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The dynamic stages of pulpal and periapical diagnosis 

The most important step before treatment can be recommended is the diagnosis. Without a proper diagnosis, we cannot treat our patient’s problems. In this essay, I will use the terms from the American Association of Endodontics, which are as follows:-

  1. Normal pulp.

  2. Reversible pulpitis.

  3. Asymptomatic irreversible pulpitis.

  4. Symptomatic irreversible pulpitis.

  5. Pulp necrosis.

  6. Apical normal tissues.

  7. Asymptomatic apical periodontitis.

  8. Symptomatic apical periodontitis.

  9. Chronic periapical abscess.

  10.  Acute apical abscess.

My perspective on the diagnosis terms that it is a dynamic progression of the different states, from the normal state to a diseased state. In this essay, we will assume that a pristine tooth is allowed to decay and progress to infect the pulp and cause apical inflammation. At different hallmarks, the diagnosis will correspond to the state of the tooth.

Imagine a tooth in its pristine condition unravaged by decay or cracks. The pulp should be vital, which means an intact blood supply and innervation. When we say we do a pulp test we are trying to ascertain if the nerve fibres are functioning and by extension a proper blood supply. Therefore, it could be reasoned if we put some electric or cold the fibers will fire their action potentials to the brain giving a painful response(the patient will say OUCH!). This pain only lasts momentarily and it is gone. We can then conclude, that the fibres are working(by extension a working blood supply) and a clinical diagnosis of a normal pulp is made.

Over time, if caries develop deep enough, the microbial toxins can reach the pulp via the dentinal tubules. This will then cause the pulp to be slightly inflamed. It is the degree of inflammation in the pulp that determines if the pulp is reversible or irreversible. But we need to confirm anyway, so we put some cold or electric and the patient will say ouch, then the pain again disappears slowly. However, this time when we see the radiograph and clinical examinations there is an obvious cause (caries). Thus we can infer that the pulp is inflamed and if we remove the source(caries), the pulp should revert to a non-inflamed state. Thus the diagnosis of reversible pulpitis is made.

However, if the decay is allowed to progress then more microbial toxins can reach the pulp and the degree of inflammation is now considered severe. What actually is happening is that the nerve fibres(A delta and C)  are sensitised; a phenomenon known as allodynia (Nerves take less stimulus to produce an action potential), at this point, a simple whiff of cold air is sufficient to trigger the painful response. Sometimes, the pulsating arteries are also sufficient to trigger the pain and give it a throbbing dull pain quality. Therefore, it could be reasoned that the pain will be constant and sufficient to disturb sleep (a classic report by patients). However, due to the lack of B fibres inside the pulp, which codes for proprioception in the mesencephalic V nucleus in the brain stem, the pain will be poorly localised and sometimes the patient cannot pinpoint which tooth is causing the pain. During clinical examination, percussing the tooth is unlikely to be tender unless the inflammation has reached near the apex and the periodontal ligament fibres start to be inflamed. If a cold or electric is placed on the tooth the pain is often intense, throbbing and lingering. This is expected and this is how we know which tooth it is. To summarize, what we read in textbooks,  “they cannot sleep”, exaggerated response to cold or electricity, and the need for constant analgesics are the classic signs of symptomatic irreversible pulpitis.

If nothing is done and the caries and microbes continue to infect the pulpal tissues and ravage the tooth, necrosis of the pulpal tissues is to be expected. Necrosis of the pulpal tissues also means that the a delta and C fibres are slowly losing their function to transmit impulses. As more and more nerve fibres become necrotic, there will less and fewer impulses generated for the brain to perceive the pain and at some point, the tooth will no longer be painful. At this point, if cold or electricity is applied to the tooth, no response is expected. However, deep down the root canals, there might still be some vital tissues too far away for the cold or electricity to stimulate. The diagnosis is thus asymptomatic irreversible pulpitis however this cannot be ascertained clinically (how can we know the last 3mm of radicular pulp is irreversibly inflamed?) and the more accurate diagnosis should be a necrotic pulp. Sometimes, when you percuss teeth like this they may respond with the tooth being more sensitive, this is because the bacterial toxins are now near the apex and are causing mild inflammation of the periodontal ligament, this is what we call tender to percussion, which means inflammation of the periodontal ligament and not exclusive to endodontic diagnosis! Thus the use of symptomatic apical periodontitis deserves special consideration.

Over time, however, the microbes will use the necrotic tissues inside the pulp and root canal spaces as a fuel source and organise themselves into biofilms “inside the root canal spaces”. These biofilms will continue to grow and advance towards the apex until they reach the apical 3rd. At this point, we can conclude there are no more A delta or C fibres inside the tooth thus any cold or electric test will yield no response. The tooth is effectively “dead”. Over time the sterile alveolar bone will receive toxins from the biofilm inside the tooth. The alveolar bone does not like this outpouring of toxins thus the immune response of the host will reorganise around the apex by removing bone and accumulating the immune cells around the apical foraminas to halt the progression of the biofilm and to prevent their invasion into the sterile bone. We can observe this in our periapical radiographs as “black circles” around the apex of a tooth. Microscopically, these black circles consist of immune cells and blood vessels. This is a state of constant repair and inflammation as the body cannot repair fully due to the biofilms inside the tooth and their continual release of toxins that the body needs to remove. The tooth may or may not be tender to percussion depending on if the inflammation is sufficient at the PDL spaces. After placing some cold and yielding no response, a large cavity is seen clinically, and  “black circles” are observed on a periapical radiograph a diagnosis of asymptomatic apical periodontitis is made.

This state of root canal infection and apical periodontitis can exist for a long time without any symptoms. The equilibrium of infection and immune response can be upset if the host immunity gets depressed or a more virulent microbe manages to reach the apical 3rd of the root canal space. At this point, the microbes will start to invade the “black circles” forming an abscess, as the abscess accumulates and there is no escape for the abscess(thick cortical plates) the pressure may push the tooth coronally. Patients often report that the tooth is more proud”. The inflammation might also be so intense that the tooth will be extremely tender to percussion. Because the PDL is rich in B delta fibres and they are also stimulated, the patient can precisely tell you which tooth is causing the pain. The diagnosis is thus acute apical abscess.

However, sometimes the cortical plates are thin and the additional inflammation may cause the buccal plate to be eroded completely, then a “pimple” forms near the apex of the tooth. This pimple acts as a valve for the abscess to depressurise itself and thus majority of the time, the tooth is not painful. They however will report a foul sweet taste that comes and goes. Clinically a draining sinus, or pimple is observed on the gingiva. Again since no living fibers exist in the pulp, no response from cold or electric is expected and “black circles” are observed on the radiographs. The diagnosis is thus chronic apical abscess.

In special cases, for multi-rooted teeth, each root can form its own diagnosis. For example in a lower molar, the mesial root can be infected and chronic periapical periodontitis and the mesial root be clinically normal periapical tissues and normal pulp.


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