Discussion

The clinical picture (radiating white lines, those are Wickham striae, with erythema and erosion in a middle-aged woman) is characteristic, but a confident diagnosis of oral lichen planus (OLP) rests on clinicopathologic correlation, because several oral conditions share this histology. [1] The biopsy shows the hallmark lichenoid interface mucositis: a band-like, predominantly lymphocytic infiltrate hugging the epithelial-connective tissue interface and confined to the superficial lamina propria, together with basal cell liquefactive (hydropic) degeneration, and scattered Civatte (colloid) bodies, and no epithelial dysplasia. [1] Supportive features include ortho- or parakeratosis and atrophic or saw-tooth rete ridges; in atrophic and erosive areas the epithelium is thinned or ulcerated and these features may be attenuated, with sub-basal separation presenting as a specific feature of the erosive form of OLP. [1]

PAS is indicated to identify superimposed candidiasis; Candida frequently colonizes OLP, acting as an aggravating factor that can worsen clinical symptoms, modulate the local immune response, and potentially increase the risk of malignant transformation. [2,3] PAS also delineates the basement membrane, which in OLP shows focal thickening and discontinuity from the interface injury. [4] This structural damage occurs because basement membrane proteins are degraded by matrix metalloproteinases and mast cell enzymes, such as chymase and tryptase, released during the local T-cell immune response. [4]

The principal differential is an oral lichenoid lesion/reaction (drug-, dental amalgam-, or GVHD-related), which tends to show a deeper or mixed infiltrate with eosinophils or plasma cells and perivascular extension, and is separated largely on clinical context. [1] Epithelial dysplasia must be actively excluded, since lichenoid dysplasia can mask premalignant change and should not be signed out as OLP. [1] Discoid lupus erythematosus also enters the differential given the interface pattern and basement membrane thickening, distinguished by a superficial and deep perivascular infiltrate plus clinical and, where indicated, direct immunofluorescence correlation. For the erosive component, direct immunofluorescence is useful to exclude an immunobullous disease (mucous membrane pemphigoid, pemphigus vulgaris) when clinically warranted.

Crucially, OLP is a recognized oral potentially malignant disorder with a low, still-debated malignant transformation risk; exclusion of dysplasia and clinical follow-up are essential. [1]

References

1. Cheng YS, Gould A, Kurago Z, Fantasia J, Muller S. Diagnosis of oral lichen planus: a position paper of the American Academy of Oral and Maxillofacial Pathology. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016;122(3):332–354.

2. Rodriguez-Archilla A, Fernandez-Torralbo S. Candida species colonization in oral lichen planus: A meta-analysis. Int J Health Sci (Qassim). 2022;16(4):58-63.

3. Sitheeque MAM, Samaranayake LP. Chronic hyperplastic candidosis/candidiasis (candidal leukoplakia). Crit Rev Oral Biol Med. 2003;14(4):253-267.

4. Juneja M, Mahajan S, Rao NN, George T, Boaz K. Histochemical analysis of pathological alterations in oral lichen planus and oral lichenoid lesions. J Oral Sci. 2006;48(4):185-193.