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Spectrum of Dentin Dysplasia in a Family

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Spectrum of Dentin Dysplasia in a Family CASE REPORT Spectrumof dentin dysplasia in a family: case report and literature review W. Kim Seow, BDS, MDSc, DDSc, PhD Stephen Shusterman, DMD Abstract The dentin dysplasias (DD),which maybe classified as type I (DD1)or type 2 (DD2),form a group of rare, inherited abnormalitiesthat are clinically distinct fromdentinogenesis imperfecta. Studies of affected families mayhelp to distinguish different types of DDand provide further insight into their etiology and clinical management.This report describes a family that showed characteristic dental features of DD1, including clinically normalcrowns in both primaryand permanentdentitions, and mobileteeth that maybe associated with prematureexfoliation. Radiographicfeatures included calcification of the pulp with crescent-shaped, radiolucent pulp remnants, short, tapering, taurodontic roots, and manyperiapical pathoses that maybe q¢sts or granulomas.A spectrumof dentin dysplasia wasnoted within the family. Strategies to prevent pulp and periapical infections and early exfoliation of the teeth include meticulousoral hygieneand effective caries-preventivemeasures. ( P ed iatr Dent16:437-42,1994) Introduction and literature review Histologically, in DD1, most of the coronal and Dentin dysplasias (DD) form a group of rare dentin mantle dentin of the root is usually reported to be abnormalities that are clinically distinct from normal, and the dentin defect is confined mainly to the dentinogenesis imperfecta. 1-3 Since its recognition in root2, s, 10 The dysplastic dentin has been reported to 19203 as "rootless teeth" and as "dentin dysplasia" by consist of numerous denticles, containing whorls of Rushton in 1933,4 the clinical features of DDhave been osteodentin that block the normal course of the den- tinal tubules,s, 10,11 well described. However, to date, relatively little is 12 knownabout the pathogenesis of the dentin defects, or A recent suggestion to subclassify DD1into four their pathological and clinical implications. As over- subdivisions based on the radiographic appearance of lapping pathological features may be present in the the pulp chambersis not likely to be clinically feasible various types of DD, studies of affected families may due to the simultaneous presence of all varieties of the help to delineate different types and provide further pulp chambers in any particular patient. Simpler sub- 13 insight into the etiology and clinical managementof classifications into either mild or severe maybe more these conditions. clinically relevant. Classificationof dentindysplasias Dentindysplasia, type II (DD2) Generally, two main classes of DD are recognized The clinical features of DD2contrast sharply with based on clinical and radiographic appearance. Shields those of DD1, and consist classically of: primary teeth et al. 2 proposed the classifications -- type I, or "dentin that have a bluish or amber discoloration, and perma- dysplasia," and type II or "anomalous dysplasia of nent teeth that appear normal;14-17 and primary teeth dentin." Witkop1 later described type I as "radicular that show total pulp obliteration, and permanent teeth dentin dysplasia" and type II as "coronal dentin dys- that show thistle-tube pulp configuration and pulp plasia" to indicate the parts of the teeth that are prima- stones14-17 in pulp chambers. rily involved. A third type of dentin dysplasia, DD3or Histologically, the affected teeth in DD2typically focal odontoblastic dysplasia, also has been proposed.S show a thin layer of normal coronal dentin and a sud- den transition to dysplastic dentin, which is sclerotic Dentindysplasia, type I (DD1) and2,3, amorphous17 with few tubules. The classical features in DD1, which have been well documented by several case reports, 3-9 are: 1) normal- Modeof inheritance appearing clinical crowns in both dentitions; 2) short, In both types of DD, the modeof inheritance is auto- conical, or absent roots that may lead to mobility and somal dominanto1, a However, there is no information early exfoliation of the teeth; 3) total obliteration of the regarding the gene defects in any type of DD. pulps except for thin, crescent-shaped pulpal remnants parallel to the cementoenamel junctions; and 4) Etiology periapical radiolucent areas, which may be granulo- The etiology of DD1remains speculative. Logan et mas or cysts associated with noncarious teeth. al. is suggested that abnormalcalcification of the pulp is Pediatric Dentistry: November/December1994 - Volume 16, Number 6 437 related to degeneration of the dental papilla, whereas Differential diagnosis Sauk and coworkers 1° postulated that premature in- Differential diagnosis of DDfrom dentinogenesis vagination of the epithelial root sheath is associated imperfecta (DI) is important, since there are several with abnormal dentin deposition. An alternative hy- overlapping features in these conditions (Table 1). pothesis8 that has received greater attention is that the DI, the mode of inheritance is also autosomal domi- primary defect in DD1resides in the ectomesenchymally nant.a0, 21 However,in DI, there is amber-gray opales- derived odontoblasts, and that the abnormal root mor- cence associated with marked attrition of both denti- phology is secondary to abnormal odontoblastic func- tions, 2°-21 whereas in DD2,the discoloration and attrition tion or differentiation. Supporting this hypothesis is a are limited to only the primary dentition, and in DD1, further suggestion that as the early formed mantle den- the teeth are clinically normal. Radiographically, DI tin is normal, and the later-formed dentin is abnormal, presents with bulbous crowns and short roots,2°-2~ the defect may be related to defective interaction of whereas DD1 shows taurodontism, and DD2 usually odontoblasts9 with the ameloblastic layer2 shows normal crown and root outlines. In addition, As is the case with DD1, the etiology of the dentin while all three entities show pulp obliteration, only defects in DD2is enigmatic. As in DD1, the change to DD2shows typical thistle-shaped pulp chambers. the formation of abnormal dentin after a period of nor- In addition to local primary defects of dentin, a few mal dentin formation suggests a genetically based de- generalized, systemic conditions may show extensive fect of an enzymesystem involved in the normal induc- obliteration of the pulp resembling the dental defects tion of odontoblast function. of DD. These generalized conditions include tumoral 22 Table. Characteristic features of dentin dysplasia and dentinogenesis imperfecta calcinosis, which shows extensive calcification of Dentin Dysplasia Dentinogenesis joints and the pulps of the (DD) Imperfecta(DI) teeth, as well as the brachio- skeletogenital23 syndrome, Type I (DD1) Type 2 (DD2) which shows mental retar- Inheritance AD AD AD dation, abnormal ribs, bone sclerosis, and hypospadias. Clinical In addition, a possibly new Appearance Prim. & perm. Prim. teeth - discolored" Prim. & perm. syndrome of dentinal dys- teeth - normal Perm. teeth - normal teeth discolored° plasia occurring with gen- Mobility ++ - eral bone sclerosis also had been24 described. Attrition - + (Prim. teeth) ++ Radiographic Case report Bulbous crowns - ++ Proband Short roots ++ + Medical and dental Taurodontism ++ histories Periapical The proband was an 8- radiolucencies ++ + + year-old male who was re- ferred by his general den- Pulp obliteration ++ ++ ++ tist for further dental Pulp remnants Horizontal Thistle-shaped Minimal pulp management, his father line at CEJ pulp chambers remaining having been previously di- Histologic agnosed with dentin dys- Mantle dentin Normal Normal Normal plasia. The medical history was noncontributory. In Coronal dentin Irregular tubules, Prim. teeth - irregular Mainly atubular particular, there was no his- whorls of tubules dentin, laminations, tory of bone disease or un- osteodentin Perm. teeth - normal somedenticles. usual bone fractures. He Root dentin True denticles, was the product of a full- excessive dentin term, uncomplicated preg- remodelling nancy, birthweight 7 lbs. His dental history re- ¯ The discolored teeth in both cases usually appearopalescent and amberor gray. vealed that eruption of the AD= autosomal dominant. primary dentition was un- 438 Pediatric Dentistry: November/December1994 - Volume 16, Number6 Figs 1, 2.Buccal views of the left (left) and right (right) posterior teeth showing the loss of periodontal attachment of the mandibular second molars, and the buccal crossbites of the maxillary primary canines. remarkable in timing and sequence. Mobil- ity of the teeth had been noticed by the par- ents. There was no history of dental infec- tion, and no restorations had been placed. General examination General examination revealed a healthy, intelligent 8-year-old of normal height (48 in.), and weight (65 lbs). His face was nor- mal, orthognathic, and symmetrical with Class 1 profile. Dental examination The patient had an early mixed denti- tion with all first permanent molars and mandibular central incisors partially erupted. The crowns of the primary teeth and erupting permanent teeth had normal shape and color, except that the cervical thirds appeared opaque. Mobility of the teeth was severe for all second primary Fig 3. Panoramic radiograph of proband showing calcification and obliteration molars and incisors, moderate in the first of all the dental pulps including those of the developing teeth. Note horizontal primary molars, and minimal in the pri- radiolucent lines approximately parallel to the cementoenamel junctions and
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