Journal
INFECTION AND IMMUNITY
Volume 68, Issue 10, Pages 5864-5868Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.68.10.5864-5868.2000
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Funding
- NCI NIH HHS [CA34196, P30 CA034196] Funding Source: Medline
- NIAID NIH HHS [R01 AI24544] Funding Source: Medline
- NIDCR NIH HHS [R29 DE10728] Funding Source: Medline
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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 x C57BL/6J)F-1 offspring were susceptible, suggesting C57BL/6J has recessive resistance alleles, while (BALB/cJ x A/J)F-1 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.
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