Denervation effectively aggravates rat experimental periodontitis

Background Nerve and its related factors in the occurrence and development of periodontitis are worthy of further study. Denervation research is a useful addition to nerve and innervation studies. The aim of this study is to establish a rat model of inferior alveolar nerve transection combined with ligature-induced periodontitis to elucidate the effects of denervation on ligature-induced rat periodontitis. Material and Methods Sixty-four Wistar rats were distributed to the four groups randomly: ligation (L); denervation (D); ligation+denervation (LD); and normal (N) as control. A ligation-inducing rat experimental periodontitis model was established in the L and LD groups. Rats in the D and LD groups also underwent the transection of the right inferior alveolar nerve simultaneously. Four weeks after the operation, the mandibles were taken out for micro-computed tomography analysis. Osteoclast number was observed through TRAP staining. The gingival tissues around the first molars were homogenized and measured by enzyme-linked immunosorbent assay for interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Collagen fibers were observed using Picro-Sirius Red staining. Nuclear factor (NF)-κB p65 and IκBα phosphorylation and osteoprotegerin (OPG)/receptor activator of NF-κB ligand (RANKL) ratio in the gingival tissues were detected by western blotting. Results Denervation strongly promoted ligature-induced alveolar bone loss in the LD group. The alveolar bone loss of the LD group was significantly increased compared with the L group. Furthermore, denervation aggravated trabecular bone breakdown in the bone specific parameters, including percentage bone area, trabecular thickness and bone mineral density. Increased TRAP-positive osteoclasts were detected in alveolar bone of the LD group. More serious collagen fiber destructions and increased expressions of IL-1β and TNF-α were found in the LD group. NF-κB p65 and IκBα phosphorylation were also significantly upregulated in the LD group. OPG/RANKL ratio in the gingival extracts was markedly decreased in the LD group compared with the L group. Decreased OPG/RANKL ratio was observed in the D group, compared with the N group. Conclusion Denervation effectively aggravates ligature-induced rat periodontitis by the NF-κB signaling pathway for excessive production of IL-1β and TNF-α and increased osteoclasts for decreased OPG/RANKL ratio. The rat model of inferior alveolar nerve transection that combined ligature-induced periodontitis provides an animal model to observe further the change of nerve-related factors in the occurrence and development of periodontitis, so as to select positive nerve-related factors to regulate inflammation and promote periodontal regeneration in the future.