Background and objective: Young mice do not develop measurable periodontal bone loss, unless heavily infected with human periodontal pathogens. However, mice with a genetically altered immune system are unable to control their own oral flora and develop periodontitis early in life. Based on the potential of the indigenous oral microbiota to cause periodontitis, we hypothesized that normal mice may ultimately develop inflammatory periodontal bone loss, i.e. as a function of age. If confirmed, this could serve as an aging model of chronic periodontitis.

Material and methods: Periodontal bone levels were measured as the distance from the cementoenamel junction to the alveolar bone crest in young mice (8-10 wk of age), old mice (>or= 18 mo of age) and mice of intermediate ages. Differential expression of inflammatory mediators in the gingivae of young and old mice was determined by quantitative real-time PCR.

Results: In comparison with young mice, old mice displayed significantly (p < 0.05) increased periodontal bone loss, accompanied by elevated expression of proinflammatory cytokines (interleukin-1 beta, tumor necrosis factor alpha and interleukin-17A) and innate immune receptors involved in the induction or amplification of inflammation (Toll-like receptor 2, CD14, CD11b, CD18, complement C5a receptor and triggering receptor expressed on myeloid cells 3).

Conclusion: Mice develop naturally induced periodontal bone loss as a function of age. This aging model of periodontitis represents a genuinely chronic model to study mechanisms of periodontal tissue destruction.