Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Pulmonary Tuberculosis II01:28

Pulmonary Tuberculosis II

Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Tuberculosis01:23

Tuberculosis

Tuberculosis (TB) remains a significant global health concern, primarily targeting the lungs and spreading through airborne transmission. Infection begins when aerosolized droplet nuclei, expelled by an individual with active TB, are inhaled by another person. These microscopic particles carry Mycobacterium tuberculosis, the causative agent of TB. Upon reaching the alveoli, the bacilli are engulfed by alveolar macrophages. However, due to their specialized lipid-rich cell wall, these pathogens...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Drug induced osteonecrosis of the jaws.

The Journal of the Tennessee Dental Association·2006
Same journal

Principles and Outcomes of Compartmental Resection in Upper Gingivobuccal Cancers.

Oral and maxillofacial surgery clinics of North America·2026
Same journal

Anatomy and Spread of Gingivobuccal Cancers.

Oral and maxillofacial surgery clinics of North America·2026
Same journal

Gingivobuccal Cancers: Demographics and Geographic Variations.

Oral and maxillofacial surgery clinics of North America·2026
Same journal

Unilateral Cleft Lip: Primary Repair.

Oral and maxillofacial surgery clinics of North America·2026
Same journal

Advances in Reconstructive Surgery for Gingivobuccal Cancers.

Oral and maxillofacial surgery clinics of North America·2026
Same journal

Etiology and Pathogenesis of Gingivobuccal Cancers.

Oral and maxillofacial surgery clinics of North America·2026
See all related articles

Related Experiment Video

Updated: Jun 28, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Wegener's granulomatosis.

Lawrence W Weeda1, Stephen A Coffey

  • 1Department of Oral and Maxillofacial Surgery, University of Tennessee, College of Dentistry, 875 Union Avenue, Memphis, TN 38163, USA. lweeda@utmem.edu

Oral and Maxillofacial Surgery Clinics of North America
|October 23, 2008
PubMed
Summary
This summary is machine-generated.

Wegener's granulomatosis (WG) is a rare disease with high mortality risk if not diagnosed and treated promptly. Early detection and intervention are crucial for managing this condition and preventing severe outcomes.

Related Experiment Videos

Last Updated: Jun 28, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Area of Science:

  • Rheumatology
  • Pulmonology
  • Otolaryngology

Background:

  • Wegener's granulomatosis (WG) is an uncommon vasculitis.
  • Delayed diagnosis and treatment significantly increase mortality risk.
  • WG can manifest with diverse symptoms, including skin, sinus, and oral mucosal lesions.

Purpose of the Study:

  • To provide clinicians with essential information on recognizing WG.
  • To outline diagnostic strategies for Wegener's granulomatosis.
  • To detail treatment approaches for managing WG.

Main Methods:

  • Literature review on WG recognition, diagnosis, and treatment.
  • Synthesis of clinical information for healthcare providers.

Main Results:

  • WG requires prompt clinical suspicion.
  • Characteristic initial presentations include mucocutaneous lesions.
  • Timely diagnosis and treatment are critical.

Conclusions:

  • Early recognition of WG is paramount.
  • Prompt initiation of treatment can mitigate life-threatening complications.
  • Clinicians must be informed to manage WG effectively.