Abstract
Background
Rheumatoid arthritis of the temporomandibular joint (TMJ-RA) has been reported to have a larger incidence range than systemic rheumatoid arthritis (RA). The presence or absence of mechanical stress (MS) is considered a factor in this. In this study, we hypothesized that TMJ-RA develops or worsens when excessive MS is applied to the temporomandibular joint of RA mouse models. We aimed to clarify the relationship between TMJ-RA and MS through morphological and histological evaluation.
Methods
Collagen antibody-induced arthritis (CAIA) was induced in male DBA/1JNCrlj 9–12 weeks old mice by administering Type II collagen antibody and lipopolysaccharide to produce RA model mice. MS was applied to the mandibular condyle. The group was separated into non-RA (control group (N = 5) and MS group (N = 5)), and RA group (CAIA group (N = 5)and CAIA MS group (N = 5)). To confirm the morphological changes in the mandibular condyle, micro-CT imaging was performed. Histological evaluation of the TMJ was performed by hematoxylin and eosin staining for condylar cartilage cell layer thickness, Safranin O staining for proteoglycans, and tartrate-resistant acidic phosphatase staining for osteoclast count. Immunohistochemical evaluation was performed to assess the localization of cartilage destruction enzymes using ADAMTS-5 (a disintegrin and metalloproteinase with thrombospondin motifs) antibody. Additionally, CD3 (cluster of differentiation), CD45, and γδ TCR (T cell receptor) antibodies were used to localize and identify the type of lymphocytes.
Results
In the CAIA MS model, a three-dimensional analysis of the temporomandibular joint by microcomputer tomography showed a crude change in the surface of the mandibular condyle. Histological examination revealed a decrease in the chondrocyte layer width and an increase in the number of osteoclasts in the mandibular condyle. T cell accumulation was observed, and γδ T cell involvement was confirmed.
Conclusions
In the CAIA model, the TMJ was less sensitive to the initiation of RA. However, the results suggested that it was exacerbated by MS, and that γδ T cells may be involved in TMJ-RA.