(i) Molecular mechanisms underlying auto-destruction of cartilage in osteoarthritis

• Published in: Current orthopaedics Vol. 10; no. 4; pp. 212 - 219
• Main Authors: Shinmei, M, Nemoto, O
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 1996
• ISSN: 0268-0890; 1532-2068
• DOI: 10.1016/S0268-0890(96)90048-1

Cartilage changes in OA consist of a slowly progressive loss of PG, increased water content, and no alteration in collagen content but a probably bigger significant change in the arrangement and the size of collagen fibers. In the normal joint, there exists a fine balance between the ongoing processes of degradation and repair. In this article, the pathogenesis of OA is viewed as a disruption of this ‘steady-state’ balance, particularly focusing on MMP-3 and TIMP-1 balance. This imbalance could be created by a variety of cytokines and growth factors which may play an important role in mediating cartilage destruction in OA. However, some of these factors are capable of mediating both stimulatory and inhibitory effects and in vivo function of these cytokines has not been clearly elucidated. Furthermore, specific inhibitors of IL-1 and TNFa exist, which, if also released from chondrocytes, may antagonize the pro-inflammatory effects of these cytokines. Thus, various cytokines produced by the chondrocyte itself are interrelated and form a complex cytokine network. We believe that expanded research in this field may result in a significantly increased understanding of the pathophysiologic processes occurring in OA. These mechanisms are probably multifaceted, but is hoped that careful analysis to interlink and relate the various components of these speculations will lead to the development of more specific and effective therapeutic agents.