What is Pulpitis?
"Pulpitis" is the medical term for the inflammation of a tooth nerve.
In order to understand the particularities of a tooth nerve inflammation, it is helpful to take a look at the anatomy of teeth. A tooth consists of:
- the dental pulp (commonly called the tooth nerve; in Latin, “pulpa”)
- the dental enamel
- and the dentin (another Latin term)
The pulp consists of nerves, lymphatic vessels, connective tissue, and blood vessels.
The dentin is interspersed with small tubules that are directly connected to the pulp.
A large tooth defect, for example due to a cavity, also means a large injury to the dentin. The probability of an inflammatory reaction of the pulp rises with the size of the dentin wound.
In general, two damage mechanisms that may cause an inflammation of the pulp can be distinguished: Infectious damaging (in case of caries, the bacteria) and non-infectious damaging (a physical/chemical damaging – for example, due to heat caused by drilling or dental chemicals).
This distinction is important for the course of the disease, because in case of an infectious cause, there is a higher risk of the caries bacteria spreading through the pulp cavity into the bone and thus causing a bone infection – as can be seen in the animation on the left.
But a bone infection may also develop in the absence of bacteria. Let’s consider the following: A tooth is cut for a crown; the cooling effect of the water is insufficient and the pulp becomes inflamed due to overheating and subsequently dies off.
The dead tissue (called necrotic tissue) is broken down by the immune system. If there is a large amount of dead tissue due to the anatomy of the individual root canals, the immune system could be overburdened by the degrading process. An insufficient amount of immune cells may then contribute to the development of an infectious reaction in the bone – as in the animation on the right.
However, in most cases, the body is able to break down the dead, non-infected tissue and the root canal subsequently calcifies (this is called, “a root sclerosis”). Years later, a root canal sclerosis may lead to a root resorption – the root “becomes” bone. Sometimes, all these processes may occur simultaneously in a tooth.
Here you see an X-ray of a tooth which had been crowned years earlier. It can be assumed that at that time, the heat of the cutting process damaged the pulp – years later, this led to a root resorption and root canal sclerosis at the anterior, shorter root; and to a bone infection at the posterior root end – the dark spot.
In order to get an even better understanding of the various outcomes of a pulpitis, it is helpful to take a closer look at the immune system. Our immune system is able to recognize and eliminate structures that are foreign to and damaging for our body.
So-called "marker cells" recognize and mark foreign structures (for example, bacteria, dead cells, cell debris, viruses, fungi).
Afterwards, the macrophages recognize these markings and remove the elements. The infection has been averted.
So it is clear that for an immune reaction, immune cells are necessary; these are located in the blood. Therefore, the focus of the inflammation must be surrounded by blood in order to fight the focus effectively.
Now the necrotic pulp tissue turns into a calcified cavity without blood vessels; there may still be cell debris attached to the walls. But blood vessels and thus immune cells are only found in the bone. Therefore, the absence of blood creates ideal conditions for bacteria (which have entered, for example, due to a deep caries), to multiply – since they are in the pulp cavity, they are basically protected from the immune system. They feed off the tissue residue and can multiply without hindrance.
At a certain point, the cell count is so large that the bacteria spread into the bone through a small opening at the root end – resulting in a bone infection. Oftentimes, the body is then no longer able to deal with the large number of bacteria and the infection progresses.
So the development of the "dead" dental nerve depends on various factors:
- The accessibility of the immune system
- the immune status of the patient
- the type, amount, and aggressiveness of the triggering cause (bacteria – yes or no)
- local factors (the anatomy of the tooth)
These different progressions of the disease also explain the different toothache characters –symptoms – pounding, pressing, dull, not locatable, etc. The transitions of these reactions are fluent; in many cases, there are several combinations, many of which may only appear after years. One should also not forget that every patient experiences pain differently.
All of these things are pointers to show dentists what they should do: Any teeth that were cut or filled must be checked semi-annually to confirm their vitality. This is done with a cold spray – more on that in the video Cold Test!
In any case, why is a “dead” tooth or a focus a threat? Well, any inflammatory reaction burdens our immune system, meaning that the body is constantly busy with “work.” Even if you do not experience any pain and neither notice nor are aware of your focus.
Moreover, if there is an infectious focus, a spreading of the bacteria may occur. These “migrating bacteria“ like to settle in places where they can escape the immune system – for example, next to artificial materials (implants, artificial heart valves...), in body parts with poor circulation (extremities of diabetics...) or on good breeding grounds (blood clots or thrombi...).
At such locations, the "spread" bacteria again cause new damage through local inflammatory reactions. That is why every focus should be treated irrespective of its developmental history – with a root canal treatment!
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