Related Experiment Video
Updated: Jul 16, 2025

Author Spotlight: Development and Evaluation of a Compound Acne Rodent Model Using C. acnes and Oleic Acid
Published on: November 1, 2024
Hidradenitis suppurativa and follicular occlusion syndrome: Where is the pathogenetic link?
Beata Jastrząb1, Jacek C Szepietowski1, Łukasz Matusiak1
1Department of Dermatology, Venereology, and Allergology, Wroclaw Medical University, Wroclaw, Poland.
Abstract:
The follicular occlusion tetrad complex encompasses several entities (hidradenitis suppurativa, acne conglobata, dissecting cellulitis of the scalp, and pilonidal cyst) that share common clinical features, risk factors, and pathophysiology. Follicular occlusion is a crucial triggering mechanism in the etiology in each of these disorders, leading to development of distinctive skin lesions such as deep-seated nodules, abscesses, comedones, and draining sinuses, often with accompanying scarring. Despite the fact that the follicular occlusion tetrad components manifest multiple similarities, they also exhibit many differences among themselves and require individual approaches and treatment.
Related Concept Videos
Skin Diseases and Disorders
Gram-positive Staphylococcus spp. and Streptococcus spp. are responsible for many of the most common skin infections. However, many...
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
Accessory Structures of the Skin: Sebaceous Glands
These glands that produce the oils on the skin and hair are holocrine glands. The mature...
Chronic Bowel Disorders: Introduction
Irritable Bowel Syndrome (IBS) is a common disorder affecting the gastrointestinal tract. The distinctive feature is recurrent abdominal pain associated with altered bowel movements, manifesting as constipation, diarrhea, or fluctuating between both. The...
Sexually Transmitted Infections
Urinary Tract Infection II: Pathophysiology

