MOLECULAR AND CELLULAR MECHANISMS OF PARODONTAL REMODELING IN TRAUMATIC OCCLUSION
Abstract and keywords
Abstract:
Objective. To systematize current data on the molecular and cellular mechanisms of periodontal tissue remodeling in response to traumatic occlusion, with a focus on key signaling pathways and promising therapeutic targets. Materials and Methods. A narrative literature review was conducted based on the analysis of publications from 2010 to 2025 in the PubMed, Google Scholar, eLibrary, and CyberLeninka databases. The selection criteria included original experimental and clinical studies, systematic reviews, and meta-analyses focusing on the pathophysiology of traumatic occlusion and related processes of mechanotransduction, bone remodeling, and impaired microcirculation. Results. The key pathogenetic factor was identified as specific pressure (force/area), rather than the absolute magnitude of the masticatory load. The tissue response is complex and phased: initial suppression of osteogenesis and metabolic imbalance are followed by the activation of osteoclastogenesis via the RANKL/RANK/OPG system, the NLRP3-IL-1β pathway, and oxidative stress mediated by the TRPM2 channel. Impaired microcirculation, ischemia, and hypoxia serve as a critical link between mechanical stress and biochemical disturbances, leading to the suppression of aerobic respiration and metabolic depression. Concurrently, compensatory and reparative processes are activated in the periodontal ligament, including the induction of heat shock proteins (HSP47, HSP70) and the remodeling of the collagen matrix involving type XII collagen. Conclusions. Traumatic occlusion is a multifactorial pathological process involving a complex cascade of molecular and cellular reactions. Effective treatment requires a comprehensive approach that combines the mandatory elimination of occlusal disorders and active anti-inflammatory therapy. Promising research directions include the development of methods targeting key molecular targets (RANKL, NLRP3, TRPM2, HSP47) and the implementation of personalized diagnostics based on biochemical markers and genetic features.

Keywords:
traumatic occlusion, periodontium, mechanotransduction, RANKL, bone resorption, periodontal ligament, HSP47, osteoclastogenesis, NLRP3
References

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