More evidence that diet has a direct link with osteoarthritis.
One important contributing factor to the pathogenesis of OA is diet: nutritional deficiency and imbalance, obesity and diabetes (resulting in hypoglycaemia or hyperglycaemia) can result in metabolic and systemic disturbances that in turn increase susceptibility to OA directly due to effects on cartilage. Recent studies suggest that cartilage damage in OA occurs coincident with metabolic dysfunction, nutrient imbalance and diabetes mellitus (Rosenbloom and Silverstein, 1996; Denko and Malemud, 1999; Okma- Keulen and Hopman-Rock, 2001). Furthermore, high carbohydrate diets and generalized vitamin deficiency cause metabolic damage to cartilage (Willhelmi, 1993b). Vitamins E, B2, and C have been shown to exert an inhibitory effect on OA in animals. Chondrotoxic damage may result from food contaminants and fluoroquinolones (Stahlmann et al., 1995, 2000;Shakibaei et al., 1996; Forster et al., 1998). Equally, mineral deficiency (i.e. calcium, magnesium, zinc, selenium and boron) can provoke skeletal damage in humans and animals.
Another joint disorder, which has a dietary component, is osteochondritis dissecans (OCD). In this disorder articular cartilage fragments separate from the articular surface and break off into the joint space (Williams et al., 1998). OCD in food-producing animals is caused by over-nutrition from excess protein and carbohydrate consumption and over supplementation (Slater et al., 1992). The overwhelming majority of musculoskeletal problems in companion animals and rapidly growing food-producing animal species are linked with a possible nutritional-related aetiology.