Association of DNA sequence-independent genetic regulatory mechanisms with apical periodontitis: A scoping review

Arch Oral Biol. 2020 Jul:115:104737. doi: 10.1016/j.archoralbio.2020.104737. Epub 2020 Apr 29.

Abstract

Objective: Different studies in the last decade have proposed that gene expression alterations that are independent of the DNA sequence may also play an important role in periapical disease. The present study aimed to assess the available evidence supporting a relationship between these alterations and apical periodontitis through a scoping review.

Design: Specific strategies were developed for different databases (MEDLINE via PubMed, Cochrane Library, Scopus, Web of Science, and Virtual Health Library) and a search performed by March 1st, 2019. The evidence sources were selected according to the eligibility criteria and underwent a critical appraisal of methodological quality.

Results: The initial search retrieved 212 references, with eight eligible articles after the removal of replicates and application of exclusion criteria. Five studies identified altered DNA methylation on inflammatory response genes (FOXP3, CXCL3, FADD, MMP2, MMP9, IFNG, IL4, IL12) on AP patients. Three others identified the alterations on the expression of several microRNAs (miR-29b, 106b, 125b, 143, 146a, 155, 198) during AP. No evidence was identified regarding mechanisms of histone methylation, or of epigenetic heritability or stability.

Conclusions: There is available evidence for the involvement of different genetic regulatory mechanisms independent of changes in DNA sequence in the development or severity of apical periodontitis. However, due to methodological limitations, further research must be performed before novel therapies and diagnostic tools for AP may arise from these data.

Keywords: Epigenomics; Periodontitis; Scoping review.

Publication types

  • Review

MeSH terms

  • Base Sequence
  • DNA Methylation
  • Gene Expression Regulation*
  • Humans
  • MicroRNAs* / genetics
  • Periapical Periodontitis* / genetics

Substances

  • MicroRNAs