Oral lichen planus and neurogenic inflammation: new observations and therapeutic implications from four clinical cases
Article first published online: 18 FEB 2014
© 2014 Wiley Periodicals, Inc.
Volume 27, Issue 4, pages 206–210, July/August 2014
How to Cite
Guarneri, F., Guarneri, C. and Marini, H. (2014), Oral lichen planus and neurogenic inflammation: new observations and therapeutic implications from four clinical cases. Dermatologic Therapy, 27: 206–210. doi: 10.1111/dth.12118
- Issue published online: 25 JUL 2014
- Article first published online: 18 FEB 2014
- neurogenic inflammation;
- oral lichen planus
Oral lichen planus (OLP) is a usually chronic and relapsing mucocutaneous disease with unknown etiology. Immunosuppressive treatment is sometimes unsatisfactory. We describe four cases of reticular OLP localized on the internal side of cheek, in the territory innervated by sensory free endings of the buccinator nerve, poorly responding to immunosuppressive treatment (topical/systemic corticosteroids, topical cyclosporin). Addition of prazepam 10 mg/day to standard therapy achieved significant improvement and clinical healing in 30–40 days. Because of the complex interplay between the nervous and immune systems, neuroinflammation, acting through conventional axon reflex and/or indirect reflex mechanism involving localized efferent vasodilatory parasympathetic fibers, could have an important pathogenic role in OLP. Such hypothesis could explain, at least partly, the spreading of lesions in OLP primarily triggered (and possibly sustained) by infections, irritants, or autoimmunity. Moreover, neuroinflammation could have a relevant role in OLP related to psychosomatic diseases, where the nervous component is the primary trigger and the main pathogen responsible for the lesions observed. Benzodiazepines modulate neuroinflammation through central, and, possibly, peripheral action. In OLP patients with mild/subclinical psychological conditions, low doses may effectively modulate neuroinflammatory pathways that are not always completely inhibited by immunosuppressive treatment and can contribute to the persistence of inflammation.