IADR Abstract Archives
Aging, Telomere Length, and Periodontitis
Objectives: Telomere shortening with age is well documented and is theorized to be the basis for cellular senescence and increased chronic diseases in aging. Periodontitis is one of these chronic diseases. We hypothesized that shortened telomere length is associated with the presence of chronic periodontitis across the lifespan.
Methods: Datasets from the 1999-2000 and 2001-2002 National Health and Nutrition Examination Survey (NHANES) were interrogated. Pocket depths and attachment loss were coupled with analysis of telomere measures and the association was estimated using SPSS. Periodontitis was defined as: ≥1 tooth with pocket depth of ≥4 mm and ≥3 mm of attachment loss occurring on the same tooth. Mean telomere lengths were compared between people with or without periodontitis (T-test). Significant differences in mean telomere lengths stratified on: Age (binned every 10 yrs, starting at age 30), Race/Ethnicity (Hispanics, Whites, Blacks, Other), and Periodontitis (Yes, No) were determined using ANOVA.
Results: For both the 1999-2000 (p=0.009) and 2001-2002 (Maxillary p=0.030 and Mandibular p=0.001) periodontitis subjects demonstrated shorter telomere lengths. ANOVA results identified a significant relationship of these differences with Race (p=0.002), Periodontitis (p=0.014), and Age (p=0.000) for the 1999-2000 sampling. Similar assessment for 2001-2002 showed this same relationship to Age (p=0.000), Periodontitis (p=0.041), and Race (p=0.000). Thus, we identified significant relationships between telomere length and periodontitis that are modified or impacted by Age and Race/Ethnicity.
Conclusions: A clear limitation of the study includes the inherent constraints of the NHANES periodontal data recorded during these sampling periods, although, our results were consistent within the available datasets. Since these differences in telomere lengths with periodontitis were observed across a broad age range, and harmonious with existing data of increased disease related to Race/Ethnicity, periodontitis may not simply be a disease of aging, but may actually transmit chronic signals that propel more rapid biologic aging.
Methods: Datasets from the 1999-2000 and 2001-2002 National Health and Nutrition Examination Survey (NHANES) were interrogated. Pocket depths and attachment loss were coupled with analysis of telomere measures and the association was estimated using SPSS. Periodontitis was defined as: ≥1 tooth with pocket depth of ≥4 mm and ≥3 mm of attachment loss occurring on the same tooth. Mean telomere lengths were compared between people with or without periodontitis (T-test). Significant differences in mean telomere lengths stratified on: Age (binned every 10 yrs, starting at age 30), Race/Ethnicity (Hispanics, Whites, Blacks, Other), and Periodontitis (Yes, No) were determined using ANOVA.
Results: For both the 1999-2000 (p=0.009) and 2001-2002 (Maxillary p=0.030 and Mandibular p=0.001) periodontitis subjects demonstrated shorter telomere lengths. ANOVA results identified a significant relationship of these differences with Race (p=0.002), Periodontitis (p=0.014), and Age (p=0.000) for the 1999-2000 sampling. Similar assessment for 2001-2002 showed this same relationship to Age (p=0.000), Periodontitis (p=0.041), and Race (p=0.000). Thus, we identified significant relationships between telomere length and periodontitis that are modified or impacted by Age and Race/Ethnicity.
Conclusions: A clear limitation of the study includes the inherent constraints of the NHANES periodontal data recorded during these sampling periods, although, our results were consistent within the available datasets. Since these differences in telomere lengths with periodontitis were observed across a broad age range, and harmonious with existing data of increased disease related to Race/Ethnicity, periodontitis may not simply be a disease of aging, but may actually transmit chronic signals that propel more rapid biologic aging.