Traumatic Occlusion Exacerbates Bone Resorption by Modifying Gene Expression in the Bone Tissue of Ligature-Induced Periodontitis in Mice.

Abstract

AIM: To clarify the molecular mechanisms of occlusal trauma in bone loss through periodontal tissue transcriptome analysis in mice with periodontitis and traumatic occlusion. MATERIALS AND METHODS: Ligature-induced periodontitis (Li) and composite resin-induced traumatic occlusion (Tra) mouse models were established (control [Co], Li, Tra and LiTra). Bone resorption was evaluated using micro-computed tomography (micro-CT). RNA-sequencing was conducted on gingiva, bone and periodontal ligament from all groups 3 days post induction. For long-term evaluation, the Co and Tra groups were maintained for 8 weeks and then analysed using micro-CT and qRT-PCR. RESULTS: Traumatic occlusion alone, sustained for 8 weeks, did not directly induce bone resorption; however, it significantly exacerbated bone resorption in mice with periodontitis. Cytokine-cytokine receptor interactions and Toll-like receptor signalling pathways were up-regulated in LiTra bone tissue. Il11, Il1rl1 and Mmp3, associated with inflammation and bone metabolism, were more highly expressed in the LiTra group than in the Li group. TNF-α signalling via NFκB and inflammatory response gene sets were enriched in the bone tissue of LiTra group. CONCLUSIONS: Traumatic occlusion accelerates bone resorption in ligature-induced periodontitis but does not independently cause significant bone loss. Occlusal trauma enhances the expression of inflammation-related genes, especially in bone with periodontitis.