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Oral lichen planus – Pathogenesis

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ORAL LICHEN PLANUS – AUTOIMMUNE PATHOGENESIS

Author: Sanketh DS, MDS

AUTOIMMUNE PATHOGENESIS

Essentially, the body’s own immune cells (lymphocytes) attack the oral mucosal cells (keratinocytes) to cause oral lichen planus. An early event in the causation of the lesion, is the unmasking of the keratinocyte antigen.

This unmasking could be induced by numerous factors like stress, drugs, bacterial or viral infections and other unknown agents. 

There are an increased number of  Langerhans cells, also called antigen presenting cells(APC), in people prone to developing oral lichen planus.

Following unmasking, Langerhans cell collects the antigen and runs to the nearest draining lymph node. Here, the Langerhans cell processes this antigen and presents it as a peptide with the help of a molecule called MHC II, to the CD4+ T lymphocytes. The CD4+ T lymphocyte recognises this peptide presented through MHC II with the help of a T-cell receptor and other co-receptors like CD4, CD 28 (on the T cell) and B7 molecule (on the Langerhans cell). Once this happens, the Langerhans cell spits out cytokines or signalling molecules called IL-12, which activates CD4+ T cell to become a mature type 1 helper T cell (Th1).

So when these Th1 cells infiltrate the tissue, they may chance encounter more APCs with the keratinocyte antigen and release IL-2 and IFN-γ.  IL-2 helps in further maturation and proliferation of Th1 cells and interferon γ signals more dendritic cells and macrophages to become vigilant. These activated macrophages and dendritic cells release pro-inflammatory cytokines like TNF-α and IL-1 to increase vascular permeability and make the blood vessels leaky. More lymphocytes may leak through these sites and march towards the site of the lesion to further fuel the cascade of reactions.  Now, IL-2 can also stimulate naïve or immature CD8+ cells to make them mature cytotoxic T lymphocytes(CTLs). These CTLs could directly recognise the antigen on the keratinocyte itself through a molecule called MHC I, or on the APCs through MHC I.

The CTLs are so called because they cause cytotoxicity. Once they recognise the peptide through MHC I, they could kill the keratinocytes by releasing perforins and grazymes. Perforins create pores on the keratinocyte and granzymes induce apoptosis of the cell.

 IL-2 also causes degranulation of adjacent mast cells to release their contents like histamine, chymase, tryptase. While histamine could cause leakiness of blood vessels and help in further escape of leukocytes, chymase activates matrix metalloproteinase 9, which in turn disrupts the basement membrane of the epithelium-connective tissue interface to help infiltration of CTLs into the epithelium.

REFERENCES

Rajendran R, Sivapathasundaram B. Shafer’s Textbook of Oral Pathology. 6 th ed. Elsevier; 2008.

Regezzi JA, Sciubba JJ, Jordan RCK. Oral Pathology: Clinical Pathologic Correlations. 5 th ed. Elsevier; 2007.

Lodi G, Scully C, Carrozzo M, Griffith S, Sugerman PB, Thongprasom K. Current controversies meeting. Part I. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100(1):40-51.

Roopashree MR, Gondhalekar RV, Shashikanth MC, George J, Thippeswamy SH, Shukla A. Pathogenesis of oral lichen planus- a review. J Oral Pathol Med 2010;9(10):729-734.

OTHER (HACKDENTISTRY) PRACTICE/STUDY RESOURCES

Oral Pathology & Medicine Question Bank 

Oral Pathology & Medicine Test Series


Oral Pathology & Medicine Illustrated Scripts


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