Abstract
The study is aimed at assessing the impact that periodontal disease and chronic hepatitis C could have on gingival crevicular fluid levels of the NLRP3 inflammasome, caspase-1 (CASP-1), and interleukin-18 (IL-18) and at evaluating whether the increased local inflammatory reaction with clinical periodontal consequences is correlated to their upregulation. Patients were divided into four groups, according to their periodontal status and previously diagnosed hepatitis C, as follows: (i) CHC group, chronic hepatitis C patients; (ii) P group, periodontal disease patients, systemically healthy; (iii) CHC + P group, patients suffering from both conditions; and (iv) H group, systemically and periodontally healthy controls. Gingival crevicular samples were collected for quantitative analysis of the NLRP3 inflammasome, CASP-1, and IL-18. CHC + P patients expressed the worse periodontal status and the highest NLRP3, CASP-1, and IL-18 levels, the difference being statistically significant (p < 0.05). The P group patients also expressed significantly more elevated NLRP3, CASP-1, and IL-18 levels, as compared to nonperiodontal patients (CHC and H groups). Chronic hepatitis C and periodontal disease could have a significant influence on the upregulation of NLRP3 inflammasome and its components, possibly contributing to an increased local inflammatory reaction and clinical periodontal consequences.
Highlights
Recent research on the complex molecular mechanisms of the inflammatory reaction has led to the development of the “inflammasome” concept, a multiprotein, oligomer compound, governing inflammation in its early stages [1, 2]
The NLRP3 complex, has a crucial role in innate immunity and inflammatory mechanisms [3, 4]. It consists of a Nod-like receptor (NLR) that mediates the activation of protease enzymes (Caspase 1 (CASP-1)) and further regulates the expression of pioneer, key, proinflammatory cytokines, such as interleukin-18 (IL-18) [3]
In the hepatitis C patients, there was a similar level of liver fibrosis, with no significant difference (p > 0:05)
Summary
Recent research on the complex molecular mechanisms of the inflammatory reaction has led to the development of the “inflammasome” concept, a multiprotein, oligomer compound, governing inflammation in its early stages [1, 2]. One of these inflammasomes, the NLRP3 complex, has a crucial role in innate immunity and inflammatory mechanisms [3, 4]. The study of this particular inflammasome (NLRP3) and its components (CASP-1 and IL-18) was chosen as a focus point of our research, considering the promising results of its assessment as a potential biomarker for the periodontal clinical status [2] and its upregulation in periodontal patients with uncontrolled type 2 diabetes [6, 8, 11]
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