AI Article Synopsis

  • Chronic periodontitis (CP) is a serious global issue linked to bone loss, associated with oral dysbiosis and an imbalance in inflammatory gene responses.
  • This research focused on the role of interleukin 10 (IL-10) gene polymorphisms in patients with CP, analyzing samples from 96 Caucasian individuals from Italy.
  • The findings revealed a connection between IL-10 gene variants and other inflammatory genes, highlighting the need for further research to enhance diagnosis and treatment strategies for periodontal disease.

Article Abstract

Chronic periodontitis (CP) is a complex pathology with a significant impact worldwide causing bone loss. Oral dysbiosis is a highly inflammatory condition associated to a long-term insulting infection and represents an underestimated CP key factor associated with an imbalance of pro-inflammatory and anti-inflammatory gene responses. The presence of a single nucleotide polymorphisms (SNPs) in the promoter region of interleukin 10 (IL-10) gene-1082, -819, and -592 was a possible determinant cause. This translational research aimed to provide outcomes on the role of IL-10 gene expression in bone loss diseases in patients affected by CP. Caucasian patients ( = 96) affected by CP were recruited from the Italian population. The subgingival samples were collected using the Bacterial Periodontal Assessment by Biomolecular Diagnostic and the characterization of a set of 15 bacterial DNA responsible of periodontitis was performed by real-time multiplex PCR. In addition, two viruses, Epstein-Barr Virus (EBV) and Herpes Simplex Virus 1 (HSV-1), and a pathogenic fungi () were included as a part of our panel. Our results confirmed an existing association between IL-10 gene polymorphisms and polymorphism of tumor necrosis factor alpha (TNFα), interleukin 1α-β-RN (IL-1α-β-RN), collagen type-l alpha (COLIA1), and vitamin D receptor (VDRs) genes in CP. Further studies are needed to improve diagnosis and endorse more effective therapeutic procedures for periodontal disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7277173PMC
http://dx.doi.org/10.3390/biomedicines8050115DOI Listing

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