What Is Pulp Necrosis?


Oral health is an important aspect of overall quality of life: aside from a pretty smile, being able to eat and speak, among many other functions your teeth provide you, are essential in everyday life. However, many diseases and conditions can lead to pulp necrosis and therefore affect your oral health: pulp necrosis is the death of the tissue and cells inside the pulp chamber, the innermost layer of the tooth.¹ Many factors like cavities (tooth decay), trauma and even ageing can lead to pulp necrosis.¹ Let’s understand more about this phenomenon and the consequences it can have on your health.

Understanding the anatomy of teeth

Human teeth are composed of a few different tissues: the outermost layer that recovers the crown is known as the enamel, a hard and mineralized tissue; also hard and mineralized is the cement layer, which covers the entirety of the roots of the teeth.² Under the enamel and the cement layers, another mineralized tissue exists, the dentin, which is rich in tubules that connect to the pulp.² The innermost layer is the pulp chamber: it is covered by odontoblasts, a type of special cells that produce dentin, but inside the pulp chamber there are a number of other cell types, such as fibroblasts (cells that produce collagen) and leukocytes (white blood cells).³ One characteristic of the pulp is that, unlike the other tissues mentioned, it is rich in blood vessels and nervous fibres: this means that the pulp is capable of sensation.³

Nervous fibres inside the pulp can be divided into two types:

  • Myelinated A-fibres that conduct fast and intense pain stimuli are usually associated with shifts in the balance of the liquid present inside the dentin tubules (due to changes in temperature).³
  • Unmyelinated C-fibres conduct slow, dull pain, and their activation is associated with changes to the pulp tissue caused by inflammation.³

Because the dental pulp is entirely covered by hard tissue, its ability to expand during inflammation to accommodate oedema is very limited: pressure builds up easily inside the pulp chamber, causing intense pain and compression of the neurovascular bundle that can lead to necrosis (cell death).³

Supporting the teeth, there are other tissues surrounding it that can be affected by pulp necrosis. The periodontal ligament is a set of elastic fibres that connect the tooth’s root through the cementum to the alveolar bone (tooth socket, the bone that surrounds the tooth) and serves to absorb the impact from chewing.⁴ 


The causes of pulp necrosis are varied. Some of them include:

  • Infection: infections caused by anaerobic and gram-negative bacteria are one of the most common causes of pulp disease; cavities, fractures, periodontal disease and dental anatomy anomalies can grant these microorganisms easier access to the pulp, and the infection spreads easily through the tissue.¹
  • Iatrogenic: sometimes dental procedures, when not adequately done, can cause pulp damage. Excess heating when using rotary instruments without proper cooling mechanisms can cause pulp injury; extensive fillings without proper pulp protection can conduct temperature changes that are also damaging; certain filling materials used years ago could also present the risk of toxicity to the pulp tissue without the presence of a seal or barrier provided by other materials.¹
  • Radiation: radiotherapy in the head and neck area can cause pulp necrosis.¹
  • Trauma: acute trauma like dislocation, cracks and fractures can cause pulp necrosis when the neurovascular bundle is damaged and the blood supply is cut off. Chronic trauma like bruxism, abrasion and orthodontic treatment can also cause pulp necrosis.¹
  • Ageing and idiopathic causes: unlike other causes, these two factors can cause the slow death of pulp cells and their substitution for collagen fibres (degenerative disorders of the pulp); this is normal with age, and sometimes can happen due to unknown (idiopathic) reasons.¹ These degenerative disorders of the pulp do not require treatment on their own.¹

Stages of Pulp Injury

  • Reversible Pulpitis: The first step of pulp necrosis is usually inflammation, a phenomenon known as pulpitis¹. Earlier stages of pulpitis can be reversible if the stimulus is removed: hypersensitivity caused by a filling material can be completely reversed if the filling is changed, for example, as the pulp is still vital and capable of healing itself.1 
  • Irreversible Pulpitis;  Later stages of pulpitis are irreversible regardless of whether or not the irritant stimulus has been removed: the pulp is still vital, but not capable of healing itself, and this results in irreversible pulpitis, which can be divided into symptomatic or asymptomatic.¹ Asymptomatic cases are the ones in which the excess fluid buildup caused by the inflammation has found an escape route, relieving the pressure inside the pulp; when there is no way to bring relief to the pressure, it builds up causing pain as symptomatic pulpitis.¹ Asymptomatic forms can happen when there is a big cavity that exposes the pulp tissue, and ulceration or hyperplasia (overgrowth) of the pulp can happen as a result.1
  • Pulp Necrosis; Necrosis is the next step. Once it reaches a point of no return, the cells of the pulp start to die (partial necrosis) until it is completely dead (total necrosis), usually starting at the pulp chamber and progressing inside the root until it reaches the apical foramen.¹ At this stage, the pulp is no longer vital and it will stop hurting, which can give the patient a false sense of security: pulp necrosis, if left untreated, can easily progress to periapical diseases such as an abscess, granuloma or a cyst.¹ Depending on whether or not there is an infection present, pulp necrosis can be classified as either septic (infected) or aseptic (non-infected).¹

Signs and symptoms

Pulp necrosis is usually associated with pain: initially, it can be described as a sharp, intense and even throbbing pain that is spontaneous and continuous.⁵ Over time, the pain can subside and become dull, though still continuous, as the pulp tissue is dying off.⁵ The affected tooth might be more or less sensitive to cold temperatures, but usually, hot temperatures exacerbate the pain.⁶ 

Cases of pulp necrosis caused by tooth decay are usually associated with large and deep cavities that are left untreated.⁶ Discoloration of the crown in a yellow, grey or brown tone can also be found in some patients.⁵ Teeth that are young and affected by large cavities can develop pulp hyperplasia, an overgrowth of pulp cells that is clinically visible as a mass that can bleed easily and causes mild discomfort to the patient.⁶ An abscess or fistula can point to pulp necrosis as well.⁶

X-rays are necessary in order to diagnose the full extent of pulp and periapical diseases.⁶

 Common findings in X-rays are:

  • Untreated deep cavities or unsatisfactory fillings with marginal infiltration⁶
  • Extensive and/or deep fillings⁶
  • Internal root resorption⁶
  • Obliteration (calcification) of the pulp chamber and/or root canal⁶
  • Unsatisfactory previous endodontic treatment (root canal treatment or RCT)⁶
  • Widening of the periodontal ligament⁶
  • The presence of periapical radiolucency (dark lesions), can point to periapical diseases such as granuloma or cyst⁶
  • The presence of periapical radiopacity (light lesions), can point to osteosclerosis, a type of response when it comes to bone infection


Diagnosis of pulp conditions is made through a combination of clinical evaluation, medical and dental history, and complementary exams like X-rays.⁶

  • Clinical evaluation of the colour of the affected tooth, whether or not there are fractures or cracks, whether or not there are cavities or previous fillings present, and if there is oedema (swelling) or presence of a fistula are points of interest that a dentist should look for.⁶ The patient’s description of the pain (if there is any) is also extremely important: how long ago has it started? Is it sharp, or dull? Is it spontaneous, or provoked by stimuli (like pressure and temperature changes)? Is it continuous or does it come and go? 
  • Clinical tests can be performed to assess pulp vitality and periapical involvement.⁶ Thermal tests are used to check vitality: usually done cold, with a dry ice spray, they can detect through the response or lack of it, if there is pulp necrosis; a dead pulp does not respond to cold or hot stimuli, but a vital pulp responds, and inflamed vital pulps usually have an exuberant response to cold stimuli.⁶ Other tests performed are percussion (both vertical and horizontal), palpation and mobility; these manoeuvres can indicate if there is periapical or even periodontal involvement in the pulp’s condition.⁶
  • X-rays are an essential diagnosing tool. Findings like widening of the periodontal ligament, obliteration of the pulp chamber and/or root canal, or presence of periapical lesions (whether radiolucent or radiopaque) can confirm a diagnosis of pulp necrosis or other conditions like cysts and granulomas.⁶ X-rays can also determine the cause of pulp necrosis: an unsatisfactory filling, a cavity, fractures or other factors that sometimes cannot be perceived clinically would not escape the eyes in an X-ray.⁶

Consequences of pulp necrosis

Pulp necrosis can lead to infection of the tooth and supporting tissues, causing numerous issues: even an aseptic necrosis can later become secondarily infected and cause issues, as the tooth loses the defence cells that should be present in the pulp, making it more vulnerable to disease.⁶

Some of the known consequences of pulp necrosis are:

  • Apical periodontitis: an inflammation of the apex of the root (periapical region), can be acute (symptomatic) or chronic (asymptomatic).¹
  • Acute dental abscess: a collection of pus that accumulates in the periapical region; the pus tends to permeate and put pressure on the surrounding tissue causing intense pain, swelling and fever.⁶ An abscess should not be treated lightly, as it brings the risk of cellulitis, Ludwig’s angina and even sepsis.
  • Chronic dental abscess: if an abscess finds a drainage point (like forming a fistula), it usually subsides the symptoms as it slowly drains the liquid from the infection, becoming a chronic infection.⁶ It can, however, become acute again if provoked by stimuli, or progress into other chronic lesions.⁶
  • Periapical granuloma: chronic infections of the periapical region can lead to the formation of granulation tissue, an amalgamation of white blood cells, bacteria and dead cells; usually asymptomatic, it slowly degrades surrounding bone tissue as it grows.⁶
  • Radicular cyst: this is a cavity filled with fluid, as a result of the osmotic pressure caused by the accumulation of dead cells and dead bacteria in an infection; as infection progresses, it induces the proliferation of the epithelial rests of Malassez, a group of cells present in the periodontal ligament responsible for repairing the area, and they proliferate into a cyst.¹ Although radicular cysts are usually asymptomatic, they can grow and become infected, causing pain.⁶
  • Internal root resorption: it can happen as a response to pulp necrosis, causing either inflammation with an increase in the size of the pulp chamber or replacement of pulp tissue to bone-like tissue.⁶
  • Bone infection: infection can spread through the surrounding bone tissue into various forms, and one of the most common ones is apical osteosclerosis, a form of osteomyelitis that causes increased bone density in a focal area.¹

Management and treatment

The first line of treatment for pulp necrosis is generally root canal treatment (RCT).⁶

Cases of reversible pulpitis (hypersensibility) can be treated by removing the stimuli, such as changing a filling and promoting proper pulp capping.⁶

If there is already an irreversible damage to the pulp or an onset of necrosis, pulpotomy (removal of the coronal pulp only) or pulpectomy (complete removal of both coronal and radicular pulp tissue, known as RCT) are options. Pulpotomy is usually advised for cases like pulp hyperplasia or earlier stages of necrosis, in which the radicular part of the pulp has not been affected yet.⁶

Most cases do require a full root canal treatment if there is already progressed necrosis, complete necrosis or periapical diseases: in these cases, the pulp is completely removed and the roots are treated and filled by a dentist⁶. Cases in which there was already an unsatisfactory RCT can be retreated.⁶

After RCT, a tooth will usually need a composite resin filling or a crown in order to be sealed and prevent secondary infection.⁶

Drugs can be used along with RCT to control infection, and antibiotics have been used to successfully subdue infection in acute abscesses.⁶ Granulomas might regress on their own after RCT and leave scarring tissue behind, but cysts require surgical removal.⁶

Alternatively, a patient might opt to extract the affected tooth. Though not ideal, extraction is an option and usually a last resort if RCT fails.


Pulp necrosis is the death of the cells that compose the pulp tissue, the innermost layer of human teeth that is responsible for sensation, protection against infection and dentin production. Common causes are infection, trauma, iatrogenic causes, radiation therapy, and ageing. Signs and symptoms include intense, continuous and spontaneous pain, with swelling or presence of fistula, discolouration of the crown, big cavities or extensive fillings. Diagnosis is made through clinical examination, tests like thermal tests (cold test) and percussion, palpation and mobility tests, along with complementary exams like X-rays, which can show the cause of the pulp necrosis (tooth decay, fractures, calcification) and/or show periapical involvement. Common consequences of pulp necrosis are apical periodontitis, dental abscess, periapical granuloma, radicular cysts, and severe infections of the face like cellulitis, Ludwig’s angina and even septicemia. Treatment usually consists of a root canal treatment (RCT) but if not possible or if the patient opts out of it, tooth extraction is also recommended.


  1. López-Marcos JF. Aetiology, classification and pathogenesis of pulp and periapical disease. Medicina Oral, Patologia Oral Y Cirugia Bucal [Internet]. 2004;9 Suppl:58–62; 52-57. Available from: https://pubmed.ncbi.nlm.nih.gov/15580137/
  2. de La Dure-Molla M, Philippe Fournier B, Berdal A. Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification. European Journal of Human Genetics. 2014 Aug 13;23(4):445–51. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4666581/
  3. A AE, Dc Y. Dental Pulp Neurophysiology: Part 1. Clinical and Diagnostic Implications [Internet]. Journal (Canadian Dental Association). 2009. Available from: https://pubmed.ncbi.nlm.nih.gov/19239745/
  4. Bath-Balogh M, Fehrenbach MJ. Illustrated dental embryology, histology and anatomy. Workbook. St Louis: Elsevier Saunders; 2011.
  5. Aldrigui JM, Cadioli IC, Mendes FM, Antunes JLF, Wanderley MT. Predictive factors for pulp necrosis in traumatized primary incisors: a longitudinal study. International Journal of Paediatric Dentistry. 2013 Jan; 23(6): 460–9.
  6. Abbott P, Yu C. A clinical classification of the status of the pulp and the root canal system. Australian Dental Journal [Internet]. 2007 Mar;52:S17–31. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1834-7819.2007.tb00522.x
This content is purely informational and isn’t medical guidance. It shouldn’t replace professional medical counsel. Always consult your physician regarding treatment risks and benefits. See our editorial standards for more details.

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Isabela Araújo Rosa

Doctor of Dental Surgery - DDS, Universidade Federal de Goiás, Brazil

Isabela is a board certified dentist in Brazil, with a background in Oral and Maxillofacial Pathology, Bioethics and Oral Medicine, and previous experience with medical writing and medical communication.

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