Abstract
The increased prevalence of osteoarthritis in Western countries is due, in part, to an aging and gradually more obese population. Obesity is a major risk factor for knee and to a lesser extent, hip osteoarthritis. The rates of disease are rising faster than can be explained by aging and obesity. This increase may be ascribed to sports-related injury or an unwillingness of patients to accept even modest joint pain that in the past probably did not trigger medical care [7]. Rates of knee replacement are rising rapidly. Effective nonsurgical treatments are desperately needed, but no treatments for osteoarthritis have been consistently shown to slow the course of disease, and there are few symptom modifying treatments considered effective — most, like exercise treatment, come with compliance issues. Vitamin D has promise as treatment for osteoarthritis, especially among those who are vitamin D deficient. Vitamin D receptors are present on chondrocytes, the cells within cartilage. Through these receptors, vitamin D may regulate matrix metalloproteinases [8]. Vitamin D deficiency inhibits bone remodeling, which may affect the bone changes that evolve with osteoarthritis. Also, deficiency may augment pain sensitivity [4] and contribute to muscle weakness. With this background, epidemiologic cohort studies [3, 5] examined the relationship of blood levels of 25-OH vitamin D, the major storage form of the vitamin, to osteoarthritis. While the initial studies suggested that vitamin D deficiency accelerated osteoarthritis disease progression [5], a later study [3] showed mixed or even negative results.
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