Vol 43 # 3 September 2011 - Kma.org.kw

September 2011
KUWAIT MEDICAL JOURNAL 177
ligament, meniscal or cartilage injuries. These injuries
occur during high activity level, often in contact
sports which include acceleration/deceleration or
rotation/pivoting movements. One example of such
a contact sport is football; the most common sport of
the world. Especially, after anterior cruciate ligament
and meniscal injuries, there is an increased risk of
developing clinical and radiological signs of OA.
In a review article Lohmander et al [6] identified 127
published articles from 1970 – 2007, 10 - 20 years after
an anterior cruciate ligament injury. These articles
were found in a Medline search by the key words
“anterior cruciate ligament, injury, osteoarthritis and
follow-up”. The prevalence of OA was found to be 50%
even after isolated anterior cruciate ligament injuries.
The Lohmander group presented, in the same report as
mentioned before [6] , a review of radiologic long term
follow-up of isolated meniscal injuries and found in 41
publications a prevalence of 50% OA after 10 – 20 years.
In another review article, Oiestad et al [7] identified 31
anterior cruciate ligament injury articles by a search
in three computer data bases (PubMed, Embase and
AMED). The number of articles retrieved originally
was 2000 but the authors made a quality scoring of the
study designs and included only 31 articles with the
highest quality score. After a mean 13.7 (10 - 27) years
follow-up, 0 - 13% of isolated anterior cruciate ligament
injuries had developed knee OA. In combined anterior
cruciate ligament and meniscal injuries, the prevalence
of OA was 21 - 48%. Even if these two review articles
are not in full agreement about the prevalence of OA
after isolated anterior cruciate ligament injuries, the
risk of long term OA is pronounced. Definitely there is
a high price for the joy of playing football. Especially
as the post-traumatic OA disease starts earlier in life
compared to most other types of OA which have a later
onset.
The innervation of the the anterior cruciate
ligament injured patient is often long-term deficient
as proprioception is affected after an injury. About
1/3 of the anterior cruciate ligament injured patients,
independent of reconstruction, do not regain the
normal muscular function of the injured limb. There
are, however, occasional reports, on non-operated
anterior cruciate ligament injured patients, who were
treated by intensive rehabilitation and recommended
a low activity level, where the long-term muscular
function was normalized [20] and long-term knee OA
was low [21] . Not only knee joint injury, but also knee
joint overload, is a risk factor for knee OA. In top
football, there is constant knee joint overload due to
the character of the game. In elite football players,
even without a documented knee injury, knee OA
was found in 30%, 10 - 20 years after the end of the
football career, while recreational football players had
the same low incidence as non-football players after
the same follow-up time [22] . Therefore, daily overload
of the knee in elite football is a negative factor for the
joint but occasional football, even in organized league
on a low level, has no such drawback.
In general, sports can be divided into low, moderate
or high demands of the knee joint where, apart from
European and American football, also basketball
and handball are examples of high knee load while
swimming and golf are examples of lower knee
load [23] .
CARTILAGE AND BONE TISSUE
OA is regarded not only as mainly a cartilage
disease, but also one that affects other tissues of a
joint, especially the bone, by subchondral sclerosis,
osteophytes and cyst formation and also the synovium
by synovitis and often increased amount of joint fluid.
Also, the ligaments are involved by time.
The bony ends, constituting the knee joint,
are covered by hyaline cartilage. This tissue has a
favourable friction coefficient which is an advantage
during load transmission [24] . The thickness of articular
cartilage varies with the pressure. The higher the peak
pressure, the thicker the cartilage and it is interesting
to note that patellar articular cartilage is the thickest in
the human body [25] . This cartilage tissue constitutes of
cartilage cells and extracellular matrix including water,
proteglycans and collagen [24,25] . There are four different
zones of articular cartilage; superficial,middle,deepand
calcified [26] . These layers have a different composition
of collagen formation and cell morphology. During
weight-bearing, water is pressed out of the extracellular
matrix, while the water returns at rest. There
is a continuous turnover in normal cartilage tissue
constituting a balance. This is a fine-tuned mechanism
which is distorted in OA when the cartilage becomes
fibrillated and by time cleft formation and areas of
necrosis appear. Mechanically mediated and cytokinemediated
pathways of cartilage degeneration have
been identified in the pathogenesis of OA [3, 24] . The
possible OA healing mechanism / response has been
studied [27-30] . There is no vascular supply or innervation
of cartilage which affect the healing properties. In the
very early stage of the OA disease, the tissue changes
can not be seen by inspection (arthroscopy) or by MRI
(radiography). Microscopy of a bone/cartilage biopsy
would, however, show early osteoarthritic findings.
By time, cartilage fibrillation and fissures will develop,
which can be seen by arthroscopy or MRI. There are
several systems used for grading of cartilage disease,
such as the Mankin ́s criteria (microscopy) or the
Outerbridge classification (inspection).
The bone tissue is affected in the early and especially
the late phase of OA. The micro-architecture of the bone
is deteriorated in all types of OA. In cancellous bone,
the form of the trabeculae are changed and the density