How caries and dental plaque are formed

To understand cariogenic pathology we have to go back to our origins, since from the beginning several evolutionary types have developed different ways to be able to grow under terrestrial gravity. Some living beings evolved in water and did not need rigid structures to maintain their body volume against gravity, for example jellyfish.

Others used protein elements such as cartilage (fish), keratin (exoskeleton of turtles), cellulose (plants), and the vast majority evolved a hard skeleton based on calcium salts to support and maintain their body under the weight of gravity. Among the latter, on the one hand we would find exoskeletons formed by calcium carbonate minerals (coral), and on the other hand those that used another much more complex mineral such as hydroxyapatite to form their endo-skeleton as in the case of mammals.

We, as mammals, have a hydroxyapatite scaffold in the form of hexagonal crystallites, which are our bricks to form the “endo-skeleton and teeth”. This brick is acid soluble, but much less so than the calcium salts of the carbonates mentioned above. In other words, our teeth are much more resistant to acid attack.

How are teeth formed?

Teeth are formed inside our bones by cells excreting a protein matrix that induces their calcium crystallization (our hydroxyapatite bricks), generating the enamel that covers the external crown.

This enamel is a-cellular and at first its hydroxyapatite crystallites are small (immature enamel), but with time they expand becoming very large, resistant and not very soluble to acid (mature enamel) with 94% calcium. The enamel covers the dentin which is cellular with 60% calcium and the rest are cells and water. At its center is the dental pulp with the life support vessels, the nerves of sensitivity or pain and the cellular bodies of the dentin.

Specifically, the enamel is formed by hydroxyapatite crystallites (94%) spatially arranged in such a way that under the microscope we observe as tufts in the internal part, called “enamel prisms or prismatic enamel”, and as if it were a compact grass called “aprismatic enamel” in the superficial or external face and in the internal interface with the dentin.

Each tooth has a very specific shape and spatial position in order to carry out its function correctly. If the chewing function is physiological, the food itself, when cut or crushed, cleans the dental surface by friction (autoclysis), leaving no residue when swallowing. In addition, there is also saliva, a wetting and cleaning agent that drags them away, leaving on the dental surface an adhered film with a protective effect known as “acquired film”, which if it is not constantly renewed will become the well-known “dental plaque” when bacteria and food debris are added.

With this introduction, it is now easier to understand how “dental caries” is formed. Dental plaque consolidated with food debris releases acids during its decomposition, producing superficial dissolution of the enamel. This enamel needs to have an acid pH below 5.5 to dissolve, the normal pH of a healthy mouth being 7.4 (an alkaline base). This pH is controlled by “saliva” through a “buffer” system (bicarbonates and phosphates), that is, the ability to neutralize the pH variations that occur when we eat.

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When we ingest any food, the pH drops a whole point, that is, from 7.4 to 6.4, and it takes about an hour to neutralize it.

What happens if you eat again before the end of that hour?

When this happens, the pH goes back down another point from the pH you had. If it was at 6.8, it would drop to pH 5.8 if everything was correct, but if the patient did not have a correct buffer system, it would need more than 2 hours to recover the initial pH, and therefore, it would be easier to reach a pH below 5.5, thus producing many areas of dissolution and leaving cavitations or concavities where the palca accumulates, colonizing with various bacteria, etc.

Among the various bacteria, we have those catalogued as “cariogenic”, mainly represented by various types of “streptococcus, lactobacillus acidophilus, actinomyces viscosus” among others, since they secrete acids and proteolytic enzymes that dissolve the enamel and dentin proteins in successive stages, thus creating clinically detectable caries. Therefore, the lesion initiated by the acids will be perpetuated by cariogenic bacteria and transformed into a CARIES. If there are no bacteria, there will be no caries.

On the other hand, the protective capacity of saliva must also be taken into account. Saliva adheres to the enamel and exposed roots of the teeth forming an insoluble film thanks to its glycoproteins that form the so-called “acquired film”. If the film is correct, it protects the teeth against acids, but at the same time it also helps bacteria to adhere, thus initiating the so-called “dental plaque” when it is not properly renewed by autoclysis or daily oral hygiene.

The initial dental plaque progresses as food debris and new bacteria are incorporated into it, thus forming a biological film where the bacteria already secrete long-chain polysaccharides that help to increase the adhesion and firmness of the plaque to the tooth. This process is intensified by the sugars that are incorporated into the mouth, feeding the biofilm bacteria and becoming more acidic (low pH), the cariogenic infection is established.

Over time, if dental plaque is not removed, its complexity increases and it is colonized not only by many types of bacteria, but also by viruses, fungi, protozoa, etc. If a dental plaque resides permanently in that area, it will start its calcification, which in the beginning is fragile-whitish and later dark in color, known as dental tartar. With the presence of tartar, pathologies known as gingivitis, which can progress to paradontopathies, are initiated.