Significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis

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.

Immunohistochemical panel of degenerated articular discs from patients with temporomandibular joint osteoarthritis

“…With respect to these features, angiogenesis within the TMJ disc has been shown as internal derangement develops 11 . Our histopathological analysis demonstrated vascular infiltration in every disc with varying degrees, and this is in line with the results from Yoshida et al 22 An animal study by Liu et al 23 indicated changes in articular cartilage matrix under excessive loading as an essential factor for the invasion of blood vessels. Tissue fragmentation was also frequently noted in our degenerated discs’ sample.…”

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

“…Recently, the significance of Chm-1 expression associated with angiogenesis during the pathogenesis of temporomandibular joint (TMJ) osteoarthritis was investigated [38]. Chm-1 protein expression was observed in the proliferative and hypertrophic zone of mandibular condylar cartilage, and chondrocyte-like cells in the TMJ disc by immunohistochemistry analyses; which is indicative of a role of Chm-1 in the regulation of TMJ remodelling via preventing blood vessel invasion of the condylar cartilage and by maintaining the integrity of the condylar cartilage and TMJ disc [28].…”

Transcriptome analyses identify key genes and potential mechanisms in a rat model of osteoarthritis

“…Three steps were followed to perform enrichment analysis of DEGs, which revealed that DEGs mainly enriched in vasculature development, response to growth factor, positive regulation of cell migration, and ECM-receptor interaction. Many studies found that vasculature development at the osteochondral junction and synovium was associated with the onset and development of OA [29, 30]. Meanwhile, some growth factors, such as VEGF and NGF, were obviously upregulated in subchondral spaces, vascular channels and chondrocytes of OA patients [31].…”