Effects of Calcium Hydroxide on Biological Activity of LPS

牙髓感染是导致根尖周炎和根尖周围骨溶解的主要原因，细菌脂多糖（LPS）在炎症和骨吸收过程中起重要作用，近年来有报道称，氢氧化钙能水解细菌脂多糖的脂质部分，本研究探讨了氢氧化钙是否能改变细菌脂多糖的生物活性，通过比较LPS和/或氢氧化钙刺激人牙周膜成纤维细胞（HPLF）6、12和24 h后炎性细胞因子IL-1 α、β、IL-6、IL-8和TNF-α的表达，探讨细菌LPS的生物学作用。结果表明：LPS刺激后HPLF各实验时间点均有IL-6、IL-8基因表达，6 h组有TNF-α基因表达，而无IL-1 α、IL-1 β基因表达。氢氧化钙抑制LPS刺激的HPLF中IL-6、IL-8和TNF-α基因的表达，提示氢氧化钙可抑制细菌LPS引起的炎症反应。

Apical periodontitis and its concomitant periapical osteolysis are caused by pulpal infection, and bacterial lipopolysaccharide (LPS) has been known to play a major role in the inflammation and the bone resorption process.Recently, it was reported that calcium hydroxide hydrolyzed the lipid moiety of bacterial LPS, resulting in the release of free hydroxy fatty acid and may alter biological activities of bacterial LPS.This study examined whether calcium hydroxide may alter the biological action of bacterial LPS through comparing the expression of inflammatory cytokine genes (IL-1 α, β,IL-6,IL-8 and TNF-α) of human periodontal ligament fibroblasts (HPLF) stimulated by LPS and/or calcium hydroxide for 6,12 and 24 hrs. The results were as follows.IL-6 and IL-8 genes in every experimental time and TNF-α gene in the 6 hours group were expressed in HPLF stimulated by LPS, but no IL-1 α or β gene were expressed. Further, calcium hydroxide inhibited IL-6, IL-8 and TNF-α gene expression in HPLF stimulated by LPS.These results suggest that calcium hydroxide inhibits the inflammatory reactions caused by bacterial LPS.