S100A8 regulates postoperative responses following tooth extraction in rats.

The reduction in alveolar ridge height and width after tooth extraction poses a substantial challenge for dental implant restoration. This study aimed to observe the roles of S100A8 in the inflammatory response and bone resorption following tooth extraction. Rat mandibular second molars were extracted. Western blotting, micro-computed tomography, tartrate-resistant acid phosphatase staining, immunohistochemistry, scanning electron microscopy (SEM), and immunofluorescence were applied to observe inflammatory responses and bone resorption after rat mandibular second molar extraction. S100A8 was overexpressed in RAW 246.7 cells, and transfection efficiency was confirmed using western blotting and immunofluorescence. Receptor Activator for Nuclear Factor-κB Ligand (RANKL)-induced osteoclastogenesis of RAW 246.7 cells and a lipopolysaccharide-stimulated environment were chosen to evaluate the roles and related mechanisms of S100A8. An increase in S100A8 expression was observed 2 weeks after molar extraction compared to normal gingival tissues. Subsequently, S100 expression decreased between the second and third weeks, coinciding with the progression of inflammatory response following tooth extraction. Positive S100A8 expression was detected in the infiltrating cells and osteoclasts. S100A8 overexpression in RAW 246.7 cells promoted tumor necrosis factor-α expression and osteoclast formation by activating nuclear factor (NF)-κB p65 signaling. In summary, S100A8 was involved in inflammatory responses and bone resorption following tooth extraction by activating NF-κB p65 signaling. Interventions targeted to decrease S100A8 levels may have therapeutic implications for minimizing post-extraction bone loss.