The dynamic stages of pulpal and periapical diagnosis
- Dr. Jimmy Chan
- Nov 14, 2023
- 6 min read
Updated: Aug 30

The most crucial step before recommending any dental treatment is accurate diagnosis. Without a proper diagnosis, we cannot treat our patients' problems. In this essay, I will use the terms from the American Association of Endodontics, which are as follows:-
Normal pulp.
Reversible pulpitis.
Asymptomatic irreversible pulpitis.
Symptomatic irreversible pulpitis.
Pulp necrosis.
Apical normal tissues.
Asymptomatic apical periodontitis.
Symptomatic apical periodontitis.
Chronic periapical abscess.
Acute apical abscess.
My perspective on the diagnostic terms is that they represent a dynamic progression of the different states of the pulp, which starts from a healthy state and progresses to a diseased state.
In this essay, we will begin with a pristine vital tooth, progress to an infected tooth, and ultimately reach an inflamed periapical tissue. As tooth decay advances closer to the pulp, corresponding changes in the pulp become evident, which can be clinically observed and tested.
Imagine a tooth in its pristine condition, unravaged by decay or cracks. The pulp should be vital, meaning it has an intact blood supply and innervation. When we perform a pulp test, we are trying to ascertain whether the nerve fibres are functioning and, by extension, whether a proper blood supply is present. Therefore, we can reason that if we apply an electrical or cold stimulus, the fibres will trigger their action potentials to the brain, resulting in a painful response (the patient will say 'OUCH!'). This pain only lasts momentarily and then disappears. 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. The microbial toxins will cause the pulp to be slightly inflamed. The degree of inflammation in the pulp determines whether the pulpal diagnosis is reversible or irreversible. However, we need to confirm this anyway, so we apply some cold or electric stimulus, and the patient will again experience pain, then, just like a normal pulp, the pain disappears almost immediately. However, this time, when we see the radiograph and in the mouth (clinical examination), there is an apparent 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 further, then more microbial toxins can reach the pulp and the degree of inflammation is now considered severe. 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 pain response. Sometimes, the pulsating arteries are also enough to trigger the pain, thus giving it a throbbing, dull pain quality. Therefore, we could reason that the pain will be constant and sufficient to disturb sleep (a classic complaint by patients). However, due to the lack of B fibres inside the pulp, which code for proprioception in the mesencephalic V nucleus in the brainstem, 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 sensation is placed on the tooth, the pain is often intense, throbbing, and lingering. This painful response is expected, and it helps us identify which tooth is affected. To summarise, 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, the 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 be fewer 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 in this manner, they may become more sensitive. This tenderness to touch is due to the bacterial toxins being near the apex and causing mild inflammation of the periodontal ligament, which is what we call tender to percussion. This phenomenon means that the periodontal ligaments are inflamed, and it is 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 that 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 tolerate this outpouring of toxins; thus, the immune response of the host will reorganise around the apex by removing bone and accumulating immune cells around the apical foramina to halt the progression of the biofilm and prevent its 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 fully repair itself due to the bacterial 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 whether the inflammation is sufficient at the PDL spaces. After placing some cold, yielding no response, a large cavity is clinically observed, and "black circles" are seen 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 between infection and immune response can be disrupted if the host's immunity becomes depressed or a more virulent microbe manages to reach the apical third 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 (due to thick cortical plates), the pressure may push the tooth coronally. Patients often report that the tooth is "more proud" (the pressure builds up at the apex, causing the tooth to be in supra occlusion). 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, resulting in a "pimple" forming near the apex of the tooth. This pimple acts as a valve for the abscess to depressurise itself, and thus, the 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 active living fibres exist in the pulp, no response to cold or electric stimulation is expected, and "black circles" are observed on the radiographs. The diagnosis is thus chronic periapical abscess.

In exceptional cases, such as multi-rooted teeth, each root can form its own diagnosis. For example, in a lower molar (Figure 8), the mesial root can become infected and develop chronic periapical periodontitis, while the distal root remains vital with clinically normal periapical tissues.
