Guangzhao Guan1, Mahmoud M Bakr2, Norman Firth3, Robert M Love4. 1. School of Dentistry, University of Otago, Dunedin, New Zealand. 2. School of Dentistry and Oral Health, Griffith University, Nathan, Australia. 3. School of Dentistry, University of Otago, Dunedin, New Zealand; School of Dentistry, University of Western Australia, Perth, Australia. 4. School of Dentistry, University of Otago, Dunedin, New Zealand; School of Dentistry and Oral Health, Griffith University, Nathan, Australia. Electronic address: R.love@griffith.edu.au.
Abstract
OBJECTIVES: The aim of this study was to identify an association or link between cyclin D1 and p27KIP1 protein expression and dysplastic changes or progression. STUDY DESIGN: Oral mucosal biopsies with a diagnosis of non-neoplastic tissue (gingivitis) (n = 10), mild to moderate oral epithelial dysplasia (n = 12), and oral squamous cell carcinoma (n = 11) were evaluated by using immunohistochemistry. Scanning software was used to determine cyclin D1 and p27KIP1 intensity of expression, location, and pattern. RESULTS: A significant increase in expression of cyclin D1 and a decrease in expression of p27KIP1 proteins were identified in oral epithelial dysplasia and less differentiated oral squamous cell carcinoma (OSCC). There was a more diffuse distribution of cyclin D1 protein expression extending from the basal cell layer into the prickle cell layers in epithelial dysplasia and extending within all epithelial layers in OSCC. Cases of oral epithelial dysplasia had moderate infrequent expression of p27KIP1. There were no p27KIP1-positive cells in OSCC. The percentage of cells with both nuclear and cytoplasmic cyclin D1 staining was higher in OSCC specimens than control groups and oral epithelial dysplasia. CONCLUSIONS: The expression of both cyclin D1 and p27KIP1 correlated with the grade of oral epithelial dysplasia and degree of OSCC differentiation. The results obtained will be verified through a basic follow-up of the cases to determine the prognosis/progression of oral dysplasia.
OBJECTIVES: The aim of this study was to identify an association or link between cyclin D1 and p27KIP1 protein expression and dysplastic changes or progression. STUDY DESIGN: Oral mucosal biopsies with a diagnosis of non-neoplastic tissue (gingivitis) (n = 10), mild to moderate oral epithelial dysplasia (n = 12), and oral squamous cell carcinoma (n = 11) were evaluated by using immunohistochemistry. Scanning software was used to determine cyclin D1 and p27KIP1 intensity of expression, location, and pattern. RESULTS: A significant increase in expression of cyclin D1 and a decrease in expression of p27KIP1 proteins were identified in oral epithelial dysplasia and less differentiated oral squamous cell carcinoma (OSCC). There was a more diffuse distribution of cyclin D1 protein expression extending from the basal cell layer into the prickle cell layers in epithelial dysplasia and extending within all epithelial layers in OSCC. Cases of oral epithelial dysplasia had moderate infrequent expression of p27KIP1. There were no p27KIP1-positive cells in OSCC. The percentage of cells with both nuclear and cytoplasmic cyclin D1 staining was higher in OSCC specimens than control groups and oral epithelial dysplasia. CONCLUSIONS: The expression of both cyclin D1 and p27KIP1 correlated with the grade of oral epithelial dysplasia and degree of OSCC differentiation. The results obtained will be verified through a basic follow-up of the cases to determine the prognosis/progression of oral dysplasia.