Czytelnia Medyczna » Nowa Stomatologia » 3/2005 » Multidisciplinary treatment of a case of dentine dysplasia. A case report

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Joanna Politowska¹, Adam Okoń², Elżbieta Jodkowska²

Multidisciplinary treatment of a case of dentine dysplasia. A case report

Multidyscyplinarne leczenie przypadku rozpoznanej dysplazji zębiny

Zakład Stomatologii Zachowawczej IS AM w Warszawie
Kierownik Zakładu: dr hab. n. med. Elżbieta Jodkowska ¹Koło Naukowe przy w Zakładzie Stomatologii Zachowawczej IS AM w Warszawie ²Zakład Stomatologii Zachowawczej IS AM w Warszawie

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INTRODUCTION

A patient who presents with dentin dysplasia is always included in the high risk group of losing teeth when young. When such cases are diagnosed they require additional care from the dentist: the patient should be constantly monitored and offered consultations with doctors of many specialties such as maxillofacial surgeons, periodontists, orthodontists and prosthetists. It is true that almost every patient comes in contact specialities they represent in his life: for example, with conservative dentistry when he is edentate, with orthodontics as a youngster, and usually with prosthetics and periodontics in the later period of his life. There are also other situations like dental trauma or a complicated extraction requiring the assistance of a dental surgeon. The question is: must patients with dentine dysplasia be monitored from the earliest years of their lives?

Dentine dysplasia is a disorder of the structure of the hard tissue of the tooth affecting mostly dentine. It is hereditary condition. It is a heritable autosomally. It affects one patient in the population of one hundred thousand. The aetiology of this disease is yet unknown. The migration of the epithelium cells of Hertwig´s sheath to the tooth germ and inducing odontoblasts to differentiate and apposition dentine can be the cause. Lesions are seen in deciduous dentition, but can also be present in permanent dentition (1, 2, 3, 4, 5, 6). Such lesions affect the crown of the tooth, its roots or both. Attributes of dentine dysplasia include: (1) proper shape and size of the crown, poor mineralization of teeth, susceptibility to attrition and sometimes increased mobility. Radiographically, this disease is manifested by: lack of root canals, the presence of dentinoma, presence of periradicular pathology and thinning of the cementum of the root. Dentine dysplasia mostly is divided into two types (1, 2, 3, 6).

Type I – concerns changes in both deciduous teeth and permanent teeth that clinically have proper shape, color and hardness. Radiographically, milk teeth demonstrate total obliteration of pulp chambers and canals, permanent ones are characterized by crescent-like shape of obliterated chambers and the presence of periapical pathology in generally caries-free teeth (5, 7, 8, 9). According to Carroll et al. type I dentine dysplasia is divided according to the progression of dysplastic changes as seen on radiographic examination. The following subtypes were proposed: 1a, 1b, 1c, 1d (4, 5). DD1a – total pulpal obliteration and no root development; DD1b – with crescent-shaped remnants of the pulp chamber and minimal root development; DD1c with two crescent-shaped radiolucent lines and significant but incomplete root development; DD1d with radiographically visible pulp chambers, oval pulp stones and bulging roots

Type II – lesions in primary dentition and permanent dentition differ. Milk teeth have brownish or blue-brown discoloration, and are susceptible to attrition. Radiographically, obliteration of the pulp chamber of milk teeth is present. Permanent teeth have the right color and root length and obliterated pulp chamber in the shape of thistle with dentinoma in it.

In fibrous dysplasia lesions are present only in primary dentition, teeth have the right color and shape. Radiographically, there are radiolucent and radiopaque areas visible in the pulp chamber and in the canals. Histologically, the condition is far from perfect but neither the shortening of the roots nor the obliteration of the chambers in the shape of the crescent can be observed (4).

All the above mentioned characteristics of the dysplastic dentition lead to tooth loss when the patient is in his 30s, 40s. Clinically, tooth decay is manifested as foci of carious lesions penetrating the obliterated chamber. Additionally there is tooth mobility of degree I or II, especially of incisors due to short roots which hold the teeth in the alveolar bone, as well as periradicular pathology even without clinical signs of caries. The treatment of patients with diagnosed dentin dysplasia requires multidisciplinary approach.

CASE REPORT

A 21-year old female was referred by her family dentist to the Maxillo-Facial Surgery clinic in Warsaw with suspected cysts in the region of teeth 14, 15, 16. Medical history revealed that the patient had no health complaints.

Clinical examination revealed the following findings:

– Extra-orally: symmetrical face, no visible abnormalities of the maxilla and mandible. Exits of trigeminal nerve not tender. Submandibular and submental lymph nodes not enlarged.

Intra-orally: the mucous membrane of the vestibule, the buccae, the floor of the mouth, the tongue, the palate with no pathology.

An OPG of the patient was taken (Fig. 1). Carious lesions of teeth 15, 37 were noted, tooth 26 was missing (the patient reported that it had been extracted due to lack of conservative treatment). Tooth 28 fully erupted while teeth 18, 38, 48 not visible in the mouth. Second degree mobility of central and lateral incisors of the mandible was noted. The patient was also consulted orthodontically.

Figure 1. The OPG.

Basing on the interview, the clinical and radiographic examination as well as consultations with orthodontists the following was concluded.

The OPG (taken in November, 2004) displayed:

– periapical lesions of teeth 15, 16,

– deep caries penetrating the remnant of the pulp chamber in tooth 15,

– almost complete obliteration of pulp chambers in all teeth,

– lack of outlines of root canals in all teeth,

– shortening and deformity of all roots,

– reduction of periodontium in all teeth,

– unerupted third molars: 18, 38, 48.

In order to further diagnose periradicular changes occipitomentale radiographs aimed at lateral nasal sinuses and the computerized tomography were taken. These X-rays failed to confirm any inflammation or pathology in the mandibular sinuses. Additionally, a periapical radiograph of tooth 15 was taken to determine the progression of caries (Fig. 2). As a result of orthodontic consultation tongue dysfunction and pathological mobility of lower incisors were observed.

Figure 2. These X-rays failed to confirm any inflammation or pathology in the mandibular sinuses.

After consultations the following treatment plan was proposed to the patient:

Conservative treatment:

1. Conditional root canal treatment of tooth 15, consisting of the removal of carious dentine and pulpal debridement from the crescent-shaped remnant chamber.

2. Treatment of caries in tooth 37.

After removing carious dentine a small pulp chamber was exposed. It was not too high but relatively wide mesiodistally. The chamber walls had the appearance of demineralised deciduous dentine. The remnant pulp was extirpated and the pulp chamber was thoroughly cleansed. After several attempts to find the root canals failed, the chamber and coronal deficiencies were restored with composite material.

Surgical treatment consisted of the incision of the oral mucosa from tooth 13 to 17 under general anesthesia with nasal intubation. The incision was continued to the vestibule of the mouth. Mucoperiosteal flap was lifted. The atrophy of bone lamina was noted around tooth 15 in a 5mm area. A bur was used to widen access to the cyst in the maxilla. The cyst was completely removed and sent for the histopathological examination.

The bur was then used to section roots of teeth 14, 15, 16 (roots were about 2mm in length). Then an attempt was made to locate and root-fill teeth 14, 15, 16, however, these canals were missing. Due to atypical structure of the teeth, young age of the patient and no pathological mobility it was decided to save teeth 14, 15, 16. No fistula to the sinus was noted. The wound was closed with sutures. Post-operative care included review appointment 7 days after the procedure, the removal of the sutures and antibiotic therapy with Augmentin.

The histopathological examination revealed chronic inflammatory cyst, which was lined with stratified squamous epithelium.

After three months the bone healed with no tooth mobility. After six months the bone defect healed uneventfully (Fig. 3).

Figure 3. After six months the bone defect healed uneventfully.

Orthodontic treatment: Schwarc´s plate with tongue barrier was planned to improve tongue function which, in consequence, diminished loosening of the incisors. After three months there was significant improvement of the tongue function, and the reduction of lower incisors mobility was indeed observed.

CONCLUSIONS

Dentinal dysplasia is usually detected during routine radiographic examination or when patients present with tenderness associated with concomitant inflammation or periapical cyst. Frequently such teeth are extracted by dental surgeons due to unrecognized dentine dysplasia, inability to locate root canals or because permanent tooth was confused with a deciduous one.

Recommended treatment includes:

Endodontic treatment of the highest number of teeth before coronal and radicular pulpal obliteration takes place.

Prevention of pulpitis, inflammation of periapical tissues and cysts, which can save teeth from extraction.

Prevention of trauma.

Prosthetic treatment before and after tooth loss.

Oral hygiene as prevention of periodontal disease and protection of hard dental tissues from caries

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Piśmiennictwo

1. Witkop C.J. Jr.: Amelogenesis imperfecta, dentinogenesis imperfecta and dentin dysplasia revisited: problems in classification. J. Oral Pathol., 1989, 17, 6, 547-553. 2.Carroll M.K., Duncan W.K.: Dentin dysplasia type I. Radiologic and genetic perspectives in a six-generation family. : Oral Surg Oral Med Oral Pathol. 1994 Sep; 78(3) :375-81. 3.Winter G.B.: Anomalies of tooth formation and eruption. (w:) Pediatric Dentistry (red.) WelburyR.R. OxFord University Press, 1999, 271-273. 4. Carroll M.K.O., et al.: Dentin dysplasia: reviev of literature and a proposed subclassification based on radiographic findings. Oral. Surg. Oral. Med. Oral. Pathol., 1991, 72, 1,119-125. 5.Kaczmarek U., Fita K.: Dysplazja zębiny. Magazyn Stomat., 2004, XIV, 5, 57-61. 6.Shields E.D., et al.: A proposed classification for heritable human dentine defects with a description of new entity. Arch Oral Biol., 1983, 18, 6, 5543-553. 7.Hulisz-Seconska M., et al.: Dysplazja zębiny typ I. Opis przypadku. Czas. Stomat. 1999, LII, 1. 8.Kaczmarczyk-Stachowska A., i wsp.: Rzadki przypadek dysplazji zębiny typu I. Czas. Stomat. 2002, LV, 3. 9.Politowska J., Okoń A.: Dysplazja zębiny. Opis przypadku. Stomat. Współcz., 2005, 1: 30-32. 10.Coke J.M., et al.: Dentinal dysplasia, Type I. Report of a case with endodontic therapy. Oral. Surg. Oral. Med. Oral. Pathol., 1979 Sep; 48(3): 262-8. 11.Seow W.K., Shusterman S.: Spectrum of dentin dysplasia in a family: case report and literature review. Pediatr. Dent., 1994 Nov-Dec; 16(6) :437-42. 12.Kalk W.W., et al.: Dentin dysplasia type I: five cases within one family. Oral. Surg. Oral. Med. Oral. Pathol. Oral. Radiol. Endod., 1998 Aug; 86(2) :175-8. 13.Petrone J.A, Noble E.R.: Dentin dysplasia type I: a clinical report. J. Am. Dent. Assoc., 1981 Dec; 103(6) :891-3.

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