using nutrition to ease the pain of osteoarthritis - HillsVet

nutrition myths and truths, facts and fallacies 

Using Nutrition to Ease the Pain of Osteoarthritis 

Ron McLaughlin, DVM, DVSc, DACVS, Department of Clinical Sciences, Mississippi State University, College of Veterinary Medicine 

Introduction 

Osteoarthritis (OA) is a progressive, degenerative disease of synovial joints characterized by pain, disability, 

destruction of articular cartilage, and bony remodeling. It is the most common cause of lameness in dogs and is 

estimated to affect 20% of the canine population over 1 year of age. The radiographic prevalence of CHD has 

been reported to be as high as 70% in golden retrievers and Rottweilers. Risk factors for developing OA include 

age, breed, genetics, trauma, obesity and developmental orthopedic conditions. 

Primary OA is rare in dogs and is the result of defective articular cartilage structure and biosynthesis. Secondary 

OA is very common and may be caused by joint trauma, inflammatory conditions, congenital and developmental 

abnormalities, and metabolic, endocrine, neuropathic, neoplastic, or iatrogenic causes. Once the disease process 

begins, a progressive cascade of mechanical and biochemical events occurs resulting in cartilage destruction, 

subchondral bony sclerosis, synovial membrane inflammation, enthesiophytosis, and the development of 

periarticular osteophytes. 

Pathophysiology 

Normal joints are composed of articular cartilage, subchondral bone, joint capsule and supporting ligaments and 

tendons. Articular cartilage is composed of sparse chondrocytes embedded in a matrix and entrapped within a 

fibrous collagen (type II) framework. The matrix is composed of proteoglycans, which are anionic and hydrophilic 

sugar molecules attached to protein backbones. They attract and hold water in a gel-like consistency. The primary 

proteoglycans in articular cartilage are chondroitin-4 sulfate, chondroitin-6 sulfate, and keratin sulfate. Aggrecan is 

a core protein with attached glycosaminoglycan side chains of chondroitin sulfate and keratin sulfate. Link protein 

is a molecule that stabilizes aggrecan 

and polymeric hyaluronic acid to form 

large macromolecular aggregates, which 

comprise the cartilage matrix (Fig. 1). 

Normal cartilage integrity is maintained 

by a balance of cytokine-driven anabolic 

and catabolic processes. However, OA 

can be initiated by a variety of physical 

stresses (i.e., trauma, obesity, DOD), 

which damage the chondrocytes and 

lead to the production of inflammatory 

mediators. These chondrocyte-derived 

metalloproteinases (MMP) include 

collagenases, stromelysins, gelatinases 

and membrane type 1 metalloproteinase. 

Also produced are aggrecanases 

(ADAM-TS4 and ADAM TS-5) and other 

proteinases. All these enzymes function to 

Figure 1: Articular Cartilage — The matrix is composed of chondrocytes, 

collagen, proteoglycans and water. White GW. DVM Best Practices, Nov. 2003. 

Used with permission.


break down cartilage matrix faster than new matrix can be produced. The products of cartilage breakdown are 

antigenic and provoke synovitis. 

Synovial macrophages and leukocytes are abundant sources of cytokines, procoagulant factors, proteinases 

and oxygen-derived free radicals including nitric oxide (NO-). Interleukin-1-beta (IL-1) and tumor necrosis 

factor-alpha (TNF-) are the predominant proinflammatory cytokines synthesized during the OA process. IL-1 

stimulates the breakdown of matrix proteins and the accumulation of degradation products. TNF- appears to 

drive the inflammatory process. Both substances induce articular cells to produce other cytokines and increase 

their own production, as well as stimulate production of proteases and prostaglandin E 2 

(PGE 2 

). Numerous 

other cytokines and growth factors are also involved in OA pathophysiology. These inflammatory cytokines 

contribute to the perpetuation and progression of arthritis by sustaining catabolic processes. Once initiated, 

these molecular and cellular pathways form a self-perpetuating cycle. 

Clinical Presentation 

Signalment: A patient’s breed, age, gender and body weight provide valuable information when assessing the 

patient’s relative risk for osteoarthritis. Rapidly growing large breed dogs, for example, are often affected with 

developmental orthopedic conditions that can lead to OA. Older dogs often demonstrate signs of OA. Obese 

animals appear more susceptible to OA and, because of their added weight, may be more debilitated by the 

disease. One long term study has documented that the prevalence and severity of osteoarthritis is greater in dogs 

with body condition scores above normal. Over the life span of these same dogs, the mean age at which 50% of 

the dogs required long-term treatment for clinical signs attributable to osteoarthritis was significantly earlier (10.3 

years, p


hip joint 

KNEE joint 

healthy hip joint 

arthritic hip joint healthy knee joint arthritic knee joint 

Figure 2: Radiographic images of healthy and arthritic hip and knee joints demonstrating typical changes 

thickening of the joint capsule, sclerosis or erosion of the subchondral bone, periarticular osteophyte formation, 

enthesiophytes, and joint mice (Fig. 2). 

Arthrocentesis and synovial fluid analysis: Synovial fluid collected from affected joints is examined for 

volume, color, clarity, viscosity, cytology, and biochemical analysis. Fluid from patients with OA may be clear or 

pale yellow and slightly turbid due to an increase in inflammatory cells. It typically contains synovial cells and 

less than 5 x 10 3 /L mononuclear cells (and a few red blood cells may also be present). Polymorphonuclear cells 

typically constitute 0-12% of cells. Synovial fluid analysis alone may not differentiate OA joints from normal 

joints (particularly in the early stages of OA), but is valuable in ruling out septic and immune-mediated arthritis. 

Physical 

Rehabilitation 

NSAID 

Adjunct 

Multimodal 

Osteoarthritis 

Management 

Weight Control 

and Exercise 

EPA-rich 

Diet 

Figure 3: Multimodal management of 

osteoarthritis 

Chondroprotectant 

Treatment Of OA 

Multimodal medical treatment is recommended for OA, including 

weight reduction, proper nutrition, exercise control, physical 

therapy, and the administration of anti-inflammatory medications, 

analgesics, and osteoarthritis disease modifying agents (Fig. 3). 

Exercise and Physical Rehabilitation: Exercise and physical therapy 

are often used as part of the treatment for OA in humans and dogs. 

Exercise reduces obesity (a primary contributor to the progression of 

OA) and controlled exercise may help improve strength and range 

of motion in joints. Exercise may also reduce the need for analgesic 

medications. Low-impact exercises such as walking and swimming 

are preferred. The activity should be initiated gradually and increased 

as joint function improves. Warm compresses, coldpacks, massage 

therapy, electrotherapy, and ultrasound are techniques used in 

treatment of both human and canine OA patients. 

Nutrition: Fish oil as a source of omega-3 fatty acids has been shown to reduce inflammation and pain in 

mammals. Certain omega-3 fatty acids have been shown to reduce the expression and activity of proteoglycandegrading 

enzymes, thereby having the potential to stop the progression of osteoarthritis (Fig.4). Damaged 

chondrocytes produce inflammatory cytokines that contribute to the progression of OA through catabolic


Physical Stress 

DOD 

Weight 

Trauma 

Structural & 

Functional 

Failure 

Cartilage 

Damage 

X 

Inflammation 

EPA 

X 

Matrix 

Damage 

Degradation caused 

by aggrecanases 

processes. Normally, arachidonic acid 

is the precursor for the synthesis of 

these inflammatory cytokines. EPA, 

an omega-3 fatty acid, competes 

with arachidonic acid for the same 

enzyme systems; and the eicosanoids 

derived from EPA promote minimal to 

no inflammatory activity. Thus, a diet 

containing n-3 fatty acids results in 

a decrease in membrane arachidonic 

acid levels and an associated decrease 

in the pro-inflammatory cytokines 

that perpetuate OA. Studies have 

documented that inflammatory 

eicosanoids produced from arachidonic 

acid are depressed when dogs consume 

foods with high levels of n-3 fatty acids, and specifically foods containing EPA. Though the exact molecular 

mechanisms for reducing inflammation (likely via resolvins and protectins) have not been fully explained, it is 

conceivable that omega-3 fatty acids modulate this process at the level of the genome or proteome. 

Four randomized, double-masked, controlled studies have been conducted in which arthritic dogs were fed a 

control food or a test food containing various levels of EPA (omega-3 fatty acid). These studies reported that the 

dogs fed the EPA-supplemented food improved in range of motion and ability to bear weight, had a decrease in 

pain and lameness, had significantly improved ability to rise form a resting position, and improved ability to run 

and play at 6 weeks. In one of these studies, biomechanical force plate analysis was also performed and found 

that dogs fed a diet containing EPA had an increase in weight bearing on the affected limb. Only 31% of the 

“control” dogs had improved weight bearing after the 90-day feeding trial, whereas 82% of dogs in the “EPA” 

group showed increased weight bearing. These clinical studies indicate that nutritional management using a 

therapeutic food supplemented with n-3 fatty acids helped improve the clinical signs of osteoarthritis in dogs as 

noted by pet owners, clinical orthopedic examination, and gait analysis of ground reaction forces. 

Disease-modifying osteoarthritis agents: These agents reportedly enhance cartilage health by providing 

the necessary precursors to maintain and repair cartilage. Many have been shown to positively affect cartilage 

matrix, enhance hyaluronate production, and inhibit catabolic enzymes. Oral disease-modifying OA agents 

typically contain glucosamine and chondroitin sulfate in various forms. 

Glucosamine is a precursor to the disaccharide unit of glycosaminoglycans, which comprise the proteoglycan 

matrix of articular cartilage. Studies using radiolabeled compounds have shown that 87% of orally administered 

glucosamine is absorbed and is eventually incorporated into the cartilage matrix. Glucosamine reportedly acts 

by providing the regulatory stimulus and raw materials for synthesis of glycosaminoglycans. Since chondrocytes 

obtain preformed glucosamine from the circulation (or synthesizes it from glucose and amino acids), adequate 

glucosamine levels in the body are essential for synthesis of glycosaminoglycans in cartilage. Glucosamine is also 

used directly for the production of hyaluronic acid by synoviocytes. In vitro biochemical and pharmacological 

studies indicate that the administration of glucosamine may normalize cartilage metabolism and stimulates 

the synthesis of proteoglycans. Clinical trials in man and animals indicate that glucosamine may have a positive 

effect on cartilage health and helps control symptoms associated with OA. 

X 

Figure 4: Pathophysiology of OA — In the dog, high levels of EPA help control 

pathways of inflammation and degradation.


Chondroitin Sulfate (CS) is the predominant glycosaminoglycan found in articular cartilage. Bioavailability 

studies have shown 70% absorption of CS following oral administration. The effect of CS on cartilage has been 

investigated in several in vivo and in vitro studies. The findings suggest that CS reduces collagenolytic activity, 

inhibits degradative enzymes, increases hyaluronate concentrations, and reduces symptoms of OA. Most 

research indicates that glucosamine and chondroitin sulfate work synergistically. Numerous studies performed 

on one such combination (Cosequin ® Nutrimax Laboratories, Inc.) have demonstrated improved synthesis of 

glycosaminoglycans and reduced proteolytic activity. Clinical trials have repeatedly shown a positive clinical 

effect in OA patients. 

Injectable disease-modifying OA agents are also available, the most common one used in dogs being Adequan ® * 

(used under license, Novartis Animal Health). Adequan is a polysulfated glycosaminoglycan (PSGAG), and studies 

have shown it has a positive anabolic effect on cartilage and decreases cartilage catabolism. 

Anti-inflammatory and analgesic medications (NSAIDs): NSAIDs are used because of their ability to 

reduce joint pain and decrease synovitis. A variety of NSAIDs are available for use in animals and are effective, 

in part, by decreasing prostaglandin synthesis through the inhibition of cyclooxygenase (COX). Newer NSAIDs 

have been shown to have no detrimental affect on the synthesis of cartilage proteoglycans in vitro at the 

recommended dosing. Drugs commonly used to control pain in dogs with OA include acetaminophen (15 mg/ 

kg q 8h), carprofen (4.4 mg/kg q 24h), etodolac (10-15 mg/kg q 24h), meloxicam (0.1 mg/kc q 8h), deracoxib 

(1-2 mg/kg q 24h), and tepoxalin (10mg/kg q 24h) among others. It is important to recognize that individual 

patients respond to specific NSAIDs quite differently. 

Corticosteroid treatment for OA remains controversial. Corticosteroids decrease the production of arachidonic 

acid, are potent anti-inflammatory agents, and decrease catabolic activity within the joint. However, 

corticosteroids may also damage cartilage (with long-term usage) by decreasing synthesis of collagen and 

matrix proteoglycans. 

Summary 

Although prevention of osteoarthritis is ideal, it is not always possible. Because osteoarthritis is a heterogeneous 

disease with diverse origins, it can present with a range of clinical manifestations. As a result, therapeutic 

recommendations should be customized for each patient. When appropriate, surgical correction of underlying 

conditions should be considered. After osteoarthritis is diagnosed, clients should be educated to foster 

realistic expectations. Osteoarthritis is usually irreversible but good management can minimize pain and slow 

progression of the disease. The goals of management include: 

✔ mitigation of risk factors 

✔ controlling clinical signs 

✔ slowing progression of the disease. 

Thus, effective treatment requires a multimodal approach, of which therapeutic nutrition is an important 

component. The goals of nutritional management include reducing inflammation and pain, enhancing cartilage 

repair, slowing cartilage degradation and providing tangible improvement in clinical signs of osteoarthritis. 

Foods designed for patients with osteoarthritis should supply age-appropriate nutrition and specific nutrients 

that may help reduce inflammation and pain, slow the degradative process, complement prescribed medications 

and provide tangible improvement in clinical signs. 

* As with all drugs in this class, side effects involving the digestive system, kidneys or liver may occur. These are normally mild, but may be serious. Pet owners should 

discontinue therapy and contact their veterinarian immediately if side effects occur. Evaluation for pre-existing conditions and regular monitoring are recommended 

for pets on any medication, including Adequan. ® Use with other NSAIDs or corticosteroids should be avoided.


Clinical Case: 

Nutritional management of osteoarthritis 

Phoebe 

History and clinical findings 

Phoebe, a 6-year-old neutered female Labrador retriever mix, was 

examined for rear limb lameness of two years duration. Clinical signs 

were mild to moderate in severity and included difficulty in rising 

from rest, limping, stiffness and reluctance to run, jump or play. No 

medications or supplements were being given by the owner. Phoebe 

weighed 75 pounds but was considered overweight with a body 

condition score of 4 on a 5-point scale. Phoebe was fed a low-calorie 

dry dog food but had access to other food sources for cats and dogs in 

the same household. 

Physical examination was normal except for the overweight body condition and orthopedic problems. A thorough 

orthopedic examination revealed the following abnormalities: 

✔ slight lameness at a walk 

✔ normal weight-bearing at rest but favors the left rear limb when walking 

✔ mild limitation in range of motion of the left hip joint 

✔ offers mild resistance when the right rear limb is elevated but bears full weight on the left hind limb 

✔ mild pain is elicited upon palpation of the left hip joint. 

A complete blood count, serum biochemistry profile and 

urinalysis were normal. Radiographs showed changes consistent 

with bilateral hip dysplasia and degenerative joint disease with 

the left coxofemoral joint more severely affected (Fig. 1). 

Questions 

Q. What are the therapeutic goals for managing patients with 

osteoarthritis or degenerative joint disease of hip joints? 

A. Therapeutic goals for managing chronic osteoarthritis or 

degenerative joint disease in the coxofemoral joints include: 

✔ Eliminating underlying causes (e.g., femoral head and 

neck excision for aseptic necrosis of the femoral head) 

Figure 1: Radiographs consistent with 

bilateral hip dysplasia and degenerative 

joint disease with the left coxofemoral joint 

more severely affected. 

✔ Setting realistic treatment expectations with Phoebe’s 

owner 

✔ Enhancing Phoebe’s quality of life by reducing pain, 

maintaining or improving activity level and improving 

joint function 

✔ Slowing disease progression by modifying cartilage 

structure and function.


Physical 

Rehabilitation 

NSAID 

Adjunct 

Multimodal 

Osteoarthritis 

Management 

Weight Control 

and Exercise 

EPA-rich 

Diet 

Figure 2: Multimodal management of 

osteoarthritis 

Chondroprotectant 

Most animals with chronic osteoarthritis or degenerative joint disease 

have irreversible changes with no opportunity to eliminate or cure 

the condition. This makes client education very important. Realistic 

expectations for both Phoebe’s owner and the veterinarian should 

acknowledge the facts that degenerative joint disease is controllable 

but not curable. A comprehensive multimodal management plan 

should focus on long-term pain management, altering disease 

progression and improving Phoebe’s quality of life (Fig. 2). 

Q. How might the overweight body condition contribute to the 

clinical problems in this dog? 

A. Osteoarthritis is often associated with abnormal forces acting on 

normal joints or normal forces acting on abnormal joints. Obesity 

may contribute to progression of degenerative joint disease and 

clinical signs by causing excess physical stress on either normal or 

abnormal joints. Additionally, recent studies have documented 

metabolic activity in adipose tissue that may be of equal or greater importance. Adipocytes secrete several 

hormones including leptin and adiponectin and produce a diverse range of proteins termed adipokines. Among 

the currently recognized adipokines are a growing list of mediators of inflammation (Fig. 3). These adipokines 

are found in human and canine adipocytes. Production of these proteins is increased in obesity, suggesting 

that obesity is a state of chronic low-grade inflammation. Low-grade inflammation may contribute to the 

pathophysiology of a number of diseases commonly associated with obesity including osteoarthritis. This might 

explain why relatively small reductions in body weight can result in significant improvement in clinical signs. 

IL-6 

IL-beta 

IGF-1 

PAI-1 

Leptin 

C 3 

Adipose Tissue 

Angiotensinogen 

TGF-b 

SAA 

TNF 

Adiponectin 

Resistin 

Figure 3. Adipocytokines and inflammatory mediators produced 

by adipocytes and adipocyte associated macrophages. C3, 

complement protein 3; IGF-1, insulin-like growth factor-1; IL, 

interleukin; PAI-1, plasminogen activator inhibitor-1; SAA, serum 

amyloid A; TNF-a, tumor necrosis factor-a; TGF-b, transforming 

growth factor-b. 

Q. Could this condition have been prevented with 

proper nutritional management? 

A. Large- and giant-breed dogs are at risk for 

developmental orthopedic disease including 

hip and elbow dysplasia, osteochondrosis and 

other conditions associated with joint instability 

or incongruity. Nutritional risk factors for 

developmental orthopedic disease include excess 

energy, fat and calcium intake during growth. Use 

of foods specifically formulated for large breed 

puppies helps manage these nutritional risk factors 

and ensure a normal, healthy growth rate. Obesity 

is recognized as a risk factor for development 

of degenerative joint disease in dogs; avoiding 

obesity can help reduce the incidence and severity 

of osteoarthritis. Recent studies have shown that 

when at-risk puppies were fed free choice during 

growth, they exhibited an increased incidence 

and severity of hip joint laxity and hip dysplasia 

compared to puppies fed in a restricted fashion. Over time, those dogs fed to maintain lean body condition 

throughout life exhibited reduced severity of osteoarthritis and a delayed need for medication compared to 

their heavier siblings.


Q. Outline a comprehensive nonsurgical management plan for Phoebe. 

A. Non-surgical management of osteoarthritis should focus on three main aspects: 

✔ Activity modification 

✔ Medications and supplements to modify joint pain and function 

✔ Nutritional management that emphasizes weight control and modifying joint inflammation 

and cartilage degradation. 

In the past, limiting activity levels in patients with osteoarthritis and degenerative joint disease was considered 

important. However, recent studies in human and veterinary patients with osteoarthritis have shown the 

benefits of exercise including decreased pain scores, improved joint function scores and less use of analgesic 

medications. Today, veterinary specialists are recommending therapeutic exercise as a way to improve quality of 

life for dogs with chronic osteoarthritis. A variety of medications and supplements are available to manage pain 

and joint function. Responses to medications and supplements vary considerably in patients with osteoarthritis 

and specific products and doses need to be individually tailored for each dog. 

Figure 4. Uptake of omega-3 fatty acids by canine chondrocytes AlA, alphalinolenate; 

EPA, eicosapentaenoate; DHA, docosahexanoate; control, serum free 

Dulbecco’s modified Eagle’s medium (DMEM). Caterson, B, Flannery CR, Hughes 

CE, et al. Mechanisms involved in cartilage proteoglycan catabolism. Matrix Biology 

2000;19(4):333-344. 

New information has been generated 

about canine osteoarthritis from in 

vitro studies with cartilage models 

and clinical studies in dogs with 

various forms of arthritis. In vitro 

cartilage studies have shown that 

canine chondrocyte membranes 

selectively store the omega-3 fatty 

acid EPA (eicosapentaenoic acid), and 

not other omega-3 fatty acids (Fig. 4). 

EPA is the most important fatty acid 

for helping manage inflammation in 

cartilage of dogs. EPA is also the only 

omega-3 fatty acid shown to inhibit 

activity of enzymes that degrade 

cartilage and helps turn off the signal 

to make degradative enzymes (Fig. 5). 

Based on these in vitro studies, clinical 

trials were performed in dogs with 

arthritis using Hill’s ® Prescription Diet ® 

j/d Canine, a food enhanced with 

levels of EPA much higher than those found in typical pet food and the only canned therapeutic pet food 

in the osteoarthritis category. Hill’s ® Prescription Diet ® j/d Canine also contains the highest levels of total 

omega-3 fatty acids,* an omega-6 to omega-3 ratio less than 1.0, high carnitine levels, added glucosamine and 

chondroitin sulfate, added antioxidant nutrients and added lysolecithin. Feeding Hill’s ® Prescription Diet ® j/d 

Canine to dogs with arthritis resulted in higher serum EPA concentrations, significant improvements in clinical 

signs observed by pet owners, improved clinical assessments of arthritis by veterinarians and improved weight 

bearing on affected limbs as measured by force plate gait analysis. Many of the dogs in the studies were not 

receiving medications or supplements in conjunction with the food. 

* Data on file. Hill’s Pet Nutrition, Inc.


Degradation 

begins with 

physical 

stress 

Degradation 

begins with 

physical 

stress 

functional 

Chondrocyte 

damage 

Chondrocyte 

damage 

High levels of omega-3 

and a low ratio of 

omega-6 to omega-3 

interrupt 

inflammation 

Structural & 

failure 

Matrix 

damage 

Inflammation 

EPA interrupts 

degradation 

Degradation 

a. Up regulation of aggrecanase enzymes and 

inflammatory mediators perpetuate cycle of 

proteoglycan breakdown and matrix damage. 

b. Appropriate levels of EPA inhibit the up 

regulation of aggrecanase enzymes at the level of 

mRNA and modulate the inflammatory response 

breaking the cycle of matrix damage. 

Figure 5. Eicosapentaenoic acid (EPA) interrupts the cycle of cartilage degradation and inflammation. 

Case management 

Hill’s ® Prescription Diet ® j/d Canine Dry pet food was dispensed for the owners to feed to Phoebe. The amount 

of food was calculated for an obese-prone animal. The owners were encouraged to deny Phoebe access to 

other sources of dog and cat food in the same household. Controlled exercise was also encouraged using walks 

on a leash. Six weeks later the owner reported improvements in all clinical problems associated with arthritis 

and improvements in Phoebe’s overall personality. The improvements observed by the owner continued at 

the three-month recheck and no pain was elicited on palpation of the left hip joint by the veterinarian. These 

improvements were noted without concurrent use of medications or supplements. Body weight and body 

condition score remained the same so client education focused on the importance of weight management with 

appropriate reductions in food, limiting access to other pet food and increased levels of exercise. 

Hill’s ® Prescription Diet ® j/d Canine is clinically proven to: 

• Improve mobility in as few as 21 days 1,2,4 

• Reduce pain in dogs with arthritis 2,3 

• Help dogs with arthritis walk, run, and play better, and climb stairs more easily 1,2,4 

• Help improve the quality of life of dogs suffering from arthritis 2,4 

Hill’s ® Prescription Diet ® j/d Canine product attributes: 

• High levels of EPA intercept the genetic signal that causes cartilage damage 

• Omega-3 fatty acids help to maintain joint health 

• High L-carnitine levels help to burn fat while maintaining lean muscle mass 

• Added glucosamine and chondroitin sulfate help to provide building blocks for cartilage repair 

• Improved taste and highly palatable nutrition help to improve compliance 

1 

Dose titration effects of omega-3 fatty acids fed to dogs with osteoarthritis (3-month feeding study), 2003. Unpublished data. 

2 

Cross AR, Roush JK, Renberg WC, et al. Effects of feeding omega-3 fatty acids on clinical signs and force plate analysis in dogs with osteoarthritis (3-month feeding study), 2004. Unpublished data. 

3 

A multi-center, practice-based study of therapeutic food and a nonsteroidal anti-inflammatory drug in dogs with osteoarthritis (3-month feeding study), 2004. Unpublished data. 

4 

Dodd CE, Fritsch DA, Allen TA, et al. Omega-3 fatty acids in canine osteoarthritis: a randomized, double-masked study (6-month feeding study), 2004. Unpublished data.


Acknowledgements 

Thanks to Dr. James Roush of Kansas State University and Dr. Tara Enwiller of Gilbert, Arizona, for providing 

information about this patient. 

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11


Ron McLaughlin, DVM, DVSc, DACVS, is Professor and Chief of Small 

Animal Surgery and Head of the Department of Clinical Sciences at Mississippi 

State University College of Veterinary Medicine. His primary areas of interest 

include the clinical areas of surgery, orthopedics and lameness. His research 

interests include orthopedics, gait analysis and biomechanics. 

®/ Hill’s, Prescription Diet and j/d trademarks are owned by Hill’s Pet Nutrition Inc. Adequan is a registered trademark owned by Luitpold Pharmaceuticals, Inc. 

Cosequin is a registered trademark of Nutrimax Laboratories, Inc. ©2008 Hill’s Pet Nutrition, Inc. 

12

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