Inhibition of Osteoblastic Cell Differentiation by Lipopolysaccharide Extract fromPorphyromonas gingivalis

Abstract

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-1β 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.

Enterococcus faecalis attenuates osteogenesis through activation of p38 and ERK1/2 pathways in MC3T3‐E1 cells

“…It is widely accepted that bacterial infections are responsible for alveolar bone destruction in periodontal disease (Nair et al 1996). Porphyromonas gingivalis LPS also significantly reduces osteoblast differentiation by inhibiting ALP, OC and osteopontin expression (Kadono et al 1999). Although E. faecalis is frequently isolated in root filled teeth with persistent periapical bone lesions, the effects of E. faecalis on osteogenesis and their underlying mechanisms are unclear.…”

Inhibitory effects of green tea polyphenol (–)‐epigallocatechin gallate on the expression of matrix metalloproteinase‐9 and on the formation of osteoclasts

“…In periodontitis, periodontal tissues are continuously challenged by periodontopathogens, such as P. gingivalis. It was shown that P. gingivalis could mediate the destruction of periodontal tissue and could be involved in alveolar bone resorption in various ways (40)(41)(42)(43)(44). In addition, the products of P. gingivalis were reported to have the ability to induce and activate host MMPs (19)(20)(21)(22)(23)(24)(25).…”

Oral Fluid–Based Biomarkers of Alveolar Bone Loss in Periodontitis

“…121,122 However, since OPN is produced by both osteoblasts and osteoclasts, it holds a dual function in bone maturation and mineralization as well as bone resorption. [123][124][125][126][127] Kido et al investigated the presence of OPN in GCF and the correlation between these levels and probing depth measures of periodontally healthy and diseased patients. Results from this study revealed that OPN could be detected in GCF, and increased OPN levels coincided with increased probing depth measures.…”