This systematic review investigates the diagnostic, prognostic, and therapeutic implications of immunohistochemical markers in dentigerous cysts (DCs) and odontogenic keratocysts (OKCs) associated with impacted third molars.

A comprehensive search strategy was employed across major databases including MEDLINE/PubMed, EMBASE, and Web of Science, from the inception of the databases to March 2024. Keywords and Medical Subject Heading (MeSH) terms such as "dentigerous cysts", "odontogenic keratocysts", "immunohistochemistry", "Ki-67", and "p53" were used. The PRISMA 2020 guidelines were followed to ensure methodological rigor. Inclusion criteria encompassed studies on humans and animals providing definitive diagnoses or specific signs and symptoms related to DCs and OKCs, with results on protein expression derived from immunohistochemistry, immune antibody, proteomics, or protein expression methods.

Of the 159 studies initially identified, 138 met the inclusion criteria. Our analysis highlighted significantly higher expressions of Ki-67 (22.1% ± 4.7 vs. 10.5% ± 3.2, p < 0.001), p53 (15.3% ± 3.6 vs. 5.2% ± 1.9, p < 0.001), and Bcl-2 (18.4% ± 3.2 vs. 8.7% ± 2.4, p < 0.001) in OKCs compared to DCs, indicating a higher proliferative index, increased cellular stress, and enhanced anti-apoptotic mechanisms in OKCs. Additionally, PCNA levels were higher in OKCs (25.6% ± 4.5 vs. 12.3% ± 3.1, p < 0.001). Genetic mutations, particularly in the PTCH1 gene, were frequently observed in OKCs, underscoring their aggressive behavior and potential malignancy.

The findings emphasize the significant role of immunohistochemical markers in distinguishing between DCs and OKCs, with elevated levels of Ki-67, p53, Bcl-2, and PCNA in OKCs suggesting a higher potential for growth and recurrence. Genetic insights, including PTCH1 mutations, further support the need for personalized treatment approaches. These markers enhance diagnostic accuracy and inform targeted therapeutic strategies, potentially transforming patient management in oral and maxillofacial surgery.

Differentiating between ameloblastoma (AB) and ameloblastic carcinoma (AC) is difficult, especially when AB has atypical cytological characteristics or an uncommon clinical history. This systematic review and meta-analysis aimed to elucidate the differential expression of immunohistochemical markers between AB and AC.

We conducted a thorough search of PUBMED and SCOPUS according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to identify cross-sectional studies that compared the expression of immunohistochemical markers in AB and AC. We used a random-effects model to analyze the risk ratios and their corresponding 95% confidence intervals (CIs). The quality of the included studies was assessed using the Newcastle-Ottawa scale. The Egger's test was used to assess publication bias.

In total, 301 articles were identified. After excluding irrelevant titles and abstracts, 86 articles were selected for full-text review. We categorized the 41 markers into proliferative and non-proliferative markers. Among non-proliferative markers, nuclear markers were differentially expressed in AB and AC. SOX2 was the only marker that significantly differentiated AB and AC, with an RR of -0.19 (CI 0.10-0.36, I2=0).

The current evidence suggests the significance of SOX2 in differentiating between AB and AC, warranting prospective confirmation in well-defined extensive studies. We highlight the paucity of high-quality replicated studies of other markers in this field. Collaborative efforts with standardized techniques are necessary to generate clinically useful immunohistochemical markers.

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.

Clinico-histopathologic assessment of patients with ameloblastoma and ameloblastic carcinoma remains the best diagnostic modality for the tumors. However, in cases where the criteria for arriving at a definitive diagnosis are not clearcut, the pathologist is faced with a dilemma and thus an imperative need for adjunct diagnostic methods.

To evaluate/compare the immunohistochemical expression of NM23 in classical, borderline (atypical) ameloblastoma and ameloblastic carcinoma and to assess usefulness of NM23 in closing diagnostic gaps between ameloblastoma and ameloblastic carcinoma.

Twenty-four (24) cases of ameloblastoma, 10 ameloblastoma with classical histopathologic features, 8 with nonclassical histopathology [atypical], and 6 cases of ameloblastic carcinoma were selected from cases seen at the Oral Pathology Laboratory of the Lagos State University College of Medicine, Nigeria. NM23 immunostaining protocol was done on the selected tissue blocks and evaluated using Sinicrope method. Analysis was done using R language.

Positive NM23 staining was observed in all cases of ameloblastoma and ameloblastic carcinoma, with more intense staining observed in the stellate reticulum-like areas than in the ameloblast-like areas. Ameloblastic carcinoma stained intensely with NM23 (100%) compared with atypical cases (37.5%) and ameloblastoma (20.0%; p = 0.04). The mean aggregate score was also significantly higher in AC (11 ± 2.4; p = 0.01). The mean aggregate score was also significant amongst growth pattern of ameloblastoma (p = 0 0.02).

The findings in this study reveal the usefulness of NM23 in differentiating ameloblastoma from ameloblastic carcinoma; a more comprehensive study with a larger sample size is recommended to corroborate or refute the findings in this study.

Four camels (Camelus dromedarius) presented to the Veterinary Teaching Hospital at King Faisal University with maxillary masses. On radiographs, the masses were multicystic and expanded the maxillary bone. The tumors were diagnosed by histopathologic examination as conventional ameloblastoma, two cases as intraosseous squamous cell carcinoma, and central odontogenic fibroma with ossification. To the authors' knowledge, this is the first report of ameloblastoma in a camel, the first detailed description of maxillary squamous cell carcinoma in camels, and the first report of central odontogenic fibroma in any animal species.

Targeted next-generation sequencing (NGS) is a well-established technique to detect pathogenic alterations in tumors. Indeed, it is the cornerstone of targeted therapy in precision medicine. We investigated the clinical utility of next-generation sequencing in real-world cases.

We retrospectively selected six representative cancer cases, wherein targeted NGS played a pivotal role in the diagnosis and treatment of patients. Additionally, we analyzed three cases with rare, unusual pathogenic alterations.

Our NGS analysis revealed that four patients had TPR-ROS1, EGFR-RAD51, and NCOA4-RET fusions and MET exon 14 skipping mutation, respectively, which can be treated with targeted therapy. Furthermore, we used NGS as a diagnostic tool to confirm the origin of unknown primary malignant tumors in two cases. Interestingly, NGS also helped us identify the following cases: patients exhibiting BRCA1 and TP53 mutations that exhibited histological and immunohistochemical characteristics consistent with endometrioid carcinoma, patients with high-grade serous carcinoma not possessing a TP53 mutation, and patients with small cell lung cancer with a ERBB2 mutation and displaying no loss of RB1.

We recommend targeted NGS for the diagnoses and targeted therapy of cancer patients.

Background: Malignant odontogenic tumours (MOTs) arise either de novo from the tooth forming tissues, their developmental residues or from existing odontogenic epithelial or mesenchymal neoplasms in the jaws. Their management requires extensive surgery due to their infiltrative nature and risk of metastasis. There is a need to understand the clinical and pathological features of MOTs to inform both treatment algorithms and prognostication. This is an area of diagnostic pathology which presents substantial difficulties in diagnosis, compounded by inconsistent use of terminology. Thus, this systematic review aimed to describe the clinical and pathological features of MOTs with a view to consolidating the literature and defining problematic areas in diagnosis and classification. Methods: An electronic database search was conducted in Web of Science, PubMed/Medline, and Embase. Additionally, the grey literature and reference lists of selected papers searched for completeness. Nine hundred and sixty articles were initially identified. Following removal of duplicates and application of inclusion/exclusion criteria, 312 articles were included for qualitative analysis. Results: The 312 articles encompassed a total of 507 patients with most lesions located within the mandible (74.3%). The most common first histological diagnosis was ameloblastic carcinoma (25.7% of all diagnoses), but there is considerable variation in how and when various diagnostic terms are used, and several misdiagnoses were reported. An initial benign diagnosis was made in 24.7% of patients, followed by a later malignant diagnosis and in this sub-group, the most common benign first diagnosis was ameloblastoma (42.4%). Cervical lymph nodes were the most common site of metastasis (9.3% of patients). With respect to distant metastasis (DM), the lungs were the most common organ affected (11.2% of DM patients) with metastasising ameloblastoma the most commonly reported tumour which metastasised to the lungs. Overall, 26.8% of patients developed recurrence. Conclusion: Overall, the quality of the literature on MOTs is poor. This review of the literature has highlighted variations in diagnostic terms and criteria which has resulted in areas of confusion with potential for misdiagnosis. This consolidation of primary data has identified key areas for targeted research including further discussion on the malignant potential of ameloblastoma.

A proper antibody panel selection is one of the most important factors to reach an adequate diagnosis in challenging cases. This retrospective study was designed to determine the contribution of immunohistochemistry (IHC) in the primary diagnosis of oral diseases in one of the main services of oral pathology in the State of São Paulo, Brazil, and to identify the most common antibodies used, and recommend diagnostic algorithms based on our experience with challenging lesions. A total of 1698 IHC stains were performed in 401 cases from a total of 28,804 cases received from public dental clinics and private dental practitioners within a period of 13 years, representing a frequency of 1.4% of IHC solicitations. Among these, 112 (28%) were mandatory to reach a final diagnosis and 255 (63.6%) were confirmative. In 34 (8.4%) cases, it was not possible to reach a conclusive/final diagnosis, even with IHC. Regarding the nature of the lesions, 210 (52.3%) were benign, 163 (40.6%) were malignant tumors, 13 (3.2%) were reactive, 10 (2.5%) were premalignant, and 5 (1.2%) were lesions of uncertain malignancy. Small amount of tissue of some incisional biopsies, overlapping features of spindle cell lesions (epithelial, neural, melanocytic, smooth muscle, endothelial, and fibroblastic/myofibroblastic cell differentiation), and overlapping features of salivary gland lesions were the most frequent challenges in which IHC stains were requested. Spindle cell lesions were the most frequent (22%) among all cases that required IHC to reach a final diagnosis. The implementation of IHC for routine practice requires a wide range of markers, proper antibody selection, and knowledge to interpret the subjectivity of staining. The inherent limitation of incisional biopsies was pointed as a reason to inconclusive diagnosis, despite a wide range of antibodies that our laboratory displays.

Due to the rarity and diversity of primary intraosseous malignancies in jawbones, we aimed to evaluate the clinicopathological features and discuss the findings of our collected cases with the literatures.

Twenty-nine patients (2000-2020) diagnosed with primary central malignancies of jawbones were selected from the database of Oral Pathology Department in our institution. Clinical features, radiographic appearance, and histopathological diagnosis of the 29 cases were analyzed.

Twenty-nine patients aged between 19 and 84 years (average, 57.4 years) with a male to female ratio of 1.2:1 were included. The most frequent site was the mandibular body and ramus, followed by the posterior maxilla and mandibular symphysis. The most common diagnosis was osteogenic sarcoma (n = 13), followed by odontogenic carcinoma (n = 7), hematologic malignancies (n = 5), salivary gland malignancies (n = 2), and neurogenic sarcomas (n = 2). The most frequent symptoms were swelling, pain, paresthesia of lower lip, and mobile tooth. Radiographically, they usually presented as ill-defined osteolytic to osteoblastic lesions depending on the amount of ossification. Wide excision comprising partial maxillectomy and segmental mandibulectomy were the most common therapeutic methods.

Despite the rarity of primary central malignancies in jawbones, the clinical features may mimic infectious process or benign lesions. Detailed history-taking, clinical and imaging examination and awareness of the patient's signs and symptoms combining with the histopathological inspection are important for early diagnosis and improved prognosis. The current data contributes a useful basis for clinical investigation regarding intraosseous malignancies occurring in the jawbones.

BACKGROUND Primary malignant ameloblastoma is a very rare tumor of the dental lamina epithelium. Similar to the benign ameloblastoma, the mass is without significant histological atypia, but the malignant type may present with metastases, most commonly to the lungs. The average age of diagnosis is 34 years, and the malignancy affects men and women equally. The tumors often present with an insidious growth and have a median survival from time of diagnosis of 17.6 years. Due to the rarity of this lesion, a standard of care has not yet been established. CASE REPORT A 38-year-old Haitian woman, who initially presented with a large primary malignant ameloblastoma of the angle of the mandible, experienced a recurrence in the floor of the mouth 30 months after surgical resection. In 2018, 2 years after the removal of the recurrent tumor, the patient presented with ascites, right-sided abdominal pain, weight loss, and a palpable liver mass. Laparoscopic exploration demonstrated a complex lateral right liver lobe cyst, suspicious for parasitic infection. Cytological analysis showed positive staining for cytokeratin 5/6, P63, and CD56, indicative of metastatic ameloblastoma of the liver. Consistent cell morphology from the primary tumor and liver cyst was also noted. Following drainage of the cyst, the patient returned to Haiti, where she died in 2020. In Haiti, she lacked appropriate local medical care, leading to the severe progression of her initial primary ameloblastoma and disease recurrence. CONCLUSIONS Malignant ameloblastoma accounts for less than 2% of all odontogenic tumors, as the benign variant is much more common. Distant metastases of these lesions are rare; to date, few cases have presented with hepatic metastases.

The World Health Organization's (WHO) updated classification of head and neck tumors (2017) defined odontogenic fibroma as a rare neoplasm. In this report, we describe an unusual, typical and rare variant of a central odontogenic fibroma with diffuse amyloid-like protein stromal deposition, and discuss the differential diagnosis with other entities. Radiographically, this lesion presented as a well-defined radiolucency of the mandible, partially cystic. Histologically, the lesion showed a unique confluence of odontogenic epithelial rests in a moderately cellular connective tissue. Immunohistochemical staining highlighted a mixture of benign epithelial and Langerhans cells within connective tissue with diffuse amyloid-like stromal deposition. The importance of recognizing this variant of odontogenic fibroma is due to its benign prognosis and clinical course.

Ameloblastoma is a locally aggressive odontogenic tumor. Etiopathogenesis and locally aggressive growth properties of ameloblastoma can be attributed to a hypoxic microenvironment conducive to tumor cell survival. Epithelial-derived follicular ameloblastoma cells (EP-AMCs) display enhanced basal autophagy, but the interplay of hypoxia and autophagy in EP-AMCs survival and ameloblastoma recurrence is unclear. We evaluated differential expression of autophagic markers in primary and recurrent ameloblastomas and hypothesized that hypoxia-induced autophagy supports EP-AMC survival. Primary and recurrent ameloblastomas were comparatively assessed for expression levels of pan-cytokeratin, Vimentin, and autophagic markers SQSTM1/p62, LC3, and pS6. EP-AMCs compared with human odontoma-derived cells (HODCs) were subjected to severe hypoxia to determine the interplay of hypoxia and autophagic process in posthypoxia survival. Pan-cytokeratin and SQSTM1/p62 were expressed by both primary and recurrent ameloblastoma epithelial cells while the ameloblastoma connective tissues displayed weak reactivity to vimentin. Under hypoxia, EP-AMC expression levels of hypoxia-inducible factor (HIF)-1α, p62, and LC3 were increased while pS6 was decreased posthypoxia. The combined decrease in pS6 and enhanced LC3 in EP-AMCs under hypoxia indicate that EP-AMCs re-establish basal autophagy under hypoxia. Taken together, these suggest a possible role of LC3-associated phagocytosis (LAP) in ameloblastoma cell survival.

Localized juvenile spongiotic gingival hyperplasia (LJSGH) is a recently described entity with distinct manifestations. Herein we report a comprehensive histopathologic study of 21 lesions and a literature review. Additionally, we propose a new term that we consider more appropriate.

LJSGH cases were retrieved and their clinicopathologic characteristics were assessed. A review of all pertinent literature was also conducted.

Eighteen patients with LJSGH (21 biopsied lesions) were identified. Microscopically, surface morphology was classified into exophytic/papillary, flat, and micropapillary (8, 7, and 6 lesions, respectively). Cases with parakeratinization (n = 9), no prominent spongiosis (n = 5), or epithelial atrophy (n = 4) were recorded. Increased vascularity, mixed inflammation with exocytosis, and cytokeratin-19 positivity were uniformly observed. Less frequent findings included pseudoepitheliomatous hyperplasia (n = 8), bacterial colonies (n = 5), acantholysis (n = 3), and dystrophic calcifications (n = 2). The literature review disclosed 201 patients with a mean age of 14.8 years (range, 3-72; 13.6% affecting adults), similar sex distribution (103:98, female:male), and predominance of the anterior maxilla (≈ 80%). Eighteen cases were multifocal (≈ 10%).

Our data suggest that the terminology could be modified, because LJSGH may be multifocal, affect older individuals, or exhibit epithelial atrophy, and the entity's odontogenic origin (as highlighted by the histopathologic and immunohistochemical findings) needs to be emphasized.

Diagnosis of odontogenic tumors can be challenging due to their rarity and diverse morphology, but when arising near the tooth, the diagnosis could be suspected. When their location is not typical, like inside the paranasal sinuses, the diagnosis is less easy. Maxillary ameloblastomas are exceedingly rare with only sparse information on their epidemiological, histological and genetic characteristics. The aim of this report is to thoroughly review the available literature in order to present the characteristics of this tumor. According to available data, maxillary ameloblastomas can occur in all ages but later than mandible ones, and everywhere within the maxillary region without necessarily having direct contact with the teeth. No sex preference has been shown. The most common histological patterns seen in this location are the follicular and plexiform ones. Maxillary ameloblastomas are locally aggressive neoplasms, thus therapy aims for excision including normal bone beyond the lesion. In contrast to mandible ameloblastomas, maxillary ones most commonly show mutations of the SMO gene. Furthermore, differential tumor diagnosis is thoroughly discussed in the present review.

Peripheral Ameloblastoma (PA) is a benign odontogenic tumor, arising from the cell rest of Serres, reduced enamel epithelium and basal cells of the surface epithelium. Peripheral ameloblastoma is a rare odontogenic neoplasm occurring commonly in the mandibular gingiva. PA clinically resembles other peripherally occurring lesions like pyogenic granuloma, peripheral ossifying fibroma, peripheral giant cell granuloma, and squamous papilloma. The recurrence rate of PA is 16-19% which demands a straight follow up. We report a case of recurrent peripheral ameloblastoma occurring in a 72-year old male located in the mandibular lingual gingiva in relation to the 44, 45 element's regions. The patient had a primary lesion excised from the same site 6 years before which was diagnosed as ameloblastoma.

A data set has been developed for the reporting of excisional biopsies and resection specimens for malignant odontogenic tumors by members of an expert panel working on behalf of the International Collaboration on Cancer Reporting, an international organization established to unify and standardize reporting of cancers. Odontogenic tumors are rare, which limits evidence-based support for designing a scientifically sound data set for reporting them. Thus, the selection of reportable elements within the data set and considering them as either core or noncore is principally based on evidence from malignancies affecting other organ systems, limited case series, expert opinions, and/or anecdotal reports. Nevertheless, this data set serves as the initial step toward standardized reporting on malignant odontogenic tumors that should evolve over time as more evidence becomes available and functions as a prompt for further research to provide such evidence.

Ameloblastic carcinoma (ACA) is a malignant neoplasm with overlapping histopathological features of benign aggressive solid multicystic ameloblastoma (SMA). This often leads to misdiagnosis with direct implication on the management protocol. The need of the hour is to adopt reliable tissue biomarkers to differentiate these lesions accurately that will help to implement an appropriate treatment modality. Few studies to differentiate ACA and SMA in literature with a limitation of a single marker and lack of availability of cases have prompted us to undertake this study. Thereby, this study is aimed at resolving the diagnostic dilemma in differentiating ACA and aggressive SMA using SOX-2, OCT-4 and CD44.

Tissue samples involved 40 archival cases of histopathologically confirmed cases of ACA (n = 20) and SMA (n = 20). The sections were subjected to immunohistochemical staining using antibodies to SOX-2, OCT-4 and CD44. Nuclear staining for SOX-2 and OCT-4 and membranous reactivity for CD44 was considered positive.

The expression of SOX-2 and OCT-4 in ACA was statistically significant when compared to SMA (P < 0.001). CD44 showed an insignificant statistical value of <0.077 in differentiating ACA and SMA. SOX-2 and OCT-4 expression in ACA showed a significant correlation coefficient of 0.616 at P < 0.004.

SOX-2 and OCT-4 could serve as independent novel markers in resolving the diagnostic dilemma between ACA and aggressive SMA.

Microcystic variant of calcifying epithelial odontogenic tumor is rare. We herein describe an additional well-documented case of microcystic CEOT. The affected patient is a Guatemalan 42-year-old female with an expansile well-defined mixed radiolucent-radiopaque lesion located in the right posterior mandible. The lesion was associated to an unerupted third molar. Histopathologic examination revealed nests and cords of moderately pleomorphic, eosinophilic polyhedral epithelial cells surrounded by a fibromyxoid stroma. The neoplastic cells showed microcystic pattern made of pseudo-glandular spaces with variable diameter. Occasional amyloid deposits and calcified acellular material were observed. Tumor cells were positive for AE1/AE3, CK14, CK19, p63, CD138, and beta-catenin. Conservative surgical resection was performed with an uneventful immediate post-surgical follow-up. After 1 year follow-up there is no evidence of recurrence. Pathologists should be aware of this unusual microcystic presentation of CEOT, which may pose a diagnostic challenge and potential diagnostic dilemma.

Ameloblastoma is a rare low-grade odontogenic tumor of epithelial origin. The World Health Organization (WHO) has defined malignant ameloblastoma (MA) as a histologically benign-appearing ameloblastoma that has metastasized. Treatment of the primary ameloblastoma usually consists of radical excision of the tumor and adjuvant radiotherapy. Chemotherapy should be used to treat metastases due to its indolent clinical course. Presented here is the case of a 43-year-old woman who was admitted to a hospital in 2006 with a large mass involving the neck and left mandible. The mass had formed over years and had been neglected. The woman was diagnosed with a primary ameloblastoma of the mandible. Surgical resection was performed, followed by adjuvant radiotherapy. In September 2016, she was admitted again, and the findings were consistent with metastases of the previously identified ameloblastoma to the lungs. The patient was evaluated for further chemotherapy with 6 cycles of cisplatin at a dose of 100 mg/m² on day 1, 5-FU at a dose of 1000 mg/m²/day on day 1-4 (3 wk), and pegylated filgrastim. The current case represents the classical course of a rare disease, which in this instance involved the common presentation of MA. This case is a valid incidence of MA based on the typical histology, findings from a lung biopsy, the immunohistochemical profile of the tumor, the typical clinical features, and a history of a previous primary disease.

This study aimed to compare the histological and immunohistochemical characteristics of ameloblastomas (AM) and ameloblastic carcinomas (AC).

Fifteen cases of AM and 9 AC were submitted to hematoxilin and eosin (H&E) and immunohistochemical analysis with the following antibodies: cytokeratins 5,7,8,14 and 19, Ki-67, p53, p63 and the cellular adhesion molecules CD138 (Syndecan-1), E-cadherin and β-catenin. The mean score of the expression of Ki-67 and p53 labelling index (LIs) were compared between the groups using the t test. A value of p<0.05 was considered to be statistically significant.

All cases were positive for CKs 5, 14 and 19, but negative for CKs 7 and 8. CKs 5 and 19 were positive mainly in the central regions of the ameloblastic islands, while the expression in AC was variable in intensity and localization. CK14 was also variably expressed in both AM and AC. Ki-67 (P=.001) and p53 (P=.004) immunoexpression was higher in AC. All cases were positive for p63, but values were higher in AC. CD138 was mainly expressed in peripheral cells of AM, with a weak positivity in the central areas, while it was positive in most areas of ACs, except in less differentiated regions, where expression was decreased or lost. E-cadherin and β-catenin were weakly positive in both AM and AC.

These results shows that Ki-67, p53 and p63 expression was higher in AC as compared to AM, suggesting that these markers can be useful when considering diagnosis of malignancy, and perhaps could play a role in malignant transformation of AM. Pattern of expression of CKs 5 and 19 in AC were different to those found in AM, suggesting genetic alterations of these proteins in malignant cells. It was confirmed that CK19 is a good marker for benign odontogenic tumors, such as AM, but it is variably expressed in malignant cases.

This article reviews a myriad of common and uncommon odontogenic cysts and tumors. The clinical presentation, gross and microscopic features, differential diagnosis, prognosis, and diagnostic pitfalls are addressed for inflammatory cysts (periapical cyst, mandibular infected buccal cyst/paradental cyst), developmental cysts (dentigerous, lateral periodontal, glandular odontogenic, orthokeratinized odontogenic cyst), benign tumors (keratocystic odontogenic tumor, ameloblastoma, adenomatoid odontogenic tumor, calcifying epithelial odontogenic tumor, ameloblastic fibroma and fibroodontoma, odontoma, squamous odontogenic tumor, calcifying cystic odontogenic tumor, primordial odontogenic tumor, central odontogenic fibroma, and odontogenic myxomas), and malignant tumors (clear cell odontogenic carcinoma, ameloblastic carcinoma, ameloblastic fibrosarcoma).

To determine how many ameloblastomas were misdiagnosed as dentigerous cysts (DCs) by correlating the radiological and histopathological features of a series of both entities.

Histopathology reports and radiological imaging of 135 DCs and 43 ameloblastomas were reviewed. Any clinical or radiological feature that suggested that the diagnosis of DC was wrong-for example, absence of an unerupted tooth-prompted review of the original histology. A total of 34 cases coded as DC at diagnosis were excluded; in the remaining 101 patients, the clinicoradiological and histopathological features were consistent with DC in 96 (95.0%). Review of the histology revealed that 4 patients had actually had odontogenic keratocysts (OKCs) and one a luminal/simple unicystic ameloblastoma (UA). One other OKC and 3 other ameloblastomas (1 luminal UA, 2 solid/multicystic) had originally been diagnosed as DC; these had been identified prior to the study. Of the 9 misdiagnosed patients, 6 were ≤20 years old. Clinically, DC had been the only, or one of the differential, diagnoses in 7 patients; in the other 2, the clinical diagnosis was radicular cyst. In none of the 4 misdiagnosed ameloblastomas was the radiology compatible with a diagnosis of DC. Incorrect terminology had been used on the histopathology request form in 5 of the 34 excluded cases where the clinical diagnosis was DC, despite the cyst being periapical to an erupted carious or root-filled tooth.

The entire clinical team must ensure that a histopathological diagnosis of DC is consistent with the clinicoradiological scenario, particularly in younger patients.

A rare case of primary intraosseous squamous cell carcinoma arising in an odontogenic keratocyst (OKC) is presented here, with the clinical and histologic features of the first biopsy showing characteristics of OKC and the second biopsy disclosing a squamous cell carcinoma. Immunoprofile of this case was compared with five cases of classical OKC by using cytokeratins CK5, CK14, and CK19, CD138, p63, Ki-67, p53, and bcl-2. Classic OKCs showed expected positivity, mainly in the basal and/or suprabasal layers with most antibodies, except for p53, which was negative, whereas the present case showed irregular positivity in all layers, indicating that this can be useful for differential diagnosis and suggesting a possible role in malignant transformation into primary intraosseous squamous cell carcinoma. In conclusion, immunohistochemical differences between the first biopsy of the present case and classic OKC suggest that immunohistochemistry can be helpful in cases with areas of subtle initial malignant transformation.