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Infection and Immunity, October 2000, p. 5864-5868, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Genetic Control of Susceptibility to Porphyromonas gingivalis-Induced Alveolar Bone Loss in Mice

Pamela J. Baker,1,* Mark Dixon,1 and Derry C. Roopenian2

Biology Department, Bates College, Lewiston, Maine 04240,1 and The Jackson Laboratory, Bar Harbor, Maine 046092

Received 20 April 2000/Returned for modification 22 June 2000/Accepted 20 July 2000

Periodontal disease affects a large percentage of the human population. Resorption of the alveolar bone of the jaw is a pivotal sequela of periodontal disease, because this bone is the attachment site for the periodontal ligaments that anchor the teeth. Using a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, a gram-negative bacterium associated with human adult periodontal disease, we provide evidence suggesting that susceptibility to such bone loss is a genetically determined trait. AKR/J, DBA/2J, and BALB/cByJ or BALB/cJ mice were highly susceptible, while A/J, A/HeJ, 129/J, SJL/J, and C57BL/6J mice were much more resistant. When susceptible BALB/cJ and BALB/cByJ mice were crossed to resistant strains, two patterns were observed. (BALBc/ByJ × C57BL/6J)F1 offspring were susceptible, suggesting C57BL/6J has recessive resistance alleles, while (BALB/cJ × A/J)F1 mice were all resistant, suggesting that A/J mice have dominant resistance alleles. These results suggest a tractable genetic basis for P. gingivalis-induced alveolar bone loss and open the possibility of exploiting the mouse model to identify loci important for host susceptibility and resistance to periodontal disease.

* Corresponding author. Mailing address: Biology Department, Bates College, Lewiston, ME 04240. Phone: (207) 786-6108. Fax: (207) 786-8334. E-mail: pbaker{at}abacus.bates.edu.

Infection and Immunity, October 2000, p. 5864-5868, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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