Periostin-deficient mice, a relevant animal model to investigate
                        periodontitis or not?

Lapérine, Olivier; Guicheux, Jérôme; Lesclous, Philippe

doi:10.1038/bonekey.2016.21

Cited by 1 publication

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“…The oral gavage model is useful for addressing a wide variety of hypotheses related to periodontal pathogenesis, ranging from the role of the host response to virulence traits of pathogens and to the interconnections of those factors with systemic parameters. The silk ligature model is more relevant to investigate mechanistic and inflammatory aspects of the host immune response to bacterial stimulus and to identify potent therapeutic targets of particular interest in this inflammatory cascade [36]. This experimental model is also the most appropriate as it mimics the start point of periodontitis, a local gingival infection where oral epithelial cells are the first-line defense.…”

Section: Discussionmentioning

confidence: 99%

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

Lapérine

Cloître

Caillon³

et al. 2016

PLoS ONE

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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.

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Section: Discussionmentioning

confidence: 99%