Biological Aging and Periodontal Disease: Analysis of NHANES (2001-2002)

Periodontitis is a chronic inflammatory disease caused by multiple potential contributing factors such as bacterial biofilm infection of the tissues surrounding the teeth and environmental determinants and a dysregulated host response for modifying and resolving the inflammation. Because periodontal disease is a major public health concern with substantial increases in the prevalence and severity in aging populations, previous studies of periodontitis tended to approach the disease as an age-associated outcome across the life span. However, few investigations have considered that, as a chronic noncommunicable disease, periodontitis may not simply be a disease that increases with age but may contribute to more rapid biologic aging.

Increasing population data supports the potential disconnect between chronological aging and biologic aging, which would contribute to the heterogeneity of aging phenotypes within chronologic ages across populations. Thus, our aim was to test whether periodontal disease affects biological aging across the life span.

The prevalence of periodontitis in the adult US population is a portion of the assessment of the National Health and Nutrition Examination Survey (NHANES), which has been ongoing since 1971 through 2-y cycles sampling populations across the country. We used NHANES 2001-2002 to test the hypothesis that the presence/severity of periodontal disease as an exposure variable would negatively affect telomere length, a measure of biological aging, and that this relationship is modified by factors that also affect the progression of periodontitis, such as sex, race/ethnicity, and smoking.

The data demonstrated a significant impact of periodontitis on decreasing telomere lengths across the life span. These differences were modulated by age, sex, race/ethnicity, and smoking within the population.

The findings lay the groundwork for future studies documenting broader effects on biological aging parameters as well as potential intervention strategies for periodontitis in driving unhealthy aging processes.

Periodontitis is a chronic inflammatory disease and dysregulated host response. Shortening of telomeres is a reflection of biologic aging. Decreased telomere lengths with periodontitis are seemingly related to chronic infection and persistent local and systemic inflammation. These findings suggest that periodontitis is not simply a disease of aging but may also transmit chronic systemic signals that could affect more rapid biological aging. Clinicians can use this outcome to recognize the role of periodontitis in driving unhealthy aging processes in patients.