Interleukin‐33 could play an important role in the pathogenesis of periodontitis

Köseoğlu, Serhat; Hatipoğlu, Mükerrem; Sağlam, Mehmet; Enhoş, Şükrü; Esen, Hacı Hasan

doi:10.1111/jre.12235

Cited by 30 publications

(40 citation statements)

References 43 publications

(94 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hence, multiple tissues are included in this region, such as the alveolar bone above the line of the apex of the two tooth roots, the periodontal ligaments (PDLs) between the adjacent two roots and the gingival tissues between the two teeth. The number of inflammatory cells and osteoclasts in the DRs was counted according to the cell morphologies, as previously reported . Briefly, the DRs in each section were divided into three equidistant parts (top, middle, and bottom); then, at 400× magnification, the cell number in three randomly selected fields of each part was obtained, and the mean cell number in the DRs was then calculated .…”

Section: Methodsmentioning

confidence: 99%

“…The number of inflammatory cells and osteoclasts in the DRs was counted according to the cell morphologies, as previously reported. 30,31 Briefly, the DRs in each section were divided into three equidistant parts (top, middle, and bottom); then, at 400× magnification, the cell number in three randomly selected fields of each part was obtained, and the mean cell number in the DRs was then calculated. 32 For determination of the number of osteoclasts in HE-stained slides, the presence of 2 or more nuclei and the osteoclast localization (adjacent to the bone surface) were used as parameters to identify osteoclasts.…”

Section: Micro-ct Scanning and Analysismentioning

confidence: 99%

See 1 more Smart Citation

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

Background Although the immunomodulatory properties of calcitriol in bone metabolism have been documented for decades, its therapeutic role in the management of periodontitis remains largely unexplored. In this study, we hypothesized that calcitriol suppresses lipopolysaccharide (LPS)‐induced alveolar bone loss by regulating T helper (Th) cell subset polarization. Methods To test this hypothesis, we determined the effect of calcitriol intervention on the development of LPS‐induced periodontitis in rats in terms of bone loss (micro‐CT analysis), local inflammatory infiltration levels, the number of osteoclasts (hematoxylin and eosin staining) and the level of osteoclastogenesis (tartrate‐resistant acid phosphatase method). Furthermore, immunohistochemistry was used to assess the expression levels of the receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin (OPG) as well as the cytokine levels of interferon‐γ (IFN‐γ), interleukin‐4 (IL‐4), IL‐17, and IL‐10 throughout the LPS‐injected region. Finally, the polarization potential of Th cells in peripheral blood was analyzed using flow cytometry. Results Calcitriol intervention decreased alveolar bone loss in response to LPS injection and inflammatory cell infiltration. Analysis of osteoclast number and RANKL and OPG expression showed that bone resorption activity was largely suppressed in response to calcitriol administration, along with decreased IL‐17 levels but increased IL‐4 and IL‐10 levels in periodontal tissues (the LPS‐injected region). Similarly, the percentages of Th2 and Treg cells in peripheral blood increased, but the percentages of Th1 and Th17 cells decreased in rats receiving calcitriol. Conclusion Our findings suggest that calcitriol can be used to inhibit bone loss in experimental periodontitis, likely via the regulation of local and systemic Th cell polarization.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Micro-ct Scanning and Analysismentioning

confidence: 99%

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…Recently, it has been also shown that TNF‐α induces IL‐33 expression in human gingival fibroblasts isolated from human periodontitis samples . In addition, increased expression of IL‐33 has been demonstrated in an experimental rat model of periodontitis . To better understand the role of IL‐33 in chronic apical periodontitis, we investigated the expression pattern of IL‐33 in both periapical granulomas and radicular cysts, as well as in healthy periapical tissues.…”

Section: Discussionmentioning

confidence: 99%

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Velickovic¹,

Pejnović²,

Petrović

et al. 2015

J Oral Pathology Medicine

View full text Add to dashboard Cite

show abstract

“…In a rat model of ligature induced-periodontitis, IL-33 expression was upregulated concomitantly to RANK-L [19]. In human, high IL-33 overexpression was recorded in the gingiva of patients affected by CP and may act as a triggering factor for the recruitment of B and T lymphocytes expressing RANK-L [20].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis

Lapérine

Cloître

Caillon³

et al. 2016

PLoS ONE

View full text Add to dashboard Cite

IntroductionChronic Periodontitis (CP) is an inflammatory disease of bacterial origin that results in alveolar bone destruction. Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP. It has been suggested that IL-33, could be of interest in CP.Objectivethe present study aims to analyze whether and how IL-33 and RANK-L and/or their interplay are involved in the bone destruction associated to CP.Material and MethodsmRNAs and protein expressions of IL-33 and RANK-L were analyzed in healthy and CP human gingival samples by immunohistochemistry (IHC) and RT-qPCR. Murine experimental periodontitis (EP) was induced using Pg infected ligature and Pg free ligature around the first maxillary molar. Alveolar bone loss was recorded by μCT. Mouse gingival explants were stimulated for 24 hours with IL-33 and RANK-L mRNA expression investigated by RT-qPCR. Human oral epithelial cells were infected by Pg for 6, 12; 24 hours and IL-33 and RANK-L mRNA expressions were analyzed by RT-qPCR.ResultsIL-33 is overexpressed in gingival epithelial cells in human affected by CP as in the murine EP. In human as in murine gingival cells, RANK-L was independently induced by Pg and IL-33. We also showed that the Pg-dependent RANK-L expression in gingival epithelial cells occured earlier than that of IL-33.ConclusionOur results evidence that IL-33 overexpression in gingival epithelial cells is associated with CP and may trigger RANK-L expression in addition to a direct effect of Pg. Finally, IL-33 may act as an extracellular alarmin (danger signal) showing proinflammatory properties in CP perpetuating bone resorption induced by Pg infection.

show abstract

Interleukin‐33 could play an important role in the pathogenesis of periodontitis

Cited by 30 publications

References 43 publications

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis

Contact Info

Product

Resources

About