ABSTRACT
Objective: The objective of this study was to assess immunohistochemically the presence of myofibroblasts both qualitatively and quantitatively in odontogenic cysts and tumors and to compare with the control cases of squamous cell carcinoma and to correlate the results with biologic behavior of these lesions. Materials and Methodology: Formalin-fixed, paraffin-embedded blocks of odontogenic cysts and tumors were retrieved from institutional archives. The sample size is 40; these include ten cases of odontogenic keratocyst (OKC) (n = 10), five cases of dentigerous cyst (n = 5), ten cases of solid ameloblastoma (n = 10), and five cases of unicystic ameloblastoma (n = 5). Ten cases of squamous cell carcinoma (n = 10) served as control. Sections were taken and stained immunohistochemically using alpha-smooth muscle actin for evaluation of myofibroblasts. The number of positive stromal cells was evaluated both for quantitative and qualitative analyses. Results: The present study showed that the mean number of myofibroblasts among the odontogenic cysts and tumors was higher in locally aggressive lesions such as OKC (23.79 ± 19.95), solid ameloblastoma (26.38 ± 17.00), and unicystic ameloblastoma (20.74 ± 14.86) which were comparable to squamous cell carcinoma (21.49 ± 9.76) when compared to benign lesions like dentigerous cyst which showed the least number of myofibroblasts (13.1 ± 7.71). Qualitatively, the staining intensity of myofibroblasts showed a significant variation within the same lesion and among different lesions. There was a distinct difference in the morphology, pattern of arrangement, and distribution of myofibroblasts among the studied lesions. Conclusion: We conclude that the increase in the number of myofibroblasts could be one of the contributory factors for the locally aggressive behavior of benign lesions such as ameloblastomas and OKCs. Further studies are suggested to understand the mechanism by which these important cellular elements exert their effects on stromal and epithelial tissue compartments.
ABSTRACT
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.
