Abstract
Recently, it has been reported that γδ T cells are associated with the pathology of rheumatoid arthritis (RA). However, there are many uncertainties about their relationship. In this study, we investigated the morphological and histological properties of peripheral as well as temporomandibular joints (TMJ) in a mouse model of rheumatoid arthritis with and without exposure to mechanical strain on the TMJ. Collagen antibody-induced arthritis (CAIA) was induced by administering collagen type II antibody and lipopolysaccharide to male DBA/1JNCrlj mice at 9−12 weeks of age, and mechanical stress (MS) was applied to the mandibular condyle. After 14 days, 3D morphological evaluation by micro-CT, histological staining (Hematoxylin Eosin, Safranin O, and Tartrate-Resistant Acid Phosphatase staining), and immunohistochemical staining (ADAMTS-5 antibody, CD3 antibody, CD45 antibody, RORγt antibody, γδ T cell receptor antibody) were performed. The lower jawbone was collected. The mandibular condyle showed a rough change in the surface of the mandibular condyle based on three-dimensional analysis by micro-CT imaging. Histological examination revealed bone and cartilage destruction, such as a decrease in chondrocyte layer width and an increase in the number of osteoclasts in the mandibular condyle. Then, immune-histological staining revealed accumulation of T and γδ T cells in the subchondral bone. The temporomandibular joint is less sensitive to the onset of RA, but it has been suggested that it is exacerbated by mechanical stimulation. Additionally, the involvement of γδ T cells was suggested as the etiology of rheumatoid arthritis.
Highlights
Rheumatoid arthritis (RA) is an autoimmune disease with a 1% prevalence worldwide
All mice injected with the collagen antibody cocktail developed inflammatory arthritis after LPS administration
As a result, compared with the control group, in the Collagen antibody-induced arthritis (CAIA) group, infiltration of inflammatory cells was observed in the synovial membrane, and a defect in the surface layer of the femur and cartilage erosion due to loss of proteoglycan in the chondrocyte layer in the chondrocyte layer was observed (Figure 2C)
Summary
Rheumatoid arthritis (RA) is an autoimmune disease with a 1% prevalence worldwide. Chronic inflammation of the joints and synovial hyperplasia, known as pannus, are observed, as well as cartilage and bone destruction by inflammatory cytokines. The detailed causes of RA have not yet been fully elucidated [1]. The involvement of gd T cells has recently been reported as one gdTcell Related Temporomandibular Joint Arthritis of the causes of autoimmune rheumatoid diseases. It is thought that gd T cells in RA patients exhibit functional characteristics similar to helper T cells, such as antigen presentation and assistance in antibody production [2]. Reports on the involvement of the TMJ are rather heterogeneous and range between 4-85% of RA patients [4–6]. Unlike RA in the limb joints, the pathogenetic mechanism of RA in the TMJ (TMJ-RA) is still unknown
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