Oral Lichen Planus

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Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.	Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.	Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.
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-b1-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-a, 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-b1, TNFa, IFN-g, 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.	ABSTRACT: Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, whiteplaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue and gingiva. Both antigen-specific and non-specific mechanisms are hypothesized to 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 Tcells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase 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. The various hypotheses proposed for pathogenesis of oral lichen planus are discussed in this review.	Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, white plaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue, and gingivae (Vincent et al., 1990; Silverman et al., 1991).
Ismail SB et al. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J Ora Sci 2007;49:89-106.	Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.	Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.
As many studies are being performed to understand the pathogenesis, potential biomarkers are being proposed to predict the onset and severity of OLP in individuals, which include CD 275 (77), serum autoantibodies to desmogleins 1 and 3 (76), urinary prokallikrein, PLUNC (78), biomarkers to predict the malignant transformation of OLP including 8-nitroguanine (79), and biomarkers to monitor therapeutic response to OLP (80).	Conclusion: Based on the pathogenesis, biomarkers are being proposed to predict the onset and severity of oral lichen planus, like CD2756, desmogleins 1 and 3; detect malignant transformation like PLUNC (Palate, lung and nasal epithelium carcinoma associated protein) and 8-nitoguanine; and monitor the therapeutic response. Analysis of current data suggests that blocking IL-12, IFN-c, TNF-a, RANTES, or MMP-9 activity or upregulating TGF-b1 activity in oral lichen planus may be of therapeutic value. More work is required for a full understanding of the etiology and pathogenesis of Oral lichen planus.	In the meantime, analysis of current data suggests that blocking IL-12, IFN-g, TNF-a, RANTES, or MMP-9 activity or up-regulating TGF-b1 activity in OLP may be therapeutic.