# Histological and Immunohistochemical Insights into Disc Perforation in the Temporomandibular Joint: A Case Report

## TL;DR

This case report examines the tissue changes in a perforated TMJ disc, revealing how mechanical stress and inflammation contribute to its degeneration.

## Contribution

The study provides novel histological and immunofluorescence insights into the mechanisms of disc perforation in TMJ disorders.

## Key findings

- Perforated disc tissue showed disorganized collagen fibers and increased fibro-chondrocytes with vascular proliferation.
- Reduced collagen type I and fibrillin-1, along with elevated MMP-3, MMP-9, and CD68, indicated ECM degradation and inflammation.
- The findings highlight biomechanical stress and inflammation as key factors in TMJ disc perforation.

## Abstract

Background/Objectives: Anterior disc displacement without reduction (ADDwoR) is a temporomandibular joint (TMJ) disorder characterized by progressive dysfunction and potential complications. Persistent displacement leads to abnormal mechanical stress, predisposing the TMJ disc to structural degeneration, including perforation. This case report aimed to examine the histological and immunofluorescence characteristics of perforated disc tissue to elucidate the mechanisms contributing to its pathology. Methods: A 50-year-old patient with bilateral ADDwoR and disc perforation underwent functional arthroplasty. Tissue samples from the perforated disc were histologically analyzed using hematoxylin–eosin and Azan Mallory staining. Immunofluorescence was performed to assess the expression of collagen type I, fibrillin-1, matrix metalloproteinases (MMPs)-3 and -9, and cluster of differentiation 68 (CD68). Results: Histological analysis revealed disorganized collagen fibres and fibro-chondrocyte cell predominance in the perilesional zone, accompanied by vascular proliferation. Adjacent tissue to perforation exhibited normal fibrous organization. Immunofluorescence showed reduced collagen type I and fibrillin-1 patterns in the perilesional area, indicating an alteration in the fibrillar component of the extracellular matrix (ECM). Increased expression of MMP-3 and MMP-9, as well as elevated numbers of CD68-positive macrophages, suggested active ECM degradation and inflammation localized to the perforation site. Conclusions: This case report underscores the critical role of biomechanical stress and inflammation in disc perforation. Decreased ECM integrity, driven by altered collagen and fibrillin composition, as well as heightened MMP activity, compromises the disc’s capacity to absorb and distribute mechanical loads. These findings advance our understanding of TMJ pathophysiology, emphasizing the need for therapeutic approaches that target both biomechanical stabilization and inflammation.