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| CASE REPORT |
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| Year : 2017 | Volume
: 8
| Issue : 1 | Page : 46-49 |
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Bilateral taurodontism in primary and permanent molars associated with hypodontia
Parmeshwarappa Poornima1, Shashikant Katkade2, Neena Indavara Eregowda1, Kenchappanavar Maheshappa Sangeeta1
1 Department of Pediatric and Preventive Dentistry, College of Dental Sciences, Davangere, Karnataka, India
2 Department of Pedodontics, ACPM Dental College, Dhule, Maharashtra, India
| Date of Web Publication | 30-Mar-2017 |
Correspondence Address:
Parmeshwarappa Poornima
Department of Pedodontics and Preventive Dentistry, Room No. 08, College of Dental Sciences, Pavillion Road, Davangere - 577 004, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0976-433X.156221
The article is to present a case of bilateral taurodontism in primary and permanent molars associated with hypodontia and to discuss the endodontic aspects. Taurodontism in permanent molars are most commonly affected and it has a very low incidence, and very fewer cases are reported in the literature in the deciduous dentition. A 12-year-old boy presented with irregularly placed tooth in upper right back region of the jaw. Orthopantomogramrevealed taurodontism in seven teeth including both primary and permanent teeth, associated with congenitally missing three premolars and permanent mandibular central incisors. Taurodontism is more frequent in nonsyndromic familial tooth agenesis. Individuals in families with second premolar and molar oligodontia are more likely to have taurodontism. Since there is a wide variation in size and shape of pulp chamber with varying degree of obliteration and canal configuration, root canal therapy becomes a challenge so it is essential to recognize and render preventive care for these teeth. Keywords: Bilateral, deciduous molars, permanent molars, taurodontism, tooth agenesis
How to cite this article:
Poornima P, Katkade S, Eregowda NI, Sangeeta KM. Bilateral taurodontism in primary and permanent molars associated with hypodontia. SRM J Res Dent Sci 2017;8:46-9 |
How to cite this URL:
Poornima P, Katkade S, Eregowda NI, Sangeeta KM. Bilateral taurodontism in primary and permanent molars associated with hypodontia. SRM J Res Dent Sci [serial online] 2017 [cited 2023 Feb 8];8:46-9. Available from: https://www.srmjrds.in/text.asp?2017/8/1/46/156221 |
| Introduction | |  |
Taurodontism is a developmental disturbance of a tooth that lacks constriction at the level of the cementoenamel junction (CEJ). It is characterized by vertically elongated pulp chamber, apical displacement of the pulpal floor and bifurcation or trifurcations of the roots.[1] The term “taurodontism” ('bull tooth') was coined from the Latin term “tauros”, which means 'bull' and the Greek term “odus”, which means 'tooth'.[2]
Shaw (1928) further classified taurodont teeth according to their severity into mild, moderate, severe (hypo-, meso- and hypertaurodont) forms, based on the apical displacement of pulpal floor [Figure 1]. Hypotaurodontism being the least pronounced form, mesotaurodontism the moderate form and hyper-taurodontism being the most severe form in which the bifurcation or trifurcation occurs near the root apices.[3] A most widely accepted and used criteria for diagnosis of taurodontism, on the basis of the distance from the lowest point of the roof of the pulp chamber 'a' to the highest point of pulp floor 'b', when divided by the distance from 'a' to root apex 'c' should be equal to or greater than 0.2 mm and/or distance from 'b' to cementoenamel junction 'd' should be greater than 2.5 mm [4] [Figure 2]. | Figure 1: Diagrammatic representation of normal (cynodontic) tooth and three subtypes of taurodontic teeth
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The etiology of taurodontism is unclear. The possible causes of taurodontism have been enumerated by Mangion [5] as follows:
- A specialized or retrograde character,
- A primitive pattern,
- A Mendelian recessive trait,
- An atavistic feature, and
- A mutation resulting from odontoblastic deficiency during dentinogenesis of the roots.
According to Hamner et al., taurodontism is caused by the failure of Hertwig's epithelial root sheath diaphragm to invaginate at the proper horizontal level.[6] In addition, it has been reported that many patients with the Klinefelter syndrome exhibit taurodontism, but it is not a constant feature of this syndrome.[7] Today, it is considered as an anatomic variant that could occur in a normal population.[4] The prevalence of taurodontism is reported to range from 2.5% to 11.3% of the human population. This range is accounted for by variations in race and differences in diagnostic criteria.[8] Taurodontism is more frequent in nonsyndromic familial tooth agenesis. Individuals in families with second premolar and molar oligodontia are more likely to have taurodontism. This association could define a subphenotype for future genetic studies of dental development. Case presented here has nonsyndromic familial tooth agenesis associated with taurodontism in multiple teeth.
Aim
It is very important for a general dental clinician to be familiar with taurodontism not only due to its clinical implications but also due to probable association with related syndromes and its management case presented here has nonsyndromic familial tooth agenesis associated with taurodontism in multiple teeth.
Background
Taurodontism is a developmental disturbance of a tooth that lacks constriction at the level of the cementoenamel junction (CEJ). It is characterized by vertically elongated pulp chamber, apical displacement of the pulpal floor and bifurcation or trifurcations of the roots.[1] The term “taurodontism” (“bull tooth”) was coined from the Latin term “tauros,” which means “bull” and the Greek term “odus,” which means “tooth.”[2]
Shaw further classified taurodont teeth according to their severity into mild, moderate, severe (hypo-, meso- and hyper-taurodont) forms, based on the apical displacement of pulpal floor [Figure 1]. Hypo-taurodontism being the least pronounced form, meso-taurodontism the moderate form and hyper-taurodontism being the most severe form in which the bifurcation or trifurcation occurs near the root apices.[3] A most widely accepted and used criteria for diagnosis of taurodontism, on the basis of the distance from the lowest point of the roof of the pulp chamber “a” to the highest point of pulp floor “b,” when divided by the distance from “a” to root apex “c” should be equal to or >0.2 mm and/or distance from “b” to CEJ “d” should be >2.5 mm [4] [Figure 2].
The etiology of taurodontism is unclear. The possible causes of taurodontism have been enumerated by Mangion [5] as follows:
- A specialized or retrograde character,
- A primitive pattern,
- A mendelian recessive trait,
- An atavistic feature, and
- A mutation resulting from odontoblastic deficiency during dentinogenesis of the roots.
According to Hamner et al., taurodontism is caused by the failure of Hertwig's epithelial root sheath diaphragm to invaginate at the proper horizontal level.[6] In addition, it has been reported that many patients with the Klinefelter syndrome exhibit taurodontism, but it is not a constant feature of this syndrome.[7] Today, it is considered as an anatomic variant that could occur in a normal population.[4] The prevalence of taurodontism is reported to range from 2.5% to 11.3% of the human population. This range is accounted for by variations in race and differences in diagnostic criteria.[8] Taurodontism is more frequent in nonsyndromic familial tooth agenesis. Individuals in families with second premolar and molar oligodontia are more likely to have taurodontism. This association could define a subphenotype for future genetic studies of dental development. Case presented here has nonsyndromic familial tooth agenesis associated with taurodontism in multiple teeth.
| Case Report | | |
A 12-year-old male child was brought to College of Dental Sciences, Davangere with complain of malposition of tooth in right posterior tooth region of the maxilla. There was no significant medical complaint in the past. Patient had a history of dental trauma and undergone treatment for the same. His intraoral examination revealed normal soft tissue appearance. Maxillary arch showed buccally erupting right maxillary first premolar, peg shaped right maxillary lateral incisor and clinically missing left maxillary lateral incisor. Mandibular arch showed retained primary central incisor in midline and clinically missing left first and second premolars and right second premolar, moderate caries on the distal surface of primary left first molar.
Orthopantomogram revealed all four permanent first molars, and primary second molars to be taurodontic [Figure 3]. All first permanent molars and primary mandibular left second molar were hyper-taurodont whereas maxillary primary second molars were meso-taurodont [Figure 4]. All permanent second molars were in developing stage and suggestive of taurodontism in future after root formation is completed. Other features include congenitally missing mandibular central incisors, right and left second premolars and maxillary right second premolar.
| Discussion | | |
Taurodontism most frequently appears as an isolated anomaly. However, its association with several syndromes also been detected (Downs, Klinefelter, Lowe, Tricho-dento-osseous, Tricho-onchyo-dental, Williams, Wolf-Hirschhorn, Seckel, Smith-Magenis, and Mohr syndrome).[1] Many of these disorders have oral manifestations, which can be detected on dental radiographs as alterations in the morphology or chemical composition of the teeth; thus, dentists may be the first to detect them.[9] Sankar et al.[10] reported the association of amelogenesis imperfecta with dental anomalies, including taurodontism, congenitally missing teeth, delayed eruption, crown resorption, pulpal calcifications and odontogenic fibromas. Shokri et al.[11] reported the prevalence of taurodont teeth as 9.29% by observation in panoramic radiograph. The author found that taurodonts were significantly more common in the maxilla (65.6%) than in the mandible (34.4%). The maxillary second molar (34.4%) was the most commonly involved tooth. Only 4 premolars were involved (12.4%). According to the morphology hypo-taurodonts were found in 24 teeth (75%) but there was no significant difference in males and females. Meso-taurodonts were found in 6 teeth, and 2 teeth were hyper-taurodont in morphology.
Many explanation for the pathogenesis of taurodont formation have been put forward from time to time, they include:
- An unusual developmental pattern;
- A delay in calcification of the pulp chamber floor;
- An odontoblastic deficiency;
- An alteration in Hertwig's epithelial root sheath, with an apparent failure of the epithelial diaphragm to invaginate at the normal horizontal levels; and
- A delayed or incomplete union of the horizontal flaps of the epithelial diaphragm.[7]
Individuals in families with second premolar and molar oligodontia are more likely to have taurodontism. In our case four permanent first molars and three primary second molars exhibited taurodontism and hypodontia involving missing three second premolars and two mandibular central incisors.
Most reports reveal that permanent teeth most frequently affected than primary.[12] In our case both deciduous and permanent molars were involved. The teeth that were diagnosed as taurodont were of both meso and hyper variety.
Ronald [13] in his cases demonstrated short, conical and misshapen roots with pulp stone in taurodontic tooth. In the presented case also pulp stone were obliterating the pulp chamber of taurodontic teeth.
Endodontic treatment in taurodontic primary teeth has been described as a complex and difficult procedure. Pulp therapy for taurodont is a challenging treatment, with increased incidence of hemorrhage during access opening that may be mistaken for perforation. Since the roots are short, and pulpal floor is placed apically, care should be taken to prevent perforation. Conventional obturating materials like zinc oxide eugenol in bulk may take longer time to resorb which may delay the natural exfoliation of the tooth. In such cases, combination of calcium hydroxide such as endoflas, vitapex can act as wonderful materials, these materials has added advantage of the faster rate of resorption due to the presence of calcium hydroxide and iodoform.[14]
Endodontic treatment in permanent teeth with taurodontism presents a challenge during negotiation, instrumentation, and obturation in root canal therapy.[15] A modified filling technique, which consists of combined lateral compaction in the apical region with vertical compaction of the elongated pulp chamber, has been proposed.[16]
| Conclusion | | |
As taurodont shows wide variation in size and shape of the pulp chamber with varying degree of obliteration and canal configuration, root canal therapy becomes a challenge. Hence, we would like to stress on the importance of diagnostic radiograph for early identification of taurodont and rendering preventive care for these teeth.
Clinical significance
Taurodontism requires special attention during cavity preparation, root canal therapy and tooth extraction. Taurodontism may complicate endodontic, orthodontic and/or prosthetic treatment planning. It presents a challenge during negotiation, instrumentation, and obturation during the root canal therapy for the endodontist. The extraction of a taurodont tooth is also difficult and complicated since the furcation is shifted to the apical area. However, it offers favorable prognosis from periodontal point of view because these teeth have to demonstrate significant periodontal destruction before the furcation involvement. In the case of prosthetic treatment of such tooth, the placement of the post for tooth reconstruction may be avoided. When used as an abutment, this tooth may not offer much stability and strength, as the surface area is smaller inside the alveolus.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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