Secondary Logo

Journal Logo

Educational Supplement

Dental Topics for Plastic Surgeons, Part Two: Abnormal Tooth Development, Conditions, and Treatment

Zajac, Jocelyn C. MD; Mantilla-Rivas, Esperanza MD; Manrique, Monica MD; Aivaz, Marudeen BS; Ramirez-Suarez, Karen I. MD; Wang, Raymond DDS; Oh, Albert K. MD; Tate, Anupama R. DMD, MPH; Rogers, Gary F. MD, JD

Author Information
doi: 10.1097/SCS.0000000000006598
  • Open


A basic dental knowledge is fundamental for several key areas of plastic surgery practice including cleft, craniofacial, orthognathic, and maxillofacial trauma. Nevertheless, there are few resources in the plastic surgery literature that provide a comprehensive review of these topics. The following review article is one of a series of articles designed to provide an overview of general dentistry and common dental abnormalities that may be encountered by practicing plastic surgeons. This section, Part II, covers abnormal dental development and related conditions that can affect the size, shape, number, or position of both the primary and permanent dentition.


Agenesis of the teeth is termed hypodontia if less than 6 teeth are missing, oligodontia if there are greater than 6 teeth absent (Fig. 1), or anodontia if there is a complete lack of primary, permanent, or both dentitions.1 Hypodontia is rare, occurring in 0.1% to 0.9% of individuals with deciduous dentition and in 3.5% to 6.5% of those with permanent dentition. In children, missing teeth most commonly occur in the maxilla, with the lateral incisor being most commonly affected; 30% to 50% of children with hypodontia of the primary dentition will have missing successor teeth in the permanent dentition because the permanent tooth bud originates from the primary tooth bud.1 This occurs more frequently in children with cleft lip and palate.1,2 In the adults, the most commonly missing teeth are the third molars followed by mandibular second premolars, the maxillary lateral incisor, maxillary second premolar, and mandibular central incisors.1 Up to 85% of subjects with hypodontia can develop lingual displacement of the canines.

Oligodontia with 6 missing teeth.

The etiology of tooth agenesis is often unclear, but it can be also associated with single gene mutations, various ectodermal syndromes (ie, Ectodermal dysplasia, odonto-onycho-dermal dysplasia), and multiple other conditions including trisomy 21 (Down syndrome), and clefts of the lip and palate.1,3 Children with anterior conical teeth, hypodontia of primary and permanent teeth, anomalies in hair, nails and skin may raise concern of ectodermal dysplasia. These patients should undergo further evaluation, and treatment.1 Treatment of tooth agenesis requires a multidisciplinary team of dentists, orthodontists, prosthodontists, and surgeons. When only a few teeth are absent the options are to open, maintain, or close the space using orthodontic appliance.1 In patients with oligodontia or anodontia, partial dentures can be constructed at an early age (2–3 years old) which may improve eating, speaking, mastication, and nutrition in these patients.1 After skeletal maturity, dental implants are possible, although a deficiency of alveolar bone in certain conditions (Fig. 2) (eg, ectodermal dysplasia) may limit this alternative.3,4

Clinical presentation of tooth agenesis in a patient with ectodermal dyplasia and characteristic “knife edge” ridge of alveolus.


Hyperdontia is defined as the development of extra, or supernumerary, teeth (Figs. 3 and 4). In Caucasians, this occurs in 0.2% to 0.8% of primary dentition and 1.5% to 3% of the permanent dentition.3 Children with supernumerary primary teeth have a 30% to 50% chance of developing a supernumerary permanent tooth in the same position. Supernumerary teeth are classified as supplemental if they are of normal size and shape (Fig. 3), or rudimentary if they have abnormal shape and diminutive. Rudimentary teeth are further described as conical (peg shaped) (Figs. 4 and 5), tuberculate (barrel-shaped anteriorly with more than one cusp), and molariform (premolar or molar-like appearance) (Fig. 6).3 Supernumerary teeth are more common in males than females, and in the maxilla compared to the mandible. If the extra tooth is located in the midline anterior maxilla, or immediately adjacent to it, it is referred to as a mesiodens. If located adjacent or distal to the normal sequence of molars, the tooth is referred to as paramolars or distomolars, respectively. Supernumerary teeth may fail to erupt and delay or prevent eruption of the permanent tooth4 and they can localized dental crowding.3

Palatal supernumerary tooth.
Mesiodens peg-shaped rudimentary supernumerary teeth 8 and 9.
Lateral peg-shaped supernumerary tooth.
Paramolars supernumerary teeth.

Supernumerary teeth can be associated with dental invagination (described below) cleft palate, and a variety of genetic conditions such as cleidocranial dysplasia (Fig. 7), oral-facial-digital syndrome type 1, and Gardner syndrome.4A single supernumerary tooth may be an odontoma, an abnormal proliferation of enamel organ cells.3 Treatment is based on the location of the supernumerary teeth and the associated symptoms. While extraction is often required, some supernumerary teeth may be left in situ if the location does not alter the normal permanent dentition and the patient is asymptomatic.4

Cleidocranial dysplasia with multiple supernumerary teeth.


Some variation in tooth size is normal, and crown size generally correlates with root size (ie, teeth with large crowns often have large, broad roots).4,5 Macrodontia refers to teeth that are physically larger than normal3 (Fig. 8) and can be associated with hyperdontia. It is seen more commonly in males, often occurs bilaterally, and is present in 1% of permanent dentition. The most commonly affected teeth are the permanent maxillary central incisors followed by the mandibular second premolars. Diffuse macrodontia has been associated with pituitary gigantism, unilateral facial hyperplasia, otodental syndrome, Klinefelter syndrome, hyperinsulinism, and hereditary gingival fibromatosis.1 Treatment of this condition depends on the underlying mechanism but includes acceptance, tooth remodeling, and tooth extraction with subsequent masking of the space with a denture, implant or bridge.1

Macrodontia of the left maxillary central incisor.

Microdontia is often associated with hypodontia and is more common in females. It is observed in 0.2% to 0.5% of patients with deciduous teeth, and is present in permanent dentition as either a single tooth (2.5%) or generalized (0.2%) form. The most commonly affected tooth is the maxillary lateral incisor, and it usually presents with a peg-shaped or conical crown (Fig. 5). Microdontia is seen in many of the hypodontia syndromes described previously and treatment options include adding composite material to reproduce the contours of a normal size crown, or porcelain veneers.4

Root length varies with race; individuals of African origin tend to have larger roots, while those of Asian origin tend to have smaller roots. Large root size is more common in males than females, and is most commonly seen in the permanent maxillary central incisors. Long root lengths are potentially at higher risk for damage during a LeFort I osteotomy.6 Short roots are most commonly seen in the permanent maxillary central incisors, and are associated with a variety of dental abnormalities. Short roots may also be seen in regional odontodysplasia, in which there is abnormal root formation, and following jaw irradiation or chemotherapy, which can disturb normal dental development.4,5


Abnormalities of tooth form have many different etiologies including erroneous developmental processes, and have multiple presentations such as fused teeth, accessory cusps, invaginated teeth, evaginated teeth, and taurodontism (Figs. 9–18).1 Conjoined teeth, also known as double teeth, fused teeth, or connate teeth, are 2 separate teeth that have been united through their dentin and sometimes pulps. They occur as a result of fusion (union of adjacent primary or permanent tooth germs through their dentine) (Figs. 9 and 10), gemination (process of separating a single tooth germ to produce 2 separate teeth) (Fig. 11), or concrescence (union of 2 teeth through the cementum without dentinal involvement) (Figs. 12 and 13).3 Concrescence, or union of 2 teeth via their cementum, may be a result of developmental or postinflammatory processes.3 It is important to determine which process is responsible for the presentation as this will determine treatment.1

A-B. Tooth fusion.
Fused teeth with decay at the interface of the 2 segments.
A-B. Tooth gemination.
Concrescence of teeth.
(A) Clinical and (B) radiographic evidence of fused mandibular premolars.
Carabelli cusps.
Talon cusp lateral incisor and dens evaginatus.
Invaginated teeth with tooth decay.
Radiograph finding of taurodism.
Enamel hypoplasia.

Conjoined teeth are present in 0.5% to 2.5% of the primary dentition, 0.3% to 0.5% in the permanent dentition, and males and females are affected equally. Radiographs will show fused crowns and/or roots, and pulp intercommunication is possible (Fig. 13B). Fusion has a familial component and is usually limited to anterior and mandibular regions. The presence of a single maxillary central incisor may appear isolated, secondary to fusion, or as part of Solitary Median Maxillary Central Incisor (SMMCI) syndrome, a condition present in 79% of patients with holoprosencephaly.1,7 Gemination occurs more commonly in the maxilla and permanent dentition. Radiographs may show a wide grown with a bifid crown on a single root. Concrescence most frequently presents in the posterior and maxillary teeth.3 The interface between the 2 segments is susceptible to the formation of dental caries (Fig. 10) and filling in the defect can prevent this problem. For conjoined teeth in the permanent dentition, the exact presentation and associated symptoms will determine treatment, which may include retaining, extracting, or surgically dividing such teeth.1 Obtaining a cone beam CT is sometimes necessary to determine treatment options when standard radiographs are insufficient.3

Abnormal development can also result in accessory or extra cusps. These may occur in both the primary and permanent dentition, and the most commonly affected teeth are the molars. Accessory cusps are most often seen on the mesiolingual surface of the permanent maxillary first molars (Carabelli cusp) (Fig. 14).8 This can also be located at the palatal surface of an anterior tooth (Talon cusp) (Fig. 15).9 Accessory cusps may obscure occlusion and look aesthetically displeasing. Teeth affected by accessory cusps are also predisposed to formation of dental caries along the interface between the cusp and palatal surface of the rest of the tooth. Treatment options include targeted grinding over a series of sessions, which will decrease the cusp height and allow for secondary dentine formation, as well as sectioning of the cusp with pulpotomy in a single visit.8,9

An invaginated tooth, or dens invaginatus, refers the phenomenon of a tooth within a tooth such that there is a lingual infolding in the crown or root of the tooth lined with enamel. This results from invagination of the enamel epithelium into the dental papilla during development (Fig. 16A).4 Invaginated teeth are rare in the primary dentition, but occur in up to 0.4% to 10% of individuals’ permanent dentition.3 They are more common in males than females, and are often bilateral. The most commonly affected tooth is the maxillary lateral incisor, followed by the maxillary central incisor and canine. This condition can lead to dental caries and pupal pathology, with sequelae including acute abscess and facial cellulitis.3 Full radiographic examination is recommended in all patients with an invaginated tooth and treatment option include sealants to prevent development of caries, endodontic treatment, or extraction.4

Evaginated teeth, or dens evaginatus, refer to teeth with outpouchings of enamel (Fig. 15), and are ascribed to abnormal evagination of the enamel epithelial and dental papilla during development.1 This phenomenon most commonly occurs in the mandibular premolars of individuals of Mongolian descent,4 and presents as a small tubercle on the occlusal surface of the tooth along the central groove or lingual ridge of the buccal cusp.9 Over time, dens evaginations tend to be fractured off or worn down, leading to pupal exposure with subsequent pathology, and periapical abscess, it may interfere with tooth eruption.8 Options for management include resin placement to smooth the surface of the evagination, excision of the tubercle followed by pulp capping, and conventional endodontic treatment. Repeated grinding of the tubercle is not recommended as it may lead to infection.10

Taurodontism, refers to the vertical enlargement of the pulp chambers that occurs at the expense of the roots (Fig. 17). It most commonly manifests in the permanent dentition and results from abnormal or failed invagination of Hertwig's root sheath, which determines root formation during development. Taurodontism is associated with multiple conditions including amelogenesis imperfecta, tricho-dento-osseous syndrome, ectodermal dysplasias, and chromosome X aneuploidy. Endodontic treatment is the main management strategy.1,3,4


Development of appropriate tooth structure is a dynamic process that can be influenced by genetic or external insults such as trauma, ionizing radiation, osteomyelitis, and chemotherapy. Acquired abnormalities in tooth structure depend upon the stage of development occurring at the time of the insult. The injury may affect multiple dental tissues, the enamel, the dentine, or a combination of the above.4,5 For example, procedures such as givoperiosteoplasty, performed in some cleft centers during primary palatoplasty to promote bony union in an alveolar cleft, can result in injury to dental structures as a result of trauma to deciduous tooth follicles during flap dissection, or injury to subsequent tooth buds from inadvertent fractures of the alveolar bone.11

Structural abnormalities that affect all tissues include arrested development of tooth germ and regional odontodysplasia. Arrested development of the tooth germ following an external insult may affect the tooth at any stage of development- roots, enamel, and/or dentine. When a permanent tooth-germ is affected by infection from an adjacent primary tooth or tooth-germ it is call a Turner tooth, and typically manifests with enamel hypoplasia and/or hypomineralization (Fig. 18). This most commonly occurs in the mandibular premolars.4


Any genetic or environmental factor that interferes with normal enamel matrix formation can lead to enamel surface defects or irregularities. Enamel formation, or amelogenesis, is a multi-step process wherein the enamel matrix is secreted by ameloblasts, the matrix calcifies and partially mineralizes, and then grows as mineral is added while water and proteins are removed.5 Enamel hypoplasia occurs when the enamel matrix is thinner than normal. In hypoplasia, the enamel will appear uniformly thin, grooved or pitted (Fig. 18). Poor enamel mineralization (hypomineralization) often occurs in conjunction with dental hypoplasia, and under-mineralized enamel looks discolored, ranging from a mottled or slightly opaque appearance to a yellow-brown color. One congenital form of this is amelogenesis imperfecta, and the enamel defects affects most, if not all, of both the primary and permanent teeth (Fig. 19). It results from a single gene mutation, and may be autosomal dominant, autosomal recessive.1,3,4 A complete absence of enamel, termed aplasia, is rare and affected teeth will have a smooth dentine layer with a red-brown color.4

Amelogenesis imperfecta.

Systemic insults affect enamel development based on the timing of the exposure, and result in a horizontal band of enamel defect along the crown causing a groove in the tooth. These irregularities are referred to as chronologic hypoplasia. Chronologic enamel defects can result from in utero insults such as endocrine disturbances (hypoparathyroidism), infections (rubella), drugs (thalidomide, tetracycline), nutritional deficiencies, metabolic and hematological disorders, among other reasons.1 Any of these insults will result in an enamel defect of the incisal area of the primary incisor crowns. This abnormality pattern is also seen in pre-term, low birth weight infants. Systemic insults occurring in the neonatal or birthing period can result in enamel defects in the primary or permanent dentition. However, occasionally, the first permanent molars may be affected as they begin to develop during this time.4

Chronologic enamel defects also occur following acute or chronic childhood illnesses such as hypothyroidism, hypoparathyroidism, renal disease, malabsorptive gastrointestinal disorders (Celiac disease), lead poisoning, and exanthematous fevers (measles). Exposure to excessive amounts of fluoride during enamel development can lead to another chronologic defect called fluorosis, a dose-dependent process of enamel mottling resulting in opacity of the enamel with associated discoloration and pitting. This occurs because fluoride causes retention of the amelogenin proteins in the enamel. Finally, local factors including dental injuries, pressure on the premaxilla from an oro-tracheal tube, infection, trauma, and cleft lip or palate may cause defects in enamel.3,4


Similar to abnormalities in enamel, dentine defects may result from environmental or genetic causes. Environmental influences include local trauma, nutritional deficiencies, tetracyclines, and chemotherapeutic agents4 or genetic causes. Vitamin D-resistant rickets follows an X-linked inheritance pattern. Histological examination shows interglobular dentine. The phenotype includes characteristics such as short stature, bowed legs, and dental abscess in the absence of caries. Abscess formation results from pulp death following exposure of the pulp horns with attrition of the teeth.3,4

Regional odontodysplasia is a generalized developmental abnormality, resulting in deformed crowns with enamel and dentine changes, large pulp chambers, and open apices.4 These teeth are referred to as ‘ghost teeth’ based on their radiological appearance of thin enamel and dentin around an enlarged radiolucent pulp (Fig. 20).3 Dentinogenesis imperfecta, also known as hereditary opalescent dentin, is inherited in an autosomal dominant manner secondary to mutations in the DSPP gene on chromosome 4.1,9 It may also be associated osteogenesis imperfecta and Ehlers Danlos syndrome. It can affect both primary and permanent dentition, although the former is more commonly involved, and teeth are typically gray, red, or brown opalescent. Enamel may erode secondary to dentinal weakness causing exposure of the dentin. Crowns become worn down over time (Fig. 21 A–C). Pupal exposure and destruction occurs in the primary dentition, predisposing to abscess formation. Imaging reveals bulbous crowns, and roots that are smaller than normal.4

Regional odontodysplasia with evidence of thin enamel and dentin around an enlarged radiolucent pulp.
Dentinogenesis imperfecta, (A) left lateral, (B) maxillar and (C) mandibular view.

Management of dentinal defects focuses on prevention of tooth erosion, maintenance of tooth height, and improvement of dental appearance. As with enamel defects, treatment should be individualized based on presentation.4


Disturbances in tooth movement often indicate a local or systemic abnormality. Eruption is the process by which a tooth moves and becomes visible in the oral cavity. Exfoliation is the process by which primary teeth are shed and replaced by permanent teeth. The normal patterns of eruption and exfoliation, as described in the previous segment of this series, are extremely consistent. For example, based on the regular timing of their eruption, the permanent first molars are often referred to as 6-year molars.5 Premature tooth eruption is uncommon. It most often occurs in children with a high birth weight, or in those with precocious puberty or other endocrine conditions.4 Babies may be born with teeth already present, or may develop teeth within the first month of life. These are referred to as natal (Fig. 22) and neonatal teeth, respectively. The most common tooth to manifest this way is the mandibular central incisor.4 The exact mechanism underlying premature eruption has not been elucidated, but these teeth are often prematurely erupted deciduous dentition.3 Natal and neonatal teeth may be extracted if they prevent feeding or cause ulceration,4 but it is often recommended that they be retained if the patient is asymptomatic.3

Mandibular central incisors natal teeth.

Delayed tooth eruption is more common than premature eruption, and may arise from congenital, systemic or local factors. There is often an underlying etiology if an infant does not have teeth by age 1 year. Systemic insults causing delayed eruption of the permanent teeth are usually identified before the eruption of the first molars, which occurs in the sixth year of age.5 Down syndrome, Turner syndrome, prematurity and low birth weight can cause delayed tooth eruption. Supernumerary teeth present in cleidocranial dysplasia can lead to delayed or absent eruption of permanent teeth (Fig. 7). Another congenital condition leading to delayed eruption includes hereditary gingival fibromatosis because erupting teeth are unable to penetrate the thickened gingiva. Systemic conditions leading to delayed eruption include nutritional deficiencies, and endocrine disorders. Local factors contributing to delayed eruption include ectopic crypt position, trauma to the primary dentition, blocked eruption pathway, and crowding often due to the presence of odontomes or supernumerary teeth. Finally, early primary tooth extraction can lead to thickening of the overlying mucosa causing iatrogenic delayed eruption. Treatment for delayed eruption of teeth involves treating any underlying systemic conditions if possible, extracting retained primary teeth, as well as obstructive odontomes and supernumerary teeth, replacing teeth that fail to erupt with prosthetics, and utilizing orthodontic treatment to ensure appropriate occlusion.4 In patients with cleft lip and/or palate, alveolar cleft bone graft provides maxillary arch continuity, bone support for the teeth adjacent to the cleft, and an osseous foundation through which lateral incisor or canine teeth can erupt.1,2

Exfoliation is a dynamic process that has multiple contributing forces such as tooth resorption, and pressure from erupting teeth. Both premature and delayed exfoliation may occur. Premature exfoliation is defined as the exfoliation of teeth in the absence of trauma in children under 5 years old, and always warrants further investigation.3 Immunodeficiency is the most common cause of early exfoliation, but other causes include hypophosphatasia, cherubism, acrodynia, hypophosphatemia, cyclical neutropenia, severe congenital neutropenia, Chediak-Higashi syndrome, leukemia, and Langerhans cell histiocytosis.4 Hypophosphatasia is a rare genetic condition of bone and mineral metabolism and all forms of this disease present with early exfoliation of the deciduous and/or permanent dentition. Aplasia or severe hypoplasia of the cementum with or without impaired dentinogenesis results in structural anomalies of the primary teeth, most commonly the incisors.1 Cherubism is another rare genetic condition associated with early exfoliation, and is caused by mutations in the adapter protein SH3BP2 on chromosome 4. Cherubism in an autosomal dominant disease that characteristically involves symmetrically developing bony lesions of the maxilla and mandible, resulting in plump, cherub-like cheeks (Fig. 23 A). This condition usually stabilizes or regresses with age, but it can be fatal. Patients will present with symmetric jaw enlargement and early exfoliation of teeth secondary to loss of bone support. Imaging shows soap-bubble lesions, or multilocular areas of bony destruction, with thinning of the cortical plate (Fig. 23B-C). Histologically, there is proliferation of fibroblasts with multinucleated giant cells and scattered hemorrhage. Workup of familial fibrous dysplasia should include a complete skeletal survey.3,12 While premature exfoliation is often the result of a congenital or systemic condition, delayed exfoliation is seen in association with local factors, such as infraocclusion, fused primary teeth, ectopically developing permanent teeth, and trauma or severe infection of the primary teeth. Infraocclusion refers to teeth that do not achieve appropriate occlusion, or teeth that have remained relatively fixed in place while the adjacent teeth continued to erupt. These may also be referred to as submerged or ankylosed teeth (Fig. 24). One common example of infraocclusion results from the failure of premolar development leading to a lack of stimulus for primary molar reabsorption and exfoliation. Surrounding permanent teeth erupt and continue to grow, but the affected primary molar becomes fixed within the alveolar bone, and does not change position appropriately. As a result, the occlusal surfaces of the affected maxillary and mandibular teeth do not meet. Studies have shown that infraoccluded teeth will usually exfoliate within expected time limits, and recommend a more conservative approach to management of these teeth. If there is no permanent successor, the primary teeth may be retained with their crowns built up. Alternatively, if extraction is pursued, the space should be maintained with orthodontic therapy to prevent future crowding.3,4

A. Clinical presentation of patient with Cherubism and characteristic cherub-like cheeks. B-C. 3D reconstruction and coronal CT-view of patient with Cherubism.
Radiographic findings of a patient with ankylosed teeth.


Discoloration of the teeth often results from systemic insults or diseases affecting the shade, translucency, and thickness of the enamel. Discoloration may be extrinsic or intrinsic. Extrinsic stains result from accumulation of a pigment along the exterior of the tooth, and can usually be removed with a surface treatment. Alternatively, intrinsic staining results from deposition of exogenous pigment within the enamel or dentine (Fig. 25), and cannot be removed with surface treatments.3 Some of the most common causes of teeth discoloration include hyperbilirubinemia, porphyria, cystic fibrosis, and tetracycline exposure.1

Intrinsic staining of teeth secondary to liver disease.


1. Dean JA, Jones JE, Walker Vinson LQA. McDonald and Avery's Dentistry for the Child and Adolescent. 10th ed. Amsterdam, Netherlands: Elsevier; 2016.
2. Rogriguez ED, Losee JE, Neligan P. Plastic Surgery: Craniofacial, Head and Neck Surgery and Pediatric Plastic Surgery. Vol 3. 4th ed. Amsterdam, Netherlands: Elsevier; 2018
3. Neville BW, Damm DD, Allen CM, et al. Oral and Maxillofacial Pathology. Amsterdam, Netherlands: Elsevier; 2015
4. Nanci A, Ten Cate AR. Ten Cate's Oral Histology: Development, Structure, and Function. 6th ed. Maryland Heights, MO: Mosby; 2003
5. Welbury R, Duggal M, Hosey M. Paediatric Dentistry. 3rd ed. Oxford, UK: Oxford University Press; 2005.
6. Kahnberg KE, Engström H. Recovery of maxillary sinus and tooth sensibility after le Fort I osteotomy. Br J Oral Maxillofac Surg 1987; 25:68–73.
7. National Institutes of Health. Genetic and rare diseases information center: single upper central incisor. Available at: Accessed March 25, 2020
8. Saap JP, Eversole LR, Wysocki GP. Developmental disturbances of the oral region. In: Contemporary Oral and Maxillofacial Pathology. Amsterdam, Netherlands: Elsevier; 2004:1–44
9. Neville BW, Damm DD, Allen CM, et al. Pathology of teeth. In: Color Atlas of Oral and Maxillofacial Diseases. Amsterdam, Netherlands: Elsevier; 2019:41–78
10. Gaynor WN. Dens evaginatus--how does it present and how should it be managed? N Z Dent J 2002; 98:104–107.
11. Berkowitz S. Cleft Lip and Palate: Diagnosis and Management. Heidelberg, Germany: Springer Verlag; 2013
12. Argyris PP, Gopalakrishnan R, Hu Y, et al. Clinicopathologic and molecular characteristics of familial cherubism with associated odontogenic tumorous proliferations. Head Neck Pathol 2018; 12:136–144.

Abnormal tooth development; dentistry; maxillofacial; plastic surgery

Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of Mutaz B. Habal, MD.