Factors involved in the T helper type 1 and type 2 cell commitment and osteoclast regulation in inflammatory apical diseases

Fukada, Sandra Yasuyo; Silva, T. A.; Garlet, Gustavo; Rosa, Adalberto Luiz; Silva, J. S. da; Cunha, Fernando

doi:10.1111/j.1399-302x.2008.00469.x

Cited by 100 publications

(150 citation statements)

References 56 publications

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“…In phase 2, the full-text of 18 studies were retrieved and evaluated. Of those, only eight 14,15,16,17,18,19,20,21 met the eligibility criteria. No additional study was identified in the reference lists of the included articles and in the grey literature.…”

Section: Study Selectionmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

“…14,15,18,21 All studies involved human periapical lesion fragments. Samples of six articles 14,15,18,19,20,21 were obtained directly through surgery and samples of the other two studies were obtained through institutional archives collected from previous surgical procedures. 16,17 Fou r a r t icles repor ted t he mea n age of participants 18,19,20,21 and five studies defined the range between 17 and 64 years.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…Samples of six articles 14,15,18,19,20,21 were obtained directly through surgery and samples of the other two studies were obtained through institutional archives collected from previous surgical procedures. 16,17 Fou r a r t icles repor ted t he mea n age of participants 18,19,20,21 and five studies defined the range between 17 and 64 years. 14,15,19,20,21 The language of the articles was predominantly English, although the studies were conducted in different countries (Brazil, United States and Serbia).…”

Section: Study Characteristicsmentioning

confidence: 99%

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Treg and Th17 cells in inflammatory periapical disease: a systematic review

et al. 2017

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The process involved in periapical lesions, which occur as an outcome of pulpal necrosis, is regulated by the immune system including regulatory T cells (Treg) and T helper 17 cell (Th17) responses. The objective of this study was to conduct a frequency systematic review to determine the presence of Treg/Th17 responses and the influence of these cells in the progression of chronic inflammatory periapical lesions in humans. A systematic computerized search was carried out in Pubmed, Medline, Web of Science and Scopus electronic databases from their date of inception through the first week of May 2017. In addition, the reference lists of the included articles and the grey literature were hand-searched. Articles that evaluated the presence and influence of Treg/Th17 in the progression of human periapical lesions were included. Study selection and the quality assessment of the included articles (using the Newcastle-Ottawa scale) were carried out by two authors. Fifty-seven titles/abstracts were screened and eight studies met the eligibility criteria and were included in this systematic review. The included studies showed large variation in the type of periapical lesion assessed, mean age, age range, type of experiment and findings regarding the participation of Th17 and Treg in the status of inflammatory periapical lesions. The studies showed the involvement of Treg in the modulation of the inflammatory response in radicular cysts and periapical granulomas. This systematic review highlights the relationship between Treg and Th17 acting in a subtle balance inhibiting or promoting the progression of human periapical lesions.

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Section: Study Selectionmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

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Treg and Th17 cells in inflammatory periapical disease: a systematic review

et al. 2017

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“…It has been shown that the symptomatic PLs are characterized by the upregulation of adhesive molecules, chemotactic factors (3), T helper (Th)1 and Th17 cytokines as well as bone resorptive cytokines such as interleukin (IL)-1, IL-6, and tumour necrosis factor (TNF)-α (2,4). On the other hand, the generation of asymptomatic PLs is followed by the Th2 immune response, which promotes PL chronicity with restriction of inflammation (5). The predominant cytokines in chronic PLs are IL-10 and transforming growth factor (TGF)-β, which are involved in healing and regression of the inflammation within PLs (2).…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal Stem Cells from Periapical Lesions Upregulate the Production of Immunoregulatory Cytokines by Inflammatory Cells in Culture / Mezenhimske matične ćelije iz periapeksnih lezija stimulišu produkciju imunoregulacijskih citokina od strane inflamacijskih ćelija u kulturi

Marković¹,

Tomić²,

Djokić³

et al. 2015

Acta Facultatis Medicae Naissensis

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The pathophysiology of periapical lesions (PLs) is under control of pro-inflammatory and anti-inflammatory (mainly immunoregulatory) cytokines. We have recently established mesenchymal stem cells (MSCs) from PLs and showed their suppressive effects on the production of proinflammatory cytokines from PLs inflammatory cells (ICs). In this work we studied the production of interleukin (IL)-10, IL-27 and transforming growth factor (TGF)-β, by PL-ICs in direct or indirect contacts with PL-MSCs. PL-ICs, which were isolated from four different asymptomatic PLs, predominantly composed of lymphocytes, followed by neutrophil granulocytes, macrophages and plasma cells. PLMSCs, expressing typical MSC markers, were co-cultivated with PL-ICs at 1:10 ratio, either in direct contact or in a transwell-system, for 24 hours. The levels of cytokines in cell-culture supernatants were tested by ELISA. The results showed that PL-MSCs up-regulated the production of all three immunoregulatory cytokines by PL-ICs. PL-MSCs stimulated the production of IL-10 and IL-27 via soluble factors, whereas the up-regulation of TGF-β required direct cell-to-cell contacts. In conclusion, our results showed for the first time the involvement of PL-MSCs in restriction of inflammation in PLs by up-regulation of immunoregulatory cytokines.

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Healing of Apical Lesions: How Do They Heal, Why Does the Healing Take So Long, and Why Do Some Lesions Fail to Heal?

Metzger

Kfir

2014

Disinfection of Root Canal Systems

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Factors involved in the T helper type 1 and type 2 cell commitment and osteoclast regulation in inflammatory apical diseases

Cited by 100 publications

References 56 publications

Treg and Th17 cells in inflammatory periapical disease: a systematic review

Treg and Th17 cells in inflammatory periapical disease: a systematic review

Mesenchymal Stem Cells from Periapical Lesions Upregulate the Production of Immunoregulatory Cytokines by Inflammatory Cells in Culture / Mezenhimske matične ćelije iz periapeksnih lezija stimulišu produkciju imunoregulacijskih citokina od strane inflamacijskih ćelija u kulturi

Healing of Apical Lesions: How Do They Heal, Why Does the Healing Take So Long, and Why Do Some Lesions Fail to Heal?

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