Association of chronic periodontitis and type 2 diabetes mellitus with salivary Del-1 and IL-17 levels

Saxena, Somil; Venugopal, Ranganath; Rao, Rachana; Yuwanati, Monal; Awasthi, H.; Jain, Megha

doi:10.1016/j.jobcr.2020.08.013

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…The level of IL-17A increased successively in saliva of healthy control group, T2DM patients and T2DM patients with chronic periodontitis, suggesting that the increase of IL-17A is one of the risk factors of chronic periodontitis in T2DM patients ( 104 , 105 ). IL-17A is also a risk factor for diabetic retinopathy in T2DM ( 106 , 107 ).…”

Section: Role Of Il-17a In the Relationship Between Periodontitis And...mentioning

confidence: 99%

Role of Interleukin-17A in the Pathomechanisms of Periodontitis and Related Systemic Chronic Inflammatory Diseases

Feng

Chen

et al. 2022

Front. Immunol.

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Periodontitis is a chronic inflammatory and destructive disease caused by periodontal microbial infection and mediated by host immune response. As the main cause of loosening and loss of teeth in adults, it is considered to be one of the most common and serious oral diseases in the world. The co-existence of periodontitis and systemic chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, inflammatory bowel disease, diabetes and so on is very common. It has been found that interleukin-17A (IL-17A) secreted by various innate and adaptive immune cells can activate a series of inflammatory cascade reactions, which mediates the occurrence and development of periodontitis and related systemic chronic inflammatory diseases. In this work, we review the role of IL-17A in the pathomechanisms of periodontitis and related systemic chronic inflammatory diseases, and briefly discuss the therapeutic potential of cytokine targeted agents that modulate the IL-17A signaling. A deep understanding of the possible molecular mechanisms in the relationship between periodontitis and systemic diseases will help dentists and physicians update their clinical diagnosis and treatment ideas.

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Section: Role Of Il-17a In the Relationship Between Periodontitis And...mentioning

confidence: 99%

Role of Interleukin-17A in the Pathomechanisms of Periodontitis and Related Systemic Chronic Inflammatory Diseases

Feng

Chen

et al. 2022

Front. Immunol.

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“…In ammation and in ammatory cell in ltration in chronic periodontitis and experimental periodontitis have been reported in many studies to increase IL-17 levels [14][15][16][17][18][19]. In particular, studies on autoimmune diseases such as psoriatic arthritis and rheumatoid arthritis have shown that secukinumab reduces IL-17 [20][21][22][23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Effects of IL-17 Inhibition with Secukinumab in Experimental Periodontitis

Taskin,

Aydinyurt,

Sancak

et al. 2023

Preprint

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Objective IL-17 plays a key role in the pathogenesis of periodontitis and systemic inflammatory diseases. This study investigates the effect of secukinumab, an IL-17 inhibitor, on the development of periodontal disease in a rat model of experimental periodontitis. Materials and Methods Experimental periodontitis was induced in rats by suturing silk around the mandibular first molar tooth (n = 32). After inducing periodontitis with ligature, the animals were divided into two groups: experimental and control. In the experimental group secukinumab was given intraperitoneally. The experiment was terminated 14 days after the induction of experimental periodontitis. Alveolar bone loss (ABL) was measured from microscope images, and the level of inflammatory cell infiltration (ICI) was analyzed by hematoxylin-eosin staining. IL-17, nuclear factor kappa B ligand receptor activator (RANKL), osteoprotegrin (OPG) levels and RANKL/OPG ratio were evaluated by immunohistochemistry. Results In the development process of experimental periodontitis, it was observed that the IL-17 inhibitor secukinumab decreased IL-17 levels, ABL, ICI and RANKL/OPG ratio (p < 0.05); and increased OPG levels (p < 0.05). No statistically significant effect of secukinumab application was observed on RANKL levels (p > 0.05). Conclusion The results obtained from this study suggested that inhibition of IL-17 with secukinumab slows down the development of periodontitis and IL-17 plays a key role as a pro-inflammatory cytokine in periodontitis pathogenesis. Clinical Relevance: This study is the first to examine the effect of secukinumab on periodontal tissues, despite of its limitations. It sheds light on the role of IL-17 in periodontal inflammation in experimental periodontitis.

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“…IL-17 and IL-23 are pro-inflammatory cytokines that can cause dysbiosis in bacterial communities and are associated with leukocyte adhesion ( Abusleme and Moutsopoulos, 2017 ). IL-17 and Del-1 have exhibited an antagonistic relationship in inflammatory effects ( Saxena et al., 2020 ; Hajishengallis and Chavakis, 2021a ). In addition, they have been observed to play a critical role in the loss of pancreatic B cells and have been shown to have pro-diabetic effects ( Mensah-Brown et al., 2006 ; Marwaha et al., 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Periodontitis induced by Porphyromonas gingivalis drives impaired glucose metabolism in mice

Kang

Zhang

Xue

et al. 2022

Front. Cell. Infect. Microbiol.

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Periodontitis has been demonstrated to be bidirectionally associated with diabetes and has been recognized as a complication of diabetes. As a periodontal pathogen, Porphyromonas gingivalis is a possible pathogen linking periodontal disease and systemic diseases. It has also been found to be involved in the occurrence and development of diabetes. In this study, 6-week-old male C57BL/6 mice were orally administered the P. gingivalis strain ATCC381 for 22 weeks. Histological analysis of the gingival tissue and quantified analysis of alveolar bone loss were performed to evaluate periodontal destruction. Body weight, fasting glucose, glucose tolerance test (GTT), and insulin tolerance test (ITT) were used to evaluate glucose metabolism disorder. We then analyzed the expression profiles of inflammatory cytokines and chemokines in gingival tissue, the liver, and adipose tissue, as well as in serum. The results showed that mice in the P. gingivalis-administered group developed apparent gingival inflammation and more alveolar bone loss compared to the control group. After 22 weeks of P. gingivalis infection, significant differences were observed at 30 and 60 min for the GTT and at 15 min for the ITT. P. gingivalis-administered mice showed an increase in the mRNA expression levels of the pro-inflammatory cytokines (TNF-α, IL-6, IL-17, and IL-23) and chemokines (CCL2, CCL8, and CXCL10) in the gingiva and serum. The expression levels of the glucose metabolism-related genes were also changed in the liver and adipose tissue. Our results indicate that oral administration of P. gingivalis can induce changes in the inflammatory cytokines and chemokines in the gingiva and blood, can lead to alveolar bone loss and to inflammatory changes in the liver and adipose tissues, and can promote glucose metabolism disorder in mice.

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Association of chronic periodontitis and type 2 diabetes mellitus with salivary Del-1 and IL-17 levels

Cited by 12 publications

References 31 publications

Role of Interleukin-17A in the Pathomechanisms of Periodontitis and Related Systemic Chronic Inflammatory Diseases

Role of Interleukin-17A in the Pathomechanisms of Periodontitis and Related Systemic Chronic Inflammatory Diseases

Effects of IL-17 Inhibition with Secukinumab in Experimental Periodontitis

Periodontitis induced by Porphyromonas gingivalis drives impaired glucose metabolism in mice

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