Abstract
Osteoarthritis (OA) is the most common joint disease that causes pain and disability in the adult population. OA is primarily caused by trauma induced by an external force or by age-related cartilage damage. Chondrocyte hypertrophy or chondrocyte senescence is thought to play a role in the initiation and progression of OA. Although chondrocyte hypertrophy and cell death are both crucial steps during the natural process of endochondral bone formation, the abnormal activation of these two processes after injury or during aging seems to accelerate the progression of OA. However, the exact mechanisms of OA progression and these two processes remain poorly understood. Chondrocyte senescence and hypertrophy during OA share various markers and processes. In this study, we reviewed the changes that occur during chondrocyte hypertrophy or senescence in OA and the attempts that were made to regulate them. Regulation of hypertrophic or senescent chondrocytes might be a potential therapeutic target to slow down or stop OA progression; thus, a better understanding of the processes is required for management.
Highlights
The simple yet complicated architecture of the articular cartilage compromises its natural capacity for self-repair [1]
This review focuses on the hypertrophic changes and cellular senescence in chondrocytes under OA conditions
Some studies report that there is no significant difference between TGFβ subtypes in suppressing hypertrophy during chondrogenesis; several other studies show that TGFβ1 is superior in suppressing hypertrophy [95,96,97]
Summary
The simple yet complicated architecture of the articular cartilage compromises its natural capacity for self-repair [1]. The cartilage, with an avascular and alymphatic nature, is composed of dense layers of extracellular matrix (ECM) containing embedded distributed chondrocytes [2]. Cartilage lines the surface of the bone and provides a low-friction surface by absorbing external pressure or stimuli, which enables painless joint movement [3]. OA accompanies progressive degradation of the articular cartilage, which leads to a loss of joint mobility and function and eventually to a low quality of life in patients due to both pain and restricted lifestyles. Cellular senescence can occur alongside hypertrophy due to similar stimuli. This review focuses on the hypertrophic changes and cellular senescence in chondrocytes under OA conditions
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