Analysis of the neoplastic nature and biological potential of sporadic and nevoid basal cell carcinoma syndrome-associated keratocystic odontogenic tumor

BACKGROUND: Keratocystic odontogenic tumor (KCOT), also known as odontogenic keratocyst, is a benign cystic neoplasm, which may be associated with nevoid basal cell carcinoma syndrome (NBCCS) and if it does, will occur as multiple cystic lesions. KCOT is locally destructive despite its bland histological features. However, the neoplastic nature of KCOT is not well established. Heparanase is an endo-d-glucuronidase enzyme that specifically cleaves heparan sulfate (HS) and the increase of its level in tumors promotes invasion, angiogenesis, and metastasis. METHODS: To investigate the neoplastic character of KCOT, we studied the localization patterns of heparanase in KCOT, focusing on the differences between sporadic and NBCCS-associated KCOTs, by immunohistochemistry and in situ hybridization. To compare the expression pattern of these cysts with non-tumorous odontogenic developmental cyst, dentigerous cyst was included. RESULTS: All the odontogenic cysts showed positive immunoreaction for heparanase protein in various intensities. The expression pattern of heparanase gene corresponded to that of protein expression. Interestingly, intense gene and protein expressions were observed in KCOT associated with NBCCS compared with sporadic ones and dentigerous cyst. CONCLUSIONS: The results implied that heparanase expression may be correlated with the neoplastic properties of KCOT, particularly in NBCCS-associated cases.     

Perlecan-rich epithelial linings as a background of proliferative potentials of keratocystic odontogenic tumor

Background:  The intraepithelial deposit of perlecan, a basement membrane-type heparan sulfate (HS) proteoglycan, has been demonstrated in neoplastic conditions such as salivary gland tumors, odontogenic tumors, and oral carcinoma in situ . Our aim was to determine whether perlecan turnover was enhanced in the lining cells of keratocystic odontogenic tumor (KCOT), which had been recently renamed from odontogenic keratocyst because of its accumulated evidence of neoplasm, as a possible background for neoplastic proliferation.
Methods:  Ten surgical specimens from each of KCOT, dentigerous cyst, and radicular cyst were examined for the expressions of perlecan core protein, HS chains, heparanase, and Ki-67 by immunohistochemistry and in situ hybridization.
Results:  In KCOT, perlecan core protein and HS chains were localized on the cell border from the parabasal to subkeratinized layers of the lining epithelium. Heparanase was localized in a similar fashion to those for perlecan and HS chains but was within the cytoplasm. mRNA signals for perlecan core protein and heparanase were mostly compatible with their protein signals. Ki-67-positive cells were localized mainly in the second basal cell layers with definitely higher labeling indices (approximately 31.3%, second layer). In contrast to KCOT, dentigerous cysts and radicular cysts had no perlecan, HS chains, and heparanase deposition in their linings with extremely lower Ki-67 indices (0.4–0.8%).
Conclusion:  The result suggests that the characteristic intra-lining-epithelial deposit of perlecan in KCOT, which has never been seen in other cystic jaw lesions, is a new evidence supporting the neoplastic nature of KCOT.     

Volumetric analysis of keratocystic odontogenic tumors and non-neoplastic jaw cysts – Comparison and its clinical relevance

The keratocystic odontogenic tumor (KCOT) is capable of causing vast osseous destruction. Histopathological examination is pivotal for diagnosis. The diagnostic process can sometimes be hindered by tissue inflammation of KCOTs with loss of defining criteria, resulting in misdiagnosis as an odontogenic jaw cyst. We discuss the possible merits of volumetric analysis when facing this particular diagnostic dilemma and for pathophysiological characterization of KCOTs. We included 114 patients, of whom 27 were histopathologically diagnosed with a KCOT and 87 with dentigerous (n = 41) and periapical cyst (n = 46). Semiautomatic segmentation and radiological analysis of preoperative cone beam computed tomography (CBCT) image data was carried out using ITK-SNAP. The mean volumetric extent of KCOTs is significantly higher compared to non-neoplastic odontogenic jaw cysts (p = 0.001). The mean volume and standard deviation for KCOTs and non-neoplastic odontogenic jaw cysts was 10381 mm³ ± 6410 and 5813 mm³ ± 4425, respectively. Volumetric analysis reveals that KCOTs significantly exceed the mean size of non-neoplastic odontogenic jaw cysts, adding an argument in favor of the neoplastic nature of KCOTs. In the case of difficult histopathological examination, lesions with a size exceeding a value of about 3000 mm³ could be considered for close clinico-radiologic follow-up.     

Differences in collagen fibres in the capsule walls of parakeratinized and orthokeratinized odontogenic cysts

Epithelial-mesenchymal interactions are thought to play an important role in the pathogenesis of odontogenic lesions. Keratocystic odontogenic tumour (KCOT) is a benign cystic neoplasm with a characteristic parakeratinized epithelial lining, which differs histologically and behaviourally from the so-called orthokeratinized odontogenic cyst (OOC). The purpose of this study was to investigate the differences in collagen fibres within the fibrous tissue walls of KCOT and OOC. Formalin-fixed paraffin-embedded tissue samples from 15 cases of KCOT and 15 cases of OOC were collected. Paraffin sections were stained with picrosirius red and observed under a standard light microscope using optical polarization. Unicystic ameloblastoma (UA, 15 cases) and subcutaneous epidermoid cysts (EC, 15 cases) were included in the study for comparative purposes. Significant difference was detected between the polarization colours in the fibrous tissue walls of KCOT and OOC (P < 0.05), whilst no significant differences were found between KCOT and UA and between OOC and EC (P > 0.05). The stromal collagen fibres of KCOT were different from those of OOC, but similar to those of UA, which suggests that the stroma of KOCT may play an important role in determining the neoplastic behaviour of the lesion through epithelial-mesenchymal interaction.     

Prognostic factors for keratocystic odontogenic tumor (odontogenic keratocyst): analysis of clinico-pathologic and immunohistochemical findings in cysts treated by enucleation

Background:  The purpose of this study was to determine prognostic factors for the recurrence of keratocystic odontogenic tumors (KCOTs) following simple enucleation by examining clinico-pathologic and immunohistochemical findings.
Methods:  Following enucleation, the frequency of recurrence among 32 subjects diagnosed with KCOT was analyzed for tumor site, radiographic and histologic features, and immunopositivity for Ki-67 and p53.
Results:  Keratocystic odontogenic tumors in four out of 32 subjects (12.5%) recurred during the follow-up period (median: 33 months, range: 7–114 months). Three out of four subjects (75.0%) among recurrent group showed high expression of Ki-67 (LI >10%) in basal layer and four (4/28; 14.3%) among non-recurrence group ( P  = 0.025). Expression of p53 among non-recurrent group was observed in 11 subjects (11/28; 39.3%), and in three subjects (3/4; 75.0%) among the recurrent group ( P  = 0.295). Hazard risk for the recurrence of KCOT was 4.02 (95% CI 1.42–18.14) for high Ki-67 expression in the basal layer by the Cox proportional hazard model ( P   =  0.009). In our study, none of the other clinico-pathologic variables were associated with the recurrence of KCOT.
Conclusion:  The results suggested that the evaluation of Ki-67 expression in KCOT at the time of pathological diagnosis might be helpful for consideration of appropriate adjunctive surgical procedures to avoid a recurrence and may serve as a prognostic marker.     

Podoplanin expression in human tooth germ tissues and cystic odontogenic lesions: an immunohistochemical study

J Oral Pathol Med (2010) 39 : 115–120
Background:  Podoplanin expression was described in mouse tooth germ and apical bud cells. The aim of this study was to analyse the podoplanin expression of human tooth germ tissues, adult teeth and odontogenic lesions immunohistochemically.
Study Design:  Nine human tooth germ biopsies and seven healthy permanent teeth extracted for orthodontic reasons were examined. Anti-podoplanin (D2-40) reactivity was investigated immunohistochemically. Five well-defined cystic odontogenic lesions (10 radicular cysts, 10 follicular cysts, three keratocystic odontogenic tumours, five ameloblastomas, and two adenomatoid odontogenic tumours) were analysed simultaneously.
Results:  Podoplanin expression was detected in the majority of epithelial and ecto-mesenchymal cells of human tooth germ tissues, odontoblasts and superficial dental pulp fibroblasts of permanent teeth. Cystic odontogenic lesions revealed positive reactions predominantly at the invasion front edge within basal epithelial layers.
Conclusion:  Podoplanin appears to be involved in the orthologic and pathologic processes of the formation of elongated cell extensions and odontoblastic fibers, in the epithelial–mesenchymal transition and local invasion during tooth germ development as well as in both reactive and neoplastic odontogenic cystic lesions.     

Prevalence of developmental odontogenic cysts in children and adolescents with emphasis on dentigerous cyst and odontogenic keratocyst (keratocystic odontogenic tumor)

Objective. To investigate the incidence and prevalence of developmental odontogenic cysts in children and adolescents and compare the features of the two most common types, dentigerous cyst and keratocystic odontogenic tumor (KCOT). Study design. A retrospective review in a series of 369 patients with all histological diagnoses of developmental odontogenic cysts in children (≤12 years) and adolescents (13–18 years) was conducted. Results. Among these, 361 (97.8%) patients were diagnosed as dentigerous cyst (n = 281) and KCOT (n = 80), with the male-to-female ratios of dentigerous cyst and KCOT both being 2:1. The average age of the patients with KCOT was older than that of those with dentigerous cyst (14.7 years vs 11.8 years, p < 0.001). Dentigerous cyst (59.1%) was more common in children, but KCOT (78.8%) was more common in adolescents (p < 0.001). Dentigerous cyst (57.6%) predominantly located on the maxilla, but KCOT (60.3%) predominantly located on the mandible (p = 0.010). Conclusions. Adolescent patients with lesions located on the mandible would favor KCOT over dentigerous cyst. This study aids in better knowledge of the prevalence of developmental odontogenic cysts in a large pediatric population, and shows that a well-supported early diagnosis is indispensable for a more adequate treatment.     

Actual Proliferating Index and p53 protein expression as prognostic marker in odontogenic cysts

Background:  The purpose of this study was to evaluate the biological aggressiveness of odontogenic keratocyst/keratocystic odontogenic tumour (KCOT), radicular cyst (RC) and dentigerous cyst (DC) by observing the actual proliferative activity of epithelium, and p53 protein expression.
Methods:  The actual proliferative activity was measured by Ki-67 Labelling Index and argyrophilic nucleolar organizing regions (AgNOR) count per nucleus. The p53 protein expression was also evaluated.
Results:  Ki-67 positive cells were observed higher in suprabasal cell layers of KCOT with uniform distribution, a few of them were predominantly observed in basal cell layer in RC and DC. The AgNOR count was significantly higher in suprabasal cell layers of KCOT. The actual proliferative activity was noted to be higher in suprabasal cell layers of KCOT. The p53 immunolabelling was dense and scattered in basal and suprabasal cell layers in KCOT. The weakly stained p53 positive cells were observed diffusely distributed in KCOT, whereas they were mainly seen in basal cell layer of RC and DC.
Conclusion:  The quantitative and qualitative differences of the proliferative activity and the p53 protein expression in sporadic KCOT may be associated with intrinsic growth potential that could play a role in its development and explain locally aggressive biological behaviour. AgNOR count and p53 protein detection in odontogenic lesions can be of great consequence to predict the biological behaviour and prognosis.     

Orthokeratinized Odontogenic Cysts Presenting as a Periapical Lesion: Report of a Case and Literature Review

Introduction

Inflammatory cysts, granulomas, abscesses, and fibrous scars represent most periapical radiolucencies. However, other less common lesions, such as orthokeratinized odontogenic cysts (OOCs), can be found at this region, and they deserve to be discussed because the prognosis for an OOC is different from that expected for the ordinary inflammatory periapical diseases.

Methods

An interesting case of OOC associated with a nonvital tooth in a 40-year-old woman is described. After a previous clinical diagnosis of a radicular cyst, the tooth was extracted, and the lesion was enucleated and submitted to microscopy examination.

Results

Because of the detection of an orthokeratinized epithelium lining, a diagnosis of OOC was concluded. After 2 years of periodic follow-up, no signs of recurrence were detected.

Conclusions

The presence of keratin in radicular lesions must be carefully evaluated to eliminate the diagnosis of lesions with more aggressive behavior, such as an OOC or even a keratocystic odontogenic tumor. Hence, histopathologic examination is mandatory to confirm the type of lesion and to differentiate other pathologic conditions, therefore establishing patients' prognoses precisely.     

Exploring the concept of “inflammatory angiogenesis” in keratocystic odontogenic tumor

Objective: The aim of the present study was to investigate the role of inflammation in angiogenesis of keratocystic odontogenic tumor (KCOT). Study Design: Twenty inflamed and 20 non-inflamed KCOTs were selected based on quantitative scoring of inflammation which was also applied on 20 radicular cysts. Microvessel density was assessed in all samples using CD34 antibody and angiogenesis was compared between the three groups. Statistical analysis was performed using one-way analysis of variance followed by post-hoc Scheffe test and P values less than 0.05 were considered significant. Results: A statistically significant difference in angiogenesis was found between radicular cysts and both inflamed and non-inflamed KCOTs (P < 0.001), but not between inflamed and non-inflamed KCOTs (P =0.347). Conclusion: Based on the results obtained in the present study, it seems that the effect of inflammation on angiogenesis in KCOT is minimal. However further investigation using other methods of evaluation is suggested to fully clarify the role of “inflammatory angiogenesis” in this neoplasm. Key words:Keratocystic odontogenic tumor, radicular cyst, angiogenesis, inflammation.     

Ameloblastoma, calcifying epithelial odontogenic tumor, and glandular odontogenic cyst show a distinctive immunophenotype with some myoepithelial antigen expression

Background:  Odontogenic neoplasms have some morphologic overlap with salivary gland neoplasms, many of which show myoepithelial differentiation. In the 1980s, an ultrastructural study identified a population of myoepithelial-like cells in calcifying epithelial odontogenic tumor. Myoepithelial derived tumors have since been shown to have distinct immunohistochemical profiles.
Methods:  We examined a series of odontogenic neoplasms, including 11 ameloblastomas, four calcifying epithelial odontogenic tumors, five glandular odontogenic cysts (GOCs), and five keratocystic odontogenic tumors with a panel of myoepithelial-associated immunohistochemical stains. We also assessed representative control examples of oral mucosa, odontogenic rests, and dentigerous cysts.
Results:  All of the neoplastic and non-neoplastic oral epithelium-derived entities share a p63-positive, high molecular weight cytokeratin (CK5/6)-positive immunophenotype. Calponin reactivity was at least focally present in two of four calcifying epithelial odontogenic tumors, three of five GOCs, and 10 of 11 ameloblastomas; the sole completely non-reactive ameloblastoma represents a lung metastasis. One case of calcifying epithelial odontogenic tumor was focally positive for glial fibrillary acidic protein. However, other more definitive markers of myoepithelial differentiation, including S-100 and smooth muscle actin, were negative. Two of three calcifying epithelial odontogenic tumors and five of five GOCs were also positive for a low molecular weight cytokeratin (CK7).
Conclusions:  Ameloblastomas, GOCs, and calcifying epithelial odontogenic tumors show a distinctive immunophenotype which overlaps with that of myoepithelial-derived salivary gland neoplasms but does not provide definitive support for myoepithelial differentiation.     

A comparative study of epithelial cell proliferation between the odontogenic keratocyst, orthokeratinized odontogenic cyst, dentigerous cyst, and ameloblastoma

OBJECTIVES: The aim of the present study was to compare the proliferation index of the epithelial cells between odontogenic keratocysts (OKC), orthokeratinized odontogenic cysts (OOC), dentigerous cysts (DC), and ameloblastomas. MATERIALS AND METHODS: The proliferation index, employing a novel cell proliferation marker IPO-38, was studied by the immunohistochemical technique in 10 OKC, seven OOC, eight DC and 10 ameloblastomas. RESULTS: The ameloblastoma had no higher labeling index (LI) of IPO-38 than the OKC (P = 0.910) but had higher LI than the OOC (P = 0.001) and DC (P = 0.000); the OKC had higher LI than the OOC (P = 0.002) and DC (P = 0.000); and the OOC had higher LI than the DC (P = 0.011). IPO-38-positive cells in the OKC and OOC were located principally in the suprabasal cell layers while the ameloblastoma were found in the peripheral portion in particularly, the follicular and plexiform types. CONCLUSION: These findings support previous studies that the proliferation indices are useful in predicting the different biological behavior of the odontogenic lesions and the OKC should be regarded as a benign tumor rather than simply an odontogenic cyst.     

Bacteriological findings in radicular cyst and keratocystic odontogenic tumour fluids from asymptomatic patients

Objective

In this study the potential presence of bacteria in radicular cyst (RC) and keratocystic odontogenic tumour(KCOT) fluids from clinically asymptomatic patients was investigated.

Materials and methods

Cyst fluids were collected by needle aspiration from 16 patients with asymptomatic osteolytic lesions (10 RCs and 6 KCOTs) undergoing surgery. All samples were transferred into tubes containing pre-reduced transport medium, delivered to the microbiology laboratory and processed within 1 h. The cysts, surgically enucleated, were sent for standard histopathological examination. Cyst fluid samples were cultured on selective and differential media in anaerobic (for about 2 weeks) and aerobic (for 24–48 h) conditions to detect viable microorganisms. After incubation, the colonies were counted, Gram-stained and identified by biochemical tests.

Results

Cultures were positive for the presence of bacteria in 15 (9 RCs, 6 KCOTs) out of 16 cases. RCs and KCOTs generally yielded low bacterial counts (10²–10⁴ CFU/ml) and were predominantly colonized by obligate anaerobes (64%), whereas less commonly by facultative anaerobes (36%). No significant differences in the detection frequencies of obligate and facultative anaerobes were evidenced between RCs and KCOTs. Propionibacterium acnes was the most common obligate anaerobe recovered both in RC and KCOT fluids. Among facultative anaerobes, Gemella morbillorum was more frequently isolated in KCOTs, whereas Staphylococcus spp. in RCs.

Conclusions

Bacteria may be present and persist within fluids of clinically asymptomatic jaw cystic lesions. The influence of bacteria and latent bacterial infection within cystic jaw lesions should be reconsidered in odontogenic cyst progression.     

Differential expression of Cyclin D1 in keratin-producing odontogenic cysts

Objetives: The aim of the present study was to analyze the expression levels of Cyclin D1 (CCD1), a nuclear protein that plays a crucial role in cell cycle progression, in a series of keratin-producing odontogenic cysts. Study Design: A total of 58 keratin-producing odontogenic cysts, diagnosed over ten years and classified according to the WHO 2005 criteria, were immunohistochemically analyzed in terms of CCD1 expression, which was quantified in the basal, suprabasal and intermediate/superficial epithelial compartments. The extent of immunostaining was measured as a proportion of total epithelial thickness. Quantified immunohistochemical data were correlated with clinicopathological features and clinical recurrence. Results: Keratin-producing odontogenic cysts were classified as 6 syndromic keratocystic odontogenic tumors (S-KCOT), 40 sporadic or non-syndromic KCOT (NS-KCOT) and 12 orthokeratinized odontogenic cysts (OOC). Immunohistochemically, CCD1 staining was evident predominantly in the parabasal region of all cystic lesions, but among-lesion differences were apparent, showing a clear expansion of parabasal compartment especially in the S-KCOT, followed to a lesser extent in the NS-KCOT, and being much more reduced in the OOC, which had the greatest average epithelial thickness. Conclusions: The differential expression of CCD1 noted in the present study suggests that dysregulation of cell cycle progression from G1 to the S phase contributes to the different aggressiveness of these lesions. However, CCD1 expression levels did not predict NS-KCOT recurrence, which is likely influenced by factors unrelated to lesion biology. Key words:Keratin-producing odontogenic cyst, keratocyst, keratocystic odontogenic tumor, nevoid basal cell carcinoma syndrome, orthokeratinized odontogenic cyst, cyclin D1, immunohistochemistry.     

Syndecan‐1 (CD 138) surface expression marks cell type and differentiation in ameloblastoma,keratocystic odontogenic tumor,and dentigerous cyst

J Oral Pathol Med (2013) 42 : 186–193 Background: The altered expression of syndecan‐1 (SD‐1), a transmembrane heparan sulfate proteoglycan, in ameloblastomas and cysts of odontogenic origin suggests that this molecule could have prognostic value in assessing the clinical outcome of those lesions. The purpose of this study was to analyze SD‐1 expression profile immunohistochemically in archival, paraffin‐embedded tissue sections of ameloblastomas and in common odontogenic cysts arising from the same locale. Methods: SD‐1 expression was investigated in 32 ameloblastomas, 26 keratocystic odontogenic tumors (KCOT), and 21 dentigerous cysts from the archives of the histopathology laboratory which were routinely processed. The cases were reviewed and assessed according to the established criteria. Sections were immunostained with monoclonal antibody against SD‐1 (CD138). Sections of normal oral mucosa, site matched, were stained in parallel as positive controls. The plasma cells in sections served as internal positive controls. Results: SD‐1 expression was observed in the epithelial and stromal elements of the sections, and the expression was significantly associated with the lesion’s extension and involvement of adjacent structures (P = 0.025). Stellate‐reticulum cells showed higher expression than the ameloblasts, which was at a significant level (P < 0.0001). Highly significant difference was reported among the three groups of lesion for the epithelial staining (P < 0.0001). The mean rank scores (Kruskal–Wallis test) of ameloblastomas were significantly lower than those of KCOT and dentigerous cysts. Non‐significant comparison was made between KCOT and dentigerous cyst groups. Conclusions: The present study revealed SD‐1 immunoreactivity in the stromal cells of ameloblastoma, KCOT, and dentigerous cysts rather uniformly. This reported SD‐1 expression by the tumor stroma is considered to be associated with poor prognosis of the lesions.     

Altered expression of cell–cell adhesion molecules β-catenin/E-cadherin and related Wnt-signaling pathway in sporadic and syndromal keratocystic odontogenic tumors

Differential diagnosis of the keratocystic odontogenic tumor (KCOT) still represents a challenging problem especially if compared with the dentigerous cyst, which is similar in clinical and radiological course. Histological assessment of this entity may therefore draw crucial attention since various radical procedures are recommended for such lesions in contrast to dentigerous cysts. Since recent reports could prove the involvement of wingless(Wnt)-signaling pathway and β-catenin in the pathogenesis of many odontogenic and neoplastic lesions indicating impairment of cell–cell adhesion, we investigated the expression of two Wnt-signaling pathways, Wnt-1 and Wnt-10A as well as β-catenin and E-cadherin along with other related proteins in both lesions. We found a significant down-regulation in the expression of cell adhesion proteins β-catenin and E-cadherin along with alteration of Wnt-1 and Wnt-10A expression in the epithelium of KCOT. We assessed a specific focal distribution pattern of p63 in the suprabasal cell layer and a significant up-regulation of cyclin D1. Furthermore, laminin α-2 was a characteristic marker labelling only the basement membrane of dentigerous cysts. These results provide a new hypothesis explaining a molecular mechanism to understand initiating and development of KCOTs and an alternative therapeutic approach, especially for syndromal patients, where these multilocal lesions may involve and destroy wide orofacial bony structures.     

Evidence of loss of heterozygosity of the PTCH gene in orthokeratinized odontogenic cyst

J Oral Pathol Med (2011) 40 : 277–280 The orthokeratinized odontogenic cyst (OOC) is an odontogenic cyst of unknown etiology. Clinical, histological, and biological differences are reported between keratocystic odontogenic tumor (KOT) and OOC. PTCH is a tumor suppressor gene related to sonic hedgehog (SHH) pathway important in embryological development. Considering that alterations in this pathway have been described in sporadic and nevoid basal cell syndrome‐associated KOT, we tested the hypothesis that OOC is also associated with loss of heterozygosity (LOH) of the PTCH gene. Seven samples of OOC and seven of KOT were included in the study. D9S287, D9S196, and D9S127 microsatellite markers located in the region of PTCH gene, at chromosome 9q, were investigated for LOH. There was loss in at least one locus in 5/7 KOT and in 4/7 OOC samples. The present finding demonstrates that, despite the existence of clinical, morphological, immunohistochemical, and biological behavior differences between OOC and KOT, both harbor similar genetic alterations at 9q.     

Survivin gene promoter polymorphism -31G/C as a risk factor for keratocystic odontogenic tumor development

Several single nucleotide polymorphisms in survivin gene promoters, notably -31G/C, have been shown to modulate the expression and activity of the survivin protein. Consequently, the -31G/C polymorphism has been identified as a risk factor for the development of several types of tumors. The aim of this study was to investigate a possible association between the -31G/C polymorphism and the risk for keratocystic odontogenic tumor (KCOT) development. DNA from 52 biopsy specimens of KCOTs and from 82 buccal swabs of healthy individuals was subjected to PCR restriction fragment length polymorphism analysis to identify individual genotypes. The distribution of genotypes in KCOT and control groups, respectively, was: GG: 30 (57.7%) vs. 26 (31.7%); CG: 17 (32.7%) vs. 45 (54.9%); and CC: 5 (9.6%) vs. 11 (13.4%), respectively. These differences were statistically significant. The G allele was more common in the KCOT group than in the control group: 76 (74%) vs. 96 (59%), respectively. Logistic regression analysis showed that GC heterozygotes had a considerably decreased susceptibility for KCOTs compared with GG homozygotes. The same was true for GC+CC vs. GG. The GG genotype of the -31G/C polymorphism might be a risk factor for KCOT development.     

Synchronous ameloblastoma and orthokeratinized odontogenic cyst of the mandible

The simultaneous occurrence of ameloblastomas with odontogenic cysts or other non-odontogenic lesions have already been described as combined lesions. However, we are unaware of any report in the English literature of simultaneous occurrence of ameloblastoma and orthokeratinized odontogenic cyst (OOC) occurring as completely distinct lesions. This report shows a case of synchronous ameloblastoma and OOC, located on posterior regions of the mandible, but in distinct sides.     

Metallothionein in the radicular,dentigerous, orthokeratinized odontogenic cysts and in keratocystic odontogenic tumor

J Oral Pathol Med (2011) 40 : 270–276 Background: Metallothionein (MT) is a protein correlated with cellular differentiation and proliferation, as well as with the inhibition of apoptosis. The aims were to report and to compare the MT expression in odontogenic cysts and keratocystic odontogenic tumor (KOT); to correlate the MT with cellular proliferation; and to evaluate the influence of the inflammation in MT. Methods: Nine cases of radicular cyst (RC), nine dentigerous cyst (DC), four orthokeratinized odontogenic cyst (OOC), and eight KOT were submitted to immunohistochemistry using anti‐MT and anti‐Ki‐67. Indexes of MT (IMT) and Ki‐67 (IK) were obtained. Lesions were grouped according to inflammation: mild‐to‐moderate (group A) and intense (group B). Results: IMT proved to be highest in RC (91%), followed by DC (89%), KOT (78%), and OOC (63%). IMT was inversely correlated with IK in KOT, and OCC, but was positively correlated with RC and DC. No differences in IMT and in IK could be observed between groups A and B. Conclusions: The higher IMT found in RC and DC compared to OCC and KOT, as well as the differences between the last ones, is possibly correlated with their different histopathological features and clinical behavior. In RC and DC, MT may play a role in cellular proliferation. However, it seems that MT is either less or is not related to proliferation in OOC and in KOT. Moreover, inflammation does not seem to alter IMT and IK.