Biomarkers of cellular senescence in bone tissue

Aim: To summarize the biomarkers of cellular senescence in bone tissue and discuss their potential relevance for clinical risk stratification and outcomes related to bone remodeling and implant osseointegration.

Materials and Methods: A narrative literature review was performed using PubMed and Google Scholar searches focused on osteoblast, osteocyte and mesenchymal stem cell senescence, DNA damage response, senescence-associated secretory phenotype, oxidative stress, and epigenetic regulation in bone. Eligible peer-reviewed publications were screened for evidence on established and emerging senescence biomarkers, detection methods (histochemical, immunohistochemical, molecular, and secretory profiling), and mechanistic links to impaired osteogenesis and enhanced osteoclastogenesis. Findings were synthesized into practical biomarker categories (molecular, cellular/tissue, and functional) with emphasis on translational implications for dental implant planning and peri-implant bone stability.

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.