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. 2016 Jan;121(1):49-57.
doi: 10.1016/j.oooo.2015.08.020. Epub 2015 Sep 5.

Smoking habits and clinical patterns can alter the inflammatory infiltrate in oral lichenoid lesions

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Smoking habits and clinical patterns can alter the inflammatory infiltrate in oral lichenoid lesions

Mohammad S Alrashdan et al. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016 Jan.

Abstract

Objective: The present immunohistochemical study aimed to investigate the possible correlation between demographic variables and clinical presentation of oral lichenoid lesions (OLL), in addition to the potential effects of these variables and smoking status on OLL inflammatory infiltrate.

Study design: A total of 53 patients with OLL were assigned, according to their smoking status at the time of diagnosis, to either a smokers group (n = 27) or a nonsmokers group (n = 26). Demographic and clinical data, including the site and pattern of the OLL, symptoms, and medical history, were analyzed. Immunohistochemical expression of clusters of differentiation, including CD3, CD4, CD8, CD68, and CD1a, was compared between the two groups.

Results: Gingival involvement in OLL was found to be significantly associated with older age. Buccal mucosa as the sole OLL site showed a significantly higher expression of CD3+ cells compared with other sites (P < .05). OLL presenting as a reticular type alone was significantly associated with less CD3+ expression (P < .05), whereas a significantly higher CD1a+ expression was seen with plaque-like type OLL (P < .05). Smoking was significantly associated with less expression of macrophages (CD68+ cells) and less clinical symptoms (P < .05 and P < .01, respectively).

Conclusion: The inflammatory infiltrate in OLL can be affected by their clinical distribution and presentation. Smoking reduces the expression of macrophages in OLL, and this may alter the immune surveillance and the mechanisms of malignant transformation.

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