| Popis: |
The temporomandibular joint (TMJ) helps move the mandible and handle the forces associated with mastication. Much like other joints in the body, the TMJ can be afflicted with disorders that impair its function. Osteoarthritis (OA), one of the most common degenerative joint diseases worldwide, has been implicated as a prevalent temporomandibular disorder with limited treatment options. Fibroblast growth factor 2 (Fgf2), a gene important in bone remodeling, has been shown to lead to murine knee OA phenotypes in its germline ablation studies. In this study, the articular chondrocyte-specific ablation of the gene is studied in the temporomandibular joint condylar cartilage of female mice using a Col2CreERT2 knockout system. Micro-CT imaging suggested phenotypic changes in the condylar head samples of the conditional knockout samples in comparison to the control. Safranin o stains on frozen sections revealed phenotypic changes in cell morphology in the deeper layers of the cKO cartilage tissues in comparison to the control. Immunohistochemistry staining indicated a significant decrease in BMP2 protein expression and increasing trends in proteins responsible for cartilage degradation such as MMP13 in cKO samples in comparison to the control. These results suggest that the conditional ablation of Fgf2 results in phenotypic disruptions in the condylar cartilage of the TMJ. Further studies would be needed to indicate the validity behind these apparent disruptions and to further evaluate the molecular markers responsible for these changes. |
