Antagonistic effect of IL1 variants in periodontitis and external apical root resorption: Evidence from a literature review.

Arch Oral Biol

Medical Genetics Department, Faculty of Medicine, University of Coimbra, Av. Bissaya Barreto, Bloco de Celas, Coimbra 3000-075, Portugal; CIMAGO (Center of Investigation on Environmental, Genetics and Oncobiology), Faculty of Medicine, University of Coimbra, Av. Bissaya Barreto, Bloco de Celas, Coimbra 3000-075, Portugal. Electronic address:

Published: November 2018

External apical root resorption (EARR) induced by orthodontic treatment and chronic periodontitis (CP) are complex phenotypes dependent on the interaction of multiple genetic and non-genetic risk factors. Apart from different environmental triggers, these phenotypes are caused by antagonistic biological mechanisms involving local immunoinflammatory reaction and alveolar bone metabolism, for which IL1 have a prominent role. Whereas EARR benefits from bone remodelling, CP is characterized by osteolytic damaged. Our aim was to verify if these two phenotypes have opposite genetic profiles, considering the most frequently analysed polymorphisms for both diseases. A review of the literature was performed searching for the association of rs1800587 from Interleukin-1 alpha (IL1A) gene and rs1143634 from interleukin-1 beta (IL1B) gene with EARR and CP. The electronic search included MEDLINE/PubMed, EBSCOhost, Cochrane and Web of Science databases. Twenty four articles met the inclusion and exclusion criteria. For IL1B polymorphism, two out of seven studies found a significant statistical association between EARR and CC genotype, whether for CP, there were eighth out of fifteen references describing a statistically significant associations with T allele. For IL1A variant, no significant association with EARR was described. In conclusion, literature review suggests that for IL1B SNP rs1143634, EARR and CP have an opposite genetic profile. For IL1A SNP, our hypothesis could not be confirmed.

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Source
http://dx.doi.org/10.1016/j.archoralbio.2018.08.006DOI Listing

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