Dental caries disease

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Introduction0:00–0:24

Dental caries disease, also called tooth decay, refers to demineralization or weakening of the teeth, and the end result of caries disease is a caries lesion.
An advanced caries lesion can progress to a point where the tooth surface forms a cavitation or a hole, which is the physical evidence of tooth breakdown.
Let's start by building a model of a tooth and its surrounding structures. In the mouth, the bone beneath the bottom row of teeth is the mandible, and the bone above the top row of teeth is the maxilla.

Physiology0:24–2:50

Both bones have an alveolus, or socket, for each tooth. The socket is lined on the inside by a periodontal ligament.
Protecting the alveolus on the outside, is a layer of soft, supportive tissue called the gingiva, or gums, that sits on top of the bone and covers the root surface from the bone to the cementoenamel junction - where the cementum and enamel come together.
The tooth itself can be roughly divided into a few parts. The first part is the root, and it sits within the alveolus.
The root is covered by cementum, which is a bonelike substance that the periodontal ligament’s fibers attach to. Next, there’s the neck, which is the transition between the root portion covered by bone and the crown.
The crown is the visible part of the tooth that protrudes from the gingiva, and it’s covered in enamel, which has such a high mineral content that it’s the hardest substance in the human body.
When the teeth are developing, enamel is made before the tooth erupts into the mouth by a group of cells called the ameloblasts that die once the tooth erupts - meaning that the teeth lose the ability to make more enamel forever.
Now, let’s fill the tooth in from the inside out. Blood vessels and nerves come from the jaw bones, and enter the center of the root through a narrow passage, called the apical foramen.
From there, they enter the soft center of the tooth, called the pulp, where they provide nutrition and sensation. The outer wall of the pulp, contains odontoblasts which are cells that secrete a bonelike substance called dentin, which is filled with protein and minerals.
The odontoblasts have long processes, or arms, that lay within tiny tubules in the dentin - like an octopus sticking its arms through a block of cement.
These tubules are important for sensory nerves as well, which use them to travel through the dentin from the pulp to the dentin-enamel junction.
Finally, there’s saliva, which is secreted from several glands in the mouth. Saliva contains bicarbonate ions, which helps to neutralize acid in the mouth, and glycoproteins like mucin which thickens the saliva.
Saliva also contains calcium and phosphate, which serve as replacement minerals, to help remineralization of the tooth surface.
So, when it comes to dental caries, there’s a tug-of-war between the pathogenic factors that promote demineralization of the tooth and protective factors that promote remineralization of the tooth.

Pathology2:50–7:51

Normally, there's a layer called the pellicle that covers the tooth, and bacteria in the mouth, like viridans group streptococci, settle on that pellicle layer.
These bacteria are called early colonizers, and they attach to the surfaces using bacterial surface proteins called adhesins.
Because they’re on the pellicle of the teeth, these bacteria come into contact with sucrose, a sugar found in various foods and drinks including table sugar.
Sucrose contains a glucose molecule bound to a fructose molecule. So the bacteria use an enzyme called glucosyltransferase to cut the bond between them, use the fructose for energy, and add the glucose to a growing chain of glucose molecules called a glucan.
Glucans allow the bacteria to attach firmly to the surface of the tooth, and form dental plaque, which is a sticky collection of bacteria, proteins from saliva, and dead cells from the lining of the mouth.
Individual bacteria multiply and form many small microcolonies that coalesce, creating a layer of dental plaque - which is a type of biofilm.
Compared to a microcolony, the bacteria in a biofilm communicate with each other via chemical signaling and together they create a complex system where some bacteria work on tunneling between the microcolonies and to the surface in order to bring in a steady supply of food.
As an analogy, if bacteria were ants, then a microcolony would be a tiny group of ants, each doing it’s own thing, whereas a biofilm would be an ant farm with complex tunnels and rooms, and each ant carrying out a specialized task.
So typically, dental plaque can form on the surface of teeth, but if the pH of the local environment around the tooth surface remains above about 5.5, enamel will not demineralize.
One factor that tips the balance towards caries progression is having less bicarbonate-rich saliva, which can result from conditions like Sjogren syndrome, radiation treatment for cancer, gastric reflux, or as a side effect of a medication or recreational drugs.
A key factor that contributes to tooth demineralization is sugar. Some bacteria ferment sucrose, and that produces lactic acid as a byproduct.
In addition, acidic foods and drinks can also cause the pH in the mouth to lower. So a drink that has lots of sugar and lots of acid, like soda which has a pH of around 3, can damage the teeth in two ways.
The bacterial population in the mouth is diverse, and if the pH in the mouth starts to decrease, it alters the balance of power.
Bacteria that thrive in a low pH, like mutans streptococci and Lactobacillus, begin to dominate. As dental plaque grows thicker, the amount of oxygen near the enamel surface begins to fall.
That makes the environment on the enamel surface favorable for facultative anaerobic bacteria, which can metabolize sugars with and without oxygen present.
If sucrose is metabolized anaerobically - without oxygen - lactic acid builds up, and it can quickly lower the pH on the enamel surface to below 5.5.
Once the environment becomes that acidic, calcium and phosphate in the enamel begin to dissolve into the fluid -filled diffusion channels between the enamel crystals, and that begins the process of demineralization.
Every time sugar enters the mouth, the bacteria are able to produce more acid, and this destruction in the subsurface continues until the surface gets so thin that it collapses - like walking on thin ice.
Intact enamel keeps bacteria out of the dentin because they do not fit through the enamel diffusion channels. However if demineralization is allowed to continue the enamel surface will cavitate to expose the dentin which will allow bacteria to enter the dentin.
Once bacteria are in the dentin it’s called infected dentin and usually requires a restoration or filling. If destruction continues into the dentin layer, then the caries lesion enlarges towards the pulp.
“” Eventually, the bacteria penetrate into the pulp, causing irritation and damage to the nerves. That’s the stage when individuals usually experience pain, although pain can also occur when the caries lesion involves the dentin layer since sensory nerve fibers travel through tubules in the dentin.
Eventually, bacteria travel down into the root canal space, and fill the entire inside of the tooth. It’s worth mentioning that formation of a caries lesion doesn’t have to begin with the enamel of the crown.
If the gingiva recedes or plaque forms between the gingiva and the root, bacteria and acids have direct access to the cementum, which is much softer than enamel and dissolves more quickly.
The demineralization of cementum and dentin can occur in a pH range of 6.2-6.8. Symptoms of dental caries include tooth pain and sensitivity, especially when chewing or drinking something that’s cold or hot, or sweet.

Symptoms7:51–8:05

If the process continues it can eventually lead to a root canal procedure or even losing a tooth. Diagnosis is usually made based on symptoms, and looking for areas of discoloration or roughness, tenderness or inflammation in the mouth, as well as using dental radiographs.

Diagnosis8:05–8:17

It’s always ideal to prevent a caries lesion from forming in the first place, and it starts with a risk assessment for identifying individuals at high risk of caries.

Prevention8:17–9:13

That includes individuals that have had a prior or current caries lesion, have problems with saliva production, have specific abnormal levels of acid-forming bacteria, like mutans streptococci and Lactobacillus, in their mouths, and those that have poor dietary habits - like frequent snacking and has a high-sugar diet.
So, treatment of dental caries disease depends on the level of risk, more specifically, reducing the pathogenic risk factors like antibacterial rinses to get rid of bacteria and increasing protective factors like products that mimic saliva.
In addition, brushing and flossing are useful because they physically remove dental plaque and deliver fluoride to the teeth to help with remineralization.
Products containing fluoride can help remineralize spots where enamel has lost its hard minerals. If the enamel surface is intact, then the caries lesion can be treated without drilling a tooth and instead using chemical remineralization.

Treatment9:13–9:52

But once the enamel surface is fully cavitated to the dentin, now the bacteria have a pathway to enter the dentin it may be necessary to remove the infected dentinal tissue and replace it with a dental filling, which allows the tooth to chew.
If the infection is so large that the entire top of the tooth needs to be removed, a dental crown can be used to replace it.
Ultimately, these restorative treatments are useful, but they alone don’t resolve the underlying cause of the caries lesion and can’t prevent new caries lesions from forming.
All right, as a quick recap. Dental caries lesions are the end result of the dental caries disease process.

Review9:52–10:35

Dental caries lesions typically form in an environment where there are lots of sugars in the mouth and a pH below 5.5 for enamel and below 6.2 to 6.8 for cementum and dentin.
That environment favors bacteria like mutans streptococci and Lactobacillus, which demineralize enamel and the dentin beneath it, and if untreated, it can eventually result in a cavitated caries lesion.
Diagnosis is done by visual inspection and radiographic imaging, and treatment and prevention involve stopping demineralization and promoting remineralization, as well as reducing levels of harmful bacteria, and restoring the surface of a tooth, if needed.