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Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate,...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...

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Related Experiment Video

Updated: Jul 11, 2026

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

Oral mucosal disease: pemphigus.

Crispian Scully1, Michele Mignogna

  • 1University College London, Eastman Dental Institute, London, UK. c.scully@eastman.ucl.ac.uk

The British Journal of Oral & Maxillofacial Surgery
|September 18, 2007
PubMed
Summary

Pemphigus vulgaris (PV) is a rare autoimmune disease characterized by IgG autoantibodies against desmoglein 3 (Dsg3). Diagnosis involves biopsy, and treatment relies on immunosuppression, with new therapies showing promise.

Area of Science:

  • Immunodermatology
  • Autoimmune Blistering Diseases

Background:

  • Pemphigus vulgaris (PV) is a rare, potentially life-threatening autoimmune disease affecting skin and mucous membranes.
  • PV exhibits a genetic predisposition, with increased susceptibility in specific ethnic groups and links to HLA class II alleles.
  • The precise initiating event remains unclear, but autoantibodies against desmoglein 3 (Dsg3) are central to its pathogenesis.

Purpose of the Study:

  • To summarize the current understanding of pemphigus vulgaris (PV) etiology, pathogenesis, diagnosis, and management.
  • To highlight the role of IgG autoantibodies against desmoglein 3 (Dsg3) in PV.
  • To discuss diagnostic methods and current/emerging treatment strategies for PV.

Main Methods:

  • Review of existing literature on pemphigus vulgaris.

More Related Videos

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Related Experiment Videos

Last Updated: Jul 11, 2026

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

  • Analysis of etiological factors, including genetic associations and autoantibody targets.
  • Examination of diagnostic techniques (biopsy, histology, immunostaining).
  • Assessment of current management strategies (immunosuppression) and novel therapeutic approaches.

    • Main Results:

    • Circulating IgG autoantibodies targeting desmoglein 3 (Dsg3) are a hallmark of PV.
    • Oral lesions are common initial manifestations, progressing to mucocutaneous involvement.
    • Diagnosis is confirmed via biopsy, histology, and immunostaining.
    • Systemic immunosuppression, primarily corticosteroids and azathioprine, is the mainstay of treatment.

    Conclusions:

    • Pemphigus vulgaris is a serious autoimmune condition with a significant genetic component.
    • Targeting desmoglein 3 (Dsg3) with autoantibodies is critical in PV pathogenesis.
    • Effective diagnosis relies on histopathological and immunological confirmation.
    • While current treatments involve immunosuppression, promising new therapies are emerging.