Ki67, CD105 and α-smooth muscle actin expression in disease progression model of oral submucous fibrosis.

AIM: The aim of this study was to investigate the expression of Ki67, CD105 and α-smooth muscle actin (α-SMA) expression in oral submucous fibrosis (OSF) and oral squamous cell carcinoma in the background of OSF (OSCC-SMF). METHODS: The study was carried out on paraffin-embedded tissues of 30 normal oral mucosa (NOM), 50 OSF cases and 105 OSCC-SMF. The immunohistochemistry was carried out to evaluate the expression of Ki67, CD105 and α-SMA antigen. RESULTS: Ki67 labelling index (LI), CD105 and α-SMA expression showed increasing trend from NOM, low-risk epithelial dysplasia (LRED), high-risk epithelial dysplasia (HRED), well-differentiated squamous cell carcinoma (WDSCC), moderately differentiated squamous cell carcinoma to poorly differentiated squamous cell carcinoma. However, there was no significant difference of α-SMA expression between HRED and WDSCC. In OSCC-SMF, Ki67 LI, CD105 and α-SMA were significantly higher in advanced clinical TNM stage, metastasis and less than 3 years patient survival as compared with early clinical TNM stage, non-metastasis and 3 years or more patient survival. CONCLUSION: Ki67 LI, α-SMA and CD105 expression alone or together correspond with the disease progression model of SMF. Hence, expression of these markers can be used as a predictive marker of clinical outcome of OSCC-SMF.

Tumor angiogenesis: role in locally aggressive biological behavior of ameloblastoma and keratocystic odontogenic tumor.

BACKGROUND: The purpose of this study was to assess and compare angiogenesis in ameloblastoma, keratocystic odontogenic tumors, dentigerous cysts, and normal oral mucosa. METHODS: Angiogenesis was assessed in 28 ameloblastoma-36 keratocystic odontogenic tumors, 28 dentigerous cysts, and 19 normal oral mucosa by measuring the mean vascular density (MVD), total vascular area (TVA) and mean vascular area (MVA). Immunohistochemistry was carried out by using CD105. RESULTS: The nonsignificant difference of MVD was noted between ameloblastoma and keratocystic odontogenic tumors (p = .174). TVA and MVA were significantly higher in ameloblastoma than keratocystic odontogenic tumors, normal oral mucosa, and dentigerous cysts (p < .001). MVD, TVA, and MVA were significantly higher in keratocystic odontogenic tumors than normal oral mucosa and dentigerous cysts (p < .001). CONCLUSION: The results suggest that tumor angiogenesis may play an important role in locally invasive aggressive biologic behavior of ameloblastoma and keratocystic odontogenic tumor. The angiogenesis could be a potent target for developing antiangiogenic therapeutic strategies, particularly in recurrent cases of odontogenic tumors.

Comparison of myofibroblasts expression in oral squamous cell carcinoma, verrucous carcinoma, high risk epithelial dysplasia, low risk epithelial dysplasia and normal oral mucosa.

The aim was to evaluate and compare the presence of myofibroblasts in oral squamous cell carcinoma (OSCC), verrucous carcinoma (VC), high-risk epithelial dysplasia (HRED), low-risk epithelial dysplasia (LRED), and normal oral mucosa (NOM). The study consisted of 37 OSCC, 15 VC, 15 HRED, 15 LRED and 15 NOM. α-smooth muscle actin (α-SMA) antibody was used to identify myofibroblasts. The α-SMA expression was not observed in NOM and LRED. The α-SMA was expressed in 97.29% of OSCC, 86.66% of VC, 46.66 % of HRED. The α-SMA expression was significantly higher in OSCC than VC (p = 0.023) and HRED (p < 0.000). The α-SMA expression was significantly higher in VC than HRED (p = 0.043). Myofibroblastic expression, as highlighted by α-SMA, is undetectable in NOM and LRED but increases as the disease progresses from potentially malignant disorders, as HRED to VC to invasive OSCC. Thus, proliferation of myofibroblasts may be used as a stromal marker of oral premalignancy and malignancy.