The pathogenesis of oral lichen planus

Sugerman, P. B., Savage, N. W., Walsh, L. J., Zhao, Z. Z., Zhou, X. J., Khan, A., Seymour, G. J. and Bigby, M. (2002) The pathogenesis of oral lichen planus. Critical Reviews in Oral Biology and Medicine, 13 4: 350-365. doi:10.1177/154411130201300405

Author Sugerman, P. B.
Savage, N. W.
Walsh, L. J.
Zhao, Z. Z.
Zhou, X. J.
Khan, A.
Seymour, G. J.
Bigby, M.
Title The pathogenesis of oral lichen planus
Journal name Critical Reviews in Oral Biology and Medicine   Check publisher's open access policy
ISSN 1045-4411
Publication date 2002-01-01
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1177/154411130201300405
Open Access Status Not yet assessed
Volume 13
Issue 4
Start page 350
End page 365
Total pages 16
Publisher Intern. and American Associations for Dental Research
Language eng
Subject 2733 Otorhinolaryngology
3500 Dentistry
Abstract Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8 cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-β1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-α, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-β1, TNF-α, IFN-γ, IL-12) and promoters (MIF, MMP-9). We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.
Keyword Hypothesis
Oral lichen planus
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: Scopus Import - Archived
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Citation counts: Scopus Citation Count Cited 377 times in Scopus Article | Citations
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Created: Fri, 26 Jan 2018, 00:36:27 EST