title: Emerging roles of immunostimulatory oral bacteria in periodontitis development.
abstract: Periodontitis is a common dental disease which results in irreversible alveolar bone loss around teeth, and subsequent tooth loss. Previous studies have focused on bacteria that damage the host and the roles of commensals to facilitate their colonization. Although some immune responses targeting oral bacteria protect the host from alveolar bone loss, recent studies show that particular host defense responses to oral bacteria can induce alveolar bone loss. Host-damaging and immunostimulatory oral bacteria cooperatively induce bone loss by inducing gingival damage followed by immunostimulation. In mouse models of experimental periodontitis induced by either Porphyromonas gingivalis or ligature, γ-proteobacteria accumulate and stimulate host immune responses to induce host damage. Here we review the differential roles of individual bacterial groups in promoting bone loss through the induction of host damage and immunostimulation.
authors.affiliation: Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
authors.forename: Yizu
authors.initials: Y
authors.lastname: Jiao
authors.affiliation: Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
authors.forename: Mizuho
authors.initials: M
authors.lastname: Hasegawa
authors.affiliation: Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI 48109, USA. Electronic address: ino@umich.edu.
authors.forename: Naohiro
authors.initials: N
authors.lastname: Inohara
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D000818:Animals; D001419:Bacteria / Q000276:immunology*; D004195:Disease Models, Animal; D051379:Mice; D009055:Mouth / Q000382:microbiology*; D010518:Periodontitis / Q000150:complications / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology
keywords: NOD1; alveolar bone absorption; innate immunity; neutrophil recruitment; pathobiont; periodontitis