REVIEW

Australian Dental Journal 2003;48:(3):156-168

Diagnosis and management of unusual dental abscesses in children

WK Seow*
encountered in primary teeth.1 In addition, dental abscesses resulting from trauma are also encountered in young children. In most children, these infections usually present as chronic inflammation which is localized to the offending tooth. In such cases, management of localized pulpal infections in the primary dentition includes root canal treatment or extraction and space maintenance. On the other hand, the treatment of a spreading, acute dental abscess centres on pain control, antibiotics, surgical drainage and removal of the source of infection, which may include endodontic treatment or extraction of the tooth. The antibiotic which is usually used for acute oral infections in children is oral amoxicillin, usually prescribed at doses of 20-40mg/kg/day, in three divided daily doses for five days.2 For the children who are allergic to penicillin, oral clindamycin at doses of 1525mg/kg/day in three or four equal daily doses is an effective alternative.2 Hospitalization and parenterallyadministered antibiotics may be required for children who show spread of the dental infection. However, some pulp infections have unusual origins which challenge diagnosis and management. Some of these infections have been referred to spontaneous abscesses because of the lack of apparent aetiological factors. Many of these unusual abscesses are associated with developmental anomalies of the teeth, either as a local aberration of tooth development, or a general manifestation of systemic conditions. In contrast, other abscesses are related to acquired conditions such as those caused by infection of the pulp due to extensive coronal destruction from pre-eruptive resorption. Occasionally, an oral abscess may result from infection of the follicle of a developing tooth through infection of the operculum or pericoronitis. As many of these unusual dental abscesses are associated with developing or newly erupted teeth, they are usually encountered in children. As the prevention of dental abscesses plays a central role in the management of these unusual entities, it is useful for the clinician to be aware of their clinical implications and the methods of abscess prevention. Recent research on these unusual conditions has greatly improved the understanding of their aetiology and
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Abstract Although the majority of dental abscesses in children originate from dental caries or trauma, a few are associated with unusual conditions which challenge diagnosis and management. Recent research findings have shed light on these unusual entities and greatly improved understanding of their clinical implications. These conditions include developmental abnormalities such as dens invaginatus in which there is an invagination of dental tissues into the pulp chamber and dens evaginatus in which a tubercle containing pulp is found on the external surface of a tooth crown. In addition, inherited conditions which show abnormal dentine such as dentine dysplasia, dentinogenesis imperfecta, and osteogenesis imperfecta predispose the dentition to abscess formation. Furthermore, spontaneous dental abscesses are frequently encountered in familial hypophosphataemia, also known as vitamin D-resistant rickets, in which there is hypomineralization of dentine and enlargement of the pulp. In addition to developmental conditions, there are also acquired conditions which may cause unusual dental abscesses. These include pre-eruptive intracoronal resorption which was previously known as pre-eruptive caries or the fluoride bomb. In addition, some undiagnosed infections associated with developing teeth are now thought to be the mandibular infected buccal cysts which originate from infection of the developing dental follicles. In the present paper, these relatively unknown entities which cause unusual abscesses in children are reviewed with the aim of updating the general practitioner in their diagnosis and management.
Key words: Dental abscess, dens invaginatus, dens evaginatus, hypophosphataemia, pre-eruptive intracoronal resorption, mandibular infected buccal cyst. (Accepted for publication 13 March 2003.)

INTRODUCTION In the paediatric patient, dental abscesses are not uncommon. Despite the decline in dental caries in past decades, many young children are still at risk for dental decay, and pulpal infections from caries are commonly
*School of Dentistry, The University of Queensland, Brisbane.
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Table 1. Developmental and acquired conditions associated with dental abscesses in children
Pathological features Developmental Abnormal morphology of crown Dens invaginatus Dens evaginatus Invagination of tooth structure into the pulp through a palatal pit. Invaginated part may contain enamel, dentine and pulp which communicates with the main pulp chamber. Cusp-like evagination of tooth structure on the occlusal surface. The evaginated cusp usually contains pulp tissue which communicates with the main pulp chamber. The pulp is filled with calcifications which resemble a mixture of cementum, bone and globular dentine. The roots are short and blunted. The pulp is totally calcified in primary dentition. In permanent dentition coronal pulps are calcified with remaining narrow channels. Bluish, brown discolouration may be noted in both dentitions. The crowns are bulbous, with short roots. Calcification of the pulp may be complete. Some types of Osteogenesis imperfecta (Types III and IV) show features of dentinogenesis imperfecta. Other types, e.g., Type I may show enlarged pulp chambers. The dentine is hypomineralized, and presents histologically as globular dentine. In addition, there are voids and channels within dentine which run from the dentine-enamel junction to the pulp. Maxillary lateral incisors Maxillary and mandibular premolars, predominantly in Asiatic races Primary and permanent dentition Primary and permanent dentition Primary and permanent dentitions affected Primary and permanent dentitions affected Primary and permanent dentitions affected Teeth most commonly affected

Abnormal structure of dentine Dentine dysplasia (Type I) Dentine dysplasia (Type II) Dentinogenesis imperfecta Osteogenesis imperfecta

Familial hypophosphataemia

Acquired conditions Pre-eruptive intracoronal resorption Resorption within the crown of an unerupted tooth which usually begins after crown formation. When the tooth erupts into the oral cavity, it usually becomes infected and resembles a large carious lesion. Infection of the follicle of a developing, partially-erupted tooth may occur from the infected operculum or pericoronitis. Primary and permanent teeth

Mandibular infected buccal cyst

First and second permanent molars, and third molars

management. Although a few of these entities are rare, others are increasingly recognized to be much more common than previously thought because they are often undiagnosed. Hence, the aim of this paper is to review these unusual conditions which are commonly associated with pulpal abscesses in children, in order to update the dental practitioner in the diagnosis and management of these entities. Developmental abnormalities of crown Table 1 presents a list of developmental and acquired conditions which are often associated with dental abscesses. As can be seen from Table 1, the abnormalities of crown morphology which are well known to cause pulpal abscesses include both invaginations and evaginations of the surface. Dens invaginatus (Dens-in-dente) Clinical and pathological features Dens invaginatus is estimated to affect about 1-2 per cent of the population, and is mainly seen in the maxillary permanent lateral incisors although it can also be located in other teeth such as supernumeraries, mandibular incisors, premolars, and molars.3-5 Occasionally, it occurs with other dental anomalies.6,7 Dens invaginatus is a developmental aberration in which an enamel-lined sac is found within a tooth
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crown or root. The sac is usually filled with pulp tissue, may be blind-ended or exits into the periodontal ligament, and causes the crown or root to be dilated.3 The abnormality is formed by invagination of the inner enamel epithelium into the dental papilla before mineralization of the crown. The site of invagination may be marked by a deep pit, usually the palatal pit of a maxillary lateral incisor, or the tip of a molar cusp.8,9 Figure 1a-1c show an abscess associated with a conical maxillary permanent lateral incisor which has a large dens invaginatus in an 11-year-old child. Pulpal infection commonly occurs when there is communication of the invaginated pulp with the oral environment. This presents soon after dental eruption in those cases which have preformed openings into the exterior, or may occur later in those teeth in which caries in the pits leads to pulpal exposure. In the case of abscesses occurring in maxillary lateral incisors without obvious causes, the presence of a dens invaginatus should always be considered. As the invagination is usually deep within the crown or root, diagnosis is usually determined only after detailed radiographic exposure.10 The periapical film may reveal an enamel-lined sac within the pulp which may appear dilated. The most challenging types of dens invaginatus are those which are small, and rotated in their long axes, so that classical radiographic appearances are not seen.
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Fig 1a. Anterior dentition of an 11-year-old boy whose maxillary left lateral incisor became abscessed due to the presence of a dens invaginatus (see Fig 1b and 1c).

Fig 1c. Radiograph of the tooth in Fig 1b. Note the thin enamel and dentine layers forming the walls of the dens invaginatus.

Fig 1b. A large dens invaginatus was found within the crown of a conical maxillary permanent lateral incisor of the patient in Fig 1a. The tooth became abscessed and was extracted because of the severity of the defect which made endodontics extremely difficult.

Management Management of dens invaginatus includes prevention of pulpal infection through early diagnosis.11 In this regard, it is recommended that all deep palatal pits on maxillary lateral incisors be investigated using periapical radiography to exclude the possibility of dens invaginatus. Figure 1d shows a double dens invaginatus discovered in the maxillary lateral incisor in a 13-year-old boy when the tooth was radiographically exposed to investigate the deep palatal pits. Before pulpal infection has occurred, such palatal pits may be cleaned, and protected with a double seal consisting of glass-ionomer cement, followed by
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Fig 1d. Periapical radiograph showing double dens invaginatus in a maxillary permanent lateral incisor in a 13-year-old boy.

composite resin. Although prophylactic removal of the dens invaginatus has been suggested by some authors,12
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Fig 2a. A maxillary second premolar which has a dens evaginatus on the occusal surface. Fig 3a. The mandibular second premolar shows remnants of a fractured dens evaginatus.

Fig 2b. In the maxillary second premolar depicted in Fig 2a, the dens evaginatus was protected by composite resin, which was placed before the tooth achieved contact with the opposing tooth.

the unpredictable results of such treatment in immature teeth do not justify this procedure as routine treatment. When pulpal involvement has occurred in a tooth with dens invaginatus, treatment options include endodontic treatment and root canal filling. The endodontic treatment may be limited to the invaginated section or extended to involve the entire pulp.5,13,14 Ultrasonic dbridement has been found to be highly useful for endodontic treatment of dens invaginatus.13 For young teeth with incompletely formed root apices, which have become abscessed due to dens invaginatus, apexification using calcium hydroxide therapy has been reported to be successful.15 Surgical root sectioning and retrograde root canal therapy has also been reported as an alternative if conventional endodontic therapy is unsuccessful.16 Dens evaginatus (Evaginated odontome) Clinical and pathological features Dens evaginatus presents as a tubercle which protrudes from the occlusal surface of a premolar tooth, or the lingual surface of an anterior tooth. This anomaly has been reported mainly in the Asiatic races, where the prevalence rate is thought be as high as 2 per cent.17 The defect is thought to be due to an outflow of the dental epithelium during tooth development to
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Fig 3b. Radiograph of the tooth in Fig 3a, showing a large diffuse periapical radiolucency associated with an incompletely calcified apex. Apexification using calcium hydroxide was successfully performed on the tooth before root canal filling.

form an accessory tubercle or cusp which is composed of enamel and dentine, and enclosing pulp tissue, which communicates with the main pulp of the tooth.18 As the tubercle is usually fragile, and fractures easily, the pulp is frequently exposed within a short time of tooth emergence.19 Figures 2a, b show dens evaginatus on the maxillary second premolar which had recently erupted. The defect is difficult to diagnose once the tubercle has fractured or abraded.17,18,20 In many cases, the defect is discovered only after a dental abscess has occurred, such as the case depicted in Fig 3a and 3b. Diagnosis
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Fig 4a. Clinical presentation of the primary dentition in a child with dentine dysplasia type I. Note the severe periodontal bone loss and abscess on the buccal of the mandibular right second primary molar.

Fig 4c. Histologic section of an exfoliated tooth from the child in Fig 4a. Note the obliteration of the pulp chamber with calcified structures resembling bone and dentine.

Fig 4b. Panoramic radiograph of the child depicted in Fig 4a. Note the severe calcification of the pulps in the entire primary dentition.

may be aided by the presence of the same anomaly in other parts of the mouth, and the exclusion of other aetiological factors such as trauma or caries. Management As in other types of crown anomalies, prevention of pulp infection can be achieved only through early diagnosis. When the characteristic tubercles or accessory occlusal cusps are noted in premolars, they should be further investigated with periapical radiographs which may show a tubercle containing enamel, dentine and pulp. If the tubercle is fractured, periapical radiolucencies are usually present (Fig 3b). The pulpal status of the teeth may be determined by the usual vitality tests. If diagnosis is made before pulpal infection has occurred, protection of the tubercle should be performed by the placement of composite resins around and on top of the tubercle (Fig 2b).21-23 This method should afford protection from cuspal wear and fracture, and should ideally be performed prior to the tooth reaching full occlusal function. Although suggested by some authors, the radical procedure of prophylactic tubercle fracture, Cvek partial pulpotomy,
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and calcium hydroxide direct pulp capping17,24 is difficult to justify due to the unpredictable outcomes of these procedures. As the majority of dens evaginatus is diagnosed after pulpal infection occurred, the management options are usually full endodontic therapy or extraction.25 As is the case with dens invaginatus, apexification of the immature tooth using calcium hydroxide is often required before root filling can be performed as pulpal infection usually occurs before root development is complete.26 Structural abnormalities of dentine As the physiology of dentine is intimately linked with the pulp, structural changes in dentine are often associated with pulp changes. Such abnormalities may be observed in children with inherited disorders of dentine such as dentine dysplasias, dentinogenesis imperfecta or mineralization defects such as rickets. In these conditions, dental abscesses are a common feature. Dentine dysplasias Clinical and pathological features The dentine dysplasias consist of a group of fairly rare conditions involving dentine only, and are often associated with abscesses.27 While dentine dysplasia is often inherited as genetic conditions involving only the teeth,28,29 a few rare dysmorphic syndromes have dental features similar to dentine dysplasia. These include tumoral calcinosis (extensive calcification of joints and teeth), and brachio-skeleto-genital syndrome (mental
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retardation, abnormal ribs, bone sclerosis and hypospadias).30 In dentine dysplasia, while there are overlapping features in the different variants, these are usually classified as Type I, or radicular dentine dysplasia and Type II or coronal dentine dysplasia to denote the respective location of the primary defect.27 The predisposition to dental abscesses in both types of dentine dysplasia is related to the pulpal obliteration found in these conditions.27 In Type I, the clinical crowns are of normal colour in both dentitions, the coronal dentine is normal, and the pulp obliteration which usually is mainly confined to the root, is severe except for thin, cresent-shaped pulpal remnants parallel to the cemento-enamel junction.27,31 The roots which are usually short, conical or absent, is associated with mobility and early exfoliation.27,32 On radiographs, there are often periapical radiolucencies, which may be granulomas or cysts.31,33 Figure 4a and 4b show the typical clinical manifestations of a child affected with Type I dentine dysplasia, while Fig 4c depicts the severe calcification of the pulp of an exfoliated primary tooth from the same child. In Type II dentine dysplasia, the primary dentition usually has a bluish or amber discolouration, but the permanent teeth are normal in colour.29,34 The primary teeth show total pulp obliteration as in Type II, but the permanent teeth have less calcifications, and the pulps classically show thistle-shaped configuration and pulp stones. Periapical abscesses are commonly encountered in these teeth.34 The pathogenesis of the dental abscesses in dentine dysplasia is the result of oral bacteria ingressing into the pulp through the dysplastic dentine after loss of enamel through caries, trauma or attrition. It is also probable that the teeth in dentine dysplasia are more likely to suffer attrition of the enamel as a result of the dysplastic dentine. Hence surface protection of the teeth through fissure sealants and steel crowns may help in preventing pulpal abscesses. In addition, pulpal infection may also occur as endo-perio lesions through severe loss of periodontal attachment in Type I dentine dysplasia (Fig 4a). Management Prevention of periodontal attachment loss is difficult in patients with dentine dysplasia due to the extremely short roots which result in poor periodontal support.27 Meticulous oral hygiene has been shown to have some success in preventing periodontal attachment loss and pulpal abscesses. Root canal treatment of severely teeth calcified teeth is also difficult, and extraction may be the only option in many cases.27 Dentinogenesis imperfecta Clinical and pathological features Dentinogenesis imperfecta (DI), is one of the most common autosomal dominant genetic disorders affecting human beings.35 According to current nomenclature, the term dentinogenesis imperfecta is
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Fig 5a. Anterior permanent teeth of a child with dentinogenesis imperfecta showing typical discolouration.

Fig 5b. Bitewing radiograph of the child in Fig 5a, showing complete obliteration of the pulps at age 13 years. Note the radiolucency situated at the furcation of the mandibular first molar.

used when this abnormality of dentine is inherited as an isolated defect of dentine.35 On the other hand, the term opalescent dentine is used when the dentine abnormality is a feature of osteogenesis imperfecta or OI.35-37 The dental abnormalities in DI and OI are associated with specific molecular defects in connective tissues of dentine and bone.35,38-41 The typical features of DI include translucent, grey or brownish crown discolouration (Fig 5a), bulbous crowns, short roots, fracturing away of enamel, severe attrition, and pulp obliteration.42 Dental abscesses encountered in DI are thought to occur from the disruption of pulpal vascular supply associated with the abnormal calcifications which result in pulp necrosis. Diagnosis of DI depends on the clinical and radiographic appearances (Fig 5a, 5b). Although both dentitions are typically affected, occasionally, only the primary dentition alone shows the discolouration. In the case of opalescent dentine occurring with OI, the clinical appearances of the primary or permanent dentition may be quite variable.43 Management Dental management of DI includes accurate diagnosis and assessment of the risk of attrition and abscess formation, and prophylactic capping of the teeth.44 As there may be a spectrum of dental manifestations in DI, sequential radiographic exposure of the teeth at intervening periods may reveal whether they are particularly prone to attrition or pulpal
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Fig 6a. Longitudinal section of an exfoliated primary tooth from a male child with XLH. Note the dentinal clefts and defects which connect the pulp with the exterior.

obliteration. In a young patient in whom the attrition rate is highly progressive, and radiographs reveal rapid pulpal obliteration, prophylactic steel crowns should be inserted on all the molars, and resin crowns on the incisors to protect the teeth from further wear.44 The posterior crowns may be inserted using a conservative technique in which there is minimal removal of tooth structure and separation of the teeth achieved by separating elastics prior to crown insertion.45 In the patient who shows excessive attrition, overlay dentures may restore occlusal vertical dimension, prevent further tooth wear, and improve aesthetics. However, as overlay dentures are a high risk factor for dental decay, extremely good preventive oral care, including daily topical fluoride treatment will need to be practiced by the patients. As in dentine dysplasia, when abscesses occur, endodontic treatment in either the primary or permanent dentitions may be problematic if there is extensive calcifications, and extractions may be the only option in such teeth.46 However, if it is desirable to retain a permanent tooth, endodontic surgery can be undertaken on teeth with extensive calcific metamorphosis, if the roots are sufficiently long, but has a guarded prognosis. In permanent teeth that require endodontic therapy and have minimal calcific pulp changes, routine endodontics may be performed. Familial hypophosphataemic rickets Clinical and pathological features X-linked hypophosphataemic rickets (XLH), also known as vitamin D-resistant rickets is one of the most common forms of rickets in developed countries.47 It is
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Fig 6b. Histologic section of the tooth in Fig 6a. Note the globular nature of the dentine which renders endodontic cleaning very difficult.

a systemic disease of particular importance in the aetiology of unusual dental abscesses.27,45,48-51 Dentists should be alerted to this condition as the systemic features may be mild, and dental abscesses may be the first presenting signs.48 In fact, a few cases are first diagnosed by dentists. The prevalence rate is usually reported to be around 1:20,000.52 In this condition, there is deficient mineralization of bone caused by a genetic defect in renal transepithelial transport of phosphate, which leads to decreased tubular reabsorption of phosphate and persistent hypophosphataemia.47,52,53 The features of rickets are the main systemic signs, but many children are not diagnosed until about 2-3 years of age when they begin to show typical features such as bowing of the legs.52 The disease is treated with large doses of oral replacement phosphate.52 Dental abscesses are frequently encountered in XLH to the extent that some patients are first diagnosed from the appearance of the spontaneous dental abscesses which are found in the absence of caries or trauma.45,48,49,51 These abscesses are due to deficiencies of dentine mineralization which results in large pulp chambers and physical defects within the dentine, as shown in Fig 6a. In many teeth, there are channels which connect the pulp horns to the amelodentinal
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amelodentinal junction, and the radiodensity of dentine approaches that of bone. Medical therapy with phosphate supplementation does not seem to have positive effects on the teeth.50 Management The main management strategy for the dental manifestations of XLH is the prevention of pulpal abscesses. In the young patient, this may be achieved through prophylactic coverage of the teeth with steel crowns in the molar teeth and composite resins in the incisor teeth. As the placement of steel crowns using conventional techniques requires removal of relatively large amounts of tooth structure, the risk of pulp exposure is high in those patients where the pulp chambers are large. To prevent this, a conservative crown technique employing the use of separating elastics and non-removal of tooth structure has been recommended for the insertion of prophylactic steel crowns for children with rickets.45 In severe cases it may be necessary to protect the occlusal surfaces of partially erupted molars with composite resins prior to insertion of steel crowns which is performed when the teeth are fully erupted.45 The steel crowns may be converted to full gold or porcelain crowns when adulthood is reached. Figure 6d shows the orthopantogram (OPG) of a child with XLH who had stainless steel crowns inserted in the permanent first molars to prevent dental abscesses. With regard to other aspects of dentistry, recent reports suggest that orthodontic treatment may be successful in children with XLH57 and implants may be also be cautiously used.58 Acquired conditions associated with dental abscesses Pre-eruptive intracoronal resorption of dentine Occasionally, the dental practitioner encounters an apparently intact, recently emerged tooth which has become abscessed, and there is a negative history of trauma or caries. Typically, such a tooth shows an ostensibly intact surface, and a large cavity within the coronal dentine just below the amelodentinal junction. Such teeth have been known by a variety of names such as occult caries, hidden caries, fluoride bombs, and fluoride syndrome.59 The terms hidden caries or occult caries refer to the fact that such lesions are thought to have originated as carious lesions, and have eluded discovery during clinical examination.60-63 On the other hand, the terms fluoride bombs or fluoride syndrome suggest that fluoride is an aetiological factor64,65 (Fig 7a). This theory states that fluoride has encouraged remineralization and the slowing of caries process in the surface enamel, masking the cavitation which progresses in dentine. In some teeth, such lesions have been discovered incidentally on radiographs before their eruption into the oral cavity and these are often erroneously referred to as pre-eruptive caries.66 More recently, the term pre-eruptive intracoronal resorption (PEIR) is used to apply to teeth showing
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Fig 6c. Bitewing radiograph of a male child who has XLH. The pulps of the teeth are large and the radiodensity of dentine is reduced.

Fig 6d. Orthopantomogram of an XLH patient who had prophylactic stainless steel crowns placed on the permanent first molars to prevent pulpal abscesses. Note the periapical and furcation radiolucencies on the primary mandibular second molars which had not been protected with steel crowns.

junction so that when the enamel is lost through attrition or caries, oral micro-organisms enter the pulp through these channels.45,49,54 Furthermore, the incompletely mineralized dentine exists in the form of globular dentine or calcospherites which trap microorganisms, and impedes mechanical endodontic cleaning (Fig 6b).49,55 Other endodontic difficulties are caused by the thin dentine which perforates easily and does not support restorative posts for prosthetic crowns. The degree of dentine mineralization in XLH and hence the risk for developing dental abscesses varies from patient to patient. Usually males are affected to a greater extent, as would be expected of an X-dominant condition, and tend to show the most severe dental changes, including taurodontism.53,56 The risks of an individual to dental abscess formation may be assessed by history and dental radiographic signs.45 Usually, the younger the patient when the first abscesses occur, the more severe the dental manifestation. In addition, the sizes of the pulp chambers of the teeth and the radiodensity of the dentine may also be determined from radiographs (Fig 6c). In the most severe cases in which the risk of abscesses is highest, the pulps are extremely large, with the pulp horns reaching the
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Fig 7a. An OPG of a 12-year-old boy who developed an abscess related to the mandibular right second molar. The tooth showed the typical appearance of a fluoride bomb (arrow). Histologic examination of the tooth showed that it to be a pre-eruptive intracoronal resorption lesion. (Radiograph courtesy of Dr Scott Smith.)

radiographs are exposed in younger subjects, an increased number of first permanent molars have also been reported to show PEIR.71,72 In the primary dentition, the prevalence is unknown as radiographs of unerupted primary teeth are seldom available. Seow and Hackley reported a 2-year-old child with an abscess in a recently erupted primary second molar which showed an intact occlusal surface, and a large resorption lesion within the coronal dentine.67 The authors suggested that it was likely to have originated as PEIR. No other cases have been reported in the primary dentition. In spite of the relatively high prevalence of this condition, the majority of lesions remain undetected until there is pulpal involvement or fracture of the cusps from extensive cavitation.68 Thus, PEIR may be an important cause of unusual pulpal abscesses in children that present within a short period of time of tooth eruption. Aetiology of pre-eruptive resorptive lesions In unerupted teeth, diagnosis of PEIR is only possible through radiographic exposure of the crowns of developing teeth. In investigations which contain serial radiographs of the same subject at different time periods, it was established that cavitation of the intracoronal dentine begins only after crown development is complete.67 Thus it may be inferred from these observations that the cavity is not the result of an intrinsic disturbance of mineralization, rather it is likely to be due to resorption of dentine tissue after mineralization. That the aetiology of the lesions is resorption of dentine is deduced from histological examination of affected teeth which often show classical signs of resorption such as osteoclasts and scalloping of the dentine margins.67,68 However, the origin of the resorption cells, as well as their pathway of entry are still unclear. It is speculated that the cells arise from undifferentiated cells of the developing dental follicle, or from the surrounding bone. They probably enter the dentine through a break in the enamel surface, such as hypoplastic pits or surface cracks or lamellae. Controlled studies, as well as individual case reports have not revealed any particular systemic factors which may predispose a child to PEIR.69,70 In particular, there is no gender or racial predilection to the condition. Also of importance is the fact that fluoride does not appear to have an aetiological role. Studies have shown that the children who have PEIR do not have any history of fluoride exposure through drinking water or fluoride supplementation.71,72 These findings confirm that those of Weerheijm et al. who showed that the prevalence of hidden lesions in a fluoridated town in Holland was over 30 per cent less compared to a non-fluoridated town in the same country.73 These findings refute the use of the term fluoride bomb to describe these lesions. Trigger factors for the resorption are also unknown, although it has been found that teeth with pre-eruptive
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Fig 7b. An OPG of a 5-year-old child with a pre-eruptive intracoronal resorption lesion in the mandibular left first permanent molar (arrow). The lesion appears as a radiolucent defect resembling caries in the dentine beneath an intact occlusal surface.

such lesions to denote the aetiology and nature of these lesions.59,67-69 Figure 7b shows typical features of a PEIR lesion in the unerupted, mandibular left first permanent molar in a 5-year-old girl. Prevalence The prevalence of PEIR can be determined using radiographs of unerupted teeth, and different prevalence figures have been reported, depending on the type and quality of radiographic exposure. In studies involving nearly 2000 OPGs and 1200 bitewings, PEIR has been found to occur in about 2-6 per cent of children and adolescents with unerupted teeth, and a tooth prevalence of about 1-2 per cent.69,70 Although any tooth in the permanent and primary dentition may be affected by PEIR, previous case reports have indicated a predominance of premolars, and second and third molars, probably due to the fact that these teeth are those most frequently observed in their unerupted states when children first present for their OPGs. In recent years, as more panoramic
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resorption are a few times more likely to be associated with ectopic eruption compared to teeth without the condition.69,70 Infection of the predecessor primary tooth has been suggested as another possible factor but is unlikely as many affected permanent teeth do not have primary predecessors. Natural history of PEIR lesions The progress of the resorption is usually slow before the tooth erupts into the oral cavity, although some lesions undergo periods of high activity. When the tooth breaks through the mucosa, micro-organisms may ingress into the resorbed cavity to cause further breakdown, so that a large carious lesion results.68 The disproportionate size of the cavity relative to the short time the tooth has been in the mouth should alert the clinician to the fact that the lesion is unlikely to be caries. In some affected teeth, the pulp is encroached soon after eruption, so that a dental abscess quickly develops. The majority of case reports suggest that there is no pain or other symptoms associated with the lesion until the pulp becomes infected (Fig 7a and 7b). If the lesion is surgically explored while the tooth is still unerupted, the tissue found within the cavity is usually connective tissue, which shows varying numbers of inflammatory cells including osteoclasts.67,68,74 In some cases, the soft tissue in the lesion connects directly with the gingival tissues through an external opening such as the buccal pit. However, it is evident from several case reports that the resorptive process usually stops when the tooth is fully erupted, when the direct communication between the lesion and the surrounding bone and soft tissues is severed. Hence in cases where the cavity is uncovered after the tooth is fully erupted, the lesion usually appears relatively empty, or filled with a friable material composed mainly decomposed dentine.75 On the other hand, if the cavity has been naturally uncovered through collapse of the cusps, the lesion takes on the appearance of a large carious cavity as it rapidly becomes colonized by the oral microbial flora. Management The management of PEIR should be centred on early diagnosis and treatment. In addition to the usual assessment of tooth presence and its position, the author recommends that all unerupted teeth on bitewings and other intra- and extra-oral radiographs be routinely scrutinized for PEIR.69,70 If an intracoronal radiolucency is detected in an unerupted, developing tooth, the tooth should be reexposed with a more detailed radiograph. For example, if an intracoronal radiolucency is detected on a panorex radiograph, an intra-oral periapical film would be required to accurately confirm the diagnosis. If the lesion is confirmed, its size and the projected time of tooth eruption should be determined. If a relatively small lesion is found in a tooth which is about to emerge, it may be monitored carefully until after tooth
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Fig 8a. An OPG of a 5-year-old child with a mandibular infected buccal cyst. Typical features of the condition include a partially erupted permanent molar, and the sclerotic buccal margin of the lesion. (Radiograph courtesy of Dr Paul Monsour.)

Fig 8b. Computerized tomography imaging scan of the mandible in the case depicted in Fig 8a, showing the buccal location of a mandibular infected buccal cyst in the buccal position, (arrow) and displacement of the molar tooth to the lingual. A similar condition may be developing on the contralateral side. (Radiograph courtesy of Dr Paul Monsour.)

eruption when the cavity may be restored using routine restorations. On the other hand, some lesions may be seen to be encroaching on the pulp even prior to tooth eruption. In these cases, it may be necessary to surgically expose the unerupted tooth to curette and restore the lesion.67 In these cases, it is recommended that the soft tissue within the lesion be sent for histopathological investigation. The prognosis of teeth affected by PEIR will depend on the size of the lesion at the time of discovery, whether there is pulpal involvement and the extent of root development. A large cavity which has encroached onto the pulp of an immature tooth with wide open root apices probably has a poor prognosis in terms of the extensive endodontic and restorative work which will be required. On the other hand, a fairly mature tooth with a PEIR lesion which is small to moderatesized should have good prognosis. These lesions may be easily restored using routine restorations. Recurrence of the resorption after curettage and restoration of the cavity has not been reported. Mandibular infected buccal cyst Clinical and pathological features The mandibular infected buccal cyst (MIBC), also known as the inflammatory paradental cyst is another
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unusual cause of dental abscesses in children and adolescents with partially erupting permanent molars.76 Since Craig first described this condition in 1976, and suggested the term paradental cyst,77 there has been debate regarding the appropriate name for this entity, although most authors agree to the term mandibular infected buccal cyst. The prevalence rate of 3 per cent reported by Ackerman et al. is probably an underestimate as many cases of MIBC are either not recognized or diagnosed as dentigerous cysts.78 Nearly all reported cases of MIBC involve the mandibular permanent first, second or third molars, although rarely, the condition may be encountered in the maxilla.79 While most cases occur unilaterally, bilateral MIBC has also been reported. In the case of the first molars, a buccal or distal location is most frequently encountered whereas in the case of third molars, the location is usually distal.79,80 In the case of the first and second permanent molars, symptoms often developed within a year of their emergence into the oral cavity. There is usually buccolingual tilting of the crown of the affected tooth, and there may be distal displacement of the crypt of the posterior adjacent tooth81 (Fig 8a and 8b). Pain, swelling and localized deep periodontal pocketing on the buccal or distal aspects are the most common symptoms in these teeth. In contrast, in the case of third molars, the time lapse between symptoms and emergence can be variable. These teeth are usually impacted and associated with previous histories of pericoronitis, and there is severe pain, swelling and trismus.81 On radiographs, the lesion usually presents as a cystlike, well-defined buccal or distal radiolucency of around 1-2cm in diameter, with a thin sclerotic rim81 (Fig 8a and 8b). Depending on the chronicity of the lesion, varying degrees of reactive bone may be seen at the margin. There is usually loss or attenuation of the lamina dura surrounding the root apices or a furcation radiolucency. In addition, there may a radiopaque inferior margin of the cyst, and attenuation of the cortical boundary of the crypt of the adjacent posterior tooth. Figure 8a shows typical radiographic features of the MIBC. In recent years, diagnosis of MIBC is further enhanced by computed tomography imaging (CT) scans82 (Fig 8b). In MIBC, the dental follicle surrounding a developing tooth, usually a mandibular molar, undergoes cystic changes due to inflammatory stimulation of the reduced enamel epithelium or the epithelial cell rests of Malassez.83 The source of the inflammation is usually the infected operculum or pericoronitis around an erupting tooth. In histologic sections, the MIBC may be distinguished by its lining of thick, proliferating, non-keratinized, stratified squamous odontogenic epithelium, and a wall composing of dense, mature fibrovascular connective tissue with an intense inflammatory cell infiltrate.78 The connective tissue of the cyst is found to be continuous with the follicle of the tooth in the majority of cases.78
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Management Although infected first and second molars were previously treated by extraction and cystic removal, a more conservative approach is currently recommended, employing antibiotics, curettage and removal of cystic contents. Retention of the affected tooth is associated with good success rates and normal healing in the majority of cases, although recurrent infection may occur in a small percentage of subjects.79 CONCLUSIONS In conclusion, although the majority of dental abscesses in children results from caries or trauma, a percentage originate from unusual conditions which range from developmental abnormalities to acquired conditions. These abscesses may be prevented by timely and accurate diagnosis and appropriate preventive measures. Knowledge of these conditions would aid the general practitioner in the differential diagnosis and treatment of these entities. REFERENCES
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Address for correspondence/reprints: Associate Professor W Kim Seow School of Dentistry The University of Queensland 200 Turbot Street Brisbane, Queensland 4000 Email: k.seow@uq.edu.au

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Australian Dental Journal 2003;48:3.