim and Wilppula: surgical reconstruction 

superior 

• Hawkins et al: equal results 

Previously Described Surgical 

Approaches 

• Since Baum 1886 > 60 procedures 

described 

• Transarticular Acromioclavicular Repairs 

– K-wires, screws, plates 

• Coracoclavicular Repairs 

– Screws, wires, sutures, tapes, allografts 

• Dynamic 

– Biceps 

Surgical Morbidity 

• Transarticular repairs 

– ACJ arthritis 

– Pin breakage – migration 

• Coraco-clavicular Repairs 

– Hardware or tape failure 

– Deltoid defects 

– Coracoid dissection 

– Failure > clavicular ascent 

• Trade bump for a scar 

3.24

Ideal ACJ Procedure 

• Anatomic 

– Replicate CHL not CAL(Weaver-Dunn) 

• No hardware 

– Small targets(coracoid), big errors(plexus) 

• Minimal morbidity 

– No deltoid detachment 

– No coracoid dissection 

• Biologic fixation 

Restore the Anatomy 

• Conoid and trapezoid ligaments 

• Base of the coracoid 


Solid Fixation 

• #5 FiberWire (Arthrex) 

– Doubled (210 lbs) 

• Biologic fixation 

Minimal Morbidity 

• Arthroscopic 

• Minimal incisions 

• Minimal dissection 

Arthroscopic Clavicular 

Stabilization (ACS) 

• Arthroscopic visualization of the base of the 

coracoid 

• Arthroscopic or open distal claviculectomy 

• Intra-articular drill guide (Arthrex) 

– Guide pin and cannulated drill through clavicle 

and coracoid 

• FiberWire retrieved arthroscopically 

ACS – Coracoid Visualization 

• Permits drilling through base 

– Variable anterior capsular anatomy 

• Foramen of Weitbrecht 

• Foramen of Rouviere 

– Posterior, anterior superior, and anterior inferior portals 

• Subscapularis bursa 

– Between SS and coracoid 

– Radiofrenquency wand clears soft tissue from coracoid 

3.25

Distal Claviculectomy 

• Eliminates risk of ACJ arthritis 

• Facilitates clavicle reduction 

• Sub-clavicular freshening 

• Prevents posterior impingement 

Intra-articular drill guide (ACL- 

Arthrex) 

• ACJ marking hook 

• Tibial drill guide 

• 2.4 mm guide pin 

• 5mm cannuated reamer 

• Nitenol suture/graft passer 


• Fiberwire #5: 

– 105 lbs per strand 

Fixation 

• Semitendinosis or Tibialis Anterior 

– Looped and tied 

Post-operative Care 

• Rotational exercises (ER and IR) 

• Sling for 6 weeks 

• Active ROM after 6 weeks 

References: 

1. Rockwood Jr., C.A.; Williams, Jr., G.R.; 

Young, D.C.: Disorders of the Acromioclavicular 

Joint. In Rockwood Jr., C.A. and Matsen III, F.A. 

(eds.): The Shoulder. 2 nd Edition. W.B. Saunders 

Company. Philadelphia, PA. p. 483-553, 1998. 

2. Bosworth, B.M.: Acromioclavicular separation: 

A new method of repair. Surg. Gyenecol. Obstet., 

73:866- 871, 1941. 

3. Kennedy, J.C.; Cameron, H.: Complete 

dislocation of the acromioclavicular joint. J Bone 

Joint Surg., 36(B): 202-208, 1954. 

4. Kennedy, J.C.: Complete dislocation of the 

3.26


SPORTS SPECIFIC OUTCOMES IN ACL SURGERY 

Wednesday, March 12, 2003 • Aotea Centre, ASB Theatre 

Chairman: Jose F. Huylebroek, MD, Belgium 

Faculty: Suzanne Werner, Sweden, Stephen Howell, MD, USA, Lars Engebretsen, MD, PhD, Norway and Jean-Claude 

Imbert, MD, France 

Lars Engebretsen, Department of Orthopaedic Surgery, Ullevål University Hospital 

Professional experience with athletes: 20 years + experience with professional athletes in all Norwegian 

Sports. National Football team doctor. Currently chief of medical coverage for Olympic Athletes. Previously 

team doctor for University of Minnesota hockey. 

I see sports depended gender difference (team handball 80% females) but also sports specific injury patterns 

(downhill versus soccer knee injuries MRI pattern) 


Our clinic does approximately 250 ACLs per year, 50% from team handball, 20% from skiing, 20% soccer, 

10% different other sports. 

We use hamstrings in patients with a history of previous patellar pain as well as in adolescents, and BPTB 

in high loading sports. 

We do not use braces on a regular base, but do use it in patients with recurvatum knees to prevent ligament 

stretching during the early healing phase. 

We allow full weightbearing as tolerated and full ROM early. Usually jogging at 8 weeks and return to practice 

at 4-6 months. No twisting sport participation until 6 months. 

Criteria for allowing running: close to normal ROM, at least 70% strength compared to normal side, walk on 

threadmill without a limp. 

Criteria for allowing jumping: full participation in proprioception rehab protocol, good hip and knee stability 

control. 

Criteria for allowing training participation: full ROM, 70% strength, no episodes of instability, normal running 

and faking patterns 

Criteria for allowing full competition: full ROM, 80% strength, no instability episodes during training, full 

running and cutting abilities. (Fitzgerald criteria) 

Value of isokinetic testing: doubtful since it has little to do with real sports participation 

Value of prevention: I believe ACL injuries can be prevented and we have done exstensive research in this 

field see www.ostrc.no 

Sport-Specific Factors in ACL Surgery and Rehabilitation 

Stephen M Howell, MD 

Sacramento, CA USA 

Evolution of ACL Reconstruction and Aggressive Rehabilitation 

My experience in ACL reconstruction began 17 years ago in August 1986. For six months I performed 

extraarticular reconstruction and because of stiffness and poor stability I then switched to an intraarticular 

3.27


autogenous DLSTG (double-looped semitendinosus and gracilis graft) combined with an extraarticular tenodesis 

and a long –leg brace for 4-6 weeks, and sports brace until mid 1987. 

Many of these earlier DLSTG grafts failed due to unrecognized roof impingement 4. I erroneously 

thought that the hamstring graft was inferior so I switched to autogenous patellar tendon with an extraarticular 

tenodesis and a long –leg brace for 4-6 weeks, and sports brace until mid 1988. The morbidity of the 

patellar tendon graft was high with stiffness, loss of quadriceps strength, and poor stability due to roof 

impingement 6. 

I learned from 1986 to 1988 that a poor result can be obtained with both a DLSTG and BTB graft when 

the surgery is poorly performed (i.e. roof impingement), and that an extraarticular reconstruction does not 

protect an impinged graft. Therefore, the return of motion and maintenance of stability was not a rehabilitation 

issue but a surgical technique issue. In other words the best rehabilitation did not correct poor surgical 

technique. 

In 1989 I switched back to the DLSTG graft after recognizing that roof impingement was the cause of the 

earlier failures as it had been for the BTB graft 5. I thought that the DLSTG graft deserved another evaluation, 

but this time I placed the tibial tunnel without roof impingement, and eliminated the extraarticular 

reconstruction. These patients had better extension and stability than the patients with the previous surgical 

technique so I thought we were on the right track 11. 

In 1990 I was strongly influenced by Dr. Don Shelbourne’s pioneering work in aggressive rehabilitation. 

We evaluated open-chain exercises and concluded they did not harm the ACL graft any more than a manual 

Lachman test 3, which was consistent with Dr. Shelbourne’s teachings. 

We published our results of aggressive rehabilitation in patients with a DLSTG graft, without a brace, 

without an extraarticular reconstruction, and a return to sport at four months using a two-incision technique. 

These knees showed no change in stability or motion between 4 months and two years confirming 

that the early return to sport with a DSLG graft was safe 10. 

In 1993 we continued with the DLSTG graft but switched to a transtibial technique to eliminate the 

morbidity from the lateral femoral incision. We confirmed that this newer technique also worked well with 

aggressive rehabilitation 7. Even though we eliminated roof impingement and used more secure fixation on 

the femur (Bone Mulch Screw) 18 and tibia (WasherLoc) 13, we observed that some patients either lost 5- 

10 degrees of flexion or had an increase in laxity 8,12. The cause of the loss of flexion and increase in laxity 

was impingement of the ACL graft against the PCL from a vertical tibial and femoral tunnel 16. We now 

center the tibial tunnel between the medial and lateral tibial spines and angle the tibial tunnel at 65 

degrees from the medial joint line of the tibia, which avoids PCL impingement 16. 

The biology of the DLSTG graft, tendon-tunnel healing, and limiting tunnel expansion has been a 

research focus since 1995. Studies suggest the DLSTG graft survives intraarticular transplantation 1, and 

that the graft relies on synovial diffusion since it does not acquire a blood supply in the first two years of 

implantation 9. Therefore, the DLSTG graft may not die or lose strength after implantation, which is consistent 

with the clinical observations that patients can safely return to unrestricted sports at 3-4 months 

7,8,10. 

A tendon heals slower to a tunnel than a bone plug during the first six weeks of implantation, which 

means that the fixation of a DLSTG graft must be BETTER than BTB 19. Because of this finding there is an 

interest in techniques that improve tendon-tunnel healing in order to increase the safety of aggressive 

rehabilitation 14,15. 

The strength of tendon-tunnel healing is better in long and snug tunnels 2, which indicates that placing 

the fixation devices not inside the tunnel (i.e. interference screw) but away from the joint line and compacting 

bone into the tunnels may promote tendon-tunnel healing 17. Our current practice is to place the 

fixation devices 25 mm away from the joint line and insert bone reamings into the femoral tunnel and a 

bone cylinder harvested from the tibial tunnel along side the DLSTG graft in the tibial tunnel to fill voids, 

increase stiffness, promote biologic fixation at the joint line, and prevent tunnel widening 18. 

Male and female athletes with ACL injuries in the NBA (ex. Spurs, Nuggets), NFL (ex. Panthers), and 

NHL (ex. Red Wings) and Division 1 college level (ex. Ohio State, Notre Dame, Georgetown, Penn State, 

Nebraska) are currently being treated using these surgical and rehabilitation principles, which include: 

• Tibial tunnel placement that prevents roof impingement 

• Tibial tunnel placement that prevents PCL impingement 

• High strength and stiff DLSTG graft 

• No extraarticular reconstruction 

• Points of fixation 25 mm from joint line 

• Bone grafting of femoral and tibial tunnel 

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• No brace 

• Return to sport at 4 months 

Rehabilitation Program 

I prefer my patients to self-administer their rehabilitation. I encourage them to get off the crutches as 

tolerated, and to walk independently by 2 weeks. At two weeks they are encouraged to go to a health club 

and use any machine that they feel comfortable on. I suggest they combine low weight and low resistance 

with high repetitions (3 sets of 25). They can begin running at 8 weeks and return to sport between 3 and 4 

months. 

The criterion for return to sport is: 

• Full extension 

• Full flexion 

• No effusion 

• Stable Lachman 

• KT-1000 MMT within 3-4 mm of the opposite knee 

• Ability to hop 85% of the distance of the normal knee with the reconstructed knee 

The full rehabilitation program can be downloaded in English or Spanish from 

http://www.drstevehowell.com/forms.cfm 

References 

1. Goradia, V. K.; Rochat, M. C.; Kida, M.; and Grana, W. A.: Natural history of a hamstring tendon autograft 

used for anterior cruciate ligament reconstruction in a sheep model. Am J Sports Med, 28(1): 40-6, 2000. 

2. Greis, P. E.; Burks, R. T.; Bachus, K.; and Luker, M. G.: The influence of tendon length and fit on the 

strength of a tendon-bone tunnel complex. A biomechanical and histologic study in the dog. Am J 

Sports Med, 29(4): 493-7, 2001. 

3. Howell, S. M.: Anterior tibial translation during a maximum quadriceps contraction: is it clinically significant? 

Am J Sports Med, 18(6): 573-8, 1990. 

4. Howell, S. M.; Clark, J. A.; and Blasier, R. D.: Serial magnetic resonance imaging of hamstring anterior 

cruciate ligament autografts during the first year of implantation. A preliminary study. Am J Sports Med, 

19(1): 42-7, 1991. 

5. Howell, S. M.; Clark, J. A.; and Farley, T. E.: A rationale for predicting anterior cruciate graft impingement 

by the intercondylar roof. A magnetic resonance imaging study. Am J Sports Med, 19(3): 276-82, 1991. 

6. Howell, S. M.; Clark, J. A.; and Farley, T. E.: Serial magnetic resonance study assessing the effects of 

impingement on the MR image of the patellar tendon graft. Arthroscopy, 8(3): 350-8, 1992. 

7. Howell, S. M., and Deutsch, M. L.: Comparison of endoscopic and two-incision technique for reconstructing 

a torn anterior cruciate ligament using hamstring tendons. Journal of Arthroscopy, 15(6): 594- 

606, 1999. 

8. Howell, S. M.; Gittins, M. E.; Gottlieb, J. E.; Traina, S. M.; and Zoellner, T. M.: The relationship between 

the angle of the tibial tunnel in the coronal plane and loss of flexion and anterior laxity after anterior 

cruciate ligament reconstruction. Am J Sports Med, 29(5): 567-74., 2001. 

9. Howell, S. M.; Knox, K. E.; Farley, T. E.; and Taylor, M. A.: Revascularization of a human anterior cruciate 

ligament graft during the first two years of implantation. Am J Sports Med, 23(1): 42-9, 1995. 

10. Howell, S. M., and Taylor, M. A.: Brace-free rehabilitation, with early return to activity, for knees reconstructed 

with a double-looped semitendinosus and gracilis graft. J Bone Joint Surg Am, 78(6): 814-25, 1996. 

11. Howell, S. M., and Taylor, M. A.: Failure of reconstruction of the anterior cruciate ligament due to 

impingement by the intercondylar roof. J Bone Joint Surg Am, 75(7): 1044-55, 1993. 

12. Howell, S. M.; Wallace, M. P.; Hull, M. L.; and Deutsch, M. L.: Evaluation of the single-incision arthroscopic 

technique for anterior cruciate ligament replacement. A study of tibial tunnel placement, intraoperative 

graft tension, and stability. Am J Sports Med, 27(3): 284-93, 1999. 

13. Magen, H. E.; Howell, S. M.; and Hull, M. L.: Structural properties of six tibial fixation methods for anterior 

cruciate ligament soft tissue grafts. Am J Sports Med, 27(1): 35-43, 1999. 

14. Rodeo, S. A.; Arnoczky, S. P.; Torzilli, P. A.; Hidaka, C.; and Warren, R. F.: Tendon-healing in a bone tunnel. 

A biomechanical and histological study in the dog. J Bone Joint Surg Am, 75(12): 1795-803, 1993. 

15. Rodeo, S. A.; Suzuki, K.; Deng, X. H.; Wozney, J.; and Warren, R. F.: Use of recombinant human bone morphogenetic 

protein-2 to enhance tendon healing in a bone tunnel. Am J Sports Med, 27(4): 476-88, 1999. 


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16. Simmons, R.; Howell, S. M.; and Hull, M. L.: Effect of the angle of the femoral and tibial tunnel in the 

coronal plane and incremental excision of the posterior cruciate ligament on anterior cruciate ligament 

graft tension: An in vitro study. Journal of Bone and Joint Surgery, In Press. 

17. Singhatat, W.; Lawhorn, K. W.; Howell, S. M.; and Hull, M. L.: How four weeks of implantation affect the 

strength and stiffness of a tendon graft in a bone tunnel: a study of two fixation devices in an extraarticular 

model in ovine. Am J Sports Med, 30(4): 506-13, 2002. 

18. To, J. T.; Howell, S. M.; and Hull, M. L.: Contributions of femoral fixation methods to the stiffness of 

anterior cruciate ligament replacements at implantation. Arthroscopy, 15(4): 379-87, 1999. 

19. Tomita, F.; Yasuda, K.; Mikami, S.; Sakai, T.; Yamazaki, S.; and Tohyama, H.: Comparisons of 

intraosseous graft healing between the doubled flexor tendon graft and the bone-patellar tendon-bone 

graft in anterior cruciate ligament reconstruction. Arthroscopy, 17(5): 461-76, 2001. 

Jean-Claude Imbert 


1. What is your professionel experience with athletes, can you give us an idea (%) what athletes (sort of 

sport) you're usually dealing with. What is their level: pro? College etc. 

Level of sport : 

Foot professional : 20 % (DI – DII – DIII) 

Amateurs : 70 % 

College : 10 % 

2. For how long have you been in practice ? 

30 years 

3. Do you see some differences in pathomechanics per sport? male or female? 

INTERNAL ROTATION CONTACT INJURIES 

NON CONTACT 

VALGUS EXTERNAL ROTATION 

SKI 

10 % 50 % 50 % 

FOOTBALL 

70 % 80 % 20 % 

OTHERS 

20 % 

4. Of all the ACL reconstructions you are doing per year, what is the (approx.) percentage of what type of 

athletes. 

Same percentage than for the consultants 

5. Do you change your technique, relating to the type of sport your pt is competing in? What do you use as 

a graft? per sport? gender? PEARLS? 

HTG for all patients (sport-gender…) Unless in case of specific contre indication or resurgery or hyperlaxity) 

6. Some type of athletes receive a brace? which type: sleeve, derotation-brace? 

I’m never bracing 

3.30

7. REHAB: all the same? when do you allow what? what are your criteria for allowing your athlete to run, to 

jump, to participate in training for contact sports, and to participate full competition? 

Home exercising for the first three months, then balanced on light sports progressive recovering under the 

medical control (sport medecine practicien). After 6 months patient is allowed to come again for jumping, 

contacts, and full competition) 

8. What do you think of the value of isocinetic testing at certain times during the postop period? MRI? 

Isocinetic testing should be usual after 6 months to estimate the fonctional value of quad ad harmstring 

groups, and further if necessary 

MRI: no MRI except in case of unusual complication, butCT scan with three dimensional reconstruction 

after 2 years. 

9. Any remarks on prevention, related to the sports you are usually dealing with? role of the referees? 

changes in rules? 

Prevention should be applied not only to the highest level, but also in small teams. 

10. Please work out the topics you are « best » in, or where you have done some research or publications: 


Topics: ACL reconstruction in female athletes. 

Prospective randomized comparative studies. 

1) comparing PT and HTG 

2) comparing HTG with 2 different femoral suspension system 

3) comparing HTG with or without interference screw in the femoral tunnel 

3.31


EMERGING TECHNOLOGIES IN KNEE SURGERY 

Wednesday, March 12, 2003 • Carlton Hotel, Carlton I 

Chairman: Masahiro Kurosaka, MD, Japan 

Faculty: Chyun-Yu Yang, MD, Taiwan, Hans-Ulrich Staeubli, MD, Switzerland , Mitsuo Ochi, MD, PhD, Japan, and 

Freddie Fu, MD, USA 

1. Introduction 

Masahiro Kurosaka (2 minutes) 

2. Computer Assisted Orthopaedic Surgery; TKA 

Chyun-Yu Yang (20 min) 


3. Computer Assisted Orthopaedic Surgery; Ligament reconstruction 

Hans-Ulrich Staeubli (20 min) 

4. Gene Therapy in Knee Surgery 

(20 min) 

5. Articular Cartilage Regeneration with Tissue Engineering Technique 

Mitsuo Ochi (20 min) 

6. Questions and Answers 

All (8 min) 

Computer assisted surgery and biological technologies such as gene therapy and tissue engineering technique 

are the forefront of emergent technologies in knee surgery. In this instructional course, experts of 

each technique and research will introduce and discuss updated advancement of these challenging knee 

surgeries. 

3.32


ARTHROSCOPIC EVALUATION AND TREATMENT OF ROTATOR CUFF INJURIES 

Wednesday, March 12, 2003 • Aotea Centre, Kupe/Hauraki Room 

Chairman: Stephen J. Snyder, MD, USA 

Faculty: Stephen Burkhart, MD, USA, James Esch, MD, USA and Alessandro Castagna, MD, Italy 

1. Snyder- Introduction of speakers and topics 

2 Castagna- Arthroscopic evaluation and treatment of partial rotator cuff tears (PASTA lesions, Bursal tears) 

3. Esch- Arthroscopic treatment of Full thickness Rotator Cuff tears, (including side-to-side lesions, 

retracted tears). 

4. Snyder- My technique for Full-thickness Cuff Repair 


5. Burkhart- Arthroscopic treatment of the Subscapularis tendon. 

6. Esch- My technique or Subscapularis Repair using two anterior portals 

7. Snyder- Learning Shoulder Arthroscopy (ALEX model, CLASroom etc.). 

Arthroscopic evaluation and treatment of partial rotator cuff tears (PASTA lesions, Bursal tears) 

A. Castagna 

Istituto Clinico HUMANITAS 

Milan, Italy 

Introduction 

The understanding and treatment of the pathology of the rotator cuff muscle-tendon complex is probably 

still the most stimulating challenge for the shoulder surgeon. Anatomy, biomechanics, presence of multiple 

layers of tissues, limited subacromial space make often difficult a precise assessment of the cuff disorders 

and therefore a proper repair. History, clinical examination and imaging will help the surgeon for an exact 

diagnosis. Imaging of the rotator cuff tears improved a lot in the last years. MRI, especially with gadolinium 

enhancement, allows a rather precise pre-op assessment. But other basic tests like X-Rays (AP, Axillary 

and Arch-View) should never skipped. 

Finally the radiologist report should be always compared by the surgeon with the history and clinical exam. 

This procedure allows to avoid over- or under- diagnosis of rotator cuff disorders. Arthroscopy demonstrated 

a great role in the assessment of rotator cuff disorders and the operative decision-making. 

General Technique of arthroscopic RC assessment 

Anatomically four tendons belonging to muscles originating from the scapula form the RC. 

Viewing from anterior to posterior they are: 

- Subscapularis 

- Supraspinatus 

- Intrarticular long head of the biceps 

- Infraspinatus 

- Teres minor 

Many authors consider the intra-articular part of the long head of the biceps functionally a part of the RC. 

3.33

The arthroscopic evaluation of RC must be done both from the articular side and the bursal side of the tendons, 

viewing through the standard posterior and anterior portals. It may help also the use of the lateral 

portal. The assessment procedure should be performed following a systematic and complete protocol of 

review of the shoulder anatomy (1). Use of a pump for distension and a controlled hypotension are very 

helpful (almost necessary) for a better view in the subacromial space. 

Intra-articular rotator cuff evaluation 

Posterior portal view (moving the scope from anterior to posterior): 

- superior margin of the subscapularis lying anterior between the glenoid and the humeral head 

- supraspinatus lying over the bicep tendon 

- intraartcular part of the long head of the biceps and its anchor on the glenoid 

- anterior aspect of the infraspinatus at his insertion near the bare area of the humeral head 


Anterior portal view (moving the scope from posterior to anterior): 

- infraspinatus and teres minor tendons 

- supraspinatus tendon 

- long head of the biceps 

- subscapularis tendon up to its insertion on the lesser tuberosity (sliding up to this point is very critical 

since the scope can easily be pulled out of the joint. This manoeuvre must be performed smoothly 

but is very important to check the subscapularis tendon insertion to the humeral head and have a look 

of its relationship with the biceps entering into the groove) 

Bursal side rotator cuff evaluation 

Bursal tissue covering the cuff tendon may confuse the view. For this reason bursectomy and removal of 

frayed tissues is requested to clear the view when a rotator cuff lesion must be clearly identified. 

The subacromial space assessment must be performed viewing from anterior, posterior and lateral portals. 

Posterior portal view (moving the scope from anterior to posterior and then lateral to medial): 

(Note: the scope must be introduced forward since the bursa is an anterior structure and the posterior 

bursa may hide the view) 


- infraspinatus tendon 

- subdeltoid shelf 

- greater tuberosity 

- musculo-tendinous junction of the cuff 

Anterior portal view (moving the scope from posterior to anterior and then from lateral to medial): 

- posterior bursa ( it is very important to remove it for a clear view in case of a repair) 






Lateral portal view (moving the scope from anterior to posterior) : 






Classifications of RC tears 

3.34

Lesions of the rotator cuff may present with different aspects, grades, morphology and severity. A lot of 

attempts were made to classify omogenously the rotator cuff tears but so far no one seems to be perfect 

(2). When looking at the cuff tendons it is important to understand: 

- full thickness or partial thickness 

- size of tear 

- number of tendons involved 

- side (articular and/or bursal) and depth of partial thickness 

- retraction of the tendons 

- quality of the tendon 

- shape of the full thickness tear 

The use of a common standard evaluation system is important for exchanging information with other surgeons, 

follow-up and proper decision-making. For the experienced arthroscopist it is possible to perform a 

precise evaluation of the rotator cuff tears. A good system of classification is the one proposed by Snyder 

that allows a systematic classification of the intraoperative findings (1) (Tab 1). Unfortunately the intratendinous 

lesions are not visible for the arthroscopist and they represent an important topic for the treatment 

of the rotator cuff decease as Fukuda demonstrated (3). 

CLASSIFICATION OF ROTATOR CUFF TEARS 


Tendon (s) involved in tear 

SS > Supraspinatus tendon 

IS > Infraspinatus tendon 

SbS > Subscapularis tendon 

RI > Rotator interval 

Location of tear 

A > Articular surface 

B > Bursal surface 

C > Complete tear, connecting A to B 

Severity of tear 

0 > Normal cuff, with smooth coverings of symposium and bursa 

I > Minimal superficial bursal or synovial irritation or slight capsular fraying in a small localized area; 

usually < 1cm 

II > Actual fraying or failure of some rotator cuff fibers in addition to synovial, bursal or capsular injury; 

usually < 2 cm 

III > More severe rotator cuff injury, including fraying and fragmentation of tendon fibers, often involving 

the whole surface of a cuff tendon (most often the supraspinatus); usually < 3 cm 

IV > Very severe partial rotator cuff tear that usually contains, in addition to fraying and fragmentation of 

tendon tissue, a sizable flap tear; usually larger in size than grade I-III and often encompass more 

than a single tendon 

Tab. I Classification of RCT as proposed by Snyder. It makes possible a standard evaluation for the arthroscopist 

Partial thickness RC tears 

Partial thickness RC tears may involve the articular side and the bursal side. Also intratendinous lesions 

may affect the cuff tendons but they are hard to be detected and treated, so far. Most of the partial tears of 

the bursal side are related to impingement with the anterior acromion. The clinical diagnosis is generally 

supported by the presence of a hooked acromion observing an outlet-view x-ray. Arthroscopically the cuff 

appears frayed like the under surface of the coraco-acromial ligament and the anterior acromion. Bursal 

inflammatory tissue is frequently observed. Some bursal side partial tears may appear like a flap floating in 

the subacromial space. The tendon avulsion from the tuberosity in these cases is frequently a consequence 

of a trauma. Preoperative diagnosis is confusing but it can be oriented by an adequate MRI study. 

Intrarticular view of the cuff doesn’t show any pathology and the final confirmation is arthroscopic. 

Intrarticular partial tears can be graded for severity of the lesion. Some present minimal fraying, some are 

deeper erosions, some may involve a relevant amount of the tendon (Tab. I). Snyder described the latter 

3.35

case with the acronym P.A.S.T.A. (Partial Articular Supraspinatus Tear Avulsion) lesion. In any case it is 

important to observe the cuff from different portals to evaluate and understand the shape and severity of 

the tear. After the tear has been assessed and understood, treatment choices are different and related to 

their severity. In the bursal side the primary treatment option is to debride the cuff and to perform an 

acromioplasty for minimal fraying of the tendon (grade AI and AII). If a significant partial bursal tear is 

observed with free-edge tendon avulsed from the tuberosity, a tendon-to-bone repair with suture anchor is 

recommended in association with an acromioplasty. In the articular aspect of the cuff, debridement of minimal 

partial tear is the adequate treatment. If after debriding the amount of left good tendon is significantly 

reduced an evaluation of the other side is necessary using the marker suture technique. If the bursal side 

tendon is frayed a full thickness tear should be induced and then a RC repair performed. If the bursal side 

tendon is healthy and strong the PASTA repair technique is an adequate treatment option. 

Arthroscopic subacromial decompression 


Arthroscopic subacromial decompression (SAD) is probably the first surgical procedure that contributed to 

make shoulder arthroscopy a popular and accepted procedure. In spite of this it may be not easy and quick 

if the surgeon doesn’t follow a logical and well know protocol. It starts with the preoperative planning with 

X-ray assessment of the acromion shape and thickness in order to be aware of the amount of bone to 

resect without under- or over treat the pathology. Intraoperative steps should always include a careful 

debridement of the subacromial space, cleaning of inflamed bursal tissue and removal of the fibrous tissue 

on the undersurface of the anterior acromion. These procedures usually induce local bleeding so it is 

important to obtain controlled low BP, perform accurate haemostasis and take advantage by the use of an 

infusion pump and bipolar electrocautery. After all the soft tissues are removed and bleeding is under control 

the bone resection procedure can be started. Several techniques have been described to perform SAD 

and can be easily found in the large amount of literature available about this topic. Our technique requires 

to prepare a lateral portal through which a motorized bone resector is introduced to prepare an "L" shaped 

through: the short limb of the "L" is represented by the anterior lateral edge of the acromion and the long 

limb of the "L" is aligned with the posterior edge of the AC joint. This will help to delineate the anterior 

part of the acromion, responsible of the impingement. The scope is then moved laterally and the motor 

posterior. The bone through will help the orientation and the lateral view will allow evaluating the amount 

of bone resection while moving from posterior to anterior and from medial to lateral. The diameter of the 

motor blade (usually 4,5 mm) will be our gauge. Final haemostasis is usually requested after the final 

smoothening of the undersurface of the acromion. 

Arthroscopic Treatment of PASTA Lesions of the Rotator Cuff 

Alex Castagna / Stephen J. Snyder, MD 

PASTA lesion is an acronym for a Partial Articular Supraspinatus Tendon Avulsion. This is a fairly common 

finding in shoulder arthroscopy that requires decision making based on the degree of tendon damage and 

the tools and skills of the surgeon. Tendon damage is seldom caused by classic impingement but more 

often by, a traction-type trauma that pulls a portion of the "footprint" attachment of the rotator cuff away 

from the humeral head. The bursal side of the tendon is usually normal. The evaluation and treatment of 

PASTA lesions is best suited to advanced arthroscopic techniques. 

1. History 

a) Patients are generally healthy and athletic. 

b) Injury is caused by either an acute event such as a fall or chronic irritation such as prolonged throwing. 

c) Symptoms include pain with activities – generally minimal pain at rest or at night. 

2. Physical Exam 

a) Tender cuff insertion 

b) Full range of motion 

c) Positive cuff stress signs 

d) +/- Weakness with cuff strength testing 

e) Impingement test unreliable 

3. Imaging 

3.36

a) X-rays are usually normal. 

b) MRI (with gadolinium) shows a defect on the articular side of the cuff attachment. The muscles 

show minimal atrophy. The bursal side of the tendon is normal. 

4. Treatment – Decision Making 

a) Diagnostic arthroscopy & bursoscopy always insert suture marker for correlation of articular and bursal 

sides. 

b) Debride frayed tissues especially on the articular side of the footprint of the cuff. 

c) Palpate cuff to assess thickness and integrity of remaining tissue. Correlate with MRI. If > 30% cuff 

tendon remains, consider transtendon repair, if < 30% good cuff remains, complete the tear and perform 

a standard tendon to bone repair. 

5. Treatment—Transtendon (PASTA) Repair 

a) Position the arm in 60 to 70 degrees of abduction. 

b) Start with the scope posterior & a Crystal® cannula anterior. 

c) Insert a spinal needle as a guide near the lateral acromial edge to determine the proper insertion 

point and angle for the anchors. (Fig 1) 

d) Drill a pilot hole with a 5/64 inch smooth pin into the prepared bone adjacent to the cartilage. 

e) Insert a Revo® 4-mm anchor loaded with one or two sutures into the pilot hole. Use single sutures if 

you are not familiar and proficient with the steps of multiple suture management. (Fig 2) 

f) Remove one strand of suture out the Crystal® cannula using a crochet hook. (Fig3) 

g) Insert a spinal needle through a healthy portion of the cuff medial to the torn surface, pass a Shuttle 

Relay® into the joint and retrieve it out the Crystal® cannula with a grasping clamp. (Fig 4) 

h) Load the suture located in the Crystal® cannula into the eyelet of the Shuttle® and carry it back 

through the tendon. (Fig 5) 

i) If a mattress stitch is desired, insert the needle through the cuff the first time 6-mm anterior to the 

anchor and a second time 6-mm posterior to the anchor and carry both limbs of the single suture back 

through. This will create a 1.2-cm mattress bridge on the bursal side of the cuff. 

j) If double sutures are used in the Revo® anchor, repeat the steps for the second suture of the first 

anchor passing the needle 1cm posterior to the first suture. Insert all additional anchors and sutures as 

needed to complete the PASTA cuff repair. Change the scope to the anterior portal and the Crystal® 

cannula posterior to insert the posterior anchors and sutures. 

k) Move the arm to the 30 degree abduction position and tie the sutures using sliding-locking knots 

progressing from anterior to posterior. (fig 6) 

l) Figure 7 is the final bursal side view after the PASTA repair has been completed using one double 

suture, one single mattress and one single simple suture. 

6. Postop Care 

a) Protect the extremity in an Ultra Sling® for four weeks. Encourage elbow, wrist and hand exercises 

from the first postop day. 

b) Allow pendulum motions and passive elevation to 90 degrees after one week. 

c) Begin gentle active elevation at 5 weeks and progress as tolerated to full activities by 4 months. 


Figure 1 

Figure 3 

Figure 5 

Figure 7 

Figure 2 

Figure 4 

Figure 6 

3.37

Making Arthroscopic Rotator Cuff Repairs Easier • My Experience and Technical Pearls 

James C. Esch, M.D. 

Tri-City Orthopaedics 

Oceanside, CA 

jesch@shoulder.com 

www.shoulder.com 

Surgeon 

Must balance skill versus ego 

Practice on a model 

Know tools 

Know suture management 


OR team 

Taught by the surgeon 

Know location of your favorite tools and anchors 

Can load suture, find correct tool 

Knows location of Plan B and Plan C tools 

Tie sliding and _ hitch knots 

Bleeding control awareness 

Inflow pressure and bag awareness 

Outflow control 

Pump nuisances 

Anesthesia BP awareness 

Is patient taking a NSAID ? 

Plan for today’s patient with a cuff tear 

Size of tear 

Pain versus weakness 

Risk of massive and superior migration 

What is your "mini-open" threshold? And experience? 

Tear Fix Size 

MRI 

Supraspinatus 

Infraspinatus 

Subscapularis 

Biceps 

Draw the size and shape on paper 

Draw Tear 

Tear Estimate 

Size 

Shape 

Does it look repairable? (Full? Partial?) 

Repair Technique 

Margin convergence 

Fixation Estimate 

Anchors 

Suture technique 

See the technique steps in your head 

See the anchor, suture through tendon, suture management, and tie knot. 

You may need to move the scope and suture for these steps. 

Exposure 

3.38

Portals and Cannulas 

Bursectomy to see 

Subacromial smoothening (decompression) 

Intra-operative Evaluation 

Probe tear after bursectomy and cleaning bony bed 

Is your Plan now the same as preoperative plan? 

Start to run the play. (You are running an option formation.) 

Margin convergence 

Handoff Techniques 

A: Direct Permanent Suture 

1. Cuff sew #2 Ethibond to ArthoPierce 

2. Other permanent handoff devices 

B: Shuttle with Crescent hooks to Blitz/Lasso 

Tie a good knot 

Anchor first 

Use 18G needle to get the angle 

I prefer anchors down a cannula 

Consider double row @ tear mobility 

Put in all at once if able 

Know suture management 

Tag ends of each suture 


Suture through tendon 

Direct trans-tendon grab of suture 

ArthroPierce and other penetrating tools 

From posterior for Infraspinatus 

From anterior for some supraspinatus 

From superior behind AC joint for U shaped SS tears 

Pass suture through tendon (if angle is good) 

Direct with Cuff Sew, Penetrators, Arthrosew 

Shuttle suture 

Use Caspari punch, crescent hooks, etc 

Postoperative care 

Immobilize long enough to heal 

Some passive motion is good 

Rehabilitation phases 

Immobilization 

Early active motion 

Late strengthening 

Conclusions: 

This is hard 

This requires thinking out the steps 

This is frustrating 

This is rewarding 

This balances your skill versus your ego 

3.39


1. Three Portals, scope posterior 

4. The scope is now in the lateral 

portal providing the “50-yard line” 

view. Note the anchor insertion portal 

adjacent to the acromion. 

2. Inside view. Scope and tools are 

moved as needed to repair the cuff 

tear. 

5. Margin convergence with a single 

pass cuff sew tool. 

3. Estimate the steps necessary for 

repair. 

6. Retrieve the suture. 

3.40

7. Tie the knot 

10. Retrieving the suture off of the 

anchor with the ArthroPierce. 


11. Final repair with two margin 

convergence sutures and two anchors. 

8. A sliding knot. 

9. A suture “handoff” from the 

ArthroPierce to the straight Cuff Sew. 

Illustration from Esch: Arthroscopic 

Rotator Cuff Repair for Smith+Nephew 

Endosocpy. 

3.41

Technique of Arthroscopic Rotator Cuff Repair 

Stephen J. Snyder, MD 

SCOI - Van Nuys, California 

Introduction 

The field of shoulder arthroscopy has progressed to the point where routine arthroscopic rotator cuff repair 

is now possible in many situations. The tools now available, including 5 mm SuperRevo anchors, excellent 

quality arthroscopic cannulas and pumps, coupled with the new surgical techniques for passing sutures 

and tying knots, have all made this advancement possible. The surgeon must develop the necessary skills 

and be supported by a well-trained team, including a skilled arthroscopic assistant, an anesthesiologist 

who is comfortable with hypotensive blood pressure regulation, and an operating room technician who 

understands and can prepare and assist with the instruments as needed. The recent availability of "Alex", 

the shoulder arthroscopic surgery simulator from Sawbones, Inc., has also accelerated the learning curve 

for those surgeons who avail themselves of it. 


The outline that follows will highlight the important steps in the repair as it is done at this time at SCOI: 

Figure 1: 

The rotator cuff tear is carefully evaluated 

with an arthroscope on both the articular and 

bursal sides, and the frayed edges of the cuff 

are debrided. The best view of the rotator 

cuff is usually "the 50 yard line" view with 

the arthroscope in a lateral subacromial 

portal which is located at the center point 

of the rotator cuff tear. 

Figure 2: 

A Spectrum‚ Crescent Suture Hook with a 

Shuttle Relay‚ suture passer is 

used to perform a side-to-side repair of 

longitudinal tears in the rotator cuff tendon. 

Figure 3: 

After passing the curved suture hook 

across the tear, a strong, long lasting 

suture is carried with the Shuttle Relay® 

back across the tear and the suture 

limbs tied together. 

Figure 4: 

The bone is lightly decorticated at the 

anatomical neck of the humerus, adjacent 

to the articular cartilage, using a high speed 

burr and/or shaver. The rotator cuff is 

mobilized to minimize tension on the 

repair. 

3.42

Figure 5: 

Figure 6: 

Figure 7: 

A small puncture wound is created adjacent 

to the lateral border of the acromion. The 

5 mm Super Revo anchor, preloaded with two 

strands of #2 braided polyester suture, is 

inserted directly through the percutaneous 

puncture wound (no cannula is needed to 

insert the anchor). The posterior anchor is 

usually inserted first. The anchor is directed 

to enter the bone in a medial direction below 

the subchondral bone at approximately a 45o angle. 

The Super Revo anchor is inserted into the 

bone until the seating ring on the driver is just 

below the surface. The vertical orientation 

mark (solid or dashed line which indicates the 

direction the anchor eyelet is facing) is 

aligned toward the cuff edge. This ensures 

that the suture passes in a direct line from the 

eyelet to the cuff without forming a twist. 

The anchor security is tested by 

pulling on the suture strands. 


Figure 8: 

The arthroscope can be positioned in the 

anterior or posterior portal but most often 

the overall visualization is best from the 

lateral acromial portal. 

Figure 9: 

A crochet hook or suture retrieval forceps i 

inserted through the anterior portal and 

retrieves the strand of the green suture that 

exits closest to the cuff. The retriever 

must pass behind (medial to) the suture limbs. 

Figure 10: A Spectrum Crescent Suture Hook is 

inserted into the posterior cannula and 

through the bursal side of the posterior edge 

of the torn rotator cuff 5 mm posterior to the 

anchor. The Shuttle Relay suture passer is 

sent through the hook and retrieved with a 

grasping forceps out the anterior cannula. 

Care must be taken to insure that the 

3.43

grasping forceps follows the same path as the 

green suture when retrieving the Shuttle 

Relay to avoid causing twists in the strands. 

Figure 11: The green suture strand is loaded into 

the eyelet of the Shuttle Relay suture 

passer outside the anterior cannula. 

The suture is then carried through the 

cuff from the articular side to the 

bursal side by withdrawing the 

opposite end of the suture passer out 

the posterior cannula. 


Figure 12: A crochet hook is used to retrieve the 

other limb of green suture into the posterior 

cannula. A switching stick is then inserted 

through the posterior cannula and the 

cannula is removed from the joint. 

Figure 13: The cannula is reinserted over the 

switching stick, leaving the sutures outside 

the cannula where they will be less likely to 

be tangled during stitching with the white 

sutures. 

Figure 14: A crochet hook or suture retrieval forceps is 

used to retrieve the limb of white suture that 

exits the anchor eyelet closest to the rotator 

cuff. The suture is pulled through the 

anterior cannula. 

Figure 15: The Spectrum Suture Hook is passed 

through the torn rotator cuff from top to 

bottom approximately 5 mm anterior to the 

anchor site. If a crescent suture hook is used 

again, it may be inserted through the 

posterior cannula. If a more angled suture 

hook is used, the posterior cannula can be 

removed and the hook passed directly 

through the portal without a cannula. The 

Shuttle Relay suture passer is passed 

through the hook and retrieved with a 

grasping forceps through the anterior cannula. 

3.44

Figure 16: The white suture strand is loaded into the 

eyelet of the Shuttle Relay suture passer 

outside the anterior cannula. The suture is 

carried through the cuff from the articular 

side to the bursal side by withdrawing the 

opposite end of the suture passer out 

the posterior portal. 

Figure 14a: Alternative method (Modified Caspari 

Suture Punch): A crochet hook is used 

to retrieve the limb of white suture that is 

closest to the cuff. The suture is pulled out 

through the lateral cannula. 


Figure 15a: Modified Caspari Suture Punch (cont): 

With the scope viewing from the anterior 

portal, a modified Caspari Suture Punch can 

be inserted through a 6 mm ClearFlex 

Cannula in the lateral portal to pass a 

Shuttle Relay suture passer from the bottom 

to top through the cuff. The suture passer is 

carried out the posterior cannula with a 

grasping forceps. 

Figure 16a: Modified Caspari Suture Punch (cont): 

The eyelet of the Shuttle Relay suture passer 

is loaded with the suture outside the 

lateral cannula and carried through the 

cuff from bottom to top by pulling on the 

opposite end. 

Figure 17: The posterior cannula is reinserted and the 

remaining white suture limb is retrieved using 

a crochet hook or suture retrieval forceps 

Figure 18: The ring handled knot pusher is threaded on 

to the green suture exiting the top of the cuff. 

It is passed into the joint to ensure there are 

no twists or obstructing soft tissue. The 

green and white suture limbs associated with 

the posterior anchor are first tied using a 

knot of choice. The second anchor is placed 

in a similar fashion, suture limbs passed, 

and tied down. 

3.45

Figure 19: The arthroscope may be moved to the 

posterior cannula for visualization. The third 

(anterior) anchor is placed in the same 

fashion and suture limbs passed through 

the cuff, usually suturing from the anterior 

portal. 


Figure 20: The illustration of the final repair shows 

three Super Revo anchors in place. Each 

anchor has two fixation points through the 

rotator cuff oriented 45o from the anchor. 

Notice the final side-to-side repair. At the 

completion of the repair, the torn end of the 

rotator cuff is tightly opposed to the bone to 

promote strong rotator cuff tendon healing. 

Arthroscopic Knot Tying Technique - Revo Knot 

Figure 1: 

Figure 2: 

Both suture tails are the same length 

and the loop-handled knot pusher is 

threaded onto the suture which has 

been passed through the soft tissue. 

This original "post" is positioned on 

the left side, shown as the darker tail 

for illustration purposes. The knot 

pusher is passed down the original 

post suture to ensure that there are no 

twists or soft tissue obstructions. 

An underhand half-hitch is placed 

around the original post and advanced into 

position on the edge of the soft tissue. 

Figure 1 Figure 2 Figure 3 

Figure 3: 

Tension is held on the post suture while a second underhand half-hitch is worked down the 

post suture to reinforce the first hitch. 

Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 

3.46 

Figure 4: 

Figure 5: 

An overhand half-hitch is next placed on the same initial post and worked down into position 

on the other two throws. 

The knot pusher and clamp are changed to the opposite suture and after checking for twists 

and soft tissue, an underhanded throw is advanced down on to the knot stack.

Figure 6: 

Figure 7: 

Figure 8: 

The knot pusher is advanced to "past point" to lock the half-hitch securely. 

A fifth overhand half-hitch is placed over the second post and worked down into position on 

the knot stack. 

Sometimes a sixth half-hitch can be used as the surgeon prefers, and the suture tails are cut 

with microscissors. 

Arthroscopic Knot Tying Technique - SMC Knot 


Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 

Figure 1: 

Figure 2: 

Figure 3: 

Figure 4: 

Figure 5: 

Figure 6: 

Thread the knot pusher on the post strand (held in the left hand) and place a clamp on the 

post. Pass the knot pusher into the joint to ensure that there are no twists or obstructing 

soft tissue. Arrange the suture so that the original post suture is short, with only 10 cm of 

the suture outside of the cannula. 

Pinch the two strands together between the thumb and index finger, crossing the loop 

strand over the post. 

Pass the loop suture under and then over both strands. 

Pass the loop strand under the post strand between the two sutures and over the top of the 

post strand in a direction away from the pinching fingers. There will be a triangular interval 

formed between the two previous looks over the post strand (red arrow). 

Feed the free end of the loop strand from bottom to top through this interval under the 

post strand. As the suture is pulled through, a "locking loop" is created (blue arrow). 

Release the thumb and index finger and place the left index finger into the "locking loop" 

from bottom to top to keep it open. Remove all slack (dress the knot) from the sutures with 

the index finger in place to avoid tightening the "locking loop" prematurely. 

Figure 7 Figure 8 Figure 9 Figure 10 Figure 11 

3.47

Figure 7: 

Figure 8: 

Figure 9: 

Pull on the post strand and use the knot pusher to guide the knot down to the tissue. Do 

not pull on the loop strand until the knot is seated. Maintain tension on the post strand 

and back off the knot pusher to assess the knot. 

Once satisfied that the knot is well seated, tighten the "locking loop" by pulling on the loop 

strand while maintaining pressure on the knot with the knot pusher. 

The "locking loop" will slide over the knot pusher and secure the knot. For further security, 

an underhand half-hitch is worked down the post suture. 

Figure 10: An overhand half-hitch is next placed on the post and worked down into position onto the 

knot stack. 

Figure 11: Suture tails are cut with microscissors. 


3.48

Subscapularis Tears:Arthroscopic 

Management/Results 

Arthroscopic Evaluation 

Normal subscap footprint 

Normal subscap/biceps relationship 

Intact medial sling for biceps (SGHL, CHL) 

The Orthopaedic Institute 

Stephen S. Burkhart, M.D. 

San Antonio, Texas 


Medial Subluxation of Biceps and 

Upper Subscap Tear 

Biceps located posterior to upper subscap 

Subscap Footprint 

2.5 cm superior-to-inferior 

1.5 cm medial-to-lateral 

Widest superiorly 

Types of Subscap Tears 

Full-thickness partial tear 

(upper subscap) 

Partial-thickness tears (PASTA-type) 

Complete tears 

Retracted adhesed tears 

3.49

Arthroscopic Subscapularis Repair 







3.50

Subcoracoid Impingement 

Full-Thickness Partial Tear 


Repair of Full-Thickness 

Partial Tear 

Partial -Thickness Tear 

(PASTA Type) 

3.51

Repair of Partial-Thickness Tear 

(PASTA-Type) 


Complete Tear 

Comma Sign 

Repair of Complete Tear 

3.52


Repair of Retracted 

Adhesed Tear 

Arthroscopic 

mobilization is 

satisfactory 

Retracted Tears 

3.53

Retracted Tears 

Slight 

medialization of 

repair (5 mm) 

satisfactory 

Do not go 

medial to 

coracoid 

Dissect Subscap from 

Coracoid Arch 


Coracoplasty 

Do coracoplasty if repair jeopardized 

by coracoid impingement 

Must have 7mm clearance between 

coracoid and subscap 

Methods 

Retrospective review 

24 Consecutive patients 

25 Arthroscopic Repairs 

Indications : 

Clinical evidence of Subscapularis tear 

(isolated or associated with larger tear) 

Results 

24 Consecutive Patients 

25 All Arthroscopic Subscapularis Repair 

M:F ratio: 17 : 7 

Mean Age: 60.7 yrs ( 41 - 78 ) 

Preop Symptoms: 18.9 months ( 1-72) 

6 Heavy Labor 

Results 

Average duration of Follow-up : 10.7 months 

Follow-up Duration > 3 months : 25 patients 

3.54

Arthroscopic Findings 

25 Shoulders 

Isolated Subscapularis 

Tear : 8 

Arthroscopic Findings 

25 Shoulders 

Combined 

with 

Posterior Cuff Tear: 17 

Average Size : 5 X 8 cm 


Clinical Outcome UCLA Score 

Pre-op Average UCLA Score : 10.7 

Post-op Average UCLA Score : 30.5 

(p < 0.0001) 

Clinical Outcome 

Forward Flexion Range 

Pre-op Average FF: 96° 

Post-op Average FF : 146° 

(p < 0.01) 

Humeral Head 

Proximal Migration 

Conclusion 

10/25 cases ( 40%) 

Before Repair 

After Repair 

Subscapularis repair can reverse proximal 

humeral migration and restore overhead 

function 

3.55

Clinical Outcome 

92% good/excellent 

results by UCLA criteria 

Conclusion 

Arthroscopic subscapularis 

repair must be tailored to the tear 

pattern 

Results of arthroscopic repair are 

equal to or better than those of 

open repair 


Thank you! 

Stephen S. Burkhart, M.D. 

San Antonio, Texas 

Arthroscopic Repair of Subscapularis Tendon Tears 

A Simple Technique 

James C. Esch, M.D. 

C. Kelly Bynum, M.D. 

Tri-City Orthopaedics 

Oceanside, CA 

jesch@shoulder.com 

www.shoulder.com 

The authors present a simplified arthroscopic direct technique for diagnosis and repair of partial subscapularis 

tendon tears. They used the anterosuperior arthroscopic portal to see the subscapularis tendon insertion 

while probing and repairing from the adjacent anterior portal. Three anatomical dissections were 

done to define the tendon insertion of the subscapularis tendon at the lesser tuberosity of the humerus. 

3.56 

The subscapularis tendon was repaired with one or two suture anchors inserted into the lesser tuberosity 

from the anterior portal while viewing from the anterosuperior portal. Suture management was via the 

standard posterior shoulder portal. A tendon penetrating-grasping device, from the anterior portal, passed 

the sutures through the displaced subscapularis tendon. The arthroscopic knots were tied from anterior 

portal.

Video of Anatomical Dissection 

Video of Subscapularis Repair 

Subscapularis tears are frequently associated with supraspinatus and infraspinatus tendon tears. The surgeon 

may not appreciate the significance of the subscapularis tendon tear when viewing from the posterior 

arthroscopic portal. Direct anterosuperior viewing and anterior probing enables the surgeon to see and 

repair these "hidden" subscapularis partial tendon tears. 

Associated with the first ten subscapularis repairs were six complete and four partial thickness supraspinatus-infraspinatus 

rotator cuff tears. There were no isolated subscapularis tears. Three patients had associated 

biceps lesions. 

The Center for Learning Arthroscopic Skills (CLASroom) 

at the Southern California Orthopedic Institute 


The Center for Learning Arthroscopic Skills 

(CLASroom) 

at the 

Southern California Orthopedic Institute 

An educational center for orthopedists and other medical professionals 

to develop and perfect their skills using technologically advanced 

arthroscopy “Dry Cadaver” ALEX models and computer simulators 

The CLAS Room is the first center of its kind – a state-of-the-art training facility 

for physicians, nurses, OR techs and 

company reps. Using lifelike 

arthroscopy models and high-tech 

computer simulators, the CLAS Room 

teaches the complex manual surgical 

skills needed to perform arthroscopy, 

through observation and repetitive 

bimanual practice. 

Stephen Snyder, MD, and his partners at 

the Southern California Orthopedic 

Institute have always been strongly 

committed to the education of other medical professionals. The CLAS Room is the latest 

step in their pursuit of educational excellence. Each year, hundreds of visitors come to 

SCOI observe and learn the latest procedures in sports medicine and arthroscopy. With the CLAS 

Room, they can now have hands-on training with the masters of arthroscopy. 

We would like to thank the following corporate sponsors for their invaluable assistance with the CLAS Room: 

Mentice Inc; Linvatec Inc.; Smith & Nephew Endoscopy; Pacific Research; Mitek Inc. and Lippincott WW Inc. 

The CLAS Room is located in SCOI’s main office in Van Nuys, California, at 6815 Noble Avenue. 

For more information on SCOI, please visit our website at http://www.scoi.com/. 

3.57

The CLAS Room includes: 

◊ Two computers – a dedicated Macintosh supercomputer, equipped with software and 

peripherals for developing and editing digital presentations, both video and PowerPoint; and 

a P.C. with a high-speed Internet connection to allow access to online data and interaction 

with other centers. 

◊ “ALEX” the Shoulder Professor – this is a lifelike arthroscopy model or “Dry 

Cadavers”(made by Sawbones, Inc.) is now able to be used with or without an arthroscopic, 

to provide a more complete hands-on training experience. “ALEX” will soon be joined by 

the new wrist, knee, ankle, elbow and spine models which provide the same experience for 

these anatomical locations as “ALEX” 

does for the shoulder. 

Three complete stations are available 

with video equipment to learn and 

practice the steps in arthroscopic 

surgery of the chosen joint. All 

necessary hand tools, suture 

anchors and disposable materials 

will be available at these stations. 


◊ 

“Sammy” – The virtual reality arthroscopic simulator produced by the 

Mentice Company of Sweden. This extraordinary computerized simulator 

is the most realistic tool currently available for learning shoulder 

arthroscopy. It is a complete 3-D 

simulation of the entire shoulder 

environment, and is a valuable aid for 

Each ALEX station is equipped with 

a scope, video player and monitor 

so the student can watch and then 

practice the operation. 

teaching eye-hand coordination, triangulation, surgical anatomy and surgical repair 

techniques. Through a force-feedback system, the surgeon experiences the same 

tactile sensations as when actually operating in the shoulder. The simulation is 

complete with “fluid” and even “blood” when a vessel is accidentally cut. The 

number of procedures that can be performed on Sammy is rapidly increasing. 

A 15-point anatomy exam, subacromial decompression, and removal of loose bodies are all 

currently available, and soon cuff and labral reconstruction, as well as capsular 

plication, will be added. 

“Sammy” the VR force feedback 

simulator allows the surgeon to 

practice arthroscopic techniques 

with the same feeling as live surgery 

◊ “Misty” – A virtual reality task simulator designed to teach bimanual 

manipulations using a series of hand tools connected to a computer. 

This simulator is remarkably useful for training all levels of surgeons to 

Be efficient and precise when operating while viewing on a video screen. 

◊ Audio and video cable links – Visitors can observer two ongoing 

arthroscopic surgeries being performed in the Center for Orthopedic 

Surgery, Inc., while simultaneously practicing on ALEX or Sammy in the 

CLASroom, and discussing ongoing cases with the surgeon. 

◊ Video teleconferencing - is also available from the CLASroom, SCOI boardroom 

and COSI surgery center to permit face-to-face interaction with other centers 

throughout the world. 

“Misty” is a bimanual task VR 

task simulator that scores the 

performance of the student and 

compares his progress to others. 

These exceptional learning tools are available to visitors at the Southern California 

Orthopedic Institute. Call Rene, Ed or Jo Ann at (818) 901-6600, ext. 3032 for information and to schedule a 

visit or log on to our web site at http://www.scoiclasroom.com./ 

3.58


ARTHROSCOPIC MANAGEMENT OF INTRA-ARTICULAR FRACTURES OF THE KNEE 

Wednesday, March 12, 2003 o Carlton Hotel, Carlton II 

Chairman: M. Nedim Doral, MD, Turkey 

Faculty: W. Jaap Willems, MD, Netherlands, Phillip Lobenhoffer, MD, Germany, Freddie Fu, MD, USA and David 

McAllister, MD, USA 

Introduction: Arthroscopic Management of Intra Articular Fractures of the Knee 

Mahmut Nedim Doral, 

O. Ahmet Atay, Onur Tetik, Gürsel Leblebicio_lu 

Hacettepe University Faculty of Medicine 

Department of Orthopaedics and Traumatology & Department of Sports Medicine 

e-mail: mn-doral@bim.net.tr 

Arthroscopic management of intraarticular fractures of the knee is a minimal invasive, more accurate, and 

outpatient procedure parallel to the technological advances. Fractures are not only important for the adolescence 

and pediatric group, but also important for the adult population. 

The main purpose of arthroscopic fixation of the intraarticular fractures is to give stability to the 

fragments and to treat the associated lesions for the restoration of the knee joint. The high degree of success 

achieved in almost all cases illustrates the amazing recuperative powers of human joints once articular 

cartilage congruence and stability is re-established together with correction of axial deformities and the 

mobilization of joints. 

EI (EI) and distal femur are the frequent zones prior to injury for the pediatric group. Also these 

problems became very frequent in the adolescence group with the increase in the level of the sportive activity. 

Avulsion fractures from EI is mostly treated with the 

arthroscopy assisted methods. Detailed evaluation of EI fracture 

and the classification according to the Meyers-McKeever system 

must be done to plan the arthroscopy-assisted treatment. 

In our practice we use transquadricipital portal for the fixation 

of EI fractures (1). But do not forget the conservative 

approaches to the EI fixation (2) 

At the same time the natural history of the elongation of 

the ACL is not clear in the literature. 

Physeal fractures that involve the distal femur must also be considered 

in the patient presented with hemarthrosis in pediatric 

and adolesence age. Magnetic resonance imaging (MRI) permits 

noninvasive evaluation of the cartilage of the growth plate and epiphysis so that diagnosis and the treatment 

of the fracture becomes more precise with the MRI. 

The most frequent intaarticular pathology for the adult group is plateau fractures of the tibia. Either 

Schatzker or Hohl classification system may be used for systematic evaluation of the fracture. Arthroscopy 

assisted treatment is mostly preferred, especially for the lower grades. 


3.59

One must keep in mind that periarticular soft tissue is a very important parameter for the planning 

of the intraarticular pathologies. Tscherne and Lobenhoffer classification system may be helpful for planning 

of the pathologies (3). 

Patellar fracture is another intraarticular fracture that may interfere with the knee unction. Arthroscopic 

assistance is helpful in the internal fixation techniques of the patellar fracture to provide and protect the 

cartilage integrity. 

Segond fracture and the chondral avulsions are the rare type of the injury but more and more participants 

in the sports bring these kinds of injuries more frequent in our daily practice. 

We can conclude that arthroscopic treatment of the intraarticular fractures of the knee joint is a 

more effective and adequate procedure with early active motion and controlled rehabilitation program. 

Under the scope of that brief knowledge it’s easy to understand arthroscopic management of major 

intraarticular fractures of the knee joint. 

An overview of the major intraarticular fractures of the knee, the classification and the mechanics of 

tibial plateau fractures. Secondly, the arthroscopic treatment of IA fractures including the arthroscopic 

techniques for the treatment of the fracture of EI. Finally, the natural history of ACL after EI fractures, the 

potential biological approach and rehabilitation will be discussed in this ICL#09. 


1-Doral MN, Atay OA, Leblebicioglu G, Tetik O. Arthroscopic fixation of the fractures of the intercondylar 

eminence via transquadricipital tendinous portal.Knee Surg Sports Traumatol Arthrosc. Nov;9(6):346-9, 2001 

2-Atay OA, Doral MN, Tetik O, Leblebicioglu G. Conservative treatment of eminentia intercondylaris fractures 

of the tibia in children. Turk J Pediatr. Apr-Jun;44(2):142-5, 2002 

3-Tscherne H, Lobenhoffer P.: Tibial plateau fractures. Management and expected results. Clin Orthop 1993 

Jul;(292):87-100 

Tibial Plateau Fractures; classification and biomechanics 

W. Jaap Willems 

Amsterdam, The Netherlands 

Several classifications for these fractures have been described. Hohl (1956) defined 6 types (undisplaced, 

Local compression,Split compression,Total,Split and Communited). Based on this system Schatzker (1979) 

described 6 types: 1)Split condylar, 2)Split and depression, 3)Joint depression, 4)Medial condylar, 

5)Bicondylar, 6)Bicondylar with diaphyseal extension. The AOgroup developed their classification, based on 

the ABC categories : A: extra-articular, B: partial intra-artcular, C: total intra-articular.In this classification 

for the tibial plateau fractures 9 subgroups are defined. The fractures of the intercondylar eminence are 

generally classified according to Meyer: undisplaced, minimally displaced ,displaced. 

The tibia plateau fracture is mostly caused by a fall; depending on the valgus or varus moments a lateral 

or medial condylar fracture exists.With rotational forces an eminence fracture can arise, comparable to an 

ACL injury, with bony detachment of the ACL on the tibial side. 

The first results on the arthroscopically assisted treatment of tibial plateau fractures is reported by Reiner 

in 1982. From the beginnings of the nineties several studies have been published. In the first decade the 

technique was used in the more simple fractures (Schatzker types 1,2 and 3 or AO type B1,B2,and B3).Later 

the more complex bicondylar fractures were treated as well with arthroscopic assistance. Nowadays the better 

visualisation, especially of the fractures in the postero-lateral part of the tibial surface as well as better 

interpretation of the concomitant pathology (cruciate ligaments, meniscus) leading to a better reduction as 

well as treatment of this concomittant pathology are seen as the great advantages of the arthropscopically 

assisted treatment of the tibialplateau fractures. The less invasive approach of the intra-articular fracture 

does not preclude a sufficient osteosynthesis, with sometimes the need of plates and screws. 

Literature: 

Schatzker J et al .(1979) : The tibia plateau fracture: the Toronto experience. Clin Orthop 138:94-104 

Reiner MJ(1982): The arthroscope in the tibial plateau fractures : its use in evaluation of soft tissue and 

bony injury. J Am Osteopath Ass. 

Fowble CD et al (1993): The role of arthroscopy in the assessment and treatment of tibial plateau frac- 

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tures.Arthroscopy 9:584-590. 

Berfeld B et al (1996): Arthroscopic assistance for uncollected tibial plateau fractures. 

Arthroscopy 12:598-602. 

The Evaluation and Natural History of Tibial Spine/ACL Avulsion Fractures 

David R. McAllister, M.D. 

University of California, Los Angeles 

Department of Orthopaedic Surgery 

Introduction 

Anatomy: 

• ACL attached to fossa anterior to the medial intercondylar eminence 

• Some ACL fibers pass beneath the transverse meniscal ligament blending with the anterior horn of 

the lateral meniscus 

Mechanism of Injury 

• Avulsions fractures in children are the result of stress on the ACL 

• Usually caused by internal rotation of the tibia, hyperflexion or hyperextension 

• Can be the result of falls from bicycles or motorbikes, sports injuries, or MVA 



• Type 1: Minimally displaced 

• Type 2: Fragment elevated but still attached 

• Type 3: Complete displacement of the fragment 

Myers and McKeever, JBJS-A, 1970 

Associated Injuries 

• Common in Adults (especially MCL injuries) 

• Uncommon in children 

Non-Operative Treatment 

• Type I & II usually non-operative treatment with immobilization in a cast for 6-8 weeks 

• 15-30 degrees of flexion to relax the posterolateral bundle of the ACL 

• Full extension to allow the femoral condyle to compress the fragment toward its fracture bed 

• Important to verify adequacy of reduction 

Operative Treatment 

• Type III fracture usually require ORIF 

• Arthrotomy 

• Arthroscopy 

Results (Baxter and Wiley, JBJS-B, 1988) 

• 42 children with anterior tibial spine fractures 

• Type 1: 8 (19%) 

• Type 2: 13 (31%) 

• Type 3: 21 (50%) 

Treatment: 

• 13: Plaster immobilization (all type I; 5 type II) 

• 15: Closed reduction (8 type 2; 7 type 3) 

• 14: Open reduction (13 type 3; 1 type 2) 

Baxter and Wiley, JBJS-B, 1988 

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Laxity: 

• Type 1: None 

• Type 2 & 3: 3-4 mm 

Loss of extension: 

• All patients lost extension (range 4-15 degrees) 

Conclusions: 

• Fractures of the tibial spine may lead to disturbance of the ACL; although asymptomatic in this study 

• Anatomic reduction does not eliminate laxity or the loss of full extension 

Results (Myers and McKeever, JBJS-A, 1970) 

• Follow up of 1959 JBJS publication 

• 70 patients with intercondylar eminence fracture 

• Types 1 and 2 treated with aspiration and casting (knee flexed 20 degrees) (80%) 

• None treated with closed reduction 

• Type 3 treated with ORIF (20%) 


• 10/22 adults had poor results 

• 46/47 children had good/excellent results 

• All type III injuries treated operatively had a good/excellent result 

Conclusions: 

• Most fractures in children have good results 

• ORIF is indicated for Type III injuries 

• Closed reduction is not indicated 

• Prognosis not so good in adults 

Summary 

• The overall prognosis is good if satisfactory reduction can be maintained 

• Can be some residual anterior laxity although when present this is usually asymptomatic 

• Can be overgrowth of medial tibial eminence 

Extension block is common and can occur with or without surgery 

The Biological Approach 

Freddie H. Fu, M.D., D.Sc. (Hon) and Volker Musahl, M.D. 

Freddie H. Fu, M.D., D.Sc. (Hon), David Silver Professor and Chairman of the Department of Orthopaedic Surgery, 

Kaufmann Building Suite 1011, 3471 Fifth Avenue, Pittsburgh, PA, 15213 

www.orthonet.upmc.edu, email: ffu@uoi.upmc.edu 

INTRODUCTION 

Limited healing capacity of ACL, PCL, central meniscus, cartilage, muscle injuries, and delayed fracture 

healing. Therapeutical approaches addressing the biological base of these injuries are mostly pre-clinical 

applications. Improving the biological healing process by means of stem cells, gene therapy, and tissue 

engineering may stimulate the healing process 

EVALUATION 

Conventional Imaging 

Limited by inability to directly visualize articular cartilage and menisci 

MRI provides non-invasive and direct visualization of bone and soft tissue structures 

MRI provides diagnostic advantage over clinical examination only in selected cases [6] 

Gadolinium enhanced MRI 

More sensitive and specific MRI technique for evaluating articular cartilage abnormalities. 

Gadolinium enhanced MRI on the composition of cartilage post ACI. At > 1 year, the grafts have GAG levels 

3.62

comparable to normal articular cartilage [4] 

Biomechanical Probes 

Measures indentation stiffness of articular cartilage 

Decrease in indentation stiffness for proteoglycan-depleted specimens compared to normal articular cartilage 

[10] 

Optical Coherence Tomography (OCT) 

Ultrasound is an echograph of ultrasonic waves; OCT is an echograph of infrared light 

Provide real-time cross-sectional imaging of articular cartilage [2] 

Detects gaps that are invisible to the arthroscope, good correlation with histomorphometric analysis 

Functional tissue engineering 

Approach to enhance tissue regeneration and provides the possibility of producing tissue that is biomechanically, 

biochemically, and histomorphologically similar to the normal 

Basic concept is based on the manipulation of cellular and biochemical mediators to affect protein synthesis 

and to improve tissue formation and remodeling 

Ultimately, the process is expected to lead to a restoration of mechanical properties [9] 

The available approaches are e.g., the use of growth factors, gene transfer technology to deliver genetic 

material, stem cell therapy, and the use of scaffolding as well as external mechanical factors 

Each of these approaches, or their combinations, offers the opportunity to enhance the healing process 


Matrices 

Protein-based polymers (e.g. fibrin, collagen) 

Carbohydrate-based polymers (e.g. PLA, PGA, hyaluronan) 

Artificial polymers (e.g. Dacron, hydroxyapatite) 

Combination polymers (e.g. crosslinging, matrix combinations) 

Matrix requirements 

Porosity (cell migration) 

Adhesion (cell attachment) 

Biodegradability 

Biocompatibility 

Bonding (tissue integration) 

Elasticity (biomechanical stability) 

Stem cells 

Cells that can turn into different tissue types, such as bone, cartilage, muscle, or tendon. 

A special stem cell population derived from muscle tissue was identified and tissue engineering approaches 

are currently under development [5] 

Biological substitutes for repair, reconstruction, regeneration, or replacement of musculoskeletal tissues 

can be engineered with muscle-derived stem cells 

For this purpose, growth factors are used, which have been shown to promote the healing of tissues of the 

musculoskeletal system. 

Growth factors 

Growth factors can be liberated by cells at the injury site (e. g. fibroblasts, endothelial cells, muscle cells, 

mesenchymal stem cells) 

Growth factors are capable of stimulating cells towards proliferation, migration, matrix synthesis and differentiation 

Growth factor application is limited by the their short biological half life, and the need for repeated and 

high dosages 

Growth factors are limited by their need for delivery to the injured site 

Among the different methods developed for local administration of growth factors, gene transfer techniques 

have proven the most promising 

3.63

(+ positive effect; - no or 

negative effect; blank not 

tested IGF-1=insulin like 

growth factor 1; bFGF=basic 

fibroblast growth factor; 

NGF=nerve growth factor; 

PDGF= platelet-derived 

growth factor; EGF= epidermal 

growth factor; TGF= 

transforming growth factor; 

BMP-2=bone morphogenic 

protein-2) 


Gene therapy 

Gene therapy transfers specific genes into the target tissue 

Successful application of gene therapy can promote production of therapeutic levels of desired proteins by 

transformed cells at the site of injury or inflammation. 

The cDNA must be packaged into a vector to enter the cell, here it is integrated into the host chromosomal 

DNA 

For expression, the desired gene has to be transcribed, translated, and secreted 

Viral and non-viral vectors are available to deliver genetic material 

Non-viral vectors, e.g. liposomes, are easy to produce and have a relatively low toxicity and immunogenicity, 

low efficiency in delivering the gene to the targeted cells 

Viral vectors present the most efficient method for gene transfer. Commonly used viruses include adenovirus, 

retrovirus, adeno-associated virus, and herpes simplex virus 

Strategies 

Strategies for local gene therapy have been extensively investigated 

Vectors can be directly injected in the host tissue, or cells in culture can be genetically altered with a vector 

(ex vivo) and transplanted [3] 

While the direct method is technically easier to achieve, the cell based ex vivo approach bares less risk, 

because gene manipulation occurs outside the body of the host 

The genetically engineered and transplanted cells supply the host not only with the desired gene expression 

but also with cells responding and participating in the healing process 

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At the experimental level, the feasibility of gene therapy was shown to the ligament insertion, meniscus, 

articular cartilage, and synovial tissue of the knee joint [1, 7, 8] 

Future directions 

Gene therapy is not yet established as a clinical therapy in Orthopedic Surgery 

Gene therapy has great potential for the treatment of musculoskeletal injuries in the future 

Phase I of the first clinical trial in orthopedics was successfully completed for human joints 

Further tissue engineering with muscle-derived stem cells and gene therapy will lead to the development of 

new treatment strategies for tissues with low healing capacities such as articular cartilage 

A large number of basic science studies and pre-clinical trials have to be completed to reach the necessary 

efficiency and safety for orthopedic applications 

REFERENCES 

1. Adachi, N., Sato, K., Usas, A., Fu, F.H., Huard, J. et al., J Rheumatol. 2002 Sep;29(9):1920-30. 

2. Chu, C.R., L.D. Kaplan, F.H. Fu, J.P. Bradley, and R.K. Studer. AOSSM, 28th Annual Meeting. 2002. 

Orlando, FL. 

3. Evans, C. and P. Robbins, J Bone Joint Surg Am, 1995. 77: p. 1103-1114. 

4. Gillis, A., A. Bashir, B. McKeon, A. Scheller, M. Gray, and D. Burstein, Investigative Radiology, 2001. 

36: p. 743-748. 

5. Huard, J., G. Ascadi, A. Jani, and et. al., Human Gene Therapy, 1994. 5: p. 949-958. 

6. Kocher, M., J. DiCanzio, D. Zurakowski, and L. Micheli, Am J Sports Med, 2001. 29: p. 292-296. 

7. Lee, J.Y., D. Musgrave, D. Pelinkovic, K. Fukushima, J. Cummins, A. Usas, P. Robbins, F.H. Fu, and J. 

Huard, J Bone Joint Surg Am, 2001. 83-A(7): p. 1032-9. 

8. Martinek, V., F.H. Fu, J. Huard, et al., J Bone Joint Surg Am. 2002 Jul;84-A(7):1123-31. 

9. Woo, S.L.-Y., K. Hildebrand, N. Watanabe, J.A. Fenwick, C.D. Papageorgiou, and J.H. Wang, Clinical 

Orthopaedics & Related Research, 1999(367 Suppl): p. S312-23. 

10. Youn, I., F. Fu, and J. Suh, The Pittsburgh Orthopaedic Journal, 1999. 10: p. 159-160. 


3.65

ICL #10 

MANAGEMENT OF THE POST MENISCECTOMY KNEE AND DECISION-MAKING 

Wednesday, March 12, 2003 o Aotea Centre, Kaikoura Room 

Chairman: Giancarlo Puddu, MD, Italy 

Faculty: Christopher Harner, MD, USA, Annunziato Amendola, MD, USA and Philippe Neyret, MD, France 

1. Meniscal Allografts – Chris Harner 

2. High Tibial Osteotomy – Ned Amendola 

3. HTO and the post meniscectomy ACL deficient knee – Philippe Neyret 


4. HTO and posterior instability – Chris Harner 

5. Antivalgus Osteotomies – Gian Carlo Puddu 

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ISAKOS 2003 

Auckland, New Zealand 

March, 2003 

Indications and Techniques 

Christopher D. Harner, MD 

Medical Director 

Center for Sports Medicine 


University of Pittsburgh 

Top 10 Orthopaedic Procedures: 

10) Debride skin/muscle/fracture 11012 

9) Total knee replacement 27447 

8) Open repair of femur fracture 27236 

7) ACL reconstruction 29888 

6) Open repair of femur fracture 27244 

5) Subacromial decompression 29826 

4) Removal of support implant 20680 

3) Carpal tunnel surgery 64721 

• Chondral debridement 29877 

1) 

1) 

Meniscectomy 

Meniscectomy 

29881 

29881 

Source: ABOS, 2002 


Rationale 

#1 goal: 

Preserve the 

meniscal and 

articular cartilage 

Save the 

Meniscus! 

Practice Profile - CDH 

Time: 14 years 

Type: Academic 

Sports Medicine / Knee 

Meniscus Transplantation: 

• 10 yr experience 

• 15-20 cases / yr (>175 

total) 

• Publications: 

– 1st 30 cases (2-10 yr f/u) 

– Lateral transplants 

– ACL + transplant 

Harner & 

Annunziata 2000 

Selection Criteria 

• Age 

• Pain (localized) 

• Previous surgery 

• Status of articular cartilage 

45° PA FWB x-ray 

Arthroscopic findings 

• Alignment 

(long cassette) 


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Graft Choice 

• Fresh-frozen, 

non-irradiated 

allografts 

(donor age 15 - 35) 

• Single tissue bank 

• Size match 

L’Insalata, 1996 

Surgical Technique 

• Arthroscopic assisted 

• “Small” arthrotomy incisions 

• Meniscus sutured with 

combined arthroscopic and 

open techniques 

• Standardized post-op rehab 


History 

• 26 y.o. male soccer player 

• twisting injury (5/97) 

– partial medial meniscectomy (6/97) 

– subtotal medial meniscectomy (1/98) 

– persistent medial joint line pain 

+ ADLs/sports 

3.68

History 

J.F. 

• 40 y/o male physician 

• Previous lateral meniscectomy 

x2 

• Lateral joint line pain 

• +ADL/work 


Post-operative Management 

• Bracing 

• Motion: CPM 0 - 90° X 4 wks 

• Partial to full weight bearing over 4 

wks 

• Return to ADLs: 8 wks 

• Return to Sports: 9 - 12 mo 

Results 

Demographics 

• 34 meniscal transplants in 31 

patients 

• Average f/u 36 mo (24 - 72) 

• 18 male, 13 female 

• Average age 28 (15 - 42) 

Subjective Rating Scales 

• Previous surgery 

1 - 4 (avg 2.4 / pt) 

• 11 isolated meniscal 

involvement 

• 20 combined with ligament 

instability 

• 100 point scale 

• Knee outcome survey 

ADL - avg 86 (79 - 92) 

Sports - avg 78 (64 - 88) 

• Lysholm - avg 84 (82 - 92) 

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IKDC Results (n = 31) 


Normal 

Nearly 

Normal 

Abnormal 

Severely 

Abnormal 

Function 

al Rating 

11 

19 

1 

0 

Activity 

Rating 

16 

14 

1 

0 

•No joint 

space 

narrowing 

over time (p 

= 0.31) 

P.B. 

9 yr s/p 

Results - Lateral Meniscus 

n = 20, 2 - 8 yr f/u: 

• IKDC: 

18% normal, 73% near normal, 9% abnormal 

• Knee Outcome Score 

ADLs 79 ± 13 

Sports 75 ± 17 

• Lysholm: 81 ± 16 

• No joint space narrowing over time 

• 18/20 would do again 

AAOS, 2001 

Conclusion 

Remains a viable 

option in: 

•Select patients 

•Joint line pain 

•Previous 

meniscectomy 

•Near “neutral” 

alignment 

•“Intact articular 

cartilage” 

T.B. 

2nd look 

1 1/2 yr s/p 

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High Tibial Osteotomy 

A. Amendola, MD 

University of Iowa Hospitals and Clinics 

The Post Meniscectomy Knee 

1. Presentation 

• Compartment pain 

• ± deformity 

• ± thrust 

2. Goals of Treatment 

• Pain reduction 

• Improvement of functional stability – not passive laxity 

• Reduction of thrust / instability 

• Improve the likelihood of success post ligamentous/cartilage or meniscal reconstructive procedures 

3. Indications – The Importance of Alignment 

Malalignment Malalignment Malalignment Malalignment 

+ + + + 

Arthrosis Instability Arthrosis Cartilage / Meniscal Transplantation 

+ 

Instability 


4. Contra-indications 

- Severe degeneration of opposite tibio-femoral compartment 

- Gross loss of motion, 70° 

- Usual medical contra-indications 

7. Pre-Operative Planning 

- Detailed history and physical exam 

- Assessment of instability 

- In-office gait analysis 

Radiographs: 

- Routine Series : - standing AP 

- standing tunnel 

- lateral 

- intra-patellar 

- Standing hip to ankle x-ray (target area is weight-bearing axis) – most important for preoperative 

planning 

8. Assessment of Alignment 

a) Femorotibial angle: (5 – 7° valgus ) measured on single weight-bearing x-rays 

b) Mechanical axis (author’s preference): measures deviation in weight-bearing line 

- Advantages and disadvantages to both methods 

- Neither is entirely accurate 

- Compare to other knee if normal 

- Intra-operative measure with fluro is important 

9. Posterior Tibial Slope 

- Bony slope is 1 – 10° 

- Soft tissue (articular slope ) is less 

- Increasing slope is similar to flexing knee 

- Keep in Mind: - Increasing posterior tibial slope increases tendency for anterior tibial translation 

- Increasing posterior tibial slope worsens ACL deficit; helps PCL deficit 

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10. Opening vs. Closing Wedge - Advantages / Disadvantages 

• Tibial Opening Wedge 

Advantages 

- Avoids proximal tib-fib joint & peroneal nerve 

- Easier to perform 2 plane osteotomy in sagittal and coronal plane 

i.e. correction of varus and hyperextension 

i.e. dealing with ACL or PCL insufficiency patterns 

- Easier operation (1 cut) 

- Does not violate anterior compartment of the leg 

Disadvantages 

- Most often requires graft 

- ? union rate 

- Not appropriate for huge ( > 2cm) corrections 


• Tibial Closing Wedge 

Advantages 

- No graft 

Disadvantages 

- Alters shape of upper tibia Æimplications for TKA 

- Difficult to control tibial slope 

- Most often slope is unintentionally decreased 

- Difficult to adjust correction intra-operatively 

- Proximal tib-fib joint violated 

- Not appropriate for huge ( > 2cm) corrections 

11. Authors Preferred Surgical Technique 

- Opening wedge 

- Puddu plate fixation 

- Autograft or allograft 

Tibial Valgus Producing Osteotomy Technique 

- Medial incision 

- Superficial MCL retracted 

- Patellar tendon retracted 

- Drill guide pin under fluoroscopic control 

- slight obliquity to orientation 

- start approximately 4cm below medial joint line 

- directed across superior aspect of tibial tubercle at patellar tendon insertion 

- to 1 cm distal to lateral joint 

- tip of fibular head helpful reference point 

- Reposition guide pin as necessary until placement is optimal (1,2 ) 

- Always perform osteotomy below guide pin (3) 

- Osteotomy should be oblique but not excessively (1) 

- Cortical cut made with small sagittal saw 

- Osteotomy completed with osteotome 

- thin, flexible osteotomes are better than traditional ones 

- leave 1cm lateral cortex as hinge 

- osteotomy should stop at least 1cm distal to lateral joint 

Technique continued 

- continuous or frequent imaging to prevent violation of lateral cortex 

- make sure both anterior and posterior cortices are penetrated 

- Gradually and carefully open osteotomy to desired width (4 ) 

- Bone grafting: 7.5mm gap or less, local or none 

> than 7.5mm, allograft or autograft (6) 

12. Alternate Fixation Options for Opening Wedge Osteotomy 

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- Other plate and screw systems 

- Bone graft only 

- External fixator / spatial frames more appropriate for huge corrections 

13. Complications 

- Haematomas 

- Failure of fixation / non-union 

- Hardware 

14. Combined ACL Deficiency / Malalignment 

Treatment Algorithms 

i) LATTERMAN and JAKOB Knee Surg Sports Traumatol Arthrosc 1996 

Group Age Pain Instability Arthroscopy Treatment 

1 >40 +++ + Subchondral bone HTO alone 

2 25-40 +-++ +-++ Severe fissuring Staged 

and fragmentation 


3

4. A. Amendola, J. R. Giffin, D.W. Sanders, J. Hirst, J.A. Johnson Osteotomy for Knee Instability: The Effect of 

Increasing Tibial Slope on Anterior Tibial Translation. Presented at American Orthopaedic Society for 

Sports Medicine Specialty Day, San Francisco, California . March 3, 2001 

The Post Meniscectomy Knee 

Ph. Neyret, T. Aît Si Selmi, T. Lootens, N.Bonin 

1/ The role of Medial Meniscus in ACL Deficient knee. 

1a/ Natural history of the ACL deficient knee. 

We know that ACL rupture leads to Osteoarthritis over time particularly if an isolated Medial Meniscectomy 

without ACL Reconstruction has been performed. 


With Henri Dejour Pierre Chambat and Deschamps, we underlined, in the past the links between ACL 

Deficient Knee and Osteoarthritis due to some biomechanical factor, particularly the status of the medial 

meniscus and the amount of the Anterior Tibial Translation. 

1b/ Osteoarthritis after ACL reconstruction 

But ACL Reconstruction can also lead to Osteoarthritis and sometimes to early and severe osteoarthritis in 

young patients. 

We reported with Henri Dejour and G Walch in 1988 that Previous Medial Meniscectomy, a delay Injury- 

Operation superior to 5 years or pre-operative degenerative changes are liable to lead to early post-operative 

osteoarthritis. 

After ACL Reconstruction, what are the radiological results at long term follow-up. reported 

Three very similar lyonnais series reported by T. Aitsiselmi, Chotel and Selva evaluated the clinical and 

radiological outcome after ACL reconstruction combined to an extra-articular tenodesis at 10 years followup. 

They also found a relationship between the medial meniscal status and radiological outcome. 

Normal 10% 

Sutured 

Partial MM 20% 

Total MM 30% 

Previous MM 60% 

If the medial meniscus was preserved it means normal of sutured at time of ACL Reconstruction, the rate 

of pre-OA or OA was 10% at 11.5 years mean follow-up. 

But if the medial meniscus was partially removed at the time of ACL reconstruction the rate of pre OA or 

OA increased to 20% and 30% in case of total meniscectomy. A previous medial Meniscectomy before the 

ACL Reconstruction was the worst eventuality : the risk of pre-OA or OA reached to 60%. 

The influence of post-operative medial meniscectomy after ACL Reconstruction in the onset of OA is still 

unknown because its frequency was very low. 

According to Shelbourne, in order of importance, articular cartilage damage, partial or total medial meniscectomy, 

and partial or total lateral meniscectomy affect the objective and subjective results from5 to 15 

years after ACL Reconstruction. 

Wu very recently, in the last issue of the American Journal of Sport Medicine, reported that at 10 years followup 

radiographic abnormalities were more common in the subgroups that had undergone meniscectomy. 

2/ The combined operation 

Henri Dejour did the Hypothesis that "ACL Deficient Knee with monopodal stance imbalance that appears 

3.74

on monopodal stance cannot be compensated for by a simple ligamentous ACL graft ". We try to better 

define the relationship between Instability and Osteothritis in a chapter of the book directed by the 

Pittburg’s team. 

2a/ Results at 10 years 

Our early results at 3 years follow-up were published in the CORR in 1994. 

But some surgeons (Jakob…) during the 90ies recommand a two stage-surgery, and the debate is still 

opened. Let me give a short overview of the publication we did in 1994. 

It was a series of 50 patients with symptoms of ACL insufficiency and varus malalignment. 44 were available 

at follow-up. 

At 3.5 years Follow-up we noted improved clinical symptoms, particularly objective and subjective stability. 

Moreover Osteoarthritis seemed to be stabilized. 

Nevertheless only one patient was able to return to competitive sport activities. 

In this series Varus malalignment was either due to medial narrowing mainly after Medial Meniscectomy, or 

due to lateral opening in case of lesions of the lateral collateral ligament. 

These two situations are completely different. In this short presentation we shall concentrate on the medial 

narrowing subgroup and then we shall discuss our present indications of the combined operation. 

2b/ Results at 10 years 


What is the long term outcome of the combined operation, ACL graft combined with a Valgus High Tibial 

Osteotomy, in one stage surgery ? 

• 1983-1999: 47 MedialFTA 

grade B: 20 grade C: 27 

• At FU: 35 knees (75%) 

Delay Injuy-op: 8y (1-33) 

Age at Operation: 32y (18-49) 

Previous medial M.: 21 (66%) 

FU: 11 years (1-16) 

- Material – Method 

The inclusion criteria were very strict. Only 47 knees with mild or moderate radiological preoperative 

changes, it means grade B or C in the IKDC classification, were operated on between 1983 and 1999. At follow-up, 

35 knees were avalaible.The mean delay Injury-Operation was 8 years with a large standard deviation. 

In 66% of cases a previous medial meniscectomy had been performed. 

A closing wedge Osteotomy was performed at the beginning of our experience and progressively we preferred 

to combine an opening wedge Osteotomy. 

- Results : 

The IKDC subjective score depends on symptoms, functional evaluation and sport activities. The average is 

79 at 11 years follow-up. 

Considering the index of satisfaction, 96% of patients considered their knee as normal or almost normal 

At follow up 42% of patients practised recreational sports and only 6% continue competitive sports. 

The final evaluation allows to underline that 60% of patients belong to the grade A or B, 34% to the grade 

C and only 6% to the grade D. 

Mean Closing Opening 

Tibial Pre-op 10.5 10.9 8.9 

Slope FU 9.4 9.5 9.3 

Radiologically we notice a tendancy to decrease the tibial slope in case of closing wedge osteotomy and a 

3.75

tendancy to increase the tibial slope in case of opening wedge osteotomy, but the difference is not statiscally 

significative, in this short series. 

We found that the residual, differential, anterior tibial transltion, 

on monopodal stance is directlty correlated with the objective 

score. In the Groups A and B the residual differential postoperative 

translation on is 2.5 mm and 5.5 mm in the groups C and D. 

It is interesting to know there is a direct relationship between the 

Anterior Tibial Translation and the tibial slope. So it is crucial 

not to increase the tibial slope when performing the Osteotomy.. 

The mean valgus correction measured on the long leg films at 

one year follow-up was 7°. 

At follow-up a loss of 2° was observed in the amount of the valgus 

correction. 

Usually we try to obtain a 2 to 4 valgus alignment. 


a b c d 

Pre-op 14 20 

3 2 

Follow-up 11 21 2 

A progression of Osteoarthritis in the medial compartment was noted in 5 Knees, 15% of cases. We do not 

establish a direct correlation between the amount of valgus correction and the progression of the 

Osteoarthritis. 

a b c d 

Pre-op 30 4 

18 2 

Follow-up 10 22 2 

A progression of Osteoarthritis in the lateral compartment was noted in 20 Knees. Severe lateral degenerative 

changes were observed in only two cases. 

We do not establish a direct correlation between the amount of valgus correction and the progression of 

the Osteoarthritis. 

2c/ Indications et technique 

What is nowadays the place of the combined operation in our practice ? 

• Firstly in case of medial narrowing without lateral opening. 

Example 1 : This patient had had an ACL Reconstruction with a good result. 

On the left knee there is a medial narrowing, grade C. Note the large amount of anterior tibial translation 

on the radiological lachman and the disappearance of the posterior clear triangle corresponding to the 

posterior horn of the medial meniscus. 

At 2 years follow-up the progression of OA seemed to be stopped and the left lower limb is well aligned 

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Example 2 : This patient had undergone a previous ACL reconstruction using a synthetic ligament and a 

medial meniscectomy. You can see there was an asymmetrical varus malalignment. At follow-up we can 

measure a 2° valgus alignment and a stabilization of the progression of Osteoarthritis. Note the complete 

control of the anterior tibial translation on the post-operative profile Xrays in monopodal stance.

Technically this operation is very simple. We harvest the Bone-Patellar tendon-Bone graft, then drill the two 

tunnels and before to pass the graft we perform an opening wedge tibial Osteotomy and then we calibrate 

again the tibial tunnel. 

To perform a combined Osteotomy is easy if one elevates the Pes Anserinus. The superficial medial collateral 

ligament is transversally cut. Two parallele pins show the direction of the future Osteotomy. 

A fluoroscopic control is absolutely necessary. 

The osteotomy is fixed with two or three staples. 

. The problem is very different in case of asymmetrical lateral opening without medial narrowing. 

Example 1 : In this patient, during the same operation we performed a combined operation and a fixation 

of the bone block of the femoral insertion of the lateral collateral ligament. 

In case of asymmetrical lateral opening due to an intersticial rupture of the lateral collateral ligament we 

recommand to perform, during the same surgery, The ACL Reconstruction, The opening wedge HTO and a 

Lateral Collateral Ligament graft, using a 6mm Bone-Patellar tendon-Bone graft harvested on the contralateral 

knee. The role of the Osteotomy is to protect the grafts and a small amount of valgus, 2 or 3 degrees is 

enough. In the absence of LCL graft an obvious hypercorrection would be required. 


Example 2 : This patient had a mild asymmetrical lateral opening, but the long leg film shows a valgus 

alignment. In this situation we decide to reconstrut the LCL and the ACL witout HTO. The result is excellent 

at 4 Years F-U. 

. The place of deflexion High Tibial Osteotomy combined with ACL Reconstruction. This option must be 

discussed when there is a grade B or C radiological changes without frontal malalignment. 

Conclusions : 

In the young athletic Acl deficient knee, one must take into account not only the symptoms (mainly instability, 

rarely pain) but also the long term outcome. 

The pre-operative clinical examination and radiological check-up allow to detect: 

- Previous Medial Meniscectomy 

- Degenerative changes or Imbalance 

- Delay Injury- Operation > 5 Years 

In such a case don’t forget to discuss the "combined operation"… Thank You. 

Bibliography 

BONIN N, AIT SI SELMI T, DEJOUR H, NEYRET Ph, 

Association Reconstruction du LCA et ostéotomie tibial de valgisation. A 11 ans de recul in « Le Genou du 

Sportif », Sauramps Medical, Montpellier 2002 : 225-235. 

BOSS A, STUTZ G, OURSIN C, GACHTER A. Anterior cruciate ligament reconstruction combined with valgus 

tibial osteotomy (combined procedure). Knee Surg. Sports Traumatol Arthrosc 1995: 3: 187-91. 

DEJOUR H, NEYRET P, BOILEAU P, DONELL ST. 

Anterior cruciate reconstruction combined with valgus tibial osteotomy. Clin Orthop 1994: 220-8. 

DEJOUR H, NEYRET P, BONNIN M. 

Instability and osteoarthristis. Knee surgery, Volume 1, 1994, Chap N° 42, "Soft Tissue Injury", Section VII, p. 

859-875. 

DEJOUR H, WALCH G, NEYRET P, ADELEINE P. 

Résultats des laxités chroniques antérieures opérées. A propos de 251 cas revus avec recul minimum de 3 

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ans. Rev. Chir. Orthop. 1988: 74: 622-636. 

DEJOUR H, DEJOUR D, AIT SI SELMI T, Chronic anterior laxity of the knee treated with free patellar graft 

and extra-articular lateral plasty : 10 year follow-up of 148 cases, Rev. Chir. Orthop. 1999: 85: 777-89. 

LATTERMANN C, JAKOB RP. 

High Tibial osteotomy alone or combined with ligament reconstruction in anterior cruciate ligament-deficient 

knees. Knee Surg. Sports Traumatol Arthrosc 1996: 4: 32-8. 

LERAT J.L., CHOTEL F, BESSE J.L., MOYEN B. 

Les résultats après 10 à 16 ans du traitement de la laxité chronique antérieure du genou par une reconstruction 

du ligament croisé antérieur avec une greffe de tendon rotulien associée à une plastie extra-articulaire 

externe. A propos de 138 cas. Rev. Chir. Orthop. 84: 712-727, 1998. 

NEYRET P, DONELL ST, DEJOUR H. 

Results of partial meniscectomy related to the state of the anterior cruciate ligament. Review at 20 to 35 

years. J.Bone Joint Surg (Br) 1993: 75: 36-40. 


NEYRET P, WALCH G, DEJOUR H. 

Intramural internal meniscectomy using the Trillat technic. Long term results of 258 operations. Rev. Chir. 

Orthop. 1988: 74: 637-46. 

NOYES FR, BARBER-WESTIN SD, NEWETT TE. 

High tibial osteotomy and ligament reconstruction for varus angulated anterior cruciate ligament-deficient 

knees. Am.J.Sports Med 2000: 28: 282-96. 

SELVA O, CHAMBAT P, TELOS WG, CASALONGA D, BONNIN M. 

Reconstruction du LCA avec un recul moyen supérieur à 10 ans. Rev. Chir. Orthop. 1997: 83. 

SHELBOURNE KD, GRAY T. 

Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the 

time of surgery : five to Fifteen-year evaluations. Am.J. Sports Med. 2000 vol 28 (4): 446-452. 

WU WM, HACKETT T, RICHMOND JC. 

Effects of meniscal and Articular Surface Status on knee Stability, Function and Symptoms after anterior 

cruciate ligament reconstruction. A long term Prospective Study. Am.J.Sports Med. 2002 vol 30(6): 845-850. 

Antivalgus Osteotomies. 

Giancarlo Puddu MD 

Clinica Valle Giulia. Roma 

I. Introduction: very often degenerative arthritis of the lateral compartment in the young or middle age 

active patient is due to a lateral meniscectomy and or to a femoro tibial malalignement in valgus that can 

be corrected with a high tibial or a distal femoral osteotomy. 

II. Indications: congenital valgus, early lateral compartment cartilage deterioration after a lateral meniscectomy, 

initial lateral arthrosis due to overweight, sport abuse and congenital valgus. 

III. Preoperative planning: can be made trough a standing radiography of both limbs which includes the 

femoral heads and the ankles. For the diagnose and indication it is very useful the P.A radiograph at 45 

degrees of knee flexion (fig. 1) and in the doubtful cases an MRI can help the decision (fig. 2). To provide a 

satisfactory clinical result, femoral or tibial osteotomy must restore the alignment of the lower extremity 

moving the mechanical axis to the 48-50% of the tibial plateau widht from medial to lateral (fig. 3). 

IV. Distal femoral osteotomy: we prefer the opening wedge lateral osteotomy, since it is easier and more 

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precise technique, using special femoral plates (Arthrex) with the same spacer of the HTO plates, but with 

seven holes, three distal and four proximal (fig. 4). . 

V. Surgical technique: a longitudinal skin incision is made on the lateral aspect of the distal third of the 

tigh, then the fascia lata is splitted longitudinally. An Homan retractor is inserted posteriorly and a special 

retractor anteriorly (fig. 5-6). Under fluoroscopy a guide pin is inserted obliquely four to six cm above the 

lateral joint line and directed medially toward the femoral origin of the medial collateral ligament (fig. 7). 

Preserving an hinge of intact cortical bone on the medial side, the osteotomy cut is open forcing the knee 

in adduction and with the wedge opener in site (fig. 8) or with a new tool "the osteotomy Jack". The chosen 

plate is positioned and fixed under a fluoroscopic control (fig. 9). Once the plate is secured to the femural 

cortex (fig. 10), the defect is filled with an autologous graft, allograft or bone substitute according with the 

preferences of the surgeon (fig. 11-12). 

VI. Medial closing wedge HTO: The correction can be obtained trough a medial closing wedge HTO if the 

resulting joint line has an obliquity not greater than 10 degrees (fig. 13-14). 

VII. Post-operative care: the knee is immobilized with a ROM brace in full extension that allows full range 

of motion when unlocked. Passive flexion extension in a CPM, quadriceps setting and straight leg raising 

exercises are begun the day after surgery. 

After the opening wedge distal femoral osteotomy partial weight bearing is allowed after 45-60 days and 

full weight bearing after 60-75 days. After the medial closing wedge HTO partial weight bearing is allowed 

after 30 days and full weight bearing after 45 days. 


VIII. Conclusions: dealing with degenerative arthritis in the young or middle age active patient with a valgus 

knee, prior any type of surgical treatment for the degenerated cartilage, it is a "must" to correct the 

femoro-tibial alignment. The Author generally prefers the opening wedge distal femoral osteotomy and in 

some special cases it is possible to make a closing wedge medial high tibial osteotomy. 

Bibliography: 

1. Brown GA, Amendola A : Radioghraphic evaluation and properative planning for high tibial osteotomies. 

In Operative Techniques in Sports Medicine W. B. Saunders. 2000, 8: pp2-14. 

2. Chambat P, Selmi TAS, Dejour D, et AL : Varus tibial osteotomy. In Operative Techniques in Sports 

Medicine. W.B. Saunders. 2000. 8: pp 44-47. 

3. Coventry MB: Proximal tibial varus osteotomy for osteoarthritis of the lateral compartment of the knee. J 

Bone Joint Surg 1987, 69A:32-38. 

4. Miniaci A, Grossmann SP, Jacob RP: Supracondylar femoral varus osteotomy in the treatment of valgus 

knee deformity. American J of Knee Surg. 1990. 2:65-73 

5. Puddu G, Franco V: Femoral antivalgus opening wedge osteotomy. In Operative Techniques in Sports 

Med. W.B. Saunders 2000. 8: pp56-60 

6. Rosenberg TD, Paulos LE, Parker RD et Al: The forty-five degree posteroanterior flexion weight-bearing 

radiograph of the knee. J Bone Joint Surg. 1988. 70A: 1479-1483. 

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TOTAL KNEE ARTHROPLASTY – NEW PERSPECTIVES ON DESIGN 

Thursday, March 13, 2003 • Aotea Centre, ASB Theatre 

Chairman: Paolo Aglietti, MD, Italy 

Faculty: David Barrett, MD, United Kingdom, Timothy Wright, PhD, USA, Kelly Vince, MD, USA, Johan Bellemans, 

Belgium, William Walsh, PhD, Australia, Mark Pagnano, MD, USA, and Fred Cushner, MD, USA 

New Perspectives on Design in Total Knee Arthroplasty 

Materials and Wear 

Timothy Wright, PhD 

Laboratory for Biomedical Mechanics and Materials 

Hospital for Special Surgery, New York, NY 


Wear is now recognized as a major threat to the longevity of metal on polyethylene total knee replacements. 

Retrieval, simulator, clinical, and numerical studies have taught us much about the modes of wear, 

the factors that affect them, and the stress conditions under which they occur. While this understanding 

should lead us to rational choices for alternate bearing materials aimed at improving wear resistance, the 

lack of a direct correlation between the amounts and type of wear and clinical performance hampers the 

process. Nonetheless, sufficient evidence exists to suggest the rationale and efficacy of several materials 

and fabrication techniques: 

• Hard bearing materials (ceramics, hard coatings, oxidized zirconium); 

• Elevated cross-linked ultra high molecular weight polyethylenes; and 

• Direct compression molded ultra high molecular weight polyethylene 

These alternatives must be considered in light of the problem that they are intended to address, the design 

and performance conditions under which they would be expected to be advantageous, and the disadvantages 

they may possess. Hard bearings, for example, would be expected to influence abrasive and adhesive 

wear mechanisms, but not markedly affect pitting and delamination types of wear. Similarly, elevated crosslinked 

polyethylenes should also improve abrasive and adhesive wear resistance (as has been shown when 

these material are used in THR acetabular components), but concern about their reduced fracture toughness 

has raised questions about their suitability. Direct compression molding has a long record of performing 

well clinically, and recent data suggest that thermal conditioning such as occurs with molding may 

provide improved wear resistance. More research is warranted, however, to create a more direct link 

between material properties and wear. Even with such research, long-term clinical use remains the only 

reliable method for assuring efficacy. 

General Reference: Wright TM and Goodman SB: Implant Wear in Total Joint Replacement: Clinical and 

Biologic Issues, Materials and Design Considerations. American Academy of Orthopaedic Surgeons, 

Rosemont, IL, 2001. 

Extraarticular tendon bone healing 

W.R. Walsh, PhD, Australia 

Biology of extraarticular tendon – bone healing 

• How does time influence the following factors 

o Mechanical properties 

o Growth factors and BMPs expression 

o Signal transduction - Smads 

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• Can we improve tendon-bone healing 

o Gene therapy 

o Non invasive stimuli 

• Rehabilitation 

• Ultrasound 

• Magnetic fields 

Fixed Bearing Cruciate Retaining Total Knee Arthroplasty 

Mark W. Pagnano, MD 

Department of Orthopedics 

Mayo Clinic 

Rochester, MN 

Whether to retain, sacrifice, or substitute for the posterior cruciate ligament remains controversial. There 

are theoretical advantages to each technique and the excellent long-term clinical results of each ensures 

that this controversy will continue. We will review the indications, technique, and results of cruciate retaining 

fixed bearing total knee arthroplasty. 


INTRODUCTION 

The controversy over retention or substitution of the posterior cruciate ligament continues. The excellent 

long-term results of total knee arthroplasties done with cemented condylar components of cruciatesacrificing, 

cruciate-substituting, and cruciate-retaining designs ensures that this debate will continue. An 

assessment of the theoretical issues and clinical results of knee arthroplasty assists in analyzing this controversy. 

Important new data from the fields of biomechanics, histology, gait analysis, radiology, and from 

the operating room have sharpened the posterior cruciate ligament debate. The interested reader can find 

a recent review article that extensively explores each of those issues.11 Historically, the potential advantages 

of posterior cruciate ligament preservation are seen as maintenance of the joint line, femoral rollback, 

proprioception, maintenance of a central contact point of articulation, and low shear stress on the 

bone-cement interface of the tibial component. The disadvantages of posterior cruciate ligament preservation 

are higher polyethylene stresses, a seesaw effect from femoral glide, difficulty in soft tissue balance, 

worse range of motion in some series, and the fact that posterior cruciate ligament retention is not always 

possible. 1 This review article will discuss the indications, technique, results, and complications of fixedbearing 

cruciate-retaining total knee arthroplasty. 

INDICATIONS 

There are certain situations where it is definitely advantageous to sacrifice the posterior cruciate ligament. 

The indications for a posterior cruciate ligament-preserving total knee arthroplasty are fixed flexion 

of less than 30∞, varus less than 20∞, and valgus less than 25∞; joint subluxation of no more than 1 cm; 

structurally intact posterior cruciate ligament; and technical ability of the surgeon. For patients with large 

fixed deformities, soft tissue balance may require sacrifice of the posterior cruciate ligament to facilitate 

proper soft tissue balancing. A surgeon's technical ability to balance the posterior cruciate ligament is 

important. A lax posterior cruciate ligament will not be functional but is preferable to an excessively tight 

posterior cruciate ligament. A tight posterior cruciate ligament will limit knee motion and may be a source 

of pain and abnormal polyethylene wear patterns. Contraindications to posterior cruciate ligament preservation 

are severe fixed deformities, technical inability to balance the posterior cruciate ligament, and 

anatomic abnormality of the posterior cruciate ligament, such as severe ligamentous degeneration and 

absent patella. 

TECHNIQUE 

Preservation and balance of the posterior cruciate ligament must be combined goals of surgery. The 

tibial attachment of the posterior cruciate ligament is located posterior and distal to the tibial plateau. 

The tibial attachment of the posterior cruciate ligament is vulnerable to injury during the tibial resection 

for total knee arthroplasty. Excessive bone resection from the proximal tibia (>1 cm) or a large posteriorly 

sloped cut may jeopardize the tibial attachment of the posterior cruciate ligament. The posterior cruciate 

ligament may be injured with a correct tibial resection by excessive posterior travel of the saw blade. 

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Placing an osteotome anterior to the posterior cruciate ligament during tibial resection will protect it. 

Once the tibial plateau bone has been removed, any remaining bone island anterior to the posterior cruciate 

ligament can be trimmed to allow placement of the tibial component. 

Balancing the posterior cruciate ligament can be difficult. A slightly lax posterior cruciate ligament is 

probably preferable to one that is excessively tight. Balance of the posterior cruciate ligament should be 

assessed after correction of any varus or valgus ligamentous imbalance. Varus or valgus imbalance can 

affect assessment of posterior cruciate ligament tension. Soft tissue balance always should be tested in 

extension and in flexion. The gap or space between the femoral and tibial cut surfaces should be within 1 

to 2 mm of each other in flexion and extension. Posterior cruciate ligament tension is assessed best with 

the trial total knee prosthesis in place. An excessively tight posterior cruciate ligament will result in (1) 

anterior translation of the tibia from beneath the femur; (2) anterior lift-off of the trial polyethylene from 

the tibia tray in flexion; and/or (3) displacement of the femoral component in flexion. A useful test of the 

relative balance of the posterior cruciate ligament is the POLO (for Pull-Out, Lift-Off) test introduced by 

Scott.2 In this test, a trial reduction is done with a stemless tibial trial and a curved tibial insert. The pullout 

portion of the test is done at 90∞ of flexion and confirms that the posterior cruciate ligament is not too 

loose if the tibial insert can not be subluxed (pulled-out) anteriorly from beneath the femur. The lift-off 

portion is done while putting the knee through a range of motion as much as 120∞ and ensuring that the 

tibial insert does not book open (lift-off) in flexion and indicate that the posterior cruciate ligament is too 

tight. Scott postulates that if the posterior cruciate ligament is not too loose and not too tight then it 

must be just right. 

If the posterior cruciate ligament is excessively tight, the tension can be decreased by several techniques. 

Increased tibial bone resection only is appropriate if the knee is tight in flexion and extension. If 

the knee is tight only in flexion, increasing tibial bone resection will leave the knee lax in extension, resulting 

in symptomatic instability. If the knee is tight only in flexion, the posterior slope of the tibial cut 

should be assessed. The tibia normally has a 3∞ to 7∞ posterior slope. The amount of posterior slope cut 

on the tibia will be dependent on the prosthetic design. Some implants have an inherent posterior slope 

in the articular geometry and will require less posterior slope than knees with a flat geometry in the sagittal 

plane. Increasing posterior slope for the tibial resection will relax the posterior cruciate ligament. 

Posterior tibial slope should not exceed 10∞ to avoid risk of injury to the tibial attachment of the posterior 

cruciate ligament. Posterior cruciate recession consists of selective release of the anterior fibers of the 

posterior cruciate ligament from their tibial attachment. Release of the anterior 10% to 20% of the posterior 

cruciate ligament will result in correct soft tissue balance. If greater than 75% of the posterior cruciate 

ligament is released, a posterior cruciate ligament-substituting prosthesis should be considered. The 

remaining 25% of the posterior cruciate ligament fibers may rupture with activity, leading to late instability.12 

If the posterior cruciate ligament is released or absent, the tibial tray should be more conforming 

because rollback does not occur. Therefore, the surgeon should match the constraints of the soft tissue 

with the inherent constraints of the knee system being used. 

RESULTS AND COMPLICATIONS 

Early ligament-retaining prostheses, such as the polycentric and geometric designs, were not able to 

provide predictable results. 

The Miller-Galante I prosthesis had a relatively flat articular geometry and multiple sizes. The objective 

was to reproduce normal knee kinematics. A study of 116 cemented prostheses at 3.5 years found 88% 

good or excellent results.16 The range of motion was 105∞. Reoperation was required in 9% of the knees, 

with revision in 6%. When inserted without cement the results with MG-I prosthesis have been termed 

problematic. Berger et al. recently reported the 11 year followup of 113 consecutive cementless Miller- 

Galante I total knees.3 Cementless femoral fixation in that study was deemed excellent while tibial components 

had a 6% rate of revision. The cementless metal-backed patella used in that series was poor with a 

30% rate of revision. Those authors now have abandoned cementless fixation in total knee arthroplasty. 

The posterior cruciate-sparing modification of the Total Condylar prosthesis was the Cruciate Condylar 

prosthesis. The same femoral component was used for the Total and Cruciate Condylar implants. The tibial 

component of the Cruciate Condylar differed from that of the Total Condylar by having a posterior cruciate 

recess posteriorly. One objective of the cruciate condylar was to encourage femoral rollback and 

motion.14 The long-term results of this design have been reported by multiple groups.5,8,13 A 9-year 

study of 144 knees found 95% good or excellent results.10 Mean knee motion was 106∞. Tibial radiolucent 

lines were present in 41%, of which 12% were progressive. Eight of the knees were failures. A review of 78 

knees in 63 patients followed for a mean of 10 years at the Mayo Clinic was done.13 Good or excellent 

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esults were achieved in 93% of knees. Mean flexion was 102∞. Radiolucent lines were present adjacent to 

57% of the knees. Using an end point of revision, survivorship was 96% at 10 years. There were no significant 

differences in survivorship, radiolucent lines, or knee scores between knees with an all-polyethylene or 

metal-backed tibial component. Complications consisted of deep sepsis in 1%, loosening in 1%, and 

supracondylar fracture in 3%. In yet another study of 42 knees followed at 11 years, 93% good or excellent 

results were achieved.5 The range of motion was 104∞. Incomplete radiolucent lines were observed in 

75%. The complication rate was 17% and the reoperation rate was 19%. 

The Kinematic condylar prosthesis had metal backing of the tibial component and separate right and 

left femoral components. The tibial plateau was flattened in the sagittal plane in an attempt to improve 

motion by encouraging femoral rollback. A study of 192 knees followed for a mean of 6 years found 88% 

good or excellent results.18 Mean knee motion was 109∞. Radiolucent lines were present adjacent to 40% 

of the tibial and 60% of the patellar components. Reoperation was done in 11 knees, of which four were for 

patellar loosening and one was for patellar fracture. In a study from the Mayo Clinic, 119 knees were evaluated 

at 10 years.9 Good or excellent results were achieved in 87%. Mean knee motion was 105∞. Joint line 

height was changed a mean of 1 mm. A 2-mm radiolucent line was identified adjacent to two patellar, one 

femoral, and one tibial component. Patellar component loosening was identified in six knees. Aseptic 

loosening of the tibial and femoral component occurred in two knees. Using an end point of revision, survivorship 

was 96% at 10 years. 

The Press Fit Condylar prosthesis was introduced with a keeled tibial component that was designed to 

resist offset loading while preserving tibial bone stock. A recent survivorship analysis of 1000 consecutive 

posterior cruciate retaining Press Fit Condylar knees revealed a 10-year survivorship free of mechanical failure 

of 98.7%.4 The Press Fit Condylar design is available in both cemented and cementless versions. A 

comparison of 51 cemented and 55 cementless Press Fit Condylar knees was done at 10 years.6 

Survivorship with revision as the end point was 96% for the cemented knees and 88% for the cementless 

knees. Knee Society scores for pain and function were 92 and 72 for the cemented knees and 88 and 66 

respectively for the cementless knees. Another 10-year followup study included 155 knees from an initial 

study group of 235 knees.17 Cementless fixation was used in more than half of the femoral components 

and less than 10% of the tibial components. Knee Society pain and function scores were 95 points and 84 

points, respectively. Survivorship to revision was reported as 92% at 10 years. 

The Anatomic Graduated Component prosthesis includes a one-piece metal-backed component with 

direct compression molded polyethylene. A multicenter study of 2001 Anatomic Graduated Component 

knees was done.15 The predominant diagnosis was osteoarthritis (91%) and the followup was from 3 to 10 

years with 71 knees having 10-year data. Knee Society pain and function scores were 75 and 86 respectively 

at last followup. A survivorship analysis (that excluded metal-backed patellar failures) predicted a 98% 10- 

year survivorship free of revision. A consecutive series of 387 knees done with the Anatomic Graduated 

Component design and using thin (4.4 mm) tibial polyethylene was reported at an average of 10 year followup. 

Survivorship with revision or loosening as the endpoint was 98.7% at 5 years, 95.4 percent at 10 

years and 94.3% at 15 years.10 

The Mayo Clinic experience with 11,606 primary total knee arthroplasties was presented at the 2002 

American Academy of Orthopaedic Surgeons annual meeting (Dallas). Of 8052 posterior cruciate-retaining 

total knee arthroplasties with a metal-backed tibial component, a 91% survivorship at 10 years was predicted. 

Therefore, the results of posterior cruciate-retaining prostheses appear durable. There appears to be 

little difference between metal-backed and all-polyethylene tibial components or between meniscal and 

fixed bearing implants. A longer duration of experience will be required to determine if these design differences 

affect long-term results. 


References 

1. Andriacchi TP, Galante JO: Retention of the posterior cruciate in total knee arthroplasty. J Arthroplasty 

3:S13-S19, 1988. 

2. Martin SD, Scott RD, Thornhill TS: Current concepts of total knee arthroplasty. J Orthop Sports Phys 

Therap 28:252-261, 1998. 

3. Berger RA, Jacobs JJ, Rosenberg AG, Barden RM, Galante JO: Problems with cementless total knee 

arthroplasty at eleven years follow-up (Abstract). J Arthroplasty 16:251, 2001. 

4. Berry DJ, Whaley A, Harmsen WS: Survivorship of 1000 consecutive cemented cruciate-retaining total 

knee arthroplasties of a single modern design: results at a mean of 10 years (Abstract). J Arthroplasty 

16:252, 2001. 

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5. Dennis DA, Clayton ML, O'Donnell S, et al: Posterior cruciate condylar total knee arthroplasty. Clin 

Orthop 281:168-176, 1992. 

6. Duffy GP, Berry DJ, Rand JA: Cement versus cementless fixation in total knee arthroplasty: Results at 10 

years of a matched group. Clin Orthop 356:66-72, 1998. 

7. Insall JN: Historical Development, Classification, and Characteristics of Knee Prostheses. In Insall JN, 

Windsor RE, Scott WN et al (eds). Surgery of the Knee. Ed 2. New York, Churchill Livingstone, 677, 1993. 

8. Lee JG, Keating EM, Ritter MA, Faris PM: Review of the all-polyethylene tibial component in total knee 

arthroplasty. Clin Orthop 260:87-92, 1990. 

9. Malkani AL, Rand JA, Bryan RS, Wallrichs SL: Total knee arthroplasty with the kinematic condylar prosthesis: 

A ten-year follow-up study. J Bone Joint Surg 77A:423-431, 1995 

10. Meding JB, Ritter MA, Keating EM, Faris PM: Total knee arthroplasty with 4.4 millimeters of tibial polyethylene: 

Average ten year follow-up study (Abstract). J Arthroplasty 16:252, 2001. 

11. Pagnano MW, Cushner FD, Scott WN: Whether to preserve the posterior cruciate ligament in total knee 

arthroplasty. J Am Acad Orthop Surg 6:176-187, 1998. 

12. Pagnano MW, Hanssen AD, Lewallen DG, Stuart MJ: Flexion instability after primary posterior cruciate 

retaining total knee arthroplasty. Clin Orthop 356:39-46, 1998. 

13. Rand JA: A comparison of metal-backed and all polyethylene tibial components in total knee arthroplasty. 

J Arthroplasty 8:307-313, 1993. 

14. Ritter MA, Gioe TJ, Stringer EA, Littrell D: The posterior cruciate condylar total knee prosthesis: A fiveyear 

follow-up study. Clin Orthop 184:264-269, 1984. 

15. Ritter MA, Worland R, Saliski J: Flat-on-flat, non-constrained compression molded polyethylene total 

knee replacement. Clin Orthop 321:79-84, 1995. 

16. Rosenberg AG, Barden RM, Galante JO: Cemented and ingrowth fixation of the Miller-Galante prosthesis. 

Clin Orthop 260:71-79, 1990 

17. Schai PA, Thornhill TS, Scott RD: Total knee arthroplasty with the PFC system: results at a minimum of 

ten years and survivorship analysis. J Bone Joint Surg 80B:850-853, 1998. 

18. Wright J, Ewald FC, Walker PS et al: Total knee arthroplasty with the kinematic prosthesis. J Bone Joint 

Surg 72A:1003-1009, 1990. 

Posterior Stabilized Knee Prostheses 

Kelly Vince MD 

General Principles 

Posterior stabilized (PS) prostheses were first introduced at the Hospital for Special Surgery in New York in 

1978 by John Insall and Al Burstein. The PS design featured a prominent tibial spine that articulated 

against a transverse cam on the femoral component. This prevented posterior dislocation in flexion (especially 

for the patellectomy patient) and mechanically enabled femoral "rollback". It eliminated"kinematic 

conflict", that resulted from retention of the posterior cruciate ligament with conforming articular surfaces. 

The PS design should be regarded as "semi-constrained" as it provides no stability to varus or valgus 

forces. 

New perspectives 

Three complications with early PS designs have largely been eliminated. Patellar fractures, complicated 7% 

of early cases. Modification of the trochlear groove and improved surgical technique have decreased this 

dramatically. Entrapment of rubbery scar on the deep surface of the quadriceps tendon, against the anterior 

edge of the trochlear groove with extensor, the so-called patellar clunk, has also largely been eliminated. 

Dislocation of the spine and cam mechanism occurred after a design modification in 1989. Attention to the 

flexion gap and design eliminated this problem. 

Two recent studies identified wear on polyethylene spine, It is unlikely however that this is a significant 

source of debris. The spine can also impinge on the anterior edge of the femoral component with hyperextension 

and may even break off producing late instability. Some of this data has probably been misinterpreted. 

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In several closely followed groups of PS implants, osteolysis was not observed in either the earliest, nonmodular 

PS designs, or in the early modular version. An isolated group with severe osteolysis has emerged. 

In some cases, with bilateral arthroplasty only one side has been affected. Shelf life and sterilization 

method have not been implicated. 

Posterior stabilization can be provided by highly conforming articulations (deep dished) or exaggerated 

anterior "lipped" polyethylene. These have the advantage of easy surgical conversion and decreased 

expense, but without the advantage of femoral rollback. As the complexity of femoral rollback, especially in 

deep flexion, is appreciated, mobile bearing, PS implants have been developed. 

The Influence of Kinematics on Maximal Flexion after TKA 

Prof. Dr. J. Bellemans 

University Hospital Pellenberg 

Katholieke Universiteit Leuven 

Belgium 

Although most surgeons agree that the functional results obtained with modern total knee arthroplasty are 

acceptable, it is clear that even with the most recent designs it is still impossible to duplicate the behaviour 

and functional performance of a normal knee. 


Recent kinematic studies have shown that modern TKA designs consistently provoke aberrant kinematics 

compared to the normal knee, mainly due to the absence of the ACL and the inability to maintain a functional 

PCL. 

With regard to roll-back, PS cam-post designs appear to perform better than PCL retaining knees, but only 

in deeper degrees of flexion, usually only beyond 90 degrees. 

Whether it is strictly necessary to try to obtain normal kinematics with our TKA designs, is still an open 

debate. 

It is clear however that the aberrant kinematics we have noted with the current designs, are the direct 

cause of the flexion limit we see in many of our patients. 

Furthermore they probably also are the basis for many of the discomforts associated with modern TKA, 

such as difficulties in stair descent, chair rise, pivoting activities, frust instabilities, etc. 

With regard to these issues, I believe there are two potential directions to improve our current TKA 

designs; (1) by introducing the concept of guided-motion (intrinsic mechanism), or (2) by maintaining or 

restoring the (extrinsic) determinants of kinematics, i.e. the cruciate ligaments, the joint configuration, and 

the extraarticular structures. 

Patella Design in TKA 

Fred Cushner, MD 

ISK Institute, New York, N.Y. USA 

The complication rate in TKA from the resurfaced patella is well described in the literature. In fact, many 

authors will leave the patella unresurfaced in an attempt to avoid patella complications following TKA. This 

presentation will focus on not only the complications but also the design issues that can decrease the 

occurrence of these complications. Design Issues for both primary as well as revision cases will also be 

reviewed. 

The initial discussion will focus on the complications that may be related to design issues. Studies 

describing synovial entrapment as well as "patella clunk" will be discussed as well as the modifications that 

have occurred with the PS design to eliminate these complications. Failure of metal backed patella will 

also be reviewed and some attention will be given to the newer metal backed designs. Optimal patella 

thickness and shape will also be reviewed. 

3.85

Current options in regards to the patella will be presented. The success of onset versus inset patella will 

be reviewed as will the research looking at the benefits of a central peg versus the three-lug design. 

Optimal patella thickness of the component will be reviewed as will proper patella placement as it pertains 

to design features. 

Design features of the trochlea will also be reviewed. The benefits of symmetrical versus asymmetrical 

designs will be discussed as will other design features such as built in external rotation, trochlea depth, 

trochlea alignment, and overall component alignment, 

The revision setting with it’s inherent bone loss presents the surgeon with a difficult problem. Surgical 

options with new patella designs that compensate for bone loss will be discussed 

New Perspectives on Design in Total Knee Arthroplasty 

Materials and Wear 

Paolo Aglietti, MD 

First Orthopaedic Clinic, 

University of Florence, Italy 


Balance between conformity and constraint is crucial to allow kinematics freedom maintaining good wear 

properties. The emergence of the mobile-bearing articulating poly surfaces in TKR reflects the efforts to 

optimised wear while dealing with complex function. Mobile bearing designs have not yet proven to provide 

better results and increased function but long-term clinical experience and laboratory data from knee 

joint simulators seem to suggest that mobile bearing designs have an advantage in reducing polyethylene 

wear (particularly pitting and delamination). Laboratory wear studies investigated correlations between 

pattern of motion of articular surfaces and wear. New mobile bearings with conforming "low-stress" articular 

geometries and motion at the undersurface create an additional challenge in minimizing top-surface 

and back-surface wear. Comparative clinical an laboratory data on wear and stresses in fixed and mobile 

bearings are showing a trend toward less amount of wear, in particular delamination, for mobile bearings. 

Errors in rotational component positioning may affect many functions of TKR especially the patello-femoral 

tracking. Mobile bearing tibial designs may be more forgiving than fixed bearing designs to minor rotational 

malalignments. 

3.86


TENDON INJURIES IN FOOTBALL (SOCCER) 

Thursday, March 13, 2003 •` Carlton Hotel, Carlton I 

Chairman: Alberto Pienovi, MD, Argentina 

Faculty: Ramon Cugat, MD, Spain and Sergio Montenegro, MD, Chile 

Tendinopatia Rotuliana – 

Aquiliana en deportista. 

Dr Sergio Montenegro 

Clínica Arauco– Clínica Dávila 

Santiago-Chile 

Patellar-Achilles 

Tendinopathy in soccer placer. 

Sergio Montenegro MD. 

Arauco Clinic-Davila Clinic 

Santiago-Chile 

Diapositiva 2: 

Slide 2. 


TENDÓN 

• Estructura anatómica de tejido conectivo fibroso 

denso y regular que ancla el músculo al hueso. 

• Funciones: 

–Transmite fuerza muscular al esqueleto con mínima 

pérdida de energía, absorbiendo golpes bruscos 

para evitar el daño muscular. 

–Rol de propiocepción. 

Diapositiva 3 

TENDÓN: TIPoS 

• Intrasinoviales 

–Tendones flexores 

• Extrasinoviales 

–T. Cuadricipital, rotuliano, aquiliano. 

Diapositiva 4. 

Tendón 

• Tejido compuesto: 

–Colágeno tipo I ( 85% peso seco del t.) 

–Colágeno tipos III, IV, V, VI, XII 

• Proteoglicanos: (polisacáridos proteicos) 

• Decorina (principal.) 

• Biglicano 

• Lumicano 

• Fibromodulina. 

• PGs : compuestos por glicosaminoglicanos 

(polímeros disacáridos. 


Tendón : Bioquímica 

• PGs en tendón: 

-Rol importante en las fibras de colágeno. 

-Rol en separar las bandas de fibras 

-Así disminuir el stress de ruptura. 

• Fibronectina (composición de la matriz celular) 

Tendon 

Anatomic structure made of connective, fibrous, 

dense tissue, which anchors muscle to bone. 

Functions: 

- It transmits muscular force to the skeleton with 

minimum loss of energy, absorbing abrupt blows 

to avoid muscular damage. 

- Propioceptive roll. 

Slide 3 

Tendon Types 

• Intrasinovial 

-Flexing Tendons 

• Extrasinovial 

-Quadricipital tendon, Patellar tendon, Achilles 

tendon. 

Slide 4 

Tendon 

Composition of the Tissue: 

- Collagen type I (85% dry weight of the total) 

- Collagen types III, IV, V, VI, XII 

- Proteoglycan: (polysaccharide proteins) 

- Decorin (principal) 

- Biglicane 

- Lumican 

- Fibromodulin 

- Proteoglycan (PGs): made up of glicosaminoglicans 

(polymeric disacharides. 

Slide 5: 

Tendon: Biochemistry 

• Proteoglycans (PGs) in tendon: 

- Important Roll in collagen fibers. 

- Roll in separating the fiber bands 

- Thus to diminish stress of rupture 

• Fibronectin (composition of the cellular matrix) 

3.87

-Rol importante en la adherencia de la matriz celular 

• Fibras elásticas: (dentro del Tendón) 

-Capacidad de absorción de golpes. 

-Mantención del patrón ondulante del colágeno. 

- Important roll in the adhesion of the cellular 

matrix. 

• Elastic Fibers: (within the tendon) 

- Capacity of absorption of traumas. 

- Maintaining of the wave pattern of collagen. 



TENDÓN 

BIoLoGÍA Y BIoMECÁNICA 

• Las propiedades MECÁNICAS están determinadas 

principalmente. por el colágeno: 

–Resistencia tisular: (directamente proporcional): 

• Contenido total de colágeno 

• Densidad de uniones (cross-links) estables. 

• organización del colágeno. 

• Diámetro fibrilar. 

–Fuerzas de Tensión: (inversamente proporcional.): 

• Contenido de colágeno tipo III. 

• Radio PG/colag. 

Slide 6: 

Tendon 

BIOLOGY And BIOMECHANICS 

The mechanical properties are determined mainly 

by collagen: 

-Tissue Resistance:(directly proportional) 

-Total contents of collagen 

-Density of unions (cross-links) stable 

-Organization of the collagen 

-Fibrillar Diameter: 

-Force Tension: (inversely proportional.) 

Contents of collagen type III. 

- Ratio Proteoglycan /collagen 

3.88 

Diapositivas: 7 

TENDINoPATIAS 

• Causas : carga de entrenamiento excesivo. 

–Con relación a: 

• Biotipo atlético. 

• Capacidad metabólica. 

• Correcta ejecución de ejercicios. 

• Apoyo correcto del pié. 

• Zapatilla adecuada. 

• Balance muscular (evaluación isokinética) 

• Superficie de entrenamiento. 

• Clima. 


LESIÓN TENDINoSA 

• Directa 

- Contusión 

- Laceración 

• Indirecta 

- Sobrecarga x tensión aguda 

- Lesión unión M-T. 

- Fractura por avulsión. 

• Lesiones por sobreuso: 

- Microtrauma repetitivo 


LESIÓN TENDINoSA 

• Degenerativa: 

- Tendinosis: 

• T. De Aquiles porción libre. 

• T. Patelar 

• Entesopatía : (más frecuente. T. Aquiles) 

- Haglund 

• Rotura (parcial o completa). 

• Inflamatoria : Peritendinitis o paratenonitis. 

• Bursitis: traumática, séptica, Enfermedad 

Slide: 7 

TENDINOPATHIES 

Causes: excesive training load. 

-In relation to: 

- Athletic Biotype. 

- Metabolical Capacity. 

- Correct performance of exercices. 

- Correct leaning of the foot 

- Adequate sport shoe. 

- Muscular Balance (isokinetic evaluation) 

- Training Surface 

- Climate 

Slide 8: 

Tendon Injury: 

Direct: 

-Contusion 

-Laceration 

Indirect: overloading by acute tension. 

M-T union injury. 

Fracture by avulsion 

Injuries caused by overuse: 

-Repetitive microtrauma 

Slide 9 

Tendon Injury: 

• Degenerative: 

-Tendinosis: 

• Achilles Tendon free portion 

• Patellar Tendon 

• Enthesopathy: (more frequent Achilles Tendon) 

-Haglund 

Rupture (partial or complete). 

Inflammatory: Peritendinitis or paratenonitis. 

Bursitis: traumatic, septic,

Sistémica. 


LESIoNES X SoBREUSo 

• Más frecuente en deportes de alta exigencia: 

–Carrera, ciclismo, remo, natación. 

• Deportes que requieren aplicación de movimientos 

explosivos: 

–Volleyball, Raquetball, Basquetball, Golf, Tenis. 

Diapositiva: 11 

LESIoNES X SoBREUSo 

• LESIoNES Centro Alto Rendimiento (2001- 

2002): 1320. 

–Lesiones tendinosas :355 (26.9%) 

Systemic disease 

Slide 10: 

INJURIES CAUSED BY OVERUSE 

More frequent in high demanding sports: 

Racing, cycling, rowing, swimming; 

sports that require applying explosive movements: 

-Volleyball, Raquetball, Basquetball, Golf, Tennis. 

Slide: 11 

Injuries by overuse. 

High Performance Center injuries (2001-2002): 

1320. 

-Tendon Injuries: 355 ( 26.9%) 

–Lesiones musculares :291 (22.1%) 

–Fracturas por stress :22 ( 1.6%) 

-Muscular Injuries : 291 (22.1%) 

-Fractures caused by stress: 22 (1.6%) 


–Periostitis :54 ( 4.1%) 

–otras (45.3%) 

598 (54.7% 


LESIoNES x SoBREUSo 

• 50 - 60% de todas las lesiones deportivas. 

• Se deben a una falla en la adaptación de las 

células y la matriz extracelular al uso repetitivo y 

cargas submáximas. 

• La capacidad adaptativa y reparativa del T. se 

puede sobrepasar cuando es estirado repetidamente 

más de 4 - 8% de su longitud original. 


LESIoNES TENDINoSAS 

• MECANISMoS: 

–1.- Stress aplicado al tendón dentro de su capacidad 

de carga fisiológica, y que excede la capacidad 

adaptativa basal de las estructuras, o, es tan frecuente 

que no hay tiempo suficiente para que el 

tejido tenga la capacidad de lograr una reparación 

intrínseca. 


LESIoNES TENDINoSAS 

• MECANISMoS: 

–2.- Aplicación brusca de carga única pesada que 

produce una lesión inicial, que debilita la estructura 

del tendón y subsecuentemente, cargas fisiológicas 

repetitivas, no permiten la maduración 

de la cicatrización del tejido. 

-Periostitis: 54 (4.1%) 

-Others: (45,3%) 

598(54.7%) 

Slide 12: 

Injuries by overuse. 

• 50 - 60% of all the sport injuries. 

• They are due to a fault in the adaptation of the 

cells and the extra cellular matrix to the repetitive 

use and submaximal loads. 

• The adaptive and repairing capacities of the tendon 

can be exceeded when it is stretched repeatedly 

more than 4 - 8% of its original length. 

Slide 13: 

Tendon Injuries: 

• Mecanisms: 

-1. - Stress applied to the tendon within its physiological 

lifting capacity, and that exceeds the basal 

adaptive capacity of the structures, or, it is so frequent 

that there isn’t enough time for the tissue to 

have the ability to obtain an intrinsic repair. 

Slide: 14 

Tendon Injuries: 

• Mecanisms: 

2. -Abrupt application of heavy unique load that 

produces an initial injury, that weakens the structure 

of the tendon and that, subsequently repetitive 

physiological loads, do not allow the maturation 

in the healing of the tissue. 

3.89


HISToPAToLoGÍA 

• TENDINITIS 

• TENDINoSIS 

• PARATENDINITIS 

• RUPTURAS PARCIALES 

• oTENDINoPATÍA: término genérico, para lesiones 

en o alrededor del tendón por sobreuso 

Slide 15: 

HISTOPATHOLOGY 

• TENDINITIS 

• TENDINOSIS 

• PARATENDINITIS 

• PARTIAL RUPTURES 

• TENDINOPATHY: generic term, for injuries in or 

around the tendon by overuse 



TENDINoSIS 

• Degeneración intrínseca tendinosa sin signos 

clínicos o histológicos de INFLAMACIÓN intratendinosa. 

• No siempre es sintomática (30% personas > 35 

años). 

• Puede debutar con la ruptura del tendón. 

• ¿Porqué en algunas personas produce dolor, 

que llegue a una indicación operatoria? 

• ¿Por qué en otras es tan asintomático, que 

llega a causar ruptura? 

Slide 16: 

TENDINOSIS 

• Intrinsic tendinose degeneration without clinical 

or histological signs of intratendon INFLAMMA- 

TION. 

• It not always is symptomatic (30% people > 35 

años). 

• Can make a debut with the rupture of the tendon. 

• Why is it so painful, in some people that it leads 

to a surgical recommendation? 

• Why in others, it’s so painless, that it leads to 

rupture? 

3.90 

Diapositivas 17: 

-SoBRECARGA REPETITIVA SoBRE TENDÓN 

-Alteración Función celular 

-Alteración Actividad Metabólica 

- Respuesta reparativa no efectiva 

-INFLAMACIÓN 

-Liberación de: PGs, citoquinas 

enzimas citolíticas 


TENDINoSIS 

• Afecta todos los componentes del tendón: 

(colágeno, fibroblastos, matriz extracelular). 

• Colágeno: 

– Lisis de fibras de colágeno. 

– Pérdida de orientación paralelismo fibras. de 

colágeno. 

– Disminución de la densidad del colágeno. 

– Microrupturas con depósitos de: Glóbulos Rojos, 

fibrina, fibronectina. 

– ondulaciones irregulares de fibras. de colágeno. 

– Aumento. Colágeno tipo III (reparación). 

– Disminución. birefrigencia ( Mo con luz polarizada). 

– Áreas de proliferación angioblástica (hiperplasia 

angiofibroblástica (Nirschl, 1979): 

• Neovascularización y aumento de celularidad. 


TENDINoSIS 

• Patrones de degeneración del colágeno: 

– Hipóxica 

– Hialina 

– Mucoide o mixoide 

Slide 17: 

-REPETITIVE OVERLOAD ON THE TENDON: 

-Alteration of Celular Function 

-Alteration of Metabolic Activity 

-Non-efective repairing answer 

-INFLAMMATION 

-Liberation of: Proteoglycans, cytokines cytolitical 

enzimes. 

Slide 18: 

TENDINOSIS 

• It afects all the components of the tendon: (collagen, 

fibroblasts, extracelular matrix). 

• Collagen: 

- Lysis of collagen fibers. 

- Loss of parallel direction in fibers of collagen. 

- Diminution of the density of the collagen. 

- Microruptures with deposits of: Red globules, 

fibrin, fibronectin. 

- Irregular fiber waves of collagen. 

- Increase collagen type III (repair). 

- Diminution birefrigerence (Optic Microscope 

with polarized light). 

- Areas of angioblastic proliferation (angiofibroblastic 

hyperplasia (Nirschl, 1979): 

• Neovascularization and increase of cellularity. 

Slide 19: 

TENDINOSIS 

• Patterns of degeneration of collagen: 

- Hypoxemia 

- Hyaline 

- Mucoid or mixoid

– Fibrinoide 

– Lipomatosa 

– Calcificaciones, fibrocartilaginosa y metaplasia 

ósea. 

Diapositivas 20: 

TENDINoSIS 

• Es el resultado final de un Nº de sutiles procesos 

patológicos con diferentes manifestaciones 

histológicas. 

• Se puede asociar a paratenonitis. 

- Fibrinoid 

- Lipomatous 

- Calcifications, fibrocartilaginous and bone metaplasia. 

Slide 20: 

TENDINOSIS 

• It is the final result of a number of subtle pathological 

processes with different histological manifestations. 

• It can be associated to paratenonitis. 


TENDINoSIS 

FACToRES ETIoLÓGICoS 

• Hipoxia tisular: Trauma repetitivo --> lesión 

microvascular. 

• Radicales libres de oxígeno --> lesión tisular. 

• Ejercicio --> aumento de temperatura intratendón 

(43-45ºC) es > que la que soportan los 

fibroblastos. 

• Edad. 

• Inmovilización 

• Hormonas (E2). 

• Drogas (corticoides, ATB fluoroquinolonas) 

alteran la matriz. 

Slide 21: 

TENDINOSIS: 

ETHIOLOGICAL FACTORS 

• Tissue Hypoxemia: Repetitive trauma --> injury 

in the microvascular structure. 

Free Radicals of Oxygen --> tissue injury. 

• Exercise --> increase of the intratendon temperature 

(43-45ºC) is > than the one that supports 

fibroblasts. 

• Age. 

• Inmovilization 

• Hormones (E2). 

• Drugs (corticoids, antibiotics fluoroquinolones) 

alter the matrix. 



TENDINoSIS 

FACToRES EXTRÍNSECoS 

• Inestabilidad articular: (hombro - m. rot.). 

• Mal alineación: 

– pronación de el tobillo 

– genu valgo 

– Aumento anteversión femoral. 

• Disminución de flexibilidad. 

• Debilidad muscular. o desbalance muscular. 

• Sobrepeso. 

• Tipo de carga (tensión, compres.,etc). 

• Patrón de carga (concéntrico, excéntrico) 

• Magnitud de la fuerza (única, repetida). 


TENDÓN EFECTo DE INMoVILIZACIÓN 

• Disminuye su fuerza tensil. 

• Disminuye resistencia. 

• Disminuye peso total. 

• A un mes: 

– Disminución de: 

• la celularidad 

• organización de fibras. de colágeno 

• Diámetro de las fibras. de colágeno. 

• Uniones de colágeno. 

• Contenido de agua y de PGs se altera. 

• No está claro el mecanismo por el cual ocurre y 

si está o no mediado por células. 

Slide 22: 

TENDINOSIS. 

EXTRINSECAL FACTORS 

• Articular Instability to: (shoulder - patellar 

movement.) 

• Bad alignment: 

- pronation of the ankle 

- genu valgo 

- Increase in femoral anteversion. 

• Diminution of flexibility. 

• Muscular Weakness or muscular inbalance. 

• Overweight. 

• Type of load (tension, compression, etc). 

• Pattern of load (concentric, excentric) 

• Magnitude of the force (unique, repeated). 

Slide 23: 

TENDON INMOVILIZATION EFECT 

• Diminishes its tensile force. 

• Diminishes resistance. 

• Diminishes its total weight. 

• To a month: 

- Diminution of: 

• cellularity 

• Organization of collagen fiber. 

• Diameter of the fibers of collagen. 

• Unions of collagen. 

• The contents of water and proteoglycans is 

altered. 

• The mechanism by which it happens is not clear 

3.91

and if it is or not mediated by cells. 


TENDoN 

EFECTo DE REMoVILIZACIoN 

• Recuperación de las propiedades bioquímicas. y 

biomecánicas. 

• Aceleración de la síntesis de colágeno y de las 

uniones. 

MoVILIZACIÓN PRECoZ MUY IMPoRTANTE PARA 

MINIMIZAR EFECToS ADVERSoS. 

Slide 24: 

Tendon 

REMOVILIZATION EFECT 

- Recovery of biochemical and biomechanical 

properties. 

- Accerelation of the synthesis of collagen and of 

the unions 

EARLY MOVILIZATION IS VERY IMPORTANT TO 

DIMINISH ADVERSE EFFECTS. 



TENDÓN 

CAMBIoS CoN LA EDAD 

• Aumenta contenido de colágeno insoluble. 

• Aumento. maduración de uniones de colágeno. 

• Aumento. diámetro de fibras de colágeno. 

• Disminuye. turn over del colageno. 

• Disminución contenido de agua y PGs. 

• Disminución. Celularidad y vascularización. 

• Desde 3a década (¿disminución? Actividad física?). 

• Si se agregan calcificación. o degeneración. 

Mucoide. 

• > susceptibilidad de lesión y < capacidad. de 

cicatrización. 

Slide 25: 

TENDON 

Aging Changes 

• The contents of insoluble collagen increases. 

• Increasing in the maturation of the unions of collagen. 

• Increasing in the diameter of the fibers of collagen. 

• The turn over of collagen decreases. 

• The contents of water and Proteoglycans 

decreases. 

• Diminution of cellularity and vascularization. 

• From the 3rd decade (diminution of physical 

activity?). 

• Calcification and Mucoid degeneration are 

added. 

• There is more susceptibility of injury and less 

capacity of healing. 

3.92 


TENDÓN 

CAMBIoS CoN LA EDAD 

• Estudios experimentales sugieren que el mantener 

el ejercicio hace más lenta estas alteraciones 

bioquímicas. 

Rodeo S.A, Isawa K. (oKU, AAoS, Sp Med 2) 


LESIoNES TENDINoSAS CLASIFICACIÓN 

• 1.-Según sitio anatómico: 

– Unión M-T 

– osteotendinoso (tenoperiostal) 

(tendinopatías de inserción). 

– En el tejido. Tendinoso. 

• 2. - Patrón histopatológico. 

• 3. - Nivel funcional. 


LESIoNES TENDINoSAS CLASIFICACIÓN 

• 3. - Nivel funcional: 

INTENSIDAD DEL DEPoRTE NIVEL 

SINToMAToLoGÍA. DEPoRTE 

Leve 1 Sin dolor Normal 

2 Dolor en ejerc. extremo, 

desaparece sin actividad. 

Slide 26: 

TENDON 

Ageing Changes 

• Experimental researches suggest that maintaining 

exercise make these biochemical alterations 

slower. 

Rodeo S.A., Isawa K. (OKU, AAOS, Sp Med 2) 

Slide 27: 

TENDON INJURIES: CLASIFICATION 

• 1-According to anatomical site: 

- Muscular –tendon union 

- Osteotendinous (tenoperiostal) (tendinopathies 

of insertion). 

- In the tendinose tissue. 

• 2. - Histopathological Pattern. 

• 3. - Functional Level. 

Slide 28: 

TENDON INJURIES CLASIFICATION 

• 3. - Functional Level: 

SPORTS 

INTENSITY LEVEL SYMTOMATOLOGY. 

Mild 1 No pain 

2 Pain in extreme sport, 

disappears without activity

Moderado 3 Duele 1-2 hrs. post-ejercicio 

4 Dolor aumenta. con cualquier 

Actividad y dura 4-6 hrs. 

Severo 5 Dolor inmediato dura 12-24 hrs. 

6 Dolor actividad. diaria 


LESIoNES TENDINoSAS DIAGNoSTICo 

• Rx. 

• Ecotomografía 

• TAC 

• RNM 

Moderate 3 It hurts for 1-2 hrs. after exercise 

4 Pain increases with any activity 

and lasts 4-6 hrs. 

Severe 5 Immediate pain lasts 12-24 hrs. 

6 Pain in daily activity 

Slide 29: 

TENDON INJURIES DIAGNOSIS 

• RADIOGRAPH 

• ULTRASONOGRAPHY 

• CT scan 

• MRI 

Diapositiva 30 

PAToLoGÍA TENDINoSA ECoGRAFÍA 

-Ventajas 

Desventajas 

** bajo costo ** alta inversión inicial 

** acceso a cualquier tend. ** experiencia 

** estudios superficiales ** resultados operador- 

** dinámico e interactivo dependiente 

** permite comparar ** artefactos (simulan 

** uso Doppler-color pato-logía) 

y angio de poder ("Powerangio") 

Slide 30: 

TENDON PATHOLOGY ULTRASONOGRAPHY 

Advantages 

Disadvantages 

** low cost ** high initial investment 

** access to any tendon ** experience 

** superficial studies ** results operating- 

** dynamic and interactive dependant 

** allows to compare ** artifacts (simulate 

** use Doppler-color and pathology) 

“Power-angio”) 



Tendinosis Rotuliana 

• Rodilla del saltador. 

• Típica lesión por sobrecarga. 

• Atletas que someten aparato. extensor a 

movimiento. intensos y repetidos : (carreras explosivas) 

– Volleyball, Basquetball, Salto alto y largo. 

• Más frecuente. en hombres entre 18 y 25 años. 

• Localización: (Ferretti A, 1986) 

– Inserción proximal T. rotuliano: 65% 

– Inserción distal cuádriceps: 25% 

– Inserción distal T. rotuliano : 10% 



TRATAMIENTo GENERAL 

• AINE / AIES 

• Fisio - KNT 

• Crioterapia post-ejercicio. 

• ondas de choque 

• Brace de tendón rotuliano. 

• Rodillera con refuerzo infrapatelar. 


TENDÓN RoTULIANo 

TRATAMIENTo QUIRÚRGICo 

• PASoS: video artroscopia asociada–Resección 

paratendón. 

–Liberación tendón e incisiones de descarga 

(tenotomías longitudinales) y escarificación (resec- 

Slide 31: 

Patellar Tendinosis 

• Jumping knee 

• Typical injury by overload. 

• Athletes who put the extensor apparatus under 

intense and repeated movements: (explosive 

races) 

- Volleyball, Basquetball, High Jump and Long Jump. 

• Its more frequent in men between 18 and 25 

years old. 

• Location: (Ferretti To, 1986) 

- Proximal Insertion of the patellar tendon.: 65% 

- Distal insertion of quadriceps: 25% 

- Distal insertion of Patellar Tendon: 10% 

Slide 32: 

Patellar Tendinosis 

GENERAL TREATMENT 

• NSAID/SAID 

• Physical therapy 

• Post-excercise Cryotherapy 

• Shock wave therapy 

• Patellar tendon Brace. 

• Knee protector with infrapatellar reinforcement. 

Slide: 42 

PATELLAR TENDON 

SURGICAL TREATMENT 

• Steps: knee arthroscopy associated - 

Paratendon resection. 

-Releasing of the tendon and incisions of unloading 

(longitudinal tenotomies) and scrafication 

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ción áreas degenerativas). 

–Resección peritenon y adherencias. 

–Resección sinovial alterada. 

–Perforaciones rótula o tibia, resección ósea– 


RESULTADoS 

• 40 Pacientes - 44 tendones. 

• Seguimiento X: 25 m (rango 3 - 60 meses) 

• Sexo: H: 36 M: 4 

• Edad : X: 28 años (rango: 17 - 46). 

• Intervenciones previas: 

–Abierta : 0 

–Artroscópica : 4 

(resection of degenerative areas). 

-Peritenon removing and adhesion removals. 

-Synovial resection altered. 

-Drillings in patella or tibia, bone resection 

Slide 47 

RESULTS 

• 40 patients - 44 tendones. 

• Follow up durring: 25 months (rank 3 - 60 months) 

• Sexo: M: 36 W 4 

• Edad: X: 28 years (rank: 17-46) 

• Previous surgeries: 

-Open: 0 

-Arthroscopics: 4 



RESULTADoS 

• Localización:–Polo proximal de rótula: 3 ( 

6,8%) 

–Polo distal de rótula: 33 (75,1%) – 

tercio medio del tendón: 5 (11,3%) 

–Inserción distal en tibia: 3 (6,8%) 

Slide 48 

RESULTS 

• Localization:- Proximal Pole of patella: 3 (6,8%) 

- Distal Pole of patella: 33 

(75,1%) – Third middle portion of the tendon: 5 

(11,3%) 

- Distal insertion in tibia: 3 (6,8%) 

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RESULTADoS 

• Deportes : 

–Fútbol : 11 (1 árbitro) 

–Atletismo : 5 ( 2 maratón) 

–Basketball : 4 

–Rugby : 3 

–Patín carrera : 4 

–Pesas : 4 

–Ciclismo : 2 

–Tenis : 3 

–Volleyball : 3 

–Hockey : 1 

–Sin deporte : 4 


RESULTADoS 

• Retorno deportivo: 

–SÍ: 34 (T) 85% No: 6 (T) 

–Tiempo promedio : 4,7 meses. 

–Nivel competitivo : 

• Igual : 30 

• Menor : 4 


- RESULTADoS 

- Complicaciones : 

- Precoces : 

- Hematoma herida: 3 

- Infección superficial: 0 

- Infección profunda: 0 

- Tardías : 

- Disestesias zona opuesta.:12 

- Dolor anterior en cuclillas: 0 

Slide 49: 

RESULTS 

• Sports: 

-Soccer: 11 (1 umpire) 

-Athletics: 5 (2 marathon) 

-Basketball: 4 

-Rugby: 3 

-Roller skate racing: 4 

-Weights: 4 

-Cycling 2 

-Tennis: 3 

-Volleyball: 3 

-Hockey: 1 

-Without sports: 4 

Slide 50: 

RESULTS 

• Sports Return: 

-YES : 34 (T) 85% NO: 6 (T) 

- Average Time : 4.7 Months 

-Competitive level: 

• Equal : 30 

• Minor : 4 

Slide 51: 

RESULTS 

- Complications: 

- Early: 

- Hematoma of the surgical incision: 3 

- Superficial Infection: 0 

- Deep Infection: 0 

- Late complications : 

- Dysesthesia opposite zone.:12 

- Ventral Pain in haunches: 0 -

- Reoperaciones: 0 

- Reinterventions: 0 

Frame 56: 


REINTEGRo ACTIVIDAD FÍSICA 

• Ausencia total de dolor 

• Movilidad articular de rodilla normal. 

• Flexibilidad muscular-tendinosa mejor que antes 

de la cirugía. 

• Equilibrio isokinético Fuerza 1-extensores de 

rodilla. 

• Déficit isokinético < al 10% con el segmento contralateral. 

• Capacidad. aeróbica normal para enfrentar la 

actividad. Física. 

• No sentir ningún tipo de temor al realizar actividad 

física. 


LESIÓN TENDINoSA PREVENCIÓN 

• Acondicionamiento físico. 

• Calentamiento previo al ejercicio. 

• Elongación pre y post actividad. 

• Evitar ejercicios unidireccionales repetidos. 

• Adaptación al terreno. 

• Equipo adecuado. 

Slide 56: 

PATELLAR Tendinosis 

RETURN TO FISICAL ACTIVITY 

• Total absence of pain. 

• Articular mobility of knee normal 

• Muscular- tendinose flexibility better than before 

the surgery. 

• Isokinetic balance strength F1- knee extensors. 

• Isokinetic deficiency < at 10% with the opposite 

segment. 

• Normal aerobic capacity to do physical activity. 

• No to feel any kind of fear while doing physical 

activity. 

Slide 68: 

TENDON INJURY PREVENTION 

• Physical Conditioning. 

• Previous warming before excercises. 

• Pre and post stretching related activities. 

• Avoid unidirectional repeating excercises. 

• Accomodating to surface. 

• Adequate equipment. 


ARTHROSCOPIC TREATMENT OF THE FIRST PATELLA DISLOCATION 

Alberto Pienovi MD 

Centro de Traumatología y Ortopedia San Isidro. ARGENTINA 

Web page: www.ctosanisidro.com 

Purpose The purpose of this study was to perform a prospective non-randomized evaluation of arthroscopic 

treatment of first patella dislocation. 

Introduction: The treatment of the first patella dislocation is still a controversial matter. 

Several papers evaluate the results of non-operative treatments and of different surgical techniques, reaching 

several conclusions. 

In this study we present and analyze the results of arthroscopic treatment using our technique in 29 cases. 

Method: Twenty-nine cases were evaluated in 28 patients. One patient was bilateral. Six of these cases 

referred a previous sensation of patella instability or laxity. The average age was 20,3 (range l6 to 36) 6 were 

men and 3 women. All patients had a previous MRI and underwent a clinical and radiographic evaluation of 

the contra lateral knee, looking for conditions that predispose this pathology. The average period between 

the accident and the surgery was of 15 days (3/32 days). The arthroscopic treatment consisted in the reparation 

of the medial retinaculum with absorbable suture plus shrinkage with radio frequency and lateral 

retinacular release using an electrobistoury. In one case the anterior tibial tubercle was transferred using a 

miniopen technique, as the patient presented a high patella 

The knee was immobilized with a brace for 3 weeks, and afterwards rehabilitation started immediately. The 

practice of contact sports was authorized 5 to 6 months postoperative. 

Results: From the 29 cases of this group, 56% presented conditions predisposing this pathology in the contra 

lateral knee. 

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The average follow-up was 26.7 months (8 lo 44), obtaining 86.21 % of excellent or very good results 

according to the UCLA evaluation table. No recurrent dislocations occurred in this group, 13.79% of the 

results were regular, corresponding to those cases presenting, after surgery, some pain or sense of instability 

when practicing sports. 

Discussion: Acute patella dislocation occurs mainly in young athletes, most of them presenting conditions 

predisposing this pathology. In these cases we expect the best results using this technique. 

Arthroscopic treatment of the first patella dislocation presents low morbility and allows an efficient and 

early recovery of its normal anatomy. We present a technique that repairs the injured tissues associated to 

an arthroscopic realignment of the patella, with predictable results. 

Arthroscopic Treatment for Patellar Tendinitis in Soccer players 

Alberto Pienovi MD 

Centro de Traumatología y Ortopedia San Isidro. ARGENTINA 

Web page: www.ctosanisidro.com 


INTRODUCTION 

Patellar tendinitis or "jumper’s knee" is an injury frequently occurring in athletes performing eccentric 

strengths of the patellar tendon. It mainly involves kicking or jumping activities, such as volleyball, basketball, 

hockey, soccer and athletics. This lesion may also be related to any physical activity that requires an 

effort of the lower extremities. 

The use of "hard" surfaces in sports fields and the wide practice of soccer have also influenced the increase 

of this pathology. 

The lesion presents micro-traumas and micro-lesions in the tendinous tissue and its osseous insertion, 

where small degenerative and necrotic areas are presented. It may resemble other tendinitis, such as those 

of the Achilles tendon or tennis elbow. 

The pathogenesis of the lesion has been poorly defined, and the physiopathology has been related to the 

clinical aspect. 

It clinically appears as spontaneous and intense pain related to physical activity, usually in the upper area 

of the tendon or in the lower pole of the patella. It may eventually be bilateral. 

X-rays may exceptionally show calcifications or an increase of density in the area. Echographies are useful 

and present an hypoechoic image, edema and peri-tendinous irregularities. The MRI allows to evaluate the 

stages and to compare images with the contralateral knee. 

The treatment is controversial even nowadays among specialists in sports medicine. It greatly depends on 

the athlete’s requirements, the sport and whether the athlete is professional or amateur. 

We consider that a pathology not responding to conservative treatment should be surgically treated, therefore 

avoiding the progression of the affection to more severe levels. 

CLASSIFICATION 

We used the clinical 4-stage classification of Blazina et al. 

Stage I: Pain after practicing sports. It does not alter the performance. 

Stage II: Pain before practicing sports. It partially decreases while practicing sports and appears again after 

finishing the effort. It decreases the athlete’s performance. 

Stage III: Pain remaining before, during and after the effort. The athlete is unable to compete. 

Stage IV: Partial or complete rupture of the tendon. 

MATERIAL AND METHOD 

Twenty-one cases are presented corresponding to twenty-one patients who underwent an arthroscopic 

treatment. Seventeen were male and four female, showing a high predominance of men. 

The cases presented here were all Stage III, being the athletes unable to practice sports normally. They all 

had undergone several previous treatments. 

The average age was twenty-three point seven years (range nineteen to thirty-two) 

They were all athletes, twelve amateur and nine collegiate. 

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The average duration of symptoms was eight months (range five to twenty-three months) 

SURGICAL TECHNIQUE 

We performed the arthroscopic surgery with local anesthesia and without tourniquet. 

Initially, an intra-articular arthroscopy allows the diagnosis and treatment of associated injuries, exploring 

the distal pole of the patella that occasionally presents hypertrophic bursitis that is debrided. 

With an eighteen needle, the maximum pain area is marked, which generally coincides with the lower pole 

of the patella. 

Two longitudinal portals, slightly oblique to allow movements, twenty-five mm over and under the area are 

enough to work at ease. A pre-tendinous cavity is created with blunt instruments. 

A wide debridement is performed until the peri-tendon is arthroscopically observed. The anterior decompression 

of the tendon is achieved by cutting longitudinally the peri-tendinous fascias with a retractile 

knife. They are generally three layers that may be independent or forming an only fascia. 

With the exposed tendon, a new debridement is performed, if necessary, and with a knife wide longitudinal 

cuts are carried out over the tendon on the same direction of its fibers. 

During the postoperative period, a brace is placed in extension position only as protection. 

Physiotherapy with active and passive mobility is indicated as tolerated. The rehabilitation program must 

be prompt and aggressive but avoiding inflammation. 

Training under resistance and strengths and return to sports vary in each patient between one to two 

months. 

We consider that the keys of the surgical technique are: 

"The creation of a conformable pre-tendinous cavity" 

"The decompression of the tendon through a wide opening of the pre-tendinous fascia" 


RESULTS 

The average follow-up was two point four years (range fourteen to thirty-seven months). 

The evaluation method was the one established by Popp et. al. with modifications. 

Excellent: full return to sports. 

Good: Sporadic symptoms 

Fair: Less competitive level 

Poor: no improvement 

Fifteen patients (seventy-one point four percent) presented excellent and very good results; four patients 

(nineteen point oh five percent) fair results with return to sports with poorer performance and two patients 

(nine point fifty-two percent) poor results. 

CONCLUSIONS 

Patellar tendinitis is a pathology that presents great clinical variations and histological degeneration of the 

patellar tendon and its osseous insertions. 

This pathology extremely disables the athlete. It initially appears unimportant, but it progressively decreases 

the athlete’s performance or leads to the interruption of sporting activities. 

The arthroscopic treatment shows good results and is indicated in stage III cases or in those cases in which 

conservative treatments have failed, therefore, preventing the progression of the pathology. 

The surgical treatment together with rehabilitation allows quicker healing and tissue regeneration. 

Arthroscopy opens a new field in the minimum invasive surgical treatment of these affections. 

3.97


KNEE MENISCUS REPAIR 

Thursday, March 13, 2003 • Carlton Hotel, Carlton II 

Chairman: Prof. Dr. med. Dieter Kohn, Germany 

Faculty: Andrew Amis, DSc, United Kingdom, Romain Seil, MD, Germany, and Uffe Joergensen, Denmark 

The questions 


Meniscus reconstruction is a routine procedure in orthopaedic sports medicine. It has been shown that 

suturing a meniscus back to the capsule will restore knee function and prevent degenerative changes at 

least for 10 years. Some studies suggest that reconstruction of the more frequent intrasubstantial tears is 

able to prevent the knee from changes as seen after meniscectomy. The reputation of partial meniscectomy 

has suffered during the past years because we have become aware that this procedure is followed by early 

degenerative changes of the joint as well. But the long term prognosis after reconstruction of intrasubstantial 

meniscal tears is still unsecure. The scientific basis of this procedure is still weak. Lots of questions 

have remained: 

Does the reconstructed meniscus function similarly or equal to an intact meniscus? 

Which types of meniscus reconstruction can prevent or delay early degenerative arthritis? 

Which lesions do better with partial resection compared to reconstruction? 

How strong must the reconstruction be to allow healing? 

How can we enhance healing if this is really necessary? 

What are the complications with the "innovative" devices? 

What are the long-term effects and side-effects of the biodegradable materials? 

Which procedures are dangerous for the hyaline cartilage. Because injury to the cartilage during reconstruction 

procedures is very common but has hardly ever been evaluated scientifically? 

Does the benefit of ease of insertion justify the costs and possible side-effects of "innovative devices"? 

ICL 13 will not solve all these problems, but we will address the following questions: 

- What is our contemporary biomechanical knowledge about meniscus function? 

- What does laboratory testing tell us about actual techniques of meniscus reconstruction? 

- What are the most effective techniques today to suture a meniscus? 

- What the are the actual techniques of non-suture meniscus repair? 

LABORATORY TESTING OF MENISCUS REPAIR 

Romain Seil, M.D. 


University Hospital 

University of Saarland 

Homburg / Saar, Germany 

The purpose of laboratory testing is to evaluate and to improve the mechanical factors of meniscus healing, 

either for meniscus sutures or for new devices for meniscus repair. In order to be as close as possible 

to the clinical setting, the biomechanical analysis of meniscus repairs can be performed at different time 

points: 

1. Immediately after repair (t = 0) in so-called time-zero cadaver studies. 

2. During the healing period (t = 0 – 12 weeks). Such studies have been performed either in tissue-culture 

models or in animal studies. 

3.98

3. After the initial healing phase (t > 12 weeks). So far, the biomechanical properties of meniscus repair at 

this period have only been addressed in animal studies. 

T = 0 

Most of the studies dealing with laboratory testing of meniscus repair have been performed as time-zero 

studies, testing the tensile fixation strength of either sutures (KOHN D, 1989; RIMMER MG, 1995; POST 

WR, 1997; SEIL R, 2000) or sutures compared to fixation devices (ALBRECHT-OLSEN PM, 1997; ASIK M, 

1997 & 2002; DERVIN GF, 1997; BARBER FA, 2000; BECKER R, 2001 & 2002; BELLEMANS, 2002; BOENISCH 

UW, 1999; SEIL R, 2000; SONG EK, 2000; ARNOCZKY SP, 2001; RANKIN CC, 2002; WALSH SP, 2001; FISHER 

SR, 2002). 

The tensile fixation strength is analyzed on a materials test system (INSTRON®, ZWICK®, MTS®). A uniaxial 

load is applied in tension to the repaired meniscus in an axis parallel to the long axis of the suture or 

the implant to be tested. The ultimate tensile load is recorded on a load-displacement curve. In most of 

the studies a complete vertical tear was created at the entire periphery of the meniscus in order to prevent 

any load transfer other than at the repair site. Usually 1 suture / device was analyzed per test. The tears 

were standardized in each study, allowing for a comparison within one study. 

The first laboratory study on meniscus repair was published in 1989 (KOHN & SIEBERT). The authors compared 

open meniscus repair techniques to arthroscopic techniques. They incriminated the circumferential 

horizontal collagen fiber orientation for the higher ultimate failure strengths (UFS) for vertical sutures compared 

to horizontal sutures. They further showed the importance of the superficial, dense fibers which 

increased the UFS of mattress sutures compared to sutures including only deeper collagen layers. Post 

(POST WR, 1997) showed that the UFS of meniscus sutures were strongly dependent on the suture material. 

In a recent study (SEIL R, 2000) we did not find any difference between horizontal and vertical PDS 2-0 

mattress sutures, whereas vertical sutures became increasingly stronger with increasing strength of the 

suture material. The UFS of horizontal sutures was limited at approximately 100 N. This suggests that the 

maximum UFS of horizontal sutures is limited by the tissue quality of the meniscus and the strength of the 

suture material, whereas the failure strength of vertical sutures depends mainly on the strength of the 

suture. 


Regarding the testing conditions there were several factors which varied from study to study and which 

might have influenced the results. There is no common agreement concerning the design of the tests, 

which makes comparisons between different studies more difficult. These variables include the type of tear, 

the age and origin of the specimen (human, bovine and porcine menisci have been used) and the crosshead 

speed (displacement rate) at which the tests were performed, varying from 50 to 750 mm/min in different 

studies. With the new fixation devices laboratory testing becomes even more complex as the UFS 

may be affected by the insertion angle of the device and the number of barbs engaged in the meniscal tissue 

(BOENISCH UW, 1999). This might explain the large variations encountered with some devices in different 

studies. These variations were especially apparent for the Meniscus Arrow® (BionX Implants Inc., 

Blue Bell, PA, USA) and the BioStinger® (Linvatec Corp., Largo, FL, USA). ARNOCZKY found a mean UFS of 

57.7 N (+/- 13.8) for the Meniscus Arrow® and 35.1 N (+/- 6.7) for the BioStinger®, whereas BARBER et al. 

found a mean UFS of 33.4 N (+/- 8.4) and of 78.3 N (+/- 30.6) respectively. Some of these devices reached 

values which were close to 2-0 UPS sutures. However, the mean UFS of new devices were generally inferior 

to sutures. 

T = 0 – 12 WEEKS 

This period corresponds to the postoperative healing phase. During this phase the operated knee may be 

protected by a brace and a specific rehabilitation program is generally applied. Two mechanical factors 

have been analyzed during this phase: the evolution of tensile fixation strength of the sutures / devices 

over time (ARNOCZKY SP, 2001; DIENST M, 2001) and the effect of repetitive loading on meniscus repairs 

(SEIL R, 2000 and 2001). 

The effect of hydrolysis time on sutures / devices has been analyzed in a tissue culture model. In these 

studies, the menisci were incubated after the repair over a defined period, after which the UFS were evalu- 

3.99

ated. Using PDS sutures DIENST et al. (2001) found a significant decrease of the UFS of nearly 50%, whereas 

the UFS of nonabsorbable suture material did not change. ARNOCZKY & LAVAGNINO (2001) found no 

decrease in UFS for the BioStinger®, the Meniscus Arrow® and the Clearfix Screw® (Mitek Products Inc., A 

Division of Ethicon, Inc., Westwood, MA, USA) over a period of 24 weeks. However, the SD staple® 

(Surgical Dynamics, Inc., Norwalk, CT, USA) and the Mitek Meniscal Repair System® (Mitek Products Inc., A 

Division of Ethicon, Inc., Westwood, MA, USA) showed a complete loss of fixation strength after 24 and 12 

weeks respectively. 

Repetitive, cyclic loading of meniscus sutures showed the appearance of a gap of 3-4 mm with a load of 40 

N between the 2 parts of the meniscus (SEIL, 2000). Furthermore, failures of the sutures occurred. Cyclic 

testing of new devices showed failures as well. No failures were noted with the Meniscus Arrow®. This was 

incriminated to the large head of the device. Compression of the repair site lead to an increase of the UFS 

of 60% (STÄRKE, 2002). 

T > 12 WEEKS 


During this phase laboratory testing of meniscus repair has essentially been performed in animal studies 

analyzing the failure strength of the scar tissue (Tab.1). Even if KAWAI (1989) found UFS after 3 months of 

up to 80 % of the intact control meniscus in dogs, most other authors found data which were far from normal. 

This shows that meniscal scar tissue does not reach its initial biomechanical properties after a period 

of 3 to 4 months. KOUKOUBIS et al. (1997) observed an increase in UFS of repaired dog menisci over a 1- 

year-period. 

Animal model Time after surgery (months) Ultimate failure strength 

Port J, 1996 Goat 4 30 % of normal tissue 

Kawai Y, 1989 Dog 3 Up to 80 % of normal 

Roeddecker K, 1994 Rabbit 3 Fibrin glue: 42 % 

Suture: 26 % 

No therapy: 19 % 

Koukoubis TD, 1997 Dog 12 SD staple > suture 

Guisasola I, 2002 Sheep 1,5 < 50 % of normal 

Tab. 1 

FORCES ACTING IN VIVO 

In vitro-testing of meniscus repair has been performed with tensile forces only. The tensile forces acting on 

meniscal repairs in vivo are unknown. Furthermore, there are not only tensile, but also compressive and 

shear forces acting on the meniscus. These complex forces are difficult to reproduce in vitro. Only few studies 

tried to analyze this important question. KIRSCH and KOHN investigated the tensile forces acting on 

posterior horn sutures of the medial meniscus in a cadaver model. They were lower than expected as they 

never exceeded 10 N. 

NEW COMPLICATIONS 

New complications have been described with the new fixation devices, among which rail-shaped chondral 

lesions on the femoral condyle after meniscus repair with Meniscus Arrows®. In a biomechanical cadaver 

study we analyzed whether meniscus sutures and different types of devices induced meniscofemoral contact 

areas and contact stresses (SEIL, 2001). We found no contact areas / stresses with conventional mattress 

sutures. However, using the Meniscus Arrow®, the Clearfix Screw® and the Meniscal Dart®, contact 

areas / stresses could be found in 89%, 54% and 29% of the analyzed cases respectively. They were significantly 

smaller / lower for those devices with a small head. 

CONCLUSIONS 

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1. The maximum failure strength of horizontal sutures is limited by the tissue quality of the meniscus AND 

the strength of the suture material, whereas the failure strength of vertical sutures depends mainly on the 

strength of the suture. 

2. The maximum failure strength of new meniscus fixation devices is generally inferior to the failure 

strength of sutures. 

3. The varying results of failure strengths for a given type of suture / fixation device between different studies 

indicates that a standardized testing model is needed. 

4. The biomechanical properties of meniscus sutures / fixation devices after meniscus repair may vary over 

time, depending on the material’s properties of the suture / fixation device. 

5. In vivo forces acting on the repair site are not completely known, but they might be lower than expected. 

6. The exact biomechanical properties of the scar tissue of a healed meniscus are unknown. 

7. The complication potential of new devices must be evaluated further. 

LITERATURE: 

ALBRECHT-OLSEN, P.; LIND, T.; KRISTENSEN, G.; FALKENBERG, B.: Failure strength of a new meniscus 

arrow repair technique: biomechanical comparison with horizontal suture. Arthroscopy., 13 : 183-187, 1997. 

ARNOCZKY SP, LAVAGNINO M. Tensile fixation strengths of absorbable meniscal repair devices as a function 

of hydrolysis time. An in vitro experimental study. Am J Sports Med, 29 (2): 118-123, 2001 

ASIK M, SENER N, AKPINAR S, DURMAZ H, GÖKSAN A. Strength of different meniscus suturing techniques. 

Knee Surg Sports Traumatol Arthroscopy, 5: 80-83, 1997 

ASIK M, SENER N. Failure strength of repair devices versus meniscus suturing techniques. Knee Surg 

Sports Traumatol Arthrosc 2002; 10 (1): 25-9 

BARBER FA; HERBERT MA: Meniscal repair devices. Arthroscopy 2000; 16 (7): 754-6 

BECKER R, STARKE C, HEYMANN M, NEBELUNG W. Biomechanical properties under cyclic loading of 

seven meniscus repair techniques. Clin Orthop 2002; (400): 236-45 

BECKER R, SCHRODER M, STARKE C, URBACH D, NEBELUNG W. Biomechanical investigations of different 

meniscal repair implants in comparison with horizontal sutures on human meniscus. Arthroscopy 2001; 

17 (5): 439-44 

BELLEMANS J, VANDENNEUCKER H, LABEY L, VAN AUDEKERCKE R. Fixation strength of meniscal repair 

devices. Knee. 2002; 9(1):11-4 

BOENISCH, U.W.; FABER, K.J.; CIARELLI, M.; STEADMAN, J.R.; ARNOCZKY, S.P.: Pull-out strength and stiffness 

of meniscal repair using absorbable arrows or Ti-Cron vertical and horizontal loop sutures. Am.J 

Sports Med, 27: 626-631, 1999. 

DERVIN, G.F.; DOWNING, K.J.; KEENE, G.C.; MCBRIDE, D.G.: Failure strengths of suture versus biodegradable 

arrow for meniscal repair: an in vitro study. Arthroscopy., 13: 296-300, 1997. 

DIENST M, SEIL R, KUEHNE M, KOHN D. Cyclic testing of meniscal sutures after in vitro culture. 20th 

Annual Meeting Arthroscopy Association of North America, Seattle, Washington, 2001 

FISHER SR, MARKEL DC, KOMAN JD, ATKINSON TS. Pull-out and shear failure strengths of arthroscopic 

meniscal repair systems. Knee Surg Sports Traumatol Arthrosc 2002; 10 (5): 294-9 

GUISASOLA I, VAQUERO J, FORRIOL F. Knee immobilization on meniscal healing after suture: an experimental 

study in sheep. Clin Orthop 2002; (395): 227-33 

KAWAI, Y.; FUKUBAYASHI, T.; NISHINO, J.: Meniscal suture. An experimental study in the dog. Clin.Orthop., 

286-293, 1989. 

KIRSCH L; KOHN D; GLOWIK A: Forces in medial and lateral meniscus sutures during knee extension – an 

in vitro study. J Biomech, 31 (Suppl.1): 1041999. 

KOHN, D.; SIEBERT, W.: Meniscus suture techniques: a comparative biomechanical cadaver study. 

Arthroscopy., 5: 324-327, 1989. 

KOUKOUBIS, T.D.; GLISSON, R.R.; FEAGIN, J.A.J.; SEABER, A.V.; SCHENKMAN, D.; KOROMPILIAS, A.V.; 

STAHL, D.L.: Meniscal fixation with an absorbable staple. An experimental study in dogs. Knee.Surg.Sports 

Traumatol.Arthrosc., 5: 22-30, 1997. 


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PORT J; JACKSON DW; LEE TQ; and SIMON TM: Meniscal repair supplemented with exogenous fibrin clot 

and autogenous cultured marrow cells in the goat model. Am J Sports Med, 24: 547-555, 1996. 

POST, W.R.; AKERS, S.R.; KISH, V.: Load to failure of common meniscal repair techniques: effects of suture 

technique and suture material. Arthroscopy., 13: 731-736, 1997. 

RANKIN CC, LINTNER DM, NOBLE PC, PARAVIC V, GREER E. A biomechanical analysis of meniscal repair 

techniques. Am J Sports Med 2002; 30(4): 492-7 

RIMMER, M.G.; NAWANA, N.S.; KEENE, G.C.; PEARCY, M.J.: Failure strengths of different meniscal suturing 

techniques. Arthroscopy., 11: 146-150, 1995. 

ROEDDECKER, K.; MUENNICH, U.; and NAGELSCHMIDT, M.: Meniscal healing: a biomechanical study. 

J.Surg.Res., 56: 20-27, 1994.SEIL, R., RUPP, S., KOHN, D. Cyclic testing of meniscus sutures. Arthroscopy 16 

(4), 1-8, 2000. 

SEIL R; RUPP S; DIENST M; MÜLLER B; BONKHOFF H; and KOHN D: Chondral lesions after arthroscopic 

meniscus repair using meniscus arrows. Arthroscopy, 2000. 

SEIL R; RUPP S; JURECKA C; REIN R; and KOHN D: Der Einfluß verschiedener Nahtstärken auf das 

Verhalten von Meniskusnähten unter zyklischer Zugbelastung. Unfallchirurg, 2000. 

SEIL, R.; RUPP, S.; and KOHN, D.: Cyclic testing of meniscal sutures. Arthroscopy, 16: 505-510, 2000. 

SEIL R, RUPP S, JURECKA C, KOHN D. Biomechanical evaluation of new meniscus fixation devices. 

ISAKOS, 14th -18th may 2001, Montreux, Switzerland 

SEIL R, RUPP S, MAI C, PAPE D, KOHN D. The footprint of meniscus fixation devices on the femoral surface 

of the medial meniscus: a biomechanical cadaver study. ISAKOS congress Montreux, 2001 

STÄRKE C, BERTH A, BECKER R. Der Einfluss axialer Kniebelastung auf die biomechanische Stabilität von 

Meniskus-Refixationstechniken. 19th Kongress der Deutschsprachigen Arbeitsgemeinschaft für 

Arthroskopie (AGA), october 11-12th, Innsbruck 2002 

SONG EK, LEE KB. Biomechanical test comparing the load to failure of the biodegradable meniscus arrow 

versus meniscal suture. Arthroscopy 15 (7): 726-732, 1999 

WALSH SP, EVANS SL, O’DOHERTY DM, BARLOW IW. Failure strengths of suture vs. biodegradable arrow 

and staple for meniscal repair: an in vitro study. Knee, 2001; 8(2): 129-33 

Treatment of Meniscus Tears in ACL-Reconstructed Knees 

K. Donald Shelbourne, MD 

Methodist Sports Medicine Center 

Indianapolis, IN 

I. Factors to consider 

• ACL intact or ACL deficient knee 

• Medial versus Lateral 

• Degenerative versus Nondegenerative 

• Stable versus Unstable 

• Treatment choices 

• Remove 

• Repair 

• Leave alone 

• Postoperative Rehabilitation – does it matter? 

II. Meniscus tears 

• Mensicus tears observed at the time of ACL reconstruction are different than tears that occur in ACLintact 

knees 

• In general, meniscus tears in ACL-intact knees have extensive degeneration 

• Meniscus tears after an acute ACL tear are traumatic and occur mostly in the posterior and peripheral 

part of the meniscus 

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• Meniscus tears in chronic ACL-deficient knees can be degenerative or nondegenerative depending on 

the number and severity of instability episodes 

• There is no correlation between joint line tenderness and meniscus tears with an acute ACL injury 

(Shelbourne et al. AJSM 1995) 

• My research and experience is mostly with patients who have ACL insufficiency 

• This presentation of my algorithm for treatment applies to meniscus tears in conjunction with ACL 

reconstruction 

III. History of treatment 

• Before arthroscopy was available, most of the meniscus tears associated with ACL instability were not 

observed or treated 

• 82-83 before using arthroscopy consistently with ACL reconstruction--35% had either a LMT or MMT 

• Expected patients to return because of meniscal symptoms at some time after ACL reconstruction – 

didn’t happen! 

• When arthroscopy was used (from 1984 on), many meniscus tears were observed 

• 67%of patients had either LMT or MMT 

• Felt compelled to either repair or remove the tears even though the tears were not symptomatic 

• Leaving the tear alone was not considered 

IV. Lateral Meniscus Tears 

• Usually incidental findings, especially with acute injury 

• Acute injury – 62% have LMT 

• Chronic – 49% 

• Found that many LMTs will heal if left in situ (FitzGibbons and Shelbourne, AJSM 1995) 

• Peripheral, posterior, or posterior horn avulsion tears 


V. Peripheral Stable Medial Meniscus Tears 

• With acute ACL injury, common tear is a peripheral undersurface tear (tension side) 

• They can be missed easily 

• Adding sutures above the tear caused the tear to "pucker" forward 

• Added vertical sutures 

• 2nd look revealed that most vertical sutures did not remain but meniscus healed 

• Current treatment is to leave the tear in situ and treat with trephination 

VI. Study by Shelbourne/Rask (Arthroscopy 2001) 

• To determine the long-term clinical sequelae of salvageable, non-degenerative, peripheral vertical 

MMTs seen at the time of ACL reconstruction 

• Meniscus tears – Stable > 1 cm but < 2 cm in length treated with abrasion and trephination 

• Meniscus tears – Unstable > 2 cm in length, treated with suture repair (> 50% of the circumference 

Subsequent arthroscopy 

Subsequent scopes 

Group N N (%) Time Post-op (years) 

Left in Situ 139 15 (10.8) 2.5 

Abrade/Trephine 233 14 (6) 2.3 

Suture 176 24 (13.6) 4.3 

No Tear 526 14 (2.9) 5.0 

• Subsequent scopes performed at a mean of 3.7 years after ACL reconstruction 

• Of patients who had subsequent arthroscopy, 45% of the AT and SITU groups and 75% of the 

SUTURE group had the procedure at > 2 years after ACL reconstruction 

Conclusions 

• Of unstable peripheral vertical MMTs treated with suture repair, 13.6% failed, with most re-tears 

occurring at greater than 2 years after repair 

• Of stable peripheral vertical MMTs treated with abrasion and trephination alone and no direct 

fixation, most (94%) remain asymptomatic at a mean of 3.6 years after treatment 

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VII. Bucket-Handle Meniscus Tears 

• Occur mostly in patients who have chronic ACL instability 

• When the meniscus becomes locked, the patient seeks treatment because of pain and lack of function 

• Found that patients who had flexion contractures from locked bucket-handle tears and then underwent 

ACL reconstruction and treatment for the locked meniscus had a high rate of arthrofibrosis 

(Shelbourne/Johnson, AJSM 1993) 

• Began doing two-staged procedures 

• Meniscus treatment followed by rehabilitation to regain full range of motion 

• ACL reconstruction as an elective procedure 

• Gave us an opportunity to evaluate meniscal healing when patients had an unrestricted rehabilitation 

program after meniscus repair 

• Initially used 8-10 sutures for the repair because we knew patients would be weight bearing quickly 

after surgery 

• Believe that weightbearing stabilizes the meniscus by pushing it to the capsule 

• Follow-up arthroscopy at the time of ACL reconstruction 

• Meniscus is healed but very few sutures present 

• Realized that the vascular access channels created from placing the sutures were key 


Approach to Repair of Bucket-Handle Meniscus Tear 

• Used a rasp and multiple needle sticks to stimulate bleeding 

• Began using 4-6 sutures in the anterior half of the meniscus 

• Left the posterior section in situ because we know these tears can heal 

• Basically converted an unstable tear to a stable tear 

Study by Shelbourne/O’Shea (AJSM, In Press) 

• Between 1987 and 1999, 1470 chronic ACLs performed 

• Eighty-eight patients had a locked bucket-handle meniscus tear that severely limited knee extension 

• The average amount of knee flexion contracture at evaluation was 20 + 10 degrees 

Results: 52 patients with 55 repairs 

Healed Partially Healed No Healing 

Meniscus Zone N N (%) N (%) N (%) 

White/white 43 21 (49) 17 (40) 5 (11) 

White/Red 11 8 (73) 2 (18) 1 (9) 

Red/Red 1 1 (100) 0 (0) 0 (0) 

Total 55 30 (54.5) 19 (34.5) 6 (11) 

• At an average follow-up of 4.3 + 3.1 years, 4 additional menisci (7%) were symptomatic and required 

meniscectomy 

• At final follow-up, 36 of 43 (83.7%) of meniscus repairs in the white/white zone remained asymptomatic 

• All repairs in the red/white and red/red zone remained asymptomatic 

• At a mean of 60 months, the average modified Noyes score was 89.9 + 8.6 (range 67-100) 

• No patients had difficulty regaining full range of motion 

• In the short-term after meniscal repair, bucket-handle tears, even in the white/white zone, appear 

healed or partially healed. 

• Only 1 of the 19 menisci that were partially healed at the time of ACL reconstruction became symptomatic 

and required removal 

VIII. Now what? 

• We know that stable peripheral MMTs can heal in situ without suture repair treatment 

• We know that repairs of unstable locked MMTs can heal well 

• Now we need to know, does the repair of large BH MMTs give better results than removal? (do they 

function like a normal meniscus) 

Repair vs. Meniscectomy: Assumptions 

• Need to "Save the mensicus" at all costs 

• Meniscectomy dooms the knee to future degenerative changes 

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• Meniscus repair has to be better than meniscectomy 

• Performed two separate studies – Bucket Handle MMT and BH LMT 

• To determine the level of superiority meniscus repair had above partial meniscectomy for isolated, 

unstable, bucket-handle meniscus tears with regard to objective and subjective results 

IX. Bucket-Handle Medial Meniscus Tears (Shelbourne/Carr, AJSM, In Press) 

• Between 1982 and 1995, 155 patients met the inclusion criteria 

• Unstable BH MMT 

• Meniscus tear > 2 cm extending in more than half of the meniscus 

• The meniscus, when probed, could be pulled into the intercondylar notch or was displaced in the notch 

Methods 

• Patients did not have any other meniscus tears, chondral damage, or other ligamentous injury 

• 56 patients underwent meniscus repair (REP group) 

• 30 nondegenerative tears 

• 26 degenerative tears 

• 99 patients had a tear that was felt to be unsalvageable (REM group) – 

• 4 nondegenerative 

• 95 degenerative 


Subjective Results 

• REM group – 87/99 patients available at 7.8 years after surgery (range 2 to 19 years) 

• REP group – 51/55 patients available at a mean of 8.9 years after surgery (range 3 to 15) 

• Total Score: Repair vs. Removal 

• REM group: 90.9 + 16.7 points 

• REP group: 90.9 + 11.6 points 

• Further evaluation for the REP group based on whether the tear was degenerative or nondegenerative 

• Not enough numbers in the REM group – almost all degenerative 

• REP group 

• Deg tear: 87.1 + 12.9 points 

• Non-deg tear: 93.9 + 9.8 points (P=0.0123) 

IKDC Results: Overall Grade 

Normal Nearly Normal Abnormal Severely Abnormal 

Group (N) N (%) N (%) N (%) N (%) 

Repaira (24) 20 (83) 3 (13) 1 (4) 0 (0) 

Nondegenerative (12) 11 (92) 1 (8) 0 (0) 0 (0) 

Degenerative (12) 9 (75) 2 (17) 1 (8) 0 (0) 

Removal (52) 41 (79) 8 (15) 3 (6) 0 (0) 

• Available for 

• REP group – 25 patients at 7.1 years p.o. 

• REM group – 56 patients at 6.0 years p.o. 

• Graded as 

• Normal 

• Nearly normal 

• Abnormal 

• Severely abnormal 

IKDC overall grade: (No patient had a grade of Severely Abnormal) 

Remove Group Repair Group 

Grade N (%) N (%) 

Normal 26 (46) 13 (52) 

Nearly Normal 25 (45) 9 (36) 

Abnormal 5 (9) 3 (12) 

3.105

Radiographic Grade: No Patient had a grade of Severely Abnormal; one patient refused x-rays) 

Remove Group Repair Group 

Grade N (%) N (%) 

Normal 41 (79) 20 (83) 

Nearly Normal 8 (15) 3 (13) 

Abnormal 3 (6) 1 (4) 

Results 

• All but one of the 15 patients who did not have a normal radiographic grade had > 5 years f/u 

• 5 patients in REP group and 1 patient in REM group required second surgery on the meniscus 

• 4 of 5 patients in the REP group had a degenerative type tear at the time of the initial treatment 


Discussion 

• Study by O’Shea showed "healing" of the meniscus or at least a low incidence of symptoms requiring 

removal (9%) 

• However, no statistically significant difference between meniscus repair and partial meniscectomy, at 

least with the follow-up of 6 to 8 years 

• Further sub-analysis based on type of tear 

• Results of degenerative tears worse than nondegenerative tears (87 vs. 94 points) 

X. Bucket-Handle Lateral Mensicus Tears (Shelbourne/Dersam) 

• Between 1982 and 1995, 91 patients had isolated, unstable bucket-handle lateral meniscus tears 

• "Isolated" means the patient did not have a medial meniscus tear or any articular cartilage damage 

Methods 

• 67 tears were seen as repairable 

• Repaired with an inside-out technique 

• Usually, 2-3 vertical sutures were used 

• 24 tears were felt to be irreparable 

• Tears usually had complex vertical and horizontal tears 

• Postoperative rehabilitation was the same program for both the repair and removal groups 

• Subjective follow-up – Modified Noyes Knee Survey 

• Objective follow-up 

• IKDC 

• Standing PA 450 weightbearing view 

Results 

• Minimum two year subjective follow-up: 

• Repair group - 57 patients, mean 7 years post-op 

• Remove group - 21patients, mean 11.1 years post-op 

• Minimum 2 year objective follow-up: 

• Repair group - 30 patients, mean 5.9 years post-op 

• Remove group - 12 patients, mean 8.1 years post-op 

Subjective scores 

Repair Group 

Category Mean ± SD Remove Group P-value 

Total Score 92.5 ± 9.4 88.7 ± 13.2 0.2014 

Pain 16.8 ± 3.1 14.0 ± 4.0 0.0478 

Swelling 8.9 ± 1.5 9.0 ± 1.3 0.8078 

Stability 19.2 ± 2.l2 19.0 ± 2.2 0.5083 

Activity 18.8 ±3.1 17.7 ± 3.9 0.0732 

3.106

IKDC Results: (No patient had a grade of Severely Abnormal) 

Overall Grade 

Radiographic Grade 

Repair Remove Repair Remove 

Grade N (%) N (%) N (%) N (%) 

Normal 16 (53) 2 (11) 26 (87) 10 (83.3) 

Nearly Normal 11 (37) 8 (42) 3 (10) 1 (8.3) 

Abnormal 3 (10) 2 (40) 1 (3) 1 (8.3) 

• Subsequent symptoms after repair: Only 2 of 67 patients (3%) required a subsequent arthroscopy 

because of symptoms of locking or catching 

Discussion 

• Although statistical significance was not found between groups for most factors, we believe the data 

indicate a trend toward worse clinical results with partial meniscectomy 

• Overall IKDC grade 

• Subjective pain score 

• These clinical differences may indicated a degenerative changes in that joint that do not appear on 

radiographs 

XI. Summary 

• This group of studies looked at the results that were specific to one type of meniscus tear 

• Patients who had other types of intraarticular damage were eliminated so that the specific results could 

be reported 

• Other reports in the literature seldom are this specific 

• Many types of meniscus tears can heal or remain asymptomatic with repair 

• Many tears can be left in situ after treatment with abrasion and trephination 

• Posterior horn avulsions 

• Peripheral medial or lateral meniscus tears 

• Most of these tears are associated with acute ACL injury 

• Many bucket-handle meniscus tears (even in the white/white zone) can be repaired without causing 

symptoms in the future 

• Fewer repaired BH lateral meniscus tears cause subsequent symptoms than BH medial meniscus tears 

• 3% lateral 

• 9% medial 

• Clinically, patients who underwent meniscectomy (lateral or medial) appeared to have inferior results 

than patients who had meniscus repair 

• Not sure how well some repairs function 

• For BH medial meniscus repairs, degenerative tears resulted in lower subjective scores than nondegenerative 

tears 

• Difficult to observe statistically significant superior results with repair versus removal, even with 8-10 

year follow-up 

• Further follow-up studies need to be specific with regard to meniscus tear type and ACL-intact or ACL 

deficient knees 


3.107


COMPLEX ISSUE IN ACL RECONSTRUCTION 

An International Perspective 

Thursday, March 13, 2003 • Aotea Centre, Kupe/Hauraki Room 

Chairman: Kai-Ming Chan, MD, Hong Kong 

Faculty: Freddie Fu, MD, USA, Savio Woo, PhD, DSc, USA, James Lam, FRCS, Hong Kong, Hans Paessler, Germany, 

Masahiro Kurosaka, Japan, Christer Rolf, United Kingdom and Hsiao-Li Ma, MD, Taiwan 

1. The ACL graft…A biological and biomechanical perspective 

Savio Woo (15 minutes) 


2. My preferred method of ACL reconstruction…Graft choice and technical pearls 

Hans Paessler (8 min) 

Masahiro Kurosaka (8 min) 

KM Chan (8 min) 

Christer Rolf (8 min) 

3. Combined ACL plus repairable meniscal injury – My preferred approach 

James Lam (8 min) 

Ma Hsiao-Li (8 min) 

4. Revision ACL surgery 

Freddie Fu (15 min) 

5. Questions and Answers 

All (10 min) 

INTRODUCTION: 

Approximately 250,000 ACL reconstructions/year in the USA alone 

80-90% success rates 

Approximately 25,000 revision ACL reconstructions/year 

Misplaced tunnels in 10-40% [4-6] 

Purpose of this Instructional Course Lecture 

Review current clinical experience, indications, techniques, results and controversies with revision 

ACL reconstruction. 

Clinical experience 

20 years 

200 ACL reconstructions/year 

30 revisions/year 

INDICATIONS 

Subjective 

Instability (ADL’s, Sports) 

Pain 

3.108

Objective 

Evidence of increased laxity on physical exam 

Evidence of increased laxity on instrumented knee testing (KT 1000) 

ETIOLOGY OF FAILURE 


Surgical technique 

Biological failure 

Biomechanical failure 

1. Surgical technique 

Technical errors 

Tunnel location 

Graft impingement 

Graft tension 

Mechanical properties of the graft [2] 

2. Biological failure 

Avascularity 

Immunology 

Stress shielding 

Bone to bone and bone to tendon healing 


3. Biomechanical failures 

Trauma (re-injury) 

Aggressive rehabilitation 

PREOPERATIVE EVALUATION 

Determine etiology, classify primary and secondary causes of graft failure, revise preoperative plan. 

History 

Symptoms (pain vs. instability) 

Previous surgical procedures (i.e. graft type, associated pathology) 

Physical exam 

Laxity patterns (assess secondary restraints) 

Anterior vs. posterior drawer 

Rotational stability 

Pivot shift test 

Varus/valgus 

Posterolateral corner 

Radiographs 

Tunnel position, size, fixation type, Fairbank’s changes 

AP, lateral 

45∞ PA FWB 

Special examinations 

MRI 

Bone scan 

CT scan 

Gait analysis 

3.109

TECHNICAL CONSDERATIONS 

Principe of treatment is not the same as in primary ACL reconstruction! 

Pre-operative planning 

Set realistic goals with patients 

Return to sports vs. ADL’s 

Beware of "knee abuser" 

Staged procedure: 

1 vs. 2 stages (bone grafting) 

Secondary restraints: 

Collaterals 

Meniscus (role for transplantation) 

Cartilage (role for osteotomy) 


Graft selection: 

Autograft vs. allograft [1] 

Computer-assisted vs. traditional planning 

Removal of hardware 

Pre-operative planning 

Leave in place if possible 

Remove hardware only with appropriate tools 

Prosthetic ligament removal in one piece 

Tunnel placement 

Femoral tunnel: 

Anterior: re-drill tunnel in correct position 

Correct: larger graft with bone graft or over-the-top position 

Posterior: convert to over-the-top position 

Tibial tunnel: 

Anterior: 

Correct: 

Posterior: 

re-drill tunnel in correct position 

larger graft with bone graft 

two stage bone grafting, large allograft 

Graft fixation 

Generally interference screws 

Alternatives (i.e. suture post, staple) 

REVISION GRAFT SELECTION 

Graft types 

Allograft (bone-patella tendon-bone, Achilles tendon) 

Autograft (bone-patella tendon-bone, hamstring tendons, quadriceps tendon) 

Graft selection 

Autograft: 

For failed allograft without technical failures 

If patient refuses allograft 

Allograft: 

For failed autografts 

For complex revision cases 

3.110

REHABILITATION 

Avoid aggressive rehabilitation! [3] 

Special considerations 

Complex cases (secondary restraints) 

Delayed allograft incorporation 

General rules 

Respect graft healing 

PWB 6-8 wks 

Return to sports after >12 month 

PITTSBURGH EXPERIENCE 

Follow up study [4] 

35 patients (25 autografts/10 allografts) 

Revision with allografts (21 PT/14 AT) 

Average follow up, 18-40 month 


Results 

Subjective (U Pittsburgh Subjective Knee Rating) 

Mean 73 (7-90), max 100 

SUMMARY 

REFERENCES 

Would have surgery again 

Yes: 83%, No 17% 

Objective (IKDC) 

B 14% 

C 50% 

D 36% 

KT-1000 laxity 

5mm 14% 

1. Careful pre-operative evaluation (gather all data) 

2. Counsel your patient 

3. Address the whole knee – not only the ACL 

4. Have different techniques available 

5. Revision is technically demanding 

6. Results are not as good as in primary reconstructions 

1. Harner, C.D., E. Olson, J.J. Irrgang, S. Silverstein, F.H. Fu, and M. Silbey, Clin Orthop, 1996(324): p. 134-44. 

2. Höher, J., S.U. Scheffler, J.D. Withrow, G.A. Livesay, R.E. Debski, F.H. Fu, and S.L.-Y. Woo. Journal of 

Orthopaedic Research, 2000. 18(3): p. 456-61. 

3. Irrgang, J.J. Clinics in Sports Medicine, 1993. 12(4): p. 797-813. 

4. Johnson, D.L., T.M. Swenson, J.J. Irrgang, F.H. Fu, and C.D. Harner, Clinical Orthopaedics & Related 

Research, 1996(325): p. 100-9. 

5. Kohn, D., T. Busche, and J. Carls. Knee Surgery, Sports Traumatology, Arthroscopy, 1998. 6 Suppl 1: p. S13-5. 

6. Musahl, V., T. Cierpinski, H. Hornung, and P. Hertel, 63. Jahrestagung der DGU, November 1999, 

Berlin, Germany, 1999. 

3.111


ELBOW ARTHROSCOPY (LIGAMENT INJURIES AND TENDINOPATHY) 

Thursday, March 13, 2003 • Aotea Centre, Kaikoura Room 

Chairman: Luigi Pederzini, MD, Italy 

Faculty: Gary Poehling, MD, USA, Gregory Bain, FRACS, Australia and Champ Baker, Jr., MD, USA 

Arthroscopic technique is becoming more and more useful in the treatment of elbow pathologies. 

Degenerative stiff elbow (DSE) and post-traumatic stiff elbow (PSE) must be considered. 

In DSE patients complain pain more than ROM deficit,while in PSE patients complain ROM deficit more 

than pain. 


Several surgical steps are described:Arthroscopic release of the posterior fossa,resection of the tip of the 

olecranon, arthroscopic release of the anterior capsule ,resection of the ipertrophic coronoid process,ulnar 

nerve release.,arthroscopic O.K. procedure, arthroscopic resection of the radial head.The Rom in DSE and 

PSE after arthroscopic treatment was evidenced in the Morrey functional arch.DSE patients at 3 years follow 

up show some mild pain and some decreased ROM.PSE patients mantain a good ROM at 3 years follow 

up.Time from trauma can influence the results. 

Elbow Osteochondral Lesions - The Role of Arthroscopy 

Poehling, Gary 

Definitions 

1. Osteochondrosis - Panner's Disease: This is a disease of the ossification center that occurs in the first 

decade of life. It is generally a self limited problem that reconstitutes itself over a year's period of time 

with very few long term problems. Observation and rest is the treatment of choice. 

2. Osteochondritis Dissecans: This is an inflammatory process effecting the articular surface. It has a peak 

incidence in 10-15 years of age. It is most commonly seen in throwing athletes and female gymnasts. 

Evaluation 

1. Range of motion 

2. Radiographs 

a. Loose bodies 

b. AVN entire capitellum - Panners age 4-10 

c. Superficial defect - OCD age 10-15 

3. Indications 

a. Failure of conservative treatment 

b. Fixed contracture greater than 10 degrees. 

c. Mechanical symptoms, locking and catching. 


1. Anterior joint - 5 mm arthroscope 

a. Proximal medial portal 

b. Anterolateral portal 

2. Posterior joint - 2.7 mm scope 

a. Mid lateral portal 

b. Adjacent portal 

3. Posterior portal - best to visualize the defect in 75% of cases. 

4. Debridement and loose body removal is treatment of choice 

5. Alternatives 

a. Headless screw 

b. Biodegradable pin 

c. Allograft 

3.112

Elbow Arthroscopy: Set-Up/Portal Anatomy and Diagnostic Arthroscopy 

Gary G. Poehling, M.D. 

Wake Forest University Health Sciences 

Winston-Salem, North Carolina 

Operating Room Set-Up & Instrumentation 

I. Patient Positioning (Figure 1) 

A. Lateral position with arm support 

B. Prone or supine position-alternative 

C. General anesthesia (preferred) 

II. Instrumentation 

A. Non-sterile upper arm tourniquet (optional) 

B. Fluid pump with pressure monitoring, 

4.5 mm/30º & 2.7/30º mm arthroscopes 

C. Motorized shaver, grasping forceps 

D. Suction basket 

E. OR set up (Figure 2) 

Figure 1 

Figure 2 


Figure 3a Figure 3b Figure 3c 

III. Technique 

A. Portals-anterior compartment 

1. Proximal medial portal (Figures 3) 

2. Anterio-lateral portal (inside out) 

3. Joint distension through mid-lateral "soft spot" using 18 ga. Spinal needle with 30-50 cc sterile 

Ringer’s Lactate solution 

- Diminished joint laxity and volume with diagnosis of contracture 

4. Establish proximal medial portal, anterior to intermuscular septum along anterior humeral shaft 

(brachialis protects anterior neurovascular structures) 

5. Arm flexion helps protect anterior neurovascular structures 

Figure 4a 

Figure 4b Figure 5 

3.113

B. Portals-posterior compartment (Figures 4a and 4b) 

1. 2.7 mm arthroscope through mid-lateral or adjacent lateral portals (see Figure 5) 

2. Use of posterior (posterior lateral or trans-triceps) portals for evaluation/instrumentation of posterior 

joint and olecranon fossa (see Figure 6) 

3. Trans-triceps portal is made with a longitudinal incision 1.5-2.0 cm proximal to olecranon process 

with elbow flexed 90º 

Figure 6a 

Figure 6b 

Figure 6c 


IV. Indications 

A. Loose bodies 

B. Osteochondritis Dessicans (OCD) 

C. Rheumatoid Arthritis - Synovectomy 

D. Contracture/Arthrofibrosis 

E. Pigmented Villinodular Synovitis (PVNS) 

F. Lateral Epicondylitis 

G. Radial Head Fractures 

H. Radial Head Resection 

I. Synovial Chondromatosis 

J. Infection/Septic Arthritis 

K. Posterolateral Instability 

V. Contraindications 

A. Advanced degenerative joint disease 

B. Previously transposed ulnar nerve prevents any medial approaches 

C. Excessive heterotopic bone 

D. Reflex Sympathetic Dystrophy (RSD) 

E. Soft tissue compromise 

References 

1. Poehling GG, Ekman EF, Ruch DS. Elbow Arthroscopy, in Oper Arth, p 821-28 

2. Menth-Chiari WA, Poehling GG, Ruch DS. Arthroscopic resection of the radial head. Arthroscopy 

1999 Mar; 15(2):226-30 

3. Moskal MJ, Savoie FH, III, Field LD. Elbow arthroscopy in trauma and reconstruction. Orthop Clin 

North Am 1999 Jan;30(1):163-77 

4. Ruch DS, Poehling GG. Anterior interosseous nerve injury following elbow arthroscopy. 

Arthroscopy 1997 Dec;13(6):756-8 

5. Day B. Elbow arthroscopy in the athlete. Clin Sports Med 1996 Oct;15(4):785-97 

6. Baker CL, Brooks AA. Arthroscopy of the elbow. Clin Sports Med 1996 Apr;15(2):261-81 

7. Ekman EF, Poehling GG. Arthroscopy of the elbow. Hand Clin 1994 Aug;10(3):453-60 

8. Gallay SH, Richards RR, O’Driscoll SW. Intraarticular capacity and compliance of stiff and normal 

elbows. Arthroscopy 1993;9(1):9-13 

9. Verhaar J, van Mameren H, Brandsma A. Risks of neurovascular injury in elbow arthroscopy: starting 

anteromedially or anterolaterally. Arthroscopy 1991;7(3):287-90 

10. Lynch GJ, Meyers JF, Whipple TL, Caspari RB. Neurovascular anatomy and elbow arthroscopy: inherent 

risks. Arthroscopy 1986;2(3):190-7 

* Illustrations by Annemarie B. Johnson, CMI 

3.114

Elbow Arthroscopy and Nerves 

Gregory Bain, Adelaide, South Australia. 

www.gregbain.com.au 

It has been recognised for some years that elbow arthroscopy has a much higher incidence of nerve injury 

than arthroscopy involving other joints. This is largely due to the close proximity of the three major nerves 

to the elbow joint. 

The ulnar nerve is at risk when introducing the medial portal particularly if the patient has a subluxating 

ulnar nerve or the patient has had a surgical anterior transposition. Injury to the ulnar nerve can occur during 

debridement of the medial gutter (Figure 1). 

The radial nerves and the posterior interosseous nerves are at risk during lateral portal placements. The 

nerves are less likely to be injured if the joint is distended and a proximal lateral portal is used. The radial 

nerve is at risk when performing an anterior capsular release, synovectomy or a radial head excision (Figure 

2). 

The median nerve passes anterior to the brachialis muscle and therefore tends to be protected during 

elbow arthroscopy (Figure 2). 

The details of the anatomy of each of the nerves with relation to the elbow joint will be presented. 

ENDOSCOPIC ULNAR NERVE RELEASE 

We have performed a cadaveric study to assess the safety and efficiency of performing an endoscopic ulnar 

nerve release at the level of the elbow with the Agee single portal endoscopic device. In a cadaveric model 

we were able to reproducibly perform a release of the arcade of Struthers, decubital retinaculum and 

Osborne’s FCU fascia. In cadaveric models there were no injuries to the ulnar nerve, its motor branches or 

articular branches. By setting the trocar into the radial side of the cubital tunnel the chance of injury to the 

motor branches is significantly reduced. 

We have been using this technique in clinical cases and found the technique to be safe and associated with 

a much more rapid rehabilitation and smaller morbidity than conventional open approaches that we had 

used previously. 


Figure 1 Figure 2 

Elbow Arthroscopy: A Long Term Follow-Up 

Champ L. Baker, Jr., MD 

The Hughston Clinic 

Columbus, Georgia 

Introduction 

• Burman reports that the elbow is unsuitable for arthroscopic exam – 1931 JBJS 

• Japanese credited for renewed interest in elbow arthroscopy with publications in the 1970’s 

• Increased popularity in the mid 1980’s 

3.115

• Accounts for 11% of arthroscopies at Mayo Clinic 

• 7.6% of orthopedists perform elbow arthroscopy 

Indications 

• Loose body/Foreign body 

• OCD 

• VEO 

• Posterior impingement 

• Synovitis 

• Arthrofibrosis 

• Diagnostic 

• DJD 

• Fracture 

• Lateral Epicondylitis 

• Radial Head Excision 

• Evaluate competency of Ulnar Collateral Ligament 

• Septic arthritis 


Contraindications 

• Severe ankylosis 

• Distortion of normal anatomy (e.g. ulnar nerve transposition) 

• Local skin infection 

Procedure 

• General Anesthesia 

• Prone position 

• Portal Placement 

– Superomedial 

– Superolateral 

– Direct lateral 

– Posterocentral 

• 2.7mm 30° arthroscope 

Post-op 

• Outpatient 

• F/U 1 week 

• Post op rehab depends on procedure 

– Regain motion #1 priority in all procedures 

Materials and Methods 

• Query of elbow arthroscopy by Champ Baker, MD 

• February 1984 – February 2001 

• Chart Review 

• Patients contacted by phone 

– Clinic Visit 

– Phone survey 

Chart Review 

• Date of birth 

• Date of surgery 

• Sex 

• Hand dominance 

• Side of procedure 

• 1º, 2º, and 3º diagnosis 

• 1º, 2º, and 3º procedures 

• Complications 

• Prior surgery 

• Repeat surgery 

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• Concomitant surgery 

• Workman’s comp 

• History of injury 

• Preop range of motion 

• Occupation 

Deleted patients 

• Concomitant open procedures (e.g. ulnar nerve transposition) 

• Diagnostic scopes 

• Deceased 

Patient Follow-up 

• Phone contact 

– Clinic visit 

• Andrews elbow scoring system 

– Subjective and objective 

• Visual analog pain scale 

• Much better, Better, Same, or Worse 

– Phone survey 

• Modified Andrews elbow scoring system 

– Subjective 

• Analog pain scale 

• Much better, Better, Same, or Worse 


Questionnaire 

Results 

• 324 elbows, 311 patients 

• 44 elbows deleted 

– 36 open 

– 5 diagnostic 

– 3 deceased 


• Ages - 11.5yo to 73.5yo (38.5 avg) 

• Sex – 206 M (74%) and 74 F (26%) 

• Hand dominance – 194 right (69%), 20 left (7%), 66 no documentation (23%) 

• Procedure side – 187 right (67%) and 93 left (33%) 

• Workman’s comp – 218 no and 62 yes 

Primary Diagnosis 

Prior Surgery 

• Prior surgery – 21 patients (7%) 

– Open procedures - 13 

– ORIF – 7 

– Scope - 1 

Concomitant surgery 

• Concomitant surgery – 20 (7%) 

– Shoulder scope – 9 

– Olecranon bursectomy – 4 

– Lateral release – 3 

– Carpal tunnel release – 2 

– CMC arthroplasty – 1 

– Ankle scope - 1 

Complications 

• Total complications – 15 (5%) 

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– Transient numbness – 6 

– Arthrofibrosis – 3 

– Neuroma – 2 

– Post-operative drainage – 2 

– Cellulitis – 1 

– Heterotopic bone – 1 

• No permanent neurovascular compromise 

Repeat Surgery 

• Repeat surgery – 26 (9%) 

– Open procedure – 17 

– Scope – 8 

– Total elbow replacement – 1 

• 4/26 patients VEO – open resection olecranon osteophyte or UCL recon 

• 3/26 open lateral release after scope release 

• 3/26 unrelated repeat procedures (e.g. radial tunnel release 1 year after loose body removal) 


Results 


• 26 elbows deleted from f/u due repeat surgery 

• 254 elbows in 242 patients possible for f/u 

• 82 elbows in 79 patients contacted 

– 52 phone interview 

– 30 clinic visit 

• 82 follow up elbows 

• Ages 11.5 - 71yo (avg. 42yr) 

• Follow up 17 – 155 mos (avg. 64.5 mos) 

• Sex, hand dominance, procedure side, workman’s compensation cases, and primary 

diagnosis analogous to total surgical population 

• Visual analog scale (0-10) 

– Daily pain avg. 1.39 (range 0-9) 

– ADL pain avg. 2.18 (range 0-8) 

– Work pain avg. 2.98 (range 0-10) 

• Andrews criteria - subjective 

– Pain avg. 18.29 (range 5-25) 

– Swelling avg. 23.17 (range 5-25) 

– Locking avg. 22.44 (range 5-25) 

– Activity limitation avg. 20.85 (range 5-25) 

• Subjective score avg. 84.76 (range 25-100) 

• 71% (58/82) elbows with good and excellent results 

• 80% (65/82) elbows better and much better 

• 74% (48/65) non-WC patients with good and excellent results 

• 75% (49/65) non-WC better and much better 

• 59% (10/17) WC patients with good and excellent results 

• 100% (17/17) WC patients better and much better 

• Good and Excellent Results 

– VEO 100% (6/6) 

– OCD 83% (5/6) 

– Loose body 75% (9/12) 

– Lateral epicondylitis 74% (23/31) 

– Synovitis 71% (5/7) 

– DJD 57% (4/7) 

– Posterior impingement 50% (1/2) 

– Arthrofibrosis 45% (5/11) 

• Better and Much Better 

– OCD 100% (6/6) 

– DJD 86% (6/7) 

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– Synovitis 86% (6/7) 

– Lateral epicondylitis 84% (26/31) 

– Loose Body 75% (9/12) 

– Arthrofibrosis 73% (8/11) 

– VEO 67% (4/6) 

– Posterior impingement 50% (1/2) 

Literature 

• Retrospective (1979-95) 

• 47 pts 

• age 3.5 – 17yo (avg age 14 yr) 

• min 2yr f/u (avg. 4.7yrs) 

• Modified Andrews elbow scoring system 

• 85% good to excellent results, 90% return to sport 

– Micheli, LJ, et. al. 

– Boston, Mass 

– Journal of Arthroscopy 2001 

• Retrospective (1977 – 1996) 

• 103 patients, mean f/u 6.2 yrs, 3 – 72yo 

• Figgie score increased from 49.3 to 89.1 

• Age didn’t affect the results 

• Pain showed the greatest improvement 

• Loose bodies, rheumatoid and septic arthritis improved the most 

• Limited improvement in degenerative arthritis 

– Jerosch, J. et al 

– Munster, Germany 

– Arch orthop trauma surg 1998 

• Retrospective (1980-1998) 

• 414 elbows with >6 week f/u 

• Chart review, survey, telephone contact (37/96 pts) 

• Major complications – permanent neurovascular injury, compartment syndrome, postop joint infection, 

loss of motion >30º 

• Minor complications – transient nerve palsy that completely resolves, drainage >5 days, superficial 

infection, loss of motion 70% good or excellent and better or much better results) a good 

procedure for OCD, loose body, synovitis, and lateral epicondylitis 

• Less predictable results for DJD, VEO, arthrofibrosis, and posterior impingement 

• Neurovascular injury can be minimized with complete knowledge of the regional anatomy of the 

elbow and careful attention to detail 

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Treatment of Lateral Epicondylitis and Soft Tissue Impingement 

Champ L. Baker, Jr., M.D. 

The Hughston Clinic 

Columbus, Georgia 

Lateral Epicondylitis Definition 

"Painful overuse tendinosis at the lateral aspect of the elbow" 

Henry J. Morris (Lancet 1882) "Lawn Tennis Arm" 

Mechanism 

Traumatic or non-traumatic mechanisms 

Often repetitive use injury 

Poor blood supply to tendon 

Insufficient healing 

Vicious cycle 

Inflammation ‡ microtear ‡ frank rupture 

Pathoanatomy 

Initially thought to be inflammatory process (tendonitis) of ECRB and 

aponeurosis at lateral epicondyle (Goldie, 1964) 

Later described by Nirschl as "Angiofibroblastic tendinosis" 

• Degenerative process 

• Granulation tissue 

• No inflammatory cells 

ECRB involved 100% 

• ECRL, EDC less commonly 

97% tendinosis 

35% gross rupture 

common extensor 

Diagnosis 

Pain and tenderness over lateral epicondyle and common extensor tendon origin 

Pain with resisted wrist extension and supination 

Pain with passive wrist flexion with elbow extended 

Radiographs usually normal 

Non-operative Treatment 

Rest 

Ice 

NSAID’s 

Counterforce brace 

Physical therapy 

Modalities 

Corticosteroid injection 

75% to 90% of pts do well 

Efficacy of Nonoperative Treatment for Lateral Epicondylitis 

Bowen, Dorey and Shapiro (American J. Orthopedics, August 2001) 

• 84 patients 

• 2.8 year follow-up 

• 25% required surgery 

• Multiple injections prognostic 

Surgical Treatment 

10-25% of patients are recalcitrant to non-op treatment 

Operative 

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• Open 

• Percutaneous 

• Arthroscopic 

Open 

Identification of pathology 

Excision tendon (ECRB) 

Decortication epicondyle 

Repair common extensor origin 

Percutaneous 

Release ECRB with #11 blade 

Local anesthesia / office or outpatient 

21 elbows in 17 patients 

20/21 normal function at 31 months follow-up 

Arthroscopic Lateral Release 

Preserves common extensor origin 

Speeds rehabilitation 

Allows intra-articular examination for chondral lesions, loose bodies, etc. 


Arthroscopic Release for Lateral Epicondylitis: A Cadaveric Model 

Kuklo, Taylor, Murphy, Islinger, Heekin and Baker 

(Arthroscopy 1999; 15(3);259-64) 

Arthroscopic resection of the ECRB and decortication of the lateral epicondyle 

10/10 successfully debrided / decorticated from 20-27mm as demonstrated by post-arthroscopic dissection 

1/10 cases over resected into subcutaneous fat 

Conclusions: 

• LCL not harmed - posterior 

• Technically feasible 

• Technically reproducible 

Arthroscopic Classification 

Type I- Deep fraying to ECRB 

Type II- Linear tears on undersurface of ECRB 

Type III- Complete avulsion of ECRB 

Arthroscopic Technique 

Prone position 

General anesthetic 

Tourniquet optional 

Equipment 

• 2.7, 4.0, 30º /70º arthroscope 

• 3.5/4.5 full radius resector / burr 

• Hand instruments / radiofrequency – monopolar 2.0 

Proximal Medial Portal 

• 2 cm proximal to the medial epicondyle 

• Adjacent to the intermuscular septum 

• Avoid the medial antebrachial cutaneous nerve 

Proximal Lateral Portal 

• 2 cm proximal and 1 cm anterior to the lateral epicondyle 

• Visualization of the anterior joint and capsule 

Operative sequence 

• Intra-articular inspection 

• Identification of ECRB origin after resection of capsule at lateral epicondyle 

• Debridement of pathologic tissue at ECRB origin 

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• Decortication of lateral epicondyle and lateral epicondylar ridge 


Arthroscopic classification and treatment of lateral epicondylitis: Two year clinical results 

Baker, Murphy, Gottlob and Curd 

(J Shoulder Elbow Surg 2000; 9;475-82) 

Patient Follow Up 

1991-1997, 42 elbows (40 patients) 

• 26 males, 14 females 

• Mean age: 42.7 yrs (18-59yrs) 

Prevalence 

• Type I Lesion: 15 (36%) 

• Type II Lesion: 15 (36%) 

• Type III Lesion: 12 (28%) 

Average length of subjective follow up: 2.04 years (1 to 5.9 years) 

Patient Follow Up - Morrey (Mayo Clinic) Elbow Evaluation 

• Pain 

• Motion 

• Strength 

• Instability 

• Function 

Results Morrey / Mayo Score (100 Points possible) 

• Overall 95 

• Type I 96 

• Type II 87 

• Type III 99 

Function Score (12 Points possible) 

• Overall 11 

• Type I 10.8 

• Type II 10.6 

• Type III 11.6 

Patient Response: 37/39 better or much better 

Arthroscopic Release for Lateral Epicondylitis 

Owens, Murphy and Kuklo (Arthroscopy 2001 Jul;17(6):582-7) 

16 patients 

• 5 Type I 

• 5 Type II 

• 6 Type III 

3 with concurrent pathology 

Return to work – 6 days 

Arthroscopic Treatment of Lateral Epicondylitis- The 4-Step Technique 

Romeo and Fox (Orthopedic Technology Review Vol 4 No. 5 Sept/Oct 2002) 

1. Resect anterior lateral capsule 

2. Resect ECRB proximal and posterior to ECRL 

3. Resect anterior to LCL 

4. Decorticate origin of ECRB 

Follow-up 


• 2 years 

• 13 of 14 extremely satisfied 

• Strength symmetrical 

Current study 

Evaluate the long-term results of arthroscopic treatment of lateral epicondylitis in terms of: 

• Patient satisfaction 

• Pain relief 

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• Return to function 

Demographics: Chart Review 


• 120 elbows 

• Male:Female ratio: 52%:48% 

• Age Range: 19-76yrs., Average age: 46 yrs. 

Mechanism: 

• Acute / Traumatic : 22% 

• Chronic / Overuse: 71% 

• Unknown: 7% 

Hand Dominance: 

• Dominant: 66% 

• Non-dominant: 24% 

• Bilateral: 10% 

Worker’s Comp: 

• Yes: 27% 

• No: 73% 

Conservative Treatment 

Non-op duration: 

• 12 mo: 29% 


Number of Injections: 

• 0: 7% 

• 1: 22% 

• 2: 18% 

• 3+: 45% 


Preop Findings 

Tenderness Lateral Epicondyle 

Pain with resisted wrist extension and supination 

ROM: 

• FROM: 72% 

• Lacks Ext: 5% 

• Lacks Flex: 7% 

• Lacks both: 12% 


Intraoperative Findings 

Baker Type: 

• Type I: 32% 

• Type II: 37% 

• Type III: 19% 

No correlation between lesion type and age, sex, etiology, length of nonoperative treatment, or arm 

dominance. 

Associated Pathology: 

• None: 41% 

• Synovitis: 34% 

• Degenerative changes: 21% 

• Loose body: 4% 

Follow Up Interval 

1-2 years: 29 pts 




>5 years: 39 pts 

Average: 49 months 


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Results 

44 pts contacted 

Average F/U 43 months 

3 failures which later required open procedure 

Visual analog scores (0-10) 

• Pain at rest: 1.2 

• Pain with ADL: 2.1 

• Pain at work: 3.2 

Results: Patient response 

Compared to pre-op: 

• Much better: 61% 

• Better: 28% 

• Same: 11% 

• Worse: 0% 

• (89% Better or Much Better) 

Results: Andrews Criteria 

Subjective score 

• Excellent: 56% 

• Good: 14% 

• Fair: 25% 

• Poor: 5% 

• (Average 85/100 points) 

Objective score 


• Good: 5% 

• Fair: 0% 

• Poor: 0% 

• (Average 98/ 100 points) 

Total score: 


• Good: 23% 

• Fair: 8% 

• Poor: 0% 

• (Average 184/200 points) 

• (92% Good or Excellent results) 

Summary Lateral Epicondylitis 

Arthroscopic treatment of lateral epicondylitis is a reliable treatment 

• Results comparable to open procedures 

• Release is feasible and reproducible 

• Arthroscopy allows complete examination and treatment of associated pathology 

• Keeps common extensor origin intact 

• Allows quicker rehabilitation 

• Grip strength maintained 

Synovial Fringe 

Remnant of confluence of radial ulnar, ulnohumeral and radial humeral joints. 

Described as a cause of tennis elbow with excision recommended in open series. 

Symptoms 

Intermittent catching, locking, loss of motion. 

No antecedent trauma. 

Pain with flexion/extension of the elbow. 

Pain localized to radial head. 

Signs 

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Pain may be present on forced hyperextension. 

Pain on forced pronation, localized to lateral radial capitellar joint. 

Pain relieved with intra-articular Xylocaine injection. 

Studies 

X-rays negative. 

No record of MRI studies. 

Treatment 

Arthroscopic release 

• Proximal medial viewing portal 

• Proximal lateral operating portal 

• Look for anterior band 

Posterior arthroscopy 

• Direct lateral portal 

• Look for › synovitis in the posterior RC joint 

• Remove fibrotic synovium 

• Look for radial chondromalacia 

Conclusions 

The presence of synovial plicae in the radiocapitellar joint must be considered in the differential 

diagnosis of painful snapping elbow. Arthroscopy confirms the diagnosis and allows excision of the 

plica. 

Always suspect in "tennis elbow". 

Arthroscopic evaluation should always include posterior radial capitellar joint 


My Practice: "Tennis Elbow" 2002 

First visit 

• History and physical confirm diagnosis 

• Rehab exercises (super seven) 

• Counterforce brace/decrease activities 

• Injection +/- 

Second visit – symptomatic 

• Injection 

• ESWT 

Third visit – failed ESWT 

• Arthroscopic release 

Thank you! 

Bibliography 

• Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic classification and treatment of lateral 

epicondylitis: 2-year clinical results. J Shoulder Elbow Surg. 2000;9:475-82. 

• Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic versus open techniques for extensor 

tendinosis of the elbow. Tech Shoulder Elbow Surg. 2000;1:184-191. 

• Kuklo TR, Taylor KF, Murphy KP, Islinger RB, Heekin RD, Baker CL Jr. Arthroscopic release for lateral 

epicondylitis: a Cadaveric model. Arthroscopy 1999;15:259-64. 

• Nirschl RP. Elbow tendinosis/tennis elbow. Clin Sports Med. 1992;11:851-70. 

• Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint 

Surg Am. 1973;55:1177-82. 

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NEW FRONTIERS IN SHOULDER ARTHROSCOPY 

Friday, March 14, 2003 • Aotea Centre, ASB Theatre 

Chairman: W. Jaap Willems, MD, Netherlands 

Faculty: Stephen Burkhart, MD, USA, George Lajtai, MD, Austria, Anthony Miniaci, MD, FRCS, Canada and Joe De 

Beer, MD, South Africa 

- Opening – Jaap Willems 

- Arthroscopic Treatment of Subscapularis Tendon Injuries – Stephen Burkhart 

- Arthroscopic Management of Acromioclavicular Dislocations – Joe De Beer 


- Arthroscopic Reconstruction of Glenoid Fractures – George Lajtai 

- Decision Making in Multidirectional Shoulder Instability – Anthony Miniaci 

- HAGL Lesions: Can They be Treated Arthroscopically – Jaap Willems 

ARTHROSCOPIC MANAGEMENT OF ACROMIOCLAVICULAR DISLOCATION 

DR JOE DE BEER 

CAPE TOWN 

In our large experience of rugby injuries it was evident that injury to the AC joint is the most common 

shoulder injury in rugby. These included Type I – V dislocations. 

Grade I Subluxation: these often lead to a painful AC joint. Management is Arthroscopic Mumford procedure, 

using two superior AC portals. This approach is also used for other forms of isolated AC joint pain 

(for e.g. "weight lifter’s shoulder") 

Grade II subluxation: Often Arthroscopic Mumford is indicated. 

Grade II subluxation: it has to be determined what the cause of the pain is in these cases: 

1 AC joint pain – pain relief after injection of local anaesthetic into AC joint.. This cause is rare in Grade III 

2 Secondary impingement of rotator Cuff due to tilting of scapula. Diagnosis made by subacromial injection 

– Arthroscopic Acromioplasty may be indicated. 

3 Traction on brachial plexus and scapular stabilisers: the most common problem – diagnosis made by 

traction on arm. Reconstruction of AC joint is indicated. (Weaver Dunn procedure) 

ARTHROSCOPIC ACROMIOCLAVICULAR RECONSTRUCTION 

This is a relatively new procedure and been described by Snyder (done via subacromial route) and Wolfe 

(done via intra-articular route). This procedure further developed by using graft material from distal clavicle 

to coracoid – viewing the coracoid from a posterior gleno-humeral portal 

CONCLUSION: 

The arthroscopic management of painful AC joint is well established and reproducible. Reconstruction of 

the AC joint arthroscopically has been developed and will soon be perfected. 

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Arthroscopic reconstruction of glenoid fractures 

Georg Lajtai MD 

Altis -Center for Sportsurgery 

Austria, Europe 

http://www.shoulder.org 

Introduction: 

Fractures of the scapular are relatively uncommon injuries, and most can be treated satisfactorily with nonoperative 

methods (1-6). 

Scapula fractures are often associated with multiple traumatic injuries which may take priority, drawing 

attention away from a treatment of the scapular fracture (2,3,6). 

Fractures of the scapula generally occur in high energy setting of vehicular trauma or fall from height. They 

are infrequent injuries compromising no more than 5 % of shoulder girdle fractures in most clinical reports. 

(2,7,8) 


This is likely because of a thick protective muscular envelope and recoil of the underlying chest wall on 

impact. Another factor is the highly mobile shoulder girdle soft tissue and bony suspensory mechanism 

where the clavicle and its articulations represent the sites of failure with most accident mechanisms. 

Displaced fractures of the acromion, scapular spine and neck have shown poorer outcomes with conservative 

treatment and for this reason operative reduction and internal fixation are usually recommended (9- 

11). 

Open reduction and internal fixation of displaced glenoid fractures have shown promising results in previous 

small series (10, 12, 13) 

Classification: 

Ideberg proposed a detailed scheme for classification that was based on a review of 338 scapula fractures 

in 322 patients (13). This scheme included fractures of the glenoid rim and the glenoid fossa. 

Classification of intraarticular glenoid fractures 

Type I: 

Glenoid rim fractures 

Typ I a: 

With anterior fracture fragment 

Typ I b: 

With posterior fracture fragment 

Type II: 

Inferior glenoid fracture involving part of the neck 

Type III: 

Superior glenoid fracture extending through the base of the coracoid process 

Type IV: 

Horizontal fracture involving both scapular, neck and body. Fractureline always runs inferior to the 

spine of the scapular 

Type V: 

Horizontal fracture (as in type IV), with an additional complete or incomplete neck fracture 

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Type VI: 

Type VI fractures are severely comminuted injuries of the glenoid fossa, caused by violent forces.(14) 

Arthroscopic reconstruction of displaced glenoid fractures 

Requirements: 

1. Trained surgeons in arthroscopic shoulder surgery 

2. Experienced surgeons in ostheosynthesis and their complications 

3. Well presorted OR-Team 

4. Having the possibility to do the reconstruction open if necessary (Instruments…) 

5. Arthroscopic pump must be available 

6. Arthroscopic instruments 

7. Cannulated screws 

8. Nurse must perfectly use the C- arm 

If there is one point not accomplished, you should not try to do this type of procedure. 


Positioning: 

The patient is positioned in the lateral decubitus position with the arm in 45 

degrees abduction and 20 degrees anteversion in a shoulder arm holder. 

The C-arm must have the possibility to change the position between the 

axial and the ap-position, so that surgeons can change the view according to 

what they need to see. 

Good arthroscopic is well as good. X ray pictures must be guaranteed otherwise 

the procedure can turn into a disaster. 

OR-Technique: 

• Standard posterior portal to the glenohumeral joint 

• Rinse the glenohumeral joint to get good visibility 

• Inspection of the joint 

• Remove debris and blood clots out of the joint and the fracture line 

• Classify the fracture and additional injuries 

• Make an anteriorsuperior and midglenoidal portal with the SPS portal system in correct position to the 

fracture fragments 

At this point the C- Arm will put in to the OR field so that an axial as well as an AP-view is possible. 

• 

At the time, when the C- Arm is correct positioned and the arthroscope looks at the fracture, the surgeon 

starts to make the reposition manoeuvre with the raspatorium - arthroscopically as well as radiologically 

controlled. 

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At the beginning of the procedure the aim is to mobilize the fracture parts - to get a perfect reduction later 

on. 

When the fracture fragments are mobilized and it is visiable that the reposition will be possible, next step 

is to change the portals, so that the arthroscope is viewing from the anterior portal. 

• Viewing from the anterior portal the next step will be, to put a Steinmann-pin through the posterial 

portal into the proximal glenoid fragment. 


This Steinmann-pin will be used as a joystick to direct the proximal fracture in correlation to the distal 

fragment. 

If the Steinmann-pin is good in place, reduction can be done on the arthroscopic as well on the radiologic 

control. 

• Put in an orientation needle 

With a K-wire you can hold the reduction and it allows a temporary fixation of the fracture fragments. 

If you are happy with the result of your reduction: 

• Make a skin incision at the Neviaser portal where your K-wire is in place and insert a cannulated screw. 

• Control your manoeuvre with x-ray and arthroscope 

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Conclusion: Arthroscopic reconstruction of glenoid fractures can be recommended in dislocated two part 

glenoid fractures type Ideberg IV and V. It is a technical demanding operative procedure, but minimal invasive 

and it allows anatomical 

reduction under arthroscopical control and stable fixation. Therefore a short postoperative rehabilitation 

and a good functional outcome can be expected. 

References: 


1. Aulicino, P. L.; Reinert. Charles; Kornberg, Markus; and Williamson, Sterling: Sisplaced intro-articular glenoid 

fractures treated by open reduction and internal fixation. J. Trauma, 26: 1137-1141, 1986. 

2. Imatani, R.J.: Fractures of the scapula: a review of 53 fractures. J. Trauma, 15: 473-478, 1975 

3. Mc Gahan, J. P., Rab, G. T.; and Dublin, Arthru: Fractures of the scapula. J. Trauma, 20: 880-883, 1980. 

4. Rowe, C. R.: Fractures of the scapula. Surg. Clin. North America, 43 : 1565-1571, 1963. 

5. Ruedl, T., and Chapman, M. W.: Fractures of the scapula and clavicle. In Operative Orthopaedics, edited 

ba

- Patient population- type of instability (voluntary, involuntary, habitual), direction (anterior, posterior, 

multi), injury pattern (traumatic, atraumatic), laxity (degree, generalized vs. focal, asymmetry) 

- Symptom definition- (Pain, Instability-subluxation/dislocation, micro) 

- Surgical pathology- capsular laxity, labral or cuff pathology, Bankart lesion, bony defects 

- More difficult than AMBRI definition- a spectrum exists even amongst these patients 

Treatment Options 

- Open Inferior Capsular Shift 

- Arthroscopic Inferior Capsular Shift and Interval Closures 

- Thermal Capsular Modification 

Open Inferior Capsular Shift 

- traditional, humeral based capsular shift 

- glenoid based procedures 

- assure shift is in north-south plane, not east-west 

- east-west shift results in loss of external rotation and potential recurrent instability 

- superior east west shift results in decreased external rotation and inferior instability-(Flask Deformity of 

capsule) 

- long term surgical results depend on patient and symptoms 

- generally the best for MDI with true instability and generalized laxity 

- approach from front in most but may want to consider posterior approach in those patients with MD laxity 

BUT posterior predominance of symptoms 


Arthroscopic Capsular Shift 

- same principles as open shift 

- glenoid based shift and therefore amount of shift is less than humeral based shifts 

- capsular tuck when labrum is intact 

- BE CAREFUL with tucks- tendency is to reduce capsular volumes in all directions which can cause stiffness(loss 

of rotational motion) or failures 

- Interval closure possible and considered important arthroscopically 

- Sometimes combined with focal or minor thermal treatment 

Thermal Capsular Modification 

- thermal energy becoming increasingly popular 

- use of laser, radiofrequency 

- laser – more expensive to use 

- requires specialized training 

- more dangerous to use 

- radiofrequency – less expensive, easier to use 

Techniques 

- depends on temperature dependent denaturation of the crystalline triple helix of type I collagen 

- time and temperature dependent 

- >65∞ causes significant denaturation of collagen 

- decrease stiffness and viscolastic behaviour of tissue for 6 weeks then recovery 

- remodeling ? is very slow and therefore may require more time to rehabilitation 

Clinical Uses 

- wide popularity because of ease of use 

- indications are not clear! 

- most reported series treat patients with mixed clinical picture 

- very few guidelines for use 

- many questions – indication for use 

- length of immobilization 

- how to treat capsule 

- location of application 

- ? complications 

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Recent Study (Miniaci et al.) 

- 19 patients with MDI with true instability 

- 2 year follow-up 

- 9/19 failures (47%) 

- 5/19 stiffness – reduced rotational motion 

- 4/19 – potential axillary nerve irritation 

- Failures – surgical revision revealed capsular deficiency in one third 

Clinical Results 

- Not good in posterior dislocation, MDI or voluntary types of instability pattern 

- Better results in anteroinferior instability, More subtle instability (subfluxation vs.Dislocaton) 


Unknown Issues 

1. ? immobilization time – will this improve failure rate or does it increase stiffness rate 

2. ? capsular stripes/dots vs. painting – will this reduce capsular damage 

3. ? avoid inferior pouch – does this reduce axillary nerve injury or does it not treat 

essential lesion of MDI (inferior capsular redundancy) 

RECOMMENDATIONS 

- need more research to determine technique and indications 

- be careful in patient selection (i.e. degrees of instability) 

- need classification of patients being treated to determine optimal method of treatment 

CLASSIFICATION 

1. MDI with true dislocations/instability 

2. MDI with PAIN but no or little instability complaints 

2a. MD laxity- asymmetric – pain +/- mild instability 

2b. MD laxity- symmetric- pain 

MDI with true dislocations/instability 

- thermal capsular modification not very successful 

- open or arthroscopic shift preferred 

- beware of other pathology 

- with voluntary instability, especially posterior an open procedure still preferred 

MDI with no instability complaints but PAIN 

- arthroscopic shift excellent 

- treat other pathology, often labral tears will give asymmetric laxity 

- thermal as an adjunct is questionable/no proof but good reports 

- when laxity is symmetric and no other pathology is identifiable may want to consider thermal treatment 

References: 

1. Altchek DW, Warren RF, Skyhar MJ and Ortiz G: T-Plasty: A Technique for Treating Multidirectional 

Instability in the Athlete. Orthop. Trans, 13:569-561, 1989. 

2. Bigliani LU: Anterior and Posterior Capsular Shift for Multidirectional Instability. Techniques Orthop, 3 

(4): 36-45, 1989. 

3. Bigliani LU, Kurzweil PR, Schwartzbach CC, Flatow EL, and Wolfe I: Inferior Capsular Shift Procedure for 

Anterior Inferior Shoulder Instability in Athletes Orthop. Trans. 13:560, 1989. 

4. Bigliani, LU, Pollock, RG, McIlveen, SJ, and Flatow, EL: The Inferior Capsular Shift Procedure for 

Multidirectional Instability of the Shoulder. American Orthopaedic Association, One Hundred and Sixth 

Annual Meeting, Coronado, California, June, 1993. 

5. Cooper RA and Brems JJ.: The Inferior Capsular Shift Procedure for Multidirectional Instability of the 

Shoulder. J. Bone and Joint Surg., 74-A: 1516-1521, Dec., 1992. 

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6. Cordasco FA, Pollock RG, Flatow EL, and Bigliani LU: Management of Multidirectional Instability. 

Operative Techniques in Sports Medicine, 4:293-300, 1993. 

7. Endo H., Takigawa T., Takata K. and Miyoshi S.: A Method of Diagnosis and Treatment for Loose Shoulder 

(in Japanese). Cent. Jpn. J. Orthop. Surg. Traumat, 1971, 14:630-2. 

8. Harryman DT, Slides JA, Harris SL., and Matsen FA: Laxity of the Normal Glenohumeral Joint: A 

Quantitative In Vivo Assessment. J. Shoulder and Elbow Surg., 1:66-76, 1992. 

9. Miniaci, A., McBirnie J. L. Thermal Capsulargraphy in the Treatment of Multidirectional Shoulder 

Instability. A Prospective Consecutive Series. (submitted publication) 

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and Treatent. IN: Instr. Course Lect. 1985: 34:232-238. 

11. Neer CS II, and Foster CR: Inferior Capsular Shift for Ivoluntary Inferior and Multidirectional Instability 

of the Shoulder. A Preliminary Report. J. Bone and Joint Surg., 62A: 897-908, 1980. 

12. Neer CS II: Shoulder Reconstruction. Saunders, Philadelphia, 1990:273-341. 

13. Norris TR, and Bigliani LU: Analysis of Failed Repair for Shoulder Instability – A Preliminary Report. IN: 

Bateman JE, and Welsh RP, Eds: Surgery of the Shoulder. Decker, Philadelphia, 1984. 

14. Treacy, S. H., Savoie, F. H., Field, L. H. Arthroscopic Treatment of Multidirectional Instability. J. Shoulder 

Elbow Surg. 8: 345-350, 1999. 


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Knee OCD 

Friday, March 14, 2003 • Aotea Centre, Kupe/Hauraki Room 

Chairman: Lars Engebretsen, MD, PhD, Norway 

Faculty: Anthony Miniaci, MD, FRCS, Canada, Lars Peterson, MD, PhD, Sweden, Jon Karlsson, MD, PhD, Sweden and 

Andre Frank, MD, France 

TREATMENT OF OCD WITH MOSAIC PLASTY 

Professor Jon Karlsson 


Although the treatment of OCD is controversial and there is no consensus in the literature, mosaic plasty, 

using osteochondral grafts is without doubt one option. This form of treatment is especially useful in case 

of large OCD, which is still in-situ. In most cases 3-4 osteochondral plugs can be used. This form of treatment 

is probably widely used today, however, there are several obvious limitations, which are still unsresolved. 

The risk of complications, including donor-site pain is one of the major draw-backs. In most cases 

the mosaic plasty is also performed as an open knee surgery, in which case arthrotomy is needed. It should 

also be born in mind that the best treatment is still unknown, as no randomised studies are yet found. 

OSTEOCHONDRITIS DISSECANS OF THE KNEE TREATED WITH AUTOLOGOUS CHONDROCYTE 

TRANSPLANTATION 

Lars Peterson, Gothenburg Universiy, Gothenburg, Sweden. 

Introduction: The etiology of osteochondritis dissecans (OCD) is still unknown, but the relations to trauma, 

repeated trauma and physical activity are discussed as possible. The treatment however varies with the age 

of the patient and the type of lesion and is a challenging clinical problem. Autologous chondrocyte transplantation 

(ACT) has been used in the treament of OCD of the knee in Gothenburg, Sweden since 1990. 

Previous reports on the treatment of OCD with ACT showed promising results. Late results (2-10 year follow-up) 

will be presented as well as complications. 

Methods: Forty-two patients with OCD were treated with ACT between September 1990 and October 1997. 

Mean age was 26 years (range 15-50) and the mean duration of symptoms was 7.5 years at the time of 

treatment. 83% had a mean of 3.2 prior surgeries. The defects were located on the medial femoral condyle 

(n=28), the lateral femoral condyle (n=13) or the femoral trochlea (n=1), the mean defect size was 5.7 cm2 

(range 1.5-12.0) and mean depth was 7.7 mm (range 4-15). At a mean follow-up of 4.8 years (range 2-10) 33 

patients were assessed clinically and 10 patients were evaluated arthroscopically. 

Results: At follow-up the clinical status were graded Good or Excellent in 86% of the patients and 84% considered 

themselves improved. Tegner-Wallgren activity score increased from mean 6.8 preoperatively to 9.3 

at follow-up and mean Lysholm score at follow-up was 73.5, compared to 44.3 preoperatively. Brittberg- 

Peterson functional VAS decreased from a mean 80.4 preoperatively to 31.6 at follow-up. At the arthroscopic 

assessment the graft was evaluated according to the Brittberg scoring system for the degree of defect 

repair, integration to border zone and macroscopic appearance with a maximum of 12 points. The mean 

score was 10.2, only one had a score less than 9. In two patients the treatment was considered as a failure, 

both of which occurred early postoperatively. Successful and unsuccessful cases will be presented. 

Discussion: The outcome after treating OCD with autologous chondrocyte transplantation is successful for 

more than 80% of the patients, the clinical status is improved and the patients consider themselves 

improved and are able to live a more active life. 

3.134

Osteochondritis Dissecans 

Clinical Treatment Options 

Anthony Miniaci, MD, FRCSC 

Professor of Orthopaedic Surgery 

Head of Sports Medicine Program 

Department of Surgery, University of Toronto 

Toronto, Ontario 

Objectives: 

At the end of this presentation the participant will be able to: 

- Understand the history and evaluation of osteochondral knee disorders specifically osteochondritis dissecans 

- Identify the efficiency of the various surgical techniques used to treat osteochondral defects and indications 

for each 

- Be able to identify the limitations and strengths of various techniques used to treat chondral and osteochondral 

pathology 


Osteochondritis Dissecans 

Localised lesion characterised by seperation of a segment of articular cartilage and its underlying subchondral 

bone 

Incidence 

-Poorly understood entity with no universally accepted etiology. 

-True incidence unknown as often spontaneous resolution without presentation. 

-Multiple joints reported but knee accounts for 75% (Pappas) 

Male:Female 2:1 (Pappas) 

Etiology 

2 Types based around physeal closure 

- Juvenile OCD 5-15yr 

-Adult OCD 15-50yr 

-Several factors implicated, 

- Trauma 

- Ischaemia 

- Genetic 

- Defects of ossification 

-? Hormonal 

Direct Trauma- As the posterolateral portion of the medial femoral condyle is affected in 85% of knees, 

direct trauma is unlikely (Aichroth) 

Indirect Trauma - Odd facet of patella articulating with area (Aichroth) 

- Impingement of tib spine on area in internal rotation (Fairbank) 

Ischemia 

-Abnormal End-artery theory of subchondral bone susceptible to emboli and ischaemia has been suggested. 

(Campbell) 

-other studies found blood supply of subchondral femur rich in anastomoses & the histology of loose bodies 

and resected fragments to NOT demonstrate evidence of OCD (Chiroff) 

Genetic 

-Suggested that OCD may represent a mild subgroup of epiphyseal dysplasia (Ribbing) 

-Associations with Perthes & Achondroplasia 

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-Familial relationships have been recorded (Stougard) 


Ossification Defects (Juvenile OCD) 

-OCD represents irregularity of ossification (Mubarak) 

-Multiple OCD lesion maybe due to an irregularity of ossification due to MED (Mubarak) 

Presentation 

-Symptoms dependent on stage of lesion 

-Early - vague pain +/- swelling, activity related 

-Late - if flap or loose body, catching & giving way 

-Effusion, tenderness, crepitus 

-External rotation of leg 

-Wilson’s sign (Flex to 90 & extend in IR, pain at 30 degrees) 

Investigations 

-Plain x-ray – notch/tunnel view required 

-Tc 99 Scan – previously described to identify & follow the course/recovery of OCD (Cahill) 

-MRI now best modality for diagnosis and following progress of lesion 

MRI Classification 

Stage I -Thickening of artic. cart. & low signal change 

Stage II-Artic. cart. breached & low signal rim behind fragment 

Stage III -Artic. cart. breached & high signal changes behind fragment 

Stage IV -Loose body (Dipaola) 

MRI 

-MRI Arthrogram better to assess breach in cartilage (Kramer) 

-Spoil Gradient Sequences for articular cart (SPGR) 

Arthroscopy 

- Arthroscopic assessment 

- Clanton & DeLee 

o Grade I - Depressed subchondral fracture 

o Grade II - OC fragment attached by an osseous bridge 

o Grade III - A detached non-displaced fragment 

o Grade IV - Displaced fragment 

Management 

-Controversy & confusion in literature as often small numbers, mix juvenile & adult and few prospective trials 

-Management dependent on 

- Age of patient 

- Stage of lesion 

Juvenile OCD- 

-Lesions in knees with open physes usually heal with conservative treatment, those that don’t are due to 

continued activity. (Cahill) 

-Ideal initial management conservative. 

- Protected wt bearing/restriction of activities (90 degree casts) 

- However, affected children often athletic & difficult to fully restrict. 

- Try to avoid impact activities 

- Chances of success with non-op treatment decrease as time of physeal closure nears 

- 50% heal within 12 months 

- Follow progress with serial MRI 

Indications for Operative Intervention 

-Symptoms persist for 6 – 12 months despite adequate non-operative treatment 

- Loose fragment 

- Progression of defect radiologically (MRI) 

- Predicted physeal closure within 6-12 months 

3.136

Adult OCD 

- Symptomatic lesions rarely heal with non-operative measures 

- Lower tolerance for operative intervention after failure of conservative measures. 

Operative Intervention 

-Stabilisation/Re-fixation of fragment 

(Clanton II, III & selected IV) 

-Excision of fragment/Reconstruction of OCD defect 

-Clanton Type II/III (IV) 

- Principles: 

- rigid fixation 

- enhance blood supply 

- re-establish congruency 

Arthroscopic Drilling: 

- Controversial for most lesions but good results reported in Juvenile 

Clanton II lesions(Aglietti) 

Internal Fixation: (open or arthroscopic) 

- Pins (Smillie) 

- K-wires (Cahill) 

- Herbert Screws (Mackie) 

- Biodegradable Rods (Dervin) 

- Corticocancellous Bone Pegs (Victoroff) 


-Additional bone grafting under articular cartilage (Anderson) 

OCD Defect 

- Poor results after excising lesion & leaving defect (Cahill) 

- Healing fibrocartilage biomechanically less resilient than articular cartilage predisposing to 

degenerative changes (Landells) 

Fragment Fixation-Technique (Miniaci) 

a) Clanton and DeLee type II and III lesions 

- Unstable lesions that fail conservative management 

- can be used in prepubertal and postpuberty patients 

- theoretical considerations 

i. stabilize fragment with K-wire, remove after fixed with 1 or 2 plugs 

ii. drill holes – stimulates blood supply 

iii. press fit 3.5 mm or 4.5 mm plugs 

- results in stable fixation 

iv. place peripheral plugs between native vascular bone and fragment so that healing of fragment 

can occur 

v. plug serves as a source of bone graft 

vi. cartilage cap on "plug" restores articular surface so end result will have continuous articular 

cartilage surface 

vii. central plug should be used for ultimate stability. This should be long enough to traverse OCD 

fragment into underlying vascular bone. 

Measure depth preoperatively. 

Ultimately provides- blood supply–drilling 

-stability-interference fixation 

-bone grafting of fibrous layer 

-congruent articular cartilage surface 

clinical results > 20 cases of OCD 

100% healing rates 

no additional fixation 

return to activity and sports by 3 to 4 months 

3.137

complete healing by 6 to 9 months 

viii. Type IV Lesions 

-Where suitable for fixation- debride bed 

-Initial stabilisation with k-wires is required before plug insertion 

b).Chronic lesions- Indications for Treatment 

- Symptomatic defect (trial of debridement) 

- Stable knee 

- Normal biomechanical alignment 

- Minimal degenerative changes 

Defect Reconstruction 

- Large osteochondral grafts 

-Autografts (Outerbridge) 

-Mosaic Autografts (Hangody, Bobic, Miniaci) 

-Allografts (McDermott) 

- Chondrocyte culture implantation- ? not as effective as a result of bone defect 


Filling of Defect – Mosaicplasty Reconstruction 

Technique – when fragment lost BE CAREFUL 

-Aim to recreate joint curvature &congruence 

-Fill defect with grafts from the periphery inwards. This allows for assessment of joint curvature and for 

central graft support 

-Central pegs will need to be longer to account for the greater height of curvature and depth of crater 

- need to sit central plugs higher, since you are reconstructing both 

a bone and cartilage defect 

- if plugs in center are not higher, then reconstruction will be flat 

- * measure center of defect on MR preoperatively to determine size 

and length of plugs 

- graft harvest from edge of patellofemoral joint (Both knees as necessary) (10-12 4.5 mm grafts from 

each knee) 

-Post-operative treatment 

- Allow knee motion but strict non-wt bearing for 6 weeks 

- Gradual wt-bearing at 6 weeks 

- return to sport 3-4 months 

-effusion can last 4 months ( painless ) 

1. Focal Traumatic Osteochondral Lesions 

- similar principles to OCD 

- in acute lesions can use plugs to fix osteochondral lesions 

- femoral condyles easiest 

- tibial lesions difficult, not practical 

- trochlear lesions usually require arthrotomy 

2. Patellofemoral Lesions 

- trochlear and patellar lesions need arthrotomy 

- usually combine with Fulkerson osteotomy and lateral release 

i. to be sure to reconstruct contour of both femoral trochlea and patella 

ii. place plugs close together to increase stability 

iii. put knee through repeat range of motion – if incongruency exists, this 

needs to be adjusted otherwise the plug heads will SHEAR off 

Optimum Surgical Conditions 

- many unknown variables at present 

- morbidity related to both donor and recipient sites as well as method of delivery 

3.138

Donor Sites 

- plug harvest location important 

- keep out tibiofemoral joint 

- 5mm on periphery of patellofemoral joint is optimal (less contact), avoids reciprocal arthrosis 

- large plugs, > 5mm fill incompletely, with fibrosis tissue 

- causes reciprocal OA in areas of weight bearing contact 

Recipient Sites 

- hole preparation crucial 

- preserve bone stock, need stable construct 

- drilling holes causes thermal necrosis 

- dilating holes preserves bone stock and reduces thermal necrosis 

- press fit plug to hole for stable construct 

- bottom out hole to avoid 

- subsidence 

- cyst formation 

- fill defect with as much articular cartilage as possible, reduces % of fibrocartilage 

- put plugs even with surrounding articular surface 

i)too proud- causes loosening and cyst formation 

ii)recessed- covered with fibrocartilage 

- ? heterotropic transfers 

- does thin cartilage become thick or vice versa 

- ? cartilage degeneration 


Graft Harvest and Delivery 

Harvest 

- do not use power trephine for harvest 

- causes cell necrosis 

- multiple small plugs allows for better reconstruction of curved surface 

- inspect plus after harvest 

i) plug integrity 

ii) fractures 

iii) obliquity 

iv) measure depth of plug 

Plug Delivery 

- press fit plugs, flush with surrounding articular surface, bottom out hole 

- manual or light pressure only to insert plugs 

- ? impaction causing cell necrosis 

- reconstruct curved surfaces, (center higher than periphery) 

- tendency is for flat reconstructions 

Basic Science/Clinical Results 

- early clinical results 

good anecdotal 

- need to define patient populations 

- at present best in patients failing other procedures (i.e. debridement, microfracture, etc.) 

- osteochondritis dissecans excellent results 

- traumatic lesions good 

- patellofemoral – fair to good 

- histologically Type II collagen preserved, bone healing of plugs provides solid structure 

- subchondral cyst formation a concern 

Future 

- ? hybrid techniques 

- ? donor site reconstruction 

3.139

REFERENCES 

Buckwalter JA, Mankin H.J. Articular cartilage: Part II: Degeneration and Osteoarthrosis, Repair, 

Regeneration, and Transplantation. JBJS- American Volume 1997; 79A:612-618. 

Rodrigo JJ, Steadman RJ, Silliman JF, Fulstone HA. Improvement of Full-thickness Chondral Defect Healing 

in the Human after Debridement and Microfracture Using Continuous Passive Motion. Am. J Knee Surg 

1994; 7:109-116. 

O’Driscoll SW, Keeley FW, Salter RB. Durability of Regenerated Articular Cartilage Produced by Free 

Autogenous Periosteal Grafts in Major Full-thickness defects in Joint Surfaces Under the Influence of 

Continuous Passive Motion. A Follow up Report at one year. JBJS 1988; 70A: 595-606. 

Hangody L. Kish G, Karpati Z, Szerb I, Udvarhelyi I, Toth J, et al. Autogenous Osteochondral Graft 

Technique for Replacing Knee Cartilage Defects in Dogs. Orthopaedics 1997; 5: 175-181. 


Bobic V. Arthroscopic Osteochondral Autograft Transplantation in Anterior Cruciate Ligament 

Reconstruction: Preliminary Clinical Study. Knee Surg. Sports Traumatology, Arthroscopy 1996; 3:262-264. 

Garrett JC. Fresh osteochondral Allografts for Treatment of Articular Defects in Osteochondritis Dissecans 

of the Lateral Femoral Condyle in Adults. Clinical Orthopaedics & Related Research 1994; 33-37. 

Hurtig M, Pearce S, Warren S, Kalra M, Miniaci A. Arthroscopic Mosaic Arthroplasty of the Equine Third 

Carpal Bone. Submitted for publication. 

Pearce S, Hurtig M, Clarnette R, Kalra M, Miniaci A. Investigation of Two Techniques for Optimizing Joint 

Surface Congruency with Mosaic Arthroplasty. Submitted for publication. 

Hurtig M, Evans P, Pearce S,Clarnette R, Miniaci A. The Effect of Graft Size and Nimber on the Outcome of 

Mosaic Arthroplasty Resurfacing: An Experimental Model in Sheep. Submitted for publication. 

References- Osteochondritis Dissecans 

Pappas AM. OCD. Clin Orthop 158;1991 

Aichroth P. OCD of the knee. JBJS 53-B;1971 

Fairbank HA. OCD. British J Surg 21;1933 

Campbell & Ranawat. OCD: the question of etiology. J Trauma6; 1966 

Chiroff & Cooke. OCD: microradiographic analysis. J Trauma 15; 1975 

Ribbing S. Hereditary ME disturbances. Actav Orth Scan 24;1955 

Stougard J. Familial occurrence of OCD. JBJS 46-B; 1961 

Mubarak & Carroll. Juvenile OCD of the knee: etiology. Clin Orthop 157; 1981 

Wilson JN. A diagnostic sign in OCD of the knee. JBJS 49-A; 1967 

Cahill & Berg. Tc-99m scintigraphy in the management of OCD. AmJ SportMed 11; 1983 

Dipaloa JD et al. Characterising OCD lesions by MRI. Arthroscopy 7;1991 

Kramer J et al. MR contrast arthrog in OCD. J Comput Assis Tomog 16;1992 

Clanton & DeLee. OCD. History, pathophys & current treatment concepts. Clin Orthop 167; 1982. 

Aglietti P et al. Arthroscopic drilling in juvenile OCD. Arthroscopy 10;1994. 

Smillie IS. The treatment of OCD. JBJS 39-B; 1957 

Cahill B. Treatment of juvenile OCD & OCD of the knee. Clin Sports Med 4;1985 

Mackie IG et al. Arthroscopic use of the Herbert screw in OCD. JBJS 72-B;1990 

Dervin GF et al. Biodegradable rods in adult OCD of knee. Clin Orthop 356; 1998 

Victoroff BN et al. Arthroscopic bone peg fixation in the treatment of OCD in the knee. Arthroscopy 12;1996 

Landells JW. The reaction of injured human cartilage. JBJS 39-B; 1957 

McDermott GB et al. Fresh small fragment osteochondral allo-grafts. Long term follow up on 1oo cases. 

Clin Orthop 197; 1985 

Outerbridge HK et al. OCD defects in the knee. Clin Orthop 377; 2000 

Berlet, Mascia, Miniaci. Treatment of unstable OCD of the knee using autogenous OC grafts. Arthroscopy 

15;1999 

3.140


HIP ARTHROSCOPY 

Friday, March 14, 2003 • Carlton Hotel, Carlton I 

Chairman: J.W. Byrd, MD, USA 

Faculty: James Glick, MD, USA, Michael Dienst, MD, Germany and Romain Seil, MD, Germany 

J.W. Byrd, MD 

y 

I. Merits of the Supine Position 

A. Effective and reproducible 

B. Utilizes existing OR equipment (standard fracture table) 

C. Positioning simple and time efficient 

D. Orientation familiar for orthopaedic surgeons 

E. Operating room layout user friendly for the surgeon and support staff 


II. 

III. 

Equipment 

A. Fracture table 

- Tensiometer for monitoring traction forces intraoperatively is the most 

important modification 

B. C-arm image intensifier 

C. 70° and 30° video-articulated arthroscopes 

D. Fluid management system 

E. Specialized hip arthroscopy cannula system 

1. Extra length cannulas 

2. Shortened bridge accommodates extra length cannulas with standard 

arthroscope 

3. Cannulated obturators 

- Allows prepositioning with spinal needle. Cannula/obturator 

assembly can be passed over a guide wire initially placed through 

the needle 

F. Extra length flexible cannulas allow passage of curved shaver blades 

G. Extra length sturdy hand instruments 

- Avoid instruments designed for other endoscopic purposes that might be 

less sturdy and at greater risk of breakage 

H. Laser exhibits distinct advantages in the hip 

1. Maneuverability 

2. Ability to effectively ablate tissue despite limits of maneuverability 

Anesthesia 

- Typically performed under general anesthetic. Epidural anesthesia is an 

appropriate alternative but requires adequate block for assuring muscle 

relaxation. 

3.141

Hip Arthroscopy: The Supine Approach 

J. W. Thomas Byrd, M.D. 

IV. Patient Positioning 

A. Placed supine on the fracture table (Figure 1) 

B. Heavily padded perineal post, lateralized against the medial thigh of the 

operative leg (Figure 2) 

1. Lateralizing the post adds a slight transverse component to the traction 

vector (Figure 3). 

2. Also lessens the likelihood of compression and possible neuropraxia of 

the pudendal nerve 


Fig. 1 

Fig. 2 

Fig. 3 

3.142




C. Operative hip positioned in extension, approximately 25° of abduction, and 

neutral rotation 

1. Slight flexion might relax the capsule and facilitate distraction, but can 

place more traction on the 

sciatic nerve and draw it 

closer to the joint, making it 

more vulnerable to injury. 

Thus, significant flexion is 

avoided during arthroscopy. 

2. Neutral rotation is important 

during portal placement 

(Figure 4) although freedom 

of rotation during 

arthroscopy can facilitate 

visualization. 

Fig. 4 

D. The contralateral extremity is abducted as necessary to accommodate 

positioning of the image intensifier between the legs. 

- Prior to applying traction to the operative leg, counter force is created by 

placing the contralateral extremity under light traction. This stabilizes 

the pelvis so that it does not shift as traction is gradually applied to the 

operative extremity. 

E. Traction is applied to the operative extremity and distraction of the joint 

confirmed by fluoroscopy. 

1. Typically about 50 pounds is applied. More force may be necessary for 

a tight joint, but should be undertaken with caution. 

2. Initially, adequate distraction (8-10 mm) may not be readily achieved. 

a. Allowing a few minutes for the capsule to accommodate to the 

tensile forces often results in relaxation of the capsule (physiologic 

creep) and adequate distraction without excessive force. 

b. Also, a vacuum phenomenon created by the capsular seal will later 

be released when the spinal needle is introduced and the joint is 

distended with fluid, which may further facilitate distraction. 

F. After confirming the ability to distract the joint, the traction is released until 

ready to begin the surgical procedure. 


3.143



V. Portals 

- The three standard portals are: Anterior, Anterolateral, and Posterolateral 

(Figures 5 and 6). 


Fig. 5 

Fig. 6 

Table 1 

DISTANCE FROM PORTAL TO ANATOMIC STRUCTURES 

(Based on Anatomic Dissection of Portal Placements in Eight Fresh Cadaver Specimens) 

Portals Anatomic Structure Average 

(cm) 

Range 

(cm) 

Anterior 

Anterior Superior Iliac Spine 

a 

Lateral Femoral Cutaneous Nerve 

b 

Femoral Nerve (level of Sartorius) 

(level of Rectus Femoris) 

(level of Capsule) 

Ascending Branch of Lateral Circumflex Femoral 

Artery 

c 

Terminal Branch 

6.3 

0.3 

4.3 

3.8 

3.7 

3.7 

0.3 

6.0-7.0 

0.2-1.0 

3.8-5.0 

2.7-5.0 

2.9-5.0 

1.0-6.0 

0.2-0.4 

Anterolatera 

l 

Posterolatera 

l 

Superior Gluteal Nerve 4.4 3.2-5.5 

Sciatic Nerve 2.9 2.0-4.3 

a 

Nerve had divided into three or more branches and measurement was made to the closest branch. 

b 

Measurement made at superficial surface of sartorius, rectus femoris, and capsule. 

c 

Small terminal branch of ascending branch of lateral circumflex femoral artery identified in three 

specimens. 

3.144




A. Anterior portal (Figure 7) 

1. Positioning 

a. Entry site is at the 

intersection of a sagittal 

line drawn distally from 

the ASIS and a 

transverse line across 

the superior margin of 

the greater trochanter 

b. Directed approximately 

45° cephalad and 30° 

Fig. 7 

towards the midline 

c. Enters the joint under the anterior margin of the acetabular labrum 

(Position is facilitated by direct arthroscopic visualization) 

2. Relationship to extraarticular anatomic structures 

a. Penetrates the sartorius and rectus femoris before entering the 

anterior capsule 

b. At the level of this portal, the lateral femoral cutaneous nerve has 

trifurcated 

i. One of these branches will usually lie close to the portal 

ii. Most branches lie lateral to the portal 

- Moving portal more laterally does not reliably avoid 

these branches 

- Moving portal medially is ill-advised because of closer 

proximity to femoral nerve 

iii. Laceration of the LFCN is avoided by utilizing careful 

iv. 

technique, not incising too deeply with the skin incision 

Although laceration can be avoided, neuropraxia of one of 

these branches may occur due to manipulation of the cannula 

and instrumentation from the anterior position (




B. Anterolateral Portal (Figure 8) 


a. Entry site is over the superior margin of the 

greater trochanter at its anterior border 

b. Direction 

i. In the AP fluoroscopic view, the 

portal passes immediately above the 

greater trochanter and then close to the 

superior surface of the 

femoral head to stay 

underneath the lateral 

acetabular labrum. 

ii. 

Accounting for normal 

femoral neck 

anteversion, with the hip 

in neutral rotation, the 

portal courses parallel to 

the floor, thus entering 

the hip joint just anterior 

to its mid-coronal plane. 

Fig. 8 

2. Relationship to the extraarticular structures 

a. The anterolateral portal lies most centrally in the "Safe Zone" for 

arthroscopy (Consequently it is the first portal established ) 

b. The portal penetrates the gluteus medius before entering the lateral 

capsule 

c. The superior gluteal nerve runs transversely an average of 4.4 cm 

cephalad to the portal 

3.146




C. Posterolateral Portal (Figure 9) 


a. Entry site is over the 

superior margin of the 

greater trochanter at its 

posterior border 

b. Directed slightly 

cephalad and anterior 

(converges toward 

anterolateral portal) 

c. Enters the joint 

underneath the 

Fig.9 

posterolateral margin 

of the labrum (Entry location is performed under direct 

arthroscopic visualization) 

2. Relationship to the extraarticular structures 

a. The portal pierces the gluteus medius and minimus before entering 

the lateral aspect of the capsule posteriorly. 

b. Like the anterolateral portal, the superior gluteal nerve averages a 

distance of 4.4 cm. 

c. It enters the capsule superior and anterior to the piriformis tendon. 

d. It lies closest to the sciatic nerve at the level of the capsule with an 

average distance of 2.9 cm. 

i. Inadvertent external rotation of the hip during portal 

placement will move the greater trochanter more posterior 

relative to the hip joint. This will unnecessarily cause the 

posterolateral portal to pass closer to the sciatic nerve. 

Consequently, external rotation is avoided during initial portal 

placement. 

ii. Hip flexion might partially relax the capsule and improve 

distraction. However this will place more traction on the 

sciatic nerve and may draw it closer to the joint, again placing 

it at more risk for inadvertent damage. Thus, inordinate hip 

flexion during hip arthroscopy should be avoided. 


3.147




VI. 

Portal Placement and Normal Arthroscopic Exam 

A. Traction is applied to the hip 

B. Anterolateral Portal 

1. Placed first because it lies most centrally in the “safe zone” for 

arthroscopy 

2. Prepositioning performed with a custom spinal needle (6", 17 gauge) 

under fluoroscopic guidance 

3. Joint is then distended with saline 

4. Important to avoid penetrating the lateral labrum with the needle 

a. The needle meets greater resistance penetrating the labrum and can 

be felt during placement. 

b. After distending the joint, if necessary, the needle can be 

repositioned closer to the femoral head, further lessening the 

likelihood of piercing the labrum. 

5. A guide wire is passed through the needle and the needle is withdrawn. 

6. The cannula/obturator assembly is then passed over the guide wire into 

the joint. (Figures 10 and 11) 

- As the assembly pierces the capsule, it is 

lifted up to avoid grazing the articular surface 

of the femoral head. 

7. The 70° arthroscope is then introduced in the 

anterolateral cannula. 

a. Use of the 70° scope allows a direct view of 

where the anterior and posterolateral portals 

enter the joint simply by rotating the lens 

anteriorly and posteriorly. 

Fig. 

b. If there is a chance that the cannula may still 

have pierced the labrum, at this point 

excessive maneuvering of the cannula should 

be minimized. 

C. Anterior Portal 

Fig. 11 

1. Prepositioned with spinal needle 

a. Facilitated by fluoroscopy 

b. Precise intracapsular positioning confirmed by direct arthroscopic 

view 

2. As the cannula/obturator assembly enters the joint, again by utilizing 

arthroscopic visualization, the labrum is avoided and the assembly is 

lifted off the articular surface of the femoral head. 

D. Posterolateral Portal 

1. Rotating the arthroscope posteriorly in the anterolateral portal allows 

viewing of the entry site for the posterolateral position. 

2. Needle placement and introduction of the cannula are then carried out in 

the standard fashion. 

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SURGICAL DEMONSTRATION 

HIP ARTHROSCOPY BY THE LATERAL APPROACH 

James M. Glick, M.D. 

I. INSTRUMENTS 

A. Traction device. 

1. Fracture table set for lateral dicubitus position 

2. Specially made traction device with tensiometer 

B. Image intensifier 

C. Hip surgical instruments 

1. 14 or 15 gauge extra long spinal needles 

2. Nitanol guide wires to fit through the needles 

3. Cannulated trochars that fit over nitanol guide wires 

4. Long 30 and 70 degree fore-oblique arthroscopes 

5. Long shaver sheaths. Diameters should be wide enough to accommodate an arthroscopic knife. 

6. Slotted cannulas 

7. Long switching sticks 

8. Arthroscopic knife (Beaver) 

9. Long motorized cutters-straight and curved with cutter on concave side. 

10. Radio frequency or laser ablative instruments 

11. Graspers 

12. Probe 

II. 

ROOM SET-UP 

A. Image Intensifier either above or below table 

B. Surgeon stands In front of patient 

C. Monitors on opposite side of table from surgeon 

Ill. TECHNIQUE 

A. Place patient on his/her side with involved leg upward 

B. Place involved leg in traction device and insert a well-padded perineal post into the crotch. 

1. Hip should be placed in slight flexion, abduction and external rotation to relax the capsule. 

2. If the diameter of the perineal post is less than 9 cm add extra padding to increase its size. A 

large diameter post will distribute the force of the traction, so it is not concentrated as much on 

the pudendal nerve. 

3. Support the lower torso. This will decrease the vertical forces on the post. 

C. Image hip joint 

D. Draw landmarks with marking pen with aid of the image intensifier 

1. Anterior superior iliac spine 

2. Greater trochanter 

E. Scrub and drape with sterile sheets and a sticky drape 

F. Find portals with long spinal needles and the aid of the image intensifier 

I. Portals 

a. Anterior paratrochanteric 

b. Posterior paratrochanteric 

c. Direct anterior 

2. First, apply 50 lbs of traction—distract at least 12mm 

3. Second, direct an extra long spinal needle into the hip joint at the proposed anterior para 

trochanteric portal, over the anterior edge of the greater trochanter with the aid of the image 

intensifier. 

a. Aspirate 

b. Inject 10cc of air to help break the suction seal which provides more distraction. 

c. Insert a nitanol guide wire into the needle and remove the needle leaving the guide wire in 

the hip joint. 

d. Make a stab incision around the guide wire. 

e. Place the arthroscope sheath with a cannulated trochar over the guide wire and direct it into 

the hip joint. Next, couple the arthroscope into the sheath. 


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4. The next two portals are made under direct vision, viewing needle entrance through the 

arthroscope. Most of the time this can be accomplished without introducing fluid into the 

joint. Occasionally a small amount of fluid might be required. These needles should be placed 

away from the labrum, to keep from damaging it. 

a. Place one needle into the proposed posterior paratrochanteric portal at the level of 

posterior edge of the greater trochanter and another needle in the direct anterior portal sight 

and watch them enter the joint. 

b. Once both needles are correctly placed in the joint the image intensifier may be removed. 

5. Prepare for arthroscopy 

a. Place inflow tubing on scope stopcock 

b. Place outflow tubing on one or the other two needles 

6. The next portals are made in a similar manner as the first: One portal for instrumentation and 

the other for outflow. 

7. Accessory portals 

a. In-between regular portal sights 

b. Outside portal sights--No further anterior than the level of the anterior superior iliac spine 

and always aim for joint when posterior. Use needles to identify the portals. 

c. Distal portals to reach the intra-capsular portion of the femoral neck. 

G. Capsulotomy--Important step In order to increase mobility of the instruments and to simplify 

instrument Insertion. 

1. Place 5.6mm cannula with cannulated trochar over nitanol wire in posterior paratrochanteric 

portal and insert into joint under direct vision. Then insert straight shaver into the cannula to 

clean the area. 

2. Next, remove the shaver and insert the arthroscopic knife through the cannula and remove the 

cannula leaving the knife in the joint. 

3. Cut the capsule as widely as possible in all directions under direct vision. 

4. After cutting the capsule, a curved shaver and other instruments should be easy to insert 

without necessitating switching sticks. 

5. If difficulty entering the joint with curved instruments is encountered, a slotted cannula may be 

inserted over a switching stick for directing these instruments into the joint. 

H. Observe hip joint and perform surgery 

1. Complete visualization by switching portals 

2. Might have to temporarily increase traction to visualize and reach depths of the joint. 

IV. TRICKS, OBSERVATIONS AND PREVENTATIVE MEASURES 

A. Relationship of portals to vital structures 

1. None near portal sights 

2. Lateral femoral cutaneous nerve is closest. 

a. Make direct anterior portal incision along the line of the nerve. 

b. Make incision just through the skin 

B. Traction device 

1. Minimize traction force to take pressure off of the pudendal and sciatic nerves 

a. Decrease traction during prep and drape 

b. Minimize hip adduction 

c. Reduce traction whenever possible--ideal amount of traction is less than 75# and like a 

tourniquet, stop after two hours. 

d. To protect the pudendal nerve, the perineal post should be at least 9 cm in diameter. Build it 

up with padding if it is not. Also make sure the pelvis is supported. 

2. Ways of keeping the traction forces at a minimum 

a. Placing hip in slight flexion, abduction and external rotation to relax the capsule. 

b. Breaking the suction seal before traction is applied 

c. Do not flex hip around a perineal post as it places a stretch on the sciatic nerve 

C. Portals to reach extra-capsular pathology or structures around the neck (tumors, pvns, synovial 

chondromatosis or loose bodies and release of the iliopsoas tendon) 

1. Patient in the lateral position. Externally rotate the hip to bring into view the lesser trochanter 

on the image intensifier 

2. Release the traction 

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3. Mark level of lesser trochanter or the area of pathology 

4. Portal for the scope is at the level of the marker and in line with the anterior para-trochanteric 

portal 

5. Portal for operating instruments below the scope portal and in line with the anterior superior 

iliac spine 

6. Line up the tips of the scope and a motorized instrument at the surgical sight on the image 

intensifier 

7. Keep the tip of the motorized instrument close to the bone and start shaving. When the 

pathology or the indicated structure comes into view appropriate surgery can be commenced. 

8. Once the space is made at the surgical sight it will become easy to exchange instruments 

9. Out flow is accomplished with the suction of the operating instruments or an accessory portal 

made distal or proximal and in between the first two portals 

D. Prevention of fluid extravasations into the retro-peritoneal space and subcutaneous tissues 

1. If possible use a pressure gauge that measures the pressure outside the joint 

2. Make sure that inflow and outflow portals do not wander outside the joint 

3. Make sure the outflow stays open and the fluid is flowing out. 

E. Prevent scuffing and labral damage 

1. Adjust the needles before making Incisions, so they are not against the femoral head 

2. Twist the scope cannula and trochar in slowly under image Intensification. If the sharp trochar 

is used, exchange it for the blunt trochar after the sharp pierces the capsule. Once the cannula 

is well into the joint, if possible, stop before it strikes the acetabular floor and insert the scope. 

3. The rest of the instruments should be inserted under direct vision. 

4. Change the needle placement if it is through the labrum before developing the portal. 

F. Reaching the deep and medial aspects of the joint 

1. Wide capsulotomy 

2. Accessory portals 

3. Curved instruments 

4. May have to increase traction 

V. REFERENCES 

A. Glick JM, Sampson TG, Hip Arthroscopy by the Lateral Approach. In: McGinty JB, ed. Operative 

Arthroscopy. 2nd ed. New York: Raven Press; 1996: 1079-1089. 

B. Glick JM, Hip Arthroscopy Using the Lateral Approach. American Academy of Orthopaedic Surgery, 

Instructional Course Lectures. 1988, 37: 223-231. 

C. Sampson TG, Glick JM, Indications and Surgical Treatment of Hip Pathology. In: McGinty JB, ed. 

Operative Arthroscopy. 2nd ed. New York: Raven Press; 1996: 1067-1078. 

D. Glick JM, Hip Arthroscopy, the Lateral Approach. In: Clinics in Sports Medicine; Ed. J. W. Thomas Byrd. 

Vol. 20, No. 4, Oct. 2001. PP 733-747. 

E. Sampson TG, Complications of Hip Arthroscopy. In: Clinics in Sports Medicine; Ed. J. W. Thomas Byrd. 

Vol. 20, No. 4, Oct. 2001. PP 831-835. 

F. Byrd JWT, Avoiding the Labrum in Hip Arthroscopy. "Arthroscopy" 16; 7: 770-773, 2000. 

G. Khapchik.V, O’Donnell, R.J. and Glick, J.M. Arthroscopically Assisted Excision of Osteoid Osteoma 

Involving the Hip. "Arthroscopy" 17; 1: 56-61, 2001. 


HIP ARTHROSCOPY WITHOUT TRACTION 

Michael Dienst, M.D. 

Department of Orthopedic Surgery 

University Hospital 

66 421 Homburg/Saar, Germany 

Email: Michael_Dienst@yahoo.de 

Over the past two decades, different hip arthroscopists around the world have been contributing to the 

development of techniques for arthroscopy of the hip joint, with most authors advocating the use of trac- 

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tion. The technique of hip arthroscopy (HA) without traction, however, has been disregarded. Recent 

reports have proposed different advantages of the non-traction technique. The low complication rate of this 

procedure has been emphasized. Whereas traction is required for inspection of the direct weight-bearing 

cartilage, the acetabular fossa and the ligamentum teres, arthroscopy without traction is ideally situated 

for evaluation of the hip joint periphery. 

This instructional course lecture presents detailed steps how to perform the non-traction technique. A systematic 

mapping of that part of the joint that can be inspected without traction is included. Indications are 

specified and illustrated with selected case examples. 


Peripheral Compartment of the Hip Joint 

Understanding of the anatomy and function of the acetabular labrum is important not only for assessment 

of integrity of the labrum but also for access to the hip joint. The labrum seals the joint space between the 

lunate cartilage and the femoral head. To overcome the vacuum force and passive resistance of the soft tissues, 

traction is needed to separate the head from the socket, to elevate the labrum from the head and to 

allow the arthroscope and other instruments access to the narrow space between the weightbearing cartilage 

of the femoral head and acetabulum. However, if traction is applied, the joint capsule with its intrinsic 

ligaments is tensioned and the joint space peripheral to the acetabular labrum decreases. Thus, in order to 

maintain the space of the peripheral hip joint cavity for better visibility and manoeverability during 

arthroscopy, traction should be avoided. 

In consequence, Dorfmann and Boyer divided the hip arthroscopically into 2 compartments separated by 

the labrum. The first is the central compartment comprising the lunate cartilage, the acetabular fossa, the 

ligamentum teres and the loaded articular surface of the femoral head. This part of the joint can be visualized 

almost exclusively with traction. The second is the peripheral compartment consisting of the unloaded 

cartilage of the femoral head, the femoral neck with the medial, anterior and lateral synovial folds 

(Weitbrecht’s ligaments) and the articular capsule with its intrinsic ligaments including the zona orbicularis. 

This area can be seen without traction and will be described subsequently. 

Positioning, Distension and Portals for Arthroscopy of the Hip Periphery 

Hip arthroscopy with and without traction can be performed in the lateral or supine position. However, the 

almost exclusive use of the anterolateral portal during HA without traction makes the supine position 

preferable. 

Free draping and a good range of movement are important to relax parts of the capsule and increase the 

intraarticular volume of the area that is inspected. This is important for safe movement of the scope in 

order to avoid damage to the cartilage of the femoral head and synovial folds and unwanted sliding of the 

scope out of the joint. The distending effect of irrigation fluid pressure is of minor importance because the 

pressure should not be increased over 70 mm Hg in order to reduce the risk of development of a severe 

soft tissue edema. 

In general, the combination of HA without traction and HA with traction is recommended. The combination 

of both techniques is important to allow a complete diagnostic arthroscopic examination of the hip. From 

my experience, the traction part should be done prior to the non-traction scope since positioning for traction 

is more demanding. In particular, exact placement of the counterpost is crucial to avoid complications. 

This can be done only under non-sterile conditions. 

For HA without traction, the patient is placed supine on a standard traction table or a standard operating 

table with an additional traction frame or robotic limb positioning device. A comprehensive overview can 

be obtained from the anterolateral portal only. Because the soft tissue mantle is relatively thin and the 

position of the portal is near the lateral cortex of the femoral neck, maneuverability of the arthroscope is 

sufficient for moving the arthroscope into the medial recess, gliding over the anterior surface of the femoral 

head to the lateral recess, and frequently passing the lateral cortex of the femoral neck for inspection of the 

posterior recess. 

First access to the hip joint periphery can be achieved with or without traction. A long needle (∆ 1-2 mm) is 

introduced via the anterolateral portal and directed to the transition between the anterior aspect of the 

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femoral head and neck. Here, the capsule is elevated from the neck which allows easier access of the needle 

into the joint. Entry to the joint is then confirmed by distension of the joint with up to 40 ml of saline, 

which leads to a visible lateral and caudal displacement of the femoral head under fluoroscopy. This is better 

seen if the hip is under moderate traction. The standard reflux test is more inconstant because of occlusion 

of the cannula by hypertrophic synovium. 

A guide wire is then inserted through the needle. The blunt guide wire can be advanced medially until it 

bounces against the medial capsule. The capsular penetration is then dilated (dilating trocars, cannulated 

trocar) and the arthroscope is introduced in the peripheral compartment under fluoroscopy. Traction (if 

applied for access) is then released and the counterpost removed. 

The knee is flexed to about 45° and held by either a specially designed long bar at the end of the table or 

an assistant – the degree of flexion, rotation and abduction of the hip joint are controlled (Fig. 1). A second 

portal is placed under arthroscopic control in the anterolateral zone. Irrigation is used to clear the view 

via the scope sheath and outflow via the additional portal. Standard and extra-long 25° and 70° lenses are 

used for the diagnostic round. 

Fig. 1: Positioning for arthroscopy of the hip joint periphery 

Diagnostic Round and Anatomy of the Peripheral Hip Joint Cavity 

Similar to the knee joint, the key to an accurate and complete 

diagnosis of lesions within the hip joint is a systematic approach 

to viewing. A methodical sequence of examination should be 

developed, progressing from one part of the joint cavity to another 

and systematically carrying out this sequence in every hip (Fig. 2). 


Fig. 2: Diagnostic round through the hip joint periphery 

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For arthroscopic examination, the peripheral compartment of the hip can be divided routinely into the following 

areas: anterior neck area (Fig. 2B-C), medial neck area (Fig. 2A), medial head area (Fig. 2D), anterior 

head area (Fig. 2E), lateral head area (Fig. 2F), lateral neck area (Fig. 2G) and posterior area (Fig. 2H). From 

my experience, the peripheral compartment can be best viewed during a diagnostic round trip starting from 

the anterior/medial surface of the femoral neck. Under slow rotation and sliding of the arthroscope over the 

femoral neck and head, the arthroscope is brought into the different areas of the peripheral compartment 

of the hip. 

Indications: 

Indications, contraindications and complications have been described in detail by Dr. Seil. I would like to 

emphasize that the indications for HA without traction do not differ from those published for the traction 

technique. In my opinion, the traction and non-traction technique should be combined to allow a complete 

diagnostic inspection of the hip joint. Particularly in synovial diseases such as chondromatosis and patients 

with unclear hip pain the combination of both techniques appear mandatory. The hip joint periphery contains 

most of the synovium of the hip joint. I have seen cases with manifestation of synovial chondromatosis 

in the peripheral compartment only. In addition, loose bodies of different origin tend to accumulated 

not only in the acetabular fossa and perilabral sulcus but also in the pouches around the femoral neck. 


Suggested Readings (Hip arthroscopy without traction): 

• Dienst M, Goedde S, Seil R, Hammer D, Kohn D. Hip Arthroscopy without Traction: In Vivo Anatomy of 

the Peripheral Hip Joint Cavity. Arthroscopy 2001; 17: 924-931. 

• Dienst M, Goedde S, Seil R, Kohn D. Diagnostic arthroscopy of the hip joint. Orthop Traumatol 2002; 

10:1-14. 

• Dorfmann H, Boyer Th, Henry P, DeBie B. A simple approach to hip arthroscopy. Arthroscopy 1988; 

4:141-142. 

• Dorfmann H, Boyer T. Arthroscopy of the hip: 12 years of experience. Arthroscopy 1999; 15:67-72. 

• Gondolph-Zink B, Puhl W, Noack W. Semiarthroscopic synovectomy of the hip. Int Orthop 1988; 12:31- 

35. Stuttgart: G. Fischer, 1995:511-571. 

• Klapper R, Dorfmann H, Boyer T. Hip arthroscopy without traction. In: Byrd JWT, editor. Operative hip 

arthroscopy. New York: Thieme, 1998:139-152. 

• Klapper RC, Silver DM. Hip arthroscopy without traction. Contemp Orthop 1989; 18:687-693. 

HIP ARTHROSCOPY 

INDICATIONS, CONTRAINDICATIONS AND COMPLICATIONS 

Romain Seil, M.D. 


Saarland University Medical Center 

Homburg / Saar, Germany 

INDICATIONS 

The indications of arthroscopy of the hip are evolving with the development of our technical skills and the 

understanding of the normal and the pathologic anatomy of this joint. Recently Byrd et al. presented an 

exhaustive table of diagnoses representing potential indications for hip arthroscopy (see below). Despite 

this large number of diagnoses most hip arthroscopies are performed for intraarticular loose bodies and 

synovial pathologies (Kelbérine & Boyer). Other diagnoses like acetabular labral tears are increasingly recognized 

and arthroscopic management of such tears has been reported to be successful (Santori & Villar; 

Mason). Currently one of the most challenging aspects of hip arthroscopy might be the understanding and 

treatment of early osteoarthritis (OA) of the hip (McCarthy J et al.; Dienst et al.), even if the therapeutic 

approach of OA must still be considered as experimental. 

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Diagnoses for Hip Arthroscopy (from: Byrd JWT, 2000) 

Arthritic disorders 

Dysplastic disease of the hip (CE angle ,20°) 

Borderline dysplastic disease of the hip (CE angle 20°-25°) 

Perthes disease 

Avascular necrosis of the femoral head: 

Synovial chondromatosis 

Sepsis 

Total hip replacement: 

Loose bodies: 

Osteochondritis dissecans 

Synovitis 

Ligamentum teres damage 

Chondral damage 

Labral pathology 

Osteochondritis dissecans 

Fibrosis 

Osteophyte 

Other 

Rheumatoid arthritis, Inflammatory arthritis, Osteoarthritis (primary, secondary to inverted 

labrum, posttraumatic, secondary to synovial chondromatosis, secondary to Perthes 

disease, secondary to dysplasia, secondary to slipped capital femoral epiphysis), Gout, 

Calcium pyrophosphate disease, Other 

Stage: I, II, III, IV, V, VI 

Articular surface: intact, fragmented 

Free fragments, Inflammatory process, Fibrosis, Soft tissue impingement, Infection 

Loosening: acetabular component, femoral component, both components 

Post-traumatic, Avascular necrosis, Synovial chondromatosis, Foreign body 

Etiology: rheumatoid arthritis, synovial chondromatosis, gout; calcium pyrophosphate disease 

(inflammatory), chemical induced, idiopathic, traumatic, pigmented villonodular synovitis, other 

Pattern: focal (pulvinar), diffuse 

Complete rupture, Partial rupture, Degenerate ligament 

Acute traumatic, Chronic traumatic 

Arthritic (Grade: I, II, III, IV) 

Location: femoral head, acetabulum, femoral head and acetabulum 

Etiology: traumatic, degenerative, idiopathic, congenital, acetabular dysplasia 

Morphology: radial flap, radial fibrillated, peripheral longitudinal, inverted, unstable 

Location: anterior, posterior, lateral, anterolateral 

Grade: stable—intact articular surface, fragmented articular surface; unstable 

Post-traumatic 

Perthes disease 

Idiopathic 

With limited range of motion 

Without limited range of motion 

Impinging 

Not impinging 


CONTRAINDICATIONS 

Recent acetabular fractures (risk of retroperitoneal and/or intraabdominal fluid extravasation). 

Severe osteoarthritis, arthrofibrosis, capsular constriction, joint ankylosis (difficult or impossible distraction 

of the joint). 

Severe obesity (difficult access to the joint, even with extra-length instruments). 

Contraindications of traction: potential stress risers in the bone from previous trauma, disease or surgery; 

soft-tissue problems (skin, vascularisation). 

COMPLICATIONS 

Complications associated with hip arthroscopy are rare (between 1.6% and 5%). Their incidence seems to 

be related to the surgeons’ experience. Most of them are related to arthroscopies of the central compartment 

of the hip which are performed with traction and mostly cause neurapraxias (Sampson). In a large 

series of 413 arthroscopies of the peripheral compartment which have been performed without traction, no 

complications have been reported (Dorfmann & Boyer). 

Complications in Hip Arthroscopy (from: Dienst M, 2002) 

Intraarticular: Instrument breakage 

Iatrogenic articular cartilage / labral lesions 

Extraarticular: 

Neurological: 

Inguinal / genital soft tissue injuries due to pressure by the traction post 

(i.e. scrotal necrosis; labia majora hematoma; vaginal lesion). 

Sensory: 

A) anterior aspect of the proximal thigh due to a lesion of the femorocutaneous 

nerve during placement of the anterior portal 

B) forefoot caused by a compression of the deep peroneal nerve in the foot holder 

C) medial aspect of the proximal thigh due to pressure on the pudendal nerve by the 

post 

Motor: 

Sciatic / femoral nerve due to prolonged and too strong traction 

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Other 

Fluid extravasations (intraabdominal / thigh) 

Heterotopic ossifications 


SELECTED REFERENCES: 

• Byrd JWT. Arthroscopy of select hip lesions. In: Byrd J (ed): Operative Hip Arthroscopy. New York, 

Thieme, 1998: 153-171 

• Byrd JWT. Complications associated with hip arthroscopy. In: Byrd J (ed): Operative Hip Arthroscopy. 

New York, Thieme, 1998: 171-176 

• Byrd JWT, Jones KS. Prospective analysis of hip arthroscopy with 2-year follow-up. Arthroscopy 16 (6), 

2000: 578-587 

• Dienst M, Gödde S, Seil R, Kohn D. Diagnostic arthroscopy of the hip joint. Orthop Traumatol 2002; 10: 

1-14 

• Dienst M, Seil R, Gödde S, Georg T, Kohn D. Arthroscopy for diagnosis and therapy of early osteoarthritis 

of the hip. Orthopade 1999; 28: 812-818 

• Dorfmann H, Boyer T. Arthroscopy of the hip: 12 years of experience. Arthroscopy 15 (1): 67-72, 1999 

• Funke EL, Munzinger U. Complications in hip arthroscopy. Arthroscopy 12 (2): 156-159, 1996 

• Griffin DR, Villar RN. Complications of arthroscopy of the hip. J Bone Joint Surg Br 1999; 81 : 604-6 

• Kelbérine F, Boyer T. L’arthroscopie de la hanche. In : Société Francaise d’Arthroscopie. Perspectives en 

arthroscopie. Vol. 2 : 39-45, 2003 

• Mason JB. Acetabular tears in the athlete. Clin Sports Med, 20 (4): 779-790, 2001 

• McCarthy JC, Noble PC, Schuck MR, Wright J, Lee JA. The role of labral lesions to development of early 

degenerative hip disease. Clin Orthop, 393: 25-37, 2001 

• McCarthy JC, Lee JA. Acetabular dysplasia: a paradigm of arthroscopic examination of chondral injuries. 

Clin Orthop, 405: 122-128, 2002 

• Sampson TG. Complications of hip arthroscopy. Clin Sports Med 20 (4): 831-835, 2001 

• Santori N, Villar RN. Acetabular labral tears: result of arthroscopic partial limbectomy. Arthroscopy 16: 

11-15, 2000 

• Villar RN. Hip arthroscopy. J Bone Joint Surg 77 B: 517-518, 1995 

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STRESS FRACTURES 

Friday, March 14, 2003 • Carlton Hotel, Carlton II 

Chairman: Gideon Mann, MD, Israel 

Faculty: Sakari Orava, MD, PhD, Finland, Ingrid Ekenman, Sweden, Peter Brukner, MD, Australia 

and Charles Milgrom, MD, PhD, Israel 

Peter Brukner, Australia - Epidemiology of Stress Fractures 

Charles Milgrom, Israel - Preventable and Inborn Causes of Stress Fracture 

Sakari Orava, Finland - Uncommon Stress Fractures and their Treatment Principles 

Ingrid Ekenman, Sweden - How Important is Accurate Diagnosis for Stress Fractures? 


Gideon Mann, Israel – Career Ending Stress Fractures of the Foot 

Charles Milgrom, Israel - Does the Asymptomatic Stress Fracture Exist? 

CAREER ENDING STRESS FRACTURES OF THE FOOT 

Gideon Mann, MD 

Meir Hospital, Kfar Saba, Israel and 

The Ribstein Center for Sport Medicine Sciences & Research, Wingate Institute, Israel 

Co-authors: S Shabat, D Morgenstern, Y Hezroni, A Finsterbush, M Nyska, N Constantini 

Introduction: 

Most stress fractures of the foot would not put in risk the sportsman's career. The few fractures that on the 

one hand occur relatively often and do tend to non-union and to long standing symptomatology are fractures 

of the Hallux Sesamoid, the Jones Fracture of the fifth metatarsal bone and fractures of the Tarsal 

Navicular. 

Sesamoid Stress Fractures 

The term "sesamoid" is derived from the Greek word "sesamum" due to the resemblance of the bone to the 

seeds of the plant Sesamum Indicum used as a purgative by the ancient Greeks (14,21). 

Sesamoid stress fractures occur in a wide variety of sports such as football, long distance running, sprinting, 

dancing, basketball, tennis and figure skating (4,5,6,7,8). 

Pathophysiology: 

Stress fractures of the sesamoid comprise approximately 5% of foot stress fractures (11). They usually 

evolve following repeated traction (2) while acute fractures could occur following both direct compression 

injuries such as a fall and traction injuries (1, 14). The stress fracture involves mostly the medial sesamoid 

(2,9,10). 

Sesamoid stress fractures have a strong tendency to non-union, probably more than any other bone (12). 

Orava and Hulkko have shown non-union in 15 of 37 cases and only 10 of 15 showed union after using 

modified foot wear and relative rest (12). 

Clinical Presentations: 

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Pain is of insidious onset and unusually long standing. It is poorly localized, occurring during or after 

activity and relieved by rest (1,2). Pain is increased by hypertension and by local pressure. 

Diagnosis: 

Diagnosis is confirmed by x-rays inclusive of an anterior-posterior projection, a lateral projection and an 

axial projection, and by a bone scan which would differentiate a fracture from a bipartite sesamoid. Serial 

x-rays in intervals of 3 weeks (1) and up to 3 or 6 months (3) would be helpful if a pre-injury x-ray showing 

no partition is unavailable, which is usually the case. 

A fractured sesamoid would usually show equal sized fragments, ragged in texture, while a bipartite 

sesamoid would have smooth and unequal fragments (1). 

75% of bipartite sesamoids are bilateral (16,17,18). 

The fracture line would usually be transverse, with osteoporotic edges which would become smoother in 

time (14). Further fragmentation could be seen (14). Both computerized tomograms (CT) (19) and magnetic 

resonance (MRI) (20) have been suggested for accurate diagnosis. 


Treatment: 

Treatment would therefore be relatively aggressive with orthoses preventing Hallux dorsiflexion, and 

padding along side with relative rest (2). If symptoms are severe a platform cast for 6 weeks with protection 

from toe dorsiflexion may be used (1,8,11), controlled by repeated x-ray (1). Others recommend a cast, 

possibly non weight bearing, for 6 weeks as the initial treatment (14, 19), with appropriate padding to 

reduce pressure on the injured bone. 

If symptoms persist bone grafting may be attempted (13). Though excision of the fractured sesamoid is 

probably more often practical (1,2,4,11) a procedure allowing return to full activity often an initial 3 week 

period of immobilization (4). Excision could be total or partial (14,15). 

Summary: 

Stress fractures of the sesamoids occur following repeated traction and usually involve the medial 

sesamoid. Acute injury caused either by crush or by traction ("Turf Toe") would involve either sesamoids. 

Pain is insidious and long standing. Diagnosis is clinical, as pain is caused by both toe dorsiflexion as by 

local pressure. Diagnosis is assisted by x-rays and bone scan and occasional CT or MRI. Radiological 

Differential Diagnosis includes bipartite or multipartite sesamoid. Clinical differential diagnosis includes 

mainly sesamoid chondromalacia. The sesamoid stress fracture has a strong tendency to non-union. 

Treatment should be initiated immediately after diagnosis and includes orthoses or cast for 6 weeks with a 

platform to prevent toe extension. 

If clinical and radiological healing fails to occur, surgical treatment by partial or total excision of the 

sesamoid should be initiated followed by 3 weeks of immobilization before gradually returning to sports. 

In selected cases, bone graft to the fracture could be considered. 

REFERENCES 

1. Linz J, Conti S, Stone D. Foot and Ankle Injuries in Sports Injuries, Fu F and Stone D, Eds. Lippincott, 

Williams & Wilkens, Philadelphia: 2001;1152-1153. 

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Harries M, Williams C, Stanish WD, Micheli LJ, Eds. Oxford: 1998;663. 

3. Scranton P. Pathologic and anatomic variations in the sesamoids. Foot Ankle 1981;1:321-6. 

4. Hulkko A, Orava S, Pellinen P, et al. Stress fractures of the sesamoid bones of the first metatarsophalangeal 

joint in athletes. Arch Orthop Trauma Surg 1985;104:113-7. 

5. Val Hal ME, Keene JS, Lange TA and Clancy WG. Stress fractures of the great toe sesamoids. Am J Sports 

Med 1982;10:122-8. 

6. Davis AW, Alexander IJ. Problematic fractures and dislocations in the foot and ankle of athletes. Clinics in 

Sports Medicine 1990;9:163-81. 

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8. McBryde AM, Anderson RB. Sesamoid foot problems in the athlete. Clinics in Sports Medicine 1988;7:51-60. 

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10. Zinman H, Keret I, Reis NI. Fractures of the medial sesamoid bone of the hallux. J Trauma 1981;21:581-2. 

11. McBryde AM. Stress fractures of the foot and ankle in Orthopaedic Sports Medicine, DeLee JC and Drez 

D, Eds. Saunders, Philadelphia: 1996;1970-7. 

12. Orava S, Hulkko A. Delayed unions and nonunions of stress fractures in athletes. Am J Sports Med 

1988;16:378-82. 

13. Anderson RB, McBryde AM. Autogenous bone grafting of hallux sesamoid nonunions. Foot Ankle 

1997;18:293-6. 

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15. Peterson L, Renstrom P. Sports Injuries, Martin Dunitz, 2001:421. 

16. Inge GAL, Ferguson AB. Surgery of the sesamoid bones of the great toe. Archives of Surgery 

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19. Biedert R. Which investigations are required in stress fracture of the great toe sesamoids? J of Ortho 

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Radiol 1994;24:37-8. 

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Jones Fracture 

Introduction 

The Jones fracture was originally described by Sir Robert Jones in 1902 (1). He described a fracture that he 

sustained himself while dancing around a tent pole. Though originally described as an acute fracture 

(2,13,14) the term is more often used inclusive of stress fractures (12,15). 

The fracture occurs at the junction of the diaphysis and the metaphysis of the fifth metatarsal often involving 

the articular facet between the fourth and fifth metatarsals but not extending distal to the facet (2). It 

is a transverse fracture best known for its nasty tendency to non-union (3-10). 

Pathophysiology and Differential Diagnosis 

The acute Jones fracture may be caused by a strong adduction force applied to the plantar flexed forefoot 

(2). Weight bearing accompanied by a pivoting force may cause an acute fracture when force is excessive, 

or a stress fracture when the force is repeated (11). It has been claimed to possibly occur more often in a 

supinated foot (3) or possibly both in the cavus foot which is more rigid and in the planovalgus foot 

because of increased stresses exerted along the lateral foot border (11,44). The fracture should be differentiated 

from a diaphyseal stress fracture which behaves similar to other metatarsal stress fractures (31) and 

from the avulsion fracture of the base of the fifth metatarsal which need virtually no treatment at all (16) 

though some would provide a walking cast for 4 weeks (17). 

Occurrence 

Metatarsal fractures are dominant in civilian sports, comprising 16% to 23% of the total number of fractures 

(18-24, 30). Figure skating has shown an incidence of 22% (32). The figures reported in the military are in 

the range of 8 to 24%, generally lower than the incidence in athletes (25-31) with some reporting only 2-8% 

(24,28-31). The exact occurrence of the true Jones fracture is not known especially as they are often reported 

alongside base or diaphyseal fractures. The acute fracture is probably more prevalent in non-athletes 

over age 21 and is equally distributed between both sexes (11). The stress variety occurs more in athletes 

aged 15 to 21 and is seen more frequently in males (11). Stress fracture of the fifth metatarsal comprises 

approximately 5% of stress fractures of the foot (46). 

Types of Fractures 

Torg in 1984 (33), following a previous publication on stress fractures of the navicular in 1982 (34), divided 

the Jones Fracture into three types: 

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I. An acute fracture, with no pre-existing pain 

II. A sub-acute fracture, when the patient complains of some degree of pre-existing pain. Cortical thickening 

and medollary sclerosis may be evident. 

III. A chronic fracture, with established non-union. 

Treatment 

The acute Jones fracture and possibly also the sub-acute (Torg type II) may be treated conservatively with a 

non weight-bearing cast for 6 week to 12 weeks (2,11,13,16,35,45,47). While some demand a full three 

months non weight bearing cast (11), others are content with a non weight bearing cast for 4 weeks followed 

by a weight bearing cast for 3 weeks (17) or possibly no cast at all if the patient is reasonably cooperative 

(31). As about one quarter of the conservatively treated fractures tend towards delayed union or 

non-union (15), surgical treatment would be preferred on occasion even for the acute stage (2). In 1994, 

Josefsson (15) pointed out that though one quarter of the conservatively treated fractures will eventually be 

treated surgically, only 12% of the acute fractures will be operated as opposed to 50% of the stress fractures. 


When displacement has occurred (35), delayed union is apparent (Torg III) (2,11,15,16,35) or the athlete 

cannot afford the lengthy conservative treatment (2) which may continue up to 5 months (16), surgical 

treatment should be considered using a large canulated 4.5 mm intramedullary screw or a large inlay bone 

graft (11,36,37,38,47). A large intramedullary screw will give a fixation strength higher than forces exerted 

at walking (39). It will hasten healing to half the time (16). A medullary screw could be inserted as an outpatient 

clinic procedure and will allow walking within 10 days, running within 6 weeks, and competing within 

9 weeks (40,47). Surgical failures would usually be accounted when using a screw that is too small or 

bone graft which is too small or failing to rim the medullary canal as required (41). Capactive coupled 

electric fields (42) and pulsed low intensity ultrasound [LUS] (43) may have a place in treating persistent 

cases and thus achieving healing of the fracture. 

Summary 

The Jones fracture was originally described in 1902 as an acute transverse fracture just distal to the base of 

the fifth metatarsal bone. The fracture could occur following an acute injury, following an acute injury 

super imposed on a partial stress fracture or as a classic stress fracture with no apparent acute trauma. 

Conservative treatment with non weight bearing with or without a cast for 6 to 12 weeks will usually suffice 

for the first two fracture types. Surgical treatment with a large intramedullary screw or inlay bone graft will 

be performed in cases of delayed union, displacement or lack of willingness of the athlete to cooperate 

with a 3 to 6 month program of conservative treatment. Surgical treatment will allow resumption of walking 

within 10 days, running within 6 weeks and competition within 9 weeks of the injury. 

REFERENCES 

1. Jones R. Fractures for the base of the fifth metatarsal bone by indirect violence. Annals of Surg 

1902;34:697-700. 

2. Brukner P, Bennell K, Matheson G. Stress Fractures, Blackwell Science:1999;178-181. 

3. Anderon EG. Fatigue fractures of the foot. Injury 1990; 21:275-9. 

4. Hulkko A, Orava S, Nikula P. Stress fracture of the fifth metatarsal in athletes. Annal Chirurg Et Gyn 1985; 

74:233-238. 

5. Dameron TB. Fractures and anatomical variations of the proximal portion of the fifth metatarsal. J Bone 

Joint Surg 1975; 57(A):788. 

6. Kavanaugh JH, Brower TD, Mann RV. The Jones fracture revisited. J Bone Joint Surg 1978; 60(A):776. 

7. Laurich LJ, Witt CS, Zielsdorf LM. Treatment of fractures of the fifth metatarsal bone. J Foot Surg 1983; 

22:207. 

8. Torg JS, Baluini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to tuberosity. 

Classification and guidelines for non-surgical and surgical treatment. J Bone Joint Surg 1984; 66(A):209. 

9. Orava S, Hulkko A. treatment of delayed and non-unions of stress fractures in athletes. Sports Injuries: 

Proceedings of the third Jerusalem Symposium, edited by G. Mann, Freund Publishing House Ltd. London, 

England1987. 

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10. Orava A, Hulkko A. Delayed unions and non-unions of stress fractures in athletes. Am J Sports Med 

1988; 16(4):378 

11. Sammarco GJ. The Jones Fracture. Instr course lect, 1993;42:201-5. 

12. Landorf KB. Clarifying proximal diaphyseal fifth metatarsal fractures. The acute fracture versus the 

stress fracture. J Am Podiatr Med Assoc 1999;89(8):398-404. 

13. Lawrence SJ, Botte MJ. Jones fractures and related fractures of the proximal fifth metatarsal. Foot Ankle 

1993;14(6): 358-65. 

14. Byrd T. Jones fracture: relearning an old injury. South Med J 1992; 85(7):748-50. 

15. Josefsson PO, Karlsson M, Redlund-Johnell I, et al. Jones fracture. Surgical versus non-surgical treatment. 

Clin Orthop 1994; (299):252-5. 

16. Clapper MF, O’Brien TJ, Lyons PM. Fractures of the fifth metatarsal. Analysis of a fracture registry. Clin 

Orthop 1995; (315):238-41. 

17. Holubec KD, Karlin JM, Scurran BL. Retrospective study of fifth metatarsal fractures. J Am Podiatr Med 

Assoc 1993; 83(4):215-22. 

18. McKeag DB, Dolan C. Overuse syndromes of the lower extremity. Phys Sportsmed 1989; 17:108-23. 

19. Warren RH, Sullivan D. Stress fractures in athletes: recognizing the subtle signs. J Musculoskel Med 

1984; 1(4):33-36. 

20. McBryde AM, Stress fractures in runners. Clin Sports Med 1985; 4(4):737-51. 

21. Matheson GO, Clement DB, McKenzie DC et al. Stress fractures in athletes. A study of 320 cases. Am J 

Sp Med 1987; 15(1):46-57. 

22. Hulkko A, Orava S. Stress fractures in athletes. Int J Sp Med 1987; 8:221-6. 

23. Brukner P, Bradshaw C, Khan K, et al. Stress Fractures: a review of 180 cases. Clin J of Sp Med 1996; 

6(2):85-9. 

24. Orava S, Hulkko A. A survey of stress fractures in Finnish athletes. Sports Injuries: Proceedings of the 

third Jerusalem Symposium, edited by G. Mann, Freund Publishing House Ltd. London, England 1987. 

25. Sahi T et al. Epidemiology, etiology and prevention of stress fractures in the Finnish defense forces and 

the frontier guard. Sports Injuries: Proceedings of the third Jerusalem Symposium, edited by G. Mann, 

Freund Publishing House Ltd. London, England 1987. 

26. Hallel T, Amit S, Segal D. Fatigue fractures of the tibial and femoral shaft in soldiers. Clinic Orthop 

1976; 118:35. 

27. Dudelzak Z, Stress fractures in military activity. The IDF army centre of physical fitness, 1991. 

28. Giladi M, et al. Publication of the Israel Defense Force Medical Corps, 1984. 

29. Giladi M, Ahronson Z, Stein M et al. Unusual distribution and onset of stress fractures in soliders. Clin 

Orthop 1985;192:142-6. 

30. Friberg O, Sahi T. Clinical biomechanics, diagnosis and treatment of stress fractures in 146 Finnish conscripts. 

Sports Injuries: Proceedings of the third Jerusalem Symposium, edited by G. Mann, Freund 

Publishing House Ltd. London, England 1987 

31. Mann G. Stress fractures in Sports Injuries. Arthroscopy and Joint Surgery, Current Trends and 

Concepts. Doral MN, Ed. Ankara:2000:307. 

32. Pecina M, Bojanic I, Dubravcic S. Stress fractures in figure skaters. Am J Sp Med 1990;18(3):277-9. 

33. Torg JS, Balduini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity: 

classification and guidelines for non-surgical and surgical management. J Bone Joint Surg 1984;66A:209-214. 

34. Torg JS, Pavlov H, Cooley LH, et al. Stress fracture of the tarsal navicular. A retrospective review of twenty-one 

cases. J Bone Joint Surg 1982;64(A):700. 

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1999;59(9):2516-22. 

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J AM Podiatr Med Assoc 1995; 85(9);473-80. 

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of the Jones fracture. Orthop Rev 1991;20(8):713, 716-7. 

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study, Foot Ankle Int 1999;20(9):560-3 

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Jones fracture. Am J Sp Med 1993;21(5):720-3. 

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base of the fifth metatarsal distal to the tuberosity: the Jones fracture. Foot Ankle Int 1996;17(8):449-57. 


3.161

42. Benazzo F, Mosconi M, Beccarisi G, et al. Use of capacitive coupled electric fields in stress fractures in 

athletes. Clin Orthop 1995;310:145-9. 

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activiites when treating stress fractures? A review of one tarsal navicular and eight tibial stress fractures. 

Iowa Orthop J 1999;19:26-30. 

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DB and Milgrom C, Eds. CRS Press, London:2001;317. 

45. Acker JH, Drez D. Non-operative treatment of stress fracture of the proximal shaft for the fifth metatarsal 

(Jones fracture), Foot Ankle 1986, 7(3):152. 




Tarsal Navicular Stress Fractures 


Introduction 

Stress Fractures of the tarsal navicular have been considered relatively unusual (37). The tendency for nonunion 

with or without avascular necrosis (1) has made this fracture unwelcome in sports medicine clinics 

(2-9). 

In 1982, Torg reviewed 21 cases of navicular stress fracture (6). Further publications by Khan (9), Kiss (10), 

Matheson (16), Benazzo (8) and Brukner (17) brought to our attention that these fractures may not be as 

rare as previously believed. 

Pathophysiology 

The Navicular bone may be repeatedly compressed between the talus and the cuneiforms during repeated 

stress (11,12). Reduced dorsiflexion of the ankle may be a contributing factor as demonstrated by Agosta 

and Morarty (11), a short first metatarsal and a long second metatarsal have also been mentioned as possible 

causes (6) but not the shape of the arch (21). Excessive sub-talar pronation has also been suggested as 

a possible contributing factor (11). The bone in this location has a sparse blood supply, which would contribute 

to its disability to withstand repeated stress (11, 13, 14). The fracture involves the dorsal middle 

third of the bone (9,10), in 96% is partial (10), 10% of the fractures involve 10% or less of the height of the 

bone (10). 

Navicular stress fractures are seen in athletes using explosive sports as jumping or sprinting, inclusive of 

figure skating, ball games and dance (33,38,39). These fractures are also seen in long distance runners if 

they use the forefoot in the footstrike (5,7,12,34,35,36). 

Epidemiology 

Previous work in the Finnish and Israeli military as summarized by Mann in 2000 (15), and in the Israel 

Border Police (18) disclosed only few navicular stress fractures. Research with figure ice-skating reported 

22% of the total stress fractures in ice-skating to be navicular stress fractures (2 of 9 cases) (20). Within the 

athletic population (8,9,10,16,17,19), navicular stress fractures comprised 3% of the total stress fractures in 

Korean athletes (19), 14.5% of stress fractures in the Australian athletes (9) and 35% of the stress fractures 

of the Australian track & field team (9). These fractures comprise approximately 3% of stress fractures of 

the foot (32). 

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Diagnosis 

Deep located pain, insidious in onset, occurring after sprinting, running or jumping should raise the suspicion 

of a navicular stress fracture (7,9,11,22). The pain may radiate to the distal forefoot medially or dorsally 

(6,11,21) and a limp may be apparent (7,21,24). Physical examination will disclose local tenderness of 

the navicular on the dorsal aspect of the foot (9,11,13) and often reduced dorsal flexion and subtalar 

motion (6,33,39). Pain may be reproduced by hopping (7). Imaging will include x-rays which are often of 

low sensitivity (9,11), inclusive of a lateral stress view if a dorsal "avulsion stress fracture" is suspected (12) 

and a planter view (25). X-rays will often show changes in the surrounding joints already on the original

views (11). X-rays have been shown by Khan to be originally positive for a fracture only in 14% of cases 

(13). The bone scan will show high sensitivity usually showing a strong reaction of the whole navicular 

bone (9,11). A computerized tomogram will disclose the fracture when the appropriate protocol is used (9, 

10, 11, 22). 1.5 mm slices are used on the axial view and 3 mm slices on the coronal view (10). The CT is 

the most accurate of the imaging method for the navicular stress fracture. The CT will also differ a stress 

reaction picked up by the bone scan from a true stress fracture (11), though 11% of these fractures will not 

be located on the original CT examination (10). Magnetic Resonance (MRI) is not often used in the diagnosis 

of navicular stress fracture though it has been used for serial follow-up of healing (23) along side local 

sensitivity (11, 23) and pain during activity (11). Diagnosis is frequently delayed 4-7 months because of the 

vague symptoms and frequently normal initial x-rays (6,42,44). 

Types of navicular stress fracture: 

Kiss evaluated CT findings in 55 stress fractures of the navicular (10). 78% were linear, 9% were linear with 

a fragment and 11% were rim fractures with an ossicle. The last type was further defined by Orava (12) who 

described a dorsal triangular fracture (stress avulsion fracture) which would benefit from surgical excision. 

Differential Diagnosis 

A bipartite navicular should be suspected according to its appearance on x-ray and CT (26). This could be 

a painful condition and a bone scan could be mildly positive. An accessory navicular would show only 

medial uptake on the bone scan, the bone would be sensitive not dorsally but rather medially and an x-ray 

would disclose the accessory bone (11). Bone reaction to stress will show uptake on the bone scan but the 

CT will be normal (11). 


In all cases, especially those with a complete fracture, avascular necrosis or Kienbuck’s Disease should be 

kept in mind, especially in youth and childhood (15). This disease involves the whole bone and is treated 

conservatively in the great majority of cases. Tarsal coalition of various types should always searched for 

clinically and radiologically (15) as they may cause excessive force on the navicular and on other tarsal 

bones. 

Treatment 

Khan in 1994 (9), summarized the treatment previously given for navicular stress fractures. The method of 

"weight-bearing rest", or stopping physical activity with or without a Weight Bearing Cast, met with a high 

rate of failure (4,6,7,13). Only 24% of 45 cases healed while weight bearing, though symptoms were largely 

alleviated (9,11). Apparently, the weight bearing did not allow osteoblastic activity to bridge the fracture 

(27,28). Treatment by "non weight bearing-cast immobilization" achieved union in 89% of 36 cases (9,11). 

Accordingly, Khan recommended treatment by non weight bearing with immobilization for 6 weeks, followed 

by 6 weeks of rehabilitation program (9,11) and followed-up on a clinical basis based on pain on 

activity and dorsal sensitivity on examination (9,11, 23). Other publications recommend similar treatment 

(5, 8). To follow up union, MRI may be used (23) or CT may be used which might show union beginning at 6 

weeks and complete union at 4 months (10). All types of treatment may be assisted by a well-fitted orthotic 

device (11). 

Surgical treatment is usually not necessary and not recommended (5,9,15). As these fractures are often 

diagnosed late, patients may often decide to reduce their physical activity and not proceed with surgical or 

other treatment (15). Patients undertaking conservative treatment should be cautioned that healing may 

take 4 (10) to 6 (9) months. Healing may possibly be assisted by pulsed low intensity ultrasound (30) or 

capactive coupled electric fields (31). 

Surgical treatment for painful persistent non-union remains an option in selected cases (5,7,43). Ha in 

1991 presented within a series of 169 fractures, 5 navicular fractures who were all treated surgically. Hulkko 

and Orava presented similar experience in their series of Finnish athletes (29) and Orava in 1993 presented 

similar experience with the dorsal-avulsion stress fracture (12). Surgical treatment will be assisted by 

opening the talo-navicular joint to locate the fracture (7,11) and marking the site with a Kirshner wire (11). 

Surgery may include internal fixation with a screw or curettage and bone graft (11). 

Overall, there seems to be a growing tendency to refer to surgical treatment in selected cases (3). Puddu et 

al, following Torg (41) and Mann (13) suggested the following outline for treatment (33): 

3.163

1. Non-complicated partial fracture and undisplaced complete fracture: non-weight bearing plaster for 6 to 

8 weeks 

2. Displaced complete fracture: treatment as above or alternatively, surgical reduction and fixation followed 

by non-weight bearing immobilization in plaster for 6 weeks. 

3. Fracture complicated by delayed union or non-union: curettage and inlaid bone grafting with internal fixation 

of unstable fragments (without attempting reduction because in general there is already a fibrous 

union). Any sclerotic fragments found must not be removed but must be fixed. After the operation, a nonweight 

bearing cast must be applied for 6 to 8 weeks. Recovery is monitored by radiographs (sometimes 3 

to 6 months are necessary). 

4. Partial fracture complicated by a small transverse dorsal fracture: the dorsal fragment may have to be 

removed. 

5. Complete fracture complicated by a widespread transverse dorsal fracture: recovery takes place by immobilization. 

Dorsal talar beaks must be removed during surgery. 


Peterson and Renstrom (44) pointed out the high rate of re-fracture, delayed union and non-union after 

surgery, which may necessitate repeated surgical procedures. The injury, the pre-existing foot anomaly (as 

sub-talar condition and reduced dorsiflexion), the surgical procedure and immobilization may all contribute 

to arthritic changes around the injured bone and enhance a disappointing and less than optimal 

final result. 

Summary 

Navicular stress fractures are apparently not unusual in athletics though they seem to be scarcely reported 

in the military. They present as vague insidious onsetting pain on activity, alleviated by rest often radiating 

distally to the forefoot. Bone scan will show strong uptake, and a CT will define the diagnosis. The great 

majority of the fractures are partial always including the dorsal middle third of the bone. Avascular necrosis, 

Kienbuck’s disease and tarsal coalition, especially subtalar coalition, should always be excluded as 

should bipartite navicular, an accessory navicular or a stress reaction. 

Athletes may decide to retire and not proceed with treatment. "Weight bearing rest" does not seem to allow 

reasonable healing and treatment should comprise of "non-weight bearing cast immobilization" for 6 weeks 

followed by 6 weeks of rehabilitation. The healing process is followed by estimating pain and local sensitivity 

and possibly repeated CT or MRI. Healing may be expected at 3 to 6 months. Occasionally, surgical 

means would be required, including internal fixation with a screw or curettage and bone grafting. 

Conservative or surgical treatment may be aided by a well-fitted orthotic. 

Surgical intervention has a relatively high occurrence of failure and complication and the patient should be 

informed of possibly less than optimal results before surgical treatment is initiated. 

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avascular necrosis in a pole vault. J Am Pod Med Assoc 1996;86(11):551-4. 

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5. Hulkko A, Orava S, Peltokallio P, et al. Stress fracture of the navicular bone. Nine cases in athletes. Acta 

Orthop Scand 1985;56:503-5. 

6. Torg JS, Pavlov H, Cooley LH, et al. Stress fracture of the tarsal navicular. A retrospective review of twenty-one 

cases. J Bone Joint Surg 1982;64(A):700-12. 

7. Fitch KD, Blackwell JB, Gilmour WN. Operation for non union of stress fracture of the tarsal navicular. J 

Bone Joint Surg 1989;71(B):105-10. 

3.164

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1992;14(1):51-65. 

9. Khan KM, Brukner PD, Kearney C, et al. Tarsal navicular stress fractures in athletes. Sports Med 

1994;17(1):65-76. 

10. Kiss ZA, Khan KM, Fuller PJ. Stress fractures of the tarsal navicular bone: CT findings in 55 cases. Am J 

of Roentgenology 1993;160:111-15. 

11. Brukner P, Bennel K, Matheson G. Stress Fractures, Blackwell Science:1999:167-73. 

12. Orava S, Karpakka J, Hulkko A, et al. Stress avulsion fracture of the tarsal navicular. An uncommon 

sport related overuse injury. Am J Sp Med 1991;19(4):392-5. 

13. Khan KM, Fuller PJ, Brukner PD, et al. Outcome of conservative and surgical management of navicular 

stress fracture in athletes. Am J of Sp Med 1992;20:657-666. 

14. Waugh W. The ossification and vascularization of the tarsal navicular and the relation to Kohler’s disease. 

J Bone Joint Surg 1958;40B:765-77. 

15. Mann G. Stress Fractures in Sports Injuries. Arthroscopy and Joint Surgery, Current Trends and 

Concepts. Doral MN, Ed. Ankara:2000:307. 

16. Matheson GO, Clement DB, McKenzie DC, et al. Stress fractures in athletes: a study of 320 cases. Am J 

of Sp Med 1987;15:46-58. 

17. Brukner P, Bradshaw C, Khan K, et al. Stress Fractures: a review of 180 cases. Clin J of Sp Med 1996; 

6(2):85-9. 

18. Mann G, Lowe J, Matan Y, et al. Shoe and insole effect on medical complaints, overuse injuries and 

stress fractures in infantry recruits – a prospective, randomized study-preliminary results. Proceedings of 

the combined congress of the international arthroscopy association and the international society of the 

knee, Hong Kong, May 1995. 

19. Ha KI, Hahn SH, Chung M, et al. A clinical study of stress fractures in sports activities. Orthop 

1991;14(10)1089-95. 

20. Pecina M, Bojanic I, Dubravcic S. Stress fractures in figure skaters. Am J Sp Med 1990;18(3):277-9. 

21. Ting A, king W, Yocum L, et al. Stress fractures of the tarsal navicular in long distance runners. Clinics in 

Sp Med 1988; 7(1):89-101. 

22. Alfred Rh, Belhobek G, Bergfeld JA. Stress fractures of the tarsal navicular. A case report. Am J Sp Med 

1992;20(6):766-8. 

23. Ariyoshi M, Nagata K, Kubo M, et al. MRI monitoring of tarsal navicular stress fracture healing – a case 

report. Kurume Med J 1998;45(2):223-5. 

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1981:9:217-18. 

25. Pavlov H, Torg JS, Freiberger RH. Tarsal navicular stress fractures: radiographic evaluation. Radiology 

1983;148:641-5. 

26. Shawdon A, Kiss ZS, Fuller P. The bipartite tarsal navicular bone: radiographic and computed tomography 

findings. Australian Radiol. 1995;39(2):192-4. 

27. Gordon TG, Solar J. Tarsal navicular stress fractures. J Am Podiatric Med Assoc 1985;75:363-6. 

28. O’Connor K, Quirk R, Fricker P, et al. Stress fracture of the tarsal navicular bone treated by bone grafting 

and internal fixation: three cases studies and a literature review. Excel 1990;6:16-22. 

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EPIDEMIOLOGY OF STRESS FRACTURES 

Peter Brukner, MD 

Stress fractures occur in association with a variety of sports and physical activities. Clinical impression 

suggests that stress fractures are more common in weight-bearing activities particularly those with a running 

or jumping component. However, it is difficult to compare the incidence of stress fractures in different 

sports or to identify the sport or activity with the greatest risk due to a lack of sound epidemiological data. 

Most of the literature in this area pertains to female runners and to male military populations. There is no 

information about stress fracture rates in the general community. 

STRESS FRACTURE INJURY RATE 

Stress fracture rates in athletes 

A number of studies have investigated stress fracture rates in athletes (Warren, Brooks-Gunn et al. 1986; 

Barrow and Saha 1988; Brunet, Cook et al. 1990; Frusztajer, Dhuper et al. 1990; Pecina, Bojanic et al. 1990; 

Cameron, Telford et al. 1992; Kadel, Teitz et al. 1992; Dixon and Fricker 1993; Goldberg and Pecora 1994; 

Johnson, Weiss et al. 1994; Bennell, Malcolm et al. 1995; Bennell, Malcolm et al. 1996). Of these, only two 

allow a direct comparison of annual stress fracture rates in different sporting populations (Goldberg and 

Pecora 1994; Johnson, Weiss et al. 1994). Johnson et al (Johnson, Weiss et al. 1994) conducted a two year 

prospective study to investigate sports related injuries in collegiate male and female athletes. In total, 34 

stress fractures were diagnosed over the study period. Track accounted for 64% of stress fractures in 

women and 50% of stress fractures in men. The stress fracture incidence rate (expressed as a case rate) in 

males was highest for track (9.7%) followed by lacrosse (4.3%), crew (2.4%) and American football (1.1%). 

The stress fracture incidence rate in women was highest for track athletes (31.1%), followed by crew (8.2%), 

basketball (3.6%), lacrosse (3.1%) and soccer (2.6%). No athlete sustained a stress fracture in fencing, 

hockey, golf, softball, swimming or tennis. 

Goldberg and Pecora (1994) reviewed medical records of stress fractures occurring in collegiate athletes 

over a three year period. Approximate participant numbers were available to allow calculation of estimated 

incidence case rates in each sport. The greatest incidence occurred in softball (19%), followed by track 

(11%), basketball (9%), lacrosse (8%), baseball (8%), tennis (8%) and gymnastics (8%). However, participant 

numbers were small in some of these sports which may have led to a bias in incidence rates. 

Both studies suggest that track athletes are at one of the highest risk for stress fracture. However, since 

neither expressed incidence in terms of exposure it may not be strictly valid to compare the risk of stress 

fracture in such diverse sports. There is only one athlete study which has expressed stress fracture incidence 

rates in terms of exposure (Bennell, Malcolm et al. 1996). This 12 month prospective study followed 

a cohort of 95 track and field athletes. Results showed an overall rate of 0.70 stress fractures per 1000 

training hours. Further research is needed to quantify incidence rates in this manner to allow more valid 

comparison between studies. 

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Retrospective studies have measured stress fractures rates in specific sporting populations, mostly runners 

and ballet dancers (Warren, Brooks-Gunn et al. 1986; Barrow and Saha 1988; Brunet, Cook et al. 1990; 

Frusztajer, Dhuper et al. 1990; Pecina, Bojanic et al. 1990; Cameron, Telford et al. 1992; Kadel, Teitz et al. 

1992; Dixon and Fricker 1993; Goldberg and Pecora 1994; Bennell, Malcolm et al. 1995). Variation in reported 

rates reflect differences in methodology particularly cohort demographics and method of data collection. 

A history of stress fracture has been reported by 13% to 52% of female runners. The lowest rate was 

found in one which included recreational as well as competitive runners. Ballet dancers are another population 

where stress fracture rates appear high with 22% to 45% of dancers reporting a history of stress fracture. 

However, most studies failed to confirm the accuracy of subject recall which may introduce bias into 

the figures reported. Nevertheless, it is clear that a stress fracture is a relatively common athletic injury. 

Stress fracture rates in the military 

Reports of the incidence of stress fractures in male recruits undergoing basic training for periods of 8 to 14 

weeks are remarkably similar and generally range from 0.9% to 4.7% (Protzman and Griffis 1977; Reinker 

and Ozburne 1979; Scully and Besterman 1982; Brudvig, Gudger et al. 1983; Gardner, Dziados et al. 1988; 

Pester and Smith 1992; Taimela, Kujala et al. 1992; Jones, Bovee et al. 1993; Beck, Ruff et al. 1996). 

However, in two particular studies involving the Israeli army, the reported incidence was 31% (Milgrom, 

Giladi et al. 1985) and 24% (Milgrom, Finestone et al. 1994). The authors attributed this much higher incidence 

to several factors including meticulous follow-up, a high index of suspicion and the use of the 

radioisotope bone scan for diagnosis. In addition, asymptomatic areas of uptake on bone scan were also 

classified as lesions which would inflate the reported figures. Stress fracture rates in female military 

recruits during basic training are generally higher than those in males ranging from 1.1% to 13.9% 

(Protzman and Griffis 1977; Reinker and Ozburne 1979; Brudvig, Gudger et al. 1983; Jones, Harris et al. 1989; 

Pester and Smith 1992; Jones, Bovee et al. 1993). 


Comparison of stress fracture rates in men and women 

It is often suggested that women sustain a disproportionately higher number of stress fractures than men. 

The relative risk of stress fracture for women compared with men from studies where stress fracture rates 

can be directly compared is shown in Figure 1. In the military, reported incidence rates over an eight week 

training period vary from 1.1% to 13.9% in women and from 0.9% to 3.2% in men. These studies consistently 

show that female recruits have a greater risk of stress fracture than male recruits with relative risks ranging 

from 1.2 to 10 (Protzman and Griffis 1977; Reinker and Ozburne 1979; Brudvig, Gudger et al. 1983; Jones, 

Harris et al. 1989; Pester and Smith 1992; Jones, Bovee et al. 1993). This increased risk persists even when 

training loads are gradually increased to moderate levels and when incidence rates are separated by age 

and race. The most likely explanation for these findings in the military is lower initial physical fitness in 

the female recruits. Other possible reasons include differences in bone density and geometry, gait, biomechanical 

features, body composition and endocrine factors, particularly estrogen status. 

In contrast, a gender difference in stress fracture rates is not as evident in athletic populations (Brunet, 

Cook et al. 1990; Cameron, Telford et al. 1992; Dixon and Fricker 1993; Goldberg and Pecora 1994; Johnson, 

Weiss et al. 1994; Bennell, Malcolm et al. 1996). Studies either show no difference between male and 

female athletes or a slightly increased risk for women, up to 3.5 times that of men. A possible confounding 

variable is that, unlike the military where the amount and intensity of basic training is rigidly controlled, it 

is difficult to assume equivalence of training between men and women in most of these studies. However, 

Bennell et al (1996) found no significant difference between gender incidence rates even when expressed in 

terms of exposure. Women sustained 0.86 stress fractures per 1000 training hours compared with 0.54 in 

men. It is feasible that a gender difference in stress fracture risk is reduced in athletes as female athletes 

may be more conditioned to exercise than female recruits and hence the fitness levels of male and female 

athletes may be closer. 

REFERENCES 

Barrow, G. W. and S. Saha (1988). "Menstrual irregularity and stress fractures in collegiate female distance 

runners." The American Journal of Sports Medicine 16(3): 209-216. 

Beck, T. J., C. B. Ruff, et al. (1996). "Dual-energy x-ray absorptiomety derived structural geometry for stress 

fracture prediction in male U.S. marine corps recruits." Journal of Bone and Mineral Research 11(5): 645- 

653. 

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Bennell, K. L., S. A. Malcolm, et al. (1995). "Risk factors for stress fractures in female track-and-field athletes: 

a retrospective analysis." Clinical Journal of Sport Medicine 5: 229-235. 

Bennell, K. L., S. A. Malcolm, et al. (1996). "The incidence and distribution of stress fractures in competitive 

track and field athletes." The American Journal of Sports Medicine 26(2): 211-217. 

Brudvig, T. J. S., T. D. Gudger, et al. (1983). "Stress fractures in 295 trainees: a one-year study of incidence 

as related to age, sex, and race." Military Medicine 148: 666-667. 

Brunet, M. E., S. D. Cook, et al. (1990). "A survey of running injuries in 1505 competitive and recreational 

runners." The Journal of Sports Medicine and Physical Fitness 30: 307-315. 

Cameron, K. R., R. D. Telford, et al. (1992). Stress fractures in Australian competitive runners. Australian 

Sports Medicine Federation Annual Scientific Conference in Sports Medicine, Perth, Australia. 

Dixon, M. and P. Fricker (1993). "Injuries to elite gymnasts over 10 yr." Medicine and Science in Sports and 

Exercise 25: 1322-1329. 

Frusztajer, N. T., S. Dhuper, et al. (1990). "Nutrition and the incidence of stress fractures in ballet dancers." 

American Journal of Clinical Nutrition 51: 779-783. 

Gardner, L. I., J. E. Dziados, et al. (1988). "Prevention of lower extremity stress fractures: a controlled trial of 

a shock absorbent insole." American Journal of Public Health 78(1563-1567). 

Goldberg, B. and C. Pecora (1994). "Stress fractures. A risk of increased training in freshman." The 

Physician and Sportsmedicine 22: 68-78. 

Johnson, A. W., C. B. Weiss, et al. (1994). "Stress fractures of the femoral shaft in athletes-more common 

than expected. A new clinical test." The American Journal of Sports Medicine 22: 248-256. 

Jones, B. H., M. W. Bovee, et al. (1993). "Intrinsic risk factors for exercise-related injuries among male and 

female army trainees." The American Journal of Sports Medicine 21: 705-710. 

Jones, H., J. M. Harris, et al. (1989). "Exercise-induced stress fractures and stress reactions of bone: epidemiology, 

etiology, and classification." Exercise and Sports Sciences Review 17: 379-422. 

Kadel, N. J., C. C. Teitz, et al. (1992). "Stress fractures in ballet dancers." The American Journal of Sports 

Medicine 20: 445-449. 

Milgrom, C., A. Finestone, et al. (1994). "Youth is a risk factor for stress fracture. A study of 783 infantry 

recruits." The Journal of Bone and Joint Surgery 76-B(20-22). 

Milgrom, C., M. Giladi, et al. (1985). "The long-term followup of soldiers with stress fractures." The 

American Journal of Sports Medicine 13(398-400). 

Milgrom, C., M. Giladi, et al. (1985). "Stress fractures in military recruits. A prospective study showing an 

unusually high incidence." The Journal of Bone and Joint Surgery 67-B: 732-735. 

Pecina, M., I. Bojanic, et al. (1990). "Stress fractures in figure skaters." The American Journal of Sports 

Medicine 18: 277-279. 

Pester, S. and P. C. Smith (1992). "Stress fractures in the lower extremities of soldiers in basic training." 

Orthopaedic Review 21: 297-303. 

Protzman, R. R. and C. G. Griffis (1977). "Stress fractures in men and women undergoing military training." 

The Journal of Bone and Joint Surgery 59-A(825). 

Reinker, K. A. and S. Ozburne (1979). "A comparison of male and female orthopaedic pathology in basic 

training." Military Medicine Aug: 532-536. 

Scully, T. J. and G. Besterman (1982). "Stress fracture - a preventable training injury." Military Medicine 

147(285-282). 

Taimela, S., U. M. Kujala, et al. (1992). "Risk factors for stress fractures during physical training programs." 

Clinical Journal of Sports Medicine 2: 105-108. 

Warren, M. P., J. Brooks-Gunn, et al. (1986). "Scoliosis and fractures in young ballet dancers: relation to 

delayed menarche and secondary amenorrhea." The New England Journal of Medicine 314: 1348-1353. 

PREVENTABLE AND INBORN CAUSES OF STRESS FRACTURE 

C. Milgrom, PhD 

Why does one person sustain a stress fracture while another person doing exactly the same training 

remains injury free? Today there exists solid epidemiological evidence to indicate that intrinsic and extrinsic 

risk factors for stress fractures exist as they do for many disease entities. 

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The principal biological role of bone is skeletal support. Genes regulating bone strength have been identified 

in lines of mice. Interbreeding of these lines results in intermediate bone strength. A similar genetic 

regulatory system may be present in humans resulting in genetic differences in bone strength. The first evidence 

that there may be a genetic basis for stress fracture was in the 1990 report of Singer et al. They 

described multiple stress fractures in monozygotic twins. Both individuals who served in the same unit, 

sustained stress fractures in the same anatomical site, with presenting symptoms in both being in the 6th 

week of training. Friedman et al have ongoing work to characterize the putative genes conferring in 

increased risk for stress fractures. 

Although medical students are taught to think of bone strength in terms of the easily measurable parameter, 

bone density, this is not the major determinant of a bone’s strength. The major determinant of a bone’s 

strength is its size. If the diameter of mid shaft tibia is increased from 22 to 27 mm, the bone’s strength in 

bending and torsion is increased 106% and compression by 50%. Tibial bone width has been found to be a 

risk factor for stress fracture. In a prospective Israeli study infantry recruits with wider tibias in the mediallateral 

plane were found to be at decreased risk for both femoral and tibial stress fractures than those with 

narrower tibias. This corresponds to the fact that the major bending moment in the tibial is in the mediallateral 

plane. The observations of this research were verified in a subsequent American military study. 

In the young, bone can be strengthen by vigorous exercise. An Israeli military study showed a mean 

increase in tibial bone density of seven per cent after fourteen weeks of vigorous training. A history of regular 

basketball playing for at least two years prior to induction into the army has been shown to markedly 

decrease the risk for stress fracture in infantry training from 20 to less than 3 per cent. Regular running 

however has never been shown to decrease the risk for stress fracture in any military study. These observations 

indicate that strengthening of bone is not an overnight phenomena and may take years to accomplish. 

It also indicates that running because it is a largely same plane repetitive activity, does not result in 

bone strengthening in muliple axes. 


It is recognized that bone reaches its maximum strength at about the age of twenty-five. The difference 

between eighteen year old and 30 year old bone can be easily seen in microscopic examination. The 

younger bone still has cartilaginous elements and is not fully mineralized. Israeli army studies have shown 

that younger infantry recruits have lower risk for stress fractures than older recruits. With each year of 

increase in recruit age between 17 and 25, the risk for stress fractures decreased by 26 per cent. An 

American study reported an opposite trend, but lack the controls and surveillance of the Israeli study. 

Other identified instrinsic anatomical risk factors for stress fractures are high external rotation of the hip 

and foot type. The low, but normal arch foot was reported to be protective for stress fractures, while the 

high cavus foot reported to have increased risk for stress fracture. Poor prior physical fitness has been 

implicated as a risk factor for stress fracture. For an athlete this factor would usually be important after a 

return from an injury or a change of activity. It has become a less important factor in military medicine, 

with many armies being volunteer forces and not universal conscripts. 

The issue of the importance of shoes and orthotics in stress fracture prevention is clouded with much myth 

and salesmanship. The large strains and strain rates that cause stress fractures of the tibia and femur are 

more the result of muscle force on the bone than the force of foot impaction. This has been shown by in 

the vivo bone strain measurements of Milgrom et al. There however is good scientific data to show that 

proper shoe gear and orthotics can lower the incidence of metatarsal stress fractures. Their role in preventing 

tibial and femoral stress fractures has not been established. 

The recent in vivo strain measurement study of Ekenman et al shows that the addition of orthotics to athletic 

shoes does not decrease and in fact increases some types of strains during running. 

From the in vivo strain gage studies of Milgrom, Burr and Ekenman there is evidence that the majority of 

tibial and femoral stress fractures are mediated through the bone remodeling response. Metatarsal stress 

fractures are more likely to be the result of pure high cyclic loading. The remodeling response occurs when 

trainees are exposed to new high strain or strain rate patterns. They attempt to strength bone by initiating 

a remodeling response, the first phase of which is bone absorption. If the high strains or strain rates continue 

during the absorption period, then stress fracture can result. Looking to the future, this seemingly 

inappropriate bone response may be possibly altered by agents such as bisphosponates. By their use the 

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amount of bone absorption may be reduced and thereby remodeling driven stress fracture incidence 

reduced. 

UNCOMMON STRESS FRACTURES AND THEIR TREATMENT PRINCIPLES 

Sakari Orava, MD, PhD, Professor, Orthopaedic surgeon 

Mehilainen Sports Clinic and Private Hospital, and Sports Trauma Research Center 

Turku, Finland 

Stress fractures usually heal well, if the diagnosis is done early and the causative factor – excessive loading 

of the bone – is adequately eliminated. However, some stress fractures in athletes are not diagnosed in 

time or in spite of the right diagnosis, exercise is started too early or continued in spite of the symptoms. 

In these cases, chronic symptoms develop, and delayed union or non union may follow. The number of 

these was estimated to be approximately 10 per cent 15 years ago. To day, due to the grown knowledge of 

stress fractures the number probably is smaller. Delayed or non unions require either a long rest from all 

physical activity or surgical treatment. 


Some stress fractures are very uncommon. The diagnosis of them may cause problems, because the differential 

diagnosis is difficult and other injuries are suspected and treated for a long time before the right 

diagnosis. These rare stress fractures are reviewed and their treatment principles discussed. 

1. Hallux sesamoid bones 

The sesamoid bones under the first metatarsophalangeal joint are very hard and tolerable bones. There are 

three possible diseases or injuries during physical exercise, that can cause pain of the sesamoid bones: 

acute fracture, stress fracture, osteochondritis or osteonecrosis of bone. The traction and compression 

stress on the sesamoid bones is high during running and jumping. The bones are not only subject to the 

pull of muscles via tendons, but they also directly bear the body weight. Stress fracture may affect the 

medial or lateral or both sesamoids. 

The diagnosis requires careful clinical examination, anteroposterior and oblique radiographs with tangential 

views of the sesamoid bones and bone scan. MRI will show bone oedema. 

Conservative treatment consists of rest from training, shoes with thick and stiff soles and special orthoses. 

Healing may take several months and some cases are painful up to two years from the onset of the symptoms. 

In cases with symptomatic non union the bone or one of the fragments can be removed. In case of 

osteonecrosis the affected bone is excised. Both sesamoids are not advised to excise. 

2. Stress fracture of anterior mid-tibia 

Slowly healing stress fracture of the anterior cortex of the mid-tibia is seen as an adaptation process of the 

cortex to physical exercise. It is seen in dancers, jumpers and runners. Only five per cent of the stress fractures 

of tibia localize at the middle of it. The fracture is caused by compressive and tensile forces. The 

patients often have a along history of mild symptoms. This stress fracture has a tendency for delayed union 

or non union and even a complete fracture may occur. 

In radiographs, a small fissure (or several) is seen transversally at the mid-tibia. The anterior cortex is usually 

thickened and hypertrophic. In tomography, CT or MRI there is a "cavity" – like "hole" inside the cortex. 

In MRI oedema of the medullary canal of tibia is also seen. 

Rest from running or jumping is several months. Supportive special orthosis can be used. Local low intensity 

ultrasound treatment and magnetic field treatment have been tried. Electrical stimulation for 3-6 

months may lead to healing, until surgical procedures are considered. In surgery, biopsy of the fracture line 

is done, drill holes with 2 mm diameter drill are made through the lateral and medial cortex. appr. five cm 

distally and proximally from the fracture line. Postoperatively lower leg orthosis is used. In chronic non- 

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unions short tension plate is set on the lateral side of the tibia. Intramedullary nailing has also been used. 

Postoperatively the above mentioned methods are still available. 

Tarsal Navicular 

The number of stress fractures of the tarsal navicular has increased during the last decade. Jumpers and 

runners, as well as gymnasts, dancers and other athletes are in the risk group to get this stress fracture. In 

midfoot pain of young athletes, navicular stress fracture should be suspected as one of the main reasons 

for prolonged pain. 

Radiograps seldom are positive in early phase. Some fractures appear suddenly with a dislocated complete 

fracture and a positive history of midfoot pain is usually obtained later from the patient. Isotope scan usually 

is positive, as well as MRI examination. In MRI intraosseous oedema often is seen also in other bones 

around the navicular bone. 

Treatment consists of rest from impact training. Magnetic field, electrical stimulation and low intensity 

ultrasound can be used. Foot orthosis or solid shoe sole may help, too. Healing time is from 2 to 4 

months. Grading with MRI as well as the history of symptoms can make the decision for operative treatment 

easier, especially, if no healing occurs during the follow-up time. Drilling of the bone across the fracture 

line and fixation with absorbable pins or screws is recommended. In complete fractures same method 

or fixation with metal screws is used. After a short non-weight bearing period full weight can be allowed 

with solid footwear. Healing after surgery until full sports capacity may take half a year. 


3. Stress fracture at the superior proximal corner of the navicular bone may become chronic and annoying. 

If the fragment is small, it will become rounded and asymptomatic during one year. If it is bigger or the 

avulsion – compression – rotation stress affects also the distal joint surface of talus, symptoms usually 

persist for a long time. Then surgical excision of the fragment may become necessary. 

Base of fifth metatarsal 

The fracture of the metatarsal five basis – Jones's fracture – is known as a risk fracture for delayed or non 

union. Stress fracture usually develops somewhat more distally as the original "Jones's fracture", to the 

proximal diaphysis. If intramedullary sclerosis occurs, the healing is disturbed. In Radiograps and in MRI 

the medullary canal obliteration can be seen. Isotope scan sometimes is only weakly positive or even negative. 

The treatment is conservative in the beginning. Non-weight bearing for three weeks is recommended and a 

good foot orthosis with whole sole bearing during the gait is recommended. If surgery is indicated, best 

results are obtained with tension band method (two 1.8 mm K-wires and a metal cerclage. 

Base of second metatarsal 

One of the uncommon stress fractures at the foot is that in the base of the 2nd MT. This bone is usually 

longer than 1.st (Morton's foot) and the patients need rising up to toes or standing toes extended (ballet 

dancers). The stress fracture of the base may become chronic, a non union develops and pain continues. 

With rest and shoe correction with elevation under the 1.st and 3.rd MT head may help and the healed 

bone itself will be stronger later. However, sometimes drilling of the sclerotic fracture area or shortening 

osteotomy in the neck of the 2.nd MT must be considered. In some cases delayed or non union develops 

also into the base of the 3rd. metatarsal. 

Toe stress fractures 

Stress fractures in toe bones are rare, The toe is swollen and gout or other inflammatory diseases are at 

first suspected. Later the radiographs show sclerosis and the right diagnosis can be made. In the proximal 

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phalanx of the big toe oblique intra-articular medial stress fractures have been described in cross country 

skiers. They are painful but heal in a few weeks with conservative treatment. 

5. Stress osteopathy of tarsal bones 

Uncommon stress oedema or osteopathy in tarsal bones may cause pain and prevent athletic exercises. 

This reaction is seen in only in MRI pictures and is located at the cuboid bone, talus, navicular and sometimes 

in cuneiforms and in the base of the 1.st and 2.nd metatarsals. It is very uncommon in athletes at the 

calcaneal bone, but the lateral side articulating with cuboid bone can be affected, too. The etiology is multifactorial 

and the oedema may last is spite of all conservative treatment methods. In chronic cases drilling 

of the affected bone / bones can be done. 

Chronic pelvic stress fractures 


In female endurance athletes a pubic stress fracture may heal very slowly. Amenorrhea is usually found in 

those athletes. Sometimes wide callus and inside it a pseudoarthrosis can be seen in all radiological examinations. 

Osteoporosis treatment with calcium and possibly D – vitamin has to be added the treatment 

protocol, in addition to the rest from training (running, jumping). If ischial bone is affected at the same 

time as pubic bone or alone, it will lead even longer healing time. 

Stress fractures of sacrum are uncommon, but can be found in runners and ball players. Sometimes this 

fracture can be bilateral. Healing, however, usually is uneventful. 

Isthmic stress fractures of lumbar vertebrae 

These stress fractures usually develop to athletes, who need repetitive maximal extension - flexion of the 

back combined with hard muscular forces or vertical jumping. They are seen in gymnasts, figure skaters, 

aerobic athletes, javelin throwers, hurdlers as well as in many other athletes. Isotope scanning in young 

athletes does not always tell the right diagnosis. MRI is more specific. examination. Follow-up is needed to 

see that spondylolisthesis will not develop. The disc lesions often connected with lumbar stress fractures 

require rest to regenerate. 

Rib stress fractures 

Some stress fractures in the ribs may last long and the diagnosis of them may be difficult. Rowers, golfers 

and many other ball or racket sport athletes can be affected. Sometimes two or even several simultaneous 

"hot spots" in the ribs can be seen in isotope scanning. Stress fracture of the first rib is an own entity with 

"TOS" – symptoms to the arm and long-lasting exertion pain. 

Uncommon stress fractures of the upper arm 

In the upper arm stress fractures are much more uncommon than in lower extremities. Difficulties with the 

diagnosis as well as treatment may come from stress fractures of carpal bones, radial epiphysis, olecranon, 

proximal humeral epiphysis and coracoid process. Those in the middle of the upper or lower arm bone diaphyses 

are easier to detect. If not diagnosed in time total fractures have occurred in some stress fractures 

(olecranon, humeral shaft). 

General diagnostic recommendations 

All of these stress fractures need special attention from physicians treating them. Because of the risk for a 

delayed union or non union, radiographs should be taken routinely, if pain suspected to come from bone 

lasts 3-4 weeks. After that isotope scanning is recommended, if symptoms do not subside. MRI has to be 

considered as the next examination in selected cases. Good examinations for bone pathology are also normal 

tomography and computerized tomography. 3 – dimensional models or the affected stress fracture site 

can also be obtained with modern imaging methods. 

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HOW IMPORTANT IS ACCURATE DIAGNOSIS FOR STRESS FRACTURES 

Ingrid Ekenman MD, PhD 

Karolinska Institute and Sabbatsberg Hospital, Stockholm, Sweden 

According to AMA, a stress fracture is a subtotal or total fracture, caused by an imbalance between outer 

repetitive and submaximal loading on one side and the remodelling of the bone on the other side. 

It has been reported that of all injuries sustained by athlete populations, stress fractures account for 

between 0.7% and 15.6%. In studies in which only runners were investigated, the relative frequency is higher: 

it ranges from 6.0% to 15.6%. In track and field athletes, stress fractures accounted for a large percentage 

of overuse injuries: 34.2% in women and 24.4% in men, as reported in one study, and 42.0% for men 

and women combined, as reported in another. 

In elite gymnasts, stress fractures accounted for 18.3% of overuse injuries in women and 9.2% in men. 

The difference in results probably reflects differences in the composition of each case series. Composition 

is affected by factors such as referral patterns; case loads; area of practise; and demographics and participation 

patterns of patients in the clinics, including training intensity, type of sport and percentage of elite 

versus recreational athletes. 


Although stress fractures are most common in lower-extremity bones, they also occur in non-weightbearing 

bones, including the ribs and upper limbs. 

Hullko and Orava found in 1988 that tibia was the most affected bone as high as 50%, followed by the 

metatarsal bones in about 28%, fibula 12%, femur 8%(including femoral neck), pelvis 1%, spine 1%. 

Milgrom et al found 1985 about the same distribution of 184 stress fractures when they examined 295 soldiers 

during one year of exercise. 

Although great variations exists in the absolute percentage of stress fractures reported at each bony site, 

the most common sites seem to be the tibia, metatarsals and fibula. 

A number of factors may influence reported distributions of stress fractures, including the patient´s gender, 

age, and type and level of activity, as well as method of stress-fracture diagnosis. 

For example, tarsal navicular stress fractures give rise to subtle clinical findings, are often missed in differential 

diagnosis of foot and ankle pain, and are rarely evident on radiographs. They will therefore be underreported 

compared with stress fractures such as ones that occur in metatarsals, for which clinical and radiographic 

diagnoses are more straightforward. 

Devas reported 1975 that when clinical examination and plain radiography are used for diagnosing stress 

fractures, the fibula, second metatarsal and calcaneus are commonly affected. 

Recent case reports of stress fractures are previously unreported sites such as the ulnar diaphysis, patella 

and neck of the seventh and eight ribs may reflect development of more sensitive imaging techniques such 

as magnetic resonance imaging (MRI) and the triple-phase isotope bone scan, as well as increased awareness 

of stress fractures. 

The typical stress fracture patient has gradual onset of pain that is activity related. If the patient continues 

to exercise, the pain will become more severe or occur at an earlier stage of exercise. If the exercise is continued 

and severity of symptoms increases, the pain may persist after exercise. 

The pain is usually well localized to the site of the fracture, though stress fractures of the neck of the femur 

commonly presents with groin pain and pain referred to the knee. 

Physical examination gives bony tenderness. This is easier to determine in bones that are relatively superficial. 

Range of joint motion is usually unaffected; the exception is when the stress fracture is close to the joint 

surface, such as stress fracture of the neck of the femur. 

Some authors have suggested that the presence of pain when therapeutic ultrasound is applied over the 

stress fracture area can be of use in detection of stress fractures. Boam et al showed that compared with 

isotope bone scan, ultrasound sensitivity was only 43% in detection of stress fractures. 

Together with the physical examination it is important to take in account the potential intrinsic factors like 

for example leg-length discrepancy, malalignment, muscle imbalance, muscle weakness or lack of flexibility. 

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In diagnosis of stress fractures, plain radiography has a poor sensitivity and a high specificity. The abnormalities 

are unlikely to be seen unless symptoms have been present for at least two to three weeks. 

When a radiograph is negative and the suspicion is high, a triple-phase bone scan is the next choice for 

investigation. It has a high sensitivity but a low specificity. Prather et al stated that the bone scan had a 

true positive rate of 100%, and false-negative scans are relatively rare. 

CT scan is a useful complement to radiographs or a bone scan for detecting fracture lines as evidence for 

stress fractures. 

MRI has been the investigation of choice. Its sensitivity is similar to that of isotope bone scan and has the 

advantage of anatomic visualization. It also differentiate between a stress fracture and a tumor and it also 

localizes the stress fracture. 

The question of accuracy when diagnosing stress fractures with the above in mind, tells us about the 

importance when differing between tumors and stress fractures and for example when diagnosing a stress 

fracture in the collum femoris, as it seems to be the most malignant kind of stress fracture. 


REFERENCES 

1.Dixon M, Fricker P. Injuries to elite gymnasts over 10 yr. Med Sci Sports Exercise 1993;25:1322-1329 

2.Brubaker CE, James SL. Injuries to runners. J Sports Med 1974;2:189-198 

3.James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med 1978;6:40-49 

4.Orava S. Stress Fractures.Br J Sports Med 1980;14:40-44 

5.Pagliano J, Jackson D. The ultimate study of running injuries. Runners world 1980;Nov:42-50 

6.Clement DB, Taunton JE, Smart GW, McNicol KL. A survey of overuse running injuries. Phys Sports Med 

1981;9:47-58 

7.Milgrom C, Giladi M, Stein M et al.Stress fractures in military recruits:a prospective study showing an 

unusually high incidense. J Bone Joint Surg 1985;67-B:732-735 

8.Devas. Stress Fractures. Edinburgh:Churchill Livingstone.1975 

9.Johansson C, Ekenman I,Tornqvist H, Eriksson E. Stress fractures of the femoral neck in athletes:the consequence 

of a delay in diagnosis. Am J Sports Med 1990;18:524-528 

10.Hulkko A, Orava S.Stress fractures in athletes.Int J Sports Med 1987;8:221-226 

11.Boam WD, Miser WF,Yuill Sc et al.Comparison of ultrasound examination with bone scintiscan in the 

diagnosis of stress fractures. J Am Board Fam Pract 1996;9(6):414-417 

DOES THE ASYMPTOMATIC STRESS FRACTURE EXIST? 

C. Milgrom, PhD 

The epidemiology and clinical presentation of stress fractures is very variable. It varies according to the 

specific bone involved, and the specific anatomic site affected within that bone. It varies according to 

whether the stress fracture is secondary to pure cyclic overloading or whether there is an intermediate 

bone remodeling response. 

There is solid epidemiological evidence available that femoral stress fractures can be asymptomatic. 

Milgrom et al, used bone scan as the basis for diagnosis of stress fracture, and found a high incidence of 

asymptomatic stress fractures of the femur in Israeli infantry recruits. Their study was prospective and 

recruits were questioned and underwent a stress fracture physical examination routinely every two weeks 

during the course of 14 weeks of basic training. According to their research protocol x-rays were also taken 

of any grade 2, 3 or 4 femoral scintigraphic foci. They found that more than half of the asymptomatic 

femoral scintigraphic foci had radiographic evidence of a stress fracture. Therefore one can not say that 

these scintigraphic foci did not represent true stress fractures. 

Milgrom et al attributed the phenomena of the asymptomatic femoral stress fracture to the low sensitivity 

of the femoral periosteum, when compared to that of the tibia or metatarsus. They stated that the tibial 

periosteum has to be very sensitive to offer protection for the very superficial anterior and medial aspect of 

the tibia. They also stated that femoral stress fracture symptoms may present as a "muscle tightness or 

ache" and maybe difficult to differentiate from similar and non-pathological feelings that normally occur 

3.174

during vigorous training. Because of this problem the "fist test" was described as an aide in femoral stress 

fracture clinical diagnosis. 

The literature supports the existence of asymptomatic fully displaced femoral stress fractures in runners. 

Michaeli et al described a case of two runners in the Boston Marathon who broke their femurs while striding 

near the end of the run. Both runners denied experiencing femoral pain before their femurs snapped 

during the run. 

Recently in Israel, we had a case of an infantry recruit who sustained an asymptomatic displaced femoral 

stress fracture during a march. He had been checked by his unit doctor, as were all of the recruits just prior 

to the march. The doctor accompanied the training unit on the march. While in mid-stride the recruit fell to 

the ground. The recruit said he could not get up. The unit doctor ordered the recruit to get up twice but the 

recruit could not. X-ray of the recruit in a nearby hospital showed a fully displaced stress fracture. 

If these studies and case reports were not enough to convince me fully that an asymptomatic femoral 

stress fracture exists, than a personal experience did. I have been running regularly since the age of 16. For 

the last 10 years I have been running about 5K three times a week. Last year we got a new dog. The dog is 

very large and I started to take her along on a leach for my runs. After about 10 weeks I developed a strange 

deep sensation in my upper thigh at night. I continued to run for another 2 weeks, but the sensation 

became stronger. During the daytime or during my runs I felt nothing abnormal. At my wife’s urging I took 

an x-ray and there it was, a proximal femoral stress fracture. This was enough to make me a believer in the 

asymptomatic femoral stress fracture and all of its clinical implications. 


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ALLOGRAFTS IN KNEE SURGERY 

Friday, March 14, 2003 • Aotea Centre, Kaikoura Room 

Chairman: Stephen Howell, MD, USA 

Faculty: Dieter Kohn, MD, Germany, Konsei Shino, MD, Japan and David Caborn, MD, USA 

Technique and Clinical Results of Meniscal Transplantation – Dieter Kohn 

Scientific Basis of Meniscal Transplantation – Steve Howell 

Technique and Clinical Results of ACL Allografts – Konsei Shino 


Scientific Basis of ACL Allografts – Steve Howell 

Technique and Clinical Results of Osteochondral Allografts – David Caborn 

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ICL #1 - ISAKOS

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