Aging, inflammation, immunity and periodontal disease.

The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the adult population over 50 years of age. Although the immune system is a critical component for maintaining health, aging can be characterized by quantitative and qualitative modifications of the immune system. This process, termed 'immunosenescence', is a progressive modification of the immune system that leads to greater susceptibility to infections, neoplasia and autoimmunity, presumably reflecting the prolonged antigenic stimulation and/or stress responses that occur across the lifespan. Interestingly, the global reduction in the host capability to respond effectively to these challenges is coupled with a progressive increase in the general proinflammatory status, termed 'inflammaging'. Consistent with the definition of immunosenescence, it has been suggested that the cumulative effect of prolonged exposure of the periodontium to microbial challenge is, at least in part, a contributor to the effects of aging on these tissues. Thus, it has also been hypothesized that alterations in the function of resident immune and nonimmune cells of the periodontium contribute to the expression of inflammaging in periodontal disease. Although the majority of aging research has focused on the adaptive immune response, it is becoming increasingly clear that the innate immune compartment is also highly affected by aging. Thus, the phenomenon of immunosenescence and inflammaging, expressed as age-associated changes within the periodontium, needs to be more fully understood in this era of precision and personalized medicine and dentistry.

The potential lifespan impact of gingivitis and periodontitis in children.

The prevalence of gingivitis in children can be similar to or greater than dental caries, but has received much less attention in understanding the long-term impact on overall health. Oral health providers must take into consideration that the clinical presentation of the gingivitis progression/severity in the primary dentition is only evident when the magnitude of the inflammatory cell infiltrate approximates the gingival surface reflected by inflamed tissues. Moreover despite its relatively benign clinical appearance, the establishment of chronic inflammation of the periodontal tissues in childhood may have the potential for local tissue destruction leading to periodontitis, and/or create an "at-risk" environment in the tissues that could adversely affect the health of these tissues across the lifespan. The present manuscript presents some fundamental information regarding the characteristics of chronic inflammation in gingival tissues of children and adolescents and speculates about the lifetime impact of gingival and periodontal infections in childhood on future oral and systemic health in the adult.

Serum Nutrient Levels and Aging Effects on Periodontitis.

Periodontal disease damages tissues as a result of dysregulated host responses against the chronic bacterial biofilm insult and approximately 50% of US adults >30 years old exhibit periodontitis. The association of five blood nutrients and periodontitis were evaluated due to our previous findings regarding a potential protective effect for these nutrients in periodontal disease derived from the US population sampled as part of the National Health and Nutrition Examination Survey (1999⁻2004). Data from over 15,000 subjects was analyzed for blood levels of cis-ß-carotene, ß-cryptoxanthin, folate, vitamin D, and vitamin E, linked with analysis of the presence and severity of periodontitis. Moderate/severe disease patients had lower cis-ß-carotene levels across all racial/ethnic groups and these decreased levels in moderate/severe periodontitis were exacerbated with age. ß-cryptoxanthin demonstrated lower levels in severe disease patients across the entire age range in all racial/ethnic groups. Folate differences were evident across the various age groups with consistently lower levels in periodontitis patients >30 years and most pronounced in females. Lower levels of vitamin D were consistently noted across the entire age range of patients with a greater difference seen in females with periodontitis. Finally, an analytical approach to identify interactions among these nutrients related to age and periodontitis showed interactions of vitamin D in females, and folate with race in the population. These findings suggest that improving specific nutrient intake leading to elevated blood levels of a combination of these protective factors may provide a novel strategy to affect the significant increase in periodontitis that occurs with aging.