Assessment of NLRP3 Gene Polymorphisms with Periodontitis as Compared with Healthy Periodontium in Iraqi Arabs Patients

Abstract

Objectives The nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome regulates the maturation and release of the cytokines as well as the activation of caspase in response to danger signals derived from pathogenic infection, tissue damage, andmetabolic changes that have a role in the pathogenesis of different diseases as periodontitis. Yet, the susceptibility to this illness could be determined by population-based genetic differences. The aim of this study was to determine whether periodontitis in Arab populations from Iraq is correlated with NLRP3 gene polymorphisms and measure clinical periodontal parameters and investigate their association with genetic polymorphisms of the NLRP3. Materials and Methods The study sample consisted of 94 participants ranging from 30 to 55 years old, both males and females who fulfilled the study's criteria. The selected participants were divided into two groups: the periodontitis group (62 subjects) and the healthy control group (32 subjects). The examination of clinical periodontal parameters of all participants was carried out, followed by a collection of venous blood for NLRP3 genetic analysis using the polymerase chain reaction–sequencing technique. Results The genetic analysis of NLRP3 genotypes at four single nucleotide polymorphisms (SNPs) (rs10925024, rs4612666, rs34777555, and rs10754557), by Hardy–Weinberg equilibrium, identified nonsignificant differences in studied groups. The C-T genotype among periodontitis was significantly different from controls, while the C-C genotype among control was significantly different from periodontitis at NLRP3 rs10925024. Overall, there were 35 SNPs in the periodontitis group and 10 SNPs in the control group for rs10925024 with significant differences versus nonsignificant differences of the other SNPs between the studied groups. Clinical attachment loss and NLRP3 rs10925024 additionally demonstrated a significant positive correlation in the periodontitis subjects. Conclusion The findings suggested that polymorphisms of the NLRP3 gene may have a role and increasing the genetic susceptibility to periodontal disease in Arabs Iraqi patients.

Diagnostic biomarkers for periodontitis (observational case-control study)

“…Related to higher levels of IL-1, IL-6, IL-8, IL-10, TNF-alpha, granulocyte colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor, which produce bone resorption in alveolar bone, activate mature osteoclasts, control bone cell proliferation, and induce osteoclasts (21,22) , destroying collagen, in particular type 1 collagen, the main form of collagen in bones (23) . This has coincided with studies done by Juluri et al (24) for PPD, Gondim et al (25) for CAL and Mahmood (26) for PPD and CAL.…”

Salivary Fractalkine Differentiating Periodontitis from Periodontally Healthy Subjects

“…Yet, there is no study investigating the concentrations of CX3CL1 and CX3R1 in saliva about periodontitis with different severities as well as different progression rates, nonetheless, similar results were obtained for both biomarkers investigated in (GCF) and the serum was obtained from patients with periodontitis [ 2 , 24 ]. Accordingly, the severity of periodontal disease may thus affect salivary CX3CL1 and its receptors.…”

“…Complex etiopathogenesis is thought to underlie damaging inflammatory diseases such as periodontitis [ 1 ]. Hence, periodontal disease is believed to arise from a range of interactions between the biofilm found in the pathogenic periodontal pockets and the immune-inflammatory responses of the host [ 2 ]. An inflammation-specific attraction of immune cells to the affected area occurs in the context of response to periodontal inflammation, which is mediated by different cytokine patterns [ 3 ].…”

The Potential Role of Reactive Oxygen Species Produced by Low-Density Neutrophils in Periodontitis

“…Periodontitis is a multifactorial progressive condition characterized by continuous destruction of periodontal tissue under the burden of a dysbiotic microflora, host immune response, environmental factors, and subject genetic suscep-tibly. 1,2 Periodontitis encompasses the existence of inflammation in the periodontal tissues, the development of periodontal pockets, a breakdown of connective tissue, alveolar bone loss, and potential tooth loss. [3][4][5][6][7] Despite their beneficial role in eradicating pathogens, inflammation is a double-edged sword; it is considered a crucial source of periodontal tissue destruction, involving leukocytes, complement, and reactive oxygen species (ROS).…”