Absence of BRAFV600E immunohistochemical expression in sporadic odontogenic keratocyst, syndromic odontogenic keratocyst and orthokeratinized odontogenic cyst.

BACKGROUND: Odontogenic keratocyst (OKC) is a unique developmental odontogenic cyst that has the potential to behave aggressively and is associated with the nevoid basal cell carcinoma syndrome. Orthokeratinized odontogenic cyst (OOC) is a distinct, uncommon odontogenic cyst. It significantly differs from OKC not only in its epithelial lining but also in proliferating kinetics, clinical, immunohistochemical and biological behaviour. BRAF gene located on chromosome 7q34 encodes a cytoplasmic serine-threonine kinase. Various immunohistochemical studies have been conducted to express the BRAFV600E gene mutation in various odontogenic cyst and tumours with varying results. The present study was conducted to evaluate the possible role of BRAFV600E in the pathogenesis of sporadic OKC, syndromic OKC and OOC by immunohistochemistry. METHODS: Formalin-fixed paraffin-embedded (FFPE) tissue blocks of 15 diagnosed cases each of sporadic OKC, syndromic OKC and OOC were retrieved from the archives of Department of Oral Pathology and subjected to immunohistochemical staining for the detection of BRAFV600E mutation using a novel rabbit monoclonal antibody clone RM8. RESULTS: Immunohistochemical analysis showed complete absence of BRAFV600E mutation in all cases of sporadic OKC, syndromic OKC and OOC. CONCLUSION: The negative immunohistochemical expression of BRAFV600E in sporadic OKC, syndromic OKC and OOC suggests that BRAFV600E plays no role in the pathogenesis of sporadic OKC, syndromic OKC and OOC.

The Role of Increased Connective Tissue Growth Factor in the Pathogenesis of Oral Submucous Fibrosis and its Malignant Transformation-An Immunohistochemical Study.

Connective tissue growth factor (CTGF), a matricellular protein of the CCN family of extracellular matrix-associated heparin-binding proteins, is highly expressed in various organ fibrosis and several malignant tumors. Although a few studies have been conducted using CTGF in oral submucous fibrosis (OSF) and oral squamous cell carcinoma, no study has demonstrated its relation with various stages of OSF and its malignant transformation. The present study investigated the possible role of CTGF in the pathogenesis of OSF and its malignant transformation by using immunohistochemistry. Ten formalin-fixed paraffin-embedded tissue blocks, each of Stage 1 OSF, Stage 2 OSF, Stage 3 OSF, Stage 4 OSF, well- differentiated squamous cell carcinoma (WDSCC) with OSF and WDSCC without OSF were stained for CTGF by immunohistochemistry. Ten cases of healthy buccal mucosa (NOM) were included as controls. The present study demonstrated a statistically significant expression of CTGF in the epithelium and connective tissue of OSF and WDSCC with and without OSF cases against its complete absence in NOM. We observed an upregulation of CTGF expression from NOM to various stages of OSF to WDSCC with or without OSF. A gradual upregulation of the CTGF expression in various stages of OSF to WDSCC (with and without OSF) against its complete absence in NOM suggests that CTGF plays an important role in the pathogenesis of OSF and its malignant transformation.

Immunohistochemical expression of stem cell markers OCT-4 and SOX-2 in giant cell tumor, central giant cell granuloma, and peripheral giant cell granuloma.

OBJECTIVES: This study aimed to evaluate and compare the immunohistochemical expression of OCT-4 and SOX-2 and to determine their use in differentiating giant cell tumor (GCT) from central giant cell granuloma (CGCG) and peripheral giant cell granuloma (PGCG). STUDY DESIGN: Formalin-fixed, paraffin-embedded tissue blocks of 10 histopathologically diagnosed cases of GCT, CGCG, or PGCG were examined for anti-OCT-4 and anti-SOX-2 antibodies. Nuclear staining of stromal mononuclear cells and multinucleated giant cells was considered positive for OCT-4 and SOX-2 expression. RESULTS: Nuclear immunoexpression of OCT-4 in stromal mononuclear cells was observed in 80% (8 of 10) of GCT cases, whereas none of the CGCG and PGCG cases showed OCT-4 immunoreactivity. SOX-2 immunoreactivity was negative in GCT, CGCG, and PGCG. CONCLUSIONS: OCT-4 immunopositivity in GCT can be used as a cancer stem cell marker to differentiate GCT from CGCG and PGCG. The presence of OCT-4 in GCT versus its complete absence in CGCG and PGCG suggests that these three conditions are separate entities. The absence of stem cell marker OCT-4 and SOX-2 raises questions regarding their role in the pathogenesis of CGCG and PGCG.