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Osteoarthritis in temporomandibular joint of Col2a1 mutant mice - PubMed
Source: pubmed.ncbi.nlm.nih.gov
Article summary:
1. Col2a1 gene mutations cause premature degeneration of knee articular cartilage in disproportionate micromelia (Dmm) and spondyloepiphesial dysplasia congenita (sedc) mice.
2. The present study analyses the temporomandibular joint (TMJ) in Col2a1 mutant mice in order to provide an animal model of TMJ osteoarthritis (OA).
3. Dmm/+ TMJs showed fissuring of condylar cartilage as early as 6 months of age, with significant staining of HtrA1, Ddr2 and Mmp-13 observed in Dmm/+ mice.
Article analysis:
The article is generally reliable and trustworthy, providing a comprehensive overview of the research conducted on Col2a1 mutant mice and their potential for providing an animal model for temporomandibular joint osteoarthritis (OA). The authors have provided detailed descriptions of the methods used to assess OA progression, including light microscopy, Mankin scoring procedure, unfolded protein response assay and immunohistochemistry. Furthermore, they have discussed the results obtained from these tests in detail, noting that Dmm/+ TMJs showed fissuring of condylar cartilage as early as 6 months of age with significant staining of HtrA1, Ddr2 and Mmp-13 observed in Dmm/+ mice. They also noted that there was an upregulation of the unfolded protein response in knee but not TMJ.
The article does not appear to be biased or one-sided; it presents both sides equally by discussing both the positive findings from their research as well as any limitations or areas for further exploration. There are no unsupported claims or missing points of consideration; all claims made are supported by evidence presented within the article itself. Additionally, there is no promotional content or partiality present; instead, the authors provide a balanced overview of their findings without attempting to sway readers towards any particular conclusion. Finally, possible risks associated with this research are noted throughout the article; for example, they discuss how upregulated UPR may exacerbate OA onset.