Background: Metabolomics is the study of metabolome which describes the full repertoire of small molecules, and the analysis of salivary metabolomics may help in identifying tumor-specific biomarkers for early diagnosis and prediction of tumor progression. The aim of the study was to evaluate the clinical utility of salivary metabolites in oral leukoplakia and oral squamous cell carcinoma.Methods: Salivary metabolomic profile of patients diagnosed with oral leukoplakia (n = 21) and oral squamous cell carcinoma (n = 22) was compared with apparently normal controls (n = 18) using Q-TOF-liquid chromatography-mass spectrometry.MassHunter profile software and Metlin database were used for metabolite identification. ANOVA to identify the regulation of metabolites between the three groups, t test (P < 0.05) to signify the changes between two groups, and chi-square test (P < 0.05) to indicate the presence or absence of metabolites in the study participants of the three groups were performed.Results: Significant upregulation of 1-methylhistidine, inositol 1,3,4-triphosphate, dglycerate-2-phosphate, 4-nitroquinoline-1-oxide, 2-oxoarginine, norcocaine nitroxide, sphinganine-1-phosphate, and pseudouridine in oral leukoplakia and OSCC was noted. Downregulated compounds in the diseased groups included l-homocysteic acid, ubiquinone, neuraminic acid, and estradiol valerate. Conclusion:A range of salivary metabolites were significantly altered in oral leukoplakia and oral squamous cell carcinoma. Further, it is necessary to evaluate the clinical utility of the individual metabolites in preventing malignant transformation of oral leukoplakia and to improve prognosis of oral squamous cell carcinoma. K E Y W O R D Sbiomarkers, leukoplakia, metabolomics, oral, oral squamous cell carcinoma, salivary diagnostics, tumor

Upregulation of L-carnitine, lysine, 2-methylcitric acid, putrescine; 8-hydroxyadenine; 17-estradiol; 5,6-dihydrouridine; and MTA suggests their diagnostic potential in oral leukoplakia and OSCC. Further, a significant upregulation of putrescine, 8-hydroxyadenine, and 5,6-dihydrouridine in OSCC than in oral leukoplakia indicates their potential role in predicting the malignant transformation of oral leukoplakia.

Oral cancer exhibits multifactorial etiology with tobacco and alcohol long been implicated as the primary risk factors. In addition, betel nut, dietary factors and poor oral hygiene have also been found to have a role in the etiology of oral cancer. Past research has uncovered a great deal of information regarding the association of exogenous bacteria with cancer. However, our definitive knowledge of the oral commensal bacteria and oral cancer link remains inadequate. In the present article, we hypothesize a causal role for oral bacterial flora in oral cancer although an indirect one. We propose that the normal bacterial flora in conjunction with the already established risk factors such as alcohol consumption may play a role in cancer development. The continued exploration of this topic may aid in better understanding of the pathogenesis of oral cancer thereby helping in appropriate treatment and better prognosis.

BACKGROUND Dentinogenic ghost cell tumor (DGCT) is an uncommon locally invasive odontogenic neoplasm. It is considered to be a solid variant of calcifying odontogenic cyst (COC). This tumor makes up for only 2%-14% of all COCs and less than 0.5% of all odontogenic tumors which owes to its rarity. The purpose of this paper was to describe a case of DGCT and the treatment adopted in our case, and to provide a review of this case in the indexed literature. CASE SUMMARY In this article, we discussed a case of 18 year old male who reported with a chief complaint of a recurrent swelling and dull aching pain in upper left back region of the jaw. Computed tomography scan was carried out which revealed hypodense lesion with a few hyperdense flecks within it suggesting the presence of calcification. On incisional biopsy, diagnosis of COC was given. After segmental resection of the lesion, histopathogically odontogenic epithelium was noted along with calcifications, ghost cells and dentinoid material. Special staining was done with van Gieson and it showed pink areas of dentinoid material and yellow colour represented ghost cells. Hence, amalgamation of careful clinical examination, use of advanced radiographic imaging and detailed histopathological examination confirmed the diagnosis of DGCT. The patient was followed up for one year and there was no recurrence of the lesion or signs of any residual tumor. CONCLUSION Radical treatment should be carried out along with mandatory long-term follow up in order to avoid recurrence in aggressive lesions.

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