Dental abscess

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Dental abscess

Pathology

Peritoneum and peritoneal cavity

Peritonitis

Pneumoperitoneum

Upper gastrointestinal tract disorders

Cleft lip and palate

Congenital diaphragmatic hernia

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Tracheoesophageal fistula

Pyloric stenosis

Sialadenitis

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Temporomandibular joint dysfunction

Dental abscess

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Warthin tumor

Barrett esophagus

Achalasia

Plummer-Vinson syndrome

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Gastrointestinal system pathology review

Congenital gastrointestinal disorders: Pathology review

Esophageal disorders: Pathology review

GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review

Inflammatory bowel disease: Pathology review

Malabsorption syndromes: Pathology review

Diverticular disease: Pathology review

Appendicitis: Pathology review

Gastrointestinal bleeding: Pathology review

Colorectal polyps and cancer: Pathology review

Neuroendocrine tumors of the gastrointestinal system: Pathology review

Pancreatitis: Pathology review

Gallbladder disorders: Pathology review

Jaundice: Pathology review

Viral hepatitis: Pathology review

Cirrhosis: Pathology review

Transcript

Content Reviewers

Rishi Desai, MD, MPH

Contributors

Charles Davis, MD

Evan Debevec-McKenney

Tanner Marshall, MS

Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses.

An abscess forms when normal tissue, like the gingiva or gums and teeth for example, is split apart and that new space is invaded by nearby pathogens like bacteria.

In a healthy mouth, normal or commensal bacteria thrive but don’t cause disease.

However, any cut or break in the mucosa is an invitation for bacteria to dive in and multiply, causing an infection.

When that happens, the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, cells release small chemicals called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6, interleukin-8, and interleukin-17, and these attract nearby immune cells.

It’s kinda like yelling for help and being heard by the nearby police.

In addition, the cytokines also dilate nearby capillaries and make them leaky - which brings more blood to the site, and allows immune cells that do show up, to easily slip out of the blood and into the tissue.

The first immune cells at the scene are neutrophils, and they release chemicals and enzymes that kill themselves and the bacteria they swallow up, creating a pool of dead bacteria and cells.

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.

Initially the dead tissue is intermixed with healthy tissue, but over time it can coalesce into a single area.

And around this pool of pus, a wall of fibrinogen - starts to harden into a barrier.

Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess...

Even though the pus is largely dead material, there are still plenty of live bacteria within the pus, which makes it highly infectious if it gets spread from one place to another.

There are a few different types of dental abscesses.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "The microbiology of the acute dental abscess" Journal of Medical Microbiology (2009)
Elsevier

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