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GWAS Study

Genome-wide association study of biologically informed periodontal complex traits offers novel insights into the genetic basis of periodontal disease.

Offenbacher S, Divaris K, Barros SP et al.

26962152 PubMed ID
GWAS Study Type
975 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

OS
Offenbacher S
DK
Divaris K
BS
Barros SP
MK
Moss KL
MJ
Marchesan JT
MT
Morelli T
ZS
Zhang S
KS
Kim S
SL
Sun L
BJ
Beck JD
LM
Laudes M
MM
Munz M
SA
Schaefer AS
NK
North KE
Chapter II

Abstract

Summary of the research findings

Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria alone have had modest success to-date. Here, we refine the CP phenotype by supplementing clinical data with biological intermediates of microbial burden (levels of eight periodontal pathogens) and local inflammatory response (gingival crevicular fluid IL-1β) and derive periodontal complex traits (PCTs) via principal component analysis. PCTs were carried forward to GWAS (∼2.5 million markers) to identify PCT-associated loci among 975 European American adult participants of the Dental ARIC study. We sought to validate these findings for CP in the larger ARIC cohort (n = 821 participants with severe CP, 2031-moderate CP, 1914-healthy/mild disease) and an independent German sample including 717 aggressive periodontitis cases and 4210 controls. We identified six PCTs with distinct microbial community/IL-1β structures, although with overlapping clinical presentations. PCT1 was characterized by a uniformly high pathogen load, whereas PCT3 and PCT5 were dominated by Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. We detected genome-wide significant signals for PCT1 (CLEC19A, TRA, GGTA2P, TM9SF2, IFI16, RBMS3), PCT4 (HPVC1) and PCT5 (SLC15A4, PKP2, SNRPN). Overall, the highlighted loci included genes associated with immune response and epithelial barrier function. With the exception of associations of BEGAIN with severe and UBE3D with moderate CP, no other loci were associated with CP in ARIC or aggressive periodontitis in the German sample. Although not associated with current clinically determined periodontal disease taxonomies, upon replication and mechanistic validation these candidate loci may highlight dysbiotic microbial community structures and altered inflammatory/immune responses underlying biological sub-types of CP.

394 European American individuals with periodontal health, 389 European American individuals with mild-moderate periodontitis, 192 European American individuals with severe periodontitis

Chapter III

Study Statistics

Key metrics and study information

975
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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