Antioxidants in osteoarthritis
Arthritis is associated with increased oxidative stress and chondrocyte-produced reactive oxygen species and decreased antioxidant
capacity.52-56 The severity of arthritic lesions is increased in the face of decreased antioxidant capacity.56
In vivo studies have shown that exposure of chondrocytes to reactive oxygen species inhibits proteoglycan and DNA synthesis
and depletes intracellular ATP.57,58 Reactive oxygen species contribute to cartilage degradation directly as well as by up-regulating the genetic expression of
MMPs and decreasing production (or activity) of tissue inhibitors of metalloproteinases.57,59 In addition, oxidative stress induced chondrocyte senescence in vitro, with reduced glucosaminoglycan production and replicative
lifespan—an effect that was reversible with antioxidant supplementation.56,60 Physiologic concentrations of vitamin E inhibited lipid peroxidation in chondrocytes and minimized oxidation-induced cartilage
degradation in vitro.59 In a different model, vitamin C was effective at reducing premature chondrocyte senescence induced by reactive oxygen species.59
While limited in number, the published studies assessing in vivo benefits of antioxidants in osteoarthritis support the in
vitro findings. A 10-year prospective cohort study showed that intake of supplemental vitamin E (P = 0.06), vitamin C (P = 0.08), and zinc (P = 0.03) independently reduced the risk for developing rheumatoid arthritis in elderly women.61 A two-year clinical trial in people with existing knee osteoarthritis evaluated the benefit of vitamin E supplementation
on cartilage degradation.62 No statistically significant differences were observed in cartilage loss, most likely due to the small sample size. However,
researchers detected directional differences with cartilage loss reduced in the vitamin E group compared with the placebo
group. A one-year study in mice genetically predisposed to developing osteoarthritis also showed a benefit from dietary antioxidants.63 Glutathione peroxidase activity was significantly increased in both the serum and synovium of mice fed a complete diet supplemented
with pyridoxine, riboflavin, selenium, and vitamins E, C, and A, confirming an antioxidant effect. The incidence of osteoarthritis
in the antioxidant-supplemented mice was decreased by one-third to one-half.63 These various studies together strongly suggest a benefit of dietary antioxidants for patients with osteoarthritis.
Other nutrients in osteoarthritis
In addition to nutrient modifications that may help in the dietary management of dogs with osteoarthritis directly, dogs need
appropriately balanced nutrition to support normal maintenance of joints and other tissues. Many people with arthritis appear
to consume nutritionally imbalanced diets. Deficiencies in antioxidant nutrients, B-vitamins, zinc, calcium, magnesium, and
selenium are frequently reported.64,65 While it's not known how many of these deficiencies contribute to osteoarthritis, these nutrients play a role in the normal
maintenance of cartilage and other tissues. Therefore, it's important that dogs with osteoarthritis receive diets that provide
complete and balanced nutrition.
Arthritis is an inflammatory condition that affects up to 20% of adult dogs. Feeding to achieve and maintain ideal body condition
can minimize the clinical signs of osteoarthritis. In addition, a balanced diet formulated to contain a high amount of long-chain
n-3 polyunsaturated fatty acids, a source of glucosamine, and abundant antioxidants may serve as a helpful adjunct to veterinary
1. Roush, J.K. et al.: Understanding the pathophysiology of osteoarthritis. Vet Med 97 (2):108-112; 2002.
2. Johnston, S.A.: Osteoarthritis. Joint anatomy, physiology and pathobiology. Vet. Clin. North Am. 27 (4):699-723; 1997.
3. McLaughlin, R.M. et al.: Medical therapy for patients with osteoarthritis. Vet Med 97 (2):135-144; 2002.
4. Anderson, R.E. et al.: Relationship between body weight gain and significant knee, hip, and back pain in older Americans. Obes. Res. 11 (10):1159-1162; 2003.