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J Dent Res. 2014 Aug;93(8):801-6. doi: 10.1177/0022034514540173. Epub 2014 Jun 16.

Impact of the Oral Commensal Flora on Alveolar Bone Homeostasis.

Author information

1
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.
2
Department of Periodontics, School of Dentistry, University of Washington, Seattle, WA 98195, USA.
3
Department of Periodontics, School of Dentistry, University of Washington, Seattle, WA 98195, USA rdarveau@u.washington.edu.

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.

KEYWORDS:

RANKL protein; helper T-cells; interleukin-17; osteoclastic bone loss; periodontium; tartrate-resistant acid phosphatase

PMID:
24935067
PMCID:
PMC4126224
DOI:
10.1177/0022034514540173
[Indexed for MEDLINE]
Free PMC Article

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