Traumatic occlusion exacerbates bone resorption by modifying gene expression in the bone tissue of ligature-induced periodontitis in mice.

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 (RNA-seq) 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, then analyzed 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 signaling pathways were upregulated 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 signaling 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.