Linh M. Nguyen

Introduction: Telomeres are nucleotide sequences found at the end of chromosomes, and their shortening is associated with chronological and biological ageing, oxidative stress and malnutrition. Shorter telomeres have been shown to be associated with periodontitis. Dietary nutrients are also influential factors in the aetiology and progression of periodontitis and other chronic inflammatory diseases. We tested the hypothesis that blood serum levels of folate, vitamin D, vitamin E, cis‐β‐carotene and/or β‐cryptoxanthin are associated with telomere lengths and periodontitis and that these relationships are modified by factors that also affect periodontitis (e.g., age, sex, smoking, race/ethnicity).Methods: Laboratory and demographic data collected by the NHANES 1999–2002 survey of 10,793 study participants were analysed. The data included age (binned every 10 years starting at age 30), race/ethnicity (White, Black, Hispanic), sex (male, female), periodontitis (none/mild, moderate/severe), vitamin levels (low, medium, high), telomere lengths (base pairs) and smoking (yes, no). Statistical analyses were performed with ANOVA tests.Results: Periodontitis was significantly associated with vitamin D, vitamin E and cis‐β‐carotene. Telomere length was significantly associated with vitamin E and cis‐β‐carotene. There were statistically significant interactions between the following vitamins and covariates on telomere length: folate and sex, vitamin D and periodontitis, vitamin D and race/ethnicity and vitamin E and sex.Conclusions: Certain blood nutrients may disrupt biological ageing, with periodontitis as a co‐morbidity. Some of these relationships are modified by demographic variables such as sex and race/ethnicity.

The objective of this study was to assess the osteoarthritis (OA) disease severity in 47 temporomandibular joints (TMJs) using a validated scale for gross signs of OA while noting the specific sites for profound disease on the donor condyle and fossa. A disease severity score of Grade 0–4, representing absent to severe disease, was awarded to each specimen’s condyle and fossa by two blinded investigators who have demonstrated interrater reliability. The mandibular fossa was more pathological compared to the mandibular condyle (* p = 0.001). When the deepest focal lesions were qualitatively assessed, it was demonstrated that the mandibular fossa was more severely degenerated than the articular eminence in 58% of donors. In this subpopulation, 74% of the severe mandibular fossa pathology was seen on the deep articular surface. When the articular eminence was the most severely degenerated region of the fossa, it was equivalently likely to see severe focal lesions on the lateral eminence (35%) or equally distributed across the entire eminence (35%). The greatest disease severity was discovered in sites of overloading, which may be associated with paranormal mandibular movements and potentially bruxism. Patients with bruxism produce significant translational movements (grinding) in the upper joint compartment and heavy vertical loading (clenching). Theoretically, this amplifies pressure and inflammation on the lateral articular surfaces and in the deep fossa.

Many chronic inflammatory diseases demonstrate demographic associations such as sex, age, and race-ethnicity. Periodontitis has been found to be increased with age and in males. This study used nonhuman primates representing a human-like model for periodontitis and examined the gingival transcriptome stratified on sex and age. Thirty-six Macaca mulatta in 4 age groups—young (17 y)—with a healthy periodontium were used to characterize gene expression in healthy gingival tissues. Gene expression was compared to clinical measures of bleeding on probing (BOP) and probing pocket depth (PPD). The results demonstrated sex differences in number of up- and downregulated genes that increased with age. Female animals generally showed elevated expression of genes related to host immunoinflammatory responses, and males showed increased expression of tissue structural genes. Gene expression correlations with BOP and/or PPD showed minimal overlap between the sexes, while male animals demonstrated substantial overlap in genes that correlated with both BOP and PPD clinical features. A cluster analysis of genes significantly different between sexes showed a clear sex and age discrimination in the young and adolescent animals. In the older groups, the genes clustered predominately by sex, irrespective of age group. A pathway analysis identified that significant gene expression patterns were quite similar in adolescent and adult animals, while the young and aged samples were quite distinct. The results confirmed substantial sex related variations in gingival tissue biology that were affected by age and observed even in adolescent animals. This suggests that “programming” of the gingival tissues related to sex can occur rather early in life and presage variations in future risk for periodontitis.

Introduction: 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. Objectives: 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. Methods: 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. Results: 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. Conclusion: 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. Knowledge Transfer Statement: 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.