Pseudomonas aeruginosa (P. aeruginosa) is associated with periapical periodontitis. The lesions are characterized by a disorder in osteoblast metabolism. Quorum sensing molecular N-(3-oxododecanoyl)-homoserine lactone (AHL) is secreted by P. aeruginosa and governs the expression of numerous virulence factors. AHL can trigger intracellular calcium ([Ca²⁺]_i) fluctuations in many host cells. However, it is unclear whether AHL can regulate osteoblast metabolism by affecting [Ca²⁺]_i changes or its spatial correlation. We explored AHL-induced apoptosis and differentiation in pre-osteoblastic MC3T3-E1 cells and evaluated [Ca²⁺]_i mobilization using several extraction methods. The spatial distribution pattern of [Ca²⁺]_i among cells was investigated by Moran's I, an index of spatial autocorrelation. We found that 30 μM and 50 μM AHL triggered opposing osteoblast fates. At 50 μM, AHL inhibited osteoblast differentiation by promoting mitochondrial-dependent apoptosis and negatively regulating osteogenic marker genes, including Runx2, Osterix, bone sialoprotein (Bsp), and osteocalcin (OCN). In contrast, prolonged treatment with 30 μM AHL promoted osteoblast differentiation concomitantly with cell apoptosis. The elevation of [Ca²⁺]_i levels in osteoblasts treated with 50 μM AHL was spatially autocorrelated, while no such phenomenon was observed in 30 μM AHL-treated osteoblasts. The blocking of cell-to-cell spatial autocorrelation in the osteoblasts provoked by 50 μM AHL significantly inhibited apoptosis and partially restored differentiation. Our observations suggest that AHL affects the fate of osteoblasts (apoptosis and differentiation) by affecting the spatial correlation of [Ca²⁺]_i changes. Thus, AHL acts as a double-edged sword for osteoblast function.

铜绿假单胞菌( P. aeruginosa ) 与根尖周炎有关。病变的特征是成骨细胞代谢紊乱。群体感应分子 N-(3-oxododecanoyl)-高丝氨酸内酯 (AHL) 由铜绿假单胞菌分泌并控制许多毒力因子的表达。AHL 可以触发许多宿主细胞中的细胞内钙 ([Ca ²⁺ ] _i ) 波动。然而，尚不清楚AHL是否可以通过影响[Ca ²⁺ ] _i变化或其空间相关性来调节成骨细胞代谢。我们在前成骨细胞 MC3T3-E1 细胞中探索了 AHL 诱导的细胞凋亡和分化，并评估了 [Ca ²⁺ ] _i使用多种提取方法进行动员。细胞间[Ca ²⁺ ] _i的空间分布模式通过空间自相关指数Moran's I进行研究。我们发现 30 μM 和 50 μM AHL 引发了相反的成骨细胞命运。在 50 μM 时，AHL 通过促进线粒体依赖性细胞凋亡和负调节成骨标记基因（包括 Runx2、Osterix、骨唾液蛋白（Bsp）和骨钙素（OCN））来抑制成骨细胞分化。相比之下，用 30 μM AHL 延长治疗促进成骨细胞分化伴随细胞凋亡。[Ca ²⁺ ] _i的高度用 50 μM AHL 处理的成骨细胞中的水平是空间自相关的，而在 30 μM AHL 处理的成骨细胞中没有观察到这种现象。50 μM AHL 引起的成骨细胞中细胞间空间自相关的阻断显着抑制了细胞凋亡并部分恢复了分化。我们的观察表明，AHL 通过影响 [Ca ²⁺ ] _i变化的空间相关性来影响成骨细胞的命运（细胞凋亡和分化）。因此，AHL 对于成骨细胞功能来说是一把双刃剑。