# The Inflammatory–Dysplastic Spectrum in Oral Lichen Planus: A Study on Six Immunohistochemical Markers

## TL;DR

This study investigates six immune markers in oral lichen planus to understand how inflammation might lead to cancerous changes in the mouth.

## Contribution

The study identifies specific immunohistochemical markers associated with dysplastic progression in oral lichen planus.

## Key findings

- IL-17 is highly upregulated in OLP lesions and correlates with inflammation intensity.
- Nuclear β-Catenin localization is linked to moderate dysplasia in OLP.
- Syndecan-4 membrane expression decreases in dysplastic lesions, while Maspin and TIMP-1 are more common in non-dysplastic cases.

## Abstract

Background/Objective: Oral lichen planus (OLP) is a chronic inflammatory, immune-mediated mucosal condition classified as a potentially malignant disorder due to its risk of progression to oral squamous cell carcinoma (OSCC). The molecular events linking chronic inflammation in OLP to epithelial dysplasia remain poorly defined. To evaluate the expression of six immunohistochemical markers: IL-17, Maspin, β-Catenin, TIMP-1, MMP-14 and Syndecan-4 in OLP specimens and to explore their association with clinicopathological features and early dysplastic changes. Methods: We conducted a retrospective, cross-sectional study including 63 cases of OLP and 20 healthy controls. Formalin-fixed, paraffin-embedded sections underwent immunohistochemical staining for the six markers. Semi-quantitative scoring of staining intensity and percentage of positive cells was performed independently by two blinded pathologists. Results: IL-17 was markedly upregulated in 82.5% of OLP lesions versus absence in controls, correlating strongly with inflammatory infiltrate intensity. β-Catenin exhibited cytoplasmic and nuclear accumulation in 88.9% of OLP samples, with nuclear localization significantly associated with moderate dysplasia. Syndecan-4 membrane expression was reduced in dysplastic lesions, while Maspin and TIMP-1 co-expression were more prevalent in non-dysplastic OLP. MMP-14 was weakly positive in 87.3% of OLP cases and correlated with neovascularization. Conclusions: Elevated IL-17 expression and nuclear localization of β-Catenin may contribute to the progression of OLP toward dysplastic transformation, with this pattern being most evident in the erosive subtype. These findings suggest that a combined immunohistochemical panel may support risk stratification in OLP, although validation in larger, prospective cohorts is warranted.