Melatonin Epigenetic Potential in Preventing Malignant Transformation of Oral Lichen Planus
NCT Number: NCT06533033
Status: ACTIVE_NOT_RECRUITING
Study Type: INTERVENTIONAL
Phases: NA
Conditions: Oral Lichen Planus
Interventions: DRUG: Rapid Release Capsules Melatoni|DRUG: Triamcinolone Acetonide ointment, Kenacort-A orabase
Sponsor: Hams Hamed Abdelrahman
Sex: ALL
Age: ADULT, OLDER_ADULT
Enrollment: 50
Study Design: Allocation: RANDOMIZED|Intervention Model: PARALLEL|Masking: SINGLE (OUTCOMES_ASSESSOR)|Primary Purpose: PREVENTION
Start Date: 2024-01-01
Completion Date: 2024-08-01
Locations: Outpatient Clinic of Oral medicine Department, Faculty of Dentistry, Alexandria University, Egypt, Alexandria, Egypt

Summary:
Background: Oral Lichen planus (OLP) is one of the most common oral diseases that has an unneglectable rate of malignant transformation. Recently malignant transformation has been definitively linked to epigenetic changes. One of those most common changes is DNA hypermethylation that causes tumor suppressor genes to downtranslate and thus carcinogenesis begins. ZNF582 gene hypermethylation is emerging as an exclusive biomarker to differentiate between normal and dysplastic changes that occur over the epithelium. Aim: To evaluate the Melatonin epigenetic potential in preventing malignant transformation of OLP. Material and methods: an epigenetic randomized clinical study will be conducted on 50 patients suffering from OLP, recruited from the outpatient clinic of Oral medicine department, Alexandria Faculty of Dentistry, Egypt. Patients will be assigned to either Control group who will receive topical corticosteroids and antifungal treatment, or test group who will receive melatonin supplement in addition to conventional treatment. All patients will be genetically evaluated for the level of DNA hypermethylation 8 weeks after treatment, and clinically evaluated for disease severity and pain, by Elsabagh scoring system 4. 8, and 12 weeks after treatment.

Primary Outcome Measures: change in DNA methylation level of tumor suppressor gene (ZNF852), The ZNF582 gene sequence will be obtained from the University of California, Santa Cruz, Genomics Institute.

website (http://genome.ucsc.edu/), and the methylation-specific PCR primers for ZNF582 will be acquired from MethPrimer (http://www.urogene.org/cgibin/ methprimer/methprimer.cgi)., up to 8 weeks|Change in oral lesions, Oral lesions will be evaluated clinically after treatment using Elsabagh et al score.

Objective mucosal lesion nature (no lesion= 0, White keratotic lesion =1, Atrophy/Erosion intermixed or not with White lesion = 2, Ulceration intermixed or not with White lesion = 3), Up to 12 weeks|Change in pain scores, Subjective pain score (no pain =0, mild pain=1, moderate pain=2, severe pain=3), Up to 12 weeks|Change in number of affected surfaces in oral cavity, Number of surfaces affected in the oral cavity other than the gingiva (only one surface affected or buccal mucosae bilaterally =0, more than one surface affected or more than both buccal mucosae=1), Up to 12 weeks|Change in gingival involvement, Gingival involvement as desquamative gingivitis (no gingival involvement = 0, narrow band (1mm) of gingival involvement or wide band in less than 6 teeth involved =1, wide band (\>1mm) of gingival involvement in more than 6 teeth involved = 2), Up to 12 weeks