Solid Ameloblastoma Research Articles

Evaluation of Paxillin Expression in Odontogenic Cysts and Tumors.

Paxillin (PXN) is one of the proteins involved in cell adhesion. PXN and integrins constitute a key site for the focal adhesion between the cell and extracellular matrix. Several studies have shown that PXN is a factor in tumor formation, progression, invasion, and metastasis. This study evaluated PXN expression in four types of odontogenic lesions with different aggressive behaviors. In this retrospective cross-sectional study, PXN expression was immunohistochemically assessed in 68 paraffin-embedded tissue samples from patients with the confirmed diagnosis of four types of odontogenic lesions, including 14 dentigerous cysts (DC), 20 odontogenic keratocyst (OKC), 16 unicystic ameloblastoma, and 18 solid ameloblastoma. The PXN expression in these samples were scored based on the percentage and intensity of immunoreactivity, and compared among the groups by Chi-square test. The PXN marker was detected in the cytoplasm of tumor cells (unicystic and solid ameloblastoma) and the epithelial layer of cysts (DC and OKC). The intensively stained marker of PXN was observed in 9 cases (64.3%) of the DC, 14 cases (70%) of OKC, 12 cases (75%) of unicystic ameloblastoma, and 13 cases (72.2%) of solid ameloblastoma. However, there was not statistical difference of PXN protein expression between DC and OKC (p Value = 0.51) and unicystic and solid ameloblastoma (p = 0.58), also the same was true for cysts and tumors (p = 0.37). The expression of PXN is not related to the biological behaviors of odontogenic lesions.

The Case for Re-Classification of Solid Ameloblastoma and Not Solid and Ameloblastoma

The Case for Re-Classification of Solid Ameloblastoma and Not Solid and Ameloblastoma

A clinicopathological analysis of 151 odontogenic tumors based on new WHO classification 2022: A retrospective cross-sectional study

Background: Odontogenic tumors are a diverse group of lesions with a variety of clinical behavior and histopathologic subtypes, from hamartomatous and benign to malignant. The study aimed to examine the clinical and pathological features of odontogenic tumors in Baghdad over the last 11 years (2011–2021). Materials and Methods: The present retrospective study analyzed all formalin-fixed, paraffin-embedded tissue blocks of patients diagnosed with an odontogenic tumor that were retrieved from archives at a teaching hospital/College of Dentistry in Baghdad University, Iraq, between 2011 and 2021. The diagnosis of each case was confirmed by examining the hematoxylin and eosin stained sections by two expert pathologists. Data from patients' case sheets were collected, including age, gender, location, and histopathological information. The type of lesions was evaluated based on the World Health Organization's most recent classification (March 2022). Results: There were 151 odontogenic tumor during this period. The most common type (39.1%) was Solid ameloblastoma. The mandibular tumors (76.8%) were more than the maxillary tumors (23.2%). The female to male ratio was 1.1:1. The most cases are found between the 2nd and 5th decades of life. Conclusions: Solid ameloblastoma was the most common odontogenic tumor, while primordial odontogenic tumor was the rarest, Odontogenic tumors were slightly more common in females than in males, the most common cases occur in the mandible., the outcome of the study gives valuable information regarding the patients' profile and type of odontogenic tumors over 11 years, which could aid in the early diagnosis and enhance the intervention.

Immunohistochemical evaluation of Glut1 in dentigerous cysts, odontogenic keratocysts, and ameloblastoma.

Glucose uptake may be considered the rate-limiting step for the growth and metabolism of the cancer cell. Studies on GLUT1 have shown that GLUT1 is involved in cell survival and proliferation in both healthy and pathological circumstances. GLUT1 expression is regarded as one of the crucial elements in the development of local aggressiveness, tumour invasiveness, and metastasis, particularly in malignant tumours. The role of glut1 in odontogenic cysts and tumours has remained uncertain. The aim of the study is to assess the expression of Glut1 in dentigerous cysts, odontogenic keratocysts, and ameloblastoma. The study was conducted in GSL Dental College. The study design was a resprospective immunohistochemical study. Formalin-fixed, paraffin-embedded blocks of histologically confirmed cases (n = 50), 10 cases of odontogenic keratocysts, dentigerous cysts, ameloblastomas solid, ameloblastomas unicystic, and dental follicles each. Brown colour staining was considered as positive staining for GLUT1. Quantitative analysis was performed by counting the number of labelled cells, and semi-quantitative analysis was conducted by assigning immunostaining intensity scores. Chi-square test was used to compare differences between the groups. A P value of ≤0.05 was considered as statistically significant. Odontogenic keratocysts and unicystic ameloblastoma showed ≥50% of label cells with strong intensity of staining. Odontogenic keratocysts and solid ameloblastoma showed sub-cellular localisation of staining in the cytoplasm and membrane. Dentigerous cysts exhibited combined nucleus, cytoplasm, and membrane sub-cellular localisation of staining. The development of ameloblastomas, odontogenic keratocysts, and dentigerous cysts appears to be influenced by GLUT-1. Variation in its expression may aid in explanation of some of the differences in biological activity of these lesions.

Localization of beta catenin across the domain of odontogenic lesions: A systematic review.

CTNNB1 gene encodes beta catenin, a transcriptional activator of Wnt pathway involved in the pathogenesis of odontogenic lesions. Though located intramembranously, its translocation into cytoplasm and nucleus could trigger cell proliferation, inhibition of apoptosis, invasion and migration of the tumour cell. Five electronic databases including MEDLINE by PubMed, Google scholar, Scopus, Trip, Cochrane library and EMBASE until 1 January 2023 without period restriction were thoroughly searched. Those articles that identified CTNNB1 mutation and beta catenin in odontogenic lesions were included for review. Risk of bias was analysed for each study using QUADAS 2 tool and Review Manager 5.3 was used to output its result. Thirty four published articles were included for data synthesis. A total of 1092 cases of odontogenic lesions were assessed for both CTNNB1 mutation and beta catenin expression. CTNNB1 mutation was observed in ameloblastoma, calcifying odontogenic cyst, calcifying cystic odontogenic tumour and all malignant odontogenic tumours. The beta catenin expression (nuclear and cytoplasmic) was maximum in odontogenic keratocyst and calcifying odontogenic cyst. The expression was variable in ameloblastomas, membranous in odontomas, calcifying cystic odontogenic tumour and nuclear in all malignant tumours. High recurrence of odontogenic keratocyst and aggressiveness of solid ameloblastoma and malignant odontogenic tumours could be associated with the nuclear translocation of beta catenin. Disparity between CTNNB1 mutation and beta catenin expression within odontogenic lesions suggests alternate routes of beta catenin activation. The review results support the unique localisation of beta catenin as a helpful diagnostic factor in the pathogenesis of odontogenic lesions.

CONSERVATIVE TREATMENT OF AMELOBLASTOMA: A CASE REPORT

Ameloblastomas are benign neoplasms of odontogenic origin that grow slowly, are locally invasive, and have high recurrence rates if not treated properly. This study aims to present a conservative approach to a clinical case of conventional solid ameloblastoma. A black 36-year-old black female patient was referred to the UFG dental school with a history of painless swelling in the left mandible and difficulty in opening the mouth. Intraoral examination showed lingual and buccal expansion of the cortical bone. Computed tomography revealed bone expansion with thinned corticals located in the left body of the mandible. An incisional biopsy was performed, accompanied by marsupialization, and the pathological examination was compatible with ameloblastoma. Due to the unsuccessful marsupialization, the taping procedure was subsequently performed under general anesthesia, and the gauze soaked in the procedure's escin were changed twice a week. The patient is undergoing follow-up with the evaluation of periodic radiographic exams. Ameloblastomas are benign neoplasms of odontogenic origin that grow slowly, are locally invasive, and have high recurrence rates if not treated properly. This study aims to present a conservative approach to a clinical case of conventional solid ameloblastoma. A black 36-year-old black female patient was referred to the UFG dental school with a history of painless swelling in the left mandible and difficulty in opening the mouth. Intraoral examination showed lingual and buccal expansion of the cortical bone. Computed tomography revealed bone expansion with thinned corticals located in the left body of the mandible. An incisional biopsy was performed, accompanied by marsupialization, and the pathological examination was compatible with ameloblastoma. Due to the unsuccessful marsupialization, the taping procedure was subsequently performed under general anesthesia, and the gauze soaked in the procedure's escin were changed twice a week. The patient is undergoing follow-up with the evaluation of periodic radiographic exams.

Stromal CD10 expression in ameloblastomas: Correlation with clinical, radiographic and histopathologic characteristics

Objectives: To describe the clinical, radiographic and histopathologic features of ameloblastoma and analyze the relationship between CD10 expression in stromal cells of ameloblastoma and clinical, radiographic and histopathologic characteristics. Materials and methods: A cross-sectional study was performed on a total of 70 cases of ameloblastoma treated at the National Odonto-Stomatology Hospital at HCM city. Results: The male to female ratio was 1.12:1. The mean age of patients was 34.6 ± 14.8 years. The mean age was 30.5 ± 13.5 years for unicystic ameloblastoma and 36.8 ± 15.2 years for solid ameloblastoma. The location of ameloblastomas showed a marked predominance in the mandible (94.3%). Swelling was the most common symptom (92.9%). 18.6% had unilocular radiolucency and 81.4% had multilocular radiolucency. There were 47 cases of ill-defined edge (67.1%). The tumor was associated with embedded teeth in 17 cases (24.3%). Root resorption was evident in 47 of 61 (77.1%) and cortical perforation was presented in 41 of 70 (58.6%). The most frequent histological patterns in solid ameloblastoma were plexiform (28.9%) and in unicystic ameloblastoma were mural (48%). There were 39/70 cases which had CD10 possitive in stromal cells. Stromal CD10 positive expression in solid ameloblastomas (64,4%) was significantly higher than in unicystic ones (40%) (p<0,05). There was statistically significant difference in tromal CD10 expression between multilocular and unilocular radiolucent ameloblastomas, between tumor with well-defined and ill- defined border, with and without cortical perforation (p<0,05). Stromal CD10 expression showed no significant difference among different histological subtypes of solid/multicystic ameloblastomas. However, there was statistically significant correlation between stromal CD10 expression and histological subtypes of unicystic ameloblastomas. Conclusions: There were significant association between stromal CD10 expression and clinical, radiographic and histopathologic characteristics of ameloblastomas. Expression CD10 by stromal cells might be correlated to local invasion of ameloblastomas.

Myofibroblasts in Odontogenic Cysts and Tumors: An Immunohistochemical Study.

The objective of this study was to assess immunohistochemically the presence of myofibroblasts both qualitatively and quantitatively in odontogenic cysts and tumors and to compare with the control cases of squamous cell carcinoma and to correlate the results with biologic behavior of these lesions. Formalin-fixed, paraffin-embedded blocks of odontogenic cysts and tumors were retrieved from institutional archives. The sample size is 40; these include ten cases of odontogenic keratocyst (OKC) (n = 10), five cases of dentigerous cyst (n = 5), ten cases of solid ameloblastoma (n = 10), and five cases of unicystic ameloblastoma (n = 5). Ten cases of squamous cell carcinoma (n = 10) served as control. Sections were taken and stained immunohistochemically using alpha-smooth muscle actin for evaluation of myofibroblasts. The number of positive stromal cells was evaluated both for quantitative and qualitative analyses. The present study showed that the mean number of myofibroblasts among the odontogenic cysts and tumors was higher in locally aggressive lesions such as OKC (23.79 ± 19.95), solid ameloblastoma (26.38 ± 17.00), and unicystic ameloblastoma (20.74 ± 14.86) which were comparable to squamous cell carcinoma (21.49 ± 9.76) when compared to benign lesions like dentigerous cyst which showed the least number of myofibroblasts (13.1 ± 7.71). Qualitatively, the staining intensity of myofibroblasts showed a significant variation within the same lesion and among different lesions. There was a distinct difference in the morphology, pattern of arrangement, and distribution of myofibroblasts among the studied lesions. We conclude that the increase in the number of myofibroblasts could be one of the contributory factors for the locally aggressive behavior of benign lesions such as ameloblastomas and OKCs. Further studies are suggested to understand the mechanism by which these important cellular elements exert their effects on stromal and epithelial tissue compartments.

Immunohistochemical expression of Ki-67 and Glypican-3 to distinguish aggressive from nonaggressive benign odontogenic tumors.

The benign neoplasms are normally slow growing, indolent with no invasive potential. However, there exist a few locally aggressive benign odontogenic tumors that have a tendency to invade and deform the surrounding structures. The exact reason for the aggressiveness of these benign neoplasms remained an enigma. Their biology and clinical expression can often be destructive and ominous. An appropriate treatment protocol needs to be followed to combat the high recurrence rate and aggressiveness of these entities. Aggressive and noniaggressive epithelial odontogenic tumors were analyzed immunohistochemically with Ki-67 and glypican 3 (GPC3). Fifty-nine cases of tumors were divided into aggressive odontogenic tumors (20 solid ameloblastomas, four unicystic ameloblastoma, and 28 keratocystic odontogenic tumors) and nonaggressive odontogenic tumors (five adenomatoid odontogenic tumors and two calcifying cystic odontogenic itumors). Statistical analysis using Pearson correlation showed Ki-67 to be a better marker for differentiating aggressive from nonaggressive odontogenic tumor as compared to GPC3 (P < 0.001, highly significant), whereas among aggressive tumors, GPC3 turned out to be more useful as compared to Ki-67 (P < 0.001, highly significant). The present study provides an insight into the different biological behavior of odontogenic tumors, which can thus be helpful in determining the therapy strategies for more aggressive odontogenic tumors.

MANDIBULAR RESECTION IN A PATIENT AFFECTED BY AMELOBLASTOMA AND IMMEDIATE RECONSTRUCTION USING A CUSTOM PROSTHESIS

Ameloblastoma is a benign, locally aggressive odontogenic tumor that can cause expansion and destruction of the cortical bone of the maxillary bones. It shows a high rate of recurrence. Eighty percent of cases appear in the mandible, and 66% of cases are located in the posterior region. The objective of this report is to present a case of an 18-year-old White female patient with ameloblastoma. The patient underwent mandibulectomy and was treated immediately with a custom prosthesis. On tomographic examination, an osteolytic lesion was noted in the left mandible compatible with ameloblastoma. Incisional biopsy of the lesion was performed, with confirmation of conventional solid ameloblastoma on anatomopathologic examination. The treatment consisted of removing the entire lesion with safety margins. Then, a personalized mandibular reconstruction plate was placed. This patient is being monitored to adapt a future implant on her prosthesis to replace the missing teeth.

CONVENTIONAL SOLID/MULTICYSTIC AMELOBLASTOMA SURGICAL TREATMENT: CASE REPORT

The present work aims to report the clinical case of a 30-year-old woman attended in the emergency room in April 2020 with a pathologic fracture of the mandible caused by extensive osteolytic injury. The patient reported an evolution of years, a history of incisional biopsy with the conclusion of solid ameloblastoma, and that less invasive treatments such as decompression and marsupialization were tried without success. On tomographic examination, the patient presented a fracture of the mandible in the branch and an expansive tumoral lesion in the branch and right body. The patient underwent emergency surgery with partial resection of the extensive mandible and temporary reconstruction of the mandibular perimeter with a 2.4-mm system reconstruction plate. The patient evolved with good healing in outpatient follow-up. The present work aims to report the clinical case of a 30-year-old woman attended in the emergency room in April 2020 with a pathologic fracture of the mandible caused by extensive osteolytic injury. The patient reported an evolution of years, a history of incisional biopsy with the conclusion of solid ameloblastoma, and that less invasive treatments such as decompression and marsupialization were tried without success. On tomographic examination, the patient presented a fracture of the mandible in the branch and an expansive tumoral lesion in the branch and right body. The patient underwent emergency surgery with partial resection of the extensive mandible and temporary reconstruction of the mandibular perimeter with a 2.4-mm system reconstruction plate. The patient evolved with good healing in outpatient follow-up.

THE CONSERVATIVE TREATMENT OF SOLID AMELOBLASTOMA—A REPORT OF TWO CLINICAL CASES

Ameloblastomas are benign tumors originating from the odontogenic epithelial and with a rare occurrence in children younger than 10 years. The tumor has a similar predominance between the third and fourth decades of life. When intraosseous, they can be classified as solid and unicystic. For solid tumors, the recommended treatment is segmental tumor resection due to its recurrence potential. The present study reports 2 cases of solid ameloblastomas in the posterior mandible region of young patients, aged 10 and 20 years old, respectively. The patients were treated with enucleation and curettage of the lesion. Both patients had intra- and extraoral swelling. In addition, cone bean tomography revealed multiloculated images. Incisional biopsy confirmed the diagnosis of solid ameloblastoma. Both patients are in clinical radiographic follow-up for about a year and are without signs of recurrence. Ameloblastomas are benign tumors originating from the odontogenic epithelial and with a rare occurrence in children younger than 10 years. The tumor has a similar predominance between the third and fourth decades of life. When intraosseous, they can be classified as solid and unicystic. For solid tumors, the recommended treatment is segmental tumor resection due to its recurrence potential. The present study reports 2 cases of solid ameloblastomas in the posterior mandible region of young patients, aged 10 and 20 years old, respectively. The patients were treated with enucleation and curettage of the lesion. Both patients had intra- and extraoral swelling. In addition, cone bean tomography revealed multiloculated images. Incisional biopsy confirmed the diagnosis of solid ameloblastoma. Both patients are in clinical radiographic follow-up for about a year and are without signs of recurrence.

Long-term follow-up of a case of multicystic ameloblastoma treated with curettage: case report / Acompanhamento a longo prazo de um caso de ameloblastoma multi-cístico tratado com curetagem: relato de caso

The conventional or multicystic solid ameloblastoma is the most common type with the majority of cases affecting the posterior region of the mandible and occurring between the third and fourth decades of life. The present study aims to report a case of multicystic ameloblastoma in which treatment by means of curettage was chosen and no evidence of recurrence was noted over 7 years of follow-up. Although the literature indicates aggressive surgical therapy as the best form of treatment for multicystic ameloblastoma, factors such as the clinical, radiographic and histopathological aspects of the lesion, patient age, postoperative morbidity, possibilities for aesthetic and functional changes must be evaluated together during treatment planning. In some cases, as in the report presented, conservative therapies such as aggressive curettage of the lesion can be effective in the long term, with no recurrence of the lesion and providing quality of life to the patient.

A meta-analysis on the presentation of Unicystic Ameloblastoma in the jaws and the consequences for their treatment

IntroductionThis meta-analysis provides reliable data on the prevalence of unicystic ameloblastomas (UA's) among solid/multicystic ameloblastomas (SMA's), as well the ratio of their presence in the maxilla and mandible and in the tooth-bearing area versus the posterior regions of the mandible, including the third molar region and ascending ramus. Material and methodsA systematic review and meta-analysis was performed according to PRISMA guideline using the strategy ((unicystic ameloblastoma) OR (((ameloblastoma) OR (solid ameloblastoma)) OR (multicystic ameloblastoma))) NOT ((((systematic review) OR (literature review)) OR (case report)) OR (Immunohistochemical)). DiscussionThe study included 3856 SMA's and 1537 UA's, which amounted to 28.5% UA's. Of the 380 cases of UA from twelve articles that mentioned the involved jaws, 355 were in the mandible and 25 in the maxilla. The preponderance for the mandible is much higher than reports from previous studies of smaller series. Only five articles mentioned the location within the mandible. The vast majority was in the posterior area. ConclusionThe consequences for treatment were discussed, with an emphasis on the approach to unicystic lesions in the posterior part of the mandible for which a protocol is suggested.

Unicystic Ameloblastoma of Mandible: A Case Report

Amelo blastoma is a neoplasm that originates from odontogenic epithelium. It is the second most common neoplasm of the oral cavity. Uni cystic ameloblastomas refer to those cystic lesions that show clinical, radio graphic, or gross features of a jaw cyst, but on histologic examination show a typical ameloblastomatous epithelium lining part of the cyst cavity, with or without luminal and/ or mural growth. Even though the lesion is not that aggressive as the solid ameloblastoma, an accurate diagnosis should be made. This lesion needs to be treated more aggressively than any other periapical lesions. This study shows that the term 'uni cystic ameloblastoma' is derived from the macro and microscopic appearance, the lesion being a well defined, often large monocystic cavity with a lining, focally but rarely entirely composed of odontogenic(ameloblastomatous epithettlium).Clinically, ameloblastoma appears as an aggressive tumor of the odontogenic tumor, more often asymptomatic, slow growing with no evidence of swelling.

Are Incisional Biopsies Reliable to Select Definitive Treatment in Patients with Ameloblastoma of the Jaws? A 15-year Interdisciplinary Retrospective Study

Ameloblastomas are tumors of odontogenic epithelium that, although benign, can have a locally aggressive course causing significant morbidity. WHO classifies ameloblastomas as 1 of 3 variants: solid/multicystic, unicystic, and peripheral. Resection, the standard treatment, is deemed curative, but can be debilitating to the patient. Unicystic subtype is considered less aggressive and could be treated with enucleation and curettage. The mercurial presentation of ameloblastomas makes the chosen treatment modality essential in decreasing the recurrence rates and associated morbidity. Definitive treatment is chosen based on an incisional biopsy, but a true diagnosis of unicystic ameloblastoma requires the entire specimen. The aim of this study is to assess the potential sampling error with an incisional biopsy and potential consequences on treatment outcomes at long-term follow-up.This is a retrospective cohort study for patients with ameloblastoma of the jaws treated at the Virginia Commonwealth University Department of Oral and Maxillofacial Surgery between 2005 to 2020. Patients with biopsy-proven ameloblastoma with a minimum of 1-year follow-up after definitive treatment and complete documentation were included. Predictor variables include radiographic findings, incisional biopsy, and histologic samples. Outcome variable is concordance between initial incisional biopsy and final treatment pathology, as well as recurrence rate.A total of 23 patients, 14 males and 9 females, met the inclusion criteria. Table 1 presents demographics and study variables for the sample. On initial incisional biopsy, 4 (17.4%) cases showed a “cystic” mention in the pathology report, 18 cases (78.3%) exhibited solid ameloblastoma, and 1 (4.3%) showed peripheral ameloblastoma. Final pathology after definitive treatment showed solid/multi-cystic ameloblastoma in 20 (87%) cases, 2 (8.7%) were unicystic, and 1 (4.3%) was peripheral ameloblastoma. Overall, initial incisional biopsy and final pathology were concordant in 21 (91%) cases. After histologic investigation, the initial biopsy for 3 (13%) cases exhibited sampling error, which is defined as the sampled tissue not being representative of the entire lesion (Table 2).Segmental resection was the definitive treatment in 14 (60.9%) cases while enucleation and curettage (E&C) were used on 6 (26.1%), and decompression followed by enucleation and curettage on 3 (13%) patients (Table 3). Postoperative follow-up from the day of definitive treatment ranged from 1 year to 15.6 years (mean 3.50 ± 3.22). Four patients (17.4%) had recurrent lesions, with 100% of them seen following conservative management (i.e., E&C or decompression with E&C). The time of recurrence after treatment ranged from 6 months to 10.75 years (mean 4.62 ± 4.25), with 1 case having more than 1 recurrence.Incisional biopsies are acceptably reliable when combined with clinical exam of the lesion and radiographic presentation to select definitive surgical treatment for ameloblastoma. The chance of sampling error should be included in the informed consent with a low threshold for second incisional biopsy when clinical/radiographic findings are not consistent with histopathological report. Consult with an oral and maxillofacial pathologist is essential, both at initial and final histopathology evaluation. Future development of less-invasive treatments that combine medical and/or surgical management, given the benign nature of ameloblastoma, will help patients achieve cure in the long term.

Cyclooxygenase-2 protein expression modulates cell proliferation and apoptosis in solid ameloblastoma and odontogenic keratocyst. An immunohistochemical study.

Cyclooxygenase-2 protein is a critically important mediator in inflammation that influences proliferation, apoptosis, angiogenesis and metastasis. Previous works showed a relationship between cyclooxygenase-2 and tumourigenesis in humans and animal models. In epithelial odontogenic tumours and cysts, increased cell proliferation and survival have been linked to its pathogenesis and tumour development. The aim of the present study was to analyse the immunohistochemical expression of cyclooxygenase-2 in solid ameloblastoma and odontogenic keratocyst and its association with proteins related to cell proliferation and apoptosis. This study was conducted on 40 cases from the Pathological Anatomy Service, University of Chile. The cases were diagnosed as solid ameloblastoma (n=21) and odontogenic keratocyst (n=19) according to WHO 2017. Slides prepared from paraffin-embedded sections were immunohistochemically stained for cyclooxygenase-2, cyclin D1, Ki-67, p63 and Bcl-2. Statistical evaluation was performed by the Shapiro-Wilk test, ANOVA Mann-Whitney test and Spearman's correlation coefficient (p<0.05). There were significant differences in the immunoexpression of cyclin D1, Ki-67 and Bcl-2 between solid ameloblastoma and odontogenic keratocyst. Likewise, there was a significant difference in the immunoexpression of p63 between follicular and plexiform histological types/subtypes of solid ameloblastoma. Lastly, there were statistical associations between cyclooxygenase-2 and Ki-67 for solid ameloblastoma and between cyclooxygenase-2 and p63 for odontogenic keratocyst. A high level of cyclooxygenase-2 is related to increased cell survival and proliferative activity in solid ameloblastoma and odontogenic keratocyst. This event might contribute to tumoural progression and local invasiveness in these lesions.

CORRELATION OF SYNDECAN 1 EXPRESSION IN SOLID AND UNICYSTIC AMELOBLASTOMA AND ITS CELLULAR COMPONENTS

<h3>Background</h3> Syndecan-1 (SDC1) is a transmembrane heparan sulfate proteoglycan (also known as CD138), participates in odontogenesis, and is known to regulate cytoskeletal organization, growth factor signaling, cell–cell adhesion, and extracellular matrix attachment. Loss of expression of SDC1 is associated with tissue invasion, metastasis, and poor prognosis. <h3>Objective</h3> To study the syndecan expression in solid and unicystic ameloblastoma and to assess and compare the distribution of the SDC1 in various cellular components of the solid multicystic and unicystic ameloblastoma and correlate with their differentiation and biological behavior. <h3>Methods</h3> Samples in this study consisted of 50 cases: 25 cases of solid multicystic ameloblastoma and 25 cases of unicystic ameloblastoma. Formalin-fixed, paraffin-embedded tissue sections were immunohistochemically analyzed for SDC1 markers. Expression of syndecan was measured under 400 × magnification in the solid ameloblastoma in epithelium where lesional cells are composed of 4 types of cellular components: peripheral basal cells of tumor nests, central stellate reticulum-like cells, and foci of squamous and granular cells. Unicystic ameloblastoma was checked for its cystic lining. Stromal expression of SDC1 was also evaluated in fibroblast-like or spindle cells. Plasma cells served as internal controls for the study. The findings were statistically analyzed. <h3>Results</h3> Comparison of the epithelial cell scoring was higher in unicystic than in solid ameloblastomas. However, the stromal expression was greater in solid ameloblastomas, moderately increased around the follicles and to a lesser extent in the deeper connective tissues. <h3>Conclusions</h3> Syndecan proved to be a useful marker to assess and compare the biologic behavior of solid and unicystic ameloblastomas.

Immunohistochemical evaluation of myofibroblasts in odontogenic keratocyst, dentigerous cyst and different clinical variants of ameloblastoma

Background: Odontogenic cysts and tumors exhibit varying degrees of aggressiveness in their biological behavior. Odontogenic keratocyst (OKC), dentigerous cyst (DC), ameloblastoma are most common odontogenic cysts and tumors to occur in the oral cavity. Myofibroblasts (MFs) in the connective tissue stroma participate in the matrix degradation process by secreting matrix metalloproteinase 2, transforming growth factor beta1 and may contribute to variation in their biological behavior. Its activity is identified by alpha-smooth muscle actin (α-SMA) marker. With this background, the present study aims to evaluate the frequency of MFs using α-SMA to determine the biological behavior of OKC, DC, and different clinical variants of ameloblastoma. Materials and Methods: A retrospective study was carried out with total of 60 samples which include 10 cases each of OKC, DC, 30 cases of different clinical variants of ameloblastomas and 10 normal mucosa taken as controls. All are stained immunohistochemically using α-SMA and were analyzed for the same. Comparison between more than 2 groups done by one way analysis of variance test with the level of significance of P ≤ 0.0001, i.e., &lt;0.05. Results: Statistically significant difference in the mean number of MFs observed between certain groups, with higher mean number in solid ameloblastoma (SA) (32.45) followed by OKC (28.79), unicystic ameloblastoma (24.53), desmoplastic ameloblastoma (7.44), and DC (1.72). Conclusion: Higher frequency of MFs noticed in SA, OKC which are key cells for connective tissue remodeling by interacting with epithelial cells and other connective tissue cells to facilitate progression of cysts and tumors thereby contributing to their biological behavior.

SOLID AMELOBLASTOMA IN MANDIBULAR REGION: A CASE REPORT

Solid ameloblastoma is an odontogenic epithelial benign neoplasia, but it is aggressive and affects mainly young adults between their third and seventh decade of life, with no predilection for sex. It is clinically characterized as a slow-growing tumor, asymptomatic and with a high recurrence rate. Radiographically, it may present as unilocular or multilocular radiolucent lesions, usually with well-defined borders similar to soap bubbles or honeycombs. This study aims to report a case of solid ameloblastoma that occurred in a 29-year-old patient, submitted to treatment of segmental mandibular resection, presenting a satisfactory result. It is fundamental to know the characteristics of the lesion and to request complementary examinations for a correct diagnosis of this pathology.