RESUMEN
Objective: This study examined the glenoid fossa in Class II and Class III malocclusions with mandibular retrusion and protrusion. Materials and Methods: A retrospective investigation examined 60 Class II and 60 Class III cephalometric radiographs. Cephalometric landmarks and glenoid fossa measurements were taken. Statistical analysis contrasted the two malocclusion groups' glenoid fossas. Results: Class II malocclusion had a much lower mean Sella-Nasion-Condylion (SNCd) angle (glenoid fossa sagittal position) than Class III (14.6° ± 1.9). Class II malocclusion had a lower mean Sella-Nasion-Gonion (SNGo) angle (32.5° ± 4.3) than Class III (36.2° ± 3.9). The SNCd angle and SNGo angle in both groups demonstrated a negative correlation, demonstrating a relationship between the glenoid fossa and the mandibular sagittal axis. Conclusion: The glenoid fossa location differs significantly between Class II malocclusion with mandibular retrusion and Class III with protrusion. Class II malocclusion has a posterior glenoid fossa, while Class III has a less posterior one. Understanding these links may help patients receive more personalized treatment.
RESUMEN
Aim: The aim of the study is to evaluate the presence of myofibroblasts quantitatively in oral epithelial dysplasia, oral squamous cell carcinoma (OSCC). Materials and Methods: Formalin-fixed, paraffin-embedded blocks were retrieved from the institutional archives. The sample size is 35 and included 15 cases of oral epithelial dysplasia (n = 15), 15 cases of squamous cell carcinoma (n = 15) and 5 cases of normal oral mucosa which served as the control (n = 5). Histologic sections were subjected to immunohistochemical analysis using alpha-smooth muscle actin, and the mean number of myofibroblasts was evaluated. Results: There were no myofibroblasts in the stroma of normal oral mucosa and oral epithelial dysplasia. Whereas all cases of OSCC showed myofibroblasts (mean ± standard deviation: 21.49 ± 9.76). This difference of myofibroblasts between OSCC and oral epithelial dysplasia was statistically significant with a P < 0.05. There was no statistically significant difference in the mean number of Myofibroblasts(MF) between 3 histologic grades of OSCC. Conclusion: The presence of myofibroblasts in the stroma of OSCC and their absence in normal oral mucosa and epithelial dysplasia reveals that these cells may play a role in cancer cell invasion and progression so the treatment strategies targeting the myofibroblasts and their by products may be beneficial in OSCC patients.
