Friday, March 23, 2012: 10:45 a.m. - 12:15 p.m.
Presentation Type: Oral Session
A paradigm in Periodontology is that periodontal disease increases in prevalence and severity with age. However, whether periodontitis is a “disease of aging” or an “aging-associated disease” remains to be delineated through more robust molecular studies of the disease during aging. Objectives: To determine the transcriptome of genes related to antigen presentation and adaptive immunity in health and periodontitis gingival tissues from Macaca mulatta across the lifespan Methods: 20 periodontally healthy M. mulatta from 3-25 years of age (5/group: young (Y) <3 yo; adolescent (AL): 3-7 yo; adult (AD): 12-15 yo; aged (AG): >17 yo) and 10 animals with periodontitis (5/group adult and aged) provided gingival tissue specimens. Gene expression was measured using the GeneChip® Rhesus Macaque Genome Array. The transcriptome was mapped to the antigen presentation pathways KEGG database for ontology comparison across the different age groups. Results: In healthy tissues, MHC I-related genes were over-expressed in both AL and AG groups (AL>AG) compared with Y and AD groups, and MHC II pathway genes were up-regulated in the AG with respect to Y and AL animals. Of note, few changes were observed in gene expression related to CD4 and CD8 T cell markers with age; although expression of the killer cell immunoglobulin receptor (KIR) related to increasing NK cell regulatory potential in these tissues was observed. In general, the over-expression of antigen presentation-related genes during periodontitis appeared fairly similar in both adult and aged animals. Interestingly, genes related to both CD8 and NK cell antigen recognition were only elevated in the aged animals with periodontitis. Conclusions: These results suggest that altered gene expression profiles related to antigen presentation pathways were noted in adolescent and aged periodontitis tissues that could reflect a susceptibility to a more aggressive gingival inflammatory response and potential for tissue destruction at these ages.This abstract is based on research that was funded entirely or partially by an outside source: NIH P20 RR020145
Keywords: Aging, Gene expression, Immune response and Periodontal disease
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