P75NTR, a neural crest stem cell marker, is continuously expressed in mesenchymal cells during tooth development. Importantly, high expression of p75NTR in the late bell stage implicates its involvement in odontogenesis and mineralization. However, the regulatory mechanisms underlying p75NTR involvement in odonto/osteogenic differentiation remain unclear. Here, we investigate the effect and potential mechanisms underlying p75NTR involvement in odonto/osteogenic differentiation. We dissected EMSCs from the first branchial arches of mice embryo and compared the proliferation and migration of p75NTR^+/+ and p75NTR^−/−EMSCs by transwell, scratch and cell counting kit 8(CCK8)assays. The differentiation ability and the involvement of nuclear factor kappa-B (NF-κB) pathway were investigated through alkaline phosphatase and immunofluorescence assay, real-time PCR, and western blot. During induction of dental epithelium conditioned medium, p75NTR^+/+ EMSCs exhibited deeper Alkaline phosphatase (ALP) staining and higher expression of odonto/osteogenic genes/proteins (e.g., dentin sialoprotein (DSPP) than p75NTR^+/+ EMSCs. Moreover, p75NTR^+/+ EMSCs exhibited higher nuclear P65 expression than p75NTR^−/−EMSCs. Inhibition of NF-κB pathway with Bay11-7082 in p75NTR^+/+EMSCs substantially decreased DSPP expression level. However, activation of NF-κB pathway with Bay11-7082 in p75NTR^−/−EMSCs enhanced DSPP expression level. Thus, p75NTR possibly plays a paramount role in the proliferation and differentiation of EMSCs via NF-κB pathway. Graphical abstract

Single cell RNA sequencing reveals mesenchymal heterogeneity and critical functions of Cd271 in tooth development

Breakage and displacement of the high-speed dental handpiece bur is one of the intraoperative complications during mandibular third molar extraction. The retained metallic fragments can trigger issues such as pain and infection. Traditional retrieval methods require extensive tissue dissection, increasing the risk of nerve injury and postoperative complications. While emerging technologies are precise, their high cost and technical complexity hinder widespread adoption. Therefore, there is an urgent need for minimally invasive and easy-to-use treatments. This retrospective study aimed to compare the clinical efficacy of magnet-assisted removal and conventional methods for retrieving broken burs during mandibular third molar surgery, as well as to analyze the associated factors and outcomes. This retrospective study analyzed 15 cases of broken burs removal divided into conventional removal (n = 7) and magnet-assisted removal (n = 8) groups. Primary outcomes included operative time and success rate; secondary outcomes encompassed 24-hour postoperative visual analogue scale (VAS) pain scores, limited mouth opening at 72 h postoperatively, and neurosensory disturbances. Compared to conventional removal, magnet-assisted removal significantly reduced operative time (P = 0.03) and showed a non-significant trend toward lower neurosensory complication rates (P = 0.036). Although the success rate of magnet-assisted removal (100%) exceeded that of conventional removal techniques (71.4%), this difference was not statistically significant. The magnet group demonstrated superior secondary outcomes, lower mean VAS scores and fewer cases of limited mouth opening. Magnet-assisted removal is a technically simple, safe, and effective minimally invasive alternative to conventional removal methods. Its advantages include reduced operative duration and potentially improved postoperative recovery.

Background: To investigate in vitro how scrapie responsive gene 1 (SCRG1) contributes to the development of temporomandibular joint osteoarthritis (TMJOA). Methods: Western blotting was used to identify protein expression. Proinflammatory cytokine levels were assessed by means of an enzyme-linked immunosorbent test. In order to find out whether chondrocytes expressed protein light chain 3B (LC3B), immunofluorescence was utilized. Results: In the TMJOA in vitro model, hydrogen peroxide (H2O2) treatment increased the expression of SCRG1, stimulated chondrocyte catabolism and inflammatory response, and blocked autophagy. In chondrocytes, SCRG1 silencing reduces the inflammatory response, catabolism, and autophagy inhibition brought on by H2O2. Concurrently, H2O2 induction triggers the nuclear factor (NF)-κB pathway and nerve growth factor receptor (NGFR). When SCRG1 is downregulated, NGFR expression is inhibited and the NF-κB pathway is blocked. Conclusions: By inhibiting NGFR and blocking the NF-κB pathway, knocking down SCRG1 can prevent H2O2-induced inflammatory response, metabolic breakdown and autophagy inhibition in chondrocytes.