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Cleft lip and palate
Congenital diaphragmatic hernia
Temporomandibular joint dysfunction
Gingivitis and periodontitis
Dental caries disease
Gastroesophageal reflux disease (GERD)
Diffuse esophageal spasm
Eosinophilic esophagitis (NORD)
Gastric dumping syndrome
Cyclic vomiting syndrome
Small bowel bacterial overgrowth syndrome
Short bowel syndrome (NORD)
Protein losing enteropathy
Small bowel ischemia and infarction
Familial adenomatous polyposis
Juvenile polyposis syndrome
Irritable bowel syndrome
Diverticulosis and diverticulitis
Non-alcoholic fatty liver disease
Cholestatic liver disease
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Primary biliary cirrhosis
Primary sclerosing cholangitis
Benign liver tumors
Pancreatic neuroendocrine neoplasms
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
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.
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