Pulp necrosis

The odontoblast cell bodies decrease in number and size before any inflammatory changes occur. The outward flow of tubular fluid can cause the nuclei of odontoblasts to be aspirated into the dentinal tubules. The odontoblasts may also be permanently damaged which causes them to release tissue injury factors which can then influence adjacent odontoblasts and underlying connective tissue. Odontoblasts can undergo vacuolization, a decrease in the number and size of the endoplasmic reticulum, and degeneration of mitochondria. It is unknown by which process (apoptosis or necrosis) the odontoblasts die.

Lymphocytes, plasma cells and macrophages comprise the initial inflammatory infiltrate. In response to bacterial assault and tissue injury non-specific inflammatory mediators are released. These inflammatory mediators include histamine, bradykinin, serotonin, interleukins (IL) and metabolites of arachidonic acid. They can interact with neuropeptides (substance P) and calcitonin gene-related peptide (CGRP) during the inflammatory response. Destruction of the nerve fibres causes neuropeptides to be released into pulp. The neuropeptides can cause an increase vascular permeability and vasodilation. The filtration of serum proteins and fluid from the vessel causes the tissue to become oedematous. The tissue pressure increases as the blood volume and interstitial fluid volume rises. The thin-walled venules are compressed and the resistance to flow in these vessels increases. This is accompanied with a decrease in blood flow causing an aggregation of red blood cells and subsequent increase in blood viscosity. This tissue also becomes ischaemic which suppresses the cellular metabolism in the area of the pulp that is affected. This causes necrosis.[8] Necrosis is a histological term that means death of the pulp.[9] It does not occur suddenly unless there has been trauma. The pulp may be partially necrotic for some time. The area of cell death enlarges until the entire pulp is necrotic. Bacteria invade the pulp which causes the root canal system to become infected.[10] Teeth that have total pulpal necrosis are usually asymptomatic except for those that have inflammation which has progressed to the periradicular tissues.

• Dental Caries
• Dental Trauma
• Dental Treatment
• Pulpitis
• Infection

The influx of bacteria and growth of a carious lesion (if gross and left untreated) inevitably leads to the centre of the tooth – the pulp chamber. Once this tissue damaging process reaches the pulp it results in irreversible changes – necrosis and pulpal infection.[12][13]

When a tooth is displaced from its normal position as a result of dental trauma, it can result in pulp necrosis due to the apical blood supply being compromised. This might be due to displacement of the tooth through avulsion or luxation. Furthermore, if the tooth is severely damaged, it could lead to inflammation of the apical periodontal ligament, and subsequently pulp necrosis.[11]

Pulpal necrosis can also occur as a result of dental treatments such as iatrogenic damage due to overzealous crown preparation – this may be due to excessive thermal insult and close proximity to the pulp during tooth preparation – or rapid orthodontic work causing excessive force.

Pulpitis is stated to be one of the stages of disease progression which leads to pulpal necrosis. This inflammation can be reversible or irreversible. Due to the enclosed nature of the pulp chamber - unlike normal inflammation - when inflamed, the increased pressure cannot be displaced to other tissues, resulting in pressure on the nerve of said tooth and tissues adjacent.[14] In irreversible pulpitis where the inflammation of pulpal tissues are not reversible, pulpal blood supply will become compromised and therefore necrosis of pulpal tissues will occur.

The pain associated with pulp necrosis is often described as spontaneous.[15] Hot temperatures are reported to have exacerbating factors, and cold temperatures are said to soothe this pain. In some cases, the pain presents as a long dull ache as this is due to necrosis of the apical nerves being the last part of the pulp to necrose. Therefore the pain is from the apical nerves, which have residual vitality remaining when the majority of the pulp is necrosed due to the supply of blood to the more medial parts of the apical nerve.[11]

In some cases of pulp necrosis there is a yellow, grey or brown crown discolouration. Dark coronal discoloration is believed to be an early sign of pulp degeneration.[16] Teeth with said discolouration need to be treated with special care and further investigations are required before pulp necrosis can be diagnosed.[11]

Alterations in the gingiva such as fistulas or abscesses and radiographic signs such as periapical lesions and external root resorption are used in some studies to diagnose pulp necrosis however other studies state that these factors alone are not enough to diagnose a necrotic pulp.[11]

Internal root resorption may be an indication of pulpal necrosis though it is not possible to diagnose accurately with radiographic presentation of this alone. This is because the pulp tissue apical to the resorptive lesion will still be vital to allow active resorption to take place, it provides the clastic cells with nutrients via a viable blood supply.[11]

Thermal testing is a common and traditional way used to detect pulp necrosis. These tests can exist in the form of a cold or hot test, which aims to stimulate nerves in the pulp by the flow of dentine liquid at changes in temperature. The liquid flow leads to movement of the odontoblast processes and mechanical stimulation of pulpal nerves.[19]

The cold test can be done by soaking a cotton pellet into 1,1,1,2 tetrofluoroethane, also known as Endo ice refrigerant spray. The cotton pellet will then be placed onto the middle third of the intact tooth surface. The clinical study done by Gopikrishna indicated the tooth to be diagnosed as having necrotic pulp if subjects felt no sensation after two 15-second applications every two minutes.[20] It is worthy to note that a control test should be performed on the adjacent tooth to ensure further accuracy of results.

The pulse oximeter test is a more accurate way to test for necrotic pulps as it primarily tests for vascular health of the pulp as compared to its nervous response.[21] This method involves taking measurements of blood oxygen saturation levels, making it non-invasive and an objective way to record patient response regarding pulpal diagnosis.[20] In a study conducted in primary and immature permanent teeth, results clearly reflected that pulse oximetry can readily differentiate between vital and non-vital, necrosed teeth.

The pulse oximeter consists of a probe containing 2 light-emitting diodes, one of which transmits red light to measure the absorption of oxygenated haemoglobin, and the other transmitting infrared light, measuring the absorption of deoxygenated haemoglobin. As both oxygenated and deoxygenated haemoglobin absorb different amounts of red and infrared light, relationships between pulsatile changes in blood volume and light absorption values can establish saturation of arterial blood. In addition, using absorption curves for both oxygenated and deoxygenated haemoglobin can determine the oxygen saturation levels.[22] For the purposes of evaluating pulp vitality, it is imperative that the probes fit the anatomical contours and shape of the measured teeth.[23]

A study was done to assess the accuracy of pulse oximetry in comparison to thermal and electrical tests. Customized pulse oximeter dental probes were placed on the crown of the tooth, with oxygen saturation values recorded after 30 seconds of monitoring each tooth. The values were taken as a positive response (ie vital pulp) within the range of 75-85% oxygen saturation and a negative response below 75%, indicating pulp necrosis.[20]

Another critically appraised topic[24] also suggests that a pulse oximeter is more accurate than cold testing in diagnosing pulp necrosis, however comments raised regarding the validity of the evidence stated that the pulse oximeter adaptors were built by the respective authors causing some degree of bias in the experiments.[24]

MRI scans have been used to detect and evaluate several head and neck regions including the Temporomandibular Joint, salivary glands, floor of the mouth, etc. In the clinical study completed by Alexandre T. Assaf, MRI scans were used to detect pulp vitality after trauma in children. The absence of re-perfusion of the dental pulp suggests the lack of revitalization of the affected teeth and hence necrosis of the pulp. In this study, MRI scans prove to be a promising tool to avoid excessive root treatment on traumatized teeth. However, a major flaw in this study is a small sample size of 7.[25]