Background: Both substance P and hypoxia-inducible factor 1 alpha (HIF-1α) are involved in inflammation and angiogenesis. However, the relationship between substance P and HIF-1α in rat periodontitis is still unknown. Methods: Ligation-induced rat periodontitis was established to observe the distribution and expression of substance P and HIF-1α by immunohistochemistry. Rat gingival fibroblasts were cultured and stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). Recombinant substance P was applied to elaborate the relationship between substance P and HIF-1α in gingival fibroblasts in vitro. Primary mouse bone marrow-derived macrophages (BMMs) were isolated and cultured to observe the effect of substance P on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis by TRAP staining. Western blotting was used to investigate the expression of HIF-1α, osteoprotegerin (OPG) and RANKL. Results: Rat experimental periodontitis was successfully established 6 weeks after ligation. Gingival inflammatory infiltration and alveolar bone loss were observed. Positive expression of substance P was found in the infiltrating cells. Higher HIF-1α levels were observed in periodontitis compared to that of normal tissues. Substance P upregulated the level of HIF-1α in gingival fibroblasts with or without 1 μg/ml LPS in vitro (*P < 0.05). Substance P upregulated the expression of HIF-1α in RANKL-stimulated BMMs in vitro. Substance P also increased the RANKL/ OPG ratio in gingival fibroblasts (*P < 0.05). Both 10 nM and 50 nM substance P promoted RANKL-induced osteoclast differentiation (*P < 0.05). Conclusion: Substance P participates in periodontitis by upregulating HIF-1α and the RANKL/OPG ratio.

Multiple idiopathic external cervical root resorption is a rare condition with numerous predisposing factors that have not yet been clearly elucidated. In addition, its diagnosis and treatment pose challenges for clinicians, and thus, the extraction of the involved teeth is commonly performed. Here, we report a 29‐year‐old pregnant woman with no contributory medical or family/social history who experienced cervical root resorption that progressed aggressively and involved all permanent teeth. This case is unique owing to the involvement of all teeth. Reports of multiple idiopathic external cervical root resorption are rare in the literature, and the pathogenesis of the condition is poorly understood. This report aims to add an additional case to the existing literature, analyse the underlying mechanisms and provide clinicians with some guidance in diagnosing cervical root resorption.

No abstract

BackgroundPeriodontal ligament‐associated protein‐1 (PLAP‐1), an important target molecule of osteoarthritis research, may affect alveolar bone resorption. The aim of our study was to detect the effect of PLAP‐1 comprehensively and systematically on alveolar bone resorption and the underlying mechanism in PLAP‐1‐knockout mouse models.MethodsWe used a PLAP‐1‐knockout (C57BL/6N‐Plap‐1−/−) mouse model to investigate the effect of PLAP‐1 on osteoclast differentiation and the underlying mechanism by adding Porphyromonas gingivalis lipopolysaccharide to stimulate bone marrow‐derived macrophages. The effect of PLAP‐1 on alveolar bone resorption and the underlying mechanism were studied using a ligature periodontitis model, with micro‐computed tomography imaging, immunochemistry, and immunofluorescence.ResultsThe in vitro analysis results demonstrated that PLAP‐1‐ knockout significantly inhibited osteoclast differentiation under both normal and inflammatory conditions. Bioinformatic analysis, immunofluorescence, and co‐immunoprecipitation showed colocalization and interaction between PLAP‐1 and transforming growth factor beta 1 (TGF‐β1). The phosphorylation of Smad1 was reduced in the PLAP‐1‐knockout‐cells compared with that in the cells from wild‐type‐mice. The in vivo analysis results demonstrated that PLAP‐1‐knockout decreased bone resorption and the levels of osteoclast differentiation markers in experimental periodontitis compared with those in wild‐type mice. Immunofluorescence staining confirmed colocalization of PLAP‐1 and TGF‐β1 in the experimental periodontitis. The phosphorylation level of Smad1 was significantly reduced in PLAP‐1 knockout mice compared with that in wild‐type mice.ConclusionsThis study revealed that the knockout of PLAP‐1 inhibits the osteoclast differentiation and decreases alveolar bone resorption through the TGF‐β1/Smad1 signaling pathway, which could serve an innovative target for the prevention and treatment of periodontitis.This article is protected by copyright. All rights reserved