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

Periodontitis;Aging;TLR2;MyD88

Paul A. Ciero, 1986-

University:University of Louisville

Department:Oral Biology

关键词: Periodontitis;    Aging;    TLR2;    MyD88;   

Others  :  https://ir.library.louisville.edu/cgi/viewcontent.cgi?article=1251&context=etd

美国|英语

来源: The Universite of Louisville's Institutional Repository

【 摘 要 】

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 TLR2-/- and MyD88-/- mice developed less periodontal bone loss compared to age-matched wild-type mice. These results indicate that TLR2 and its adaptor MyD88 contribute to periodontal bone loss in aged mice, implicating these molecules as potential targets for drug therapies in the treatment of periodontitis.