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Dental abscess



Gastrointestinal system


Peritoneum and peritoneal cavity
Upper gastrointestinal tract disorders
Lower gastrointestinal tract disorders
Liver, gallbladder and pancreas disorders
Gastrointestinal system pathology review

Content Reviewers:

Rishi Desai, MD, MPH

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.

The first one is called a periapical abscess, and it’s located at the apical foramen of the tooth.

A periapical abscess begins when bacteria gain entry into the dental pulp of the tooth through an opening caused by dental caries or from trauma.

The inflammation then spreads and causes necrosis or tissue death throughout the entire length of the dental pulp.

And if it goes on without treatment - like a root canal, then the infection ultimately reaches the apical foramen of the tooth.

Subsequently, the infection reaches the periapical tissues and at that point, it’s considered apical periodontitis, which is inflammation of the periapical tissues which secure the tooth in its socket.

The infection usually develops into an abscess as the pus coalesces, and it can involve nearby structures like the alveolar bone and adjacent teeth.

Sometimes periapical abscesses become quiescent, meaning that they don’t grow much but the bacteria remain alive within the abscess cavity.

In that situation, it’s called chronic inflammation, and it’s where a periapical granuloma forms from this walled-off area.

In fact, technically, the term “granuloma” is a misnomer in this case since these lesions don’t look like normal granulomas under a microscope.

During this stage where there’s a stalemate between the infection and the immune system, if the infection gains the upper hand, then it’s called an acute apical abscess.

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