Immunosenescence and inflammaging: Conspiracies against alveolar bone turnover

ObjectiveInflammaging and immunosenescence are characteristics of senescent immune system alterations. This review provides insights into inflammaging and immunosenescence in periodontitis and focuses on the innerlink of inflammaging and immunosenescence in alveolar bone turnover from a perspective of cell-cell interaction. MethodsThis review is conducted by a narrative approach to discuss the effect of inflammaging and immunosenescence in aging-related alveolar bone loss. A comprehensive literature research in PubMed and Google was applied to identify reports in English. ResultsInflammaging is concerned with abnormal M1 polarization and increasing circulating inflammatory cytokines, while immunosenescence involves reduced infection and vaccine responses, depressed antimicrobial function, and infiltration of aged B cells and memory T cells. TLR-mediated inflammaging and altered adaptive immunity significantly affect alveolar bone turnover and aggravate aging-related alveolar bone loss. Besides, energy consumption also plays a vital role in aged immune and skeletal system of periodontitis. ConclusionsSenescent immune system exerts a significant function in aging-related alveolar bone loss. Inflammaging and immunosenescence interact functionally and mechanistically, which affects alveolar bone turnover. Therefore, further clinical treatment strategies targeting alveolar bone loss could be based on the specific molecular mechanism connecting inflammaging, immunosenescence, and alveolar bone turnover.

Automated summary

This review discusses the role of inflammaging and immunosenescence in periodontitis, with a focus on the connection between inflammaging and immunosenescence in alveolar bone turnover. The results show that the senescent immune system plays a significant role in aging-related alveolar bone loss. Inflammaging and immunosenescence interact functionally and mechanistically, affecting alveolar bone turnover. Therefore, clinical treatment strategies for alveolar bone loss could be developed based on the specific molecular mechanism connecting inflammaging, immunosenescence, and alveolar bone turnover.