Substance P Enhances the Inhibition of Osteoblastic Cell Differentiation Induced by Lipopolysaccharide From <i>Porphyromonas gingivalis</i>

Azuma, Hideki; Kido, Jun‐ichi; Ikedo, Dai; Kataoka, Masatoshi; Nagata, Toshihiko

doi:10.1902/jop.2004.75.7.974

Cited by 55 publications

(46 citation statements)

References 44 publications

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“…Our data also showed that LPS strongly inhibits the expression of Runx2 mRNA in mouse osteoblast MC3T3-E1 cells. These results are consistent with the results reported by previous studies (Azuma et al, 2004;Tomomatsu et al, 2009).…”

Section: Discussionsupporting

confidence: 94%

Toll-like receptor-4-dependence of the lipopolysaccharide-mediated inhibition of osteoblast differentiation

Liu

Huang

et al. 2016

Genet. Mol. Res.

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pathogenic factor affecting bone fracture healing. Therefore, the effect of LPS on bone metabolism is relevant for bone healing. In this study, we investigated the effect of LPS on the expression of Toll-like receptor (TLR)-4 (an LPS receptor) by using real-time quantitative PCR and western blotting. We also examined the regulatory role of LPS in osteoblast differentiation by measuring the ALP activity, matrix mineralization, and ALP, OCN, and Runx2 mRNA (essential factors affecting osteoblast differentiation) expression in LPS-treated mouse osteoblast MC3T3-E1 cells. We also evaluated the effect of TLR-4 on LPS-mediated inhibition of osteoblast differentiation using RNA interference. LPS promotes TLR-4 mRNA and protein expression in MC3T3-E1 cells (P < 0.05, P < 0.01 or P < 0.001), and inhibits osteoblast differentiation by downregulating matrix mineralization and ALP activity (P < 0.05, P < 0.01 or P < 0.001), and suppressing the expression ALP, OCN, and Runx2 mRNA in MC3T3-E1 cells (P < 0.05 or P < 0.01). Conversely, RNAi-mediated TLR-4 knockdown abrogates the LPS-mediated inhibition of osteoblast differentiation (P < 0.05 or P < 0.01). In summary, LPS was shown to inhibit osteoblast differentiation by suppressing the expression of ALP, OCN, and Runx2 in a TLR-4-dependent manner. The results of this study may provide insights into the signal pathway of LPS-induced bone loss or delayed bone fracture healing.

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Section: Discussionsupporting

confidence: 94%

Toll-like receptor-4-dependence of the lipopolysaccharide-mediated inhibition of osteoblast differentiation

Liu

Huang

et al. 2016

Genet. Mol. Res.

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“…15,16) Much attention was paid to removal of endotoxin from recombinant protein solution after purification. We used a rapid, easy-to-follow procedure and effectively reduced the endotoxin level to less than 0.2 EU for further use in cell experiments, according to the manufacture's instructions for the Endotoxin Removal Kit.…”

Section: Resultsmentioning

confidence: 99%

Effect of a Novel Recombinant Protein of FibronectinIII7-10/Cadherin 11 EC1-2 on Osteoblastic Adhesion and Differentiation

Yuan

Zhou

Zhu

et al. 2009

Bioscience, Biotechnology, and Biochemistry

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“…P. gingivalis LPS, lipids, metabolic products and sonicated extracts can inhibit the differentiation and osteogenesis of osteoblasts [5-10], and modulate RANKL (receptor activator of nuclear factor-kappaB ligand) and/or OPG (osteoprotegerin) expression in osteoblasts to indirectly stimulate osteoclastogenesis [11-14]. Recently, our laboratory has established that P. gingivalis can invade osteoblasts and inhibit their maturation and mineralization in vitro [15], and fimbriae play an important role in mediating the initial invasive process [16].…”

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model

Zhang¹,

Ju²,

Rigney

et al. 2014

BMC Oral Health

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BackgroundPorphyromonas gingivalis has been shown to invade osteoblasts and inhibit their differentiation and mineralization in vitro. However, it is unclear if P. gingivalis can invade osteoblasts in vivo and how this would affect alveolar osteoblast/osteoclast dynamics. This study aims to answer these questions using a periodontitis mouse model under repetitive P. gingivalis inoculations.MethodsFor 3-month-old BALB/cByJ female mice, 109 CFU of P. gingivalis were inoculated onto the gingival margin of maxillary molars 4 times at 2-day intervals. After 2 weeks, another 4 inoculations at 2-day intervals were applied. Calcein was injected 7 and 2 days before sacrificing animals to label the newly formed bone. Four weeks after final inoculation, mice were sacrificed and maxilla collected. Immunohistochemistry, micro-CT, and bone histomorphometry were performed on the specimens. Sham infection with only vehicle was the control.ResultsP. gingivalis was found to invade gingival epithelia, periodontal ligament fibroblasts, and alveolar osteoblasts. Micro-CT showed alveolar bone resorption and significant reduction of bone mineral density and content in the infected mice compared to the controls. Bone histomorphometry showed a decrease in osteoblasts, an increase in osteoclasts and bone resorption, and a surprisingly increased osteoblastic bone formation in the infected mice compared to the controls.ConclusionsP. gingivalis invades alveolar osteoblasts in the periodontitis mouse model and cause alveolar bone loss. Although P. gingivalis appears to suppress osteoblast pool and enhance osteoclastic bone resorption, the bone formation capacity is temporarily elevated in the infected mice, possibly via some anti-microbial compensational mechanisms.

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Substance P Enhances the Inhibition of Osteoblastic Cell Differentiation Induced by Lipopolysaccharide From Porphyromonas gingivalis

Abstract: These findings suggest that SP inhibits osteoblastic cell differentiation and may be related to bone metabolism in periodontal diseases under conditions of stress.

Cited by 55 publications

References 44 publications

Toll-like receptor-4-dependence of the lipopolysaccharide-mediated inhibition of osteoblast differentiation

Toll-like receptor-4-dependence of the lipopolysaccharide-mediated inhibition of osteoblast differentiation

Effect of a Novel Recombinant Protein of FibronectinIII7-10/Cadherin 11 EC1-2 on Osteoblastic Adhesion and Differentiation

Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model

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