IADR Abstract Archives
Innate Lymphoid Cells as Potential Therapeutic Candidates Promoting Socket Preservation
Objectives: Tooth extraction causes morphological changes in alveolar bone, hindering prosthodontic and dental implant treatments. Innate lymphoid cells (ILCs) regulate bone metabolism during periodontitis progression. To date, their potential involvement in socket healing after tooth extraction remains unknown. In the present study, we aimed to elucidate the specific role of ILCs in socket healing after tooth extraction.
Methods: Maxillary first molars of wild-type mice were extracted, and changes in ILC populations and cytokine levels in the socket surrounding the extracted tooth were analyzed using single-cell RNA sequencing and flow cytometry. The ILCs in these sockets were histologically characterized using immunohistochemistry. The same molars were extracted from Il2rg-/-Rag2-/- mice lacking ILCs, and bone formation in the socket was evaluated using micro-computed tomography. Mouse bone marrow-derived mesenchymal stem/stromal cells (BMSCs) were cultured with interleukin (IL)-13, and cell mineralization was visualized using alizarin red S staining. IL-13 was intravenously administered to wild-type mice concomitantly with tooth extraction, and bone formation was assessed.
Results: The number of type 2 ILCs (ILC2s) within the extracted tooth socket was significantly higher than that of ILC1s and ILC3s (P<0.05). IL-13 secretion by ILC2s significantly increased after tooth extraction (P<0.05), and IL-13-producing ILC2s were observed near the bony walls of the socket. ILC-deficient mice exhibited significant impairment in bone formation in the socket compared to wild-type mice (P<0.05). IL-13 supplementation also significantly enhanced BMSC mineralization, thereby promoting bone formation in the sockets of wild-type mice (P<0.05).
Conclusions: Overall, these results suggest that ILC2s enhance bone formation in sockets after tooth extraction by promoting BMSC osteogenesis via IL-13 secretion. ILC2s thus represent a novel therapeutic candidate for socket preservation and promotion of desired prosthodontic outcomes.
Methods: Maxillary first molars of wild-type mice were extracted, and changes in ILC populations and cytokine levels in the socket surrounding the extracted tooth were analyzed using single-cell RNA sequencing and flow cytometry. The ILCs in these sockets were histologically characterized using immunohistochemistry. The same molars were extracted from Il2rg-/-Rag2-/- mice lacking ILCs, and bone formation in the socket was evaluated using micro-computed tomography. Mouse bone marrow-derived mesenchymal stem/stromal cells (BMSCs) were cultured with interleukin (IL)-13, and cell mineralization was visualized using alizarin red S staining. IL-13 was intravenously administered to wild-type mice concomitantly with tooth extraction, and bone formation was assessed.
Results: The number of type 2 ILCs (ILC2s) within the extracted tooth socket was significantly higher than that of ILC1s and ILC3s (P<0.05). IL-13 secretion by ILC2s significantly increased after tooth extraction (P<0.05), and IL-13-producing ILC2s were observed near the bony walls of the socket. ILC-deficient mice exhibited significant impairment in bone formation in the socket compared to wild-type mice (P<0.05). IL-13 supplementation also significantly enhanced BMSC mineralization, thereby promoting bone formation in the sockets of wild-type mice (P<0.05).
Conclusions: Overall, these results suggest that ILC2s enhance bone formation in sockets after tooth extraction by promoting BMSC osteogenesis via IL-13 secretion. ILC2s thus represent a novel therapeutic candidate for socket preservation and promotion of desired prosthodontic outcomes.