Fig. 1
Schematic diagram of the cross-talk between cellular senescence and OA. Characteristic manifestations of joint degeneration are as follows: senescent subchondral bone with decreased bone density, reduced bone mass and thinning, senescent infrapatellar fat pad with inflammatory changes, senescent chondrocytes with decreased function accompanied by increased matrix degradation, senescent synoviocytes with diminished function and chronic synovitis, and senescent stem cells with diminished function and genetic stability. Alterations in senescent cells include telomere attrition, DNA instability, vacuolization of the cytoplasm, endoplasmic reticulum stress, mitochondrial dysfunction and alterations in the cell membrane. The characteristic pathology of OA includes reconstruction of the subchondral bone, synovial hyperplasia, cartilage damage, and inflammatory changes in the infrapatellar fat pad. The inflammatory mediators form a bridge of communication between cellular senescence and OA, and senescent cell-associated secretory phenotypes (SASP) play a critical role in this process
