Aberrant activation of the PI3K/Akt signalling pathway, a major driving force of diverse cellular processes has been implicated in tumour development and progression. Here, we report that astaxanthin (AXT), a potent antioxidant ketocarotenoid prevents cancer hallmarks by inhibiting PI3K/Akt and the associated downstream NF‐κB and STAT‐3 signalling pathways in SCC131 and SCC4 oral cancer cells as well as in the hamster buccal pouch carcinogenesis model. Using small molecule inhibitors of NF‐κB, STAT‐3 and PI3K and by overexpression of PI3K, we provide evidence to show that AXT inhibits NF‐κB and STAT‐3 signalling and cancer hallmarks by restraining the kinase activity of PI3K/Akt. Additionally, AXT downregulated the noncoding RNAs (ncRNAs), miR‐21 and HOTAIR that influence PI3K/Akt signalling emphasising its modulatory effects on epigenetic regulation. Ethyl cellulose‐based AXT nanoparticles showed greater chemotherapeutic efficacy in the hamster oral carcinogenesis model compared to native AXT. We suggest that AXT prevents cell proliferation, apoptosis evasion, invasion and angiogenesis by intercepting the crosstalk between the PI3K/Akt, NF‐κB and STAT‐3 signalling circuits both in vitro and in vivo. Astaxanthin that abrogates the PI3K/Akt signalling axis, a central hub that orchestrates acquisition of cancer hallmarks is a promising candidate for anticancer drug development.

Background:Cytological reports of ameloblastoma are relatively rare in the literature. Appropriate cytologic diagnosis may play a significant role in its preoperative presumptive diagnosis, especially when incisional biopsy findings are inadequate.Aim:To systematically study the detailed cytomorphologic features of ameloblastoma and to evaluate the role of fine needle aspiration cytology (FNAC) in its preoperative diagnosis.Materials and Methods:In this study, FNAC was done on 26 cases of intra-osseous jaw lesion, clinically diagnosed as odontogenic tumor or developmental odontogenic cysts and detailed cytopathological interpretation was carried out and the results were correlated with the corresponding histopathology.Results:Of the 26 cases, 15 were found to be ameloblastoma and sensitivity of FNAC in the diagnosis of ameloblastoma was found to be 86.6%. None of the intra-osseous jaw lesion was false positively diagnosed as ameloblastoma in FNAC and hence the specificity was found to be 100%.Conclusion:Presence of cohesive epithelial cell clusters exhibiting smaller basaloid cells with peripherally placed tall columnar cells and occasional large squamous cells either adjoining the basaloid epithelial clusters or in isolated group aids in the specific cytological diagnosis of ameloblastoma and FNAC offers an excellent diagnostic aid that may play a significant role in preoperative presumptive diagnosis of ameloblastoma along with incisional biopsy.

The central odontogenic fibroma (COF) is a rare benign odontogenic mesenchymal tumor of jaw bones. The World Health Organization (WHO) recognizes two variants of COF namely: 1) Epithelial-rich type (WHO) and 2) epithelial-poor type (simple type). Rare variants like ossifying COF, COF associated with giant cell lesions, and amyloid have been documented. This article presents a case of an epithelial-rich variant of COF in a 24-year-old female. It presented as a bony swelling of the maxilla and appeared as a mixed lesion in radiographs. Histopathology showed a highly cellular fibrous connective tissue stroma with plump fibroblasts and long strands of odontogenic epithelium exhibiting mild eosinophilic to clear cytoplasm. Numerous cementum-like hematoxyphilic calcifications of various sizes akin to dentin or acellular cementum were observed. We believe that clinical and radiographic features of this case may add valuable knowledge to the already existing literature.

No abstract

Reactive proliferations of the gingiva comprise lesions such as pyogenic granuloma (PG), inflammatory fibroepithelial hyperplasia (IFH), peripheral ossifying fibroma (POF), and peripheral giant cell lesion. Osteopontin (OPN) has a dual role, it promotes mineralization when it is bound to solid substrate, and on the other hand, it inhibits mineralization when it is seen in association with solution.Objectives The study aimed to evaluate the expression of osteopontin in normal gingival tissue and different types of focal reactive proliferations of gingival tissue, and its role in the development of calcification within it.Material and Methods The presence and distribution of osteopontin was assessed using immunohistochemistry in five cases of normal gingival tissue and 30 cases of focal reactive proliferations of gingiva.Results There was no expression of osteopontin in normal subjects. Few cases of pyogenic granuloma, inflammatory fibroepithelial hyperplasia, and all the cases of peripheral ossifying fibroma showed positivity for osteopontin in the inflammatory cells, stromal cells, extracellular matrix, and in the calcifications.Conclusion The expression of osteopontin in all the cases of peripheral ossifying fibroma speculates that the majority of the cases of peripheral ossifying fibroma originate from the periodontal ligament cells. The treatment modalities for peripheral ossifying fibroma should differ from other focal reactive proliferations of gingiva.

Context:The epithelium atrophy, as the oral submucous fibrosis (OSMF) progresses, is believed to be an after effect of stromal fibrosis, hyalinization, decrease in vascularity and cellularity and is considered as “ischemic atrophy.” Due to hypoxia, caspase-3 get activation and subsequent decrease in viable cell count can occur.Aims and Objectives:To determine caspase-3 expression in various grades of OSMF and oral squamous cell carcinoma (OSCC) to find out whether upregulation of apoptosis is responsible for the epithelial changes in OSMF.Subjects and Methods:The control tissue (15 samples from normal oral mucosa) and study group comprising 97 cases of OSMF of different grades and OSCC associated with OSMF were stained with caspase-3 antibody, and the percentage of positive cells was calculated using ImageJ software.Statistical Analysis:The results obtained were statistically analyzed using ANOVA and Tukey's honest significance difference test and Mann–Whitney U-test.Results:There was a nuclear expression of caspase-3 in basal and parabasal layers of normal epithelium. There was cytoplasmic expression of caspase-3 in OSMF without dysplasia, total absence of caspase-3 expression in dysplastic epithelium and in majority cases of OSCC. The caspase-3 percentage was increased in OSMF (0%–53%) when compared with OSCC (0%–8%). The statistical comparison of caspase-3 among normal, OSMF and OSCC patients revealed significant correlation (P < 0.00010). The comparison within different grades of OSMF and between dysplastic and nondysplastic epithelium OSMF also showed significance (P < 0.019).Conclusions:The decreased expression of caspase-3 in disease progression reflects its role in the malignant transformation.

No abstract

Background:The present study is aimed at analyzing the expression of inducible nitric oxide synthase (iNOS) in the epithelial lining of odontogenic keratocyst (OKC), dentigerous cyst (DC), radicular cyst (RC) in order to understand the possible role of iNOS with special reference to its neoplastic nature and local aggressive of cysts.Aim:The primary aim of the following study is to analyze the immunohistochemical expression of iNOS and secondary aim is to compare the iNOS expression, pattern and intensity of staining among the epithelial linings of OKC, DC and RC.Materials and Methods:iNOS in the epithelial lining cells were analyzing in 10 OKC's, 10 DC's and 10 RC's using immunohistochemistry. The percentage of positive cells was assessed and presented as mean ± standard deviation. The correlation with respect to the intensity and percentage of staining within the epithelial linings of OKCs, DCs and RCs was carried out using (analysis of variance and Student's t-test) Chi-square test.Results:Staining intensity of iNOS portion was seen in the entire thickness of the epithelial linings of OKC, whereas in DC's only one case had entire thickness of the epithelial lining staining and in RC's none of the cases showed entire thickness of staining. On comparing the staining intensity of iNOS between OKC, DC and RC groups, using Chi-square test, there was a statistically significant difference between these groups (P < 0.01). On analyzing the immuno-reactivity of iNOS in OKC, DC and RC there was a positive variable expression iNOS between the cysts.Conclusion:iNOS was over expressed in OKCs when compared with DC and RC suggesting that iNOS may contribute to the aggressive behavior of OKC. This is yet another evidence to support that OKC is the neoplasm.