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Clin Oral Investig ; 25(3): 1291-1297, 2021 Mar.
Article in English | MEDLINE | ID: mdl-32594309

ABSTRACT

BACKGROUND AND OBJECTIVES: Treg and TH17 cells influence the inflammatory process in periodontal diseases and could also play in a similar pattern, an essential role in immune-inflammatory mechanisms involved in the destruction of the peri-implant tissues, peri-implantitis. Therefore, this study evaluated the levels of RORγT and FOXP3 gene expression in subjects with peri-implantitis and healthy peri-implant tissues. METHODS: A total of 35 subjects with implant-supported restorations in both diseased and healthy clinical conditions (n = 15 healthy; n = 20 peri-implantitis) were included in this study. Peri-implantitis was defined as probing depth > 5 mm, bleeding on probing and/or suppuration, and peri-implant bone loss >4 mm. Peri-implant tissue biopsies were collected for analysis of the mRNA, RORγT, and FOXP3 expression levels. The samples were submitted to total RNA extraction, treatment with DNAse, and cDNA synthesis. Subsequently, real-time PCR reaction was performed to evaluate the levels of RORγT and FOXP3 gene expression to the reference gene. These were analyzed by the non-parametric Mann-Whitney method with a level of significance of 5%. RESULTS: Higher gene expression levels of the transcription factors RORγT and FOXP3 were detected in the tissues affected by peri-implantitis when compared with healthy tissues (p < 0.05). CONCLUSIONS: The present study demonstrated the possible existence of a hybrid TH17-Treg profile, based on the gene expression of transcription factors inducing differentiation of these cells. Further studies must be designed to gain a better understanding of the immunological mechanisms involved in the pathogenesis of peri-implantitis. CLINICAL RELEVANCE: The levels of RORγT and FOXP3 transcription factors that were linked to cells with the FOXP3+RORγT+ phenotype could be used as a predictor of peri-implantitis progression.


Subject(s)
Dental Implants , Peri-Implantitis , Humans , Immunity , T-Lymphocytes, Regulatory , Th17 Cells
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