Chcesz wydać pracę habilitacyjną, doktorską czy monografię? Zrób to w Wydawnictwie Borgis – jednym z najbardziej uznanych w Polsce wydawców książek i czasopism medycznych. W ramach współpracy otrzymasz pełne wsparcie w przygotowaniu książki – przede wszystkim korektę, skład, projekt graficzny okładki oraz profesjonalny druk. Wydawnictwo zapewnia szybkie terminy publikacji oraz doskonałą atmosferę współpracy z wysoko wykwalifikowanymi redaktorami, korektorami i specjalistami od składu. Oferuje także tłumaczenia artykułów naukowych, skanowanie materiałów potrzebnych do wydania książki oraz kompletowanie dorobku naukowego.

© Borgis - Nowa Stomatologia 2/2016, s. 106-119 | DOI: 10.5604/14266911.1208249
*Dominika Szczepanek1, Katarzyna Emerich1, 2
Treatment methods for selected complications of dentin dysplasia type I – a report of five cases
Metody leczenia wybranych powikłań dysplazji zębiny typu I – opis pięciu przypadków
1Pediatric and Family Dental Clinic, University Dental Center, Medical University of Gdańsk
Head of Clinic: Professor Katarzyna Emerich, BDS, PhD, DSc
2Chair and Department of Paediatric Dentistry, Medical University of Gdańsk
Head of Chair and Department: Professor Katarzyna Emerich, BDS, PhD, DSc
Streszczenie
Dysplazja zębiny typu I jest chorobą genetyczną, dziedziczoną autosomalnie dominująco, występującą 1/100 000 urodzeń. Charakteryzuje się nieprawidłową morfologią koron oraz zmianami w budowie korzeni zębów: skróceniem, nieprawidłowym kształtem, częściowym lub całkowitym brakiem komór miazgi, obecnością torbieli oraz rozchwianiem zębów. Wiąże się to z utrudnionym lub niemożliwym do wykonania leczeniem endodontycznym oraz szybką utratą ruchomych zębów. Praca pokazuje wybrane metody leczenia powikłań dysplazji zębiny oraz zasady profilaktyki pozwalające utrzymać zęby jak najdłużej w jamie ustnej. Najważniejsze dla prawidłowego leczenia jest trafne postawienie diagnozy. O ile na podstawie badania zewnątrzustnego bardzo trudno jest postawić diagnozę, to po wykonaniu zdjęcia ortopantomograficznego nie powinno być wątpliwości. Lecząc pacjenta z dysplazją zębiny, należy przede wszystkim zadbać o profilaktykę przedwczesnej utraty zębów. Należy regularnie wykonywać skaling pozwalający uniknąć stanów zapalnych oraz eliminować wszystkie węzły urazowe i przedwczesne kontakty.
Wobec konieczności leczenia endodontycznego związanego z bólem lub zmianami okołowierzchołkowymi należy zastosować kiretaż otwarty lub zamknięty. Leczenie ortodontyczne oraz protetyczne jest dość ryzykowne ze względu na obciążenie zębów dodatkowymi siłami. Należy dążyć do poprawy warunków w jamie ustnej oraz jak najdłuższego utrzymania własnych zębów pacjenta, nawet rozważając często niestandardowe metody leczenia.
Summary
Dentin dysplasia, type I, is a genetic disorder inherited as an autosomal dominant trait. The incidence has been estimated at 1/100,000 births. DDI is characterized by the presence of teeth with abnormal crown morphology without rudimentary root development: shortened root length, abnormal shape, partial or total obliteration of the pulp chamber, periapical radiolucent areas or cysts and loosening of the teeth. This results in more complex or impossible endodontic treatment and a rapid loss of loose teeth.
This paper describes methods for the treatment of selected complications of type I dentin dysplasia as well as prevention strategies aimed at preserving the teeth for the longest possible time. A correct diagnosis is essential for proper treatment planning.
It is very difficult to make a diagnosis based only on intraoral examination but with OPG there should be no doubts. The most important aspect in the treatment of dentin dysplasia type I is to prevent premature loss of teeth. Scaling should be performed regularly to avoid inflammatory conditions. Moreover occlusal trauma and premature occlusal contacts should be eliminated. If endodontic treatment associated with pain or periapical changes is necessary, open or closed curettage should be performed. Orthodontic and prosthetic treatment methods are quite risky due to additional forces applied on the teeth. Therefore, we should strive to improve dental condition in the oral cavity and preserve the patient’s own teeth for as long as possible, even if non-standard methods of treatment are needed.
Introduction
Dentin dysplasia is a genetic disorder of teeth occurring in 1 per 100,000 births. It is often observed throughout several generations of family members. The disorder exhibits sex-unlinked, autosomal dominant inheritance. It is probably related to gene mutation on chromosome 4q 13-21. This location corresponds to locus dentinogenesis imperfecta, therefore the symptoms of dentin dysplasia type I and II are similar. It is believed that an abnormal migration of Hertwig’s epithelial root sheath cells into the dental papilla contributes to the development of dentin dysplasia. These cells induce abnormal osteoblasts differentiation, leading to excessive dentin deposition and pulp chamber obliteration (1-4).
Three types of dysplasia have been distinguished based on clinical and radiological symptoms. Type I dentin dysplasia, also known as radicular dysplasia, will be discussed in more detail below.
Type II dentin dysplasia, also known as coronal dentin dysplasia (2-4), is often confused with amelogenesis imperfecta. Both, permanent and deciduous teeth are affected. Normal shape of the crown, characteristic amber or blue colour and a rapid enamel abrasion are observed in deciduous teeth. The roots are of normal length and shape (1-3). The crowns of the permanent teeth have slightly altered colour and the enamel susceptibility to abrasion is lower compared to deciduous teeth. The teeth exhibit lower susceptibility to caries and lower responsiveness to thermal stimuli. No pathological mobility or marginal periodontal lesions are observed (4). The roots of the teeth affected by dysplasia type II show normal morphology. However, an X-ray reveals characteristic shell-like appearance. The pulp chamber in molars may be crescent-shaped, while single-rooted teeth may be thistle-tube shaped. Pulp stones, which rarely develop in dental canals, may be found in the chamber (2-4).
Dentin dysplasia type III, i.e. fibrous dysplasia, is a combination of type I and II dysplasia. The disorder is very rare. Both the chamber and the root are of normal structure. Normal appearance of the enamel and the presence of dental chamber give rise to many difficulties in the diagnosis of the disease. Fibrous dentin in the pulp chamber as well as rearrangement of collagen, which is only present in the predentin, are the only characteristic features (2-4). Dentin dysplasia type I, also known as radicular dysplasia, often remains undetected in clinical practice due to normal coronal morphology as well as resistance to caries and abrasion (2-5). Patients attend to the dentist due to cervical exposure or teeth mobility. Dentin dysplasia is usually diagnosed accidentally, based on OPG. X-ray images show shortened tooth roots, partially or completely obliterated pulp chamber and pulp stones in the 1/3 of the periapical chamber. Pathological lesions also affect the parodontium, manifesting in horizontal bone atrophy, thinning of the bone structure around the roots as well as the presence of cysts (5, 6). Furthermore, patients with the above-described radiographic image may sometimes experience throbbing pain increasing with temperature and in the horizontal position, i.e. symptoms typical of gangrene (2, 3). The observed clinical symptoms include fistulas in the region of the affected teeth despite obliterated pulp and the absence of canal lumens (5).
Four subtypes of type I dentin dysplasia have been distinguished: Ia, Ib, Ic, Id. Subtype Ia corresponds to the most advanced disease – the teeth have no roots, while only residual roots are present in subtype Ib. Subtype Ic is characterised by shortened roots, while normal root length and the presence of pulp stones in the pulp chamber are observed in subtype Id (2). Patients often do not realize for many years that they suffer from dentin dysplasia. Symptoms such as exposed cervical dentin or tooth mobility are attributed to periodontitis. Currently, the wide use of panoramic radiographs allows for an accidental detection of the disease (5). However, this usually happens at the stage of permanent, often residual, dentition. Currently, the increasing number of patients deciding for orthodontic treatment have a panoramic radiograph performed, which allows to detect dentin dysplasia already at the stage of mixed dentition (7, 8). Radiological image of dentin dysplasia in deciduous dentition is extremely rarely encountered by a dentist.
Aim
The aim of this paper was to familiarize the reader with the clinical manifestations of dentin dysplasia based on the description of two families affected by this disorder. In the first case, type I dentin dysplasia was observed in siblings (brother and sister); in the second case, the disease affected two sisters and a daughter of one of them.
Case reports
A 12-year boy was reported to the Paediatric and Family Dental Clinic of the University Dental Center, Medical University of Gdańsk, referred by his orthodontist for dental treatment. The orthodontist began treatment with removable dental braces. However, he discontinued treatment and referred the patient to a specialist pedodontic center after performing a panoramic radiograph. The boy’s parents reported no systemic diseases, allergies or chronic use of medications. Intraoral examination revealed no abnormalities, but a typical picture of mixed dentition, which is usually found in a 12-year-old child. Dental crowns were of normal shape, size and structure (fig. 1), covered with properly developed, hard, shiny and smooth enamel. Permanent teeth, except for 2nd and 3rd molars and 36, 43, 44 and 45 as well as persistent deciduous teeth 53 and 63 were found in the oral cavity. The teeth 32, 31, 41 and 42 had second-degree mobility. Caries was present in the fissures of teeth 16, 26 and 46. The patient delivered a panoramic radiograph (fig. 2) taken a few months earlier, showing a different status of dentition compared to that of the day of examination. The OPG showed root shortening in all permanent teeth and complete pulp chamber obliteration in teeth 25, 26, 36, 32, 31, 41 and 42. A crescent-shaped brighter area could be seen in the coronal portion of the chamber in the remaining permanent teeth, indicating partial chamber obliteration. Periapical lesions and bone thinning were identified in teeth 36, 32, 41 and 46. Based on dental examination and a characteristic radiological image, type I dentin dysplasia was diagnosed. Treatment plan was presented: thorough hygiene instructions and non-traumatic tooth brushing training, treatment of teeth affected by caries, extraction of persistent and worn deciduous teeth as well as orthodontic consultation with a specialist in the treatment of patients with dentin dysplasia. Medical history collected from the patient and his parents provided important information on the loss of tooth 36, which was extracted a few months earlier. The patient reported to the endodontist due to idiopathic pain persisting for a few days. The pain neither resolved when consuming cold beverages, nor was increased by warm stimuli. After X-ray examination, the dentist began endodontic treatment. An attempt to localize dental chamber or the root canal ortifice failed. As the pain persisted, extraction was performed. Deciduous teeth were extracted under infiltration anaesthesia with 4% articaine during several subsequent visits. In the first permanent molars, medium carious lesions were removed and cavities filled with composite material. Fluoride varnish was applied after treatment completion. The patient reported for a follow up every 3 months; no new carious lesions were observed and a very good hygiene was maintained. The boy does not report pain or gingival bleeding. Fluoride preventive treatment is regularly performed during visits. Since dentin dysplasia is inherited as an autosomal dominant trait and occurs among family members, particular emphasis was put on the search for other cases of the disorder among the family members when collecting medical history. It was found that a very rapid loss of previously mobile teeth was experienced by the father and the grandmother of the patient.
Fig. 1. The intraoral conditions presented by patient 1 (a 12-year-old boy)
Fig. 2. A panoramic view of patient 1 (a 12-year-old boy)
The patient’s 17-year-old sister also complained of increased tooth mobility and frequent gingival bleeding. She reported no systemic diseases, allergies or pharmacotherapy. The patient remains under the care of the Orthodontic Clinic at the University Dental Center, Medical University of Gdańsk. No abnormalities were found during intraoral examination. Normal coronal structure of the permanent teeth 17-27, 37-47 and tooth 63, with hard, glossy and smooth enamel without pathological lesions. Crossbite of teeth 13 and 43 (fig. 3). Gingival recession in teeth 44, 45, 34 and 35; 4 mm periodontal pockets were observed. Despite very good hygiene, absence of calculus or soft dental deposits, bleeding occurred at teeth 43 and 36 on probing. Second-degree tooth mobility was found in teeth 24, 34, 35, 44, 45 and 46. Teeth 18-28, 37-48 are present on the panoramic radiograph (fig. 4). The roots are shortened, which is typical of dysplasia. Teeth 17, 13-23, 26, 36, 35, 31, 42 and 44 have partially obliterated pulp giving a typical crescent shape within the crowns. The canals of the remaining teeth are completely obliterated. Periapical lesion may be seen in tooth 46, however, the patient reports no pain symptoms. Caries is present on the biting surface of tooth 36. Location of tooth 23 on the radiological image relative to the location in the oral cavity indicates that the image is out of date. The patient receives orthodontic treatment at the Orthodontic Clinic at the University Dental Center, Medical University of Gdańsk. Orthodontic microimplant was placed in the hard palate, orthodontic bracket was placed on tooth 23 (fig. 5). Hygiene instructions with emphasis on non-traumatic tooth brushing techniques were provided due to bleeding during tooth brushing and gingival recessions. During the visit, debridement of medium-deep caries on tooth 36 biting surface was performed and the cavity was filled with composite material. Finally, fluoride varnish was applied to the teeth. Regular follow-up visits every 3 months and fluoride preventive treatment were recommended. Three days after the visit, the patient reported to the Clinic due to pain affecting all teeth. The pain increased during ingestion of warm beverages. Dental examination revealed no abnormalities. A cold test (ethyl chloride) showed reduced response to cold, which is typical of dentin dysplasia. Full mouth subgingival scaling was performed due to unknown pain location. Pockets were rinsed with 0.9% NaCl solution, then metronidazole was applied. The patient felt a relief. Follow-up and revisit were recommended in case the symptoms recurred. The pain recurred after 3 weeks (the severity increased with warm and decreased with cold). This time, the patient provided the precise location of symptoms, i.e. tooth 35, which showed weaker response to ethyl chloride. Radiovisiography was performed and revealed widened periodontal ligament space and periapical lesion in tooth 35 (fig. 6). External curettage through the periodontal pocket (4 mm) and root planing were performed after infiltration anaesthesia with 4% articaine due to the absence of carious lesions and obliterated chamber and canals. Washing with 0.9% NaCl solution was performed and dexadent/metronidazole were applied. The patient was instructed to attend another visit if the pain persisted. The patient was informed about the prognosis as well as the potential need for tooth extraction if the symptoms persisted. She reported for another follow-up after 3 months. She maintains a very good hygiene, reports no gingival bleeding during tooth brushing or pain. Dental examination revealed no carious lesions. Fluoride varnish was applied to the teeth. The patient regularly attends follow-up visits, during which fluoridation is performed. No pain episodes occur. The patient also remains under the care of the Orthodontic Clinic. Although dentin dysplasia is a very rare disease (1 per 100,000 births), we managed to find another family whose members are affected by this disorder: a women (36 years), her 6-year-old daughter and her 34-year-old sister. The 36-year-old patient is in good general health, reports no allergies or chronic pharmacotherapy. She was diagnosed with dentin dysplasia in 2007. The woman began to experience dental problems typical of dentin dysplasia already in the primary school. She observed increased mobility of the lower incisors. At the age of 15 years, the patient reported to the dentist due to submental oedema. Intraoral examination revealed tooth 41 periapical oedema and fistula. The dentist attempted root canal treatment leaving the tooth open. Unable to identify the pulp chamber or the canal ortifice, he performed an X-ray radiograph. The image showed root shortening, thinning of the bone structure in the periapical area and obliterated root canal. The patient was referred for further treatment to the Periodontal Clinic, where panoramic X-ray was performed as well as basic blood tests and an endocrine profile were recommended. Blood cell count revealed high leukocytosis, while the endocrine profile did not derive from normal. Clindamycin and antiseptic irrigations were used for abscess treatment. The treatment was ineffective, therefore the tooth was extracted. The loss of tooth 47 occurred later in time, yet under similar circumstances. First, pain typical of gangrene occurred and was followed by abscess formation and, consequently, extraction was performed after an unsuccessful attempt of endodontic treatment. The periodontal care involved regular scaling and prophylactic procedures. Tooth 41 reconstruction was very important for the patient. Initially, a removable partial prosthesis was inserted in the gap. The woman felt discomfort related to the mobile prosthesis. She also noticed increased mobility of the surrounding teeth and progressive gingival recession. In 2007, the patient presented at a Surgical Clinic for consultation regarding the possible use of implants. Here, a thorough diagnostics was run and type I dentin dysplasia was for the first time diagnosed. The patient was informed about the causes of the disease, prognosis and treatment options as well as missing tooth reconstruction. It was decided to reconstruct teeth 41 and 47 using implants. The loss of tooth 41 more than 10 years before and the use of prosthesis resulted in significant bone loss. Autologous bone graft followed by implant placement was necessary. For tooth 47, only implant placement was performed due to a sufficient amount of bone. In 2009, the pregnant patient lost tooth 47 implant as a result of peri-implantitis. She didn’t decide for another implantation.
Fig. 3. The intraoral conditions presented by patient 2 (a 17-year-old girl)
Fig. 4. A panoramic view of patient 2 (a 17-year-old girl)
Fig. 5. An orthodontic microimplant in patient 2 (a 17-year-old girl)
Fig. 6. RVG of periapical lesions in tooth 35 in patient 2 (a 17-year-old girl)
Currently, the patient reports dental hypersensitivity, mobility and bleeding during tooth brushing. She regularly (twice a year) attends follow-up visits, undergoes scaling and sandblasting. The current panoramic radiograph confirms the diagnosis of type I dentin dysplasia (fig. 7): characteristic root shortening, crescent shape within the crowns indicating partial pulp chamber obliteration, periapical lesions at teeth 24 and 26 with no carious lesions, widened periodontal ligament space at tooth 25. Tooth 41 is replaced by an implant, while a gap remains within tooth 47.
Fig. 7. A panoramic view of patient 3 (a 36-year-old woman)
The patient’s 6-year-old daughter has been under orthodontic care since 2011. The lack of erupted tooth 71 at the age of 2 years was the reason for attending a dentist. The mother did not suffer from any diseases during pregnancy and had a natural birth at due date. The girl has no systemic diseases and does not receive chronic medication. As indicated in medical history, first deciduous teeth erupted at the age of 18 months and these were upper central incisors, which were followed by lower lateral incisors. Dental examination was performed during the visit, however, panoramic X-ray was postponed due to the young age of the patient. The patient attended follow-up visits at 6-month intervals up to the age of 5 years. No caries was detected, deciduous teeth did not show mobility. Fluoride preventive treatment was performed during visits. Panoramic X-ray performed at the age of 5.5 years revealed characteristic deciduous root shortening and the presence of undeveloped permanent tooth buds (fig. 8). The patient is still under constant dental care. Follow-up panoramic X-rays are planned in the future to assess the progression of permanent teeth dentin dysplasia as well as to plan prevention strategy aimed at the longest possible maintenance of patient’s own teeth.
Fig. 8. A panoramic view of patient 4 (a 5-year-old girl)
A 34-year-old sister is the last patient described in this paper. Type II dentin dysplasia can be diagnosed based on panoramic X-ray. As usual, root shortening, pulp chamber and root canal obliteration as well as a periapical lesion at tooth 46 may be observed (fig. 9). Appropriately endodontically treated tooth 31 with a distinct shortening of the root is noteworthy. Medical history indicated that the patient was treated for abscess and fistula in the region of tooth 31. Effective endodontic treatment was initiated. This was followed by resection of the periapical lesion with a retrograde filling of the canal. According to the patient, the procedure was performed many years ago. Currently, thinning of the bone structure can be seen. The long-term maintenance of the tooth in the socket may be considered a success.
Fig. 9. A panoramic view of patient 5 (a 34-year-old woman)
Discussion
Genetic factors underlying dentin dysplasia do not allow for full recovery or elimination of the cause of disease. The dentist can implement symptomatic treatment or prevent complications. As shown in the presented cases, a correct diagnosis is crucial (2-10). Radiological image of dentin dysplasia is very characteristic, therefore the diagnosis should not be difficult. Problems encountered by patients can be divided into periodontal (dental mobility, gingival bleeding during tooth brushing, gingival recession, pathological periodontal pockets) and endodontic (gangrenous pain, periapical lesions, abscesses). These complications result in the loss of teeth, which requires reconstruction (prosthetic and implant treatment). Furthermore, patients with dentin dysplasia need an improvement in aesthetics, which sometimes requires orthodontic treatment. Prevention is the second most important aspect after a correct diagnosis (2, 3, 5-7). Patients with type II dentin dysplasia show greater resistance to caries than those with normal teeth (5). However, regular check-ups every 3-6 months and preventive fluoride treatment are necessary (2, 5, 6). The role of the dentist is to instruct patients on how to effectively and non-traumatically brush their teeth. Hygiene is of key importance since inflammation, which manifests in bleeding, accelerates gingival recession and can lead to increased tooth mobility (3-5). The dentist should always check the presence of plaque and calculus during follow-up visits. Professional teeth cleaning as well as pointing out hygienic shortcomings to the patient may be necessary (6). In the case of significant dental mobility, all factors that could potentially contribute to this pathology, i.e. occlusal trauma, premature occlusal contacts, parafunctions, should be eliminated (2). Sometimes the presence of malocclusion increases dental mobility. Therefore, it is worth considering orthodontic treatment, which poses a great challenge for the orthodontist. Orthodontic treatment of patients with dentin dysplasia is very controversial. Root shortening in the teeth that are not well anchored in the bone should be taken into account. The thinned structure of the bone surrounding the teeth does not allow using forces necessary for tooth repositioning. Orthodontists are concerned about complications in the form of increased gingival recession, lowered bone level or accelerated tooth loss. Treatment is often discontinued in cases described in the literature (8). However, due to the high dental awareness of patients as well as their aesthetic requirements, the aspect of orthodontic treatment is more frequently mentioned (7). The described 17-year-old patient receives orthodontic treatment. In this case the orthodontist departed from standard treatment with braces due to the risk of an overload caused by the applied forces. The aim of the treatment was to relocate the upper canines with very long roots into the dental arch and their correct alignment. Since an orthodontic microimplant was used, the applied forced did not affect other teeth with shortened roots. Although the patient is still under treatment, first effects in the form of appropriate canine alignment may be observed. Long-term effects are to be expected in the future. Another complication that can occur in patients with dentin dysplasia are periapical lesions, bone cysts and bone thinning unrelated to deep caries leading to pulpitis (3, 6). The probable cause may be related to periodontal pocket infections (2, 3, 6). Unawareness of this aspect as well as undiagnosed dentin dysplasia may consequently lead to an incorrect treatment. A 12-year-old patient lost tooth 36 due to suspected gangrene. The endodontist attempted, based on the symptoms, standard root canal therapy by opening the tooth and searching for the chamber and canal orifices. The search was unsuccessful and the patient continued to complain of pain. Therefore extraction was performed. For his sister, other non-standard therapeutic method described in the literature was used (3). External curettage, root planning and local antibiotic therapy were used as abnormally formed periodontium could have accounted for infection. The patient no longer felt the pain. However, such treatment should be monitored and it should be borne in mind that prognosis is uncertain in such cases (3). Perhaps the tooth will have to be extracted or a resection of the periapical lesion will have to be performed in the future (6). Extraction had to be performed in another, a 36-year-old patient, who was also diagnosed with dentin dysplasia, due to periapical lesion, abscess and fistula. Resection of the root was performed in her sister (a similar case), and the tooth was left in the oral cavity. As indicated in the literature, resection should be a method of choice for an appropriate length of the root (3, 6). It may be seen in the described patient that the root is much shorter, however, extraction could be an alternative for the applied treatment. Time has shown that it was worth performing the procedure. Premature tooth loss is inevitable in patients with dentin dysplasia. Prolonged maintenance of teeth in the oral cavity using all available means is considered a therapeutic success. However, if tooth loss does occur, the missing teeth should be reconstructed. This is important due to both, aesthetic reasons and a reduced load on the remaining teeth. There are two therapeutic options, i.e. the use of prosthesis or implants, to choose from. Dental implant treatment is a relatively new method for the reconstruction of missing teeth. Two implants were used in the described case of a 36-year-old patient. The patient was informed that the risk of implant rejection was higher due to the diagnosed dentin dysplasia. Thus, as in the case of tooth 41, the implant has been maintained for 8 years. Unfortunately, the implant of the tooth 47 was lost. Cases of dental implant treatment may be also found in the literature (8, 10). Unfortunately, it is too early to describe the effects of this type of treatment.
Conclusions
Type II dentin dysplasia is a rare genetic disorder with autosomal dominant inheritance. It very often affects family members. If the disorder is diagnosed in one family member, it is necessary to perform examination of siblings and parents. Correct diagnosis early in life allows for the treatment aimed at the longest possible maintenance of teeth in a satisfactory condition. The treatment of endodontic complications is difficult and involves high risk of failure. Pain relief is the determinant of success as no other means for the control of therapeutic effects are available. The loss of teeth is very common and inevitable in some cases. Reconstruction using a permanent dental prosthesis is not always possible, whereas a mobile prosthesis causes discomfort. Although dental implants significantly contribute to aesthetics and comfort improvement, the prognosis for implants is uncertain due to the fact that the method is relatively new and there are no studies on long-term implant maintenance in the oral cavity of patients with dentin dysplasia. Early diagnosis and appropriate prevention are essential to maintain the teeth in the oral cavity for the longest possible time.
Piśmiennictwo
1. Cameron AC, Widmer RP (red. wyd. pol. U. Kaczmarek): Stomatologia dziecięca. Elsevier Urban & Partner, Wrocław 2013. 2. Syryńska M, Janiszewska-Olszowska J: Dziedziczna dysplazja zębiny typu Ic – opis 3 przypadków. Czas. Stomat 2005; 7: 520-524. 3. Tkacz I, Mielnik-Błaszczak M, Pels E, Borowicz J: Dysplazja zębiny – opis przypadku. Nowa Stomatol 2012; 2: 58-63. 4. Boguszewska-Gutenbaum H, Grzybowska A, Janicha J, Valipour Kolti F: Dysplazja zębiny – opis jednostki chorobowej. Nowa Stomatol 2009; 14: 82-89. 5. Ozer S, Ozden B, Ozden FO, Gunduz K: Dentinal dysplasia type I: A case report with a 6-year follow up. Case Rep Dent 2013, 659084: 1-3. 6. Toomarian L, Mashhadiabbas F, Mirkarimi M, Mehrdad L: Dentin displasia type I: a case report and review of the literature. J Med Case Reports 2010; 4: 1-6. 7. Bespalez-Filho R, De Azambuja Berti Couto S, Souza PHC et al.: Ortodontic treatment of a patient with dentin dysplasia type I. Am J Orthood Dentofacial Orthop 2013; 143: 421-425. 8. Fulari SG, Tambake DP: Rootless teeth: Dentin dysplasia type I. Contemp Clin Dent 2013; 4: 527-530. 9. Nettem S, Nettemu SK, Basha K, Venkatachalapathi S: Implant – based oral rehabilitation of a variant model of type I dentinal dysplasia: A rare case report. Dent Res J 2014; 11: 513-517. 10. Depprich RA, Ommerborn MA, Handschel JGK et al.: Dentin displasia type I: a challenge for treatment with dental implant. Head & Face Medicine 2007; 3(31): 1-5.
otrzymano: 2016-05-06
zaakceptowano do druku: 2016-05-26

Adres do korespondencji:
*Dominika Szczepanek
Poradnia Stomatologii Dziecięcej i Rodzinnej Uniwersyteckie Centrum Stomatologiczne GUMed
ul. Elizy Orzeszkowej 18
80-208 Gdańsk
tel. +48 663-337-821
dominika.borecka@gmail.com

Nowa Stomatologia 2/2016
Strona internetowa czasopisma Nowa Stomatologia