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Apparition de la maladie parodontale précoce chez la souris déficiente à la sélectine P/E
Author(s) -
Niederman R.,
Westernoff T.,
Lee C.,
Mark L. L.,
Kawashima N.,
UllmanCuller M.,
Dewhirst F. E.,
Paster B. J.,
Wagner D. D.,
Mayadas T.,
Hynes R. O.,
Stashenko P.
Publication year - 2001
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1034/j.1600-051x.2001.028006569.x
Subject(s) - periodontitis , dental alveolus , medicine , immunology , cytokine , tooth loss , disease , leukocyte adhesion deficiency , connective tissue , periodontal fiber , animal studies , immune system , pathology , dentistry , integrin alpha m , oral health , cd18
Background: Retrospective and correlation studies suggest that early‐onset periodontal disease may be due to a deficiency in phagocyte function, a pathogenic oral biofilm, and/or dysregulated gingival cytokine expression. Increased susceptibility to periodontal disease is therefore thought to result from multiple risk factors. Methods: We tested this hypothesis prospectively using P/E‐selectin adhesion molecule deficient mice that mimic the human syndrome leukocyte adhesion deficiency II. Results: Our studies demonstrate that, in comparison to wild type animals, P/E −/− mice exhibit: spontaneous, early onset alveolar bone loss which is significant by 6 weeks of age; a 10‐fold elevation in bacterial colonization of their oral cavities; and elevated gingival tissue levels of the bone resorptive cytokine IL‐1α. Alveolar bone loss is completely prevented by prophylactic antibiotic therapy. Conclusions: These experiments provide the first prospective evidence for the multiple risk factor hypothesis of periodontal disease, and validate the first animal model for early onset periodontitis in which both the microbiota and host response can be systematically manipulated. P/E −/− animals should be useful in testing the virulence of putative periodontal pathogens, in determining the role of host resistance factors in periodontitis, in exploring the proposed relationship(s) between infection mediated alveolar bone loss and systemic health disorders, and exploring their genetic relationships.