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Periapical radiolucencies are some of the most common radiographic lesions encountered in clinical practice.Most periapical radiolucent lesions are of endodontic origin and result from the destruction of bone secondary to a necrotic pulp.When tissue obtained from these lesions is submitted for pathological examination, the diagnosis most often will be periapical granuloma, periapical cyst, and occasionally periapical scar or periapical abscess. Lesions of non-endodontic origin may mimic the typical periapical lesion associated with a necrotic pulp. Such nonendodontic periapical lesions may be diagnosed as a cyst or a benign aggressive, benign fibro-osseous, or malignant lesion. It is impossible to differentiate among this plethora of pathologic entities without the submission of tissue for histopathological examination. In addition, many of these pathologic entities possess different behaviors and may require more aggressive treatment and additional follow-up.
Therefore, it is important to submit any tissue that is obtained from the apical region of a tooth for microscopic examination. According to the guidelines of the American Association of Endodontists, the microscopic examination of a periradicular lesion is indicated at any time that tissue can be harvested.1 However, previous data suggest that the selective submission of tissue obtained from periapical lesions is a common practice.2 The authors will briefly describe the variety of pathologic entities that may be included in the differential diagnosis of a periapical radiolucency.
The most important developmental odontogenic cyst to rule out in the differential diagnosis of a periapical radiolucency is the odontogenic keratocyst (OKC). In the most recent World Health Organization (WHO) publication,3 the odontogenic keratocyst has been reclassified as keratocystic odontogenic tumor (KCOT). The histopathology of KCOT is rather distinctive. It presents as a cystic lesion with a uniform six- to eight-cell-layer thick epithelial lining and a corrugated luminal parakeratin surface. In addition, the basal cells of the epithelium are palisaded with hyperchromatic nuclei.Varying amounts of keratin may be noted within the lumen of the cyst. The cyst wall is most often comprised of un-inflamed fibrous connective tissue.
There have been previous reports in the literature of KCOT presenting as a periapical radiolucency.6-10 KCOT is a developmental lesion that arises from rests of dental lamina. The importance of this particular lesion is that it requires at least a 7-year follow-up after treatment, which typically consists of enucleation and curettage followed by peripheral ostectomy, to evaluate for recurrences. Long-term follow-up is necessary because although most recurrences occur within 5 years, recurrences have been reported as long as 7 years from the initial diagnosis and treatment. Recurrent KCOTs typically result from remnants of the cyst wall that have not been thoroughly excised. So-called daughter cyst remnants within this incompletely excised tissue may give rise to additional KCOTs. In a retrospective study of nonendodontic periapical lesions, KCOTs were the most commonly diagnosed, representing 42.3% of the total.11
Multiple KCOTs may be associated with the Gorlin syndrome (nevoid basal cell carcinoma syndrome). In addition to the jaw cysts, the most significant complication for patients with this syndrome is the development of multiple basal cell carcinomas on both sun-exposed and non-sunexposed skin.Many patients with Gorlin syndrome will present with their first KCOT before the age of 17. Furthermore, KCOTs associated with the syndrome may present either synchronously (simultaneously) or metachronously (at different times).
A developmental non-odontogenic cyst that may be misdiagnosed as a lesion of endodontic origin is the nasopalatine duct cyst. The nasopalatine duct cyst, or incisive canal cyst, is the most common developmental nonodontogenic cyst of the oral region. It arises from remnants of epithelium within the incisive canal and, therefore, typically presents between the maxillary central incisors.The nasopalatine duct cyst may present as a well-defined radiolucency apical to the maxillary central incisors.12-13 In many cases teeth in association with a nasopalatine duct cyst will be vital; however, if a cyst is large enough it may devitalize one or more of the teeth in the region, thus mimicking a lesion of endodontic origin.
Falling under the category of a benign aggressive lesion, the central giant cell granuloma is the one that most commonly may present as a periapical radiolucency. 6,14-18 Previously, these lesions were thought to represent a reparative process, hence the original name of central giant cell reparative granuloma. Currently, the etiology for these lesions remains unknown. Although not all central giant cell granulomas display an aggressive clinical course, an additional consideration is that the histopathology of central giant cell granuloma is identical to that of the brown tumor of hyperparathyroidism. Central giant cell granulomas are most often diagnosed in patients under the age of 30 in the posterior mandibular region and also classically may occur in the anterior mandible crossing the midline. Occasionally, central giant cell granulomas may also occur in the anterior maxillary region.
Additional benign aggressive lesions that have been reported as periapical radiolucencies include Pindborg tumor (calcifying epithelial odontogenic tumor), Langerhans cell disease, and central odontogenic fibroma.14,19-21
The most common benign fibro-osseous lesion that may mimic a lesion of endodontic origin is an early periapical cementoosseous dysplasia. This lesion typically presents at the apices of the mandibular incisors in young and middle-aged African- American females. Periapical cementoosseous dysplasia often has a multifocal presentation, making it less of a diagnostic challenge.However, there have been cases of solitary lesions previously reported.22-23 The key to discerning periapical cemento- osseous dysplasia from a lesion of endodontic origin is to perform pulp vitality testing in addition to a thorough clinical history and evaluation of the radiographic presentation. The lamina dura associated with teeth involved by periapical cementoosseous dysplasia should be intact, unlike that seen with a lesion of endodontic origin. Over time these lesions will display varying amounts of mineralized material (cementum and bone) that further distinguishes them from a periapical radiolucency associated with a nonvital tooth. Once the vitality of the tooth or teeth in question has been validated to confirm the diagnosis of periapical cemento-osseous dysplasia, no further treatment is indicated.
Other, less common benign fibro-osseous lesions to consider in the differential diagnosis of periapical radiolucency would be cemento-ossifying fibroma and benign cementoblastoma. Although both of these typically present as well-defined mixed radiolucent/radiopaque lesions, initially they may present as well-defined periapical radiolucent lesions. The cementoblastoma is a benign neoplasm of cementum that most often occurs in association with the apex of a mandibular first molar during the second and third decades.
Although uncommon, both primary and metastatic malignancies should be included in the differential diagnosis of a periapical radiolucency. The most common primary malignancy to arise in bone, with the exception of hematopoietic malignancies such as leukemia or lymphoma, is osteosarcoma.Other primary intraosseous malignancies that have been reported include salivary gland adenocarcinoma and antral carcinoma. A wide range of metastatic lesions have been reported to mimic lesions of endodontic origin.Metastatic lesions to the jaws most often represent carcinomas including breast, lung, prostate, kidney, or colon.19,20,24-38 Typical radiographic and clinical features that suggest a malignancy include a lesion with poorly defined or ragged borders, spiking root resorption, uniform widening of the periodontal ligament space around one or more teeth, tooth mobility, pain or paresthesia, and failure of the lesion to resolve after endodontic therapy.
Case Study
A 45-year-old African-American man presented to the clinic with a chief complaint of gingival swelling of the anterior maxillary region for the past several years.He reported that it had increased and subsequently decreased in size during that time, and recently had increased in size during the previous 2 months.He reported a previous history of trauma to the area in question.The patient's medical history was noncontributory. His social history was significant for being a recovering cocaine addict.He was not taking any medications and reported no known drug allergies.
The extraoral examination was within normal limits. The intraoral examination revealed a 7-cm buccal swelling with sinus tract formation, which had been present for approximately 6 months, at the apex of tooth No. 10 (Figure 1). It was slightly firm and nontender upon palpation. Radiographic examination revealed a radiolucent lesion from the midline of the left maxilla to the apex of tooth No.13 and the remaining roots of tooth No. 9 (Figure 2). Probing depths were within normal limits. Pulp vitality testing was performed on teeth Nos. 10 through 14 (Table 1). Root canal treatment was performed on tooth No. 10, and after 1 year the radiolucency did not diminish in size. The patient subsequently underwent enucleation of a cystic lesion at the apex of tooth No.10 followed by an apicoectomy. The surgical procedure consisted of a midcrestal intrasulcular incision followed by a vertical releasing incision from the mesial of tooth No.10 to the distal of tooth No.13. The surgical procedure consisted of a midcrestal intra-sulcular incision from the distal of tooth No. 13 to the mesial of tooth No. 10 and continuing as a mid-crestal incision to the midline; then a vertical releasing incision was made at the midline. A full-thickness mucoperiosteal flap was elevated to expose the lesion (Figure 3 and Figure 4). After the cyst was enucleated it was submitted for histopathologic examination (Figure 5).The area was debrided by opening a flap and cleaning the area with a surgical curette.Any visible remnants of the granuloma were withdrawn from the bony cavity. An apicoectomy was performed and sealed with an intermediate restorative material. A bone graft was not placed because of the patient's limited financial resources. The flap was repositioned with interrupted sutures. Postoperative instructions and anti-inflammatory medications were provided to the patient.
The histopathologic examination revealed a cyst lined by nonkeratinized stratified squamous epithelium. The cyst wall consisted of fibrous connective tissue that supported an infiltrate of lymphocytes and plasma cells (Figure 6). Extravasated red blood cells, collections of a brown globular foreign material suggestive of hemosiderin, and cholesterol granuloma formation were also observed (Figure 7). This was consistent with a diagnosis of periapical cyst. Although it would have been ideal to have a follow-up radiograph at 6 months, because this case was completed at an academic setting in an endodontic postgraduate clinic, the patient was lost to follow-up.
Discussion
By far, most periapical radiolucencies result from the devitalization of teeth representing various entities including periapical cyst, periapical granuloma, periapical abscess, or periapical scar. Occasionally, though, dentists must also consider other less common pathologic entities presenting as periapical radiolucencies that have been reviewed.
Pulpal inflammation ultimately may lead to irreversible pulpitis and pulpal death. Four categories of noxious stimuli leading to pulpal inflammation include: mechanical damage, thermal injury, chemical irritation, and bacterial infection.39 Pulp death leads to the development of a periapical granuloma. A periapical granuloma, or chronic apical periodontitis, is comprised of chronically inflamed granulation tissue. Inflammation may stimulate the epithelial rests of Malassez to proliferate, thus forming an epitheliumlined cyst, or periapical cyst. Periapical cyst, which is synonymous with radicular cyst, is the most common cystic lesion occurring in the jaws. Patients will generally be asymptomatic, unless there is an exacerbation of acute inflammation.
In this particular case the differential diagnosis in addition to periapical cyst may also include chronic apical periodontitis (periapical granuloma), odontogenic keratocyst (KCOT), and central giant cell granuloma. If the tooth had been vital, periapical cyst or granuloma could have been ruled out.
A periapical cyst radiographically cannot be distinguished from a periapical granuloma. The periapical cyst may present as either a well-defined or poorly defined noncorticated radiolucency. Root resorption is not uncommon. Bony expansion may also be noted in larger lesions. A comprehensive medical and dental history, clinical examination, and radiographic examination should be performed to develop a proper differential and definitive diagnosis. This will allow for the development of a proper treatment plan.
Initially, treatment should consist of conservative management by root canal therapy. Resolution of the lesion with a nonsurgical protocol should be achieved within 6 months to 1 year.Appropriate clinical and radiographic follow-up is necessary to document resolution of the lesion. If the lesion does not resolve after root canal therapy, an apicoectomy procedure with retrofill will be necessary.40 Any tissue excised should be submitted for histopathologic examination. Retrofill can be accomplished using amalgam, intermediate restorative material, or super ethoxy benzoic acid.41 An alternative to apicoectomy would be extraction of the tooth and curettage of the extraction socket to remove any soft tissue.
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About the Authors
Peter J. Giannini, DDS, MS
University of Nebraska Medical
Center College of Dentistry
Lincoln, Nebraska
Howard B. Gross, DDS, MSD
University of Pennsylvania
School of Dental Medicine
Philadelphia, Pennsylvania
Private Practice in Periodontics and Dental Implants
Philadelphia, Pennsylvania
Loven A. Litchmore, DMD, MPH
Temple University,
Maurice H. Kornberg School of Dentistry
Philadelphia, Pennsylvania
Brett M. Strong, DDS
Private Practice in Endodontics
Round Rock, Texas