Epigenetic mechanisms in odontogenic tumors: A literature review

ObjectiveEpigenetic mechanisms, such as DNA methylation, regulate important biological processes as gene expression and it was suggested that these phenomena play important roles in the carcinogenesis and tumor biology. The aim of this review is to provide the current state of knowledge about epigenetic alterations, focusing mainly on DNA methylation, reported in odontogenic tumors.DesignLiteratures were searched based in the combination of the following keywords: odontogenic tumors, epigenetics, DNA methylation, histone modifications, non-coding RNA, microRNA, DNA methyltransferases. Electronic databases (Medline/PubMed, Scopus and Web of Science) were screened.ResultsThe analysis of epigenetic alterations in different tumors has rapidly increased; however, limited information is available about epigenetic mechanisms involved in the formation of odontogenic tumors. DNA methylation is the most studied epigenetic modification in these tumors and the participation of non-coding RNA’s in odontogenic tumors has been recently addressed. Differential expression of DNA methyltransferases, altered DNA methylation patterns and aberrant expression of non-coding RNA’s were reported in odontogenic tumors.ConclusionsCurrent studies suggest epigenetics as an emerging mechanism, possibly implicated in etiopathogenesis of odontogenic tumors. Deeper understanding of the epigenetic abnormalities in these tumors could show potential applications as biomarkers or therapeutic possibilities in the future.     

Osteosarcoma of the jaws--a series from Kaduna, Nigeria

15 primary and one metastatic osteosarcoma of the jaw bones in Nigerians are described. The age range was typical of this tumour; most cases were in the mandible. Clinical and radiographic features were often diagnostic but the microscopic appearances were varied and problematical. No metastases were detected and effective surgical treatment depended upon the degree of spread in soft tissue. Inoperable tumours had infiltrated the pharyngeal and tonsillar area. Some resected cases survived for one year or more.     

Analysis of the pattern of maxillofacial fractures in Kaduna, Nigeria

There are considerable differences in the reported worldwide pattern of maxillofacial fractures. In the more developed countries of Europe, violence followed by road crashes are the predominant causes while in the developing world the causative factors are reversed with most being the result of road crashes. Interestingly, recent data indicated a 3:1 male:female ratio worldwide. Between 1991 and 2000, 443 cases of maxillofacial fractures were seen at the Maxillofacial Unit, Ahmadu Bello University Teaching Hospital, Kaduna, Nigeria. Road crashes were responsible for 246 cases (56%) followed by falls, 24% (n=108). In a previous report from this centre in 1980, 241 fractures were seen each year, so our lower rate of 44 cases a year is because the number of centres for the treatment of such injuries in Nigeria has increased. There has also been a fourfold increase in the number of women with facial fractures in this largely Moslem population, which reflects their greater exposure during the past 20 years. More patients were seen with mandibular than middle-third fractures, because more of the latter died. This shows that while more centres for treatment are available for patients with maxillofacial trauma, the lack of enforcement of legislation on the use of seat belts, drunken driving and inadequate emergency medical care have continued to cause considerable mortality and morbidity from these injuries in Nigeria. It is also difficult to compare data among centres because of inconsistent terminology.     

Peripheral epithelial odontogenic tumors: a review

Peripheral (extraosseous or soft tissue) odontogenic tumors are rare lesions that occur in the soft tissue overlying the tooth-bearing areas of the mandible and the maxilla. A review of the English-language literature revealed only 48 well-documented cases of peripheral epithelial odontogenic tumors. Thirty-two were peripheral ameloblastomas; six were peripheral adenomatoid odontogenic tumors; nine were peripheral calcifying epithelial odontogenic tumors; and one was a peripheral squamous odontogenic tumor. An additional four cases were reported as peripheral ameloblastomas in extragingival locations, but their odontogenic origin is debatable. Although the peripheral ameloblastoma is histologically similar to its central counterpart, it differs in its clinical features and biologic behavior. It does not exhibit an aggressive, destructive behavior and does not invade the underlying bone. Conservative excision of the tumor with minimal but adequate margins is the treatment of choice and recurrences are uncommon. This benign biologic behavior appears to be true also for lesions diagnosed as peripheral calcifying epithelial odontogenic tumors and undoubtedly is true for the peripheral adenomatoid odontogenic tumors.     

Amyloid-like material in odontogenic tumors.

Various types of odontogenic tumors (epithelial, mesodermal, and mixed tumors) were studied for the presence of amyloid material. Highman's Congo red and Wolman's standard toluidine blue methods were used for diagnosing amyloid. Of all types of odontogenic tumors studied, only the calcifying epithelial odontogenic tumors contained material that might be interpreted as amyloid-like.     

Necrotizing fasciitis of odontogenic origin in Ibadan, Nigeria

We reviewed eight patients with necrotizing fasciitis of odontogenic origin. There were three women and five men, mean age 58 (range 46-72), and none had any associated medical condition such as diabetes. All cases had symptoms of toothache for a mean duration of 34 days (range 26-42) before they sought treatment. Infection originated in the molar teeth region, and initially presented as an odontogenic or periodontal abscess. The clinical features of necrotizing fasciitis became apparent only after the superficial fascia had been invaded. The transient unusually reddish hue for a dark skin might be explained by the fact the deep fascia and muscles were affected before the superficial fascia and skin. Necrosis of the skin began in the submandibular region and progressed downwards. The necrotic area was less than the extent of infection. Antimicrobial treatment, debridement, and fasciotomy improved healing. Delay before appropriate treatment had an adverse affect on outcome, and one patient died.     

Classification of odontogenic tumours. A historical review

Using the term odontome for any tumour arising from the dental formative tissues, Broca suggested a classification of odontogenic tumours (OTs) in 1869. From 1888 to 1914, Bland-Sutton and Gabell, James and Payne modified tumour terminology, while maintaining Broca's odontome concept. Thoma and Goldman's classification (1946) divided the OTs into tumours of ectodermal, mesodermal and mixed origin and abolished the general term odontome. The Pindborg and Clausen classification (1958) based on the idea that the reciprocal epithelial-mesenchymal tissue interactions were also operating in the pathogenesis of OTs. In 1966, WHO established a Collaborating Centre for the Histological Classification of Odontogenic Tumours and Allied Lesions (including jaw cysts) headed by Dr Jens Pindborg. In 1971, the first authoritative WHO guide to the classification of OTs and cysts appeared followed in 1992 by a second edition. In 2002, Philipsen and Reichart produced a revision of the 1992-edition and in 2003, the editors of the WHO Blue Book series: 'WHO Classification of Tumours' decided to produce a volume on the Head and Neck Tumours including a chapter on Odontogenic Tumours and Bone Related Lesions. In July of 2005 this volume was published by IARC, Lyon.     

Ameloblastoma: clinical features and management of 315 cases from Kaduna, Nigeria

This paper reviews 315 cases of ameloblastoma seen and managed at the Oral and Maxillofacial Clinic of Ahmadu Bello University Hospital, Kaduna, Nigeria over a 20-year period. The data collected on age at presentation, sex distribution, clinical presentation and modalities of treatment are analysed and discussed.A male preponderance was found, with peak presentation in the third and fourth decades of life. Few patients presented with mucosal ulceration, while some presented atypically with expansion of either the lingual or buccal cortical plate of the mandible. Resection of the lesion with dento-alveolar bone and preservation of the lower border of the mandible is effective conservative management in patients with an intact lower border. We do not recommend curettage or enucleation because of the frequency of recurrence. One hundred percent success was recorded in the patients rehabilitated using autogenous bone grafts. Where practicable, bone grafting should be done immediately to avoid the common complications of displacement of bony remnants and occlusal disharmony that occur when grafting is delayed.     

Polyoma virus-induced murine odontogenic tumors.

Neonatal mouse pups were injected subcutaneously with polyoma virus to induce odontogenic tumors. This treatment resulted in a spectrum of tumors that arose in organs dependent upon epithelial-mesenchymal interactions for their organogenesis, which included the teeth, salivary glands, thymus, and lacrimal glands. In addition, several odontogenic tumors with a histologic resemblance to ameloblastoma were identified and analyzed with respect to the presence of markers specific for various stages of ameloblast differentiation. Immunodetection analyses of the odontogenic tumors identified fibronectin and laminin, typical of basement membrane organization during early tooth organogenesis. These same tumors failed to express amelogenin, a gene whose expression is limited to differentiated ameloblasts. In contrast, a 47 kDa enamelin-like polypeptide was identified with the use of an antienamelin antibody. These data were interpreted to suggest that the polyoma virus truncated the differentiation pathway for these odontogenic tissues at an early stage of their development and retained the expression of basement membrane components and the enamelin-like polypeptides, yet excluded expression of amelogenin gene products. This observation suggests that polyoma viral transformation may dysregulate odontogenic tissue interactions and produce tumors composed of cells arrested at a specific stage in their development.     

Frequency of odontogenic cysts and tumors: a systematic review

A systematic review of the literature from 1993 to 2011 was undertaken examining frequency data of the most common odontogenic cysts and tumors. Seven inclusion criteria were met for the paper to be incorporated. In the preliminary search 5231 papers were identified, of these 26 papers met the inclusion criteria. There were 18 297 odontogenic cysts reported. Of these there were 9982 (54.6%) radicular cysts, 3772 (20.6%) dentigerous cysts and 2145 (11.7%) keratocystic odontogenic tumors. With the reclassification of keratocystic odontogenic tumor in 2005 as an odontogenic tumor, there were 8129 odontogenic tumors reported with 3001 (36.9%) ameloblastomas, 1163 (14.3%) keratocystic odontogenic tumors, 533 (6.5%) odontogenic myxomas, 337 (4.1%) adenomatoid odontogenic tumors and 127 (1.6%) ameloblastic fibromas. This systematic review found that odontogenic cysts are 2.25 times more frequent than odontogenic tumors. The most frequent odontogenic cyst and tumor were the radicular cyst and ameloblastoma respectively.     

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提要：颌骨内的胚胎性成牙组织常为牙源性肿瘤的组织来源。因此,颌骨是人类骨骼中最好发上皮性肿瘤的部位,并且常伴有牙体样组织形成。牙源性恶性肿瘤发病率低,缺乏临床及病理诊断经验,需与多种来源类型的肿瘤鉴别诊断,这些侵袭性病损具有较高的复发倾向,生物学行为等方面具有特殊性。本文着重讨论牙源性恶性肿瘤的病理学诊断。     

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牙源性囊肿与牙源性肿瘤是口腔颌面部较为常见的疾病。由于临床表现的多样性,易与其他类型的颌面部囊肿或肿瘤相混淆,而且不同类型的牙源性囊肿和肿瘤其治疗方案也有所区别,所以牙源性囊肿及肿瘤的术前诊断对于其治疗方案的选择起着关键的作用,而在其诊治的过程中,影像学检查起到了非常重要的作用;不同类型的牙源性囊肿及肿瘤的影像学表现也各具特征。本文对常见的牙源性囊肿(牙源性角化囊肿等)及肿瘤(成釉细胞瘤、恶性成釉细胞瘤等)的影像学表现结合实际的影像学图片作简单的介绍,比较各种影像学检查在上述疾病诊断中所具有的优点,以期望能将CT、MRI及全景片等影像学检查手段更好的运用于上述疾病的诊治中。     

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由于颌骨内的成牙组织常可作为囊肿和肿瘤的组织来源,因此颌骨是人类骨骼中最好发上皮性囊肿和肿瘤的部位。这类牙源性病损好发于年轻人,可造成颌骨及邻近组织的破坏,导致口腔颌面部外形改变,某些侵袭性病损具有较高的复发倾向,可对患者的生存质量及心理健康造成严重影响。本文着重讨论几种常见的牙源性囊肿与牙源性肿瘤的病理学诊断。     

A retrospective review of treatment of the odontogenic keratocyst.

PURPOSE: The purpose of this study was to evaluate different surgical treatment methods for odontogenic keratocysts and the outcome of those treatments over a 25-year period. PATIENTS AND METHODS: A retrospective review was performed of 40 patient charts treated at the University of Iowa Hospitals and Clinics (Iowa City, IA) from 1977 to 2002 with the diagnosis of odontogenic keratocyst. Demographic data were collected along with lesion location, symptoms present at initial presentation, surgical treatment rendered, length of follow-up, and incidence of recurrence. RESULTS: Surgical treatments included enucleation, enucleation with Carnoy's solution, peripheral ostectomy, peripheral ostectomy with Carnoy's solution, and en bloc resection. Recurrence was found in 9 to 40 patients. Seven of 9 recurrences (78%) occurred in 5 years or less, with 2 (22%) occurring more than 5 years after initial treatment. Patients treated with enucleation had a recurrence rate of 54.5% (6 of 11 patients). One of 2 patients treated with enucleation and Carnoy's solution had a recurrence. Those treated with peripheral ostectomy had a recurrence rate of 18.2% (2 of 11). Peripheral ostectomy with Carnoy's solution had no recurrences (0/13). CONCLUSION: Treatment of an odontogenic keratocyst with peripheral ostectomy, with or without the use of Carnoy's solution, had a significantly lower rate of recurrence. Treatment with enucleation, with or without the use of Carnoy's solution was associated with a significantly higher recurrence rate.     

Molecular pathology of odontogenic tumors

Odontogenic tumors are lesions derived from the elements of the tooth-forming apparatus and are found exclusively within the jawbones. This review represents a contemporary outline of our current understanding of the molecular and genetic alterations associated with the development and progression of odontogenic tumors, including oncogenes, tumor-suppressor genes, oncoviruses, growth factors, telomerase, cell cycle regulators, apoptosis-related factors, regulators of tooth development, hard tissue-related proteins, cell adhesion molecules, matrix-degrading proteinases, angiogenic factors, and osteolytic cytokines. It is hoped that better understanding of related molecular mechanisms will help to predict the course of odontogenic tumors and lead to the development of new therapeutic concepts for their management.