ArticleExperimental and therapeutic medicine2017
Significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- OX40L in endothelial cells promotes temporomandibular joint subchondral bone angiogenesis and osteoclastogenesis in mice.Bone & joint research · 2026Article
- Angiogenesis in temporomandibular joint osteoarthritis: an update on mechanisms and research advances.Frontiers in medicine · 2026Review
- Effects of Hyaluronic Acid (HA) and Platelet-Rich Plasma (PRP) on Mandibular Mobility in Temporomandibular Joint Disorders: A Controlled Clinical Trial.Biomolecules · 2024Article
- Piezo1 Affects Temporomandibular Joint Osteoarthritis by Influencing pSmad3.Frontiers in physiology · 2022Article
- Emerging role of integrated PET-MRI in osteoarthritis.Skeletal radiology · 2021Review
- Inhibition of mTORC1 in the rat condyle subchondral bone aggravates osteoarthritis induced by the overly forward extension of the mandible.American journal of translational research · 2021Article
- Expression of Dickkopf-related Protein 1 in Patients with Temporomandibular Osteoarthritis after Treatment with Hyaluronic Acid.Current medical science · 2020Article
- Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease.Cellular and molecular life sciences : CMLS · 2019Review
- Transcriptome analyses identify key genes and potential mechanisms in a rat model of osteoarthritis.Journal of orthopaedic surgery and research · 2018Article
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Authors and funding
5 authors.
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Abstract
We studied the significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis (TMJOA). Fifteen 8-week-old female Sprague-Dawley rats were selected to establish TMJOA models of gradually induced occlusal disorders. Five rats were sacrificed at 4, 8 and 16 weeks, and histological exam was conducted along with micro-computed tomography observation on the condyle specimen. The distribution and number of new blood vessels breaking were observed through the tidemark through CD34 immunofluorescence staining. The proliferation of chondrocytes were detected through Ki67 immunohistochemical staining, and the differentiation functions of chondrocytes were observed through PTHrP and IHH immunohistochemical staining. The degradation functions of cartilage matrix were observed through matrix metalloproteinase (MMP)-9 immunohistochemical staining to detect the expression of vascular growth promotion and inhibition factors with vascular endothelial growth factor (VEGF), CTGF and CHM-1 immunohistochemical staining and screen differentially expressed genes through gene chip analysis method. It was found that the condyle tissue full thickness, fiber layer thickness and calcified cartilage layer thickness were significantly increased with time (P<0.05). Bone mineral density, trabecular thickness and Tb.Sp were also increased significantly with time, BS/BV and trabecular number were decreased significantly with time (P<0.05). The new blood vessels reached the deep layer of calcified cartilage until the tide line was broken and non-calcified cartilage was invaded. The number of vessels were increased significantly with time (P<0.05). Ki67, PTHrP and IHH-positive rates were increased significantly (P<0.05). MMP-9, VEGF, CTGF and CHM-1 were increased significantly (P<0.05). VEGF, CTGF and CHM-1 mRNA were upregulated differentially with the expressed genes. In conclusion, the new blood vessels may be important in the pathogenesis of TMJOA.
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