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Oral Diseases Oct 2019The aim of the present study was to assess the outcomes of radical and conservative treatment approaches of solid/multicystic and unicystic ameloblastoma in terms of... (Meta-Analysis)
Meta-Analysis
OBJECTIVES
The aim of the present study was to assess the outcomes of radical and conservative treatment approaches of solid/multicystic and unicystic ameloblastoma in terms of recurrence rates.
MATERIAL AND METHODS
A systematic review and meta-analysis was conducted based on the PRISMA statement. Search was performed using PubMed, Embase, SCOPUS, and Web of Science for articles published from January 1969 until March 2018. Quality assessment of the selected articles was conducted using the Quality Appraisal of Case Series Studies Checklist. The meta-analysis was performed using the MedCalc program.
RESULTS
The search strategy yielded 6,984 articles; 20 studies met the eligibility criteria and were included in the meta-analysis. The pooled recurrence rate of solid/multicystic ameloblastomas following radical treatment was 8%, while conservative treatment caused recurrences in 41%. For unicystic ameloblastomas, these values were 3% and 21%, respectively. The risk of recurrences in both types of ameloblastomas following radical treatment was lower than following conservative treatment.
CONCLUSIONS
The present study showed statistically significant differences in recurrence favoring radical treatment for both unicystic and solid/multicystic ameloblastoma. The solid/multicystic type showed more recurrences than the unicystic type. Unfortunately, since only retrospective studies were available, the evidence is less strong as wished for.
Topics: Ameloblastoma; Checklist; Conservative Treatment; Humans; Jaw Neoplasms; Neoplasm Recurrence, Local; Netherlands; Retrospective Studies; Treatment Outcome
PubMed: 30548549
DOI: 10.1111/odi.13014 -
Ear, Nose, & Throat Journal Sep 2021
Topics: Adolescent; Adult; Child; Female; Humans; Male; Mandibular Neoplasms; Medical Illustration; Odontoma; Young Adult
PubMed: 31760790
DOI: 10.1177/0145561319890175 -
Fetal and Pediatric Pathology Apr 2023Ameloblastic fibro-odontoma (AFO) is a benign odontogentic tumor without an aggressive behavior, unlike the similar ameloblastic fibroma. A 9-year-old boy, with tooth...
Ameloblastic fibro-odontoma (AFO) is a benign odontogentic tumor without an aggressive behavior, unlike the similar ameloblastic fibroma. A 9-year-old boy, with tooth eruption failure, underwent enucleation and curettage of a well-defined variable radiolucent and radio-opaque right mandible lesion. There was odontogenic epithelium with peripheral palisading in a loose myxoid stroma as well as a disorganized component of dentin, enamel, and cementum, features of an AFO. AFO is an odontogenic mixed tumor of epithelium and mesenchyme.
Topics: Male; Humans; Child; Odontoma; Mandibular Neoplasms; Epithelium; Head; Connective Tissue
PubMed: 35748698
DOI: 10.1080/15513815.2022.2088910 -
The Pan African Medical Journal 2021Pleomorphic adenoma is a benign mixed tumor, which is composed of myoepithelial and epithelial cells. A fibrous capsule separates these cells from the surrounding...
Pleomorphic adenoma is a benign mixed tumor, which is composed of myoepithelial and epithelial cells. A fibrous capsule separates these cells from the surrounding tissues. Pleomorphic adenoma is the most common salivary gland tumour accounting for 40-70% of all major and minor salivary gland tumours. It is also the commonest minor salivary gland benign tumours accounting for 70% of all tumours. Hard palate is the commonest site followed by upper lip, buccal mucosa, tongue, floor of mouth, retromolar trigone. This case report discusses a case of pleomorphic adenoma of hard palate in an old man after complete excision of the tumour, which was confirmed by a biopsy specimen.
Topics: Adenoma, Pleomorphic; Adult; Humans; Male; Palatal Neoplasms; Palate, Hard
PubMed: 33912316
DOI: 10.11604/pamj.2021.38.146.26508 -
Endocrine Sep 2023Parathyroid carcinoma (PC) is an extremely rare malignant tumor of the parathyroid glands, accounting for less than 1% of primary hyperparathyroidism, commonly... (Review)
Review
Parathyroid carcinoma (PC) is an extremely rare malignant tumor of the parathyroid glands, accounting for less than 1% of primary hyperparathyroidism, commonly characterized by severe and unmanageable hypercalcemia, aggressive behavior, high metastatic potential, and poor prognosis. PC manifests prevalently as a sporadic tumor and only occasionally it is part of congenital syndromic and non-syndromic endocrine diseases. Molecular pathogenesis of this form of parathyroid tumor is not fully elucidated and it appears to be caused by multiple genetic and epigenetic drivers, differing among affected patients and not yet clearly stated in distinguishing PC from the benign parathyroid adenoma (PA). Congenital forms of PC have been prevalently associated with germline heterozygous loss-of-function mutations of the CDC73 tumor suppressor gene, both in the context of the hyperparathyroidism jaw-tumor syndrome (HPT-JT) and of the isolated familial hyperparathyroidism (FIPH). Currently, surgical en bloc resection of affected gland(s) and other involved structures is the elective therapy for both primary and recurrent PC. However, it usually results ineffective for advance and metastatic disease, and a high percentage of post-operative recurrence is reported. Targeted medical therapies for surgically untreatable PC, based on the molecular profile of PC samples, are, therefore, needed. The characterization of genetic and epigenetic alterations and deregulated pathways in PC samples will be of fundamental importance to tailor treatment for each patient. Here, we reviewed main findings on molecular pathogenetic aspects of PC, and the current state of the art of therapies.
Topics: Humans; Parathyroid Neoplasms; Tumor Suppressor Proteins; Neoplasm Recurrence, Local; Jaw Neoplasms; Hyperparathyroidism, Primary
PubMed: 37160841
DOI: 10.1007/s12020-023-03376-w -
Atlas of the Oral and Maxillofacial... Sep 2023
Review
Topics: Child; Humans; Bone Transplantation; Mandible; Mandibular Neoplasms; Mandibular Reconstruction; Free Tissue Flaps; Treatment Outcome
PubMed: 37500201
DOI: 10.1016/j.cxom.2023.04.002 -
International Journal of Molecular... Oct 2021Parathyroid tumors are rare endocrine neoplasms affecting 0.1-0.3% of the general population, including benign parathyroid adenomas (PAs; about 98% of cases),... (Review)
Review
Parathyroid tumors are rare endocrine neoplasms affecting 0.1-0.3% of the general population, including benign parathyroid adenomas (PAs; about 98% of cases), intermediate atypical parathyroid adenomas (aPAs; 1.2-1.3% of cases) and malignant metastatic parathyroid carcinomas (PCs; less than 1% of cases). These tumors are characterized by a variable spectrum of clinical phenotypes and an elevated cellular, histological and molecular heterogeneity that make it difficult to pre-operatively distinguish PAs, aPAs and PCs. Thorough knowledge of genetic, epigenetic, and molecular signatures, which characterize different parathyroid tumor subtypes and drive different tumorigeneses, is a key step to identify potential diagnostic biomarkers able to distinguish among different parathyroid neoplastic types, as well as provide novel therapeutic targets and strategies for these rare neoplasms, which are still a clinical and therapeutic challenge. Here, we review the current knowledge on gene mutations and epigenetic changes that have been associated with the development of different clinical types of parathyroid tumors, both in familial and sporadic forms of these endocrine neoplasms.
Topics: Adenoma; Cyclin-Dependent Kinase Inhibitor p27; Epigenesis, Genetic; Fibroma; Humans; Hyperparathyroidism; Hyperparathyroidism, Primary; Jaw Neoplasms; Multiple Endocrine Neoplasia Type 1; Multiple Endocrine Neoplasia Type 2a; Mutation; Parathyroid Neoplasms; Proto-Oncogene Proteins; Tumor Suppressor Proteins
PubMed: 34681865
DOI: 10.3390/ijms222011206 -
Pathologie (Heidelberg, Germany) Jul 2023Maxillofacial tumours cover a broad spectrum of lesions, including neoplasms, hamartomatous changes and developmental disorders. Since the beginning of 2022, a beta... (Review)
Review
Maxillofacial tumours cover a broad spectrum of lesions, including neoplasms, hamartomatous changes and developmental disorders. Since the beginning of 2022, a beta version of the 5th edition of the WHO classification for head and neck tumours has been available online, and a print version is expected to be published in mid-2023. From a conceptual point of view, little has been changed compared to the 4th edition; the sort order of lesions is more rigorously arranged according to benign and malignant behaviour and identical tumour types are no longer described redundantly in different chapters depending on their location. The diagnostic criteria are now summarized as "essential" and "desirable", and in addition to the clinical features, imaging is now also incorporated, providing an interdisciplinary approach to the classification. A few new entities are included for the first time. This article gives an overview of the main changes introduced in the new WHO classification with a special emphasis on fibro-osseous lesions of the craniofacial skeleton.
Topics: Humans; World Health Organization; Head and Neck Neoplasms; Jaw Neoplasms; Bone and Bones; Hamartoma
PubMed: 37179260
DOI: 10.1007/s00292-023-01195-4 -
QJM : Monthly Journal of the... Aug 2019
Topics: Adult; Ameloblastoma; Cone-Beam Computed Tomography; Hemangioma; Humans; Male; Mandibular Neoplasms
PubMed: 31120127
DOI: 10.1093/qjmed/hcz117 -
Journal of Oral Biosciences Jun 2022Ghost cells (GCs) are cells with distinct intracytoplasmic keratinization, which leads to the preservation of the cellular outline with a clear area corresponding to the... (Review)
Review
BACKGROUND
Ghost cells (GCs) are cells with distinct intracytoplasmic keratinization, which leads to the preservation of the cellular outline with a clear area corresponding to the previous nucleus location. GCs may show various patterns, such as degeneration, tissue granulation, and calcification. Their true nature and the mechanism regulating the conversion of odontogenic epithelial cells into GCs remain unclear. GC keratinization is different from normal keratinization as they are larger than keratotic squames, are frequently vacuolated, and have prominent nuclear membrane remnants. Few cystic lesions, odontogenic tumors, and non-odontogenic tumors, such as calcifying odontogenic cyst, craniopharyngioma, pilomatrixoma, odontoma, dentinogenic ghost cell tumor, and ghost cell odontogenic carcinoma, exhibit GCs as a typical feature. The Wnt and Notch signaling pathways play a role in the histogenesis of the neoplasms.
HIGHLIGHT
The review clarifies the various proposed hypotheses of the histogenesis of GCs, including molecular pathogenesis. Diagnostic workup for the identification of GCs, including special staining and immunohistochemistry, has been extensively discussed. A stepwise algorithm for identifying odontogenic and non-odontogenic lesions containing GCs has been proposed. Additionally, the prognostic role of GCs in the lesions has been elucidated.
CONCLUSION
Among the various hypotheses of the origin of GCs, we suggest that aberrant keratinization is the most accepted based on various immunohistochemical studies and special staining characteristics. GCs are a distinct characteristic entity of many odontogenic and non-odontogenic lesions; however, it remains controversial whether their presence has any pathognomonic role in the biological nature of these lesions.
Topics: Hair Diseases; Humans; Jaw Neoplasms; Odontogenic Cyst, Calcifying; Odontogenic Tumors; Pituitary Neoplasms; Skin Neoplasms
PubMed: 35398253
DOI: 10.1016/j.job.2022.03.005