DVM, PhD, DACVIM, DACVN
Dr. Bartges is from West Virginia and a graduate of Marshall University. After receiving his DVM in 1987 from the University of Georgia, in 1993 he completed an internship and dual residency in internal medicine and nutrition and received a PhD degree from the University of Minnesota. He then joined the faculty at the University of Georgia, and in 1997 joined the faculty at the University of Tennessee, where he remained until 2015. At Tennessee, he was Professor of Medicine and Nutrition, held the Acree Endowed Chair of Small Animal Research, and served as interim department head. He then served as an internist, nutritionist, and academic director at Cornell University Veterinary Specialists in Stamford CT and an Adjunct Clinical Professor of Medicine at Cornell University. He joined the faculty at The University of Georgia in 2016 and is currently Professor of Medicine and Nutrition in the Department of Small Animal Medicine and Surgery. He is board certified in small animal internal medicine and nutrition. Dr. Bartges is internationally known for his research and publications in veterinary nephrology and urology and nutrition. He has published approximately 350 peer-reviewed manuscripts, research abstracts, review articles, and book chapters and is the primary editor of Nephrology and Urology of Small Animals, along with Dr. Dave Polzin. He has spoken at approximately 250 meetings, many of which were international. His focus is on minimally invasive procedures and on clinical research in urinary tract diseases and nutrition.Read Articles Written by Joe Bartges
DVM, DACVIM (Nutrition), CVA
Dr. Raditic is a board-certified veterinary nutritionist. She was a professor for both the nutrition and the integrative medicine services at the University of Tennessee College of Veterinary Medicine and is currently the owner/founder of Nutrition and Integrative Medicine Consultants, which offers independent consulting and education. With a professional career that includes the roles of general practitioner, practice owner, academician, and independent veterinary nutritionist/consultant, she offers personal and unique perspectives on the role of nutrition, supplements, and integrative care for veterinary patients.
Updated April 2023Read Articles Written by Donna Raditic
Osteoarthritis is a common problem among dogs and increases with age. Nutrition can be one tool for preventing and managing osteoarthritis in dogs. This article discusses the role of 4 nutritional approaches that are used to prevent or treat this disease. The value of some approaches remains uncertain, and research is ongoing. This article summarizes current research findings and provides references for more in-depth review.
The role of nutrition in development of musculoskeletal disease in growing dogs has been recognized for decades. Developmental orthopedic disease (DOD) refers to a group of skeletal abnormalities that affect primarily fast-growing, large, and giant breed dogs. Risk factors among dogs already at genetic risk are nutrient excess (calcium and energy) and rapid growth (overfeeding and excess energy in diet).1-5 Increased risk for DOD has been associated with dietary calcium >3% on a dry matter basis, despite an appropriate calcium-to-phosphorous ratio.2 Another cause of excess calcium intake is client-provided treats and/or calcium-containing supplements. For example, 2 level teaspoons of calcium carbonate (10 to 15 antacid tablets) added to a large breed puppy’s daily intake doubles the calcium intake. Diets formulated for growth of large and giant breed dogs contain less energy and calcium and higher protein than growth diets for smaller dogs. Commercial diets for puppies at risk for DOD display the following statement from the Association of American Feed Control Officials (AAFCO): “[Pet food name] is formulated to meet the nutritional levels established by the AAFCO Dog Food Nutrient Profiles for growth/all life stages including growth of large-size dogs (70 lbs or more as an adult).” In addition, prevention of DOD in dogs has been associated with restricted food intake during growth, which slows the rate of growth without reducing adult body size.6,7
Obesity is the condition of having accumulated body fat that negatively affects health, including increased risk for osteoarthritis. Obesity can result in osteoarthritis because of the excess forces placed on joints and articular cartilage, which may lead to inactivity and further weight gain. Thus, a vicious cycle ensues. But perhaps more clinically relevant, adipose tissue is metabolically active and pro-inflammatory; therefore, obesity may contribute to inflammation.8-12 The negative effects of excess weight may be obvious in an obese dog, especially when obesity-related disease is present, but should not be overlooked in an overweight but otherwise clinically healthy dog.
Body Condition Score
Assigning a body condition score (BCS) and muscle condition score is essential for preventing the conditions of being overweight (BCS 6-7/9) or obese (BCS 8-9/9). Quantitatively, obesity is defined as exceeding ideal body weight by 30% or more.
Risk for Osteoarthritis
Several studies have demonstrated a relationship between overweight and obese dogs and osteoarthritis;9 however, a cause and effect has not been found.13,14 A long-term study of 48 dogs fed the same diet found that those fed 25% less quantity experienced longer delay to development of chronic disease, including osteoarthritis.15 They also weighed less, had better BCS, and lived an average of 1.8 years longer. Maintaining optimal or slightly lean body condition may lower risk of developing osteoarthritis, reduce the severity of osteoarthritis, and delay onset of clinical signs of osteoarthritis in dogs.
Other studies have shown improved mobility after weight loss among obese dogs with osteoarthritis.16,17 In these studies, improvement was noticed after modest weight loss of at least 6% body weight.
Weight loss may have additional value for dogs when combined with rehabilitation and physical therapy. One clinical trial evaluated 29 adult dogs that were overweight or obese (BCS of 4/5 or 5/5) and had clinical and radiographic signs of osteoarthritis.18 All dogs were fed the same diet; however, those that received intensive physical therapy, including transcutaneous electrical nerve stimulation, obtained greater weight reduction and better mobility than those that received home-based physical therapy.18
Degenerative osteoarthritis involves an inflammatory component, which might be modified by the addition of nutritional components, specifically omega-3 (n-3) fatty acids, to the diet. Eicosanoids derived from n-6 fatty acids, for the most part, have vasoactive and pro-inflammatory effects. Arachidonic acid (an n-6 fatty acid) is incorporated into cell membranes and when metabolized yields prostaglandins, leukotrienes, and thromboxanes of the 2 and 4 series. Many drugs used to treat degenerative osteoarthritis inhibit conversion of arachidonic acid to these eicosanoids. Metabolism of n-3 fatty acids yields eicosanoids of the 3 and 5 series, which are less vasoactive and less pro-inflammatory. Substituting an n-3 fatty acid in the membrane may decrease these responses. In addition to modulating cytokines, n-3 fatty acids reduce expression of cyclooxygenase-2, lipoxygenase-5, aggrecanase, matrix metalloproteinases 3 and 13, interleukin-1α and -1β, and tumor necrosis factor α.19-23 Novel oxygenated products, called resolvins (resolution phase interaction products), and docosatrienes (generated from n-3 fatty acids), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) have been identified as resolving inflammation in exudates and tissues,24-26 including the tissues involved in osteoarthritis.27-32
One study of 18 dogs with experimentally induced and surgically repaired transection of the left cranial cruciate ligament found that consumption of a high n-3 diet was associated with lower serum concentrations of cholesterol, triglycerides, and phospholipids; lower synovial concentration of prostaglandin E2; better ground reaction forces; and fewer radiographic changes of osteoarthritis compared with consumption of a high n-6 diet or a control diet.33,34 Synovial membrane fatty acid composition mirrored the fatty acid composition of the diets consumed. Studies of dogs with osteoarthritis found associations between high n-3 diets and improved ability to rise from a resting position and play,35 improved peak vertical force values and subjective improvement in lameness and weight bearing,36 and the ability to tolerate more rapid reduction of carprofen dosage,37 compared with dogs fed control diets. A study of 48 dogs that underwent tibial plateau-leveling osteotomy for cranial cruciate ligament disease found that those fed a commercial diet with increased n-3 fatty acids had lower synovial inflammatory cytokine concentrations than did dogs fed a maintenance diet, with or without receiving postoperative rehabilitation therapy. Decreased progression of osteoarthritis was noted for dogs fed the increased n-3 diet and for dogs that underwent rehabilitation in this38 and in another39 study.
Supplements given to dogs with osteoarthritis are often underdosed. Giving n-3 fatty acid supplements or feeding diets containing increased n-3 fatty acid levels to dogs with osteoarthritis is beneficial when the appropriate doses of EPA and DHA are delivered. When administering n-3 fatty acids, use the sum of EPA (a 20-carbon n-3 fatty acid) and DHA (a 22-carbon n-3 fatty acid) rather than the total amount of n-3 fatty acids. Recommended dosage is up to 175 mg of the sum of EPA and DHA per kilogram of body weight. A more accurate dosage is based on metabolic body weight: 310 mg of the sum of EPA and DHA per kilogram of body weight raised to the 0.75 power.40 The National Research Council safe upper limit is approximately 200 mg of the sum of EPA and DHA per kilogram of body weight or 370 mg of the sum of EPA and DHA per metabolic body weight.
Initially high dosages of n-3 fatty acids often result in diarrhea. Therefore, we often start with 600 to 900 mg of the sum of EPA and DHA per kilogram of body weight for a few weeks and then increase slowly to 120 to 170 mg of the sum of EPA and DHA per kilogram of body weight.
Although flaxseed is often recommended as a source of n-3 fatty acids (because it contains α-linolenic acid), it is not a good source of n-3 fatty acids in dogs because dogs can convert less than 10% of α-linolenic acid to EPA.40
Chondromodulating agents are purported to slow or alter progression of osteoarthritis. They are used for dogs with osteoarthritis when cartilage damage is present but before fibrocartilage has developed. Beneficial effects of chondromodulating agents may include a positive effect on synthesis of cartilage matrix and hyaluronan as well as an inhibitory effect on catabolic enzymes in osteoarthritic joints.41 These agents may also be beneficial when used prophylactically for dogs prone to osteoarthritis. Chondromodulating compounds fall into 2 categories: Food and Drug Administration-approved agents that can have label claims of clinical effects (e.g., polysulfated glycosaminoglycan) and products considered to be nutritional supplements, which legally cannot claim any medical benefits (e.g., glucosamine and chondroitin sulfate). Although many of these products are administered as supplements or alternative treatments, some (e.g., glucosamine and green-lipped mussel) are incorporated into pet foods.
Glucosamine and Chondroitin Sulfate
Glycosaminoglycans are a major component of joint cartilage and glucosamine is a glycosaminoglycan precursor; therefore, supplemental glucosamine may help rebuild cartilage.42-48 However, data concerning the clinical effects of glucosamine-chondroitin sulfate on osteoarthritis are conflicting.49-59 In a clinical trial comparing glucosamine hydrochloride and chondroitin sulfate with carprofen in 35 dogs with osteoarthritis, the carprofen-treated dogs showed improvement in 5 subjective measures while dogs treated with glucosamine-chondroitin sulfate showed improvement in 3 of 5 measures but only at the final assessment.60 A 60-day trial of 71 dogs with osteoarthritis assessed subjective and objective measures comparing carprofen, meloxicam, glucosamine-chondroitin, and placebo.61 Results indicated that objectively measured variables improved significantly for dogs that received carprofen and meloxicam but not for those that received glucosamine-chondroitin or placebo. Subjective findings of veterinarians agreed with findings of objective evaluation, but subjective assessment by clients identified improvement with meloxicam only.61 On the basis of these results, reviews have concluded that the clinical evidence of benefit of glucosamine and chondroitin sulfate in dogs with osteoarthritis is weak.49-51
Many dog foods formulated and marketed for adult dogs, geriatric dogs, and growing large breed dogs contain glucosamine and chondroitin sulfate, but the exact amounts are often not readily available. In terms of evaluating glucosamine and chondroitin sulfate inclusion in a manufactured dog food, questions have arisen over whether these agents are bioavailable and in enough quantity to provide benefit. These compounds are not recognized as essential by AAFCO and thus are not included in dog nutrient profiles. They are considered “generally regarded as safe” ingredients.
New Zealand green-lipped mussel (Perna canaliculus) is a rich source of glycosaminoglycans, although its proposed benefit is thought to be from its anti-inflammatory effects.62 Research findings have been discrepant, possibly because of differences in product stabilization. A stabilized lipid extract more effectively inhibits inflammation than a nonstabilized extract.63 Early studies, which used nonstabilized products, found no beneficial effect of green-lipped mussel on arthritis. By 1986, dried mussel extracts stabilized with a preservative became available, and addition of green-lipped mussel to the diet was associated with significant improvement in subjective arthritis scores,64 reduced joint swelling and joint pain,65 improved mobility (but not as much as dogs that received carprofen),66 and improved clinical signs (but not musculoskeletal scores)67 compared with dogs that received placebo. However, although systematic reviews of agents used to treat osteoarthritis in dogs found the data regarding the benefits of green-lipped mussel extract in dogs to be promising, uncertainties existed relating to the scientific quality of the data and no definitive relationship has been proven between clinical improvements and the therapy.50,51
In summary, 4 nutritional approaches may help prevent or treat osteoarthritis in dogs.
- Diets aimed at preventing developmental orthopedic disease may help prevent later development into osteoarthritis.
- Weight loss for overweight and obese dogs not only decreases the mechanical wear and tear on joints but decreases systemic inflammation that accompanies osteoarthritis.
- Omega-3 fatty acids (specifically EPA and DHA) beneficially modulate the inflammatory response.
- Chondromodulating agents maintain cartilage integrity and facilitate repair of damaged cartilage.
1. Hazewinkel HAW. Skeletal disease In: Wills JM, Simpson KW, eds. The Waltham Book of Clinical Nutrition. Tarrytown, NY: Pergamon, 1994;395-423.
2. Hazewinkel HAW, Goedegebriure S, Poubs P, et al. Influences of chronic calcium excess on the skeletal development of growing Great Danes. JAAHA 1985;21:377-391.
3. Lauten SD. Nutritional risks to large-breed dogs: from weaning to the geriatric years. Vet Clin North Am Small Anim Pract 2006;36:1345-1359, viii.
4. Smith GK, Paster ER, Powers MY, et al. Lifelong diet restriction and radiographic evidence of osteoarthritis of the hip joint in dogs. JAVMA 2006;229:690-693.
5. Nap RC, Hazewinkel HA, Voorhout G, et al. Growth and skeletal development in Great Dane pups fed different levels of protein intake. J Nutr 1991;121:S107-113.
6. Alexander JE, Wood LLH. Growth studies of Labrador Retrievers fed a caloric dense diet: time-restricted versus free choice feeding. Canine Practice 1987;14:41-47.
7. Kealy RD, Lawler DF, Ballam JM, et al. Effects of diet restriction on life span and age-related changes in dogs. JAVMA 2002;220:1315-1320.
8. Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Am J Clin Nutr 2006;83:461S-465S.
9. Pang SS, Le YY. Role of resistin in inflammation and inflammation-related diseases. Cell Mol Immunol 2006;3:29-34.
10. Otero M, Lago R, Gomez R, et al. Leptin: a metabolic hormone that functions like a proinflammatory adipokine. Drug News Perspect 2006;19:21-26.
11. Zoran DL. Obesity in dogs and cats: a metabolic and endocrine disorder. Vet Clin North Am Small Anim Pract 2010;40:221-239.
12. Marshall W, Bockstahler B, Hulse D, et al. A review of osteoarthritis and obesity: current understanding of the relationship and benefit of obesity treatment and prevention in the dog. Vet Comp Orthop Traumatol 2009;22:339-345.
13. Edney ATB, Smith PM. Study of obesity in dogs visiting veterinary practices in the United Kingdom. Vet Rec 1986;118:391-396.
14. Janssen I, Mark AE. Separate and combined influence of body mass index and waist circumference on arthritis and knee osteoarthritis. Int J Obes (Lond) 2006:1223-1228.
15. Kealy RD, Lawler DF, Ballam JM, et al. Evaluation of the effect of limited food consumption on radiographic evidence of osteoarthritis in dogs. JAVMA 2000;217:1678-1680.
16. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. JAVMA 2000;216:1089-1091.
17. Burkholder WJ, Taylor L, Hulse DA. Weight loss to optimal body condition increases ground reactive force in dogs with osteoarthritis. Compen Contin Educ Pract Vet 2000;23:74.
18. Mlacnik E, Bockstahler BA, Muller M, et al. Effects of caloric restriction and a moderate or intense physiotherapy program for treatment of lameness in overweight dogs with osteoarthritis. JAVMA 2006;229:1756-1760.
19. Hurst S, Zainal Z, Caterson B, et al. Dietary fatty acids and arthritis. Prostaglandins Leukot Essent Fatty Acids 2010;82:315-318.
20. Curtis CL, Hughes CE, Flannery CR, et al. n-3 fatty acids specifically modulate catabolic factors involved in articular cartilage degradation. J Biol Chem 2000;275:721-724.
21. Curtis CL, Rees SG, Cramp J, et al. Effects of n-3 fatty acids on cartilage metabolism. Proc Nutr Soc 2002;61:381-389.
22. Curtis CL, Rees SG, Little CB, et al. Pathologic indicators of degradation and inflammation in human osteoarthritic cartilage are abrogated by exposure to n-3 fatty acids. Arthritis Rheum 2002;46:1544-1553.
23. Zainal Z, Longman AJ, Hurst S, et al. Relative efficacies of omega-3 polyunsaturated fatty acids in reducing expression of key proteins in a model system for studying osteoarthritis. Osteoarthritis Cartilage 2009;17:896-905.
24. Serhan CN, Arita M, Hong S, et al. Resolvins, docosatrienes, and neuroprotectins, novel omega-3-derived mediators, and their endogenous aspirin-triggered epimers. Lipids 2004;39:1125-1132.
25. Hong S, Gronert K, Devchand PR, et al. Novel docosatrienes and 17S-resolvins generated from docosahexaenoic acid in murine brain, human blood, and glial cells. Autacoids in anti-inflammation. J Biol Chem 2003;278:14677-14687.
26. Meduri GU, Carratu P, Freire AX. Evidence of biological efficacy for prolonged glucocorticoid treatment in patients with unresolving ARDS. Eur Respir J Suppl 2003;42:57s-64s.
27. Xu ZZ, Ji RR. Resolvins are potent analgesics for arthritic pain. Br J Pharmacol 2011.
28. Lima-Garcia J, Dutra R, da Silva K, et al. The precursor of resolvin D series and aspirin-triggered resolvin D1 display anti-hyperalgesic properties in adjuvant-induced arthritis in rats. Br J Pharmacol 2011.
29. Xu ZZ, Zhang L, Liu T, et al. Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med 2010;16:592-597.
30. James M, Proudman S, Cleland L. Fish oil and rheumatoid arthritis: past, present and future. Proc Nutr Soc 2010;69:316-323.
31. Calder PC. Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’ PUFA, inflammatory processes and rheumatoid arthritis. Proc Nutr Soc 2008;67:409-418.
32. Calder PC. n-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr 2006;83:1505S-1519S.
33. Bartges JW, Budsberg SC, Pazak HE, et al. Effects of different n6:n3 fatty acid ratio diets on canine stifle osteoarthritis. Orthopedic Research Society 47th Annual Meeting; 2001.
34. Budsberg SC, Bartges JW, Pazak HE, et al. Effects of different N6:N3 fatty acid diets on canine stifle osteoarthritis. Veterinary Orthopedic Society 28th Annual Meeting; 2001.
35. Roush JK, Dodd CE, Fritsch DA, et al. Multicenter veterinary practice assessment of the effects of omega-3 fatty acids on osteoarthritis in dogs. JAVMA 2010;236:59-66.
36. Roush JK, Cross AR, Renberg WC, et al. Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis. JAVMA 2010;236:67-73.
37. Fritsch DA, Allen TA, Dodd CE, et al. A multicenter study of the effect of dietary supplementation with fish oil omega-3 fatty acids on carprofen dosage in dogs with osteoarthritis. JAVMA 2010;236:535-539.
38. Verpaalen VD, Baltzer WI, Smith-Ostrin S, et al. Assessment of the effects of diet and physical rehabilitation on radiographic findings and markers of synovial inflammation in dogs following tibial plateau leveling osteotomy. JAVMA 2018;252:701-709.
39. Baltzer WI, Smith-Ostrin S, Warnock JJ, et al. Evaluation of the clinical effects of diet and physical rehabilitation in dogs following tibial plateau leveling osteotomy. JAVMA 2018;252:686-700.
40. Bauer JE. Therapeutic use of fish oils in companion animals. JAVMA 2011;239:1441-1451.
41. McNamara PS, Johnston SA, Todhunter RJ. Slow-acting, disease-modifying osteoarthritis agents. Vet Clin North Am Small Anim Pract 1997;27:863-881.
42. Chan PS, Caron JP, Orth MW. Effects of glucosamine and chondroitin sulfate on bovine cartilage explants under long-term culture conditions. Am J Vet Res 2007;68:709-715.
43. Lippiello L, Han MS, Henderson T. Protective effect of the chondroprotective agent Cosequin DS on bovine articular cartilage exposed in vitro to nonsteroidal antiinflammatory agents. Vet Ther 2002;3:128-135.
44. Gouze JN, Bordji K, Gulberti S, et al. Interleukin-1beta down-regulates the expression of glucuronosyltransferase I, a key enzyme priming glycosaminoglycan biosynthesis: influence of glucosamine on interleukin-1beta-mediated effects in rat chondrocytes. Arthritis Rheum 2001;44:351-360.
45. Dodge GR, Jimenez SA. Glucosamine sulfate modulates the levels of aggrecan and matrix metalloproteinase-3 synthesized by cultured human osteoarthritis articular chondrocytes. Osteoarthritis Cartilage 2003;11:424-432.
46. Ali AA, Lewis SM, Badgley HL, et al. Oral glucosamine increases expression of transforming growth factor beta1 (TGFbeta1) and connective tissue growth factor (CTGF) mRNA in rat cartilage and kidney: Implications for human efficacy and toxicity. Arch Biochem Biophys; 2011.
47. Phitak T, Pothacharoen P, Kongtawelert P. Comparison of glucose derivatives effects on cartilage degradation. BMC Musculoskelet Disord 2010;11:162.
48. Silbert JE. Dietary glucosamine under question. Glycobiology 2009;19:564-567.
49. McKenzie BA. What is the evidence? There is only very weak clinical trial evidence to support the use of glucosamine and chondroitin supplements for osteoarthritis in dogs. JAVMA 2010;237:1382-1383.
50. Aragon CL, Hofmeister EH, Budsberg SC. Systematic review of clinical trials of treatments for osteoarthritis in dogs. JAVMA 2007;230:514-521.
51. Sanderson RO, Beata C, Flipo RM, et al. Systematic review of the management of canine osteoarthritis. Vet Rec 2009;164:418-424.
52. Sofat N, Beith I, Kumar PG, et al. Recent clinical evidence for the treatment of osteoarthritis: what we have learned. Rev Recent Clin Trials; 2011;6(2):114-126.
53. De Silva V, El-Metwally A, Ernst E, et al. Evidence for the efficacy of complementary and alternative medicines in the management of osteoarthritis: a systematic review. Rheumatology (Oxford) 2011;50:911-920.
54. Wandel S, Juni P, Tendal B, et al. Effects of glucosamine, chondroitin, or placebo in patients with osteoarthritis of hip or knee: network meta-analysis. BMJ 2010;341:c4675.
55. Sawitzke AD, Shi H, Finco MF, et al. Clinical efficacy and safety of glucosamine, chondroitin sulphate, their combination, celecoxib or placebo taken to treat osteoarthritis of the knee: 2-year results from GAIT. Ann Rheum Dis 2010;69:1459-1464.
56. Pirotta M. Arthritis disease – the use of complementary therapies. Aust Fam Physician 2010;39:638-640.
57. Petersen SG, Saxne T, Heinegard D, et al. Glucosamine but not ibuprofen alters cartilage turnover in osteoarthritis patients in response to physical training. Osteoarthritis Cartilage 2010;18:34-40.
58. Lee YH, Woo JH, Choi SJ, et al. Effect of glucosamine or chondroitin sulfate on the osteoarthritis progression: a meta-analysis. Rheumatol Int 2010;30:357-363.
59. Giacovelli G, Rovati LC. Glucosamine and osteoarthritis. Conclusions not supported by methods and results. BMJ 2010;341:c6338.
60. McCarthy G, O’Donovan J, Jones B, et al. Randomised double-blind, positive-controlled trial to assess the efficacy of glucosamine/chondroitin sulfate for the treatment of dogs with osteoarthritis. Vet J 2007;174:54-61.
61. Moreau M, Dupuis J, Bonneau NH, et al. Clinical evaluation of a nutraceutical, carprofen and meloxicam for the treatment of dogs with osteoarthritis. Vet Rec 2003;152:323-329.
62. Gibson RG, Gibson SL, Conway V, et al. Perna canaliculus in the treatment of arthritis. Practitioner 1980;224:955-960.
63. Butters DE, Whitehouse MW. Treating inflammation: some (needless) difficulties for gaining acceptance of effective natural products and traditional medicines. Inflammopharmacology 2003;11:97-110.
64. Servet E, Biourge V, Marniquet P. Dietary intervention can improve clinical signs in osteoarthritic dogs. J Nutr 2006;136:1995S-1997S.
65. Bui LM, Bierer TL. Influence of green lipped mussels (Perna canaliculus) in alleviating signs of arthritis in dogs. Vet Ther 2003;4:397-407.
66. Hielm-Bjorkman A, Tulamo RM, Salonen H, et al. Evaluating complementary therapies for canine osteoarthritis part I: green-lipped mussel (Perna canaliculus). Evid Based Complement Alternat Med 2009;6:365-373.
67. Pollard B, Guilford WG, Ankenbauer-Perkins KL, et al. Clinical efficacy and tolerance of an extract of green-lipped mussel (Perna canaliculus) in dogs presumptively diagnosed with degenerative joint disease.
N Z Vet J 2006;54:114-118.