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Pulp necrosis

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198:(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 449:, 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. For the purposes of evaluating pulp vitality, it is imperative that the probes fit the anatomical contours and shape of the measured teeth. 532:
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.
480:, 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. 104:
5-20mm Hg, marked increases in pressure in the pulp due to inflammation can go up to 60mm Hg. 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. A common clinical sign associated with the histopathology will be varying levels of suppuration and purulence.
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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.
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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
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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
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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
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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
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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
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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. Teeth with said discolouration need to be treated with special care and further investigations are required before pulp necrosis can
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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
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Another critically appraised topic 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
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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
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The pain associated with pulp necrosis is often described as spontaneous. 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
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The dental pulp is located in the centre of a tooth, made up of living connective tissue and cells. It is surrounded by a rigid, hard and dense layer of dentine which limits the ability of the pulp to tolerate excessive build up of fluid. Normal interstitial fluid pressure in the pulp ranges from
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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".
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which suppresses the cellular metabolism in the area of the pulp that is affected. This causes necrosis. Necrosis is a histological term that means death of the pulp. It does not occur suddenly unless there has been trauma. The pulp may be partially necrotic for some time. The area of cell death
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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
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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. This altered translucency in the tooth is due to
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levels, making it non-invasive and an objective way to record patient response regarding pulpal diagnosis. 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.
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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.
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enlarges until the entire pulp is necrotic. Bacteria invade the pulp which causes the root canal system to become infected. Teeth that have total pulpal necrosis are usually asymptomatic except for those that have inflammation which has progressed to the periradicular tissues.
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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
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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.
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of the tooth, with oxygen saturation values recorded after 30 seconds of monitoring each tooth. The values were taken as a positive response (i.e. vital pulp) within the range of 75-85% oxygen saturation and a negative response below 75%, indicating pulp necrosis.
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tissues, resulting in pressure on the nerve of said tooth and tissues adjacent. 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.
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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".
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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
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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".
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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.
123:, 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 1384:
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".
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necrotic pulp if subjects felt no sensation after two 15-second applications every two minutes. It is worthy to note that a control test should be performed on the adjacent tooth to ensure further accuracy of results.
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Following the spread of local inflammation, chemical mediators such as IL-8, IL-6 and IL-1 are released from necrotic tissues leading to further inflammation and odema, which advances to total necrosis of the pulp.
139:. 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 492:. 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. 429:
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. This method involves taking measurements of blood
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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.
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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
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comprise the initial inflammatory infiltrate. In response to bacterial assault and tissue injury non-specific inflammatory mediators are released. These inflammatory mediators include
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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".
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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
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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".
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Peterson, K.; Söderström, C.; Kiani-Anaraki, M.; Lévy, G. (June 1999). "Evaluation of the ability of thermal and electrical tests to register pulp vitality".
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technique. A disadvantage of this was that it required multiple visits over a prolonged time and there could be an increased risk of cervical
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Munshi, A.; Hegde, Amitha; Radhakrishnan, Sangeeth (January 2003). "Pulse oximetry: a diagnostic instrument in pulpal vitality testing".
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disease progressions which occur in stages; normal healthy tissue becomes inflamed (i.e. pulpitis) which if left untreated leads to
143:, a decrease in the number and size of the endoplasmic reticulum, and degeneration of mitochondria. It is unknown by which process ( 1951: 1760: 1431:
Mainkar, Anshul; Kim, Sahng G. (May 2018). "Diagnostic Accuracy of 5 Dental Pulp Tests: A Systematic Review and Meta-analysis".
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Bjørndal L (July 2008). "The caries process and its effect on the pulp: the science is changing and so is our understanding".
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preparation – this may be due to excessive thermal insult and close proximity to the pulp during tooth preparation – or rapid
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Jafarzadeh, Hamid; Rosenberg, Paul A. (March 2009). "Pulse Oximetry: Review of a Potential Aid in Endodontic Diagnosis".
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Levin, LG; et al. (December 2009). "Identify and Define All Diagnostic Terms for Pulpal Health and Disease States".
69:. This altered translucency in the tooth is due to disruption and cutting off of the apical neurovascular blood supply. 112:
also be lost. The periapical lesion will enlarged with time and consequently, the pulp will be diagnosed as necrotic.
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and discolouration of the tooth. Tests for a necrotic pulp include: vitality testing using a thermal test or an
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JACOBSEN, INGEBORG (August 1980). "Criteria for diagnosis of pulp necrosis in traumatized permanent incisors".
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Pulpal necrosis can also occur as a result of dental treatments such as iatrogenic damage due to overzealous
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Berggreen E, Bletsa A, Heyeraas KJ (September 2007). "Circulation in normal and inflamed dental pulp".
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There are additional signs of pulp necrosis which may be detected during radiographic assessment:-;
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Yu, C; Abbott, PV (2007). "An overview of the dental pulp: its functions and responses to injury".
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Smaïl-Faugeron V, Glenny AM, Courson F, Durieux P, Muller-Bolla M, Fron Chabouis H (May 2018).
1996: 1921: 1841: 1734: 120: 58: 1045:"Predictive factors for pulp necrosis in traumatized primary incisors: a longitudinal study" 2135: 2050: 2003: 732: 438: 270: 73: 215:– this can occur with or without the involvement of bacteria. It is the result of various 8: 2085: 2010: 1847: 1823: 1714: 1709: 1677: 1673: 410: 1311: 813:
Goodell, GC; Tordik, PA; Moss, D (December 2005). "Pulpal and periradicular diagnosis".
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have been used to detect and evaluate several head and neck regions including the
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and infection and finally resulting in loss of pulp tissue (i.e. pulpless canals)
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Aldrigui JM, Cadioli IC, Mendes FM, Antunes JL, Wanderley MT (November 2013).
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Pulpal regeneration can be considered if the following criteria are met:
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disruption and cutting off of the apical neurovascular blood supply.
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Hargreaves KM, Goodis HE, Tay FR, Seltzer S (February 2012).
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The most basic treatment for teeth with pulpal necrosis is
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Pulp necrosis arises due to the cellular death within the
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Apexogenesis is not applicable as there is apical closure
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to die and cause initiation of an inflammatory response.
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clastic cells with nutrients via a viable blood supply.
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Incomplete root development and incomplete apex closure
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Periodontitis as a manifestation of systemic disease
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The pulse oximeter consists of a probe containing 2
1340: 719:Rechenberg DK, Galicia JC, Peters OA (2016-11-29). 306:Pulp necrosis may or may not arise with symptoms. 812: 660:(4th ed.). Oxford: Oxford University Press. 33:is a clinical diagnostic category indicating the 2122: 1038: 1036: 553:"Dental Pulp Necrosis MeSH Descriptor Data 2018" 309:Signs and symptoms of pulpal necrosis include; 1612: 1526:"Guide to Clinical Endodontics 6th edition". 1086:International Journal of Paediatric Dentistry 1049:International Journal of Paediatric Dentistry 1033: 655: 483: 413:and mechanical stimulation of pulpal nerves. 1077: 965: 916: 929:The Cochrane Database of Systematic Reviews 682: 555:. National Library of Medicine. 6 July 2009 385: 27:Tissue death within the interior of a tooth 1626: 1619: 1605: 1430: 547: 545: 72:Sequelae of a necrotic pulp include acute 49:. It is often the result of many cases of 1060: 948: 899: 754: 744: 376: 1126: 971: 881: 777: 190:. They can interact with neuropeptides ( 1952:Combined periodontic-endodontic lesions 1761:Combined periodontic-endodontic lesions 1485:Journal of Cranio-Maxillofacial Surgery 1300:Journal of Clinical Pediatric Dentistry 542: 367: 206: 14: 2123: 1540: 1011:. Hanover Park, IL: Quintessence Pub. 420: 1600: 1426: 1424: 1249: 1247: 1245: 877: 875: 873: 871: 869: 867: 865: 863: 831: 301: 1932:Generalized aggressive periodontitis 714: 712: 651: 649: 607: 605: 527:. The apical barrier technique with 1528:American Association of Endodontics 1312:10.17796/jcpd.26.2.2j25008jg6u86236 276: 24: 1927:Localized aggressive periodontitis 1421: 1242: 1228:10.1111/j.1600-9657.1999.tb00769.x 1141:10.1111/j.1600-0722.1980.tb01231.x 901:10.1111/j.1834-7819.2007.tb00522.x 860: 792:10.1111/j.1834-7819.2007.tb00525.x 523:due to an increase in exposure to 465:3-Tesla Magnetic Resonance Imaging 273:, and subsequently pulp necrosis. 25: 2147: 1129:European Journal of Oral Sciences 709: 646: 602: 98: 1942:Necrotizing periodontal diseases 1583: 1185:10.1111/j.1600-9657.2011.01100.x 1009:Seltzer and Bender's Dental Pulp 640:10.1111/j.1601-1546.2010.00249.x 588:10.1111/j.1600-9657.2011.01100.x 403: 263: 254: 1534: 1519: 1475: 1377: 1334: 1291: 1207: 1163: 1120: 1000: 825: 613:"Dental Pulp Cavity Definition" 196:calcitonin gene-related peptide 154: 130: 941:10.1002/14651858.CD003220.pub3 882:Abbott PV, Yu C (March 2007). 806: 771: 697:(6): 325–333. September 2017. 656:Soames JV, Southam JC (2005). 619: 566: 289:work causing excessive force. 269:to inflammation of the apical 13: 1: 1947:Abscesses of the periodontium 1483:magnetic resonance imaging". 535: 445:, and the other transmitting 1756:Chronic apical periodontitis 746:10.1371/journal.pone.0167289 394: 37:of cells and tissues in the 7: 1871:Calcifying odontogenic cyst 292: 91:Treatment usually involves 10: 2152: 1876:Glandular odontogenic cyst 1751:Acute apical periodontitis 1555:10.1016/j.joen.2017.03.003 1497:10.1016/j.jcms.2015.06.010 1445:10.1016/j.joen.2018.01.021 1399:10.1016/j.joen.2012.06.012 1355:10.1016/j.joen.2008.12.006 1269:10.1016/j.joen.2006.12.003 986:10.1016/j.joen.2008.02.037 846:10.1016/j.joen.2009.09.032 529:mineral trioxide aggregate 509:Mineral Trioxide Aggregate 484:Management & Treatment 345:Extensive/deep restoration 2020: 1960: 1912: 1900: 1884: 1856: 1819: 1789: 1743: 1702: 1691: 1635: 888:Australian Dental Journal 780:Australian Dental Journal 461:bias in the experiments. 226: 2131:Acquired tooth disorders 2071:Linear gingival erythema 1969:A. actinomycetemcomitans 386:Internal root resorption 331:Increased tooth mobility 328:Internal root resorption 186:(IL) and metabolites of 151:) the odontoblasts die. 474:Temporomandibular Joint 358: 2066:Horizontal bony defect 1892:Cracked tooth syndrome 1781:Vertical root fracture 1543:Journal of Endodontics 1433:Journal of Endodontics 1387:Journal of Endodontics 1343:Journal of Endodontics 1257:Journal of Endodontics 974:Journal of Endodontics 834:Journal of Endodontics 377:Abscess and/or fistula 115:The pulp can respond ( 1922:Chronic periodontitis 1842:Chronic periodontitis 1735:Pink tooth of Mummery 1720:Irreversible pulpitis 439:light-emitting diodes 411:odontoblast processes 121:irreversible pulpitis 59:irreversible pulpitis 2106:Vertical bony defect 2051:Gingival enlargement 1643:Caries (tooth decay) 490:root canal treatment 368:Crown discolouration 316:Crown discolouration 271:periodontal ligament 207:Aetiology and Causes 86:electric pulp tester 74:apical periodontitis 2086:Periodontal disease 1848:Periodontal disease 1820:Gingiva/periodontal 1725:Reversible pulpitis 1715:Internal resorption 1710:External resorption 1678:Internal resorption 1674:External resorption 1216:Dental Traumatology 1173:Dental Traumatology 894:(1 Suppl): S17-31. 737:2016PLoSO..1167289R 691:Pediatric Dentistry 576:Dental Traumatology 421:Pulse Oximeter Test 117:reversible pulpitis 2081:Periodontal pocket 1976:Capnocytophaga sp. 1807:Periapical abscess 1771:Periapical abscess 515:calcium hydroxide 302:Signs and symptoms 65:and/or periapical 47:bacterial invasion 2118: 2117: 2114: 2113: 1815: 1814: 1692:Pulp/periapical ( 1098:10.1111/ipd.12372 1062:10.1111/ipd.12019 1018:978-0-86715-480-1 980:(7 Suppl): S2–5. 840:(12): 1645–1657. 786:(1 Suppl): 4–16. 667:978-0-19-852794-7 628:Endodontic Topics 525:calcium hydroxide 431:oxygen saturation 217:connective tissue 16:(Redirected from 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1776:Phoenix abscess 1739: 1687: 1682:Root resorption 1663:Hypercementosis 1631: 1625: 1591:Medicine portal 1589: 1584: 1582: 1579: 1578: 1539: 1535: 1525: 1524: 1520: 1480: 1476: 1429: 1422: 1382: 1378: 1339: 1335: 1296: 1292: 1252: 1243: 1212: 1208: 1168: 1164: 1125: 1121: 1082: 1078: 1041: 1034: 1019: 1005: 1001: 970: 966: 935:(5): CD003220. 921: 917: 880: 861: 830: 826: 811: 807: 776: 772: 717: 710: 688: 687: 683: 668: 654: 647: 624: 620: 611: 610: 603: 571: 567: 558: 556: 551: 550: 543: 538: 486: 478:salivary glands 467: 423: 406: 397: 388: 379: 370: 361: 304: 295: 279: 266: 257: 229: 209: 157: 133: 101: 95:or extraction. 28: 23: 22: 15: 12: 11: 5: 2149: 2139: 2138: 2133: 2116: 2115: 2112: 2111: 2109: 2108: 2103: 2098: 2093: 2088: 2083: 2078: 2073: 2068: 2063: 2058: 2053: 2048: 2043: 2038: 2033: 2027: 2025: 2018: 2017: 2015: 2014: 2007: 2000: 1993: 1986: 1979: 1972: 1964: 1962: 1958: 1957: 1955: 1954: 1949: 1944: 1939: 1934: 1929: 1924: 1918: 1916: 1907: 1905:periodontology 1898: 1897: 1895: 1894: 1888: 1886: 1882: 1881: 1879: 1878: 1873: 1868: 1862: 1860: 1854: 1853: 1851: 1850: 1845: 1835: 1829: 1827: 1817: 1816: 1813: 1812: 1810: 1809: 1804: 1802:Radicular cyst 1799: 1793: 1791: 1787: 1786: 1784: 1783: 1778: 1773: 1768: 1763: 1758: 1753: 1747: 1745: 1741: 1740: 1738: 1737: 1732: 1727: 1722: 1717: 1712: 1706: 1704: 1697: 1689: 1688: 1686: 1685: 1665: 1660: 1655: 1650: 1645: 1639: 1637: 1633: 1632: 1624: 1623: 1616: 1609: 1601: 1595: 1594: 1577: 1576: 1533: 1518: 1474: 1439:(5): 694–702. 1420: 1376: 1349:(3): 329–333. 1333: 1306:(2): 141–145. 1290: 1263:(4): 411–414. 1241: 1222:(3): 127–131. 1206: 1179:(5): 379–385. 1162: 1135:(4): 306–312. 1119: 1092:(5): 432–442. 1076: 1032: 1017: 999: 964: 915: 859: 824: 805: 770: 708: 681: 666: 658:Oral pathology 645: 618: 601: 565: 540: 539: 537: 534: 504: 503: 500: 485: 482: 466: 463: 447:infrared light 427:pulse oximeter 422: 419: 405: 402: 396: 393: 387: 384: 378: 375: 373:be diagnosed. 369: 366: 360: 357: 353: 352: 346: 343: 333: 332: 329: 326: 317: 314: 303: 300: 294: 291: 278: 275: 265: 262: 256: 253: 252: 251: 248: 243: 240: 235: 228: 225: 208: 205: 156: 153: 132: 129: 100: 99:Histopathology 97: 82:radicular cyst 78:dental abscess 26: 9: 6: 4: 3: 2: 2148: 2137: 2134: 2132: 2129: 2128: 2126: 2107: 2104: 2102: 2099: 2097: 2094: 2092: 2091:Periodontitis 2089: 2087: 2084: 2082: 2079: 2077: 2074: 2072: 2069: 2067: 2064: 2062: 2059: 2057: 2054: 2052: 2049: 2047: 2044: 2042: 2039: 2037: 2034: 2032: 2029: 2028: 2026: 2023: 2019: 2013: 2012: 2008: 2006: 2005: 2001: 1999: 1998: 1997:P. intermedia 1994: 1992: 1991: 1990:P. gingivalis 1987: 1985: 1984: 1980: 1978: 1977: 1973: 1971: 1970: 1966: 1965: 1963: 1959: 1953: 1950: 1948: 1945: 1943: 1940: 1938: 1935: 1933: 1930: 1928: 1925: 1923: 1920: 1919: 1917: 1915: 1911: 1908: 1906: 1901:To be grouped 1899: 1893: 1890: 1889: 1887: 1883: 1877: 1874: 1872: 1869: 1867: 1864: 1863: 1861: 1859: 1855: 1849: 1846: 1843: 1839: 1838:Periodontitis 1836: 1834: 1831: 1830: 1828: 1825: 1818: 1808: 1805: 1803: 1800: 1798: 1795: 1794: 1792: 1788: 1782: 1779: 1777: 1774: 1772: 1769: 1767: 1764: 1762: 1759: 1757: 1754: 1752: 1749: 1748: 1746: 1742: 1736: 1733: 1731: 1730:Pulp necrosis 1728: 1726: 1723: 1721: 1718: 1716: 1713: 1711: 1708: 1707: 1705: 1701: 1698: 1695: 1690: 1683: 1679: 1675: 1671: 1670: 1666: 1664: 1661: 1659: 1656: 1654: 1651: 1649: 1646: 1644: 1641: 1640: 1638: 1634: 1630: 1629:tooth disease 1622: 1617: 1615: 1610: 1608: 1603: 1602: 1599: 1592: 1581: 1572: 1568: 1564: 1560: 1556: 1552: 1548: 1544: 1537: 1529: 1522: 1514: 1510: 1506: 1502: 1498: 1494: 1490: 1486: 1478: 1470: 1466: 1462: 1458: 1454: 1450: 1446: 1442: 1438: 1434: 1427: 1425: 1416: 1412: 1408: 1404: 1400: 1396: 1392: 1388: 1380: 1372: 1368: 1364: 1360: 1356: 1352: 1348: 1344: 1337: 1329: 1325: 1321: 1317: 1313: 1309: 1305: 1301: 1294: 1286: 1282: 1278: 1274: 1270: 1266: 1262: 1258: 1250: 1248: 1246: 1237: 1233: 1229: 1225: 1221: 1217: 1210: 1202: 1198: 1194: 1190: 1186: 1182: 1178: 1174: 1166: 1158: 1154: 1150: 1146: 1142: 1138: 1134: 1130: 1123: 1115: 1111: 1107: 1103: 1099: 1095: 1091: 1087: 1080: 1072: 1068: 1063: 1058: 1054: 1050: 1046: 1039: 1037: 1028: 1024: 1020: 1014: 1010: 1003: 995: 991: 987: 983: 979: 975: 968: 960: 956: 951: 946: 942: 938: 934: 930: 926: 919: 911: 907: 902: 897: 893: 889: 885: 878: 876: 874: 872: 870: 868: 866: 864: 855: 851: 847: 843: 839: 835: 828: 820: 816: 809: 801: 797: 793: 789: 785: 781: 774: 766: 762: 757: 752: 747: 742: 738: 734: 730: 726: 722: 715: 713: 704: 700: 696: 692: 685: 677: 673: 669: 663: 659: 652: 650: 641: 637: 633: 629: 622: 614: 608: 606: 597: 593: 589: 585: 582:(5): 379–85. 581: 577: 569: 554: 548: 546: 541: 533: 530: 526: 522: 521:root fracture 518: 517:apexification 512: 510: 501: 498: 497: 496: 493: 491: 481: 479: 475: 471: 462: 458: 455: 450: 448: 444: 440: 435: 432: 428: 418: 414: 412: 404:Thermal Tests 401: 392: 383: 374: 365: 356: 351: 347: 344: 342: 338: 337: 336: 330: 327: 325: 321: 318: 315: 312: 311: 310: 307: 299: 290: 288: 284: 274: 272: 264:Dental Trauma 261: 255:Dental Caries 249: 247: 244: 241: 239: 238:Dental Trauma 236: 234: 233:Dental Caries 231: 230: 224: 222: 218: 214: 204: 201: 197: 193: 189: 185: 181: 177: 173: 169: 165: 161: 152: 150: 146: 142: 141:vacuolization 138: 128: 126: 122: 118: 113: 109: 105: 96: 94: 89: 87: 83: 79: 75: 70: 68: 62: 60: 56: 52: 51:dental trauma 48: 44: 40: 36: 32: 31:Pulp necrosis 19: 18:Necrotic pulp 2011:T. denticola 2009: 2004:T. forsythia 2002: 1995: 1988: 1983:F. nucleatum 1981: 1974: 1967: 1961:Pathogenesis 1729: 1667: 1636:Hard tissues 1546: 1542: 1536: 1527: 1521: 1488: 1484: 1477: 1436: 1432: 1390: 1386: 1379: 1346: 1342: 1336: 1303: 1299: 1293: 1260: 1256: 1219: 1215: 1209: 1176: 1172: 1165: 1132: 1128: 1122: 1089: 1085: 1079: 1055:(6): 460–9. 1052: 1048: 1008: 1002: 977: 973: 967: 932: 928: 918: 891: 887: 837: 833: 827: 818: 814: 808: 783: 779: 773: 728: 724: 694: 690: 684: 657: 631: 627: 621: 579: 575: 568: 557:. Retrieved 513: 505: 494: 487: 468: 459: 451: 436: 424: 415: 407: 398: 389: 380: 371: 362: 354: 350:pulp capping 334: 308: 305: 296: 280: 267: 258: 213:pulp chamber 210: 164:plasma cells 158: 155:Inflammation 134: 131:Odontoblasts 125:odontoblasts 114: 110: 106: 102: 90: 71: 67:radiolucency 63: 39:pulp chamber 30: 29: 2136:Endodontics 1824:Periodontal 634:(1): 2–11. 443:haemoglobin 287:orthodontic 192:substance P 184:nterleukins 168:macrophages 160:Lymphocytes 93:endodontics 2125:Categories 2061:Gingivitis 2036:Edentulism 2022:Pathologic 1833:Gingivitis 1744:Periapical 1694:Endodontal 559:2018-10-24 536:References 339:Untreated 176:bradykinin 2101:Recession 1914:Diagnoses 1858:Bone cyst 1790:Ungrouped 1648:Attrition 1627:Acquired 1505:1010-5182 1453:0099-2399 1407:0099-2399 1363:0099-2399 1320:1053-4628 1277:0099-2399 1236:1600-4469 1193:1600-4469 1149:0909-8836 1027:794664259 470:MRI scans 395:Diagnosis 348:Previous 250:Infection 200:ischaemic 180:serotonin 172:histamine 145:apoptosis 2041:Fremitus 2031:Calculus 2024:entities 1797:Pulpitis 1653:Abrasion 1571:21655918 1563:28511779 1513:26165761 1461:29571914 1415:22892732 1371:19249589 1328:11874005 1285:17368329 1201:22233180 1114:48359961 1106:29896799 1071:23331274 994:18565367 959:29852056 910:17546859 854:19932339 815:Clinical 800:17546858 765:27898727 725:PLOS ONE 703:29179372 676:57006193 596:22233180 293:Pulpitis 246:Pulpitis 221:necrosis 149:necrosis 1766:Fistula 1658:Erosion 1530:. 2016. 1469:4262028 1157:6934614 950:6494507 756:5127562 733:Bibcode 324:fistula 322:and/or 320:Abscess 2096:Plaque 1703:Pulpal 1569:  1561:  1511:  1503:  1467:  1459:  1451:  1413:  1405:  1369:  1361:  1326:  1318:  1283:  1275:  1234:  1199:  1191:  1155:  1147:  1112:  1104:  1069:  1025:  1015:  992:  957:  947:  908:  852:  798:  763:  753:  701:  674:  664:  594:  341:caries 227:Causes 194:) and 55:caries 1903:from 1885:Other 1567:S2CID 1465:S2CID 1110:S2CID 454:crown 283:crown 43:tooth 41:of a 35:death 1559:PMID 1509:PMID 1501:ISSN 1457:PMID 1449:ISSN 1411:PMID 1403:ISSN 1367:PMID 1359:ISSN 1324:PMID 1316:ISSN 1281:PMID 1273:ISSN 1232:ISSN 1197:PMID 1189:ISSN 1153:PMID 1145:ISSN 1102:PMID 1067:PMID 1023:OCLC 1013:ISBN 990:PMID 955:PMID 933:2018 906:PMID 850:PMID 796:PMID 761:PMID 699:PMID 672:OCLC 662:ISBN 592:PMID 425:The 359:Pain 313:Pain 166:and 57:and 1551:doi 1493:doi 1441:doi 1395:doi 1351:doi 1308:doi 1265:doi 1224:doi 1181:doi 1137:doi 1094:doi 1057:doi 982:doi 945:PMC 937:doi 896:doi 842:doi 788:doi 751:PMC 741:doi 636:doi 584:doi 182:, i 147:or 80:or 2127:: 1680:, 1676:, 1565:. 1557:. 1547:43 1545:. 1507:. 1499:. 1489:43 1487:. 1463:. 1455:. 1447:. 1437:44 1435:. 1423:^ 1409:. 1401:. 1391:38 1389:. 1365:. 1357:. 1347:35 1345:. 1322:. 1314:. 1304:26 1302:. 1279:. 1271:. 1261:33 1259:. 1244:^ 1230:. 1220:15 1218:. 1195:. 1187:. 1177:28 1175:. 1151:. 1143:. 1133:88 1131:. 1108:. 1100:. 1090:28 1088:. 1065:. 1053:23 1051:. 1047:. 1035:^ 1021:. 988:. 978:34 976:. 953:. 943:. 931:. 927:. 904:. 892:52 890:. 886:. 862:^ 848:. 838:35 836:. 819:27 817:. 794:. 784:52 782:. 759:. 749:. 739:. 729:11 727:. 723:. 711:^ 695:39 693:. 670:. 648:^ 632:17 630:. 604:^ 590:. 580:28 578:. 544:^ 511:. 476:, 178:, 174:, 162:, 119:, 76:, 61:. 53:, 1844:) 1840:( 1826:) 1822:( 1696:) 1684:) 1672:( 1620:e 1613:t 1606:v 1573:. 1553:: 1515:. 1495:: 1471:. 1443:: 1417:. 1397:: 1373:. 1353:: 1330:. 1310:: 1287:. 1267:: 1238:. 1226:: 1203:. 1183:: 1159:. 1139:: 1116:. 1096:: 1073:. 1059:: 1029:. 996:. 984:: 961:. 939:: 912:. 898:: 856:. 844:: 821:. 802:. 790:: 767:. 743:: 735:: 705:. 678:. 642:. 638:: 615:. 598:. 586:: 562:. 20:)

Index

Necrotic pulp
death
pulp chamber
tooth
bacterial invasion
dental trauma
caries
irreversible pulpitis
radiolucency
apical periodontitis
dental abscess
radicular cyst
electric pulp tester
endodontics
reversible pulpitis
irreversible pulpitis
odontoblasts
dentinal tubules
vacuolization
apoptosis
necrosis
Lymphocytes
plasma cells
macrophages
histamine
bradykinin
serotonin
nterleukins
arachidonic acid
substance P

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