Periodontal inflammation and bone loss in aged mice

Abstract

Background and objective-Young mice do not develop measurable periodontal bone loss, unless heavily infected with human periodontal pathogens. However, mice with 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.

Oral health in geroscience: animal models and the aging oral cavity

“…In another study, we recently published that alveolar bone levels decline only a very slight amount in C57BL6/ JNia mice between 2 and 3 months of age and 9-10 months of age; however, by 22-24 months, a substantial decline in alveolar bone levels has occurred . These data are consistent with a prior study by Liang et al (Liang et al, 2010) who showed loss of alveolar bone in 18-month-old mice compared to 2-month-old mice. A simple pairwise comparison of 2-month-old mice to 9-10-month-old mice would not have uncovered this large age-related decline in alveolar bone, however.…”

Age-associated changes in innate immunity and their impacts on inflammatory disease.

“…However, none of these diseases have been linked to age-associated alterations in Del-1 expression, which could be responsible for dysregulated chronic recruitment of neutrophils to affected tissues. Aging mice, like aging humans, can naturally develop periodontal bone loss [74,84]. We therefore examined whether age-related mouse periodontitis is associated with changes in Del-1 expression.…”

“…To our knowledge, the abrogation of periodontitis in Oel-r / --IL-17R- [4,[93][94][95] and in mouse periodontitis models [74,96]. IL-17…”

“…In this regard, the elderly show inappropriately high periodontal inflammatory responses relative to young individuals following comparable de novo biofilm formation [84]. A similar condition may apply to old mice which develop overt periodontitis [74]. From a mechanistic viewpoint, little is known regarding the impact of aging on innate immunity and inflammatory diseases [82,84].…”

“…Therefore, periodontitis represents an attractive model to determine the role of Oel-1 in neutrophil-mediated chronic inflammation with impact on systemic diseases. Old age and age-associated inflammation are factors that contribute to increased prevalence and severity of periodontitis in humans and mice [74,75]. Our overall hypothesis is that age-associated reductions in Oel-1 expression leads to excessive recruitment of neutrophils and increased IL-17 A production in periodontal tissues, resulting in enhanced periodontal inflammation and periodontal bone loss.…”