Conclusions: Bone cellular senescence is characterized by increased SA-β-gal activity, upregulation of cell-cycle inhibitors (p16INK4a, p21CIP1/WAF1, p53-related pathways), persistent DNA damage signaling, and a proinflammatory secretory phenotype that promotes osteoclast activation and suppresses osteogenesis. Tissue-level changes include reduced osteoblast function, osteocyte loss, and a shift toward resorptive remodeling reflected by an elevated RANKL/OPG ratio. Emerging signals (e.g., selected long non-coding RNAs and innate immune sensors such as TLR9) may complement classic markers in future panels. Integrating senescence-related biomarkers into clinical assessment may support individualized protocols for patients with biologically compromised bone and inform targeted preventive strategies.
Ostrianko et al. (Sun,) studied this question.