RESUMO
Objective: To observe and compare the radiographs of spiral CT and cone-beam CT (CBCT) in the imaging of temporomandibular joint osteoarthrosis (TMJOA) and to explore the difference between CBCT and spiral CT in detection accuracy so as to provide references for clinical diagnosis and treatment. Methods: A total of 52 patients with TMJOA diagnosed in the Department of Oral and Maxillofacial Surgery, General Hospital of Chinese PLA, from January 2018 to December 2019 were selected. There were 10 males and 42 females, with an average age of 38.6 years (21-70 years). All patients underwent spiral CT and CBCT examinations. Two oral radiologists and two oral and maxillofacial surgeons measured and evaluated the joint spaces and condylar bone lesions of each side of temporomandibular joint. According to the presence or absence of osteoarthrosis, the patients were divided into osteoarthrosis group (92 sides) and non osteoarthrosis group (12 sides). The mean size of joint spaces and the detection rate of lesions were compared between the two groups. SPSS 20.0 was used to analyze the data. Results: There was no significant difference between the measurements of joint space size and joint position in the spiral CT group and the CBCT group (P>0.05). The mean size of the anterior space and the ratio of the posterior condyle in the osteoarthrosis side were larger than that in the normal side. The LR index was smaller in the osteoarthrosis side than that in the normal side indicating that the position of the posterior condyle in the osteoarthrosis side was deviated. However, the difference was not statistically significant (P>0.05). Both spiral CT and CBCT showed good consistency in displaying condylar osteopathy. The most common types of condylar osteopathy was surface defect. The detection rates of defects by spiral CT were surface erosion (85.6%, 89/104), articular surface flattening and shortening (82.7%, 86/104), subcortical sclerosis (40.4%, 42/104), osteophyte (40.4%, 42/104) and subcortical cyst (11.5%, 12/104) respectively. The detection rates of defects by CBCT were surface erosion (88.5%, 92/104), articular surface flattening and shortening (86.5%, 90/104), subcortical sclerosis (35.6%, 37/104), osteophyte (41.3%, 43/104) and subcortical cyst (11.5%, 12/104). There was no statistical difference between the two groups (P>0.05), respectively. Conclusions: Both spiral CT and CBCT showed good accuracies in displaying the osteopathy of TMJOA and the sizes of the joint spaces measured by spiral CT and CBCT were basically the same. Both spiral CT and CBCT could be used as a routine diagnostic method for TMJOA.
RESUMO
OBJECTIVE: Satb1 regulates chromatin structure and gene expression, and is aberrantly expressed in many tumors. However, there is still no report about Satb1 functions in peripheral nerve injury until now. In this study, we explored the regulatory effect of Satb1 on Schwann cells. MATERIALS AND METHODS: MTT assay, transwell assay, and flow cytometry assay were respectively used to determine Schwann cell viability, migration, and apoptosis. The mRNA and phosphorylation levels of Satb1 and SHIP1 were assessed by RT-PCR and Western blotting analysis, respectively. The correlation between Satb1 and SHIP1 was examined by ChIP assay. The expressions of PI3K/AKT pathway related factors were detected by Western blotting. RESULTS: In the present study, we found that knock-out of Satb1 significantly inhibited cell viability and migration, and promoted Schwann cells apoptosis. Conversely, over-expression of Satb1 promoted cell viability, migration, and inhibited apoptosis. Satb1 inhibited SHIP1 expression by recruiting HDAC1. Furthermore, results showed that Satb1 activated the PI3K/AKT signaling pathway by inhibiting the expression of SHIP1. SHIP1 showed significant reversal effects on the regulatory roles of Satb1 in Schwann cells. Over-expression of Satb1 and SHIP1 inhibited cell viability, migration, and promoted apoptosis. CONCLUSIONS: Our study demonstrated that the Satb1 knock-out could inhibit the activation of PI3K/AKT pathway by up-regulating SHIP1, thus inhibiting cell viability and migration, and promoting Schwann cell apoptosis.