Age-associated periodontal bone loss in normal and TLR2- or MyD88-deficient mice

AGE-ASSOCIATED PERIODONTAL BONE LOSS IN NORMAL AND TLR2OR MYD88-DEFICIENT MICE Paul A. Ciero November 21,2011 Age-related alterations in innate immunity are poorly understood. The identification of those mechanisms, which are dysfunctional in old age, will shed light on potential therapeutic strategies for chronic inflammatory diseases prevalent in the elderly, such as periodontitis. Mice naturally develop chronic periodontitis as a function of age, which is characterized by periodontal bone loss. TLR2, a pattern-recognition receptor of leukocytes which mediates inflammatory responses in the periodontium, was expressed at higher levels in the gingivae of old mice (~18 months) compared with young mice (8 to 10 weeks). MyD88 is a signaling adaptor protein for TLR2 and other TLRs. We thus hypothesized that age-associated periodontal bone loss may be mediated through TLR2 and MyD88 and tested this hypothesis in appropriate gene knockout mice. Periodontal bone levels were measured as the distance from the cementoenamel junction to the alveolar bone crest. Aged TLRZand MyD88--