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 Table of Contents  
REVIEW ARTICLE
Year : 2016  |  Volume : 6  |  Issue : 3  |  Page : 112-118

Dental Anomalies: An Update


Department of Pediatric Dentistry, Oral and Dental Research Center, Kerman University of Medical Sciences, Kerman, Iran

Date of Web Publication7-Dec-2016

Correspondence Address:
Fatemeh Jahanimoghadam
Department of Pediatric Dentistry, Oral and Dental Research Center, Kerman University of Medical Sciences, Kerman
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2321-8568.195316

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  Abstract 

Dental anomalies are usual congenital malformation that can happen either as isolated findings or as a part of a syndrome. Developmental anomalies influencing the morphology exists in both deciduous and permanent dentition and shows different forms such as gemination, fusion, concrescence, dilaceration, dens evaginatus (DE), enamel pearls, taurodontism or peg-shaped laterals. All These anomalies have clinical significance concerning aesthetics, malocclusion and more necessary preparing of the development of dental decays and oral diseases. Through a search in PubMed, Google, Scopus and Medline, a total of eighty original research papers during 1928-2016 were found with the keywords such as dental anomaly, syndrome, tooth and hypodontia. One hundred review titles were identified, eighty reviews were retrieved that were finally included as being relevant and of sufficient quality. In this review, dental anomalies including gemination, fusion, concrescence, dilaceration, dens invaginatus, DE, taurodontism, enamel pearls, fluorosis, peg-shaped laterals, dentinal dysplasia, regional odontodysplasia and hypodontia are discussed. Diagnosing dental abnormality needs a thorough evaluation of the patient, involving a medical, dental, familial and clinical history. Clinical examination and radiographic evaluation and in some of the cases, specific laboratory tests are also needed. Developmental dental anomalies require careful examination and treatment planning. Where one anomaly is present, clinicians should suspect that other anomalies may also be present. Moreover, careful clinical and radiographical examination is required. Furthermore, more complex cases need multidisciplinary planning and treatment.

Keywords: Dental anomaly, hypodontia, syndrome, tooth


How to cite this article:
Jahanimoghadam F. Dental Anomalies: An Update. Adv Hum Biol 2016;6:112-8

How to cite this URL:
Jahanimoghadam F. Dental Anomalies: An Update. Adv Hum Biol [serial online] 2016 [cited 2019 Oct 22];6:112-8. Available from: http://www.aihbonline.com/text.asp?2016/6/3/112/195316


  Introduction Top


Anomaly (irregular) is opposite from what is known as normal. Disturbance of the epithelium and mesenchyme can markedly alter the normal odontogenesis leading to the developmental anomaly of teeth. Depending on the developmental stage in which the difference has taken place, various anomalies could take place, for example, anomalies of number, structure, size and/or shape. [1] A majority of uncommon dental anomalies occur during childhood years. Developmental dental anomalies are classified according to their abnormalities in number, shape, colour, structure, texture, eruption, exfoliation and position. [2] Local as well as systemic factors may be responsible for these developmental anomalies. Such effects may begin before or after birth, therefore both the dentition might be affected. [3]

More than 300 genes have been identified to be expressed in teeth that are responsible for odontogenesis. Defects in these genes have been found to be one of the reasons for variation of the morphology of tooth. [4] Diagnosing dental abnormality needs a thorough evaluation of the patient, involving a medical, dental, familial and clinical history. Clinical examination and radiographic evaluation and in some of the cases, specific laboratory tests are also needed. [3] Dental anomalies including the number of teeth involve hypodontia (one or more missing teeth), oligodontia (six or more missing teeth), anodontia (complete absent of teeth) and hyperdontia (one or more extra teeth, also identify as supernumeraries). Variations in the size of teeth include microdontia (teeth smaller than normal) and macrodontia (enlargement of the teeth compare to normal). Both these situations may be either generalised to all the teeth or isolated to one or several teeth. Alterations in the morphology of teeth include double teeth (fusion and gemination), talon cusp, dens evaginatus (DE) and dens invaginatus (DI) (dens in dente). [4] Early diagnosis of dental anomalies should allow for more comprehensive prolonged treatment planning, more proper prognosis and in certain instances, less extensive interception. [5]


  Methods Top


A search was performed through PubMed, Google Scholar, Scopus and Medline for different dental anomalies. One hundred review titles were identified, eighty papers were retrieved that were finally included as being relevant and of sufficient quality. A total of eighty original research papers that have been published from 1928 to 2016, with the keywords such as dental anomaly, syndrome, tooth and hypodontia were selected. Information from selected articles was extracted and classified to assess the significance of different dental anomalies.


  Discussion Top


Description of the anomalies

Gemination


Tannenbaum and Alling in 1963 determined gemination as the formation of equivalent of two teeth from the same follicle, with evidence of an endeavour for the teeth to be completely separate. [6]

Gemination also determined as twin teeth, twin formations, joined teeth, fused teeth or dental twinning is commonly seen in the maxillary anterior area. [7],[8]

Geminated teeth arise from an endeavour at the division of a single tooth germ by invagination, results a single tooth with two completely separated crowns; or a large, incompletely separated crown having a single root and root canal. [9] This condition can be confirmed radiographically. [10] The anomalous tooth has an enlargement in mesial-distal diameter than normal and is counted as one. [10],[11] However, the total number of teeth in dental arch is also normal. [10]

The aetiology of geminated teeth stays unknown but nutritional deficiency, endocrine influences, infectious/inflammatory progress, excessive ingestion of medicines, congenital diseases; local trauma and ionising radiation are included as causative factors. [8]

Clinically, gemination happening in the anterior tooth side causes aesthetic disorders related to tooth alignment, spacing and arch asymmetry. The presence of deep grooves on the surface forms it susceptible to caries and periodontal problems by facilitating bacterial plaque accumulation. The eruption of adjacent tooth may also be obstacle. [9]

Fusion

Pindborg defined fusion as the combination between dentin and enamel of two or more separate developing teeth. [12] Fusion is developmental anomaly of dental hard tissue and defined as the joining of two developing tooth germs resulting in a single large tooth structure different treatment methods can be used according to the requirements of situation. [13] This anatomic abnormality happens more often in deciduous dentition with a predilection for the anterior region. [10]

Fusion can be complete (total/true fusion) or incomplete (partial/late fusion), it depends on level of development. [10],[11] If fusion starts before calcification stage, the teeth unite completely and the crown incorporates enamel, dentin, cementum and pulp of both the teeth. Incomplete fusion happens at a later level and resultant tooth may exhibitive separate crowns and limited to root alone with combined or separate pulp canals. [14]

Different theories have been put forward to describe the aetiology of fusion. It has been suggested that when the tooth germs are too close together they come in contact and fuse as they develop because of the physical pressure or force generated during growth. The other theories suggested the use of thalidomide or occurrence of viral infection while pregnancy. [15] A genetic aetiology has also been included. [16] Fusion has been noted with congenital anomalies like cleft lip and also in X-linked congenital conditions. Some dental and non-dental abnormalities such as supernumerary teeth, hypodontia, peg-shaped incisors, dens in dente, nail disorders, syndactyly, successional conical teeth, macrodontia and double permanent teeth have been attendant with fusion. [17],[18]

On some occasions, two independent pulp chambers and root canals can be seen. However, fusion can also be the union of a normal tooth bud to a supernumerary tooth germ. [19] Fusion may cause aesthetic disorders and occlusal disturbances due to crowding and irregular morphology and shape, respectively. The presence of deep grooves may prepare for caries or periodontal diseases and cause early pulp exposure. The larger root mass and increased surface region would result in late resorption and subsequently bring late or ectopic eruption of the permanent successors. [10]

Concrescence

Concrescence is determined as the cemented combination of two adjacent teeth without confluence of the underlying dentin showing independent pulp chambers and root canals. [20],[21] It may happen before or after the teeth have erupted. This condition can frequently be attributed to trauma or crowding of teeth. [22] If the condition happens while developmental stage, it is called true/developmental concrescence and achieved/post-inflammatory concrescence if after root formation. [23],[24]

Concrescence is seen often in the posterior maxillary region. The developmental pattern frequently involves a second molar tooth in which its roots closely approximate to the adjacent impacted third molar. [24] Few cases have shown the concrescence of a third molars and a supernumerary tooth. [21]

It is suspected that space restriction while developmental stage, local trauma, too much occlusal force, or local infection after development play an important role in the happening of concrescence. [21],[25] True concrescence is attributed to the close proximity of developing roots of the adjacent teeth whereas achieved concrescence may result from a chronic inflammatory response to a non-vital tooth. [23] The combination may vary from one small site to a solid cemented mass along the whole extent of approximating root surfaces. [21]

Radiographic examination is necessary when concrescence is suspected clinically. Although in cases of superimposition of two closely approximated teeth, additional radiographic projections at different angulations may be required. [21]

Concrescence should be identified to reduce the risk of complications associated with surgical procedures. [25] It may also affect the extraction of an adjacent tooth and may cause fracture the tuberosity or floor of the maxillary sinus. In such cases, sectioning of tooth should be considered to reduce adverse and unexpected outcomes. [23]

Dilaceration

The term dilacerations was first used by Tomes in 1848, and it is defined as a deviation or bend in the linear relationship of a crown of a tooth to its root. Based on this definition, dilacerations is distinguished from the rarely used term flexion, which is defined as a tooth with a hooked or a bent root. [26] It is an abnormal angulation or bend in the root and less frequently, the crown of a tooth. Most cases are idiopathic and have no clinical feature. [27] Dilaceration can occur in both permanent and primary dentitions, however in the latter is very low. [28],[29] The prevalence rate is greater in posterior teeth and in the maxilla. [30] Mentioned by some authors, a tooth is considered to have a dilaceration towards mesial or distal direction if there is a 90° angle or more along the axis of the tooth or root, whereas others determined dilaceration as a deflection from the normal axis of the tooth of 20°. The most accepted reason of dilaceration is acute mechanical injury to the primary predecessor tooth that head to the dilaceration of the underlying developing succedaneous permanent tooth. [31] Crown dilaceration is rarer than root dilacerations. Crown dilacerations are usually observed in the permanent maxillary incisors followed by mandibular incisors. Clinically, the maxillary incisors show a lingual deviation during the mandibular incisors incline labially. [32] Crown dilaceration is the reason of a developmental anomaly in which there has been an abrupt change in the axial inclination between the crown and the root of a tooth. Two possible reason of dilacerations are trauma and developmental disturbances, and it has also been suggested that it might be associated with some developmental syndromes. [33] The other possible contributing factors that have been noted such as scar formation, developmental anomaly of the tooth germ, facial clefting, advanced root canal infections, ectopic development of the tooth germ and lack of space and area, effect of anatomic formations (e.g., cortical bone of the maxillary sinus, mandibular canal, or nasal fossa, which might perverse the epithelial diaphragm), presence of an adjacent cyst, tumour, or odontogenic hamartoma, mechanical interposition with eruption (e.g., from an ankylosed primary tooth that does not resorb), tooth transplantation, extraction of primary teeth and hereditary and genes factors. [31],[34],[35]

Identification and diagnosis of dilaceration often needs radiographs taken at different angulations. [36] Mesial or distal root curvatures of dilacerated roots are perspicuity discernible on periapical radiographs. However, if the curvature lies in a labial-buccal direction, the central X-ray beam crosses almost parallel to the deviating area of the root giving a 'bulls eye' like appearance, [29] but still periapical radiographs are the most appropriate way to diagnose the presence of root dilacerations. [37] Clinical identification of dilaceration is necessary because it can lead to non-eruption, longer retention of predecessor tooth or conceivable apical fenestration of the buccal or labial cortical plate. [29] Dilaceration makes a challenge for endodontic or orthodontic treatment as well as discomfort in extraction. [38]


  Dens Invaginatus Top


DI also determines as the pregnant woman anomaly, wide compound odontoma, and dens in dente, happens as a consequence of an invagination on the external surface area of the tooth crown before calcification. The endodontic treatment of invaginated teeth may be challenging cause of difficulties in accessing the root canals and also reason of complex variations of internal morphology. [39],[40] The invagination ranges from a short pit limited to the crown to a deep invagination into the root, at times widening to or beyond the root apex. The most severe forms are odontome-like and are mostly termed invaginated odontomes. [41] Most of the cases are encountered in maxilla with the maxillary lateral incisors being mostly affected, followed by central incisors, premolars, canines and molars. [40],[42] The classical radiographic appearance of coronal DI is a pear-shaped invagination of enamel and dentin with a narrow structure at the opening on the surface area of the tooth. The in folding of the enamel lining is more radio-opaque than the surrounding tooth construction aiding easy recognition. [43]

Oehlers et al. grouped coronal DI into three types according to the radiographic appearance such as:

  • Type I: An enamel-lined minor form happening within the confines of the crown not extending beyond the cementoenamel junction (CEJ)
  • Type II: An enamel-lined form which invades the root but remains limited as a blind sac. It may or may not connect with the dental pulp
  • Type IIIA: A form which crosses through the root and connected laterally with the periodontal ligament space through a pseudo-foramen. There is usually no communication with the pulp, which lies also compressed within the root
  • Type IIIB: A form which crosses through the root and perforating at the apical region through a pseudo-foramen. The invagination may be completely lined by enamel, but mostly cementum will be found lining the invagination. [44]


A radicular form of DI has also been defined by Oehlers et al. which is thought to arise because of the proliferation of Hertwig's root sheath. The root of this kind of tooth is enlarged which can be demonstrated radiographically. [45]

Infection, trauma, pressure or difficulty from the growing dental arch is thought to be responsible for DI. [39] A focal failure of growth or a proliferation of a part of the inner enamel epithelium may be included in the invagination. [46],[47] Ohlers suggested a distortion of the enamel organ and further protrusion of a part of the enamel organ resulting in the formation and shaping of enamel-lined channel. [44]

The invagination acts as a channel for entrance of irritants and microorganisms; and prepare for the development of dental caries. Since the thickness of enamel is less, pulp necrosis happens at an earlier age. Coronal DI can also go ahead to abscess formation, retention of neighbouring teeth, cysts, internal resorption, cellulitis, etc. [48]


  Dens Evaginatus Top


DE is a developmental aberration of a tooth resulting in formation of one accessory cusp whose morphology of shapes has been determined as abnormal tubercle, elevation, protuberance, excrescence, extrusion or a bulge. It is also mentioned to as tuberculated cusp, accessory tubercle, occlusal tuberculated premolar, Leong's premolar, evaginatus odontoma and occlusal pearl. [49],[50] Currently, DE is the preferable terminology and was first recommended by Oehlers et al. in 1967. [44] This unusual anomaly projects above the adjacent tooth surface area, exhibitive enamel covering a dentinal core that commonly contains pulp tissue; occasionally having slender pulp horn which extends to different distances within the dentinal core. [50],[51] The tubercles of DE have been differentiated from the cusp of carabelli which is a normal anatomical formation and is differentiated from DE by the absent of a pulp core. [50]

The happening of DE shows too much racial differences with a higher spreading among people of mongoloid origin. [52] It is commonly associated with the occlusal surface area of premolars. Schulze (1987) distinguished the following five types of DE for posterior teeth by the location and area of the tubercle. [50],[53]

  1. A cone-like enlargement of the lingual cusp
  2. A tubercle on the disposed plane of the lingual cusp
  3. A cone-like enlargement of the buccal cusp
  4. A tubercle on the disposed plane of the buccal cusp
  5. A tubercle arising from the occlusal surface area obliterating the central groove.


When DE appears in the anterior region area, it is commonly observed on the lingual surface and is known as a talon's cusp. [50] Early diagnosis and management of DE are necessary to prevent occlusal interference, compromised aesthetics, carious developmental grooves, periodontal problems because of excessive occlusal forces, or irritation of the tongue while speech and mastication. [54] Mitchell was the first to identify this anomaly in 1892, which was later named talon by Mellor and Ripa because of its resemblance to an eagle's talon. [55] It is usually seen in the maxillary lateral incisors region and has been associated with syndromes such as Rubinstein and Taybi, Berardinelli-Seip, Mohr, Ellis-van Creveld, Sturge-Weber and incontinentia pigmenti achromians. [56] It differentiated in size, shape, length and mode of attachment to the crown and ranges from an enlarged cingulum to a large, well-delineated cusp extending beyond the incisal region of the tooth. [41] The cusp is composed of normal enamel and dentin including varying extensions of pulp tissue. It may also communicate with the incisal edge to produce a T-form or, if more cervical, a Y-shaped crown contour. [42] Talon cusp is an unusual anomaly, whose etiology may be disturbances in the morph differentiation stage. Talon cusp is a rare entity in which a prominent wisplike structure originates from the cervical area of lingual or labial surfaces of the anterior teeth, happening lingually with the most frequency. [57]

Hattab et al. classified talons' cusps into three types based on the degree of cusp shapes formation and extension: [58]

  • Type 1: Talon - refers to a morphologically well-delineated accessories cusp that prominently projects from the palatal (or facial) surface area of a primary or permanent anterior tooth and extends at least half the distance from CEJ to the incisal edge
  • Type 2: Semi talon - refers to an additional cusp of a millimeter or more extending less than half the distance from CEJ to the incisal edge region. It may blend with the palatal surface area or stand away from the rest of the crown
  • Type 3: Trace talon - an enlarged or eminent cingula and their variations, i.e., conical, bifid or tubercle-like.


The DE or talons cusp may have fracture or be abraded as soon as the tooth comes into occlusion, exposing the pulp. [15] Hence, early identification of this anomaly and prompt treatment should be instituted to avoid endodontic complications.

Enamel pearls

Enamel which is normally confined to the anatomic crowns of human teeth may be found ectopically on the root, either as cervical enamel projections or enamel pearls. [58],[59] Enamel pearl is determined as an ectopic globule of enamel that is firmly attached to the tooth root. [60] Enamel pearls may include completely of enamel connected to cementum or root dentin or may indicate incorporation of a cone of dentin with or without pulpal extension, the last two are referred to as composite enamel pearls and the composite type without pulpal extension is the most usual type of macroscopically detected enamel pearls. [61] It has been mentioned to as an enameloma, enamel droplet, enamel nodule, enamel exostoses and enamel globule. It is found usually on the roots of maxillary molars, particularly the third molars adjacent to the furcation or furrow of the root. [59]

Enamel which is usually restricted to the anatomic crowns of human teeth may be found ectopically on the root, either as cervical enamel projections or enamel pearls. These developmental aberrations in tooth morphology may prepare the affected area to plaque accumulation and consequently brings periodontal breakdown. Early diagnosis of these anomalies may meliorate the prognosis of the involved teeth. Enamel pearl is determined as an ectopic globule of enamel that is firmly connected to the tooth root. The size of clinically recognizable enamel pearls may vary from 0.3-4 mm. Risnes (1974) observed enamel pearls on 2.28% molars of 8854 teeth examined grossly. The enamel pearls happened more usually on the roots of maxillary molars, especially third molars. The usual site of area of the enamel pearl is adjacent to the furcation or furrow of the root, especially the bifurcation or trifurcation locations of maxillary and mandibular molars. Maxillary 2 nd and 3 rd molars are more usually included than the first molars. [61]

Advanced localised periodontal destruction has been attendant with cervical enamel projections and enamel pearl, preparing for attachment loss. [62]

Taurodontism

Witkop determined taurodontism as teeth with large pulp chambers in which the bifurcation or trifurcation has displacement apically, so that the chamber has bigger apical-occlusal height than in normal teeth and lacks the constriction at the level of CEJ. The distance from the trifurcation or bifurcation of the root to the CEJ is bigger than the occlusal-cervical distance. [63]

This anomaly was first mentioned in the remnants of prehistoric hominids by de Terra in 1903 and by Gorjanovic-Kramberger and Aldoff in 1907. [64] Pickerill in 1909 noted this in modern man. [65] Although the term 'taurodontism' was first used by Sir Arthur Keith in 1913 to defined the teeth of prehistoric people, the Neanderthals and Heidelberg. [26] He coined this term from the Latin word tauro (for bull) and Greek term dont (for tooth) due to the morphological resemblance of affected tooth to the tooth of ungulates or cud chewing animals. Shaw has classified taurodontism arbitrarily based on comparative degree of apical displacement of floor of pulp chamber into hypo, meso and hyper-taurodontism. [66]

Peg-shaped laterals

A peg lateral is an undersized, tapered, maxillary, small, lateral incisor. [67] The tooth is conical in shape; broadest cervically and tapers incisally to a blunt point. An uncommon happening is that of a peg-shaped maxillary central incisor. Peg-shaped teeth grow from a single lobe instead of four. The peg-shaped laterals are predominantly genetically defined and can also be caused because of endocrinal disturbances. [68] Peg-shaped laterals may be attendant with other dental anomalies such as tooth agenesis, canine transposition and over-retained primary teeth. Studies of identical twins have showed that missing teeth and peg-shaped lateral incisor might be a varied expression of the same genetic trait. [67],[69] Early management of the peg-shaped laterals is important because of psychological problems in children as well as for the correct development of the stomatognathic system. [68]

Fluorosis

Fluorosis is a cosmetic situation that affects the teeth. It is happened due to overexposure to fluoride during the first 8 years of life. This is the time when most permanent teeth are being formed completely. [70]

Reason of the dental fluorosis is the increasing in concentration within the fluoride microenvironment of the ameloblasts while enamel formation. Fluorosis is increasing in mostly the enamel proteins amelogenin and enamelin. In such an anomaly, both primary and permanent dentition are effected. Symptoms of fluorosis range from tiny white specks or streaks that may be unnoticeable to dark brown stains and rough, pitted enamel that is difficult to clean. Teeth that are unaffected by fluorosis are smooth and glossy. They should also be a pale creamy white. There are ways of management of these anomaly such as, genetic counselling, preservation of molar teeth with stainless steel crowns or nickel chrome or gold onlays, composite resin veneers over anterior teeth, certain treatment with porcelain and precious metal must be delayed until late adolescence. [70],[71]


  Dentinal Dysplasia Top


Dentinal dysplasia (DD) is frequent determined as rootless teeth. Clinical specification includes very short or absent roots but the crowns are normal clinically, pulpal obliteration similar to dentinogenesis imperfecta and often periapical radiolucencies surrounding the defective roots. In such an anomaly all teeth and both dentitions are affected. Management of this anomaly using prosthetic rehabilitation is an effective treatment. [3]

In general, two main classes of DD are identified based on clinical and radiographic appearance. [4] Witkop proposed the classifications - Type I, or 'dentin dysplasia', and Type II or 'anomalous dysplasia of dentin'. Witkop later determined Type I as 'radicular dentin dysplasia' and Type II as 'coronal dentin dysplasia' to show the parts of the teeth that are primarily involved. It is a rare anomaly of unknown aetiology that affects approximately one patient in every 100,000. Histologically, in DD1, most of the coronal and mantle dentin of the root is frequently reported to be normal, and the dentin defect is limited mainly to the root. [72] The third type of dentin dysplasia, DD3or 'focal odontoblastic dysplasia', also has been proposed. [73]

Regional odontodysplasia

Regional odontodysplasia (RO) is a rare developmental anomaly that affects the primary and permanent dentitions. This disturbance is generally localised in only one arch and its aetiology is unknown yet. Clinically, the affected teeth have an abnormal shape and are typically discoloured. Radiographically, these teeth show a ghost-like aspect. This anomaly tends to effect several adjacent teeth within a particular segment of the jaw, and usually does not cross the midline. [74] RO mostly involves one quadrant and affects the maxilla twice as frequently as the mandible, [75] with the left maxillary quadrant being the most frequently affected quadrant. [76] It has a predilection for the central and lateral incisors, with higher prevalence in females. [77] Treatment planning must be designed separately for each individual case. It depends on many factors such as the patient's age, medical history, involvement extension, teeth eruption, aesthetics and the development stage of this anomaly. [75]

Hypodontia

Congenitally missing teeth (CMT), or as usually named hypodontia, is a highly prevalent feature. Besides an unfavourable appearance, patients with missing teeth mostly suffer from malocclusion, periodontal damage, insufficient alveolar bone growth, less chewing ability, inarticulate pronunciation and other problems. [78] Hypodontia is more prevalent in women so it is necessary to manage these teeth aesthetically. The frequency rate of hypodontia is variable in different sexes and races. Physical disruption of dental lamina may cause obliteration of tooth buds and agenesis of tooth. This condition is seen in orofaciodigital syndrome, Ellisvan syndrome and cleft lip and palate. It can also be the result of metabolic misbalance that causes dental agenesis. Finally, hereditary defect of the underlying mesenchyme may lead to hypodontia. [79] The treatment plan for CMT is challenging and requiring multidisciplinary approach to achieve a successful outcome. A paediatric dentist often initiates interdisciplinary treatment by the diagnosis of hypodontia and maintenance of the primary teeth. Definitive treatment plan is usually determined after the eruption of all permanent teeth. [80]


  Conclusion Top


Developmental anomalies of the teeth require careful examination and treatment planning. Where one anomaly is present, clinicians should suspect that other anomalies may also be present. Developmental dental anomalies show variations and no two anomalies of the same types are alike. Hence, knowledge of various criteria which have been put forward for the identification and classification of the different anomalies is essential to diagnose the condition and perform appropriate treatment.

Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.

 
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Abstract
Introduction
Methods
Discussion
Dens Invaginatus
Dens Evaginatus
Dentinal Dysplasia
Conclusion
References

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