Objective: It is currently considered that the defect of mitotic spindle caused by centrosome abnormalities may be one of the reasons for the development of aneuploidy in tumors. This study attempted to elucidate the possible role of centrosome defects in the development and progression of OSCC by investigating the frequency of centrosome amplification in oral precancerous lesions and OSCC.
Methods: Formalin-fixed, paraffin-embedded tissues of 12 cases of normal oral epithelium, 22 case of dysplasia with different degree epithelium dysplasia and 32 cases of OSCC with different differentiation were investigated for centrosome status by using indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The differences and the change trend of centrosome status in these groups were statistically analyzed by SPSS10.0.
Results: Normal oral epithelium showed normal centrosomes in epithelium cells, while 16 of 22 cases (72.73%) of dysplasia (DYS) and 27 of 32 cases (84.38%) of OSCC showed the evidence of centrosome amplification and morphological abnormalities characterized by huge size, clump or supernumerary centrosomes in a fraction of epithelium or tumor cells. The percentage of cells with abnormal centrosomes increased gradually from mild-dysplasia epithelium to poorly differentiated OSCC, which positively correlated with the histologicalcytologic grade of oral precancerous lesions and OSCC (P < 0.01).
Conclusion: Centrosome amplification was an early event and that might play a role in the establishment and perhaps the progression of OSCC. There might be some direct relationship between centrosome defects and the cellular morphological phenotype characteristics of dysplasia and OSCC. Centrosome amplification could be served as an alternative diagnostic indicator of dysplasia and the intervention of centrosome cycle might serve as a particular way for the prevention and treatment of OSCC in the future.