Endothelial Cells Inhibit BMSc Osteogenesis In Peri-Implantitis

The relationship between bone resorption and angiogenesis in peri-implantitis remains unclear. This study established a peri-implantitis model in beagle dogs and isolated bone marrow mesenchymal stem cells (BMSCs) and endothelial cells (ECs) to investigate the osteogenic capacity of BMSCs in the presence of ECs and explore the underlying mechanisms. A ligature-induced peri-implantitis model was validated, with bone loss assessed via micro-computed tomography (micro-CT). Cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA). BMSCs and ECs were isolated and cultured to evaluate angiogenesis, osteogenesis-related protein expression, and NF-κB signaling pathway activity. At 8 weeks post-surgery, peri-implant gingival swelling and micro-CT-confirmed bone resorption were observed. The peri-implantitis group exhibited significantly elevated levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), angiotensin II (ANGII), and vascular endothelial growth factor (VEGF) compared to controls. In vitro, BMSCs co-cultured with inflammatory ECs (IECs) demonstrated reduced osteogenic differentiation capacity and upregulated expression of NF-κB pathway-related cytokines. Under peri-implantitis conditions, endothelial cells inhibit BMSC osteogenic differentiation via the NF-κB signaling pathway, suggesting a potential therapeutic target for peri-implantitis management.