Abstract
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/BxN 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/BxN 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/BxN mice secreted inflammatory cytokines (IL-6 and IL-1β) and expressed degradative mediators such as matrix metalloproteinases (MMPs). K/BxN 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.
Highlights
The upper part of the temporomandibular joint (TMJ) is formed by the temporomandibular fossa or glenoid fossa, and the lower part is formed by the mandibular condyle
fibroblast-like synoviocytes (FLSs) are mesenchymal resident cells that have been described in recent decades as active players in cartilage damage through proliferative/invasive properties and the secretion of inflammatory (e.g., interleukin-6 (IL-6)) and degradative (e.g., matrix metalloproteases (MMPs)) mediators.[3]
Characterization of K/BxN mice detected in the TMJ of K/BxN mice (Fig. 1h, i and Supplementary Fig. 3b–f) in comparison with the TMJ of controls (Fig. 1k, l and Several murine arthritis models have been reported in the Supplementary Fig. 3a)
Summary
The upper part of the temporomandibular joint (TMJ) is formed by the temporomandibular fossa or glenoid fossa, and the lower part is formed by the mandibular condyle. An ellipsoidal articular disc composed of fibrous connective tissue divides the joint into two parts: the upper and the lower articular cavities. These cavities are limited by the synovial membrane and filled with fluid. Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic articular inflammation (driving swelling, stiffness, and pain) and sometimes accompanied by extra-articular manifestations. FLSs (or type B synoviocytes) are mesenchymal resident cells that have been described in recent decades as active players in cartilage damage through proliferative/invasive properties (so-called “pseudo-tumoural” behavior) and the secretion of inflammatory (e.g., interleukin-6 (IL-6)) and degradative (e.g., matrix metalloproteases (MMPs)) mediators.[3]
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