Osteoarthritis: toward a comprehensive understanding of pathological mechanism

Di Chen(Rush University Medical Center), Jie Shen(Washington University in St. Louis), Weiwei Zhao(Rush University Medical Center), Tingyu Wang(Shanghai Jiao Tong University), Lin Han(Drexel University), John L. Hamilton(Rush University Medical Center), Hee‐Jeong Im(Rush University Medical Center)
Bone Research
January 17, 2017
Cited by 1,206Open Access
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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.


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