DELAYED WOUND HEALING IN AUTOIMMUNE VASCULITIS: A HISTOPATHOLOGICAL STUDY

Abstract

Autoimmune vasculitides are systemic disorders marked by blood vessel inflammation and frequently complicated by delayed wound healing. This histopathological study aimed to elucidate the underlying mechanisms contributing to impaired tissue repair in patients with autoimmune vasculitis. Skin biopsy samples were obtained from patients presenting with non-healing cutaneous ulcers and compared to control samples. Histological analysis revealed dense infiltration of neutrophils, macrophages, and lymphocytes in the wound beds, indicating persistent inflammation. Immunohistochemical staining showed elevated TNF-α levels and a predominance of pro-inflammatory (M1) macrophages, reinforcing the role of chronic inflammation in delaying wound closure. Vascular integrity was significantly compromised, as evidenced by reduced CD31 expression, while increased α-SMA expression indicated pathological vascular remodeling. These findings suggest that endothelial dysfunction impairs nutrient and oxygen delivery to the wound site, further exacerbating tissue damage. Additionally, Masson’s trichrome staining demonstrated excessive collagen deposition and fibrosis, while elevated matrix metalloproteinase activity highlighted ongoing extracellular matrix degradation. The combined effects of prolonged inflammation, vascular disruption, and fibrotic remodeling establish a hostile microenvironment that hinders the normal wound healing cascade. Although the study’s modest sample size limits generalizability, the findings underscore critical pathological features that could be targeted for future therapeutic intervention. These insights provide a foundation for developing immunomodulatory and vascular-stabilizing strategies to improve wound outcomes in patients with autoimmune vasculitis.