机构地区:[1]INSERM(French National Institute of Health and Medical Research),UMR 1260,Regenerative NanoMedicine(RNM),FMTS,Strasbourg,France [2]INSERM,UMR 1109,Immuno Rhumatologie Moléculaire(IRM),FMTS,Strasbourg,France [3]Fédération Hospitalo-Universitaire(FHU)OMICARE,Universitéde Strasbourg,Strasbourg,France [4]Facultéde Chirurgie Dentaire,Universitéde Strasbourg(UDS),8 rue Ste Elisabeth,Strasbourg,France [5]Pole de Médecine et Chirurgie Bucco-Dentaires,Hopitaux Universitaires de Strasbourg(HUS),1 place de l’Hopital,Strasbourg,France [6]ICube UMR 7357,Universitéde Strasbourg,CNRS,FMTS,4 rue Kirschleger,Strasbourg,France [7]Department of Biomedical Engineering,Core Facility Micro-and Nanotomography,Biomaterials Science Center(BMC),University of Basel,Gewerbestrasse 144123,Allschwil,Switzerland
出 处:《International Journal of Oral Science》2020年第1期59-67,共9页国际口腔科学杂志(英文版)
基 金:This work was funded by the INSERM。
摘 要:Rheumatoid arthritis(RA) is an autoimmune disease affecting 1% of the world population and is characterized by chronic inflammation of the joints sometimes accompanied by extra-articular manifestations. K/Bx N mice, originally described in 1996 as a model of polyarthritis, exhibit knee joint alterations. The aim of this study was to describe temporomandibular joint(TMJ)inflammation and damage in these mice. We used relevant imaging modalities, such as micro-magnetic resonance imaging(μMRI)and micro-computed tomography(μCT), as well as histology and immunofluorescence techniques to detect TMJ alterations in this mouse model. Histology and immunofluorescence for Col-I, Col-II, and aggrecan showed cartilage damage in the TMJ of K/Bx N animals, which was also evidenced by μCT but was less pronounced than that seen in the knee joints. μMRI observations suggested an increased volume of the upper articular cavity, an indicator of an inflammatory process. Fibroblast-like synoviocytes(FLSs)isolated from the TMJ of K/Bx N mice secreted inflammatory cytokines(IL-6 and IL-1β) and expressed degradative mediators such as matrix metalloproteinases(MMPs). K/Bx N mice represent an attractive model for describing and investigating spontaneous damage to the TMJ, a painful disorder in humans with an etiology that is still poorly understood.Rheumatoid arthritis(RA) is an autoimmune disease affecting 1% of the world population and is characterized by chronic inflammation of the joints sometimes accompanied by extra-articular manifestations. K/Bx N mice, originally described in 1996 as a model of polyarthritis, exhibit knee joint alterations. The aim of this study was to describe temporomandibular joint(TMJ)inflammation and damage in these mice. We used relevant imaging modalities, such as micro-magnetic resonance imaging(μMRI)and micro-computed tomography(μCT), as well as histology and immunofluorescence techniques to detect TMJ alterations in this mouse model. Histology and immunofluorescence for Col-I, Col-II, and aggrecan showed cartilage damage in the TMJ of K/Bx N animals, which was also evidenced by μCT but was less pronounced than that seen in the knee joints. μMRI observations suggested an increased volume of the upper articular cavity, an indicator of an inflammatory process. Fibroblast-like synoviocytes(FLSs)isolated from the TMJ of K/Bx N mice secreted inflammatory cytokines(IL-6 and IL-1β) and expressed degradative mediators such as matrix metalloproteinases(MMPs). K/Bx N mice represent an attractive model for describing and investigating spontaneous damage to the TMJ, a painful disorder in humans with an etiology that is still poorly understood.
关 键 词:DAMAGE alterations INFLAMMATION
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...