Physiological Occlusal Force Promotes Heme Oxygenase-1 to Repair Periodontal Injury in a Rat Model of Replanted Teeth

Abstract

Objective The physiological occlusal force generated by mastication plays a critical role in tooth replantation after complete avulsion by promoting periodontal ligament healing. Heme oxygenase-1 (HO-1), a classical cytoprotective factor, exhibits mechanoresponsive expression in periodontal ligament cells (PDLCs). This study aims to investigate whether occlusal force can reduce replacement root resorption during the healing of periodontal ligament in replanted teeth and its potential mechanisms. Methods A tooth avulsion model was established in occlusal group rats and occlusal deprivation group rats. The healing of periodontal ligament was evaluated at 7 and 28 days post-replantation using micro-computed tomography, histological analysis, and immunohistochemistry. PDLCs were isolated to construct the injured periodontal ligament cells (iPDLCs) model. Following the application of cyclic tensile force, collagen synthesis level and the expression changes of HO-1 and transforming growth factor-beta 1 (TGF-β1) were assessed. Results The physiological occlusal force reduced replacement root resorption, promoted periodontal healing and the conversion of type III collagen (COL Ⅲ) to type I collagen (COL Ⅰ), and increased HO-1 expression in the periodontal ligament of replanted rat teeth. The cyclic tensile force (4% strain, 0.5 Hz) applied for 4 hours upregulated the expression of HO-1, COL Ⅰ, and COL III in iPDLCs. Enhanced HO-1 expression increased the levels of TGF-β1, COL I, and COL III, whereas inhibition of HO-1 or blockade of TGF-β1 reduced COL I and COL III expression. Simultaneous upregulation of HO-1 and inhibition of TGF-β1 resulted in decreased COL I and COL III expression. Conclusion Physiological occlusal force may be associated with reduced replacement root resorption and elevated HO-1 expression, while also promoting collagen synthesis in the injured periodontal ligament. Low deformation with short-term cyclic tensile force induces HO-1 expression, thereby promoting COL I and COL III synthesis in iPDLCs. This process is closely associated with the TGF-β1 signaling pathway.