Objective: The purpose of this study was to observe the effect of hyperocclusion on the remodeling of gingival tissues and detect the related signaling pathways.
Design: Hyperocclusion models were established by tooth extraction in mice. The mice were sacrificed at 3, 7, 14, 28, or 56 days after the surgery, and the left mandibular first molars with gingival tissues were isolated and examinations were focused on the gingival tissues. Apoptotic cells were examined using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) technology. Proliferating cells, p65, inflammatory cytokines, and β-catenin were detected using immunohistochemical methods.
Results: A series of apoptosis and proliferation responses were triggered in stressed gingival tissues. It was observed that the levels of p65, proinflammatory factors including interleukin-1β and tumor necrosis factor-α in extraction group were higher compared with those from mice with intact dentition, and peaked on days 14, 14 and 7 respectively. The expression of β-catenin was increased under hyperocclusion situations, peaked on day 14, and declined to the initial levels over time.
Conclusions: The results of this study suggest that hyperocclusion causes remodeling of the gingival tissues by activating a series of adaptive responses. Both nuclear factor kappa B and Wnt/β-catenin signaling pathways may be responsible for those adaptive responses though the exact mechanism is not clear.
Keywords: Gingival tissues; Hyperocclusion; Mechanical stress; NF-κB signaling pathway; Wnt/β-catenin signaling pathway.
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