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Interdisciplinary Perspectives on Infectious Diseases
Volume 2009 (2009), Article ID 864359, 6 pages
Research Article

B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection

1Biology Department, Bates College, Lewiston, ME 04240, USA
2Immunology/Inflammation/Hematology Section, The Jackson Laboratory, Bar Harbor, ME 04609, USA

Received 13 June 2009; Revised 25 July 2009; Accepted 10 August 2009

Academic Editor: Robert Burne

Copyright © 2009 Pamela J. Baker et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Periodontal disease is one of the most common infectious diseases of humans. Immune responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh- mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans. P. gingivalis-infected normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD activated B cells and CD T cells in immune normal mice compared to IgD deficient mice. These data suggest that IgD is an important mediator of alveolar bone resorption, possibly through antigen-specific coactivation of B cells and CD T cells.