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Oral Lichen Planus (OLP)

Oral Lichen Planus (OLP) is a chronic and persistent disease that afflicts 1–2% of the population (3). A chronic course is typical, and spontaneous resolution is uncommon. The disease most frequently occurs in middle-aged females. This disease is uncommonly seen in younger patients. Approximately 15% of OLP patients develop cutaneous lesions and approximately 20% have concomitant genital lesions. Oral involvement may be seen in up to 60% of patients with cutaneous LP. OLP rarely occurs in children (1). The etiology and pathogenesis of OLP has not been fully understood, but it is thought to arise from a chronic immune response involving CD4 + and CD8 + T lymphocytes with keratinocyte apoptosis (5). 

The main risk of OLP is malignant transformation of the lesions, ranging from 0.4% to up to 12.5% in the erythematous and erosive types (4)

Clinical Features

  • Clinical presentation of OLP is usually bilateral symmetric or asymmetric, located on buccal mucosa, tongue, lips and/or gingiva. Usually, the lesions show characteristic Wickham’s striae; white lines forming a lace-like network (2). Clinically, six types of OLP, namely reticular, plaque-like, papular, atrophic/erosive, ulcerative, and bullous types, can be identified. Two or more types of OLP can occur simultaneously in a patient.

Diagnosis

  • Diagnosis of OLP is established by clinical examination with histopathologic confirmation. Direct immunofluorescence (DIF) examination is used to rule out autoimmune diseases (e.g., pemphigus, pemphigoid). Histopathologic diagnosis confirms the clinical diagnosis of OLP. The correlation between clinical and histopathologic diagnosis is crucial for definitive diagnosis of OLP. OLP necessitates additional biopsy for direct immunofluorescence assessment and/or histopathologic evaluation, so continued clinical follow-up after the initial biopsy is essential.

  • The histopathologic features of OLP are characteristic and composed of hyperkeratosis of the epithelium, hydropic or liquefaction degeneration of basal epithelial cells, atrophy or acanthosis of spinous epithelial cells, saw-tooth epithelial ridges, a homogeneous eosinophilic deposit at the epithelium-connective tissue junction, and a band-like lymphocytic infiltrate in the superficial lamina propria. Degenerating keratinocytes may be seen in the area of the epithelium and connective tissue interface and have been termed colloid, cytoid, hyaline or Civatte bodies (1). 

  • DIF is a diagnostic adjunct for OLP lesion. The characteristic DIF finding for OLP lesion is a deposit of fibrinogen in a shaggy pattern at the basement membrane zone in the absence of immunoglobulin and complement (3). DIF is often necessary to differentiate OLP from mucous membrane pemphigoid and pemphigus vulgaris. DIF finding for mucous membrane pemphigoid is a linear deposition of immunoglobulins (IgG, IgA or IgM) or complement 3 (C3) at the basement membrane zone of the epithelium, and that for pemphigus vulgaris is a lattice-like (or chicken wire) deposition of immunoglobulins (IgG or IgM) or C3 in the intercellular areas among epithelial cells (1)

Management

  • Asymptomatic lesions do not require treatment. However, annual follow-up to assess for clinical transformation and self-resolution. Treatment besides proper oral hygiene and eliminating rough, jagged dental surfaces also involves avoiding irritating foods. For symptomatic lesions, topical corticosteroids are the first-line local treatment. Additional options for local therapy include topical calcineurin inhibitors and intralesional corticosteroid injections. The systemic agents (e.g., prednisone) are usually reserved for recalcitrant cases.

Oral Lichen Planus (OLP) Tests

Selected References

  1. Cheng, Y. S. L., Gould, A., Kurago, Z., Fantasia, J., & Muller, S. (2016). Diagnosis of oral lichen planus: a position paper of the American Academy of Oral and Maxillofacial Pathology. Oral surgery, oral medicine, oral pathology, and oral radiology, 122(3), 332-354.

  2. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol. 2002; 46:207–14. 

  3. González‐Moles, M. Á., Warnakulasuriya, S., González‐Ruiz, I., González‐Ruiz, L., Ayén, Á., Lenouvel, D., ... & Ramos‐García, P. (2021). Worldwide prevalence of oral lichen planus: A systematic review and meta‐analysis. Oral diseases, 27(4), 813-828.

  4. Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005; 100:164–78. 

  5. Nogueira PA, Carneiro S, Ramos-E-Silva M: Oral lichen planus: an update on its pathogenesis. Int J Dermatol. 2015;54(9):1005–10. 10.1111/ijd.12918 

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