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Microbiology and Biotechnology Letters

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Molecular and Cellular Microbiology / Biomedical Sciences  |  Pathogenesis and Host-Microbial interactions

Microbiol. Biotechnol. Lett. 2016; 44(4): 557-562

https://doi.org/10.4014/mbl.1608.08010

Received: August 31, 2016; Accepted: September 21, 2016

치주염 유발 세균 Aggregatibacter actinomycetemcomitans와 Porphyromonas gingivalis에 의한 committed osteoclast precursor 분화 증가

Augmented Osteoclastogenesis from Committed Osteoclast Precursors by Periodontopathic Bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis

Ok-Jin Park , Yeongkag Kwon , Cheol-Heui Yun and Seung Hyun Han *

11Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul 08826, Republic of Korea , 2Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea

Abstract

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Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis are gram-negative bacteria frequently found in lesions from patients with periodontitis manifesting alveolar bone loss. Lipopolysaccharides are a major virulence factor of gram-negative bacteria. Bone resorption is known to be regulated by bacteria and their virulence factors. In the present study, we investigated the effects of A. actinomycetemcomitans and P. gingivalis on bone resorption. Heat-killed A. actinomycetemcomitans (HKAa) and heatkilled P. gingivalis (HKPg) induced bone loss in the femurs of mice after intraperitoneal administration. HKAa and HKPg augmented the differentiation of committed osteoclast precursors into osteoclasts, while they inhibited the differentiation of bone marrow-derived macrophages into osteoclasts. Concordant with the effects of the heat-killed whole cells, LPS purified from A. actinomycetemcomitans and P. gingivalis also augmented osteoclast differentiation from committed osteoclast precursors but attenuated it from bone marrow-derived macrophages. Taken together, these results suggest that the whole cells and lipopolysaccharides of A. actinomycetemcomitans and P. gingivalis induce the differentiation of committed osteoclast precursors into osteoclasts, potentially contributing to bone resorption in vivo.

Keywords: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, lipopolysaccharide, osteoclast, bone loss

References

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  1. Arai F, Miyamoto T, Ohneda O, Inada T, Sudo T, Brasel K, et al. 1999. Commitment and differentiation of osteoclast precursor cells by the sequential expression of c-Fms and receptor activator of nuclear factor kappaB (RANK) receptors. J. Exp. Med. 190: 1741-1754.
    Pubmed KoreaMed CrossRef
  2. Feng X, McDonald JM. 2011. Disorders of bone remodeling. Annu. Rev. Pathol. 6: 121-145.
    Pubmed KoreaMed CrossRef
  3. Flemmig TF. 1999. Periodontitis. Ann. Periodontol. 4: 32-38.
    Pubmed CrossRef
  4. Irfan UM, Dawson DV, Bissada NF. 2001. Epidemiology of periodontal disease: a review and clinical perspectives. J. Int. Acad Periodontol. 3: 14-21.
    Pubmed
  5. Kang J, de Brito Bezerra B, Pacios S, Andriankaja O, Li Y, Tsiagbe V, et al. 2012. Aggregatibacter actinomycetemcomitans infection enhances apoptosis in vivo through a caspase-3-dependent mechanism in experimental periodontitis. Infect. Immun. 80:2247-2256.
    Pubmed KoreaMed CrossRef
  6. Kim J, Yang J, Park OJ, Kang SS, Kim WS, Kurokawa K, et al. 2013. Lipoproteins are an important bacterial component responsible for bone destruction through the induction of osteoclast differentiation and activation. J. Bone. Miner. Res. 28: 2381-2391.
    Pubmed CrossRef
  7. Kopydlowski KM, Salkowski CA, Cody MJ, van Rooijen N, Major J, Hamilton TA, Vogel SN. 1999. Regulation of macrophage chemokine expression by lipopolysaccharide in vitro and in vivo. J. Immunol. 163: 1537-1544.
    Pubmed
  8. McArdle A, Marecic O, Tevlin R, Walmsley GG, Chan CK, Longaker MT, et al. 2015. The role and regulation of osteoclasts in normal bone homeostasis and in response to injury. Plast. Reconstr. Surg. 135: 808-816.
    Pubmed CrossRef
  9. Mogensen TH. 2009. Pathogen recognition and inflammatory signaling in innate immune defenses. Clin. Microbiol. Rev. 22:240-273.
    Pubmed KoreaMed CrossRef
  10. Munford RS. 2008. Sensing gram-negative bacterial lipopolysaccharides:a human disease determinant? Infect. Immun. 76:454-465.
    Pubmed KoreaMed CrossRef
  11. Papapanou PN. 1996. Periodontal diseases: epidemiology. Ann. Periodontol. 1: 1-36.
    Pubmed CrossRef
  12. Park OJ, Cho MK, Yun CH, Han SH. 2015. Lipopolysaccharide of Aggregatibacter actinomycetemcomitans induces the expression of chemokines MCP-1, MIP-1alpha, and IP-10 via similar but distinct signaling pathways in murine macrophages. Immunobiology 220: 1067-1074.
    Pubmed CrossRef
  13. Park OJ, Yang J, Kim J, Yun CH, Han SH. 2015. Enterococcus faecalis attenuates the differentiation of macrophages into osteoclasts. J. Endod. 41: 658-662.
    Pubmed CrossRef
  14. Park OJ, Yi H, Jeon JH, Kang SS, Koo KT, Kum KY, et al. 2015. Pyrosequencing analysis of subgingival microbiota in distinct periodontal conditions. J. Dent. Res. 94: 921-927.
    Pubmed CrossRef
  15. Ready D, D'Aiuto F, Spratt DA, Suvan J, Tonetti MS, Wilson M. 2008. Disease severity associated with presence in subgingival plaque of Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Tannerella forsythia, singly or in combination, as detected by nested multiplex PCR. J. Clin. Microbiol. 46:3380-3383.
    Pubmed KoreaMed CrossRef
  16. Rodan GA. 1998. Bone homeostasis. Proc. Natl. Acad. Sci. USA 95: 13361-13362.
    Pubmed KoreaMed CrossRef
  17. Rogers JE, Li F, Coatney DD, Rossa C, Bronson P, Krieder JM, et al. 2007. Actinobacillus actinomycetemcomitans lipopolysaccharidemediated experimental bone loss model for aggressive periodontitis. J. Periodontol. 78: 550-558.
    Pubmed KoreaMed CrossRef
  18. Takami M, Kim N, Rho J, Choi Y. 2002. Stimulation by toll-like receptors inhibits osteoclast differentiation. J. Immunol. 169:1516-1523.
    Pubmed CrossRef
  19. Trouillet-Assant S, Gallet M, Nauroy P, Rasigade JP, Flammier S, Parroche P, et al. 2015. Dual impact of live Staphylococcus aureus on the osteoclast lineage, leading to increased bone resorption. J. Infect. Dis. 211: 571-581.
    Pubmed CrossRef
  20. Van Dyke TE, Sheilesh D. 2005. Risk factors for periodontitis. J. Int. Acad. Periodontol. 7: 3-7.
    Pubmed KoreaMed
  21. Varoga D, Wruck CJ, Tohidnezhad M, Brandenburg L, Paulsen F, Mentlein R, et al. 2009. Osteoblasts participate in the innate immunity of the bone by producing human beta defensin-3. Histochem. Cell Biol. 131: 207-218.
    Pubmed CrossRef
  22. Wright JA, Nair SP. 2010. Interaction of staphylococci with bone. Int. J. Med. Microbiol. 300: 193-204.
    Pubmed KoreaMed CrossRef
  23. Zhang W, Ju J, Rigney T, Tribble G. 2014. Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model. BMC Oral. Health. 14: 89.
    Pubmed KoreaMed CrossRef
  24. Zou W, Bar-Shavit Z. 2002. Dual modulation of osteoclast differentiation by lipopolysaccharide. J. Bone. Miner. Res. 17: 1211-1218.
    Pubmed CrossRef

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