Osteoarthritis: toward a comprehensive understanding of pathological mechanism

Abstract

Osteoarthritis (OA) is the most common degenerative joint disease and a major cause of pain and disability in adult individuals. The etiology of OA includes joint injury, obesity, aging, and heredity. However, the detailed molecular mechanisms of OA initiation and progression remain poorly understood and, currently, there are no interventions available to restore degraded cartilage or decelerate disease progression. The diathrodial joint is a complicated organ and its function is to bear weight, perform physical activity and exhibit a joint-specific range of motion during movement. During OA development, the entire joint organ is affected, including articular cartilage, subchondral bone, synovial tissue and meniscus. A full understanding of the pathological mechanism of OA development relies on the discovery of the interplaying mechanisms among different OA symptoms, including articular cartilage degradation, osteophyte formation, subchondral sclerosis and synovial hyperplasia, and the signaling pathway(s) controlling these pathological processes.

Osteoarthritis: Towards better treatment through understanding disease mechanisms

A better understanding of the molecular mechanisms underpinning osteoarthritis should enable the development of new treatment strategies. In a review article, Di Chen from the Rush University Medical Center in Chicago, USA, and colleagues discuss the causes of this common degenerative joint disease, which include injury, obesity, aging, and genetics, and the various techniques used to elucidate the biochemical changes implicated in osteoarthritis-associated pain and disability. These include studying the disease in a range of mouse models, and investigating human cells and tissue in the laboratory. Even though significant progress has been made in recent years, many questions remain about the pathological processes involved in the initiation and progression of osteoarthritis. Tackling these unknowns could lead to interventions that restore degraded cartilage or slow down disease development.

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