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J Endod. 2011 Apr;37(4):455-9. doi: 10.1016/j.joen.2011.01.009.

Genetic predisposition to persistent apical periodontitis.

Author information

1
American Board of Endodontics, Case Western Reserve School of Dental Medicine, Cleveland, Ohio, USA.

Erratum in

  • J Endod. 2011 Jun;37(6):887.

Abstract

INTRODUCTION:

The proinflammatory cytokine interleukin (IL)-1 is a key regulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. Allele2 of IL-1β is associated with a four-fold increase in IL-1β production. The aim of this case-control study was to evaluate the gene polymorphism of IL-1β in the pathogenesis of endodontic failure. We hypothesized that the gene polymorphism (allele2 of IL-1β) would influence host response and enhance inflammatory reactions predisposing to persistent apical periodontitis (PAP).

MATERIALS AND METHODS:

Subjects with at least 1 year of follow-up after root canal therapy (RCT) were recalled. Inclusion and exclusion criteria were applied, and 34 subjects with signs/symptoms of PAP with otherwise acceptable RCT were included. Sixty-one controls showed healing with acceptable RCT. Genomic DNA from buccal mucosa was amplified by polymerase chain reaction followed by restriction fragment length polymorphism to distinguish the alleles of IL-1β gene polymorphism.

RESULTS:

A significant difference in the distribution of the polymorphic genotype among cases (70.6%) and controls (24.6%) (P < .001, Pearson χ(2)) was shown.

CONCLUSIONS:

These findings suggest that specific genetic markers associated with increased IL-1β production may contribute to increased susceptibility to PAP.

PMID:
21419289
PMCID:
PMC3845962
DOI:
10.1016/j.joen.2011.01.009
[Indexed for MEDLINE]
Free PMC Article

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