Dens evaginatus

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Dens evaginatus
Other namesTuberculated cusp, accessory tubercle, occlusal tuberculated premolar, Leong's premolar, evaginatus odontoma, occlusal pearl [1] [2]
Specialty Dentistry

Dens evaginatus is a rare odontogenic developmental anomaly that is found in teeth where the outer surface appears to form an extra bump or cusp.

Contents

Premolars are more likely to be affected than any other tooth. [3] It could occur unilaterally or bilaterally. [1] Dens evaginatus (DE) typically occurs bilaterally and symmetrically. [4] This may be seen more frequently in Asians [3] (including Chinese, Malay, Thai, Japanese, Filipino and Indian populations). [4]

The prevalence of DE ranges from 0.06% to 7.7% depending on the race. [3] It is more common in men than in women, [3] more frequent in the mandibular teeth than the maxillary teeth. [1] Patients with Ellis-van Creveld syndrome, incontinentia pigmenti achromians, Mohr syndrome, Rubinstein-Taybi syndrome and Sturge Weber syndrome are at a higher risk of having DE. [3] [2]

Signs and symptoms

It is important to diagnose DE early and provide appropriate treatment to help prevent periodontal disease, caries, pulpal complications [3] and malocclusion. [2] It occurs on the cingulum/occlusal surface of the teeth. The extra cusp can cause occlusal interference, displace of the affected tooth and/or opposing teeth, irritates the tongue when speaking and eating and decay the developmental grooves. [2] Temporomandibular joint pain could be experienced secondarily due to occlusal trauma caused by the tubercle. [1] [2]

This cusp could be worn away or fractured easily. [1] [4] [2] In 70% [4] of the cases, the fine pulpal extension were exposed which can lead to infection, [4] pulpal necrosis and periapical pathosis.

Associated anomalies

Cause

The cause of DE is still unclear. [2] There is literature indicating that DE is an isolated anomaly. During the bell stage of tooth formation, DE may occur as a result of an unusual growth and folding of the inner enamel epithelium and ectomesenchymal cells of dental papilla into the stellate reticulum of the enamel organ. [5] [4]

Diagnosis

Diagnosis of DE can be difficult when there is no signs and symptoms of necrotic or infected pulp. [1] It is a challenging task to differentiate between a true periapical lesion and a normal periapical radiolucency of a dental follicle of an immature apex. [1]

Classification

The anterior DE tubercles have an average width of 3.5mm and length of 6.0mm, [4] while posterior tubercles have an average 2.0mm in width and length of up to 3.5mm. [4] If the cusp of Carabelli is present, the tooth associated are often larger mesiodistally and it is not uncommon that a DE involved tooth has an abnormal root pattern. [4]

There are 4 different ways to classify/ categorize DE involved teeth.

  1. Schulge (1987) classification, teeth falls into 5 categories according to the location of the tubercles [4] [2]
    • Tubercle on the inclined plane of the lingual cusp
    • Cone-like enlargement of the buccal cusp
    • Tubercle on the inclined plane of the buccal cusp
    • Tubercle arising from the occlusal surface obliterating the central groove
  2. Lau's classification, divide teeth into groups according to their anatomical shape [4] [2]
    • Smooth
    • Grooved
    • Terraced
    • Ridged
  3. Oehlers classification, teeth categorized depending on the pulp contents within the tubercle (histological appearance of the pulps were examined) [4] [2]
    • Wide pulp horns (34%)
    • Narrow pulp horns (22%)
    • Constricted pulp horns (14%)
    • Isolated pulp horn remnants (20%)
    • No pulp horn (10%)
  4. Hattab et al. classification [2]
    • Anterior teeth
      • Type 1 - Talon, a well defined additional cusp that projects palatally and extends at least half the distance from the cementoenamel junction (CEJ) to the incisal edge
      • Type 2 - Semitalon, an additional cusp that extends less than half the distance from the CEJ to the incisal edge
      • Type 3 - Trace talon, prominent cingula
    • Posterior teeth
      • Occlusal DE
      • Buccal DE
      • Palatal DE/ Lingual DE

Management

If the tooth involved is asymptomatic or small, no treatment is needed [3] and a preventative approach should be taken.

Preventative measures [3] include:

For teeth with normal pulp and mature apex, reduce the opposing occluding tooth. [4] Reinforce the tubercle by applying flowable composite. [4] [2] Occlusion, restoration, pulp and periapex assessment should be done yearly. [4] When there is adequate pulp recession, tubercle can be removed and tooth can be restored. [4]

For teeth with normal pulp and immature apex, reduce the opposing occluding tooth. [4] Apply flowable composite to the tubercle. [4] Occlusion, restoration, pulp and periapex assessment should be done every 3–4 months until the apex matures. [4] When there is signs of adequate pulp recession, tubercle can be removed and tooth can be restored. [4]

For teeth with inflamed pulp and mature apex, conventional root canal treatment could be carried out and restored accordingly. [4]

For teeth with inflamed pulp and immature apex, shallow MTA pulpotomy could be performed and then restore with glass ionomer and composite. [4]

For teeth with necrotic pulp and mature apex, conventional root canal therapy could be done and restored. [4]

For teeth with necrotic pulp and immature apex, MTA root-end barrier could be carried out. Glass ionomer layer and composite could be used to restore the tooth. [4]

If there is occlusal interference, the opposing projection should be reduced. [3] [2] Make sure that the tubercle does not contact other teeth in all excursive movement. [2] This is usually done over a few appointments, 6 to 8 weeks apart to allow the formation of reparative dentin to protect the pulp. [3] Fluoride varnish should be applied onto the ground surface. [7] [6] [3] [4] Recall the patient for follow-up after 3, 6 and 12 months. [3]

In some cases, extraction [ citation needed ] could be considered (e.g. for orthodontic purposes, failed apexification) [2]

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Dens invaginatus (DI), also known as tooth within a tooth, is a rare dental malformation found in teeth 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.

Dentin dysplasia teeth hard tissue disease characterized by presence of normal enamel but atypical dentin with abnormal pulpal morphology

Dentin dysplasia (DD) is a rare genetic developmental disorder affecting dentine production of the teeth, commonly exhibiting an autosomal dominant inheritance that causes malformation of the root. It affects both primary and permanent dentitions in approximately 1 in every 100,000 patients. It is characterized by presence of normal enamel but atypical dentin with abnormal pulpal morphology. Witkop in 1972 classified DD into two types which are Type I (DD-1) is the radicular type, and type II (DD-2) is the coronal type. DD-1 has been further divided into 4 different subtypes (DD-1a,1b,1c,1d) based on the radiographic features.

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Attrition (dental) loss of tooth substance caused by tooth-to-tooth contact

Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging. Advanced and excessive wear and tooth surface loss can be defined as pathological in nature, requiring intervention by a dental practitioner. The pathological wear of the tooth surface can be caused by bruxism, which is clenching and grinding of the teeth. If the attrition is severe, the enamel can be completely worn away leaving underlying dentin exposed, resulting in an increased risk of dental caries and dentin hypersensitivity. It is best to identify pathological attrition at an early stage to prevent unnecessary loss of tooth structure as enamel does not regenerate.

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Dental pertains to the teeth, including dentistry. Topics related to the dentistry, the human mouth and teeth include:

Apical foramen

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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. It is often the end result of many cases of dental trauma, caries and irreversible pulpitis.

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.

Regenerative endodontics

Regenerative endodontic procedures (REPS) 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 REPS is to regenerate the tissues and the normal function of the dentin-pulp complex.

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 3 4 5 6 7 8 9 10 11 Echeverri EA, Wang MM, Chavaria C, Taylor DL (July 1994). "Multiple dens evaginatus: diagnosis, management, and complications: case report". Pediatric Dentistry. 16 (4): 314–7. PMID   7937267.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 Hülsmann M (March 1997). "Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment considerations". International Endodontic Journal. 30 (2): 79–90. doi:10.1111/j.1365-2591.1997.tb00679.x. PMID   10332241.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Manuja N, Chaudhary S, Nagpal R, Rallan M (June 2013). "Bilateral dens evaginatus (talon cusp) in permanent maxillary lateral incisors: a rare developmental dental anomaly with great clinical significance". BMJ Case Reports. 2013: bcr2013009184. doi:10.1136/bcr-2013-009184. PMC   3702862 . PMID   23813995.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 Levitan ME, Himel VT (January 2006). "Dens evaginatus: literature review, pathophysiology, and comprehensive treatment regimen". Journal of Endodontics. 32 (1): 1–9. doi:10.1016/j.joen.2005.10.009. PMID   16410059.
  5. Borie E, Eduardo; Oporto V, Gonzalo; Aracena R, Daniel (June 2010). "Dens evaginatus in Hemophilic Patient: A Case Report". International Journal of Morphology. 28 (2): 375–378. doi: 10.4067/S0717-95022010000200006 . ISSN   0717-9502.
  6. 1 2 Bazan MT, Dawson LR (September 1983). "Protection of dens evaginatus with pit and fissure sealant". ASDC Journal of Dentistry for Children. 50 (5): 361–3. PMID   6580300.
  7. 1 2 Koh ET, Ford TR, Kariyawasam SP, Chen NN, Torabinejad M (August 2001). "Prophylactic treatment of dens evaginatus using mineral trioxide aggregate". Journal of Endodontics. 27 (8): 540–2. doi:10.1097/00004770-200108000-00010. PMID   11501594.
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