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Oral lichenoid lesion

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ORAL LICHENOID LESIONS: PATHOGENESIS, CLINICAL FEATURES, HISTOPATHOLOGY AND TREATMENT

Author: Sanketh DS, MDS

INTRODUCTION & ETIOLOGY

Oral lichen planus (OLP) is a chronic mucosal disorder of autoimmune pathogenesis, for which the etiology is yet unknown. While OLP could be clinically diagnosed beyond doubt when manifesting in its characteristic “bilateral & reticular” form, there may be instances where certain lesions may clinically appear very similar but lack certain classic characteristics of OLP or may have a specific etiologic factor. Such lesions are a group of mucosal diseases called “oral lichenoid lesions (OLL)”.

OLLs have been classified into 4 types them being 1) oral lichenoid contact lesions due to amalgam restorations, 2) OLLs due to drugs, 3) OLL in graft versus host disease(GVHD) and 4) an unclassified type of OLL that may lack one or more clinical aspects of OLP. For example patients may manifest with erythematous changes limited to the gingiva without signs of “classic” OLP elsewhere in the oral cavity, or lesions may be unilateral in presentation. In addition, there have also been reports of arecanut and betel quid chewing causing these lesions.  

PATHOGENESIS

Oral lichenoid lesions due to amalgam, drugs and betel quid take a long period of time to manifest, usually in the order of months to years. Hence these OLLs are hypothesized to be type IV hypersensitivity reactions where the amalgam, mercury, drug or betel quid products bind with the oral keratinocyte surface proteins, inducing a cell-mediated auto-immune response.

Langerhans cell may pick the antigen from an oral keratinocyte and present them to a naïve CD4+ T cell activating them to become mature CD 4+ T cell. The active CD4+ T cell produces cytokines IL-2 and IFN-γ. Further, IL-2 may stimulate naïve CD 8+ T cells to become activated cytotoxic cells. An activated CD 8+ T cell could recognise the antigen in the oral keratinocyte and on recognition destroys the keratinocyte by releasing perforins and grazymes. Perforins create pores on the keratinocyte and granzymes induce apoptosis of the cell.  

GVHD occurs in recipients of allogenic bone-marrow transplantation. The immune-competent T cells present in the donor marrow recognise the host/recipient antigens as foreign and react against them.  

CLINICAL FEATURES

OLL due to amalgam restorations

These OLLs manifest as reticular white striae, papules or plaques with or without erosions (red areas) or ulcerated areas. They are commonly located posteriorly on the buccal mucosa and lateral border of the tongue where the mucosa comes in contact with the restoration. These lesions have an anatomic relationship to the restoration and are typically unilateral on the same side of the restoration and are never bilateral. OLLs due to amalgam restorations are seldom present on the gingiva, palate or other oral sites. However, the diagnosis may become difficult when there are multiple amalgam restorations.

Key to diagnosis: Unilateral lesion in close association with the amalgam restoration together with histolopathology.

OLL due to drugs

Numerous drugs like anti-malarials, anti-hypertensives, NSAIDs and anti-microbials have been reported to cause OLL. These OLLs may manifest as desquamative lesions, reticular white striae, white plaques with or without erosions (red areas) or ulcerated areas. There may or may not be burning sensations to hot and spicy foods.

Key to diagnosis: Lichenoid drug reactions could pose problems during diagnosis. Not only do they take several months to manifest post the use of the drug, but also do not subside immediately after the drug’s withdrawal. This makes it difficult to establish a “cause-effect” relationship between the drug and the lesion. However it has been suggested that these lesions tend to be mostly unilateral and ulcerative.

OLL due to GVHD

These lesions present as erythematous, ulcerated and desquamative areas, with white keratotic striae or plaques. Patients complain of pain and burning sensation to hot and spicy foods.

Key to diagnosis: History of bone marrow transplantation and other systemic manifestations of GVHD.

OLL due to arecanut and betel quid

These lesions may present as fine white wavy, parallel striae that do not criss-cross unlike OLP and sometimes may radiate from a central erythematous area.

Key to diagnosis: The lesions commonly manifest on the buccal mucosa and the gingivo-buccal sulcus corresponding to the placement of the quid. The lesion may regress on cessation of the habit.

HISTOPATHOLOGY

The histopathological features of OLLs are very similar to OLP with a few differences. OLLs have an epithelium that may be hyperkeratotic, atrophic or ulcerated with basal cell degeneration. Typically all OLLs except OLLs in GVHD have sub-epithelial inflammation that may extend deep into the stroma. The inflammatory infiltrate is mixed consisting of lymphocytes, plasma cells, neutrophils and eosinophils. In addition there may be subtle differences among the different OLLs themselves.

a) OLLs due to amalgam restorations may have lymphoid follicle aggregates scattered in the stroma.
b) OLLs in GVHD have sparse sub-epithelial inflammation confined to the upper stroma and perivascular cuffing by lymphocytes.
c) OLLs due to drugs may have an increased number of apoptotic or colloid bodies in the epithelium.

DIAGNOSIS

When you encounter a white lesion that has wavy striae; check if the lesion has classic OLP features, i.e. a bilateral reticular lesion on the buccal mucosa. If so, it fulfils a clinical diagnosis of OLP. If the lesion shows atypical features, ie is unilateral and has an etiological agent like amalgam, betel quid, drugs or GVHD associated, it could be clinically diagnosed as OLL . A biopsy could be done if in doubt, to check for microscopic features. Apart from certain similar features, OLLs could be differentiated from OLP by the presence of dense inflammation extending deep into the stroma, mixed inflammatory infiltrate, lymphoid aggregates and perivascular cuffing! 

REFERENCES

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

Neville BW, Damm DD, Allen CM, Chi A. Oral and Maxillofacial Pathology. South Asian ed. Elsevier; 2016.

Kamath VV, Setlur K, and Yerlagudda K. Oral Lichenoid Lesions – A Review and Update. Indian J Dermatol. 2015; 60(1): 102.

Hiremath SK,  Kale AD, Charantimath S. Oral lichenoid lesions: Clinico-pathological mimicry and its diagnostic implications. Indian J Dent Res. 201;22(6):827-34.

Robledo-Sierra J. Oral lichen planus: A study of associated factors with special reference to thyroid disease. Doctoral Thesis, Institute of Odontology, Sahlgrenska Academy at University of Gothenburg,2015.

Reichart PA, Warnakulasuriya S. Oral lichenoid contact lesions induced by areca nut and betel quid chewing: a mini review. J Investig Clin Dent. 2012;3(3):163-6.

Anand R, Dhingra C,  Menon I, Prasad S. Betel nut chewing and its deleterious effects on oral cavity. J Cancer Res Ther. 2014;10(3):499-505.

Patil S, Rao RS, Sanketh DS, Warnakulasuriya S. Lichenoid dysplasia revisited – evidence from a review of Indian archives. J Oral Pathol Med. 2015;44(7):507-14.

OTHER (HACKDENTISTRY) PRACTICE/STUDY RESOURCES

Oral Pathology & Medicine Question Bank 

Oral Pathology & Medicine Test Series


Oral Pathology & Medicine Illustrated Scripts


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