rtrophic form of arthritis, but is now known to include a process where the normal balance between cartilage synthesis and degradation is disrupted, usually with an inflammatory component (6).
Articular cartilage distributes loads over the bone surface to provide a low-friction surface for bones to move over. OA is a disease process that is characterized by the uncoupling of the normal balance of degradation and repair in the articular cartilage and subchondral bone which leads to abrasion of the articular cartilage with a formation of new bone at and around the joint surfaces. This process results in functional deterioration of the joint. Repair responses include a bony outgrowth at the joint margins, called osteophytes, which are derived from bone or calcified cartilage (6).
OA is classified into three major subsets, generalized OA (GOA; bony enlargement of the distal and proximal interphalangeal joints of the hand), large joint OA, and erosive OA (hand interphalangeal involvement). Large joint OA of hips and knees can occur in the context of GOA or in isolation. When hips are affected in the context of GOA, joint involvement usually occurs bilaterally with a central loss of joint space. Some cases of hip OA can result in clear-cut radiographic and symptomatic improvement; these usually have the central form of the disease. Most cases of hip OA are superior pole OA; this form is more common in men and is unassociated with GOA. It is mainly unilateral with cartilage loss in the superior pole of the joint with a tendency for femoral head migration superolaterally or medially. Some suggest that 40 percent to 90 percent of adult hip OA is from subtle developmental abnormalities of the hip to include the following: acetabular dysplasia, congenital hip dislocation, Legg-Calve-Perthes disease, and slipped capital femoral epiphysis (6).
Confounding factors in human epidemiological studies of OA include individual variat...