Changes of the condylar position after modified disk repositioning: A retrospective study based on magnetic resonance imaging.

OBJECTIVE: This study aimed to explain the malocclusion resulting from the changes in condylar position after unilateral open disk repositioning surgery. STUDY DESIGN: Patients treated with unilaterally modified temporomandibular joint disk repositioning were reviewed. All patients underwent magnetic resonance imaging (MRI) before and immediately after surgery. Occlusion was checked, and the changes in the joint space and condylar position were measured by using MRI. The paired t test was used for analysis. RESULTS: Thirty-two patients were included in the final analysis. The incidence rates of the posterior open bite in the affected side were 100%, 87.5%, 71.9%, 9.4%, 3.1%, and 3.1% at 0, 3, and 7 days and 3 and 6 months, and at the last follow-up after surgery, respectively. Mean distances of the condylar movements were 2.67 and 0.32 mm in the affected joints and normal joints, respectively. There were significant differences for the anterior (P = .03), superior (P < .001), and posterior (P < .001) joint spaces of the affected joints as demonstrated by MRI. CONCLUSIONS: The joint spaces significantly increased postoperatively, in addition to the changes in condylar position in anterior and inferior movements, leading to posterior open bite; however, the position returns to normal 3 months after surgery. We concluded that disk repositioning, when done unilaterally, results in stable occlusion over time.

Skull Base Erosion Resulting From Primary Tumors of the Temporomandibular Joint and Skull Base Region: Our Classification and Reconstruction Experience.

PURPOSE: We sought to introduce our classification and reconstruction protocol for skull base erosions in the temporomandibular joint and skull base region. PATIENTS AND METHODS: Patients with neoplasms in the temporomandibular joint and skull base region treated from January 2006 to March 2017 were reviewed. Skull base erosion was classified into 3 types according to the size of the defect. RESULTS: We included 33 patients, of whom 5 (15.2%) had type I defects (including 3 in whom free fat grafts were placed and 2 in whom deep temporal fascial fat flaps were placed). There were 8 patients (24.2%) with type II defects, all of whom received deep temporal fascial fat flaps. A total of 20 patients (60.6%) had type III defects, including 17 in whom autogenous bone grafts were placed, 1 in whom titanium mesh was placed, and 2 who received total alloplastic joints. The mean follow-up period was 50 months. All of the patients exhibited stable occlusion and good facial symmetry. No recurrence was noted. CONCLUSIONS: Our classification and reconstruction principles allowed reliable morpho-functional skull base reconstruction.

Injecting vascular endothelial growth factor into the temporomandibular joint induces osteoarthritis in mice.

It is unclear whether vascular endothelial growth factor (VEGF) can initiate osteoarthritis (OA) in the temporomandibular joint (TMJ). In this study we evaluated the effects of intra-articular injection of exogenous VEGF in the TMJ in mice on the early stage. Forty-eight male Sprague-Dawley mice were equally divided into 3 groups. In the vegf group, the mice received an injection of VEGF solution (50 µL) in the TMJ once a week over a period of 4 weeks. In the sham group, the mice received an injection of saline (50 µL). The control group did not receive any injection. Four mice from each group were sacrificed at 1, 2, 4, and 8 weeks. Gradual prominent cartilage degeneration was observed in the vegf group. Additionally, this group showed higher expressions of metalloproteinase (MMP)-9, MMP-13, receptor activator of nuclear factor-kappa-B ligand (RANKL), and a higher number of apoptotic chondrocytes and VEGF receptor 2 (VEGFR2)-positive chondrocytes. Micro-computed tomography (CT) revealed prominent subchondral bone resorption in the vegf group, with a high number of osteoclasts in the subchondral bone. In vitro study demonstrated that VEGF can promote osteoclast differentiation. In conclusion, our study found that VEGF can initiate TMJ OA by destroying cartilage and subchondral bone.