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Related Experiment Video

Updated: Jun 16, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

The pathogenesis of systemic sclerosis revisited.

Matthias Geyer¹, Ulf Müller-Ladner

¹Department of Rheumatology and Clinical Immunology, Justus-Liebig-University of Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany.

Clinical Reviews in Allergy & Immunology

|January 21, 2010

Summary

Systemic sclerosis (SSc) is a chronic autoimmune disease with unknown causes, leading to excessive collagen buildup and vascular issues. Its complex pathophysiology involves immune system imbalances, vascular dysfunction, and connective tissue activation, resulting in various organ manifestations.

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Area of Science:

Rheumatology
Immunology
Pathophysiology

Background:

Systemic sclerosis (SSc) etiology remains enigmatic despite known infectiological, environmental, and genotypic factors.
SSc is a chronic autoimmune disease characterized by excessive collagen deposition and obliterating angiopathy.
Pathophysiology involves immune system imbalances, vascular dysfunction, and activated connective tissue cells.

Purpose of the Study:

To elucidate the complex interplay of factors contributing to SSc pathophysiology.
To summarize the mechanisms underlying SSc development and progression.
To correlate pathophysiological mechanisms with clinical manifestations observed in SSc patients.

Main Methods:

Review of existing literature on SSc etiology and pathophysiology.
Analysis of the interplay between immune, vascular, and connective tissue components.
Correlation of pathophysiological findings with clinical symptoms.

Main Results:

SSc pathophysiology stems from a complex interplay of immune dysregulation, vascular dysfunction, and fibroblast activation.
This interplay leads to impaired vascular response, excessive extracellular matrix deposition, and immunological disarrangement.
These mechanisms explain diverse clinical manifestations like Raynaud's phenomenon, digital ulcers, and organ-specific symptoms.

Conclusions:

The etiology of SSc is multifactorial and complex, involving intricate interactions between the immune system, vasculature, and connective tissue.
Understanding these pathophysiological pathways is crucial for explaining the wide spectrum of clinical symptoms in SSc patients.
Further research is needed to fully unravel the enigmatic etiology and develop targeted therapies for systemic sclerosis.