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.

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
savage_sugarman.pdf savage_sugarman.pdf application/pdf 212.02KB 0

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 2002-07-01
Year available 2002
Sub-type Critical review of research, literature review, critical commentary
Open Access Status File (Author Post-print)
Volume 13
Issue 4
Start page 350
End page 365
Total pages 16
Place of publication USA
Publisher International and American Associations for Dental Research
Language eng
Subject C1
320899 Dentistry not elsewhere classified
730112 Oro-dental and disorders
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-beta1-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-alpha, 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-beta1, TNF-alpha, IFN-gamma, 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 Dentistry, Oral Surgery & Medicine
Oral Lichen Planus
Versus-host Disease
Transforming Growth Factor-beta-1
Experimental Allergic Encephalomyelitis
Migration Inhibitory Factor
Collagen-induced Arthritis
Experimental Autoimmune Encephalomyelitis
T-cell Subsets
Bone-marrow Transplantation
Glucose-induced Apoptosis
Q-Index Code C1
Institutional Status UQ
Additional Notes This document is a journal review.

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Excellence in Research Australia (ERA) - Collection
School of Dentistry Publications
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 284 times in Thomson Reuters Web of Science Article | Citations
Google Scholar Search Google Scholar
Created: Wed, 15 Aug 2007, 03:01:31 EST