The adenomatoid odontogenic tumour: an update of selected issues.

The aim of this update was to present the recent notable progress within remaining questions relating to the adenomatoid odontogenic tumour (AOT). Selected issues that were studied included the following: (i) AOT history and terminology, (ii) the so-called peripheral AOT, (iii) AOT and the gubernaculum dentis and (iv) the so-called adenomatoid odontogenic cyst (AOC). The earliest irrefutable European case of AOT was described in 1915 by Harbitz as 'cystic adamantoma'. Recently, Ide et al. have traced two Japanese cases with irrefutable proof described by Nakayama in 1903. The so-called peripheral (gingival) variant of AOT seems to cover a dual pathogenesis, both an 'erupted intraosseous' and an 'extraosseous' (gingival) one. In 1992, we theorized that the generally unnoticed gubernaculum dentis (cord and canal) seems to be involved in the development of AOT. Ide et al. have concluded that the dental lamina in the gubernacular cord seems to be an embryonic source of the vast majority of AOTs. The suggestion by Marx and Stern to change the nomenclature of AOT to adenomatoid odontogenic cyst (AOC) is critically discussed. The present authors agree on the background of the work of several groups of researchers and WHO/IARC classifications that the biology of the follicular variant of AOT is already fully explained and does not make room for any change in diagnostic terms. Further, there is no reason to change terminology in this case where improvements or conditions to better clinical management are not an issue.

Pulse or hyaline ring granuloma. Review of the literature on etiopathogenesis of oral and extraoral lesions.

Since the late 1950s, reports on an unusual giant-cell granulomatous lesion affecting the jaws, lungs, stomach and intestines have been published. Histopathologically, the lesions showed the presence of structureless hyaline rings with multinucleated giant cells. The aim of this review was to summarize the literature on the etiopathogenesis of the so-called oral and extraoral pulse or hyaline ring granuloma. Literature was searched using PubMed and Medline. In addition, hand search was performed. Search words were oral and extraoral hyaline ring granuloma, giant-cell hyaline angiopathy, pulse granuloma and chronic periostitis. Numerous terms for hyaline ring granuloma have been introduced over time (1971-2008). One hundred seventy-three cases of oral hyaline ring granuloma have been retrieved from the literature. In the mandible, 72.3% occurred . Two theories for etiopathogenesis have been proposed: (1) the origin of the hyaline rings is due to a foreign material (pulse and legumes) having penetrated the oral mucosa or gastrointestinal tract and lungs (exogenous theory) and (2) the rings are due to hyaline degenerative changes in walls of blood vessels (endogenous theory). Experimental production of oral and extraoral hyaline ring granulomas is consistent with the exogenous origin. Particles or remains of leguminous cells having been implanted or aspirated into human tissues whether located to the oral cavity or throughout the entire digestive tract and respiratory system are thought to be causative. Pulse or hyaline ring granulomas are rare but are well-defined oral and extraoral lesions due to implantation of the cellulose moiety of plant foods in contrast to the starch components.

Adenomatoid odontogenic tumors: an analysis of 67 cases in a Thai population.

OBJECTIVE: The aim of this study was to determine the biologic profile of the adenomatoid odontogenic tumor (AOT) in a Thai population. STUDY DESIGN: Sixty-seven cases of AOT registered from January 1974 to May 2006 were studied retrospectively. Age, sex, variants of AOT, site and extent of tumors, associated impacted teeth, initial clinical diagnoses, clinical presentations, and duration of symptoms were analyzed. RESULTS: All AOT cases were intraosseously located, of which 55.2% were follicular and 44.8% extrafollicular. The 2 variants together were found more frequently in the maxilla than in the mandible, with a ratio of 2:1. Females were affected more often than males, with a ratio of 1.8:1. The peak incidence (56.7%) was found in the second decade of life. The majority of AOT lesions (68.7%) was found in the anterior jaws. Adenomatoid odontogenic tumors were observed more often on the left side of jaws (50.7% vs. 38.8%). Canines were the most common teeth associated with follicular AOT (67.5%), and the maxillary canines alone accounted for 51.3% of all cases. The majority of our patients presented with a painless swelling and with duration of symptoms of 6 months and longer. CONCLUSIONS: The distribution and characteristics of AOT in a Thai population are similar to the findings found in other populations. Interestingly, in this series we observed a case involving an impacted deciduous canine and a case associated with an impacted maxillary third molar.

An updated clinical and epidemiological profile of the adenomatoid odontogenic tumour: a collaborative retrospective study.

BACKGROUND: Adenomatoid odontogenic tumour (AOT) is a benign odontogenic jaw lesion. The aim of this study was to update the biological profile of AOT. MATERIAL AND METHODS: Cases published in the literature and cases in files of co-authors were included. RESULTS: 550 new cases were retrieved, and of a total of 1082 cases analysed, 87.2% were found in the second and third decades. The M:F ratio was 1:1.9. 70.8% were of the follicular variant (extrafollicular: 26.9%, peripheral: 2.3%). 64.3% occurred in the maxilla. 60% of follicular AOTs were associated with unerupted canines. Nineteen cases of AOT (2.8%, M:F ratio was 1:1.4) were associated with embedded third molars. Twenty-two peripheral AOTs (2.3%, M:F ratio was 1:5.3) were recorded. The relative frequency (RF) of AOT ranged between 0.6% and 38.5%, revealing a considerably wider AOT/RF range than hitherto reported (2.2-7.1%). CONCLUSIONS: This updated review based on the largest number of AOT cases ever presented, confirms the distinctive, although not pathognomonic clinicopathological profile of the AOT, its worldwide occurrence, and its consistently benign behaviour.

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.

Oral erythroplakia--a review.

Oral erythroplakia (OE) is considered a rare potentially malignant lesion of the oral mucosa. Reports entirely devoted to OE are very few, and only two reviews none of which are of recent date have been published. Only the true, velvety, red homogeneous OE has been clearly defined while the terminology for mixed red and white lesions is complex, ill-defined and confusing. A recent case control study of OE from India reported a prevalence of 0.2%. A range of prevalences between 0.02% and 0.83% from different geographical areas has been documented. OE is predominantly seen in the middle aged and elderly. One study from India showed a female:male ratio of 1:1.04. The soft palate, the floor of the mouth and the buccal mucosa is commonly affected. A specific type of OE occurs in chutta smokers in India. Lesions of OE are typically less than 1.5 cm in diameter. The etiology of OE reveals a strong association with tobacco consumption and the use of alcohol. Histopathologically, it has been documented that in OE of the homogenous type, 51% showed invasive carcinoma, 40% carcinoma in situ and 9% mild or moderate dysplasia. Recently, genomic aberrations with DNA aneuploidy has been demonstrated. p53 mutations with different degrees of dysplasia may play a role in some cases of OE. Transformation rates are considered to be the highest among all precancerous oral lesions and conditions. Surgical excision is the treatment of choice. Data on laser excision are not available. Recurrence rates seem to be high, reliable data are, however, missing. More studies on OE are strongly needed to evaluate a number of so far unanswered questions. The natural history of OE is unknown. Do OEs develop de novo or are they developing from oral leukoplakia through several intermediate stages of white/red lesions? The possible role of fungal infection (Candida micro-organisms) is not clear as is the possible role of HPV co-infection in the development of OE. More data on incidence and prevalence, biological behaviour and adequate treatment are urgently needed.

Adenomatoid odontogenic tumor mimicking a periapical (radicular) cyst: a case report.

The adenomatoid odontogenic tumor (AOT) is a benign (hamartomatous), noninvasive lesion with slow but progressive growth. A rare subvariant of the extrafollicular type of AOT may mimic periapical disease radiographically. We report on a 15-year-old girl with a periapical radiolucent lesion affecting teeth 7 and 8 initially suspicious of periapical disease, although clinical findings seemed to indicate a nonendodontic lesion. An exploratory surgical approach was chosen, and the final diagnosis of the removed noncystic tissue mass was microscopically confirmed to be an AOT.