Osteoarthritis: toward a comprehensive understanding of pathological mechanism.
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.
Department of Biochemistry, Rush University Medical Center , Chicago, IL, USA.
Di
D
Chen
Department of Orthopaedic Surgery, Washington University , St Louis, MO, USA.
Jie
J
Shen
Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA; Department of Orthopaedics & Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Weiwei
W
Zhao
Department of Pharmacy, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine , Shanghai, China.
Tingyu
T
Wang
School of Biomedical Engineering, Science, and Health Systems, Drexel University , Philadelphia, PA, USA.
Lin
L
Han
Department of Biochemistry, Rush University Medical Center , Chicago, IL, USA.
John L
JL
Hamilton
Department of Biochemistry, Rush University Medical Center , Chicago, IL, USA.
Hee-Jeong
HJ
Im