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International Journal of Clinical ISSN: 1939-5833 Volume 7, Number 4 © Nova Science Publishers, Inc.

TOOTH ABNORMALITIES: AN OVERVIEW OF MORE THAN 20 DEVELOPMENTAL AND ACQUIRED DISORDERS

Abbas Shokri1, Hamed Mortazavi2,, Maryam Baharvand, and Amir Movahhedian3 1Department of Oral & Maxillofacial Radiology, Dental School, Hamadan University of Medical Sciences, Hamadan, Iran 2Department of Oral & Maxillofacial Medicine, Dental School, Shahid Beheshti University of Medical Sciences, Tehran, Iran 3Shahid Beheshti University of Medical Sciences, Tehran, Iran

ABSTRACT

This paper was aimed to describe a number of abnormalities, which dental practitioners in every discipline might encounter.To accomplish this review article the last versions of dental textbooks addressing the topic were first studied. Thereafter, the MeSH keywords of "tooth", "tooth abnormalities", "dental anomalies", "tooth disease", and "teeth disease" were searched in databases of Pubmed/Medline, Scopus, and EMBASE to find relevant original, review, and case reports. Finally, the subjects from articles were compared with authorized textbooks and compiled to the present review.We described 28 entities of teeth abnormalities of developmental and environmental origin as well as their treatment modalities. This article as a practical review could help dentists renew their knowledge about the field and arrive at more accurate diagnoses and treatment plan.

Keywords: tooth, tooth abnormalities, dental anomalies, tooth disease, teeth disease

Clinical Significance

Every dental practitioner is very likely to encounter patients having abnormalities in their teeth in terms of structure, number, size, position, and morphology. Hence, appropriate knowledge of such pathologies is mandatory for correct diagnosis and treatment plan.

Correspondence to: Department of Oral & Maxillofacial Medicine, Dental School, Shahid Beheshti University of Medical Sciences, Daneshjoo Blvd, Tabnak St, Chamran Highway,Tehran, Iran. Zip code: 1983963113, Work phone: +98-21-29902311, Work fax: +98-21-22403194, E-mail: [email protected] 348 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

INTRODUCTION

Dental anomalies represent a wide spectrum of disorders divided into two subgroups: acquired and developmental abnormalities [1]. The etiology of dental anomalies has not been known thoroughly yet [2, 3], but it seems that both environmental and genetic factors could be involved [4-6]. Developmental anomalies are categorized into five groups including abnormalities in size, number, morphology, structure, and position of teeth [6-12]. This paper was aimed to describe a number of tooth abnormalities, which dental practitioners in every discipline might encounter.

LITERATURE SEARCH

We used various general search engines such as Google, Google Scholar, and Yahoo as well as bibliographic databases such as PubMed, PubMed central, Medline Plus, Med Know, EBSCO, Science Direct, Scopus, WebMD, EMBASE, and three authorized textbooks to find relevant topics by means of medical subject headings keywords such as "tooth", "tooth abnormalities", "dental anomalies", "tooth disease", and "teeth disease". The search was accomplished in 2013 and limited to English-language articles published over the last 50 years in both medical and dental journals. Totally, 312 articles were identified. After provisional assessment of the titles and abstracts by two reviewers, 110 articles were selected as relevant to the topic, and 80 were available for us of which 75 were used in our review. After compilation of information from relevant articles and updated textbooks, we categorized tooth abnormalities into two subgroups of acquired and developmental abnormalities with further sub classifications in each subgroup. Meanwhile, a brief treatment modality for each entity was provided.

DEVELOPMENTAL DISORDERS

Teeth Number Anomalies

Hypodontia Lack of tooth formation is one of the most common developmental disorders with a prevalence of 1.6-9.6% in . However, this rate increases to 20% when third molar is considered. is uncommon among with a prevalence of 0.5-0.9%, and if happens usually lateral incisors are involved. Missing of a primary tooth increases the chance of its succeeding permanent tooth to be missed [1]. Hypodontia is associated with , increased freeway space and the remaining deciduous teeth. The most common form of hereditary hypodontia is autosomal dominant, which the mean number of missing teeth is more than two. Except for the third molar, mandibular second premolars, maxillary second premolars and mandibular central incisors are the most commonly missing teeth [1]. Tooth Abnormalities 349

Hypodontia affects women more than men. Apart from third molars, hypodontia has a range of 0.3-11.3% according to epidemiological studies. This wide range could be attributed to racial, age, and geographical differences among studied populations [2]. Based on another study, prevalence of hypodontia in deciduous and permanent teeth was reported 1% and 3- 8.5% respectively [13]. A study on 12-18 years old children found that white people were more affected by hypodontia compared to blacks, and the most common missing tooth among the study population was third molar [8]. Treatment of hypodontia would be replacing missing teeth by prostheses. In some patients, prior orthodontic treatment helps lessen need for restorative procedures or obtain better results [1].

Hyperdontia Prevalence of supernumerary teeth is 0.1-3.8% among white people, and a little higher in Asian population. affects primary teeth less often (0.3-0.8%). Although single tooth hyperdontia occurs more frequently in permanent teeth and in 95% of cases in the anterior , numerous non-syndromic supernumerary teeth are quite common in . Most supernumerary teeth are seen in the jaws;however some have been reported in gingiva, maxillary tuberosity, soft , maxillary sinus and nasal cavity. Despite hypodontia, hyperdontia is associated to and is twice more common as in men than women [1]. The etiology is unknown, but it is seen in some families more commonly. An association between hyperdontia and some syndromes or developmental disorders such as cleidocranial dysplasia, Gardner’s syndrome and or cleft palate has been suggested [13]. A study in Turkey revealed that 84 supernumerary teeth were seen in 69 radiographs, which nine of them were deciduous and 75 were permanent teeth. The most common affected site and teeth were premaxilla (67%) and mesiodense respectively. Meanwhile, supernumerary teeth had a prevalence of 2.7% among Turkish children [11]. In a study in Greek population, prevalence of hyperdontia was reported 1.8% and mesiodense was the most common type among supernumerary teeth [14]. In a similar study in India prevalence of hyperdontia was reported 1.4% [5]. Extraction of supernumerary teeth in mixed dentition is the standard treatment of hyperdontia [1].

Size Abnormalities

Microdontia This term is just used when teeth are smaller than usual; when the jaw is bigger than usual as a result of spacing between teeth and teeth look smaller this is called relative microdontia, which represents jaw enlargement but not true microdontia. True generalized microdontia is uncommon, but it can occur as a sporadic finding in Down syndrome, pituitary dwarfism and some rare hereditary anomalies. Single microdontia is often seen in maxillary lateral incisors, which usually has a peg-shaped on a normal-height root. The prevalence of microdontia has a range of 0.8-8.4% in different populations and it seems to be of autosomal dominant inheritance with incomplete penetration [1]. 350 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

Solitary microdontia often involves maxillary lateral incisors and third molars. In a survey in Japan, 1.9% of students had microdontia [15]. No treatment is necessary unless for esthetic reasons. In this case, peg-shaped lateral incisors could be restored by porcelain restorations [1].

Macrodontia The term macrodontia (megalodontia, megadontia) is justified when teeth are larger than usual, and not when teeth with normal size are placed in a small jaw or in case of gemination and fusion. True generalized macrodontia may be along with gygantism. True localized macrodontia may be seen in facial hemihypertrophy. The etiology is unknown, and there is no need for any treatment unless for esthetic reasons [1, 16].

Positional Anomalies

Transposition This is a situation in which two teeth displace when teeth are not in their proper position in dental arch. Transposition is common in canines and first premolars followed by lateral incisors. Sometimes second premolar erupts between the first and second molar. Transposition of central and lateral incisors is rare. Transposition has not been reported among primary teeth. This anomaly can be associated with hypodontia, supernumerary teeth and remaining deciduous teeth [16]. A studyon Turkish population aged 12-27 years old demonstrated the prevalence of transposition as 0.27% with the female: male ratio of 2.2:1. In addition, the most common transposition occurred between canine and lateral incisors (60%), which was more frequent in the left side [17]. In another study, 88% of transpositions were unilateral with greater prevalence in maxilla than mandible. Moreover, the most common transposition occurred between maxillary canine and first premolar (83%) followed by maxillary canine and lateral incisor (73%)[18].

Morphological Anomalies

Concrescence occurs when root of two or more teeth attach to each other by . Both primary and permanent teeth can be affected. Although etiology is unknown, many authors believe that lack of enough space during development, trauma, abnormal occlusal forces and local infections after development have important roles. If this occurs during development it is called true concrescence. If it happens later it is called acquired concrescence. Maxillary molars are the most affected teeth. Involved teeth might erupt incompletely or remain erupted. Prevalence is equal in both sexes [16]. There is no need for treatment unless root connection results in delayed eruption. In this case surgical extraction is recommended [1].

Fusion arises from union of tooth germs. Some experts believe that this happens when tooth germs come too close to each other or contact while erupting or connect to each other before calcification. However, the others believe that physical forces and pressure Tooth Abnormalities 351

during tooth formation make tooth germs contact. Genetic basis of this anomaly is probably autosomal dominant with low penetration. Women and men are affected equally. Fusion usually causes decrease in teeth number. Fusion can involve both permanent and deciduous teeth; however it is more common in primary teeth. In addition, fusion is more common in anterior teeth in both dentitions [1]. Size of a fused tooth varies from normal to twice of a normal tooth [16]. Bilateral fusion of mandibular primary teeth was reported to be more prevalent in lateral incisors and canine followed by central and lateral incisors. Sometimes fusion is accompanied with missing of succeeding teeth [19]. A case of fused mandibular third molar to a supernumerary tooth has been reported as well [20]. Usually there is no need for treatment. If necessary, extraction is done to prevent eruption problems [1].

Gemination (Double Teeth) It often involves anterior teeth; however premolars and molars can be affected. In most cases there is a deep groove with various depths involving all or a part of crown or root. This groove indicates attachment line between two tooth germs [21]. Germination is more frequent in primary teeth and anterior region. There is no sex predilection. Enamel or may be hypocalcified or hypoplastic in this abnormality [16]. The prevalence of double teeth in the primary and permanent dentition ranges from 0.4% to 0.9 % and 0.1% to 0.2 %, respectively [4,5]. Geminated teeth are mostly unilateral, so that bilateral presentation of this phenomenon is very rare with the prevalence of 0.01% to 0.04% in the primary, and 0.05% in the permanent dentition [21]. It is suggested that fissures of involved teeth be sealed in order to prevent caries. In most cases the tooth crown is reshaped with or without full crowns [1].

Taurodontism

Taurodontism is enlargement of root trunk and chamber of multi- root teeth as a result of apical movement of pulp floor and tooth furcation. Diagnosis is usually based on radiographic findings. Some researchers have reported taurodontism in premolar teeth though others believe that taurodontism does not affect premolars [1]. Taurodontism is found in primary and permanent dentition, but it is more common in permanent teeth (molars and premolars). This entity could be observed in single or multiple teeth both unilaterally and bilaterally [16]. Taurodontism might present distinctively or as a sign of a syndrome. It is found in association with cleft lip, cleft palate and hypodontia. There is no need for treatment for taurodontism [1].

Dilaceration

Dilaceretion is an angulation or an abnormal curve in root or rarely in crown. Although most of cases are idiopathic, it seems that in some cases calcified portion of tooth germ is displaced after trauma and the rest of tooth forms with an abnormal angulation. often occurs as a result of avulsion or intrusion of deciduous teeth at the age of four. 352 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

Dilaceration due to trauma is usually seen in anterior teeth, which results in functional and esthetic problems. With less prevalence it may be caused by adjacent odontogenic tumors or hamartoma[1].Diagnosis of dilacerated teeth is important in root canal therapy; otherwise the treatment will fail [22]. According to a study, prevalence of dilaceration was reported 3.8%, mostly seen in mandibular third molar, mandibular first molar and maxillary third molar, respectively [23]. Maxillary and mandibular incisors had the lowest prevalence [24]. is the best way for diagnosing dilacerations. In the case of mesial or distal curve they will be seen perfectly in a periapical radiograph. Extraction of dilacerated tooth necessitates radiograph prescription as well [16].Mild dilacerations in permanent teeth don’t need treatment. Teeth with delayed eruption or eruption disorder could be guided to proper place by orthodontic treatment [1].

Supernumerary Roots This term is used when there are extra roots compared to tooth normal anatomy. All the teeth and both dentitions can be affected. The most involved teeth are maxillary and mandibular permanent molars especially third molar and mandibular canine and premolars. In many cases supernumerary roots are divergent and could be seen in radiographs easily. Sometimes extra roots are small and superimposed on other roots; therefore it is hard to recognize them. No treatment is necessary, but it is mandatory to diagnose before extraction or root canal therapy [1].

Dens Evaginatus It is a rare dental anomaly, which features an extra cusp or tubercle on the occlusal surface of the tooth. It is mostly seen in premolars; however it can also affect canines, molars and incisors. Mandible is involved five times more often than maxilla. It results from abnormal proliferation of inner enamel epithelium into stellate reticulum. The tubercle has a central dentinal part surrounding a pulp tissue with various forms, and the pulp might not exist in some cases [1].Prevalence of Dent evaginatus was reported to be 1-4%, and it is more common in some races such as American Indians, Eskimos, Chinese, Japanese, Thais and Pilipino [25].On radiographic view, occlusal table reveals a tubercular surface and usually with a cuspal pulp extension. The extra cusp often causes occlusal interference resulting in clinical problems. In an extensive research, over 80% of extra cusps had and in more than 25% of patients pulpal disease was seen. was also common [1]. In case of pulp exposure due to attrition and fracture pulp necrosis would be possible featured by peri-apical radioluency [16]. often leads to occlusal interference and pulp necrosis. To prevent pulp involvement occlusal adjustment by minimal removal of dentin and using stannous fluoride is suggested [1].

Dens Invaginatus This anomaly also known as dens in dent is a developmental problem resulting from enamel organ invagination into dental papilla before calcification stage. It begins from crown and sometimes extends down to root. It is most frequent in the maxillary lateral incisors and with lower possibility in maxillary centrals, premolars, canines, and rarely molars. Clinically, this anomaly is seen in the crown at the lingual pit, which makes the tooth susceptible to decay. A radiopaque invagination similar to enamel density extending from cingulum to root canal is observed in radiographs. This defect shows a broad spectrum of morphological Tooth Abnormalities 353

variations, from loop shaped to pear shaped, mild radiolucent structure to a complete tooth within another one. This entity is easily diagnosed, because the invaginated enamel layer has more opacity compared to surrounding structures. It is divided into three categories based on the severity of invagination: in type one a small enamel-covered structure formed inside the crown, which has not reached the CEJ. Type two features enamel- covered structure like a closed cavity, which might affect the root and be in contact with the pulp. Type three is a severe form, which extends through the root length without pulp involvement [26]. Double invaginatus is a rare form where two invaginations take place in one tooth. It causes rapid extension of decay and involvement of the pulp chamber. Oral microorganisms might attack the pulp chamber through and result in periapical pathoses. The patients are often asymptomatic, not aware of the condition, and usually identified by routine intra oral radiographs. In some studies an association between dens invagination and taurodontism, microdontia, gemination, supernumerary teeth and dentinogenesis imperfecta was found [26].Dens invaginatus is a common tooth anomaly with the prevalence of 0.25- 1.5% among maxillary lateral incisors [26]. Radiographs often discover this anomaly. Root invaginatus has a lower prevalence, and is harder to diagnose. This anomaly can be diagnosed by means of radiographs even before eruption [16]. In type one, the orifice of dens invaginatus should be restored to prevent decay and pulp . Root canal therapy is needed in type three dens invaginatus [1].

Structural Anomalies

Dentinogenesis Imperfecta It is a primary developmental disorder in dentin, which enamel may be thinner than normal as well. The prevalence of dentinogenesis imperfecta is equal in both sexes, and it can affect primary and permanent dentitions [16]. Dentinogenesis imperfecta is one of the most common hereditary disorders in dentin formation. In the United States of America the prevalence is reported one in 8000 people. It is inherited as an autosomal dominant pattern, and accidental incidence due to gene mutation is rare. In this anomaly a basic defect occurs in regulating structural proteins in a way that a mesodermal defect causes abnormality in papilla of both primary and permanent teeth [1]. It is divided into three types: type I is associated with osteogenesis imperfecta, type II is not related to osteogenesis imperfecta, and type III or Brandy wine is a rare type with abnormal enlargement of pulp, which is called “shell teeth”. In recent years it became clear that dentinogenesis imperfecta and osteogenesis imperfecta are two distinct entities without any relation, hence a new classification is suggested: type I (including type II) and type II (including type I and II) [27]. Teeth with nearly normal crowns and roots in terms of size and morphology respond well to full coverage restorations [1].

Amelogenesis Imperfecta

Amelogenesis imperfecta is a series of genetic defects affecting the structure and clinical appearance of all or most of teeth by a rather similar pattern, and may be along with structural or biochemical changes in other parts of the body. It is enamel developmental disorder 354 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al. featured by hypoplasia, hypomineralization or both. Patients have discolored hypersensitive teeth, which are prone to destruction. This may occur before or after eruption. Hereditary patterns of this disorder can be autosomal dominant, autosomal recessive, X-linked or sporadic. The prevalence could be various from one in 14000 in the United States to one in 700 in North of Sweden [28]. According to a study, amelogenesis imperfecta is a genetic anomaly associated with anomalies such as taurodontism, congenital missing teeth, delay in eruption and crown attrition [29]. Patients with generalized with insufficient enamel thickness need full crown. For patients with short crowns, complete denture is the only satisfying treatment [1].

Tooth Impaction

Eruption is a continuous process of tooth movement from the start point to the functional position. Teeth with delayed eruption before emerging in the mouth are considered impacted. Some authors call un erupted teeth due to a physical barrier as impacted and those having no necessary erupting forces as embedded [1].Impaction in deciduous teeth is rare, but second molars are mostly affected. Ankylosis has an important role in the pathogenesis of impaction [24]. In permanent dentition, the most commonly affected teeth are mandibular third molars followed by maxillary third molars and canines. Impaction is often because of teeth crowding and insufficient development of maxillofacial structures. Other reasons are cysts, tumors, trauma, reconstructive surgery etc. [1]. A study in Greece regarding third molar impaction demonstrated that common causes of were insufficient space, remained primary teeth and inappropriate esthetic restorations, respectively. According to this study after third molars most impactions happened in maxillary canines followed by premolars [14]. Another study in China about impaction of mandibular second molars showed that in all cases except one, impactions were of mesio angular type, and the range of mesial inclination was between 13-57 degrees [30]. In a study in Babol (North of Iran), the prevalence of impaction was reported as 9.65%, and slightly higher in women. Maximum rate of impaction found in mandibular third molar (63%) followed by maxillary canine (17%). In addition, prevalence of impaction in mandible (66%) was more than maxilla (34%) [31]. Treatments of impacted teeth are: follow up, teeth eruption by orthodontic forces, transplantation and surgical extraction [1].

Acquired Tooth Disorders

Tooth Ankylosis It is an anomaly where an attachment between alveolar bone and cementum or dentin takes place before or after eruption [32, 33]. According to another definition, stopping of eruption after immerging is called ankylosis [1]. The etiology has not been known yet; however different factors such as genetic, trauma to bone or periodontal ligament, local defect in vertical growth of bone, local metabolism disorders and local inflammation are suggested [32]. Tooth Abnormalities 355

Ankylosis may occur at any age. According to reported studies, the highest prevalence is among 8-9- year- old children [32-35]. Any teeth could be affected, but mandibular primary first molar, mandibular primary second molar, maxillary primary first molar, and maxillary primary second molar are involved most commonly. Ankylosis is uncommon among permanent teeth. If primary ankylosed tooth shows delayed exfoliation it must be extracted. Prosthetic treatment is recommended to increase length of clinical crown of primary ankylosed tooth without any succeeding teeth and permanent ankylosed tooth [1].

RESORPTION

Resorption is defined as destruction of tooth structure due to osteoclastic activation, which is divided to internal and external types according to the affected surfaces [16].

Internal Resorption

It occurs in pulp chambers or root canals and causes loss of surrounding dentin. This could be either transient, self- limited or progressive. The reason is unknown, but it could be related to inflammation of pulpal tissue. Lesions can be as a round or oval radiolucency or located along the crown and root. Border of lesions might be either well defined and smooth or scalloped. The lesion might be completely radiolucent and homogenous [16, 36-38]. If the entire pulp is taken out by root canal therapy before exposure of the lesion to the periodontal ligament, internal resorption will be stopped [1].

External Resorption

It is a condition, which the outer root surface or the crown surface of an un-erupted tooth is lost. In this anomaly, cementum, dentin and pulp are involved over the time. This can affect one or more and rarely the entire teeth. Its etiology is unknown; however inflammatory lesions, tumors, cysts, mechanical pressures, etc could contribute to this entity. It is common in apical and cervical sites. If it starts from the apex, there will be a smooth resorption, which causes thickening of apex, but if it occurs as a result of periapical inflammatory lesions, lamina dura will be lost. A common reason of root external resorption is an adjacent un erupted tooth [16, 38-42]. The first measure for the treatment of external resorption is identification and elimination of predisposing factors. Cervical lesion can be exposed by surgery; then the soft tissue is removed and the tooth is restored [1].

Hypercementosis

Hypercementosis (cementum hyperplasia) is a non-neoplastic aposition of excessive cementum on the root. Radiographically, affected teeth show thickness and rounding of the apices [43]. As cementum and dentin have the same radiopacity determining the exact amount of excessive cementum is difficult. Enlarged root is surrounded by radiolucent space of 356 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al. periodontal ligament and lamina dura. Hypercementosis could affect one or more teeth or may be seen as a generalized process in mouth [44,45]. It is often seen in adults and its prevalence rises with increasing age. According to studies the most affected teeth are mandibular molars, mandibular and maxillary second premolars and mandibular first premolars [1,14]. Radiographic features of hypercementosis are considered in differential diagnosis with [46]. Hypercementosis does not need any treatment, but some teeth must be sectioned before extraction [1].

Pulp Stone

Pulp stones are calcified foci in dental pulp. Microscopically, it is seen in more than half of the young teeth and nearly all people older than 50 years old. is a common radiographic finding and may occur in one or more teeth. Its cause is unknown [1,47]. In radiographs they appear in different shapes of radio-opaque structures within the pulp chamber or root canals. These stones don’t have a fix number or shape and can be round, oval or similar to pulp chamber’s shape. Their outline might be well or ill- defined. They can be seen in all teeth, but molars are often affected [16, 48, 49].

Pulpal Sclerosis

Despite pulp stones, it is a generalized form of pulp and root canal calcification. The cause is unknown, but it is related to aging. The pattern of calcification is amorphous, non- organized and like parallel strips or columns of calcified material [50, 51]. This can occur as a reaction to dental caries as well [51]. Pulpal calcification does not require any special treatment [1].

Tooth Fluorosis

Using large amount of fluoride could result in enamel defects named tooth fluorosis. Although fluoride causes permanent , it also increases tooth resistance to decay, because of combination of fluoride and developing enamel and producing fluorapatite crystals that are more resistant to dissolution by acids. Effect of fluoride on causing enamel defect is applied on enamel structure by trapping of amelogenin protein, which results in hypomineralization followed by enamel hypomaturation and increasing surface pitting. This new structure results in alteration of light reflection and creation of white spots sometimes together with yellow to dark brown discoloration. In the past, mild to moderate fluorosis was called mottled enamel [1]. Tooth fluorosis is depending on fluoridation of water supply. Water fluoridation in Tehran and Semnan was reported 0.3 mg F/L and 1.3 mg F/L, respectively, according to Meyer- Lueckel study. Prevalence of fluorosis was significantly high in Semnan [53]. Similar studies were accomplished in other cities of Iran [54, 55, 56].Yellow to brown discoloration can be treated by microabrasion, but white spots need restorative treatment [1]. Tooth Abnormalities 357

Attrition

Attrition is a because of opposing primary or permanent teeth contact during or mastication. Incisal, occlusal and lingual surfaces of maxillary anterior teeth along with labial surface of mandibular anterior teeth mostly involved. It is observed as smooth and shiny surface matching with teeth contacts [1]. In Yadav study prevalence of attrition among people between 18 and 55 years old was reported 88%, which was increased by age and more frequent in men. A direct relationship between attrition and tenderness of masticatory muscles, pain and limited mouth opening was also found [57-60]. Normal attrition does not require any treatment unless the loss of tooth structure is remarkable. The treatment includes elimination of tooth sensitivity, identifying causes of attrition and protecting the remaining tooth structure [1, 61].

Abrasion

Abrasion is a kind of pathologic tooth or restoration wears due to external mechanical trauma such as brush, pencil, toothpick, pipe handle, ouch, chewing tobacco, nuts and inappropriate use of dental floss. According to Van'tSpijker study prevalence of abrasion varied from 0.3% in age of 20 to 17% in age of 70 [61]. The appearance is different depending on the cause of abrasion. For example toothbrush creates a cervical horizontal groove on buccal surfaces of the tooth. Abrasion has well defined borders and a smooth and hard surface [1,62]. Materials with maximum resistance against wear should be used to restore abrasion areas [1,62].

Erosion

Erosion is loss of tooth structure due to chemical agents of non-bacterial origin seen at facial and palatal surfaces of maxillary anterior teeth and facial and occlusal surface of mandibular posterior teeth. Classic sign of erosion is a concavity in dentin surrounded by projected enamel ridges. Active sites of erosion have a clean surface while the passive sites are discolored by stains [63]. Moimaz reported erosion in 0.6% in 4-6 year- old children with equal rate in both sexes. Six- year old children were mostly involved and lingual and occlusal surfaces were more affected [64]. In another study by Huew, erosion was observed in 40.8% of 12- year- old children, which 32.5% of them were limited to enamel and in 0.3% of cases even the pulp was exposed [65]. In erosion cases, preventive measurements to decrease the effect of acidic agents and increase resistance of oral cavity against acids must be done. There should be one- hour period between brushing and use of acidic foods and beverages in order to prevent wear of weak enamel [1, 66]. 358 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

Syphilitic Hypoplasia

Congenital syphilis results in specific enamel hypoplasia that is rare nowadays. Affected anterior teeth called Hutchinson’s incisors have narrow incisal edge and their maximum diameter is on middle one third of the crown. Middle part of the incisal edge usually has a hypoplastic notch. Posterior teeth that are involved are called mulberry molar and have small occlusal table and undeveloped cusp looking like berries [67, 68].

Molar Incisor Hypomineralization

This disorder has been considered as a distinct entity since three decades ago, and had not been diagnosed before. Patients with this disorder have enamel defect on one or more of their first molar, appearing as white, yellow or brown spots, which is clearly distinguished from adjacent enamel. Defected enamel is often soft, porous, fragile, and is easily chipped off. Affected molars are sensitive to cold, heat and mechanical trauma. Incisors might get involved as well, but this would be milder. The cause of this phenomenon is unknown, and its prevalence was reported 3.3% to 25% in different communities [69, 70]. In a study by Cho in Hong Kong this disorder was found in 8.2% of primary school children. The most affected age was 12 and the most affected teeth were permanent maxillary first molars, permanent mandibular first molars and permanent maxillary central incisors [71].

CONCLUSION

Diagnosing of teeth disorders is accomplished by means of clinical examination, imaging and sometimes genetic evaluation. Treatment of teeth anomalies consists of wide range of modalities from simple restorative treatments to prosthodontics and surgery depending on the extent of functional disability.

REFERENCES

[1] Neville R, Damm D, Alen C, Bouquot J. Oral and maxillofacial pathology. St. Louis:Saunders, 2009; 49-106. [2] Dahlberg AA. Dental morphology and evolution. Chicago: University of Chicago Press, 2000; 257-62. [3] Jones JH, Manson DK. Dental manifestation of systemic disease. J. Oral Manif. Sys. Dis. 1998; 19; 3-24. [4] Meon R. in primary dentition: case report. Singapore Dent J 1999; 15: 32-4. [5] Gupta SK, Saxena P, Jain S, et al. Prevalence and distribution of selected developmental dental anomalies in an Indian population. J. Oral Sci. 2011; 53: 231- 238. [6] Jelka J, Ilija S, Domagoj G, et al. The prevalence of oral and dental anomalies in children with developmental disturbance. Acta Stomat. Croat. 2002; 79-83. Tooth Abnormalities 359

[7] Lunardelli S E, Peres M A. Prevalence and distribution of developmental enamel defects in the primary dentition of pre-school children. Braz. Oral Res.2005; 19; 144-9. [8] Harris EF, Clark LL. Hypodontia. An epidemiologic study of American black and white people. Am. J. Orthod. Dentofacial. Orthop. 2008; 134: 761-7. [9] Hall RK, The prevalence of developmental defects of (DDE) in a pediatric hospital department of dentistry ovulation (part 1). Adv. Dent. Res. 2001; 3: 114-9. [10] Pedreira EN, Gallotini MC, Cardoso CA. Radiographic study dental anomalies in Brazilian patients with neuropsychomotor disorders. J. Appl. Oral Sci. 2007; 15: 524-8. [11] Esenlik E, Sayin M.O, OnurAtilla A. Supernumerary teeth in Turkish population. Am. J. Orthod. Dentofacial. Orthop. 2009; 136: 848-52. [12] Sisman Y, Uysal T, Gelgor IE. Hypodontia. Does the prevalence and distribution pattern differ in orthodontic patients? Eur. J. Dent. 2007;1: 167 -73. [13] Peker I, Kaya E, Darendeliler-Yaman S. Clinic and radiographical evaluation of non- syndromichypodontia and hyperdontiain permanent dentition. Med. Oral Patol. Oral Cir.Bucal. 2009; 14:e393-7. [14] Fardi A, Kondylidou-Sidira A, Bachour Z, et al. Incidence of impacted and supernumerary teeth-a radiographic study in a North Greek population. Med. Oral Patol. Oral Cir.Bucal. 2011; 16:e56-61. [15] Hölttä P, Alaluusua S, Saarinen-pihkala UM, Peltola J, Hovi L. Agenesis and microdontia of permanent teeth as late adverse effects after stem cell transplantation in young children. Cancer 2005; 103:181-90. [16] White Sc, Pharoah Mj. Oral radiology principles and interpretation. Missouri: Mosby/Elsevier, 2009; 282-293. [17] Celikoglu M, Miloglu O, Oztek O. Investigation of tooth transposition in a non- syndromic Turkish anatolian population: Characteristic features and associated dental anomalies. Med. Oral Patol. Oral Cir.Bucal. 2010; 15:716-20. [18] Ely NJ, Sherriff M, Cobourne MT. Dental transposition as a disorder of genetic origin. Eur. J.Orthod.2006; 28:145-51. [19] Tewari N, Pandey R K. Bilateral fusion in primary mandibular teeth: A report of two cases. J. Indian Soc.Pedod. Prev. Dent. 2011; 29:50-2. [20] Taheri J B, Baharvand M, Vahidi-GhahrodiA R. Unilateral fusion of a mandibular third molar to a super-numerary tooth. J. Dent. Tehran. Univ. Med. Sci. 2005; 2: 33-35. [21] Shokri A, Baharvand M, MortazaviH.The largest bilateral germination of permanent maxillary central incisors: report of a case. J.Clin. Exp. Dent. 2013; 5: 295-7. [22] Malcić A, Jukić S, BrzovićV, et al. Prevalence of root dilacerations in adult dental patients in Croatia. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 2006; 102: 104-9. [23] Chohayeb AA. Dilaceration of permanent upper lateral incisors: frequency, direction, and endodontic treatment implications. Oral Surg. Oral Med. Oral Pathol. 1983; 55: 519-20. [24] Sawamura T, Minowa K, Nakamura M. Impacted teeth in the maxilla: usefulness of 3D Dental-CT for preoperative evaluation. Eur. J.Radiol. 2003; 47:221-6. [25] Stecker S, DiAngelis AJ. Dens evaginatus: a diagnostic and treatment challenge. J. Am. Dent. Assoc.2002; 133: 190-3. [26] Zengin AZ, Sumer AP, Celenk P. Double dens invaginatus: report of three cases. Eur. J. Dent. 2009; 3: 67-70. 360 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

[27] Bhandari S,Pannu k. Dentinogenesis imperfecta: a review and case report of a family over four generations. Indian J. Dent. Res. 2008; 19: 357-61. [28] Crawford PJ, Aldred M, Bloch-Zupan A. Amelogenesis imperfecta. Orphanet. J. Rare Dis 2007; 2: 17. [29] Marie A, Collins, Sally M. Dental anomalies associated with amelogenesis imperfecta. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 1999; 88: 358-64. [30] Cho SY, Ki Y, Chu V, Chan J. Impaction of permanent mandibular second molar in Ethnik Chinese school children. J. Can. Dent. Assoc. 2008; 74: 521. [31] Haghanifar S, Emamverdizadeh P. Radiographic evaluation of impacted teeth prevalence Dental faculty of Babol 2004-2006. Journal of Gasr-e-Baran 2009; 1: 14- 17. [32] Suprabha BS, PaiSM. Ankylosis of primary molar along with congenitally missing first permanent molar. J. Indian Soc. Pedod. Prev. Dent. 2006; 24: S35-7. [33] Bertl MH, Weinberger T, Schwarz K, et al. Resonance frequency analysis: a new diagnostic tool for dental ankylosis. Eur. J. Oral Sci. 2012; 120: 255-8. [34] Silvestrini Biavati A, Signori A, Castaldo A, et al. Incidence and distribution of deciduous molar ankylosis, a longitudinal study. Eur. J. Paediatr. Dent. 2011; 12: 175-8. [35] Loriato LB, Machado AW, Souki BQ, Pereira TJ. Late diagnosis of dentoalveolar ankylosis: impact on effectiveness and efficiency of orthodontic treatment.Am. J. Orthod. Dentofacial. Orthop. 2009; 135:799-808. [36] Fernandes M, de Ataide I, Wagle R. part I - pathogenesis and case series of internal resorption. J. Conserv. Dent. 2013; 16: 4-8. [37] Mohammadi Z, Yazdizadeh M, Shalavi S. Non-surgical repair of internal resorption with MTA: a case report. Iran Endod. J. 2012; 7: 211-4. [38] Nunes E, Silveira FF, Soares JA, et al. Treatment of perforating internal root resorption with MTA: a case report. J. Oral Sci. 2012; 54: 127-31. [39] Shokri A, Mortazavi H, Salemi F, et al. Diagnosis of simulated external root resorption using conventional intraoral film radiography, CCD, PSP, and CBCT: A comparison study. Biomed. J. 2013; 36: 18-22. [40] Utneja S, Garg G, Arora S, et al. Nonsurgical endodontic retreatment of advanced inflammatory external root resorption using mineral trioxide aggregate obturation.Case Rep. Dent. 2012; 2012: 624792. [41] Jensen JL, Solheim T, Koppang HS, et al. Aggressive external root resorption of the entire dentition accompanied by osteolysis: a case report. Int. J. Prosthodont. 2012; 25: 459-64. [42] Shaban B, Mortazavi H, Shahvali E, Latifian B. Dental replantation. Journal of Army University of Medical Sciences of the I. R. Iran 2010; 8: 148-153. [43] Woodmansey K, Naidu A, Lerner L. Focal hypercementosis affecting a mandibular molar: a case report. Gen. Dent. 2011; 59: e196-9. [44] Schätzle M, Tanner SD, Bosshardt DD. Progressive, generalized, apical idiopathic root resorption and hypercementosis.J.Periodontol. 2005; 76: 2002-11. [45] Seed R, Nixon PP. Generalised hypercementosis: a case report. Prim. Dent. Care 2004; 11: 119-22. [46] Napier Souza L, Monteiro Lima Júnior S, Garcia Santos Pimenta F J, et al. Atypical hypercementosis versus cementoblastoma. Dentomaxillofac. Radiol. 2004; 33: 267-70. Tooth Abnormalities 361

[47] Nanjannawar GS, Vagarali H, Nanjannawar LG, et al. Pulp stone--an endodontic challenge: successful retrieval of exceptionally long pulp stones measuring 14 and 9.5 mm from the palatal roots of maxillary molars. J. Contemp. Dent. Pract. 2012; 13: 719- 22. [48] Marwaha M, Chopra R, Chaudhuri P, et al. Multiple pulp stones in primary and developing permanent dentition: a report of 4 cases. Case Rep. Dent. 2012; 2012:408045. [49] Çolak H, Çelebi AA, Hamidi MM, et al. Assessment of the prevalence of pulp stones in a sample of Turkish Central Anatolian population. Scientific World Journal. 2012; 2012: 804278. [50] Farges JC, Joffre A, Magloire H. Response of odontoblastic and pulpal cells to carious lesions. C. R.Seances Soc. Biol. Fil. 1993; 187: 582-95. [51] Massler M. Pulpal reactions to dental caries.Int. Den.t J.1967; 17: 441-60. [52] Jung S, Minoux M, Manière MC, et al. Previously undescribed pulpal and periodontal ligament calcifications in systemic sclerosis: a case report.Oral Surg. Oral Med. Oral Pathol. Oral Radiol. 2013; 115: e47-51. [53] Meyer-Lueckel H, Bitter K, Shirkhani B, et al. Prevalence of caries and fluorosis in adolescents in Iran. Quintessence Int. 2007; 38: 459-65. [54] Ramezani GH, Valaei N, Eikani H. Prevalence of DMFT and fluorosis in the students of Dayer city (Iran). J. Indian Soc.Pedod. Prev. Dent. 2004; 22: 49-53. [55] Imandel K, Khodabandeh A, Mesghaly A, et al. Epidemiology of fluorosis in the Borazjan area of Iran. I. Fluoride content in drinking water. Southeast Asian J. Trop. Med. Public Health. 1977; 8: 87-8. [56] Taheri J B, Baharvand M, Gholami-Koohestani M. Evaluation of students’ oral health status in Rezvanshahr, Iran in 2001. The Journal of Islamic Dental Association of IRAN (JIDA) 2003; 15: 59-67. [57] Yadav S. A Study on prevalence of dental attrition and its relation to factors of age, gender and to the signs of TMJ dysfunction. J. Indian Prosthodont. Soc. 2011; 11: 98- 105. [58] Mortazavi H, Javadzadeh A, Delavarian Z, Zare-Mahmoodabadi R. Myofascial Pain Dysfunction Syndrome (MPDS). Iran J.Otorhinol.2010; 22: 131-36. [59] Mortazavi H, Latifian, B. A review in myofascial pain dysfunction syndrome and its prominence in military personnel. HBI Journals. 2009; 7: 137-142. [60] Javadzade Bolouri A, Delavarian Z, Mortazavi H, et al. The effect of combination therapy with fluoxetine and clonazepam in myofacial pain dysfunction syndrome. Aust. J. Basic & Appl. Sci. 2011; 5: 520-525. [61] Van'tSpijker A, Rodriguez J M, Kreulen C M, et al. Prevalence of tooth wear in adults. Int. J. Prosthodont. 2009; 22: 35-42. [62] Hara AT, Lippert F, Zero DT. Interplay between experimental dental pellicles and Stannous-Containing toothpaste on dental erosion-abrasion. Caries Res. 2013; 47: 325- 329. [63] McCarthy R. Dental erosion--current perspectives for general practice. J. Ir. Dent. Assoc. 2012; 58: 241-4. [64] Moimaz S, Araújo P, Chiba F, et al. Prevalence of deciduous tooth erosion in childhood. Int. J. Dent.Hyg. 2013; 11: 226-30. 362 Abbas Shokri, Hamed Mortazavi, Maryam Baharvand et al.

[65] Huew R, Waterhouse PJ, Moynihan PJ, et al. Dental erosion among 12 year-old Libyan schoolchildren. Community Dent. Health 2012; 29: 279-83. [66] Buczkowska-Radlińska J, Łagocka R, Kaczmarek W, et al. Prevalence of dental erosion in adolescent competitive swimmers exposed to gas-chlorinated swimming pool water. Clin. Oral Investig.2013; 17: 579-83. [67] Putkonent T. Dental changes in congenital syphilis. Relationship to other syphilitic stigmata. Acta. Derm. Venereol. 1962; 42: 44-62. [68] Putkonent T, Niranen E. Congenital syphilitic molars in the light of measurement results. Arch. Klin. Exp. Dermatol. 1961; 212: 495-505. [69] Weerheijm KL. Molar incisor hypomineralisation (MIH). Eur. J. Paediatr. Dent. 2003; 4: 114-20. [70] Ivanović M, Zivojinović V, Sindolić M, et al. Molar incisor hypomineralisation in the first permanent teeth. Srp. Arh. Celok. Lek. 2007; 135: 472-7. [71] Cho SY, Ki Y, Chu V. Molar incisor hypomineralization in Hong Kong Chinese children. Int. J. Paediatr. Dent. 2008; 18: 348-52.