10.5455/ejfs.196581 Developmental anomalies of teeth and ... › 69fd › dd579e87640... · was the...

Eur J Forensic Sci ● Apr-Jun 2016 ● Vol 3 ● Issue 2 39

European Journal of Forensic Sciences

DOI: 10.5455/ejfs.196581

www.ejfs.co.uk

INTRODUCTION

Forensic odontology is an integral part of the forensic fraternity, and one of its primary applications is to establish the identity of individuals: perpetrators of a crime and victims of disasters [1,2]. Disasters can be both natural or man-made [3] and may result in damages of unimaginable magnitudes [3-5]. The primary objective of forensic odontologists after disasters or in crime scenes is to collect dental information from the deceased, compare ante-mortem and post-mortem dental information [6,7] and find similarities among them to establish identities of deceased victims. Dental identification is primarily

used to confirm the identities of unknown persons when identification by other means such as DNA or fingerprints is not possible in disaster situations that result in skeletonization, decomposition, severe burning [8] or charring [9] of the individuals beyond recognition, especially in disasters that involve multitude of casualties [10].

The advantages of using teeth in establishing identities of people are because they are durable [11] and are capable of resisting damage unlike the other structures of the body [1,12]. Previous studies on the subject have described methods involved in collecting and examining dental evidence [13], but little

Developmental anomalies of teeth and their applications in forensic odontologyMithun Rajshekar1, Thejaswini Mithun2, Jose Joy Idiculla3, Marc Tennant4

Review Article

ABSTRACTForensic odontologists are often part of disaster victim identification teams that help in establishing the identity of victims. There may be situations when forensic odontologists get summoned to establish or confirm identities of victims after mass disasters whose identities cannot be established by any other means, identify individuals in crime scenes, or even be used as corroborative evidence. The primary objective of a forensic odontologist at a disaster site/crime scene is to establish the identity of a deceased victim by comparing ante-mortem and post-mortem records. The objective of this article is to briefly explain the clinical and radiological features of developmental dental anomalies and associated syndromes and highlight their role in victim identification. The authors emphasize the roles of dental practitioners and forensic odontologists in victim identification by examining and recording dental features that may assist in establishing the identity of deceased individuals during disasters or otherwise.

KEY WORDS: Forensic sciences, forensic odontology, dental anomalies, dental evidence, disaster victim identification

1Menzies Research Institute Tasmania, Tasmanian Institute for Law Enforcement Studies, University of Tasmania, Hobart, Australia, 2Oral Health Services Tasmania, Hobart, Australia,3Department of Oral Medicine, Oral Diagnosis and Oral Pathology, Faculty of Dentistry, Melaka Manipal Medical College Jalan Batu Hampar, Bukit Baru, Malaysia, 4Centre for Rural and Remote Oral Health, University of Western Australia, Perth, Australia

Address for correspondence:Address for correspondence: Mithun Rajshekar, Menzies Research Institute Tasmania, Tasmanian Institute for Law Enforcement Studies, University of Tasmania, Hobart, Australia. E-mail: [email protected]

Received: Received: July 16, 2015

Accepted: Accepted: September 15, 2015

Published: Published: October 12, 2015

Rajshekar, et al. Dental anomalies and their role in forensics

40 Eur J Forensic Sci ● Apr-Jun 2016 ● Vol 3 ● Issue 2

research has been conducted on quantifying the information required to establish a positive identification. Disaster victim identification charts suggested by the Interpol [14] require forensic odontologists to identify and record all available dental findings [7], but these charts have limited number of dental features printed on them for forensic odontologists to collect and record. Additionally, working in stressful conditions such as in disaster zones can result in failing to record vital information that may be used to establish a person identity. As experts, it is essential for us to be able to identify all types of information on dental features that can be observed in a deceased person, those including dental anomalies.

Dental anomalies can be vital pieces of information that can be used to identify a person if and when that information has been recorded in the ante-mortem dental records. Historically, dental characteristics have been of utmost value in distinguishing several hominid fossils, and one of the most outstanding finds was that of the Neanderthals. Apart from various other differences and similarities between the modern man and the Neanderthal, one feature that stood apart was the taurodont, a developmental anomaly found in the human dentition features of which are explained further in the article [15]. The aim of this paper is to briefly describe some important dental anomalies and their manifestations in the oral cavity. The authors of this article accentuate the importance of recording such information that has the potential to play an important role in establishing the identities of unknown persons who cannot be identified by any other means due to the nature of a certain disaster.

METHODOLOGY

This article focuses on dental anomalies and their role in establishing identities of unknown victims of disasters or other crimes. The authors advocate the importance of dental features such as developmental anomalies of teeth and associated syndromes and utilizing this information to simplify and ameliorate the person identification process. Some common and uncommon dental anomalies that can be identified in human dentitions have been presented further. An intense literature search from online resources such as PubMed, Medline along with online resources at the University of Tasmania was performed to collect appropriate literature for this review article.

Dental Anomalies and Their Presentations

The anomalies presented in this article are classified according to their extent of changes to teeth. These changes are: (a) Surface abnormalities, (b) shape abnormalities, (c) changes in position, and (d) increase or decrease in a number of teeth. These anomalies have been briefly explained based on their modes of diagnosis. Dental anomalies that can be assessed or diagnosed clinically are:

Surface Abnormalities

Mottled enamel

Chalky white or dull white patches seen on the surface of teeth are characteristics of mottled enamel. Most often, severely

affected teeth present themselves with a characteristic unglazed white. The teeth glow when exposed to light due to loss of normal translucency. Weakening of teeth is seen due to loss of enamel material and restorations is often unsuccessful in such cases [16,17].

Enamel hypoplasia

Enamel hypoplasia is one of the most common abnormalities of human dentition [18] and can be observed as round or band like irregularities on the dental enamel and may change color to yellow or brown due to external pigmentation. It is considered to occur as the result of a disturbance caused during the stage of active enamel formation [19-21] and can be classified into hereditary and environmentally induced enamel hypoplasia [22]. These anomalies are seen to occur both in primary and permanent dentition. A variation of enamel hypoplasia is Turners hypoplasia, which unlike other developmental anomalies affects just one tooth which is often referred to as Turner’s tooth [23].

Amelogenesis imperfecta

Amelogenesis imperfecta [Figure 1] is a developmental anomaly of the enamel [24,25] as a result of either hypoplasia or hypo-mineralization or both affecting almost all the teeth present. The enamel of affected teeth is often discolored, and is sensitive and is inclined to disintegrate easily. This condition is genetically derived [26,27] and is easily diagnosed with a thorough family history [25].

Dentinogenesis Imperfecta

Dentinogenesis imperfecta is a hereditary dysplastic condition affecting the dentin of teeth affecting both deciduous and permanent dentitions [28]. It has a genetic predisposition and is directly inherited from the affected parent(s) [29]. It has been previously known as hereditary opalescent dentin [28-30], hereditary hypoplasia of the dentin or odontogenesis imperfecta [29]. The crowns of affected teeth range from blue to brown in color and radiographically, the affected teeth appear to have bulbous crowns and short constricted roots [30].

Shape Abnormalities

Talon cusp

It is also called dens evaginatus or evaginated odontoma. It is an additional cusp like structure and shaped like an eagles talon [Figure 2a and b]. It usually projects from the cingulum of teeth mostly, the maxillary and mandibular incisors and are visible on clinical inspection. When viewed as a radiograph, it contains all normal characteristics of a normal tooth-the enamel, dentin including a pulp horn. It has been reported in both males and females and only in permanent teeth [31-33]. Apart from being called as the above, they have also been described under various other names in the past, some of them being supernumerary cusp, occlusal enamel pearl, interstitial cusp, odontome of the axial core, and tuberculated premolar [33].



Paramolar and distomolar teeth

Supernumerary teeth found in the molar region are classified as distomolars and paramolars [34]. Paramolars [Figure 3a] are presented as vestigial teeth buccal to the molars [35] and distomolars [Figure 3b] are usually presented as the fourth molar [34].

Cusp of carabelli

As the name suggests, cusp of carabelli [Figure 4] is a tubercle [36] or cusp like structure present on the mesiolingual surface of the upper first molars [37] and can either be found unilaterally or bilaterally [38] but with no sexual dimorphism [39]. The structure can appear as a furrow or pit, a slight protuberance or as a fully formed cusp like structure [Figure 7] [38].

Fusion

Fusion of teeth [Figure 5a-c] or synodontia is a phenomenon where two separate teeth fuse to become one. This may either be partial fusion or complete fusion. Identifying fused teeth is part clinical and part radiographic [40].

Germination

Germination [Figure 6a-c] is the phenomenon where one tooth fails to divide completely often leading to bifid crowns on a single set of root or roots. Identification is the appearance of two crowns at the place of one. The results can be confirmed using radiographs [40].

Peg shaped lateral incisors

An anomaly affecting the maxillary lateral incisors [Figure 7a-c], where the crown size is evidently reduced and is associated with the tapering of the incisal edge giving it a peg shaped appearance [41]. It is 1.35 times more prevalent in females as compared to males and can be seen in either of the upper quadrants [42].

Figure 1: Dentition affected by Amelogenesis imperfecta

Figure 4: Cusp of carabelli seen on the right maxillary fi rst molar

Hutchinson’s incisors

Hutchinson’s incisors are very similar to the peg shaped laterals, but only to occur in individuals affected by congenital syphilis and on the permanent central incisors instead of the lateral incisors. The incisors may be distinguished from normal incisors based on their greyish enamel, the smallness of their size and generally rounded in shape. Another feature of the Hutchinson’s incisors is the presence of a notch on the incisal edges, but it may be lost due to accelerated dental wear associated with congenital syphilis [43]. A similar developmental anomaly associated with permanent molars in individuals affected with congenital syphilis is Moon’s

Figure 2: (a and b) Talons cusp in relation to 12

a b

Figure 3: Supernumerary teeth (a) paramolar, (b) distomolar distal to 28

b

a



molars. Affected permanent first molars are usually smaller and dome shaped with cusps placed closer than normal. They have also been called bud molars [43] and mulberry molars [44].

Retained deciduous teeth

Clinically, deciduous teeth can be retained in their positions longer than normal [Figure 8]. This may be seen in cases both with and without a successor tooth [45]. Retained deciduous teeth can result in transposition of teeth [46] which has been explained further in the article.

Mesiodens

Mesiodens [Figure 9] are the most common found supernumerary teeth in both the primary and permanent dentitions [47]. They are found in the incisor regions between the maxillary central

incisors [48,49] and can be unilateral or bilateral. Mesiodens are diagnosed by panoramic radiographs, but can be suspected in cases involving retained primary incisors or ectopic eruptions of the incisors [47].

Change in Position

Tooth transposition

Tooth transposition [Figure 10] can be best described as the phenomenon where adjacent teeth interchange their positions. It technically means that space normally occupied by a specific tooth is no longer occupied by that tooth but the adjacent tooth. One must be sure that the tooth is not an ectopic tooth before diagnosing the transposed tooth as such [46,50].

Submerged tooth

Submerged teeth [Figure 11] occur as a result of partial eruption or retention of teeth at the absence of a physical barrier [51-53]. Other terms used to describe the phenomenon are secondary retention, half retention or even re-impaction. The etiology of this anomaly remains unknown; however, studies have suggested a strong genetic predisposition. A tooth may be classified as

Figure 8: Retained deciduous canine in the upper left quadrant

Figure 9: Mesiodens between upper right and left central incisors

Figure 5: Fusion of (a) molar tooth with supernumerary, (b) maxillary premolar with fused roots, (c) premolars

a b c

Figure 6: (a) Germination of 42, (b) germination of teeth molar tooth, (c) germination of teeth molar tooth

a b c

Figure 7: (a, b and c) Peg shaped lateral incisors

a b

c



submerged when the marginal ridges of the particular tooth are at least 0.5 mm below the marginal ridge of the adjacent teeth. The most commonly affected teeth are the deciduous mandibular second molars [54] and are clinically visible. Another reason for teeth to be submerged or partially erupted is because of teeth ankylosis. Ankylosis is a dental phenomenon where the cementum or dentin of teeth are fused with the alveolar bone preventing it from erupting completely [52,55,56].

Increase or Decrease in Number of Teeth

Supernumerary teeth

Supernumerary teeth [Figure 12a-c] are the presence of more than the usual number of teeth in the oral cavity [57]. Super numerary teeth most often occur in the pre-maxilla region. They can be seen both in permanent and deciduous teeth. In normal, they resemble normal teeth but they may also be conical in shape [58].

Dental agenesis

Dental agenesis [Figure 13] is the congenital absence of teeth [59] often associated with terms such as hypodontia, oligodontia, and anodontia [60]. It is one of the commonest dental anomalies affecting humans [61] and the second mandibular premolar is the most common affected tooth. It

is also observed with lateral maxillary incisor and the second maxillary premolar [62]. Dental agenesis is often associated with other oral anomalies [62], some of which have been discussed below in the anomalies section.

Some Dental Anomalies are Best Observed or Diagnosed Radiographically

Tooth impactions

Teeth are considered to be impacted when their eruption is delayed due to radiographic or clinical obstructions [63] [Figure 14]. All teeth can potentially be impacted; however, it has been found that third molars, maxillary canines, premolars and maxillary central incisors are most commonly affected. It is a common phenomenon among people today, but impacted teeth are found in skulls that are from the prehistoric age. In a recent excavation in Croatia, an adult female skull dated between 2700 and 24BC was found [64] and it was observed that the maxillary canine was impacted in bone and was established as an important finding. Impacted teeth have been considered to be evolutionary variations of teeth and have been reported widely in previous excavations, which mean it has been a feature for thousands of years [64].

Dens invaginatus

Furthermore, referred as dens in dente or dens telescopes, dens ivaginatus [65] is a rare developmental abnormality of teeth

Figure 10: Tooth transposition

Figure 11: Submerged toothFigure 13: Dental agenesis in the mandibular anterior region

Figure 12: (a,b and c) Supernumerary teeth

a b

c



where the teeth affected display an infolding of enamel before mineralization of the soft tissue and may extend all the way to the root. The appearance may range anywhere from a loop to pear shape or a tooth within a tooth. The teeth most often affected are the maxillary lateral incisors [66]. It can be diagnosed radiographically by looking for radio-opaque invagination that may extend from the cingulum to the root [65].

Odontoma

Odontomas are the most commonest [67] of odontogenic tumors that are clinically asymptomatic. They can occur as a compound or complex odontomas [68] depending on their structural presentation. Compound odontomas [Figure 15a] are anatomically, and structurally similar to normal teeth, however, complex odontomas [Figure 15b] display an irregularity in their structure [69]. Compound odontomas often occur in the anterior region of the oral cavity closer to the incisors and the canines, whereas complex odontomas normally occur closer to the pre-molar and molar regions of the oral cavity and associated more with the permanent teeth and are generally rare in association with deciduous teeth [70]. Radiographically, they appear as single or multiple radio-opaque lesions. At times, odontomas may cause secondary disturbances such as impaction or retention of teeth [69,70].

Enamel pearls

Enamel pearls [Figure 16] are pearl like projections of the enamel of teeth and they may either be found on the crown or the root [71]. The size of enamel pearls vary, but there have been

reports of more than one enamel pearl found on a tooth and in rare instances up-to four pearls on a tooth [72]. These pearls can be visually identified when they are present on the enamel surface and appear on a radiograph when they occur on the root surface. Ectopic enamel pearls are normally associated with periodontal destruction in molars and hence can be used as markers to identify people with periodontal diseases [73]. Enamel pearls have been occasionally found in primary dentition in the past [74].

Taurodontism

Taurodontism or “bull like teeth” [Figure 17] is a dental anomaly characterized by large pulp chambers and short roots that furcate at the lower thirds of the root the etiology of which involves both genetic and environmental factors [15,75,76]. It is usually seen in molars with an increased distance of more than 2.5 mm and can be diagnosed radiographically. It is one of the common features found both in the modern man and the Neanderthal [15,77].

Tooth dilaceration

Tooth dilaceration [Figure 18a and b] is an acute deviation of the long axis of the tooth on either the root or the crown [78]. Third molars are the most common teeth that are dilacerated, with the maxillary lateral incisors coming in second [79]. Tooth

Figure 14: An orthopentamogram of an impacted upper canine Figure 16: Enamel pearl on a maxillary molar

Figure 17: Taurodontism in relation to 36 and 46 along with multiple impactionsFigure 15: (a) Compound odontoma, (b) complex odontoma

a b



dilacerations have been seen in the primary dentition [80] and can be observed radiographically.

Concresence

Concresence [Figure 19a and b] is a condition of teeth where the neighboring teeth are attached to one another only by their cementum. Concresence has been reported as occurring in both the crown as well as the roots of teeth and can be diagnosed radiographically [81-83].

Hypercementosis

Furthermore called as cementum hyperplasia, hypercementosis [Figure 20] is expressed by excessive deposition of cementum on root surfaces of teeth and can be diagnosed radiographically [84,85].

Dentin Dysplasia

Dentin dysplasia describes a rare developmental defect of teeth usually characterized by a defective root form with a pulp chamber that may be partially or fully obliterated by whorl like dentine [86]. Dentinal dysplasia can be diagnosed through radiographs [86,87].

Listed above are some of the dental anomalies that occur in the oral cavity. These anomalies often present themselves as solitary occurrences, but sometimes these anomalies can occur in groups to form syndromes. Syndromes associated with dental anomalies can be used in identifying unknown persons. Table 1 shows characteristic features of a few syndromes associated with dental manifestations. These syndromes have been categorized based on their rarity of occurrence.

DISCUSSION

Dental agenesis is the most common developmental anomaly affecting humans [61]. Crouzon syndrome and Treacher Collins syndrome are the most common syndromes that manifest with dental abnormalities. These findings are based on syndromes

that have been listed in this article; however, there are many more syndromes with dental manifestations that can be added to the list.

Establishing identities of individuals as part of forensic investigations are a result of collaborative efforts between various teams. These teams often consist of specialists from various fields of criminal investigations, such as the law enforcement departments, pathologists, odontologists, and anthropologists amongst others [158]. Dental variations among people are noted to be unique, and this knowledge will guide us in achieving positive identifications of people involved in disasters [159]. The process of using dental evidence in establishing identities of people primarily involves examining and collecting vast numbers of dental features present in the dentitions of the deceased persons [160] and comparing them with their previous dental records. Complete and well maintained dental records with reports on dental anomalies can be accessed by the investigating team while establishing the identities of people.

It is crucial to understanding the importance of additional features such as dental anomalies and their potential in achieving positive identification of victims during or

Figure 18: Dilaceration of (a) upper left canine, (b) upper right central incisor

a b Figure 19: (a and b) Concrescence on maxillary molar

a b

Figure 20: (a and b) Hypercementosis on mandibular molar tooth

a b



after disasters [98]. Both general dental practitioners and forensic odontologists must ensure that all developmental anomalies and associated syndromes (if and when present) are recorded in the ante-mortem clinical dental records as well as the post-mortem records [161]. This information will be significant when forensic odontologists compare ante-mortem and post-mortem dental records to establish the identity of an individual for forensic investigations. The authors of this article suggest that, in addition to examining and recording information on existing dental anomalies and associated syndromes, it is also vital to conduct further research on estimating incident rates for the occurrence of such dental anomalies and associated syndromes for different communities or populations and integrate those incident

rates into a matrix where the probability of their occurrence in a population can be calculated. This will increase the ability of forensic odontologists to establish positive person identifications.

CONCLUSION

Forensic odontology is the culmination of wide knowledge of all the intraoral structures and deriving information on how these structures function as a unit and applying it in forensic investigations. Dental characteristics and features have set individuals apart from one another, and these features and their variations or similarities could help us in identifying unknown individuals during disasters or any situation that

Table 1: Characteristic dental features of syndromes associated with oral and dental manifestations and the rarities of their occurrencesSyndrome Oral manifestations Rarity of occurrence

Hutchinson-gilford progeria syndrome

Hutchinson-Gilford progeria syndrome is associated with an increased mandibular angle (upto about 150°) Gorlin and Sedano in 1968 suggested that the lack of developmental space in both the maxilla and mandible lead to severe dental crowding. Delayed eruption of teeth, localized enamel hypoplasia of the permanent central incisors, and periodontits have been previously reported along with reduction in the size of pulp chambers [88]

Extremely rare [89-92]

Rubinstein-Taybi syndrome

Common dental findings with Rubinstein-Taybi Syndrome include micrognathia [93], retrognathia [94], presence of Talons cusp [94], crowding, and narrow palate leading to anterior and posterior cross bites [95]

1/125000 live births [93]

Kabuki syndrome Kabuki syndrome is represented by cleft lip/cleft palate [96-98] along with a bifid uvula. Malocclusion is seen which may range from micrognathia or retrognathia. Other features seen are high arched palate, with wide spacing of teeth, delayed tooth eruption and abnormalities such as neonatal teeth, screwdriver shaped incisors [96,97] teeth with enlarged pulp chambers and cone shaped teeth [97-99]

Rare with 350 cases around the world [98,100]

Axenfeld-rieger syndrome

Is characterized by anodontia [101], microdontia [101,102], maxillary hypoplasia along with abnormally shaped and abnormally implanted teeth [103,104]

Rare (1:200,000) [104-106]

Hallerman-streiff syndrome

Hallerman-Streiff syndrome is characterized by microstomia [107] severe malocclusion [108], enamel hypoplasia [108], premature fracture of permanent teeth, hypodontia and presence of neonatal teeth [109]

Rare<1/1,000,000 [108-111]

Blepharo-chelio-dontic syndrome

The common manifestations are the presence of bilateral cleft lip or bilateral cleft palate [112,113]. Oligodontia and microdontia[113] have been seen in at-least half of all the cases reported [112,114]

Rare (<1/1,000,000) [112,115-117]

Russell silver syndrome

This syndrome is characterized by the presence of microdontia[118] a high arched narrow palate[119] and associations of cleft palate along have been reported along with a triangular shaped face [120-123]

Rare (1:100,000) [124-126]

EVC The syndrome has wide dental manifestations including neonatal teeth, partial anodontia [127,128], gingival hypertrophy, malocclusion, labiogingival frenulum hypertrophy, serrations on the incisal margins, conical teeth, premature eruptions of teeth, enamel hypoplasia and hypodontia [129]

Rare around 5.2/100,000 of live births in UAE alone [127,129-131] and 1/60,000 in a general population [132]

Incontinentia pigmenti (Bloch-Sulzberger syndrome)

Cases of Incontinentia pigmenti (Bloch-Sulzberger syndrome) are reported to have delayed tooth eruption, retained deciduous (which may be inter related) hypodontia associated with malformed crowns of lower incisors (mostly cone shaped) [133-135]. Cleft lip and cleft palate have been reported in the past [136]

Rare [134-138]1-9/1,000,000

Apert syndrome Presence of a Byzantine-arched palate [139], ectopic eruptions, severe crowding and shovel shaped incisors[139] are class characteristics of Apert Syndrome [140,141]

Rare [139,142,143] (15.5/1,000,000)

Downs syndrome Is characterized by anomalies such as high arched palate, peg shaped laterals, hypoplasia[144] taurodontia, hypodontia, partial anodontia along with a pseudo class III malocclusion [145,146]

Relatively rare 1.15-1.62/1000 (based on a report by Zeuten et al. 1973) [147,148]

Variant Carvajal syndrome

Has been reported with the presence of premature resorption of deciduous roots along with extensive caries along with localized absence of permanent teeth [149]

Rare [150,151]

Treacher Collin syndrome

Often associated with cleft palate [152-154] with anterior open bite [155] Common [152,153] 1:50,000 live births

Crouzon syndrome Crouzon syndrome is commonly associated with dental agenesis.The syndrome exhibits dental malocclusion, maxillary hypoplasia and retruded upper lip. Association of dental malformations like Angles class III, open bite cross bite has also been noted [62]

Common (1/25000)[156] to Rare (16.5/1,000,000) [157]

EVC: Ellis-van creveld syndrome



requires identification of individuals based on teeth. Dental practitioners and forensic odontologists share the responsibility of ensuring that a complete and thorough examination of the oral cavity must be performed for all possible findings to be recorded . Dental practitioners must record and save all findings in secure folders to facilitate easy retrieval when required. Forensic odontologists that assist with identifying victims after disasters or otherwise have a responsibility to extract and record all possible information from the victims and compare it with detailed dental records when available, to ensure a scientific, faster yet efficient positive identification. Finally, identifying all potential dental features and include them in comparing ante-mortem and post-mortem records is the key to establishing positive identities of unknown individuals.

ACKNOWLEDGMENTS

The authors would like to thank Dr. Robert Anthonappa, Pedodontist (UWA) for providing us with Figures 18a, 5c, 2b, 4, 14, Dr. Kiran Kumar HS, Prosthodontist, Sri Hasanamba Dental College and Hospital, Hassan, India for Figures 1 a-c, 2, 10, 3 and b, 13, 12c, 8, 7a-c, 9, 11, 17, and Dr. Jose Joy Idiculla for Figures 20,19, 18b, 16, 15a and b, 12a and b, 6a-c, 5a and b.

REFERENCES

1. Avon SL. Forensic odontology: The roles and responsibilities of the dentist. J Can Dent Assoc 2004;70:453-8.

2. Rajshekar M, Kruger E, Tennant M. Bite-marks: Understanding the role of general practitioners in forensic identification. J Int Oral Health 2012;4:8.

3. Rajshekar M, Tennant M. The role of the Forensic odontologist in disaster victim identification: A brief review. Malaysian J Forensic Sci 2014;5:78-85.

4. Lucina H. Disaster victim identification and anatomy. AXIS 2009;1:26-40.

5. Xavier M, Bento A, Costa A, Corte-Real A, Veloso C, Sampaio L, et al. Primary teeth as DNA reference sample in disaster victim identification (DVI). Forensic Sci Int Genet Suppl Ser 2011;3:e381-e2.

6. Hill AJ, Hewson I, Lain R. The role of the forensic odontologist in disaster victim identification: Lessons for management. Forensic Sci Int 2011;205:44-7.

7. Rajshekar M, Tennant M. Dental evidence in Forensic investigations: What we see and what we don’t. Scott J Arts Soc Sci Sci Stud 2013;16:9.

8. Kolude B, Adeyemi BF, Taiwo JO, Sigbeku OF, Eze UO. The role of forensic dentist following mass disaster. Ann Ib Postgrad Med 2010;8:111-7.

9. Valenzuela A, Martin-de las Heras S, Marques T, Exposito N, Bohoyo JM. The application of dental methods of identification to human burn victims in a mass disaster. Int J Legal Med 2000;113:236-9.

10. Pretty IA, Sweet D. A look at forensic dentistry – Part 1: The role of teeth in the determination of human identity. Br Dent J 2001;190:359-66.

11. Wright M. Disaster victim identification. Aust J Disaster Manage 1992;7:1-3.

12. Carl KL. Forensic odontology. Hong Kong Med Diary 2008;13:16-20.13. Stavrianos C, Georgaka E, Sarafidis G, Aroni D, Vasiliadis L,

Tretiakov G, et al. Dental and oral features useful in identification. Res J Med Sci 2012;6:33-41.

14. International Criminal Police Organization. Disaster Victim Identification Guide. Bad Arolsen: Interpol; 2009.

15. Hayashi Y. Endodontic treatment in taurodontism. J Endod 1994;20:357-8.

16. Smith MC, Lantz EM, Smith HV. The cause of mottled enamel, a defect of human teeth. Agricultural Experiment Station. June 10, 1931 ed. Tucson, Arizona: University of Arizona; 1931. p. 253-82.

17. McKay FS. Twentieth-century challenges. An investigation of mottled teeth. Public Health: The Development of a Discipline. New Brunswick, NJ: Rutgers University Press; Vol. 2. 2011. p. 123.

18. Nikiforuk G, Fraser D. The etiology of enamel hypoplasia: A unifying concept. J Pediatr 1981;98:888-93.

19. Pindborg JJ. Pathology of The Dental Hard Tissues. Phiadelphia: W.B Saunders Co; 1970.

20. Evans MW. Furtherobservations of dental defects in infants subsequent to maternal rubella during pregnancy. Obstet Gynecol Surv 1948;3:58.

21. Bhushan BA, Garg S, Sharma D, Jain M. Esthetic and endosurgical management of Turner’s hypoplasia; A sequlae of trauma to developing tooth germ. J Indian Soc Pedod Prev Dent 2008;26 Suppl 3:S121-4.

22. El-Najjar MY, DeSanti MV, Ozebek L. Prevalence and possible etiology of dental enamel hypoplasia. Am J Phys Anthropol 1978;48:185-92.

23. Geetha Priya PR, John JB, Elango I. Turner’s hypoplasia and non-vitality: A case report of sequelae in permanent tooth. Contemp Clin Dent 2010;1:251-4.

24. Aldred MJ, Savarirayan R, Crawford PJ. Amelogenesis imperfecta: A classification and catalogue for the 21st century. Oral Dis 2003;9:19-23.

25. Crawford PJ, Aldred M, Bloch-Zupan A. Amelogenesis imperfecta. Orphanet J Rare Dis 2007;2:17.

26. Collier PM, Sauk JJ, Rosenbloom SJ, Yuan ZA, Gibson CW. An amelogenin gene defect associated with human X-linked amelogenesis imperfecta. Arch Oral Biol 1997;42:235-42.

27. Bäckman B, Holmgren G. Amelogenesis imperfecta: A genetic study. Hum Hered 1988;38:189-206.

28. Roberts E, Schour I. Hereditary opalescent dentine (Dentinogenesis imperfecta). Am J Orthodont Oral Surg 1939;25:267-76.

29. Ivancie GP. Dentinogenesis imperfecta. Oral Surg Oral Med Oral Pathol 1954;7:984-92.

30. Sapir S, Shapira J. Dentinogenesis imperfecta: An early treatment strategy. Pediatr Dent 2001;23:232-7.

31. Mellor JK, Ripa LW. Talon cusp: A clinically significant anomaly. Oral Surg Oral Med Oral Pathol 1970;29:225-8.

32. Hamasha AA, Safadi RA. Prevalence of talon cusps in Jordanian permanent teeth: A radiographic study. BMC Oral Health 2010;10:6.

33. Yip WK. The prevalence of dens evaginatus. Oral Surg Oral Med Oral Pathol 1974;38:80-7.

34. Dubuk AN, Selvig KA, Tellefsen G, Wikesjö UM. Atypically located paramolar. Report of a rare case. Eur J Oral Sci 1996;104:138-40.

35. Dahlberg AA. The paramolar tubercle (Bolk). Am J Phys Anthropol 1945;3:97-103.

36. Kraus BS. Carabelli’s anomaly of the maxillary molar teeth; Observations on Mexicans and Papago Indians and an interpretation of the inheritance. Am J Hum Genet 1951;3:348-55.

37. Hassanali J. Incidence of Carabelli’s trait in Kenyan Africans and Asians. Am J Phys Anthropol 1982;59:317-9.

38. Alvesalo L, Nuutila M, Portin P. The cusp of Carabelli. Occurrence in first upper molars and evaluation of its heritability. Acta Odontol Scand 1975;33:191-7.

39. Falomo OO. The cusp of Carabelli: Frequency, distribution, size and clinical significance in Nigeria. West Afr J Med 2002;21:322-4.

40. Mahabob MN, Kumar BS, Raja S. Fusion: A diagnostic dialoma rare case reports. J Integr Dent 2012;1:1-5.

41. Baccetti T. A controlled study of associated dental anomalies. Angle Orthod 1998;68:267-74.

42. Hua F, He H, Ngan P, Bouzid W. Prevalence of peg-shaped maxillary permanent lateral incisors: A meta-analysis. Am J Orthod Dentofacial Orthop 2013;144:97-109.

43. Hillson S, Grigson C, Bond S. Dental defects of congenital syphilis. Am J Phys Anthropol 1998;107:25-40.

44. Jacobi KP, Cook DC, Corruccini RS, Handler JS. Congenital syphilis in the past: Slaves at Newton Plantation, Barbados, West Indies. Am J Phys Anthropol 1992;89:145-58.

45. Aisenberg MS. Studies of retained deciduous teeth. Am J Orthodont Oral Surg 1941;27:A179-84.

46. Ely NJ, Sherriff M, Cobourne MT. Dental transposition as a disorder of genetic origin. Eur J Orthod 2006;28:145-51.

47. Russell KA, Folwarczna MA. Mesiodens – Diagnosis and management of a common supernumerary tooth. J Can Dent Assoc 2003;69:362-6.

48. Sykaras SN. Mesiodens in primary and permanent dentitions. Report of a case. Oral Surg Oral Med Oral Pathol 1975;39:870-4.



49. Asaumi JI, Shibata Y, Yanagi Y, Hisatomi M, Matsuzaki H, Konouchi H, et al. Radiographic examination of mesiodens and their associated complications. Dentomaxillofac Radiol 2004;33:125-7.

50. Chattopadhyay A, Srinivas K. Transposition of teeth and genetic etiology. Angle Orthod 1996;66:147-52.

51. Antoniades K, Kavadia S, Milioti K, Antoniades V, Markovitsi E. Submerged teeth. J Clin Pediatr Dent 2002;26:239-42.

52. Biederman W. Etiology and treatment of tooth ankylosis. Am J Orthodont 1962;48:670-84.

53. Darling AI, Levers BG. Submerged human deciduous molars and ankylosis. Arch Oral Biol 1973;18:1021-40.

54. Herman E. Evaluation and management of ankylosed teeth. New York State Dent J 1964;30:327-33.

55. Andersson L, Blomlöf L, Lindskog S, Feiglin B, Hammarström L. Tooth ankylosis. Clinical, radiographic and histological assessments. Int J Oral Surg 1984;13:423-31.

56. Biederman W. The incidence and etiology of tooth ankylosis. Am J Orthodont 1956;42:921-6.

57. Flint EG. Supernumerary teeth. Am J Orthodont Oral Surg 1939;25:135-53.

58. Roger-Hall HT. Supernumerary Teeth. London: The Dental Gazette; 1939. p. 489-93.

59. Polder BJ, Van’t Hof MA, Van der Linden FP, Kuijpers-Jagtman AM. A meta-analysis of the prevalence of dental agenesis of permanent teeth. Community Dent Oral Epidemiol 2004;32:217-26.

60. Silva Meza R. Radiographic assessment of congenitally missing teeth in orthodontic patients. Int J Paediatr Dent 2003;13:112-6.

61. De Coster PJ, Marks LA, Martens LC, Huysseune A. Dental agenesis: Genetic and clinical perspectives. J Oral Pathol Med 2009;38:1-17.

62. S t a v r o p o u l o s D, B a r t z e l a T, Ta r n o w P, M o h l i n B , Kahnberg KE, Hagberg C. Dental agenesis patterns in Crouzon syndrome. Swed Dent J 2011;35:195-201.

63. Aitasalo K, Lehtinen R, Oksala E. An orthopantomographic study of prevalence of impacted teeth. Int J Oral Surg 1972;1:117-20.

64. Rajic S, Muretic Z, Percac S. Impacted canine in a prehistoric skull. Angle Orthod 1996;66:477-80.

65. de Sousa SM, Bramante CM. Dens invaginatus: Treatment choices. Endod Dent Traumatol 1998;14:152-8.

66. Hülsmann M. Dens invaginatus: Aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J 1997;30:79-90.

67. Budnick SD. Compound and complex odontomas. Oral Surg Oral Med Oral Pathol 1976;42:501-6.

68. Or S, Yücetas S. Compound and complex odontomas. Int J Oral Maxillofac Surg 1987;16:596-9.

69. de Oliveira BH, Campos V, Marçal S. Compound odontoma – Diagnosis and treatment: Three case reports. Pediatr Dent 2001;23:151-7.

70. Yeung KH, Cheung RC, Tsang MM. Compound odontoma associated with an unerupted and dilacerated maxillary primary central incisor in a young patient. Int J Paediatr Dent 2003;13:208-12.

71. Chrcanovic BR, Abreu MH, Custódio AL. Prevalence of enamel pearls in teeth from a human teeth bank. J Oral Sci 2010;52:257-60.

72. Cavanha AO. Enamel pearls. Oral Surg Oral Med Oral Pathol 1965;19:373-82.

73. Risnes S, Segura JJ, Casado A, Jiménez-Rubio A. Enamel pearls and cervical enamel projections on 2 maxillary molars with localized periodontal disease: Case report and histologic study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:493-7.

74. Kupietzky A, Rozenfarb N. Enamel pearls in the primary dentition: Report of two cases. ASDC J Dent Child 1993;60:63-6.

75. Casamassimo PS, Nowak AJ, Ettinger RL, Schlenker DJ. An unusual triad: Microdontia, taurodontia, and dens invaginatus. Oral Surg Oral Med Oral Pathol 1978;45:107-12.

76. Hamner JE 3rd, Witkop CJ Jr, Metro PS. Taurodontism; Report of a case. Oral Surg Oral Med Oral Pathol 1964;18:409-18.

77. Seow WK, Lai PY. Association of taurodontism with hypodontia: A controlled study. Pediatr Dent 1989;11:214-9.

78. Jafarzadeh H, Abbott PV. Dilaceration: Review of an endodontic challenge. J Endod 2007;33:1025-30.

79. Chohayeb AA. Dilaceration of permanent upper lateral incisors: Frequency, direction, and endodontic treatment implications. Oral Surg Oral Med Oral Pathol 1983;55:519-20.

80. Kilpatrick NM, Hardman PJ, Welbury RR. Dilaceration of a primary tooth. Int J Paediatr Dent 1991;1:151-3.

81. Mader CL. Concrescence of teeth: A potential treatment hazard. Gen Dent 1984;32:52-5.

82. Sugiyama M, Ogawa I, Suei Y, Tohmori H, Higashikawa K, Kamata N. Concrescence of teeth: Cemental union between the crown of an impacted tooth and the roots of an erupted tooth. J Oral Pathol Med 2007;36:60-2.

83. Foran D, Komabayashi T, Lin LM. Concrescence of permanent maxillary second and third molars: Case report of non-surgical root canal treatment. J Oral Sci 2012;54:133-6.

84. Shafer W, Hine M, Levy B. A Textbook of Oral Pathology. 3rd ed. Philadelphia: WB Saunders Co.; 1974. p. 217.

85. Weinberger A. The clinical significance of hypercementosis. Oral Surg Oral Med Oral Pathol 1954;7:79-87.

86. Logan J, Becks H, Silverman S Jr, Pindborg JJ. Dentinal dysplasia. Oral Surg Oral Med Oral Pathol 1962;15:317-33.

87. Tidwell E, Cummingham CJ. Dentinal dysplasia: Endodontic treatment, with case report. J Endod 1979;5:372-6.

88. Hennekam RC. Hutchinson-Gilford progeria syndrome: Review of the phenotype. Am J Med Genet A 2006 1;140:2603-24.

89. Pollex RL, Hegele RA. Hutchinson-Gilford progeria syndrome. Clin Genet 2004;66:375-81.

90. Eriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, Scott L, et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 2003;423:293-8.

91. De Sandre-Giovannoli A, Bernard R, Cau P, Navarro C, Amiel J, Boccaccio I, et al. Lamin a truncation in Hutchinson-Gilford progeria. Science 2003;300:2055.

92. Merideth MA, Gordon LB, Clauss S, Sachdev V, Smith AC, Perry MB, et al. Phenotype and course of Hutchinson-Gilford progeria syndrome. N Engl J Med 2008;358:592-604.

93. Castriota-Scanderbeg A, Dallapiccola B. Rubinstein-Taybi syndrome. Abnormal Skeletal Phenotypes: From Simple Signs to Complex Diagnoses. New York: Springer; 2005. p. 856-8.

94. Gardner DG, Girgis SS. Talon cusps: A dental anomaly in the Rubinstein-Taybi syndrome. Oral Surg Oral Med Oral Pathol 1979;47:519-21.

95. Wiley S, Swayne S, Rubinstein JH, Lanphear NE, Stevens CA. Rubinstein-Taybi syndrome medical guidelines. Am J Med Genet A 2003;119A:101-10.

96. Petzold D, Kratzsch E, Opitz Ch, Tinschert S. The Kabuki syndrome: Four patients with oral abnormalities. Eur J Orthod 2003;25:13-9.

97. Adam MP, Hudgins L. Kabuki syndrome: A review. Clin Genet 2005;67:209-19.

98. Teixeira CS, Silva CR, Honjo RS, Bertola DR, Albano LM, Kim CA. Dental evaluation of Kabuki syndrome patients. Cleft Palate Craniofac J 2009;46:668-73.

99. Mhanni AA, Cross HG, Chudley AE. Kabuki syndrome: Description of dental findings in 8 patients. Clin Genet 1999;56:154-7.

100. Matsumoto N, Niikawa N. Kabuki make-up syndrome: A review. Am J Med Genet C Semin Med Genet 2003;117C:57-65.

101. Shields MB. Axenfeld-Rieger syndrome: A theory of mechanism and distinctions from the iridocorneal endothelial syndrome. Trans Am Ophthalmol Soc 1983;81:736-84.

102. Alward WL. Axenfeld-Rieger syndrome in the age of molecular genetics. Am J Ophthalmol 2000;130:107-15.

103. Fitch N, Kaback M. The Axenfeld syndrome and the Rieger syndrome. J Med Genet 1978;15:30-4.

104. Dressler S, Meyer-Marcotty P, Weisschuh N, Jablonski-Momeni A, Pieper K, Gramer G, et al. Dental and craniofacial anomalies associated with axenfeld-rieger syndrome with PITX2 mutation. Case Rep Med 2010;2010:621984.

105. Tümer Z, Bach-Holm D. Axenfeld-Rieger syndrome and spectrum of PITX2 and FOXC1 mutations. Eur J Hum Genet 2009;17:1527-39.

106. Hjalt TA, Semina EV. Current molecular understanding of Axenfeld-Rieger syndrome. Expert Rev Mol Med 2005;7:1-17.

107. Chen H. Hallermann-Streiff syndrome. Atlas of Genetic Diagnosis and Counseling. Totowa, NJ: Humana Press; 2006. p. 469-72.

108. Junewick J. Hallerman-streiff syndrome michigan 2010. Available from: http://www.advancedradteaching.com/teachingfiles/406. [Last cited on 2015 May 25].

109. Junewick J. Hallerman-Streiff Syndrome Michigan: Advanced Radiology Services Teaching; 2010. p. 1-5. Available from: http://www.admin.advancedradteaching.com/teachingfiles/406.pdf. [Last cited on 2015 May 25].

110. Orphanet. Hallermann-Streiff syndrome. France; 2006. Available from: http://www.orpha.net/consor/cgi-bin/Disease_Search.php?lng=EN&data_id=2019&Disease(s)%20concerned=Hallermann-



Streiff-Francois-syndrome&title=Hallermann-Streiff-Francois-syndrome&search=Disease_Search_Simple. [Last cited on 2014 July 18].

111. Neki AS. Hallermann-Streiff syndrome. Indian J Ophthalmol 1993;41:83-4.

112. Yen MT, Lucci LM, Anderson RL. Management of eyelid anomalies associated with Blepharo-cheilo-dontic syndrome. Am J Ophthalmol 2001;132:279-80.

113. Valdéz-de la Torre MH, Quintana-García M, Canún S. Blepharo-cheilo-dontic (BCD) syndrome in two Mexican patients. Am J Med Genet 1999;85:157-9.

114. Gorlin RJ, Wiedemann HR. Blepharo-cheilo-dontic (BCD) syndrome. Acta Ophthalmol Scand Suppl 1996;22.

115. Orphanet. Blepharo-Cheilo-Odontic syndrome. France; 1997. Available from: http://www.orpha.net/consor/cgi-bin/Disease_Search.php?lng=EN&data_id=1934&Disease_Disease_Search_diseaseGroup=Blepharo-cheilodontic-&Disease_Disease_Search_diseaseType=Pat&Disease(s)/group%20of%20diseases=Blepharo-cheilo-odontic-syndrome--Blepharocheilodontic-syndrome-&title=Blepharo-cheilo-odontic-syndrome--Blepharocheilodontic-syndrome-&search=Disease_Search_Simple. [Last cited on Dec 2014].

116. Retna RN, Sockalingam S. Clinical manifestation of blepharocheilodontic (BCD) syndrome: A case review. Sains Malaysiana 2013;42:85-8.

117. Iida A, Narai S, Takagi R, Ono K, Ikeda N. Blepharo-cheilo-dontic (BCD) syndrome: Case report. Cleft Palate Craniofac J 2006;43:237-43.

118. Cullen CL, Wesley RK. Russell-Silver syndrome: Microdontia and other pertinent oral findings. ASDC J Dent Child 1987;54:201-4.

119. Fuleihan DS, Der Kaloustian VM, Najjar SS. The Russell-Silver syndrome: Report of three siblings. J Pediatr 1971;78:654-7.

120. Patton MA. Russell-Silver syndrome. J Med Genet 1988;25:557-60.121. Saal HM. Russell-Silver syndrome. Management of Genetic

Syndromes. Seattle, WA: University of Washington; 1993.122. Eggermann T, editor. Russell–Silver syndrome. American Journal

of Medical Genetics Part C: Seminars in Medical Genetics; Hoboken, NJ: Wiley; 2010.

123. Wollmann HA, Kirchner T, Enders H, Preece MA, Ranke MB. Growth and symptoms in Silver-Russell syndrome: Review on the basis of 386 patients. Eur J Pediatr 1995;154:958-68.

124. Christoforidis A, Maniadaki I, Stanhope R. Managing children with Russell-Silver syndrome: More than just growth hormone treatment? J Pediatr Endocrinol Metab 2005;18:651-2.

125. Kariminejad MH, Bozorgmehr B. Russell-Silver Syndrome. Genetics in the 3rd Millennium 2006;4:740-1.

126. Anderson J, Viskochil D, O’Gorman M, Gonzales C. Gastrointestinal complications of Russell-Silver syndrome: A pilot study. Am J Med Genet 2002;113:15-9.

127. Lichiardopol C, Militaru C. Ellis-van Creveld syndrome. Rom J Morphol Embryol 2006;47:363-6.

128. Mundlos S, Horn D. Ellis–Van Creveld Syndrome. Limb Malformations. Berlin: Springer; 2014. p. 46-8.

129. Baujat G, Le Merrer M. Ellis-van Creveld syndrome. Orphanet J Rare Dis 2007;2:27.

130. Ali BR, Akawi NA, Chedid F, Bakir M, Ur Rehman M, Rahmani A, et al. Molecular and clinical analysis of Ellis-van Creveld syndrome in the United Arab Emirates. BMC Med Genet 2010;11:33.

131. Shilpy S, Nikhil M, Samir D. Ellis Van Creveld syndrome. J Indian Soc Pedod Prev Dent 2007;25 Suppl: S5-7.

132. Chen H. Ellis-van Creveld Syndrome. Atlas of Genetic Diagnosis and Counseling. Totowa, NJ: Humana Press; 2006. p. 350-4.

133. Landy SJ, Donnai D. Incontinentia pigmenti (Bloch-Sulzberger syndrome). J Med Genet 1993;30:53-9.

134. Ehrenreich M, Tarlow MM, Godlewska-Janusz E, Schwartz RA. Incontinentia pigmenti (Bloch-Sulzberger syndrome): A systemic disorder. Cutis 2007;79:355-62.

135. Shotts N, Emery AE. Bloch-Sulzberger Syndrome (incontinentia pigmenti). J Med Genet 1966;3:148-52.

136. Vogt J, Matheson J. Incontinentia pigmenti (Bloch-Sulzberger syndrome). A case report. Oral Surg Oral Med Oral Pathol 1991;71:454-6.

137. Sulzberger MB, Fraser J, Hutner LL. Incontinentia pigmenti (bloch-sulzberger): Report of an additional case, with comment on possible relation to a new syndrome of familial and congenital anomalies. Arch Dermatol Syphilol 1938;38:57-69.

138. Orphanet. Incontinentia pigmenti France: Orphanet; 2013. Available from: http://www.orpha.net/consor/cgi-bin/OC_Exp. php?Lng=GB&Expert=464. [Last cited on Dec 2014].

139. Soanca A, Dudea D, Gocan H, Roman A, Culic B. Oral manifestations in Apert syndrome: Case presentation and a brief review of the literature. Rom J Morphol Embryol 2010;51:581-4.

140. Kreiborg S, Cohen MM Jr. The oral manifestations of Apert syndrome. J Craniofac Genet Dev Biol 1992;12:41-8.

141. Park WJ, Theda C, Maestri NE, Meyers GA, Fryburg JS, Dufresne C, et al. Analysis of phenotypic features and FGFR2 mutations in Apert syndrome. Am J Hum Genet 1995;57:321-8.

142. Cohen MM Jr, Kreiborg S, Lammer EJ, Cordero JF, Mastroiacovo P, Erickson JD, et al. Birth prevalence study of the Apert syndrome. Am J Med Genet 1992;42:655-9.

143. Chen H. Apert syndrome. Atlas of Genetic Diagnosis and Counseling. Totowa, NJ: Humana Press; 2006. p. 61-9.

144. Scully C. Down’s syndrome: Aspects of dental care. J Dent 1976;4:167-74.

145. Hennequin M, Faulks D, Veyrune JL, Bourdiol P. Significance of oral health in persons with Down syndrome: A literature review. Dev Med Child Neurol 1999;41:275-83.

146. Jaspers MT. Taurodontism in the Down syndrome. Oral Surg Oral Med Oral Pathol 1981;51:632-6.

147. Zeuten E, Nielsen J, Nielsen A. Prevalence of Down’s syndrome. Hereditas 1973;75:136-8.

148. Roizen NJ, Patterson D. Down’s syndrome. Lancet 2003 12;361:1281-9.149. Barber S, Day P, Judge M, Toole EO, Fayle S. Variant Carvajal

syndrome with additional dental anomalies. Int J Paediatr Dent 2012;22:390-6.

150. Yusuf P, Abdul Aziz AH. Carvajal syndrome – A rare variant of naxos disease in two saudi siblings. Pediatr Ther 2013;3:1.

151. Nehme N, El Malti R, Roux-Buisson N, Caignault JR, Bouvagnet P. Evidence for genetic heterogeneity in Carvajal syndrome. Cell Tissue Res 2012;348:261-4.

152. Dixon J, Trainor P, Dixon MJ. Treacher Collins syndrome. Orthod Craniofac Res 2007;10:88-95.

153. Dixon MJ. Treacher Collins syndrome. J Med Genet 1995;32:806-8.154. Jones MC. Treacher collins syndrome. Management of Genetic

Syndromes. New Jersey: Wiley-Blackwell; 2005.155. Poswillo D. The pathogenesis of the Treacher Collins syndrome

(mandibulofacial dysostosis). Br J Oral Surg 1975;13:1-26.156. Ahmed I, Afzal A. Diagnosis and evaluation of Crouzon syndrome.

J Coll Physicians Surg Pak 2009;19:318-20.157. Cohen MM Jr, Kreiborg S. Birth prevalence studies of the Crouzon

syndrome: Comparison of direct and indirect methods. Clin Genet 1992;41:12-5.

158. Chandra Shekar BR, Reddy CV. Role of dentist in person identification. Indian J Dent Res 2009;20:356-60.

159. Sweet D. Interpol dvi best-practice standards – An overview. Forensic Sci Int 2010;201:18-21.

160. Adams BJ. Establishing personal identification based on specific patterns of missing, filled, and unrestored teeth. J Forensic Sci 2003;48:487-96.

161. Naiman M, Larsen AK Jr, Valentin PR. The role of the dentist at crime scenes. Dent Clin North Am 2007;51:837-56, vii.

Source of Support: Nil, Confl ict of Interest: None declared.

10.5455/ejfs.196581 Developmental anomalies of teeth and ... › 69fd › dd579e87640... · was the...

Documents

Transcript of 10.5455/ejfs.196581 Developmental anomalies of teeth and ... › 69fd › dd579e87640... · was the...