Oral Lichen Planus Workup

Updated: Oct 02, 2017
  • Author: Jaisri R Thoppay, DDS, MBA, MS; Chief Editor: Jeff Burgess, DDS, MSD  more...
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Laboratory Studies

The history, typical oral lesions, and skin involvement are usually sufficient to diagnose oral lichen planus (OLP), although laboratory studies and biopsy may be required (see Procedures).

Direct immunofluorescence testing can help in distinguishing erosive or the rare bullous oral lichen planus from pemphigus vulgaris, benign mucous membrane pemphigoid, dermatitis herpetiformis, and linear immunoglobulin A (IgA) disease. The most characteristic feature of oral lichen planus is shaggy linear fibrin distribution.

Some studies show an increased incidence of C albicans infection in patients with oral lichen planus. Periodic acid-Schiff (PAS) staining of biopsy specimens and candidal cultures or smears may be performed. However, these tests may be of limited clinical value because oral C albicans is present in more than 70% of the population as a common organism in oral flora. The presence of C albicans and the oral load of this organism do not aid either the diagnosis or the treatment of oral lichen planus.


Other Tests

Skin patch testing may be helpful in identifying a contact allergy in some patients with oral lichen planus (OLP). [33] The current recommendation is to use a standard series; a dental prosthesis series; and a metal salt series that includes gold, mercury, and palladium salts as well as other salts of metals used in dental restorations. Late readings, or those obtained at 10 and 17 days after the application of the skin patch, may be required.

The most common allergy is related to mercury contained in amalgam restorations. Compared with patients with lesions in other locations, patients with lesions near the amalgam restoration have a higher rate of positive patch test results to mercury. When the amalgam restorations are removed, patients with a positive result have higher remission rates (47-100% depending on the study) than those of patients without this positive result.

Although the assessment of hepatic function in the treatment of otherwise healthy southern European and Japanese patients with oral lichen planus may be warranted, similar screening in British and American patients appears to be of limited benefit. Formal studies are still ongoing. Consider hepatic biochemical testing only when patients have proven oral lichen planus and suspected liver disease.



Biopsy may be required to exclude malignancy or to differentiate between oral lichen planus (OLP) and other white or chronic ulcerative oral lesions, including reactive keratoses, chronic hyperplastic candidosis, epithelial dysplasia, discoid lupus erythematosus, gastrointestinal disease (including oral Crohn disease), and anemic states.


Histologic Findings

Histopathologic examination of lesional tissue is the most relevant investigation in cases of oral lichen planus (OLP).

Consistent findings include a bandlike subepithelial mononuclear infiltrate consisting of T cells and histiocytes, increased numbers of intraepithelial T cells, and degenerating basal keratinocytes that form colloid (Civatte, hyaline, cytoid) bodies, which appear as homogenous eosinophilic globules. Variable findings include parakeratosis, acanthosis, and sawtooth rete pegs.

Degeneration of the basal keratinocytes and disruption of the anchoring elements of the epithelial basement membrane and basal keratinocytes (eg, hemidesmosomes, filaments, fibrils) weakens the epithelial-connective tissue interface. As a result, histologic clefts (ie, Max-Joseph spaces) may form, and blisters on the oral mucosa (bullous lichen planus) may be seen at clinical examination. B cells and plasma cells are uncommon findings.

Immunoglobulin or complement deposits are not a consistent feature of oral lichen planus, although fibrin is deposited in a shaggy linear pattern in the basement membrane zone. Colloid bodies contain fibrin, immunoglobulin M (IgM), C3, C4, and keratin. Laminin and fibronectin staining may be absent in areas of heavy fibrin deposition and colloid body formation. This finding suggests basement membrane damage in these areas.

In oral lichen planus, electron microscopy is used principally as a research tool. The ultrastructure of the colloid bodies suggests that they are apoptotic keratinocytes, and studies using the end-labeling method revealed DNA fragmentation in these cells. Electron microscopy shows breaks, branches, and duplications of the epithelial basement membrane in oral lichen planus.