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, 5 (4), 229-241

Age and Periodontal Health - Immunological View

Affiliations

Age and Periodontal Health - Immunological View

J L Ebersole et al. Curr Oral Health Rep.

Abstract

Purpose of the review: Aging clearly impacts a wide array of systems, in particular the breadth of the immune system leading to immunosenescence, altered immunoactivation, and coincident inflammaging processes. The net result of these changes leads to increased susceptibility to infections, increased neoplastic occurrences, and elevated frequency of autoimmune diseases with aging. However, as the bacteria in the oral microbiome that contribute to the chronic infection of periodontitis is acquired earlier in life, the characteristics of the innate and adaptive immune systems to regulate these members of the autochthonous microbiota across the lifespan remains ill defined.

Recent findings: Clear data demonstrate that both cells and molecules of the innate and adaptive immune response are adversely impacted by aging, including in the oral cavity, yielding a reasonable tenet that the increased periodontitis noted in aging populations is reflective of the age-associated immune dysregulation. Additionally, this facet of host-microbe interactions and disease needs to accommodate the population variation in disease onset and progression, which may also reflect an accumulation of environmental stressors and/or decreased protective nutrients that could function at the gene level (ie. epigenetic) or translational level for production and secretion of immune system molecules.

Summary: Finally, the majority of studies of aging and periodontitis have emphasized the increased prevalence/severity of disease with aging, all based upon chronological age. However, evolving areas of study focusing on "biological aging" to help account for population variation in disease expression, may suggest that chronic periodontitis represents a co-morbidity that contributes to "gerovulnerability" within the population.

Keywords: aging; environment; immunology; nutrition; periodontitis.

Conflict of interest statement

Conflict of Interest All authors declare no conflicts of interest.

Figures

Figure 1:
Figure 1:
Schematic of interactions of genetics and host responses that contribute to age-associated diseases (originally published in [159]).
Figure 2:
Figure 2:
Schematic of the host-microbe interactions in periodontitis. Includes identification of both modifiable (eg. smoking, diabetes, etc.) and non-modifiable (eg. sex, race/ethnicity, age) factors that could modulate the oral microbiome and host response to the microbiome components. Also, of note is the potential that aging substantively affects the modifiable components, as well as the composite interactions of aging in controlling responses and disease expression related to sex and race/ethnicity across the population (modified from [159]).
Figure 3:
Figure 3:
(A) Proposed antigenic diversity of P. gingivalis within the human population, reflected by individual differences in antibody response profiles to specific P. gingivalis strains. Additionally, the impact of age (in years) on these response patterns is shown. The bars denote group means from ≤35 years (n=87), 36–50 years (n=151) and >50 years (n=58) subjects and the vertical practice describe 1 SEM for the groups. The lines denote significant differences at p<0.05. The P. gingivalis strains are: ATCC33277, FCD381, W50, W83, A7A1–28, and A7436. (B) Levels of selected nutrients in blood of subjects >65 years of age derived from the NHANES 1999–2004 dataset. Periodontitis was defined as a site with clinical attachment loss (CAL) ≥3 mm and a periodontal pocket ≥4 mm. NHANES (1999–2004) used the partial-mouth periodontal examination protocol to sample teeth and sites [–183]. The protocols randomly selected two quadrants of the mouth and specified 2 to 3 sites per tooth for measurement of pocket depth, attachment loss, and bleed on probing. In 1999–2000, two sites per tooth (mid-facial and mesio-facial) were measured, while three sites per tooth (mid-facial, mesio-facial and distal) were measured in 2001–2002 and 2003–2004. The bars denote group means [Normal (no periodontitis), n=1019–1453; Perio, n=133–220] and the vertical brackets enclose 1 SEM. The asterisk (*) denote significant differences at p<0.05. (C) Measured telomere length compared to standard reference DNA [Mean telomere length relative to standard reference DNA (T/S) ratio; https://wwwn.cdc.gov/Nchs/Nhanes/2001-2002/TELO_B.htm]. The points denote group mean levels and the vertical brackets enclose 1 SEM. The asterisk (*) denote significant differences at p<0.05.

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