Differential regulation of blood vessel formation between traumatic temporomandibular joint fibrous ankylosis and bony ankylosis in a sheep model.

OBJECTIVES

Clinical and experimental studies show that the etiology of traumatic temporomandibular joint (TMJ) fibrous ankylosis and bony ankylosis are associated with the severity of trauma. However, how the injury severity affects the tissue differentiation is not clear. We tested the hypothesis that angiogenesis affects the outcomes of TMJ trauma, and that enhanced neovascularization after severe TMJ trauma would promote the development of bony ankylosis.

METHODS

Bilateral condylar sagittal fracture and discectomy were performed for each sheep, with the glenoid fossa receiving either severe trauma to induce bony ankylosis or minor trauma to induce fibrous ankylosis. At days 7, 14, 28, and 56 after surgery, total RNA was extracted from the ankylosed callus. Temporal gene expressions of several molecules functionally important for blood vessel formation were studied by real-time PCR.

RESULTS

Histological examination revealed a prolonged hematoma phase and a lack of cartilage formation in fibrous ankylosis. mRNA expression levels of HIF-1α, VEGF, VEGFR2, SDF1, Ang1, Tie2, vWF, CYR61, FGF2, TIMP1, MMP2, and MMP9 were distinctly lower in fibrous ankylosis compared with bony ankylosis at several time points.

CONCLUSIONS

Our study indicates that inhibition of angiogenesis after TMJ trauma might be a promising strategy for preventing bony ankylosis in the future.