Association of Functional Gene Polymorphism with Apical Periodontitis

• Does individual genetic makeup play a role in apical periodontitis? Gene polymorphism has been suggested to result in differences in cellular expressions that resulted in inflammation, and, thus, the aim of this systematic review was to evaluate if such relationship exists.
• The qualities of the included studies were evaluated according to a modified suggested guideline specific for quality assessment scale for genetic association studies by Nibali.
• Eight articles were identified, and the results of the present review suggest that although some authors have reported that some biologic markers may play a role in apical periodontitis, others have not supported this association.
• Limitations were noted in the current studies by not judiciously matching selected case/control groups, balancing or adjusting for confounders (such as smoking, diabetes, and body mass index), using the Hardy-Weinberg Equilibrium, providing power calculation for a given sample size, correcting for false-positive (type I) error, or providing odds ratios with confidence intervals.
• The results of this review suggest polymorphism and biological modifiers by which some individuals, if challenged by bacterial accumulations, may have a more vigorous immunoinflammatory response, leading to apical periodontitis. More research in this area is warranted.

IntroductionTo date, only a few studies have searched for relationships between genetic polymorphism and periapical microbial infection. Thus, the purpose of this systematic review was to evaluate the relationship between host modifying factors and their association with apical periodontitis.MethodsTwo reviewers independently conducted a comprehensive literature search. The MEDLINE, Embase, Cochrane, and PubMed databases were searched. Additionally, the bibliographies of all relevant articles and textbooks were manually searched.ResultsEight articles were identified and included in this review. The results of the present review suggest that although some authors have reported that some biologic markers may play a role in apical periodontitis, others have not supported this association. Limitations were noted in the current studies by not judiciously matching selected case/control groups, balancing or adjusting for confounders (such as smoking, diabetes, and body mass index), using the Hardy-Weinberg Equilibrium, providing power calculation for a given sample size, correcting for false-positive (type I) error, or providing odds ratios with confidence intervals. The results of this review suggest polymorphism and biological modifiers, by which some individuals, if challenged by bacterial accumulations, may exhibit a more vigorous immunoinflammatory response, leading to apical periodontitis.ConclusionsMore research in this area is warranted to determine greater specificity in these possible interactions.