Cxcl10 Mediates Osteoblast Inhibition In Periodontitis-Related Bone Loss

The Role of CXCL10 in Osteoblast Regulation During Periodontal Bone Destruction Bioinformatics analysis identified key osteogenic genes in periodontitis. Gingival tissues from healthy individuals and periodontitis patients were analyzed for CXCL10 expression and clinical correlations. MC-3T3 E1 cells were treated with CXCL10 or LPS, and osteogenic activity was assessed via ALP/ARS staining, RT-qPCR, and immunohistochemistry. A total of 134 genes differentially expressed during osteogenesis in periodontitis were identified, with the top ten upregulated hub genes including CXCL10, CXCL8, CXCR4, CXCL12, and TLR4. More important, CXCL10 expression was significantly elevated in periodontal inflammatory tissues (P < 0.001) and positively correlated with probing depth (PD) (r = 0.588, P < 0.01), clinical attachment loss (CAL) (r = 0.580, P < 0.01), and alveolar bone resorption (ABR) (r = 0.509, P < 0.05). CXCL10 stimulation led to reduced ALP and ARS staining, and decreased expression of osteogenic markers Runx2, Col1a1, and Ocn. In contrast, pro-inflammatory cytokines IL-6, TNF-α, and IL-1β were upregulated following high-concentration CXCL10 exposure. CXCL10 plays a crucial role in periodontal bone destruction by partially inhibiting osteoblast proliferation and differentiation while promoting inflammation. These findings suggest that CXCL10 may serve as a potential therapeutic target for periodontitis.