Duloxetine hydrochloride-induced oral lichenoid reaction: a case report

Objective: To report the first case of duloxetine hydrochloride [DH]-induced oral lichenoid drug reaction [OLDR]

Clinical Presentation and Intervention: A 57-year-old male patient presented with painful ulcerative lesions on the bilateral buccal mucosa of 2-year duration. The patient was on multiple drug therapy for his systemic ailments. After thorough evaluation for possible medical ailments and with the physician's consent, withdrawal of DH was done. The oral lesions were resolved after 2 weeks

Conclusion: In this case, DH induced OLDR

Melanin: A scavenger in gingival inflammation.

Background: One of the major direct or indirect targets of ultraviolet exposure of skin is the melanocyte or the melanin -forming cell. Epidermal melanocytes act as a trap for free radicals. Based on the protective role of melanocytes in medical literature, the role of melanin pigmentation in gingiva needs to be elucidated. Periodontal pathogens and their products demonstrate the ability to induce the generation of reactive oxygen species. Hence purpose of this study was to unravel the protective role of melanin (if any) against the gingival inflammation. Materials and Methods: A total of 80 subjects; 20 in each group were selected. The selection of subjects regarding gingival pigmentation was based on Dummett's scoring criteria 0, 3. A complete medical, dental history and an informed consent were obtained from the patients. After evaluation of clinical parameters the GCF was collected using microcapillary pipettes at the selected sites. IL-1β levels were quantitated using ELISA. Results: In non-pigmented healthy and gingivitis groups, there was a positive correlation between plaque index, gingival index and bleeding index versus IL-1β level: indicating an increase in the biochemical mediator of inflammation corresponding to an increase in the clinical parameters of inflammation. Also a positive correlation was found between the gingival index and bleeding index versus the IL-1β levels in the pigmented healthy group. The pigmented gingivitis groups showed a negative correlation between the plaque index, gingival index and bleeding index. Conclusions: The clinical markers of inflammation such as gingival index, bleeding index was of low numerical value in pigmented group than in the non-pigmented group, supposedly due to the protective action of melanin. The negative correlation of clinical markers of inflammation to the IL-1β levels in the pigmented gingivitis group could possibly be attributed to the protective role of melanins.