Orthodontic treatment relies on the application of mechanical forces to achieve tooth movement, but these forces interact with periodontal tissues in complex ways, often exacerbating or being influenced by inflammatory processes. This conceptual paper proposes an integrative mechanistic framework that synthesizes inflammatory signaling, mechanotransduction pathways, and alveolar bone remodeling into a unified causal pathway. Key constructs include orthodontic mechanical forces that initiate mechanotransduction via cellular sensors, leading to the release of inflammatory mediators such as cytokines (e.g., interleukin-1, tumor necrosis factor-α) and prostaglandins (e.g., prostaglandin E2). These mediators, in turn, modulate bone remodeling through osteoclastogenesis and osteoblast activity, while bidirectional feedback loops amplify tissue responses, potentially resulting in periodontal degradation if dysregulated. The framework highlights how inflammation serves as both a response to and a modulator of mechanical stress, explaining variable clinical outcomes in orthodontic interventions. By integrating cellular and molecular biology with tissue biomechanics, this model addresses gaps in understanding the bidirectional causal pathways between force application and inflammatory feedback. It offers theoretical implications for optimizing orthodontic strategies to minimize tissue damage and enhance remodeling efficiency, without relying on empirical data. This synthesis provides a bold, mechanistic foundation for future research in periodontology and orthodontics.
