Pulp necrosis

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Pulp necrosis is a clinical diagnostic category indicating the death of cells and tissues in the pulp chamber of a tooth with or without bacterial invasion. [1] It is often the end result of many cases of dental trauma, caries and irreversible pulpitis.

Contents

In the initial stage of the infection, the pulp chamber is partially necrosed for a period of time and if left untreated, the area of cell death expands until the entire pulp necroses. The most common clinical signs present in a tooth with a necrosed pulp would be a grey discoloration of the crown and/or periapical radiolucency. This altered translucency in the tooth is due to disruption and cutting off of the apical neurovascular blood supply. [2]

Sequelae of a necrotic pulp include acute apical periodontitis, dental abscess or radicular cyst and discolouration of the tooth.[ citation needed ] Tests for a necrotic pulp include: vitality testing using a thermal test or an electric pulp tester. Discolouration may be visually obvious, or more subtle.

Treatment usually involves endodontics or extraction.[ citation needed ]

Histopathology

The dental pulp is located in the centre of a tooth, made up of living connective tissue and cells. [3] It is surrounded by a rigid, hard and dense layer of dentine [3] which limits the ability of the pulp to tolerate excessive build up of fluid. Normal interstitial fluid pressure in the pulp ranges from 5-20mm Hg, marked increases in pressure in the pulp due to inflammation can go up to 60mm Hg. [4] The rise in pressure is commonly associated with an inflammatory exudate causing local collapse of the venous part of microcirculation. Tissues get starved of oxygen thus causing venules and lymphatics collapse which may lead to localized necrosis. [5] A common clinical sign associated with the histopathology will be varying levels of suppuration and purulence. [6]

Following the spread of local inflammation, chemical mediators such as IL-8, IL-6 and IL-1 [7] are released from necrotic tissues leading to further inflammation and odema, which advances to total necrosis of the pulp. [5]

Further stages of destruction of pulp necrosis often leads to periapical pathosis, causing bone resorption (visible on radiographs) following bacterial invasion. The apical periodontal ligament (PDL) space widens and becomes continuous with apical radiolucency; the lamina dura of the apical area will also be lost. [7] The periapical lesion will enlarged with time and consequently, the pulp will be diagnosed as necrotic.

The pulp can respond (reversible pulpitis, irreversible pulpitis, partial necrosis, total necrosis) in a variety of ways to irritants. This response depends on the severity and duration of the irritant involved. If the irritant is severe or persists for a sustained amount of time it can cause the odontoblasts to die and cause initiation of an inflammatory response.

Odontoblasts

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.

Inflammation

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.

Aetiology and Causes

Pulp necrosis arises due to the cellular death within the pulp chamber – this can occur with or without the involvement of bacteria. [1] It is the result of various connective tissue disease progressions which occur in stages; normal healthy tissue becomes inflamed (i.e. pulpitis) which if left untreated leads to necrosis and infection and finally resulting in loss of pulp tissue (i.e. pulpless canals) [11]

Causes

Dental Caries

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]

Dental Trauma

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]

Dental Treatment

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

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.

Signs and symptoms

Pulp necrosis may or may not arise with symptoms.

Signs and symptoms of pulpal necrosis include;

There are additional signs of pulp necrosis which may be detected during radiographic assessment:-;

However, in some cases there may be no radiographic signs. For example, pulp necrosis caused by dental trauma which may only manifest/present itself with time, resulting in clinical changes. [11]

Pain

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]

Crown discolouration

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]

Abscess and/or fistula

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

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]

Diagnosis

There are a plethora of ways to diagnose pulp necrosis in a tooth. The diagnosis of pulp necrosis can be based on the following observations: negative vitality, a periapical radiolucency, a grey tooth discoloration and even peri-apical lesions. [17] This altered translucency in the tooth is due to disruption and cutting off of the apical neurovascular blood supply. [18]

Thermal Tests

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.

Pulse Oximeter Test

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]

3-Tesla Magnetic Resonance Imaging

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]

Management & Treatment

The most basic treatment for teeth with pulpal necrosis is root canal treatment. This involves the use of biologically accepted mechanical and chemical treatment of the root system, followed by the placement of a root filling, allowing healing of the periradicular tissues to occur.

Pulpal regeneration can be considered if the following criteria are met:

  1. Incomplete root development and incomplete apex closure
  2. Apexogenesis is not applicable as there is apical closure

Pulpal regeneration involves the removal of the necrotic pulp followed by the placement of medicament into the root canal system until it is non-symptomatic. Apical bleeding is then induced to create a clot at the apex which will be sealed by Mineral Trioxide Aggregate. [26]

In an immature permanent tooth pulpal necrosis causes the development of the root to stop. This causes the walls of the root to become fragile and thin which can make these teeth more prone to cervical root fracture and ultimately the tooth may be lost. These teeth in the past were treated with the calcium hydroxide apexification technique. A disadvantage of this was that it required multiple visits over a prolonged time and there could be an increased risk of cervical root fracture due to an increase in exposure to calcium hydroxide. The apical barrier technique with mineral trioxide aggregate was then used. The advantage of this technique over apexification was that it shortened the number of appointments and the healing outcomes were better. A disadvantage of both these techniques was that it did not allow the root to mature and so regenerative endodontic procedures (REPs) were utilised. A systematic review conducted by Kahler, et al (2017) showed similar clinical outcomes for teeth treated with REPs versus calcium hydroxide apexification/MTA apical barrier technique. They suggested that it should be considered as a first line treatment option in immature teeth with pulpal necrosis. They did state that a thorough discussion with the patient would be necessary as teeth treated with REP’s can show variable root maturation and adverse outcomes. [27]

Related Research Articles

<span class="mw-page-title-main">Root canal</span> Hollow part of the root of a tooth

A root canal is the naturally occurring anatomic space within the root of a tooth. It consists of the pulp chamber, the main canal(s), and more intricate anatomical branches that may connect the root canals to each other or to the surface of the root.

<span class="mw-page-title-main">Toothache</span> Medical condition of the teeth

Toothache, also known as dental pain, is pain in the teeth or their supporting structures, caused by dental diseases or pain referred to the teeth by non-dental diseases. When severe it may impact sleep, eating, and other daily activities.

<span class="mw-page-title-main">Pulp (tooth)</span> Part in the center of a tooth made up of living connective tissue and cells called odontoblasts

The pulp is the connective tissue, nerves, blood vessels, and odontoblasts that comprise the innermost layer of a tooth. The pulp's activity and signalling processes regulate its behaviour.

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels, the nerves, and connective tissue inside a tooth and provides the tooth's blood and nutrients. Pulpitis is mainly caused by bacterial infection which itself is a secondary development of caries. It manifests itself in the form of a toothache.

A pulp polyp, also known as chronic hyperplastic pulpitis, is a "productive" inflammation of dental pulp in which the development of granulation tissue is seen in response to persistent, low-grade mechanical irritation and bacterial invasion of the pulp.

<span class="mw-page-title-main">Condensing osteitis</span> Medical condition

Condensing osteitis is a periapical inflammatory disease that results from a reaction to a dental related infection. This causes more bone production rather than bone destruction in the area. The lesion appears as a radiopacity in the periapical area hence the sclerotic reaction. The sclerotic reaction results from good patient immunity and a low degree of virulence of the offending bacteria. The associated tooth may be carious or contains a large restoration, and is usually associated with a non-vital tooth. It was described by Dr. Carl Garré in 1893.

Dens invaginatus (DI), also known as tooth within a tooth, is a rare dental malformation where there is an infolding of enamel into dentine. The prevalence of condition is 0.3 - 10%, affecting more males than females. The condition is presented in two forms, coronal and radicular, with the coronal form being more common.

<span class="mw-page-title-main">Periapical cyst</span> Medical condition

Commonly known as a dental cyst, the periapical cyst is the most common odontogenic cyst. It may develop rapidly from a periapical granuloma, as a consequence of untreated chronic periapical periodontitis.

<span class="mw-page-title-main">Root canal treatment</span> Dental treatment

Root canal treatment is a treatment sequence for the infected pulp of a tooth which is intended to result in the elimination of infection and the protection of the decontaminated tooth from future microbial invasion. Root canals, and their associated pulp chamber, are the physical hollows within a tooth that are naturally inhabited by nerve tissue, blood vessels and other cellular entities. Together, these items constitute the dental pulp.

Apical periodontitis is typically the body's defense response to the threat of microbial invasion from the root canal. Primary among the members of the host defense mechanism is the polymorphonuclear leukocyte, otherwise known as the neutrophil. The task of the neutrophil is to locate and destroy microbes that intrude into the body – anywhere in the body – and they represent the hallmark of acute inflammation.

<span class="mw-page-title-main">Pulpotomy</span>

Pulpotomy is a minimally invasive procedure performed in children on a primary tooth with extensive caries but without evidence of root pathology. The minimally invasive endodontic techniques of vital pulp therapy (VPT) are based on improved understanding of the capacity of pulp (nerve) tissues to heal and regenerate plus the availability of advanced endodontic materials. During the caries removal, this results in a carious or mechanical pulp exposure (bleeding) from the cavity. During pulpotomy, the inflamed/diseased pulp tissue is removed from the coronal pulp chamber of the tooth leaving healthy pulp tissue which is dressed with a long-term clinically successful medicament that maintains the survival of the pulp and promotes repair. There are various types of medicament placed above the vital pulp such as Buckley's Solution of formocresol, ferric sulfate, calcium hydroxide or mineral trioxide aggregate (MTA). MTA is a more recent material used for pulpotomies with a high rate of success, better than formocresol or ferric sulfate. It is also recommended to be the preferred pulpotomy agent in the future. After the coronal pulp chamber is filled, the tooth is restored with a filling material that seals the tooth from microleakage, such as a stainless steel crown which is the most effective long-term restoration. However, if there is sufficient remaining supporting tooth structure, other filling materials such as amalgam or composite resin can provide a functional alternative when the primary tooth has a life span of two years or less. The medium- to long-term treatment outcomes of pulpotomy in symptomatic permanent teeth with caries, especially in young people, indicate that pulpotomy can be a potential alternative to root canal therapy (RCT).

<span class="mw-page-title-main">Tooth resorption</span> Medical condition

Resorption of the root of the tooth, or root resorption, is the progressive loss of dentin and cementum by the action of odontoclasts. Root resorption is a normal physiological process that occurs in the exfoliation of the primary dentition. However, pathological root resorption occurs in the permanent or secondary dentition and sometimes in the primary dentition.

Dental pulpal testing is a clinical and diagnostic aid used in dentistry to help establish the health of the dental pulp within the pulp chamber and root canals of a tooth. Such investigations are important in aiding dentists in devising a treatment plan for the tooth being tested.

A phoenix abscess is an acute exacerbation of a chronic periapical lesion. It is a dental abscess that can occur immediately following root canal treatment. Another cause is due to untreated necrotic pulp. It is also the result of inadequate debridement during the endodontic procedure. Risk of occurrence of a phoenix abscess is minimised by correct identification and instrumentation of the entire root canal, ensuring no missed anatomy.

<span class="mw-page-title-main">Pulp stone</span>

Pulp stones are nodular, calcified masses appearing in either or both the coronal and root portion of the pulp organ in teeth. Pulp stones are not painful unless they impinge on nerves.

<span class="mw-page-title-main">Regenerative endodontics</span> Dental specialty

Regenerative endodontic procedures is defined as biologically based procedures designed to replace damaged structures such as dentin, root structures, and cells of the pulp-dentin complex. This new treatment modality aims to promote normal function of the pulp. It has become an alternative to heal apical periodontitis. Regenerative endodontics is the extension of root canal therapy. Conventional root canal therapy cleans and fills the pulp chamber with biologically inert material after destruction of the pulp due to dental caries, congenital deformity or trauma. Regenerative endodontics instead seeks to replace live tissue in the pulp chamber. The ultimate goal of regenerative endodontic procedures is to regenerate the tissues and the normal function of the dentin-pulp complex.

<span class="mw-page-title-main">Pulp capping</span>

Pulp capping is a technique used in dental restorations to prevent the dental pulp from necrosis, after being exposed, or nearly exposed during a cavity preparation, from a traumatic injury, or by a deep cavity that reaches the center of the tooth causing the pulp to die. When dental caries is removed from a tooth, all or most of the infected and softened enamel and dentin are removed. This can lead to the pulp of the tooth either being exposed or nearly exposed which causes pulpitis (inflammation). Pulpitis, in turn, can become irreversible, leading to pain and pulp necrosis, and necessitating either root canal treatment or extraction. The ultimate goal of pulp capping or stepwise caries removal is to protect a healthy dental pulp and avoid the need for root canal therapy.

In the dental specialty of endodontics, periradicular surgery is surgery to the external root surface. Examples of periradicular surgery include apicoectomy, root resection, repair of root perforation or resorption defects, removal of broken fragments of the tooth or a filling material, and exploratory surgery to look for root fractures.

Periapical granuloma, also sometimes referred to as a radicular granuloma or apical granuloma, is an inflammation at the tip of a dead (nonvital) tooth. It is a lesion or mass that typically starts out as an epithelial lined cyst, and undergoes an inward curvature that results in inflammation of granulation tissue at the root tips of a dead tooth. This is usually due to dental caries or a bacterial infection of the dental pulp. Periapical granuloma is an infrequent disorder that has an occurrence rate between 9.3 to 87.1 percent. Periapical granuloma is not a true granuloma due to the fact that it does not contain granulomatous inflammation; however, periapical granuloma is a common term used.

Apexification is a method of dental treatment to induce a calcific barrier in a root with incomplete formation or open apex of a tooth with necrotic pulp. Pulpal involvement usually occurs as a consequence of trauma or caries involvement of young or immature permanent teeth. As a sequelae of untreated pulp involvement, loss of pulp vitality or necrotic pulp took place for the involved teeth.

References

  1. 1 2 "Dental Pulp Necrosis MeSH Descriptor Data 2018". National Library of Medicine. 6 July 2009. Retrieved 2018-10-24.
  2. ↑ Lauridsen E, Hermann NV, Gerds TA, Ahrensburg SS, Kreiborg S, Andreasen JO (October 2012). "Combination injuries 3. The risk of pulp necrosis in permanent teeth with extrusion or lateral luxation and concomitant crown fractures without pulp exposure". Dental Traumatology. 28 (5): 379–85. doi:10.1111/j.1600-9657.2011.01100.x. PMID   22233180.
  3. 1 2 "Dental Pulp Cavity Definition".
  4. ↑ Berggreen E, Bletsa A, Heyeraas KJ (September 2007). "Circulation in normal and inflamed dental pulp". Endodontic Topics. 17 (1): 2–11. doi:10.1111/j.1601-1546.2010.00249.x.
  5. 1 2 Soames JV, Southam JC (2005). Oral pathology (4th ed.). Oxford: Oxford University Press. ISBN   978-0-19-852794-7. OCLC   57006193.
  6. ↑ "Pulp Therapy for Primary and Immature Permanent Teeth". Pediatric Dentistry. 39 (6): 325–333. September 2017. PMID   29179372.
  7. 1 2 Rechenberg DK, Galicia JC, Peters OA (2016-11-29). "Biological Markers for Pulpal Inflammation: A Systematic Review". PLOS ONE. 11 (11): e0167289. Bibcode:2016PLoSO..1167289R. doi: 10.1371/journal.pone.0167289 . PMC   5127562 . PMID   27898727.
  8. ↑ Yu, C; Abbott, PV (2007). "An overview of the dental pulp: its functions and responses to injury". Australian Dental Journal. 52 (1 Suppl): 4–16. doi:10.1111/j.1834-7819.2007.tb00525.x. PMID   17546858.
  9. ↑ Goodell, GC; Tordik, PA; Moss, D (December 2005). "Pulpal and periradicular diagnosis". Clinical. 27.
  10. ↑ Levin, LG; et al. (December 2009). "Identify and Define All Diagnostic Terms for Pulpal Health and Disease States". Journal of Endodontics. 35 (12): 1645–1657. doi:10.1016/j.joen.2009.09.032. PMID   19932339.
  11. 1 2 3 4 5 6 7 8 Abbott PV, Yu C (March 2007). "A clinical classification of the status of the pulp and the root canal system". Australian Dental Journal. 52 (1 Suppl): S17-31. doi: 10.1111/j.1834-7819.2007.tb00522.x . PMID   17546859.
  12. ↑ Smaïl-Faugeron V, Glenny AM, Courson F, Durieux P, Muller-Bolla M, Fron Chabouis H (May 2018). "Pulp treatment for extensive decay in primary teeth". The Cochrane Database of Systematic Reviews. 2018 (5): CD003220. doi:10.1002/14651858.CD003220.pub3. PMC   6494507 . PMID   29852056.
  13. ↑ Bjørndal L (July 2008). "The caries process and its effect on the pulp: the science is changing and so is our understanding". Journal of Endodontics. 34 (7 Suppl): S2–5. doi:10.1016/j.joen.2008.02.037. PMID   18565367.
  14. ↑ Hargreaves KM, Goodis HE, Tay FR, Seltzer S (February 2012). Seltzer and Bender's Dental Pulp. Hanover Park, IL: Quintessence Pub. ISBN   978-0-86715-480-1. OCLC   794664259.
  15. 1 2 Aldrigui JM, Cadioli IC, Mendes FM, Antunes JL, Wanderley MT (November 2013). "Predictive factors for pulp necrosis in traumatized primary incisors: a longitudinal study". International Journal of Paediatric Dentistry. 23 (6): 460–9. doi:10.1111/ipd.12019. PMID   23331274.
  16. ↑ Moccelini BS, de Alencar NA, Bolan M, Magno MB, Maia LC, Cardoso M (June 2018). "Pulp necrosis and crown discoloration: a systematic review and meta-analysis". International Journal of Paediatric Dentistry. 28 (5): 432–442. doi:10.1111/ipd.12372. PMID   29896799. S2CID   48359961.
  17. ↑ JACOBSEN, INGEBORG (August 1980). "Criteria for diagnosis of pulp necrosis in traumatized permanent incisors". European Journal of Oral Sciences. 88 (4): 306–312. doi:10.1111/j.1600-0722.1980.tb01231.x. ISSN   0909-8836. PMID   6934614.
  18. ↑ Lauridsen, Eva; Hermann, Nuno Vibe; Gerds, Thomas Alexander; Ahrensburg, Søren Steno; Kreiborg, Sven; Andreasen, Jens Ove (2012-01-11). "Combination injuries 3. The risk of pulp necrosis in permanent teeth with extrusion or lateral luxation and concomitant crown fractures without pulp exposure". Dental Traumatology. 28 (5): 379–385. doi:10.1111/j.1600-9657.2011.01100.x. ISSN   1600-4469. PMID   22233180.
  19. ↑ Peterson, K.; Söderström, C.; Kiani-Anaraki, M.; Lévy, G. (June 1999). "Evaluation of the ability of thermal and electrical tests to register pulp vitality". Dental Traumatology. 15 (3): 127–131. doi:10.1111/j.1600-9657.1999.tb00769.x. ISSN   1600-4469.
  20. 1 2 3 Gopikrishna, Velayutham; Tinagupta, Kush; Kandaswamy, Deivanayagam (April 2007). "Evaluation of Efficacy of a New Custom-Made Pulse Oximeter Dental Probe in Comparison With the Electrical and Thermal Tests for Assessing Pulp Vitality". Journal of Endodontics. 33 (4): 411–414. doi:10.1016/j.joen.2006.12.003. ISSN   0099-2399. PMID   17368329.
  21. ↑ Munshi, A.; Hegde, Amitha; Radhakrishnan, Sangeeth (January 2003). "Pulse oximetry: a diagnostic instrument in pulpal vitality testing". Journal of Clinical Pediatric Dentistry. 26 (2): 141–145. doi:10.17796/jcpd.26.2.2j25008jg6u86236. ISSN   1053-4628. PMID   11874005.
  22. ↑ Jafarzadeh, Hamid; Rosenberg, Paul A. (March 2009). "Pulse Oximetry: Review of a Potential Aid in Endodontic Diagnosis". Journal of Endodontics. 35 (3): 329–333. doi:10.1016/j.joen.2008.12.006. ISSN   0099-2399. PMID   19249589.
  23. ↑ Dastmalchi, Nafiseh; Jafarzadeh, Hamid; Moradi, Saeed (September 2012). "Comparison of the Efficacy of a Custom-made Pulse Oximeter Probe with Digital Electric Pulp Tester, Cold Spray, and Rubber Cup for Assessing Pulp Vitality". Journal of Endodontics. 38 (9): 1182–1186. doi:10.1016/j.joen.2012.06.012. ISSN   0099-2399. PMID   22892732.
  24. 1 2 Mainkar, Anshul; Kim, Sahng G. (May 2018). "Diagnostic Accuracy of 5 Dental Pulp Tests: A Systematic Review and Meta-analysis". Journal of Endodontics. 44 (5): 694–702. doi:10.1016/j.joen.2018.01.021. ISSN   0099-2399. PMID   29571914. S2CID   4262028.
  25. ↑ Assaf, Alexandre T.; Zrnc, Tomislav A.; Remus, Chressen C.; Khokale, Arun; Habermann, Christian R.; Schulze, Dirk; Fiehler, Jens; Heiland, Max; Sedlacik, Jan (September 2015). "Early detection of pulp necrosis and dental vitality after traumatic dental injuries in children and adolescents by 3-Tesla magnetic resonance imaging". Journal of Cranio-Maxillofacial Surgery. 43 (7): 1088–1093. doi:10.1016/j.jcms.2015.06.010. ISSN   1010-5182. PMID   26165761.
  26. ↑ "Guide to Clinical Endodontics 6th edition". American Association of Endodontics. 2016.
  27. ↑ Kahler, B; et al. (July 2017). "An Evidence-based view of the Efficacy of Treatment Approaches for Immature Permanent Teeth with Pulp Necrosis Health and Disease States". Journal of Endodontics. 43 (7): 1052–1057. doi:10.1016/j.joen.2017.03.003. PMID   28511779. S2CID   21655918.
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