Association of Polymorphism in IL-18 Gene with Periodontitis in Uyghur Adults in Xinjiang and Evidence from Six Case‐Control Studies with a Comprehensive Analysis

Shan, Chao; Ma, Ting; Wang, Ting Ting; Wu, Long; Abasijiang, Aisaiti; Jin, Zhao

doi:10.1080/08820139.2020.1841222

Cited by 11 publications

(5 citation statements)

References 32 publications

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“…Severe acute respiratory syndrome coronavirus may also aggravate periodontal pocket formation by enhancing the expression of pro-inflammatory cytokines, including IL-1b, and the dissemination of periodontal pathogens, and increased IL-1b release may exacerbate coronavirus disease 2019 lung infection (219,220). Likewise, IL18 polymorphisms are associated with susceptibility to periodontitis, and increased IL-18 levels in chronic periodontitis may positively correlate with periodontal destruction (153,(221)(222)(223).…”

Section: Inflammasomes In Periodontitismentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

Ling

Jiang

2021

Front. Immunol.

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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Section: Inflammasomes In Periodontitismentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

Ling

Jiang

2021

Front. Immunol.

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“…The results by Tanaka et al [ 26 ] suggest the association between the IL-18 promoter rs1946518 polymorphism and periodontitis in young Japanese women. Shan et al have found the association between IL-18 gene polymorphisms and susceptibility to periodontitis in a Uyghur population [ 27 ]. In a Brazilian population, an association was found between IL-18 (rs187238 and rs1946518) and chronic periodontitis [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

IL-18 Gene rs187238 and rs1946518 Polymorphisms and Expression in Gingival Tissue in Patients with Periodontitis

et al. 2022

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Periodontitis is a chronic disease with disturbed balance between the immune and inflammatory response of the host to bacteria. Many studies have shown that proinflammatory cytokines play a significant role in the pathogenesis of periodontal disease. In this study, we examined the association between the IL-18 gene rs187238 and rs1946518 polymorphisms and periodontitis in non-smoking and smoking patients. This study enrolled 200 patients with periodontitis (130 non-smokers and 70 smokers) and 156 control subjects (124 non-smokers and 32 smokers). There were no statistically significant differences in the distribution of the rs187238 and rs1946518 IL-18 genotypes and alleles between patients with periodontitis and control subjects, between smoking patients with periodontitis and smoking control subjects, and between non-smoking patients with periodontitis and non-smoking control subjects. There were no statistically significant differences in clinical parameters in relation to the IL18 rs187238 genotypes. In patients with the IL18 rs1946518 GG genotype, we observed increased values of bleeding on probing (BoP) and periodontal probing depth (PPD), compared to subjects with the TT genotype. In patients with periodontitis, we observed statistically significant decreased expression of the IL-18 gene in comparison with healthy subjects (0.231 ± 0.163 vs. 0.663 ± 0.197, p = 0.0008). In addition, the IL-18 gene expression in gingival tissue in patients with periodontitis correlated positively with the number of remaining teeth. The results of our study suggest that the IL-18 rs187238 and rs1946518 polymorphisms are not significant risk indicators of periodontitis in our population. However, in patients with the IL18 rs1946518 GG genotype, we observed increased values of BoP and PPD, compared to subjects with the TT genotype. In addition, in gingival tissue of patients with periodontitis, we have detected decreased expression of IL-18. The gingival expression of IL-18 in patients with periodontitis correlated positively with number of remaining teeth. The above results suggest that IL-18, in addition to its pro-inflammatory effects in periodontal disease, may also exhibit protective properties.

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“…The most periodontitis-related SNPs have been studied in the Toll-like receptor-2 (TLR-2) [16], TLR-4 [17], Fc-γ receptor (FCGR2A) [18], interleukin-1 (IL-1) [19][20][21], IL-4 [22], IL-6 [23][24][25], IL-10 [23,26], IL-18 [27,28], vitamin D receptor [11,29], tumor necrosis factor alpha (TNFA) [30][31][32], matrix metalloproteinase (MMP) [33,34], and cyclo-oxygenase-2 (COX-2) [35].…”

Section: Periodontitis-related Genetic Variation 21 Snps In Inflammat...mentioning

confidence: 99%

Epigenetics and Stem Cells Applications in Periodontal Therapy

Kafa

2024

Recent Advances and Future Perspectives in Periodontology [Working Title]

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While periodontitis is closely linked with pathogen outgrowth, many patients have the risk of recurrence after therapy. Variations of inflammatory genes are associated with an increased susceptibility of periodontitis. Epigenetics can regulate these gene expression. In this chapter, we will highlight on the potential role of epigenetic changes in different facets, more particularly in genes involved in inflammation. Epigenetics act through remodeling of chromatin and can selectively activate or inactivate genes, determining their expression. Epigenetics could play an essential role in understanding the mechanism of gene-environment interactions, and the factors which stimulate periodontitis and reduce its response to therapy are now the subject of many studies. Also, mesenchymal stem cells (MSCs) are a promising source to regenerate periodontal tissues. They could be a good alternative to the adopted therapies, ignoring the artificial biomaterial limitations. They could be considered as a natural process for periodontium regeneration and has an immunomodulatory role to resolute the infection. For this reason, it is necessary to investigate and evaluate MSCs applicability in humans, and their clinical approach involved in regeneration of periodontal tissues.

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Association of Polymorphism in IL-18 Gene with Periodontitis in Uyghur Adults in Xinjiang and Evidence from Six Case‐Control Studies with a Comprehensive Analysis

Cited by 11 publications

References 32 publications

Inflammasomes in Alveolar Bone Loss

Inflammasomes in Alveolar Bone Loss

IL-18 Gene rs187238 and rs1946518 Polymorphisms and Expression in Gingival Tissue in Patients with Periodontitis

Epigenetics and Stem Cells Applications in Periodontal Therapy

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