Abstract and Introduction

Abstract

Osteoarthritis is often a progressive and disabling disease, which occurs in the setting of a variety of risk factors – such as advancing age, obesity, and trauma – that conspire to incite a cascade of pathophysiologic events within joint tissues. An important emerging theme in osteoarthritis is a broadening of focus from a disease of cartilage to one of the 'whole joint'. The synovium, bone, and cartilage are each involved in pathologic processes that lead to progressive joint degeneration. Additional themes that have emerged over the past decade are novel mechanisms of cartilage degradation and repair, the relationship between biomechanics and biochemical pathways, the importance of inflammation, and the role played by genetics. In this review we summarize current scientific understanding of osteoarthritis and examine the pathobiologic mechanisms that contribute to progressive disease.

Introduction

Osteoarthritis (OA) is characterized by a progressive loss of articular cartilage accompanied by new bone formation and, often, synovial proliferation that may culminate in pain, loss of joint function, and disability. A variety of etiologic risk factors and pathophysiologic processes contribute to the progressive nature of the disease and serve as targets of behavioral and pharmacologic interventions. Risk factors such as age, sex, trauma, overuse, genetics, and obesity can each make contributions to the process of injury in different compartments of the joint. Such risk factors can serve as initiators that promote abnormal biochemical processes involving the cartilage, bone, and synovium, which over a period of years result in the characteristic features of OA: degradation of articular cartilage, osteophyte formation, subchondral sclerosis, meniscal degeneration, bone marrow lesions, and synovial proliferation.

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