Kadono H, Kido J, Kataoka M, Yamauchi N, Nagata T
Department of Periodontology and Endodontology, Tokushima University School of Dentistry, 3-18-15 Kuramoto, Tokushima 770-8504, Japan.
Infect Immun. 1999 Jun;67(6):2841-6. doi: 10.1128/IAI.67.6.2841-2846.1999.
Lipopolysaccharide from Porphyromonas gingivalis (P-LPS), an important pathogenic bacterium, is closely associated with inflammatory destruction of periodontal tissues. P-LPS induces the release of cytokines and local factors from inflammatory cells, stimulates osteoclastic-cell differentiation, and causes alveolar bone resorption. However, the effect of P-LPS on osteoblastic-cell differentiation remains unclear. In this study, we investigated the effect of P-LPS extract prepared by the hot-phenol-water method, on the differentiation of primary fetal rat calvaria (RC) cells, which contain a subpopulation of osteoprogenitor cells, into osteoblastic cells. P-LPS extract significantly inhibited bone nodule (BN) formation and the activity of alkaline phosphatase (ALPase), an osteoblastic marker, in a dose-dependent manner (0 to 100 ng of P-LPS extract per ml). P-LPS extract (100 ng/ml) significantly decreased BN formation to 27% of the control value and inhibited ALPase activity to approximately 60% of the control level on days 10 to 21 but did not affect RC cell proliferation and viability. P-LPS extract time-dependently suppressed the expression of ALPase mRNA, with an inhibitory pattern similar to that of enzyme activity. The expression of mRNAs for osteocalcin and osteopontin, matrix proteins related to bone metabolism, was markedly suppressed by P-LPS extract. Furthermore, P-LPS extract increased the expression of mRNAs for CD14, LPS receptor, and interleukin-1beta in RC cells. These results indicate that P-LPS inhibits osteoblastic-cell differentiation and suggest that LPS-induced bone resorption in periodontal disease may be mediated by effects on osteoblastic as well as osteoclastic cells.
牙龈卟啉单胞菌(P - LPS)的脂多糖是一种重要的病原菌,与牙周组织的炎症性破坏密切相关。P - LPS可诱导炎性细胞释放细胞因子和局部因子,刺激破骨细胞分化,并导致牙槽骨吸收。然而,P - LPS对成骨细胞分化的影响仍不清楚。在本研究中,我们研究了通过热酚 - 水法制备的P - LPS提取物对原代胎鼠颅骨(RC)细胞分化的影响,这些细胞含有骨祖细胞亚群,可分化为成骨细胞。P - LPS提取物以剂量依赖性方式(每毫升0至100 ng P - LPS提取物)显著抑制骨结节(BN)形成和成骨细胞标志物碱性磷酸酶(ALPase)的活性。在第10至21天,P - LPS提取物(100 ng/ml)可使BN形成显著降低至对照值的27%,并将ALPase活性抑制至对照水平的约60%,但不影响RC细胞增殖和活力。P - LPS提取物随时间依赖性地抑制ALPase mRNA的表达,其抑制模式与酶活性相似。骨钙素和骨桥蛋白(与骨代谢相关的基质蛋白)的mRNA表达被P - LPS提取物显著抑制。此外,P - LPS提取物增加了RC细胞中CD14(LPS受体)和白细胞介素 - 1β的mRNA表达。这些结果表明,P - LPS抑制成骨细胞分化,并提示牙周疾病中LPS诱导的骨吸收可能是通过对成骨细胞和破骨细胞的作用介导的。