Esophageal Lichen Planus-Contemporary Insights and Emerging Trends

Abstract

Background: Lichen planus (LP) is a common inflammatory disease affecting skin, mucous membranes, hairs, and nails, with an unpredictable course involving remissions and relapses. LP is a Type-I-Inflammation disease involving IFN-γ and IL-17 as key inflammatory mediators. Materials and Methods: We searched PubMed/MEDLINE and Google Scholar search engines for studies on the esophageal manifestation of lichen planus over an unlimited time frame. Articles were searched with combinations of Medical Subject Heading (MeSH) terms. Given the limited number of publications, no exclusion criteria were applied. Results: Esophageal lichen planus (ELP) is an underreported manifestation of LP that primarily affects middle-aged women. Its prevalence among LP patients remains to be defined. Though potentially clinically silent, ELP can significantly impact patient wellbeing and serve as a precursor to esophageal squamous cell carcinoma. While dysphagia is the primary symptom, the condition may also remain subclinical. The endoscopic hallmarks of ELP are mucosal denudation and tearing, trachealization, and hyperkeratosis. Chronic disease progression may lead to scarring esophageal stenosis. Histologically, ELP shows mucosal detachment, T-lymphocytic infiltrations, epithelial cell apoptosis (Civatte bodies), dyskeratosis, and hyperkeratosis. Fibrinogen deposits along the basement membrane zone distinguish ELP from various immunological esophageal diseases. There is currently no standardized therapy available. Topical steroids lead to symptomatic and histologic improvements in two-thirds of patients. Severe or refractory cases require immunosuppressive therapy, whereas JAK-inhibitors represent a promising emerging option. Endoscopic dilation helps symptomatic stenosis. Considering ELP's precancerous potential, timely diagnosis and treatment are crucial in preventing complications, such as stenosis or invasive esophageal squamous cell carcinoma. Conclusions: ELP is an underdiagnosed and underreported manifestation of LP. While it may remain clinically silent, it can nevertheless significantly affect patients' wellbeing and life expectancy. This narrative review aims to initiate multidisciplinary cooperation among gastroenterologists, dermatologists, oral health professionals, and histopathologists to support clinical diagnosis and management.

Keywords: JAK inhibitors; autoimmunity; dysphagia; eosinophilic esophagitis; esophageal epidermoid metaplasia; esophagitis; lichen planus; precancerous condition; squamous cell carcinoma.

Figure 1

Endoscopic findings in esophageal lichen planus. (A): trachealization; (B): trachealization and fragile mucosa; (C): hyperkeratosis; (D,E): tearing; (F,G): tearing and localized denudation of the mucosa; (H,I): tearing and spacious denudation of the mucosa.

Figure 2

Histopathologic features of ELP: band-like lymphocytic infiltrate in the superficial tunica propria, most prominent at the rete ridges, spilling over to the squamous epithelium (A). Scattered epithelial apoptosis (Civatte bodies, (B)). Intraepithelial CD3-positive T-cells (C) enriched in a CD8-positive subpopulation (D). Focal detachment of the squamous epithelium from the tunica propria (E). Example of a case with intraepithelial lymphocytes (F) composed of CD4-positive T-cells (G) and only a small number of CD8-positive cells (H). (A,B,E,F): hematoxylin and eosin; (C,D,G,H): immunohistochemical stains for CD3, CD4, or CD8. Original magnification: (A,F) ×400, (B) ×1000, (C,D,G,H) ×250, (E) ×100.

Figure 3

Dissection of the esophageal squamous epithelium at the junctional zone associated with confluent inflammatory infiltrates (A–C) Abundant CD3-positive T-cells (D) predominantly expressing CD4 in this case (E). Increased Ki67-positive proliferation fraction of the squamous epithelium (F). (A–C): hematoxylin and eosin; (D–F): immunohistochemical stains for CD3, CD4, or Ki67. Original magnification (A) ×100, (B,C) ×650, (D–F) ×250.

Figure 4

Conditions mimicking ELP: Lymphocytic gastritis (A) associated with a lichenoid esophagitis (B) with numerous CD3-positive T-cells (C); eosinophilic esophagitis (D) and erosive Candida esophagitis (E) characterized not only by a granulocytic but also by a CD3-positive T-cell component (F). (A,B,D): hematoxylin and eosin; (E): periodic acid Schiff reaction; (C,F): immunohistochemical stains for CD3. Original magnification: (A–F) ×400.