The role of synovial macrophages and macrophage-produced mediators in driving inflammatory and destructive responses in osteoarthritis.

摘要

Osteoarthritis (OA), one of the most common diseases among mammals, can be considered to be part of the aging process. It is characterized pathologically by focal areas of damage on articular cartilage centered on load-bearing areas in association with the formation of new bone at the joint margins, changes in subchondral bone, and synovitis. Mechanical factors, such as obesity or a history of joint trauma, are recognized risk factors for OA, as are certain endogenous factors, such as type II collagen mutations and acetabular dysplasia. OA is the world's leading cause of chronic disability not only for the elderly but also for individuals of working age. Given the huge economic and personal burdens of OA and the fact that this disease is the major cause of the increasing demand for joint replacements, there is an urgent need for disease-modifying treatments to stop or slow the development and progression of OA. For this to be possible, however, additional knowledge is needed about the pathogenesis of disease initiation and progression in OA.