Analysis of Interleukin 17A in periapical abscess and granuloma lesions

Ferreira, Luciana Gonçalves Valente; Rosin, Flávia Cristina Perillo; Corrêa, Luciana

doi:10.1590/1807-3107bor-2016.vol30.0034

Cited by 16 publications

(12 citation statements)

References 24 publications

(34 reference statements)

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“…, Ferreira et al . ). As described above, it is evident these molecular changes orchestrate the inflammatory process once it has been initiated and precede the presentation of clinical symptoms.…”

Section: Introductionmentioning

confidence: 97%

“…For example, interleukin [IL]1-a, IL-1b, IL-2, prostaglandin [PGE]-2, tumour necrosis factor [TNF]-a, interferon [IFN]-ɣ and macrophage inflammatory protein [MIP]-1b are considered potent stimulators of osteoclastic activity (M arton & Kiss 2000, Metzger 2000 whereas high concentrations of IL-4, IL-5, IL-6, IL-10 and IL-13 are reported to antagonistically suppress apical bone resorption (Stashenko et al 1987, Fukada et al 2009, Popovska et al 2017. Furthermore, increased levels of IL-17A have been associated with the development of radicular cysts and abscesses (Ajuz et al 2014, Ferreira et al 2016). As described above, it is evident these molecular changes orchestrate the inflammatory process once it has been initiated and precede the presentation of clinical symptoms.…”

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confidence: 99%

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A systematic review of methods used to sample and analyse periradicular tissue fluid during root canal treatment

et al. 2019

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Aim The primary aim was to identify techniques used to sample and analyse periradicular tissue fluid (PTF) in permanent teeth diagnosed with apical disease during root canal treatment. Secondly, to identify the types of inflammatory mediators studied using this approach. Methodology Data Sources: PubMed, EMBASE, Cochrane Library, Science Direct, Web of Science and OpenGrey. Eligibility Criteria: Clinical studies published until 1 June 2018 which utilized orthograde techniques to sample and analyse PTF were included. Cell culture, laboratory or animal studies and those concerned with investigating inflammatory mediator activity from within healthy or diseased pulp tissue, and not periradicular tissues, were excluded. Study appraisal and methods: In accordance with PRISMA guidelines, data were extracted on study characteristics, target mediators, sampling and assay techniques and the parameters associated with the PTF sampling and eluting protocol. A qualitative synthesis was conducted, and studies were critically appraised using a modified version of the Cochrane risk of bias tool. Results Study Characteristics: From 251 studies, 33 were eligible for inclusion. Sampling techniques included the use of paper points (n = 27), fine needle aspiration (n = 4) and filter strips (n = 2). Assay techniques included enzyme‐linked immunosorbent assay (n = 18), quantitative polymerase chain reaction (n = 9), radioimmunoassay (n = 4), colorimetric assay (n = 2), immunofluorometric assay (n = 1) and cytometric bead array (n = 1). Forty‐five different inflammatory mediators were targeted at the proteomic/metabolomic (n = 25) or transcriptomic level (n = 9). Limitations: Significant heterogeneity exists within the methodology, and only 5 studies disclosed unambiguous information about their PTF sampling and eluting protocols. Conclusions Paper points and proteomic/metabolomic analysis are currently the preferred methods for studying and analysing PTF during root canal treatment. The most studied analytes were IL‐1β and TNF‐α. Implications: Further research is required to develop an optimized PTF sampling and eluting protocol to overcome methodological heterogeneity, and future studies are advised to follow a standardized approach to reporting their methodology.

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Section: Introductionmentioning

confidence: 97%

mentioning

confidence: 99%

A systematic review of methods used to sample and analyse periradicular tissue fluid during root canal treatment

et al. 2019

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“…The results indicated that there were a significantly higher number of CD4 + /IL-17 + positive cells compared with CD8 + /IL-17 + cells both in the periapical abscesses and granulomas using double immunofluorescence staining. Abscess regions in the lesions exhibited the highest labelling area for IL-17, which was also densely expressed in neutrophils (Ferreira et al 2016). Another study analysed the expression of different Th subset cytokines or markers (IFN-c, TNF-a, IL-17, IL-21, IL-23, IL-33, IL-4, IL-9, IL-10, IL-22 and FOXp3) via real-time PCR array in PGs and control samples and revealed multiple cytokine clusters accountable for lesions with active and inactive status (as determined by RANKL/OPG expression ratio) (Araujo-Pires et al 2014).…”

Section: Human Studiesmentioning

confidence: 95%

“…Abscess regions in the lesions exhibited the highest labelling area for IL‐17, which was also densely expressed in neutrophils (Ferreira et al . ). Another study analysed the expression of different Th subset cytokines or markers (IFN‐γ, TNF‐α, IL‐17, IL‐21, IL‐23, IL‐33, IL‐4, IL‐9, IL‐10, IL‐22 and FOXp3) via real‐time PCR array in PGs and control samples and revealed multiple cytokine clusters accountable for lesions with active and inactive status (as determined by RANKL/OPG expression ratio) (Araujo‐Pires et al .…”

Section: Review Of Identified Publicationsmentioning

confidence: 97%

The Presence and involvement of interleukin‐17 in apical periodontitis

2019

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Apical periodontitis (AP) is a chronic inflammatory disease characterized by periapical tissue inflammation and destruction of the associated alveolar bone. It is caused by microbial infections within the root canal and the resultant host immune responses in the periapical tissues. The proinflammatory cytokine interleukin (IL)‐17 has been shown to play an important role in many inflammatory diseases. There is increasing evidence of the presence of IL‐17 in AP, which might be associated with disease pathogenesis. Moreover, several animal studies indicate the potential role of IL‐17 in periapical inflammation and the resultant bone resorption in AP. This article reviews recent studies regarding the collective in vitro, in vivo and clinical evidence of the presence and involvement of IL‐17 in AP. A search related to IL‐17 in apical periodontitis was conducted on PubMed, EMBASE and Web of Science databases using keywords and controlled vocabulary. Two independent reviewers first screened titles and abstracts and then the full texts that were included. A total of 25 papers were identified, of the 25 included articles, 7 involved laboratory studies on cell cultures, 11 involved animal experimentations, and 7 were observational studies using human clinical samples. In conclusion, evidence for the presence of IL‐17 in AP from human and animal models is clear. However, there is relatively little information currently available that would highlight the specific role of IL‐17 in AP.

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“…Para-dental g ranuloma is considered an asymptomatic chronic lesion, although sporadic acute cases associated with secondary infections have been reported elsewhere 1,2 . The immune response in periapical lesions is frequently investigated to understand not only the relationship between their pathogenesis and microbiota, but also why some lesions are resistant to non-surgical endodontic treatment 3,4 .…”

Section: Introductionmentioning

confidence: 99%