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 Table of Contents  
Year : 2015  |  Volume : 7  |  Issue : 6  |  Page : 499-503  

Clinical evaluation of nonsyndromic dental anomalies in Dravidian population: A cluster sample analysis

1 Department of Oral Pathology, Vivekanandha Dental College for Women, Tiruchengo, Tamil Nadu, India
2 Department of Oral and Maxillofacial Pathology and Microbiology, Mahe Institute of Dental Science and Hospital, Mahe, U.T. of Puducherry, India
3 Undergraduate Dental student, Vivekanandha Dental College for Women, Tiruchengode, Tamil Nadu, India
4 Department of Community Dentistry, Chettinad Dental College and Hospital, Chennai, Tamil Nadu, India

Date of Submission28-Apr-2015
Date of Decision28-Apr-2015
Date of Acceptance22-May-2015
Date of Web Publication1-Sep-2015

Correspondence Address:
Dr. Andamuthu Yamunadevi
Department of Oral Pathology, Vivekanandha Dental College for Women, Tiruchengo, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-7406.163517

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Aim: To record the prevalence rate of dental anomalies in Dravidian population and analyze the percentage of individual anomalies in the population. Methodology: A cluster sample analysis was done, where 244 subjects studying in a dental institution were all included and analyzed for occurrence of dental anomalies by clinical examination, excluding third molars from analysis. Results: 31.55% of the study subjects had dental anomalies and shape anomalies were more prevalent (22.1%), followed by size (8.6%), number (3.2%) and position anomalies (0.4%). Retained deciduous was seen in 1.63%. Among the individual anomalies, Talon's cusp (TC) was seen predominantly (14.34%), followed by microdontia (6.6%) and supernumerary cusps (5.73%). Conclusion: Prevalence rate of dental anomalies in the Dravidian population is 31.55% in the present study, exclusive of third molars. Shape anomalies are more common, and TC is the most commonly noted anomaly. Varying prevalence rate is reported in different geographical regions of the world.

Keywords: Dental anomalies, Dravidian population, Talon′s cusp

How to cite this article:
Yamunadevi A, Selvamani M, Vinitha V, Srivandhana R, Balakrithiga M, Prabhu S, Ganapathy N. Clinical evaluation of nonsyndromic dental anomalies in Dravidian population: A cluster sample analysis. J Pharm Bioall Sci 2015;7, Suppl S2:499-503

How to cite this URL:
Yamunadevi A, Selvamani M, Vinitha V, Srivandhana R, Balakrithiga M, Prabhu S, Ganapathy N. Clinical evaluation of nonsyndromic dental anomalies in Dravidian population: A cluster sample analysis. J Pharm Bioall Sci [serial online] 2015 [cited 2022 Jun 26];7, Suppl S2:499-503. Available from:

Odontogenesis is a complex process which involves the interaction of the epithelium derived from the first arch and the ectomesenchyme of the neural crest cells resulting in the formation of tooth. [1] Various genes are involved in determining the number, shape, position and size of each tooth. Any mutations in these genes occurring due to metabolic or other pathological conditions and environmental alterations result in the occurrence of dental anomalies. [2] These dental anomalies have varying proportion of occurrence in different geographical regions and at times, they can be a potential source of orthodontic problems. In severe forms, they can modify the craniofacial morphology and skeletal patterns also.

Thus, the present study is aimed to record the prevalence rate of dental anomalies in Dravidian population and to determine the occurrence of varying proportions of individual dental anomalies in Dravidian population.

   Methodology Top

This descriptional cross-sectional study included 250 students of Dravidian origin, studying at Vivekanandha Dental College for Women, Namakkal, India. All the students studying in the I, II, III years of the dental course were included in the study, and their age range was within 17-21 years. Subjects of non-Dravidian origin, nonwilling subjects, subjects who had undergone orthodontic treatment, subjects with syndromes, if any were excluded from the study. Thus, among the 250 students, 244 were fitting the inclusion criteria and were included in the study. Also, third molars were excluded from analysis, since the eruption would not be completed in the age group of selected study subjects (17-21 years). Informed consent was obtained from each subject and the purpose of the study was made clear to them.

Using sterile mouth mirror, explorer, cotton the oral cavity was examined clinically by two examiners under proper light source. The presence or absence of dental anomalies was noted down in case history format, customized for the study. Radiographs, if taken previously in these subjects, for other dental treatment needs were also analyzed. The dental anomalies, after being recorded, were classified in terms of number, size, shape, position/location, and others. The numerical count of observed anomalies was transferred to excel sheet and their total and individual proportions were calculated.

   Results Top

Among the 244 female students, anomalies were noted in 77 (31.55%) individuals and 11 persons (4.5%) had more than one anomalies. 54 persons showed variation in shape (22.1%), 21 subjects had size anomalies (8.6%), eight showed anomalies in number of teeth (3.2%), and 1 person (0.4%) had canine in abnormal location (ectopic canine), while retained deciduous was seen in 4 students (1.63%).

Among the shape anomalies, Talon's cusp (TC), dens evaginatus, peg laterals (PL), and supernumerary cusps were noticed. Number anomalies in terms of hyperdontia and hypodontia, size anomalies in terms of microdontia and macrodontia were seen. The percentage of individual anomalies observed were tabulated [Table 1].
Table 1: Prevalence rate of dental anomalies in the study subjects

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   Discussion Top

Odontogenesis involves complex interaction of genes in determining the number (transforming growth factor-ß, bone morphogenic protein [BMP], fibroblast growth factor [FGF], epithelial growth factor, sonic hedgehog family, wingless [Wnt] Drosophila family genes are involved mainly in initiation process), tooth type (Dlx-1, Dlx-2 and Barx-1 are expressed in posterior regions, whereas Msx-1, Msx-2 and Dlx-2 are seen in anterior regions), and tooth position (FGF-8, pituitary homeobox-2, BMP-4 in the oral epithelium and Pax-9 in the tooth mesenchyme). [1] Thus, mutation in these genes cause related anomalies, which may affect a single tooth, few teeth, or the whole dentition and the related structures (e.g., ectodermal dysplasia). [2] Dental anomalies can also result from environmental factors (e.g., trauma, infection) or a combination of genetic and environmental factors. Their clinical presentation is varying and most of the dental anomalies are occurring in asymptomatic milder forms, hardly requiring any treatment. Yet, few anomalies may be a source of potential orthodontic problems, periodontal problems, etc., and warrants prompt treatment.

The occurrence of dental anomalies was studied previously in various populations and known to differ with geographical and ethnic variations. Variation in prevalence rate also depends on method of examination and age of study population. From our study results, the obtained prevalence rate in Dravidian population was about 31.55%, which on comparison [Table 2] was, less than that of Marati population (39.20%), [3] Saudi Arabia (45.1%), [4] Jothpur (36.7%), [5] Thailand (38.6%) [6] and Turkey (56.4%) [7] study results and this variation was greatly owed to difference found in number anomalies [Table 2].
Table 2: Prevalence rate of dental anomalies in various study population

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Number anomalies

Number anomalies were about only 3.2% in our study, contrary to the highest percentage noted in other studies [Table 2]. The marked decrease in the proportion of anomalies in tooth number in the present study might be due to our study method. Third molars, which are most commonly missing teeth, are excluded from the study and radiographic evaluation of dental anomalies is not done in all cases to rule out hyperdontia (e.g., mesiodens) or impacted teeth.


Two percentage of study population were with hypodontia and maxillary laterals were the most commonly missing teeth (excluding third molars, 2.8-7.4%, [8] is reported in literature). Bilaterally missing laterals [Figure 1] and occurrence of microdontic lateral incisor on one side and absence of lateral incisor on the opposite side [Figure 2] were noteworthy findings, since such combination is reported in several studies. [4] This combined anomalous nature (microdontia of lateral incisor on one side and absence of laterals on other side) is the result of similar genetic defect on both the teeth at varying degrees. [4]
Figure 1: Bilaterally missing maxillary lateral incisors

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Figure 2: Microdontia on right maxillary lateral incisor and absence of lateral incisor on left side

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The occurrence of tooth agenesis have racial prediliction (Blacks < Whites < Asians [9]) and even gender variation (females > males [9] ). Hypodontia is reported to be rare in deciduous dentition (slightly more than 1%) and in such occurrence, the successor permanent teeth are also nearly always absent. [8] Hypodontia is known to be more common in first and second degree relatives, than in the general population.

Mutations of genes such as Msx-1 (at loci 4p16.1) cause specific hypodontia or oligodontia, nonsense mutation of Msx-1 gene is associated with combination of tooth agenesis and cleft lip and/or cleft palate. [10] Mutation in Pax-9 gene at loci 14q12-q13 is related with agenesis of permanent molars with or without involving primary teeth. [11] Colorectal cancer and tooth agenesis is associated with mutation in AXIN 2 gene at loci 17q23-24. [12]

Environmental factors like irradiation, administration of chemotherapy for malignant disorders during tooth development stages can cause hypodontia, the effect being depending on the age of the patient and administered drug dosage. [13]


1.2% of hyperdontia was seen in our study (other reports - [1-3%] [13] ), being more common in the posterior molar and premolar region. In contrast, mesiodens is the most common hyperdontic teeth in the literature [13] and many theories were proposed for the occurrence of hyperdontic teeth. They are thought to be a part of postpermanent dentition, occurring due to proliferation of dental lamina. [14] Being known to occur simultaneously in monozygotic twins, [15] brook in 1984, [16] put forward a combination of genetic and environmental factors for their occurrence and no mutated gene was found to be associated with hyperdontia.

Size anomalies


Prevalence of isolated microdontia in literature is between 1% and 8%, [13] and 6.6% is noticed in the present study. Maxillary lateral incisors were reduced mesio-distally and most frequently involved in this anomaly. PLs are a form of microdontic teeth, where shape is also altered. It is common in >1% of general population, [13] and 1.63% in our study [Figure 3]. PLs are inherited as autosomal dominant trait and it is notable that if both the parents are with PLs, their homozygous child will present with complete anodontia of succedaneous teeth. [17] Except for variation in crown, these teeth remain normal in root portion and have a healthy long-term prognosis, requiring no treatment. On patient's concern about esthetics, the treatment options can be considered.
Figure 3: Peg laterals in left maxillary lateral incisor

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Larger teeth or macrodontia was observed in 2% of our study population, and all are localised form, noticed in the maxillary central incisors bilaterally.

Shape anomalies

Talon's cusp
"Talon's cusp are well-delineated additional cusp on the surface of an anterior tooth and extends 1/2 the distance from cement enamel junction to incisal edge." [13] We had high prevalence rate of this anomaly (14.34%) and results, similar to our findings were noted in the other Indian race, Marati [3] population also. Thus, TC might be the most prevailing racial marker in Indian races, especially in Dravidian and Marati population.

Maxillary lateral incisors followed by central incisors were more commonly affected in our subjects and the proposed pathophysiology is that hyperproliferation of the anterior ends of dental lamina during odontogenesis leads to TC. [18] TC is also a part of syndromes like Rubeinstein-Taybe syndrome [2] and Berardinelli Seip syndrome. [18]

Supernumerary cusps

Supernumerary cusps (5.73%) were seen in maxillary and mandibular first and second molars and premolars. Fifth cusp in mandibular second molar, prominent cusp of carabelli, considered to be normal variants were noted in many subjects. Three cusps in maxillary second premolars and mandibular first premolars were also found. Sixth cusp in mandibular first molar, termed as tuberculum intermedium [19] was noted in one case and literature had related this anomaly with metabolic disorders like type I diabetes mellitus. [20] A single case of dens evaginatus (central tubercle or Leong's premolar) was observed unilaterally in mandibular second premolar [Figure 4]. Anticipating periodontal problems, due to improper occlusal force, grinding of opposing teeth or this tubercle can be done. [13]
Figure 4: Dens evaginatus on right mandibular second premolar

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Lingually erupted canine occurred in a single subject (0.4%) in association with retained deciduous canine. Retained deciduous teeth will cause delay in eruption of successors and also affect their path of eruption. Their early detection is necessary to facilitate orthodontic treatment.

   Conclusion Top

Prevalence of dental anomalies in the Dravidian population is 31.55%, exclusive of third molars. Shape anomalies are more common in the dentition of Dravidian population, followed by size and number anomalies. TC is the most commonly observed dental anomaly. Variation in prevalence rate of different anomalies is observed with geographical and racial variations. Further studies including larger sample population from both the genders and usage of radiological aids can aid in better visualization of the condition.

Financial support and sponsorship


Conflicts of Interest

There are no conflicts of interest.

   References Top

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Shafer WG, Hine MK, Barnet ML. Developmental disturbances. In: Rajendran R, Sivapathasundaram B, editors. Textbook of Oral Pathology. 7 th ed. New Delhi: Reed Elsevier India Private Limited; 2012.  Back to cited text no. 2
Kathariya MD, Nikam AP, Chopra K, Patil NN, Raheja H, Kathariya R. Prevalence of dental anomalies among school going children in India. J Int Oral Health 2013;5:10-4.  Back to cited text no. 3
Afify AR, Zawawi KH. The prevalence of dental anomalies in the western region of Saudi Arabia. ISRN Dent 2012;2012:837270.  Back to cited text no. 4
Patil S, Doni B, Kaswan S, Rahman F. Prevalence of dental anomalies in Indian population. J Clin Exp Dent 2013;5:e183-6.  Back to cited text no. 5
Kositbowornchai S, Keinprasit C, Poomat N. Prevalence and distribution of dental anomalies in pretreatment orthodontic Thai patients. KDJ 2010;13:92-100.  Back to cited text no. 6
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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.  Back to cited text no. 9
Satokata I, Maas R. Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development. Nat Genet 1994;6:348-56.  Back to cited text no. 10
Stockton DW, Das P, Goldenberg M, D′Souza RN, Patel PI. Mutation of PAX9 is associated with oligodontia. Nat Genet 2000;24:18-9.  Back to cited text no. 11
Aswathyraj R, Deepa MS, Farooqi AH, Brahmanandan A. Genetics and tooth anomalies - An update. Oral Maxillofac Pathol J 2013;4:ISSN 0976-1225.  Back to cited text no. 12
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. 2 nd ed. Philadelphia: WB Saunder′s Company; 2002.  Back to cited text no. 13
Regezi JA, Sciubba J. Oral Pathology. Clinical-Pathologic Correlations. 2 nd ed. Philadelphia: WB Saunders; 1993.  Back to cited text no. 14
Brook AH. A unifying aetiological explanation for anomalies of human tooth number and size. Arch Oral Biol 1984;29:373-8.  Back to cited text no. 15
Rubin MM, Nevins A, Berg M, Borden B. A comparison of identical twins in relation to three dental anomalies: Multiple supernumerary teeth, juvenile periodontosis, and zero caries incidence. Oral Surg Oral Med Oral Pathol 1981;52:391-4.  Back to cited text no. 16
Witkop CJ Jr. Agenesis of succedaneous teeth: An expression of the homozygous state of the gene for the pegged or missing maxillary lateral incisor trait. Am J Med Genet 1987;26:431-6.  Back to cited text no. 17
Solanki M, Patil SS, Baweja DK, Noorani H, Pk S. Talon cusps, macrodontia, and aberrant tooth morphology in Berardinelli-Seip syndrome. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:e41-7.  Back to cited text no. 18
Schied RC, Weiss G. Woelfel′s Dental Anatomy. 8 th ed. Philadelphia: Library of Congress Cataloging in Publication Data; 2010. p. 331.  Back to cited text no. 19
Yamunadevi A, Basandi PS, Madhushankari GS, Donoghue M, Manjunath A, Selvamani M, et al. Morphological alterations in the dentition of type I diabetes mellitus patients. J Pharm Bioallied Sci 2014;6:S122-6.  Back to cited text no. 20


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]


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