Interleukin-1β is a potential therapeutic target for periodontitis: a narrative review

Cheng, Ran; Wu, Zhiwu; Li, Mingming; Shao, Meiying; Hu, Tao

doi:10.1038/s41368-019-0068-8

Cited by 156 publications

(112 citation statements)

References 159 publications

(165 reference statements)

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“…Although periodontitis, as with CVD, does not exhibit the classic signs of rare autoinflammatory diseases including unpredictable fevers, skin rashes, and joint damage, severe periodontitis is characterized by increased levels of IL-1β [41][42][43][44][45] and CRP, [46][47][48] which are consistent with other common autoinflammatory diseases. 49 In recent years, investigators have used large clinical databases to ask whether the presence of a specific disease that increases systemic inflammation also increases the risk for future CVD or type 2 diabetes.…”

Section: Implications For Treating Periodontal Diseasementioning

confidence: 94%

Future of preventing and managing common chronic inflammatory diseases

Kornman

2020

Journal of Periodontology

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Chronic inflammation has emerged as a key factor that contributes to some common chronic diseases and reduces lifespan. Studies have identified multiple types of chronic inflammation ranging from autoimmune disease, which attacks specific tissues, to autoinflammatory diseases, which cause low-grade systemic inflammation and contribute to several common chronic diseases. This article highlights new perspectives on the role of chronic inflammation in cardiovascular disease (CVD). Such information is being leveraged to develop new treatment strategies for CVD and may inform how periodontal disease influences CVD.

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Section: Implications For Treating Periodontal Diseasementioning

confidence: 94%

Future of preventing and managing common chronic inflammatory diseases

Kornman

2020

Journal of Periodontology

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“…In addition, IL-1 increases PGE2 synthesis in fibroblasts, indirectly inducing the expression of RANKL as well. IL-1 has, therefore, a long-lasting effect on osteoclastogenesis, which leads to bone resorption [90].…”

Section: Il-1mentioning

confidence: 99%

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

et al. 2020

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Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiological processes and inflammatory diseases including osteoporosis. The aim of the review was to evaluate the role of alarmins in osteoporosis. A bibliographic search of the published scientific literature regarding the role of alarmins in osteoporosis was organized independently by two researchers in the following scientific databases: Pubmed, Scopus, and Web of Science. The keywords used were combined as follows: “alarmins and osteoporosis”, “RAGE and osteoporosis”, “HMGB1 and osteoporosis”, “IL-1 and osteoporosis”, “IL 33 and osteopororsis”, “S100s protein and osteoporosis”. The information was summarized and organized in the present review. We highlight the emerging roles of alarmins in various bone remodeling processes involved in the onset and development of osteoporosis, as well as their potential role as biomarkers of osteoporosis severity and progression. Findings of the research suggest a potential use of alarmins as pharmacological targets in future therapeutic strategies aimed at preventing bone loss and fragility fractures induced by aging and inflammatory diseases.

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“…O fluido gengival é um exsudato parecido com o plasma e que, no transcorrer de sua passagem pelos tecidos até os tecidos periodontais, são capturados mediadores inflamatórios envolvidos na resposta tecidual destrutiva, sendo importante na fisiopatologia da doença periodontal. De forma geral, os níves de IL-1β encontram-se elevados em sítios acometidos pela doença periodontal quando comparados a sítios sadios (Cheng et al, 2020).…”

Section: Resultsunclassified

“…Atualmente está bem estabelecida a relação entre a progressão da doença periodontal e altos níveis de citocinas, numerosas citocinas estão envolvidas nessa rede e participam da fisiopatologia, porém essa rede não está completamente estabelecida. Neste contexto, estudos têm demonstrado que os mediadores inflamatórios mais consistentemente associadas com periodontite são: IL-1β, IL-6, TNF-α e PGE2 (Cheng et al, 2020) A IL-1 é secretada em duas formas moleculares, α e β (no fluido extracelular), por inúmeras células incluindo macrófagos, células b, neutrófilos, fibroblastos e células epiteliais, ambas as formas possuem efeitos pró-inflamatórios e, dependendo de uma série de fatores, podem induzir reabsorção óssea, uma vez que tem sido demonstrado que a IL-1 é idêntica estruturalmente ao fator de ativação osteoclástica, sendo, também, potente inibidor de formação óssea. A IL-1β está presente em maior concentração nos tecidos periodontais e fluido gengival de sítios acometidos pela doença periodontal, quando comparados aos sítios saudáveis, além de estar correlacionada com o avanço da lesão estável para a lesão progressiva (Goutoudi et al, 2004).…”

Section: Introductionunclassified

O papel da interleucina-1beta na fisiopatogenia da doença periodontal: uma revisão de literatura

Fróes

Pasquinelli

Quintela

et al. 2020

RSD

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The bacteria involved in the gingival inflammatory process induce inflammatory responses characterized by the release of mediators, for example, interleukins, the cytokines involved in the course of development of periodontal disease are not yet fully established. The increase in the amount of interleukin-1beta (IL-1β) is correlated, in the periodontal lesion, with the progression from the stable lesion to the progressive lesion. The purpose of this literature review was to evaluate IL-1β and its influence on the development of periodontal disease. Initially, 860 articles from the following databases were evaluated in this literature review: Pubmed, Lilacs, Scielo, Web of Science, Embase and Cochrane. The search terms were: periodontal disease and IL-1β; periodontitis and IL-1β; oral health and IL-1β; gingivitis and IL-1β. With the adopted criteria, 28 articles were included in this literature review. The observed results showed that IL-1β is the one that most relates to the activity of the disease, since patients with periodontitis have a higher frequency of a genotype associated with increased production. These cytokines can be generated by immune cells, such as lymphocytes and monocytes in the medullary cavity or by other bone cells, particularly cells of the osteoblastic lineage. We conclude that IL-1β is directly related to the progression of periodontal disease, promoting the entry of inflammatory cells to the sites of infection and high levels of IL-1β are related to bleeding rates, probing depth and clinical level of insertion changed.

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Interleukin-1β is a potential therapeutic target for periodontitis: a narrative review

Cited by 156 publications

References 159 publications

Future of preventing and managing common chronic inflammatory diseases

Future of preventing and managing common chronic inflammatory diseases

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

O papel da interleucina-1beta na fisiopatogenia da doença periodontal: uma revisão de literatura

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