Mechanisms of inflammatory cell activation in periodontitis-induced bone destruction and advances in targeted interventions

Abstract

Periodontitis is a leading cause of tooth loss in adults, characterized primarily by alveolar bone destruction driven by dysregulated host immune-inflammatory responses. Central to this pathological process is the aberrant activation of inflammatory cells within the periodontal microenvironment. This review comprehensively summarizes the activation phenotypes, functions, and interaction networks of key inflammatory cells including macrophages, neutrophils, T cells, and B cells in periodontitis. It elucidates the molecular and cellular mechanisms by which these activated cells contribute to bone destruction through the release of inflammatory mediators and regulation of osteoclastogenesis and osteoclast function. Furthermore, the review highlights recent advances in targeted therapeutic strategies aimed at modulating inflammatory cell activation, encompassing small molecule inhibitors, biologics, and cell-based therapies. By integrating current knowledge on inflammatory cell dynamics and targeted interventions. This review aims to identify key therapeutic targets within inflammatory cell networks to guide the development of precision therapies for periodontitis.