The effect of lipopolysaccharide from the oral bacterium Bacteroides gingivalis on osteoclastic resorption of sperm-whale dentine slices in vitro

Sismey-Durrant, Helen J.; Hopps, Rosamund M.

doi:10.1016/0003-9969(87)90106-3

Cited by 22 publications

(11 citation statements)

References 10 publications

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“…Although the influence of LPS on osteoclasts and bone resorption has been studied extensively (9, 28–30), the underlying effects of P. gingivalis LPS on osteoblasts and the bone repair process are less well defined. Some studies have indicated that P. gingivalis LPS and sonicated bacterial extracts inhibit various osteogenic parameters, such as alkaline phosphatase activity, collagen synthesis and bone nodule formation, implying that periodontal pathogens inhibit bone formation (5, 31–33).…”

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Lipopolysaccharide alters decorin and biglycan synthesis in rat alveolar bone osteoblasts: consequences for bone repair during periodontal disease

Roberts

Moseley

Sloan

et al. 2008

European J Oral Sciences

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A prime pathogenic agent associated with periodontitis is lipopolysaccharide (LPS) derived from Porphyromonas gingivalis. This study investigated the effects of P. gingivalis LPS on osteoblasts, which are responsible for alveolar bone repair. Bone cells were obtained from explants of rat alveolar bone chips and cultured with 0–200 ng ml−1 of P. gingivalis LPS. Porphyromonas gingivalis LPS significantly increased cell proliferation and inhibited osteoblast differentiation, as judged by reduced alkaline phosphatase activity. Analysis of biglycan mRNA and protein levels indicated that P. gingivalis LPS significantly delayed the normally high expression of biglycan during the early stages of culture, which are associated with cell proliferation and early differentiation of progenitor cells. In the presence of P. gingivalis LPS, decorin expression by the alveolar bone cells was reduced during periods of culture relating to collagen fibrillogenesis and mineral deposition. Analysis of glycosaminoglycan chains conjugated to these proteoglycans suggested that in the presence of P. gingivalis LPS, dermatan sulfate persisted within the matrix. This study suggests that P. gingivalis LPS influences the expression and processing of decorin and biglycan in the matrix, altering alveolar bone cell activity and osteoblast phenotype development. The consequences of this altered expression in relation to hindering bone repair as part of the cycle of events during periodontal disease are discussed.

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confidence: 99%

Lipopolysaccharide alters decorin and biglycan synthesis in rat alveolar bone osteoblasts: consequences for bone repair during periodontal disease

Roberts

Moseley

Sloan

et al. 2008

European J Oral Sciences

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“…LPS of P. gingivalis (P-LPS) stimulates the differentiation and activity of osteoclastic cells by mediating inflammatory cytokines and factors such as interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-␣), and prostaglandin E 2 (PGE 2 ) and finally induces bone resorption (8,20,45,58). LPS is also known to increase the release of inflammatory osteolytic factors from osteoblastic cells and to stimulate alveolar bone resorption by an indirect effect through the action on osteoblastic cells as well as a direct effect on osteoclastic cells (25,36,46). Physiological bone remodelling is controlled by a balance between bone formation and resorption.…”

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Inhibition of Osteoblastic Cell Differentiation by Lipopolysaccharide Extract fromPorphyromonas gingivalis

et al. 1999

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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.

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“…Lipopolysaccharide (LPS) of Porphyromonas gingivalis, a pathogenic bacterium of periodontal disease, has been considered an important pathogenic component of the organism in the initiation and development of periodontal diseases, because bacterial LPS is known to be a potent stimulator of inflammatory cytokine production and bone resorption (2,12,18,21,31). One target of LPS is the human gingival fibroblast, a cell that play an important role in the remodeling of periodontal soft tissues.…”

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CD14-mediated signal pathway of Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts

et al. 1996

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Lipopolysaccharide (LPS) induces expression of inflammatory cytokines in monocytes/macrophages via CD14, one of the LPS receptors, which is expressed predominantly in these cells. It has been demonstrated thatPorphyromonas gingivalis LPS (P-LPS) also is able to induce inflammatory cytokines in human gingival fibroblasts. Therefore, it is important to determine whether CD14 is expressed in gingival fibroblasts and to define the P-LPS-mediated signal-transducing mechanism in the cells. In this study, we observed unexpectedly by immunohistochemical, Western blotting (immunoblotting), and Northern (RNA) blotting assays that CD14 is expressed at high density in human gingival fibroblasts. P-LPS-induced expression of the monocyte chemoattractant protein 1 (MCP-1) gene in the cells was inhibited markedly by treatment with anti-human CD14 antibody and was completely was inhibited by herbimycin A, a potent inhibitor of tyrosine kinase. The inhibitor also dramatically inhibited monocyte chemotactic activity of and MCP-1 production by the cells. Furthermore, P-LPS-induced expression of the MCP-1 gene in the cells also was blocked by inhibitors of two transcription factors, i.e., curcumin, an inhibitor of AP-1, and pyrolidine dithiocarbamate, an inhibitor of NF-B. Both inhibitors inhibited monocyte chemotactic activity in the culture supernatant of P-LPS-treated cells. Gel shift mobility assay showed stimulation of the AP-1 and NF-B contents in P-LPS-treated cells. This study is the first to demonstrate the expression of CD14 in human gingival fibroblasts and to show that the signal-transducing pathway of P-LPS in the cells is mediated by CD14.

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The effect of lipopolysaccharide from the oral bacterium Bacteroides gingivalis on osteoclastic resorption of sperm-whale dentine slices in vitro

Cited by 22 publications

References 10 publications

Lipopolysaccharide alters decorin and biglycan synthesis in rat alveolar bone osteoblasts: consequences for bone repair during periodontal disease

Lipopolysaccharide alters decorin and biglycan synthesis in rat alveolar bone osteoblasts: consequences for bone repair during periodontal disease

Inhibition of Osteoblastic Cell Differentiation by Lipopolysaccharide Extract fromPorphyromonas gingivalis

CD14-mediated signal pathway of Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts

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