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Potential role of TP 63 in apical periodontitis development
Author(s) -
Souza L. C.,
Crozeta B. M.,
Guajardo L.,
Brasil da Costa F. H.,
SousaNeto M. D.,
Letra A.,
Silva R. M.
Publication year - 2019
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.13133
Subject(s) - single nucleotide polymorphism , periodontitis , medicine , haplotype , radicular cyst , genotyping , pathology , allele , genotype , biology , genetics , cyst , gene
Aim To investigate the expression of TP 63 in apical periodontitis ( AP ) tissues and the association of single nucleotide polymorphisms ( SNP s) in the TP 63 gene with AP using a case‐control dataset. Methodology Expression of TP 63 in human AP lesions (apical abscess, radicular cyst, periapical granuloma) was evaluated using immunohistochemistry. A case‐control association study was performed to assess the association of TP 63 polymorphisms in individuals having AP with or without associated pain. Cases were defined as subjects with deep caries and AP ( n = 151) and subjects with symptomatic apical periodontitis or acute apical abscess ( n = 124). Subjects without AP ( n = 169) and asymptomatic ( n = 196) were used as controls, respectively. Saliva samples were collected as source of genomic DNA . Twelve SNP s in the TP 63 gene were selected for genotyping using Taqman chemistry in real‐time PCR . Data analysis was performed using PLINK software. The Bonferroni method was applied to correct for multiple testing; α ≤ 0.004 indicates significant differences between groups. Results TP 63 expression was evident in apical abscesses and radicular cysts, while weaker expression was observed in periapical granulomas. Positive expression was observed in mononuclear cells in the granulation tissues of all AP lesions. Regarding the presence of AP , a trend for allelic association was observed for rs16864812 and rs9810322 ( P = 0.04) and rs9810322 genotypes were also nominally associated with AP under a dominant model ( P = 0.04). When considering the presence of periapical pain, a trend for allelic and genotypic association was observed for rs10155037 ( P = 0.03). Haplotypes were also associated with AP and periapical pain ( P ≤ 0.05). Conclusions Apical periodontitis is a complex multifactorial condition and it is likely that multiple genes and environmental effects may influence its susceptibility, progression or both. TP 63 variants may play a role in AP pathogenesis and susceptibility, individually or interactively with other genes. Additional studies in other populations and functional studies are needed to improve understanding of the role of TP 63 in AP .