Two-stage extraction by partial grinding of impacted mandibular third molar in close proximity to the inferior alveolar nerve

BACKGROUND Extraction of impacted third molars often leads to severe complications caused by damage to the inferior alveolar nerve(IAN).AIM To proposes a method for the partial grinding of an impacted mandibular third molar(IMM3)near the IAN to prevent IAN injury during IMM3 extraction.METHODS Between January 1996 and March 2022,25 patients with IMM3 roots near the IAN were enrolled.The first stage of the operation consisted of grinding a major part of the IMM3 crown with a high-speed turbine dental drill to achieve sufficient space between the mandibular second molar and IMM3.After 6 months,when the root tips were observed to be away from the IAN on X-ray examination,the remaining part of the IMM3 was completely removed.RESULTS All IMM3s were extracted easily without symptoms of IAN injury after extraction.CONCLUSION Partial IMM3 grinding may be a good alternative treatment option to avoid IAN injury in high-risk cases.

PPAR-γactivation promotes xenogenic bioroot regeneration by attenuating the xenograft induced-oxidative stress

Xenogenic organ transplantation has been considered the most promising strategy in providing possible substitutes with the physiological function of the failing organs as well as solving the problem of insufficient donor sources.However,the xenograft,suffered from immune rejection and ischemia-reperfusion injury(IRI),causes massive reactive oxygen species(ROS)expression and the subsequent cell apoptosis,leading to the xenograft failure.Our previous study found a positive role of PPAR-γ in antiinflammation through its immunomodulation effects,which inspires us to apply PPAR-γ agonist rosiglitazone(RSG)to address survival issue of xenograft with the potential to eliminate the excessive ROS.In this study,xenogenic bioroot was constructed by wrapping the dental follicle cells(DFC)with porcine extracellular matrix(p ECM).The hydrogen peroxide(H_(2)O_(2))-induced DFC was pretreated with RSG to observe its protection on the damaged biological function.Immunoflourescence staining and transmission electron microscope were used to detect the intracellular ROS level.SD rat orthotopic transplantation model and superoxide dismutase 1(SOD1)knockout mice subcutaneous transplantation model were applied to explore the regenerative outcome of the xenograft.It showed that RSG pretreatment significantly reduced the adverse effects of H2O2on DFC with decreased intracellular ROS expression and alleviated mitochondrial damage.In vivo results confirmed RSG administration substantially enhanced the host’s antioxidant capacity with reduced osteoclasts formation and increased periodontal ligament-like tissue regeneration efficiency,maximumly maintaining the xenograft function.We considered that RSG preconditioning could preserve the biological properties of the transplanted stem cells under oxidative stress(OS)microenvironment and promote organ regeneration by attenuating the inflammatory reaction and OS injury.

PTHrP promotes subchondral bone formation in TMJ-OA

PTH-related peptide(PTHr P) improves the bone marrow micro-environment to activate the bone-remodelling, but the coordinated regulation of PTHr P and transforming growth factor-β(TGFβ) signalling in TMJ-OA remains incompletely understood. We used disordered occlusion to establish model animals that recapitulate the ordinary clinical aetiology of TMJ-OA. Immunohistochemical and histological analyses revealed condylar fibrocartilage degeneration in model animals following disordered occlusion. TMJ-OA model animals administered intermittent PTHr P(i PTH) exhibited significantly decreased condylar cartilage degeneration. Micro-CT,histomorphometry, and Western Blot analyses disclosed that i PTH promoted subchondral bone formation in the TMJ-OA model animals. In addition, i PTH increased the number of osterix(OSX)-positive cells and osteocalcin(OCN)-positive cells in the subchondral bone marrow cavity. However, the number of osteoclasts was also increased by i PTH, indicating that subchondral bone volume increase was mainly due to the i PTH-mediated increase in the bone-formation ability of condylar subchondral bone.In vitro, PTHr P treatment increased condylar subchondral bone marrow-derived mesenchymal stem cell(SMSC) osteoblastic differentiation potential and upregulated the gene and protein expression of key regulators of osteogenesis. Furthermore, we found that PTHr P-PTH1R signalling inhibits TGFβ signalling during osteoblastic differentiation. Collectively, these data suggested that i PTH improves OA lesions by enhancing osteoblastic differentiation in subchondral bone and suppressing aberrant active TGFβsignalling. These findings indicated that PTHr P, which targets the TGFβ signalling pathway, may be an effective biological reagent to prevent and treat TMJ-OA in the clinic.