Implant dentures become the first choice for denture restoration in patients with tooth loss. However, oral implants often fail in osteoporosis (OP) patients. Melatonin (MT) induces osteogenic differentiation of bone mesenchymal stem cells (BMSCs), suggesting its therapeutic potential in OP treatment. Long non-coding RNA H19 induces osteogenic differentiation of BMSCs, while its regulatory mechanism in MT-involved osteogenic and adipogenic differentiation of BMSCs remains elusive. Ovariectomized (OVX) rat was used to construct an OP model, and bone quality was assessed. Meanwhile, the expression of H19, miR-541-3p, MT and adiponectin (APN) was examined by quantitative reverse transcription-PCR (qRT-PCR) or ELISA. The adipogenic and osteogenic differentiation of BMSCs were determined by oil red O staining and alizarin red S staining, respectively. The targeting relationships between H19, miR-541-3p and APN mRNA were predicted by bioinformatics and confirmed by RNA immunoprecipitation and dual-luciferase reporter assay. The results showed that MT, H19 and APN were down-regulated, while miR-541-3p was up-regulated in the OVX rat model. At the cellular level, MT reduced adipogenic differentiation, heightened osteogenic differentiation of BMSCs, and activated Wnt/β-catenin pathway, which were reversed by the MT2 selective inhibitor 4-P-PDOT. Overexpressing H19 facilitated the osteogenic differentiation and inhibited the adipogenic differentiation of BMSCs mediated by MT, while H19 knockdown or overexpressing miR-541-3p had the opposite effect. Moreover, H19 functioned as a competitive endogenous RNA and sponged miR-541-3p, and miR-541-3p targeted APN. Overall, MT modulates the osteogenic and adipogenic differentiation of BMSCs by mediating H19/miR-541-3p/APN axis, providing a new reference for the targeted therapy of OP.

A considerable number of patients with prominent mandibular angle have mandibular third molar impaction that needs surgical removal. Mandibular reduction is a popular and effective surgery to correct prominent mandibular angle, but it has been rarely performed simultaneously with impacted third molar extraction. In order to decrease the number of operations and suffering of patients, safely performing these 2 operations together is necessary and important. From January 2016 to June 2018, patients received mandibular reduction and impacted mandibular third molar extraction together were retrospectively reviewed. Forty-seven patients receiving long-curve mandibular reduction (n = 12) or simple mandibular reduction (n = 35) were included in this study. A total of 65 impacted mandibular third molars were extracted during mandibular reduction. One patient had hematoma within facial soft tissue which reabsorbed spontaneously. Seven patients who underwent long-curve mandibular reduction reported transient inferior lip numbness for several weeks. No infection or poor wound healing was reported. No immediate or delayed mandibular fracture occurred. All the patients were satisfied with both the aesthetic result of mandibular reduction and the unnecessity of receiving a secondary surgery to extract the impacted third molar. Simultaneously performing mandibular reduction and impacted mandibular third molar extraction can effectively reduce the number of operations and patients’ suffering. It is also safe with adequate pre-op assessment, professional surgical knowledge, proper use of surgical instruments, meticulous surgical procedures, and correct post-op care.

Background and objectives Periodontitis is a chronic multifactorial inflammatory disease associated with dental plaque biofilms. Slit guidance ligand 2 (SLIT2) has been shown to guide neuronal migration, regulate the inflammatory response and cancer progression. However, the role of SLIT2 in periodontitis is poorly understood. In this study, we investigated the expression of SLIT2 in the gingiva of periodontitis and its role in periodontitis progression. Methods Gingiva and gingival crevicular fluid (GCF) were collected from healthy people and periodontitis patients. Immunohistochemistry and enzyme‐linked immunosorbent assay (ELISA) were used to analyze SLIT2 secretion level. Healthy human gingival fibroblasts (hGFs) were isolated and the expression of SLIT2 in lipopolysaccharide (LPS)‐treated hGFs was detected. The effect of SLIT2 on inflammation was analyzed using western blot and immunofluorescence. SLIT2 knockdown (KD) and overexpression assays in hGFs were performed to investigate the role of SLIT2 in the LPS‐induced inflammatory response. Results Gingival tissues and GCF of periodontitis patients displayed higher expression of SLIT2. Similarly, SLIT2 was upregulated in hGFs in an inflammatory environment (LPS treatment). In addition, SLIT2 treatment increased the expression of the inflammatory mediators interleukin‐6 (IL‐6) and IL‐8 in hGFs. Mechanistically, SLIT2 stimulated the activation of nuclear factor‐κB (NF‐κB) signaling, as well as LPS. Lastly, SLIT2 KD impaired LPS‐induced IL‐6 production in hGFs, while SLIT2 overexpression amplified the inflammatory response. Conclusion SLIT2 may be involved in the aggravation of periodontitis by activating NF‐κB signaling in hGFs.