title: Impact of the Oral Commensal Flora on Alveolar Bone Homeostasis.
abstract: Homeostasis of healthy periodontal tissues is affected by innate and adaptive immunosurveillance mechanisms in response to the normal oral flora. Recent comparisons of germ-free (GF) and normal specific-pathogen-free (SPF) mice have revealed the impact of host immunosurveillance mechanisms in response to the normal oral flora on alveolar bone height. Prior reports that alveolar bone height is significantly less in normal SPF mice compared with their age- and strain-matched GF counterparts suggest that naturally occurring alveolar bone loss is a normal component of healthy periodontal tissue homeostasis. In this report, histomorphometric analyses confirmed increased alveolar bone loss and revealed increased numbers of TRAP+ osteoclastic cells lining the alveolar bone surface in SPF compared with GF mice. Increased numbers of RANKL+ cells and IL17+ cells in the periodontium of SPF mice demonstrate possible molecular mechanisms mediating the up-regulated osteoclastogenesis and alveolar bone loss in SPF mice compared with GF mice. Increased numbers of T-lymphocytic cells and T-helper cells in the junctional epithelium of SPF mice compared with GF mice suggest that the adaptive immune response contributes to physiologic alveolar bone loss in the healthy periodontium. This GF animal model study notably begins to elucidate the impact of host immunosurveillance mechanisms in response to the normal oral flora, mediating catabolic alveolar bone homeostasis in the healthy periodontium.
authors.affiliation: Department of Periodontics, School of Dentistry, University of Washington, Seattle, WA 98195, USA Department of Preventive Dentistry and Dental Public Health, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, Aichi, 464-8650, Japan Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8558, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Irie
authors.affiliation: Department of Periodontics, School of Dentistry, University of Washington, Seattle, WA 98195, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Novince
authors.affiliation: Department of Periodontics, School of Dentistry, University of Washington, Seattle, WA 98195, USA rdarveau@u.washington.edu.
authors.forename: R P
authors.initials: RP
authors.lastname: Darveau
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D056704:Adaptive Immunity / Q000276:immunology; D016301:Alveolar Bone Loss / Q000276:immunology / Q000473:pathology; D000539:Alveolar Process / Q000276:immunology* / Q000473:pathology; D000818:Animals; D001419:Bacteria / Q000276:immunology*; D017252:CD3 Complex / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D002452:Cell Count; D004846:Epithelial Attachment / Q000276:immunology / Q000473:pathology; D005856:Germ-Free Life; D006706:Homeostasis / Q000276:immunology*; D007113:Immunity, Innate / Q000276:immunology; D007157:Immunologic Surveillance / Q000276:immunology; D020381:Interleukin-17 / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D018655:Lymphocyte Count; D051379:Mice; D009055:Mouth / Q000382:microbiology*; D009504:Neutrophils / Q000276:immunology; D010010:Osteoclasts / Q000473:pathology; D053245:RANK Ligand / Q000032:analysis; D013047:Specific Pathogen-Free Organisms; D013601:T-Lymphocytes / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D017252:CD3 Complex; D015704:CD4 Antigens; D020381:Interleukin-17; D007527:Isoenzymes; D053245:RANK Ligand; C505689:Tnfsf11 protein, mouse; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase
keywords: RANKL protein; helper T-cells; interleukin-17; osteoclastic bone loss; periodontium; tartrate-resistant acid phosphatase