RESUMO
Calcifying odontogenic cyst (COC), once called calcifying cystic odontogenic tumor, is classified under the category of odontogenic cysts. However, the proliferative capacity of the lesional epithelium and consistent nuclear ß-catenin expression raise questions about its current classification. This study aimed to determine whether COC would be better classified as a neoplasm in the histologic and molecular context. Eleven odontogenic lesions diagnosed as COC or calcifying cystic odontogenic tumor were included in this study. The growth patterns of the lesional epithelium were analyzed histologically in all cases. ß-catenin immunohistochemistry and molecular profiling using Sanger sequencing and whole-exome sequencing were performed in 10 cases. Of the 11 cases studied, histologic features reminiscent of so-called adenoid ameloblastoma were observed in 72.7% (8/11), and small islands of clear cells extended into the wall in 36.4% (4/11). Intraluminal and/or mural epithelial proliferation was found in 72.7% of the cases (8/11). Nuclear ß-catenin expression was observed focally in all 10 cases studied, mainly highlighting epithelial cells forming morules and adjacent to dentinoid. CTNNB1 hotspot mutations were detected in 60.0% of the cases (6/10). All the remaining cases had frameshift mutations in tumor-suppressor genes involved in the WNT pathway, including APC and NEDD4L. Recurrent WNT pathway mutations leading to nuclear translocation of ß-catenin and distinct epithelial growth patterns found in COC are the neoplastic features shared by its solid counterpart, dentinogenic ghost cell tumor, supporting its classification as a tumor rather than a cyst.
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Mutação , Cisto Odontogênico Calcificante , Via de Sinalização Wnt , Humanos , Feminino , Masculino , Cisto Odontogênico Calcificante/patologia , Cisto Odontogênico Calcificante/genética , Adulto , Via de Sinalização Wnt/genética , Pessoa de Meia-Idade , beta Catenina/genética , beta Catenina/metabolismo , Ameloblastoma/genética , Ameloblastoma/patologia , Ameloblastoma/metabolismo , Adolescente , Adulto Jovem , Neoplasias Maxilomandibulares/genética , Neoplasias Maxilomandibulares/patologia , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/análise , Tumores Odontogênicos/genética , Tumores Odontogênicos/patologia , Idoso , CriançaRESUMO
BACKGROUND: Despite recent advances in the use of immune checkpoint blockade (ICB) across various cancer types, its efficacy in odontogenic carcinomas remains unexplored. This study aims to investigate PD-L1 expression and the tumor immune microenvironment (TIME) in odontogenic carcinomas to determine the therapeutic potential of ICB and the significance of immune markers. METHODS: The expressions of PD-L1 and T cell markers (CD3, CD8, and FOXP3) were visualized by immunohistochemistry in 21 tissue samples of odontogenic carcinomas. Tumoral PD-L1 expression and the density and spatial distribution of T cell subsets were evaluated, from which TIME was determined. The associations of the variables with clinicopathological and prognostic factors were statistically analyzed. RESULTS: PD-L1 was positively expressed in 52.4% (11/21) of the cases studied. Among tumor types, ameloblastic carcinoma showed significantly higher PD-L1 expression (p = 0.016). TIME based on the intratumoral and stromal T cell distribution was immune-inflamed in 61.9% (13/21) and immune-excluded in 38.1% (8/21), with no immune-desert cases. PD-L1 expression was associated with the densities of all intratumoral T cell subsets (p = 0.03 for CD3, p = 0.03 for CD8, and p = 0.008 for FOXP3) but not with those of stromal T cells. High PD-L1 expression was associated with larger tumor size (p = 0.021), while the intratumoral CD8/CD3 ratio was inversely correlated with tumor size (p = 0.048). CONCLUSION: These findings indicate the involvement of adaptive immune resistance in a subset of odontogenic carcinomas and support the therapeutic potential of ICB in patients with these rare malignancies.
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Carcinoma , Neoplasias Bucais , Tumores Odontogênicos , Humanos , Antígeno B7-H1/metabolismo , Inibidores de Checkpoint Imunológico , Linfócitos T/metabolismo , Neoplasias Bucais/patologia , Tumores Odontogênicos/patologia , Fatores de Transcrição Forkhead , Carcinoma/patologia , Microambiente Tumoral , Linfócitos T CD8-Positivos/patologia , Biomarcadores TumoraisRESUMO
An epithelial odontogenic tumor called adenoid ameloblastoma (AA) has recently been included in the new WHO classification. However, AA has considerable overlapping features with a preexisting entity, dentinogenic ghost cell tumor (DGCT). This study compared the clinical, histologic, and molecular characteristics of AA and DGCT. Eight cases of odontogenic tumors initially diagnosed as AA or DGCT were included in this study. Quantitative histologic analysis, ß-catenin immunohistochemistry, and molecular profiling using next generation sequencing were performed. Additionally, accumulated clinical data of AA and DGCT were statistically analyzed. Nuclear ß-catenin accumulation was detected in all cases in common, although the tumors studied histologically consisted of varying combinations of the AA-like phenotype, ghost cells, and dentinoid. However, CTNNB1 hotspot mutations were not found in any case. Instead, loss-of-function mutations in tumor suppressor genes involved in the WNT pathway, including the APC, SMURF1, and NEDD4L genes, were found regardless of histologic type. In addition, KRT13 mutations were detected in 2 cases with a high proportion of ghost cells. Finally, a literature analysis revealed clinical similarities between the previously reported cases of AA and DGCT. These findings suggest that from a clinical and molecular point of view, AA and DGCT represent a histologic spectrum of WNT pathway-altered benign odontogenic tumors rather than 2 distinct tumors. Moreover, previously unidentified keratin mutations may be associated with ghost cell formation found in specific types of odontogenic lesions.
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Tonsila Faríngea , Ameloblastoma , Tumores Odontogênicos , Humanos , Ameloblastoma/genética , Ameloblastoma/patologia , beta Catenina/genética , Tonsila Faríngea/patologia , Via de Sinalização Wnt/genética , Tumores Odontogênicos/genética , Tumores Odontogênicos/patologia , Ubiquitina-Proteína LigasesRESUMO
BACKGROUND: Surgical management for chondrosarcoma of the temporomandibular joint (TMJ) is challenging due to the anatomical location involving the facial nerve and the functional joint. The purpose of this case series was to analyze the largest number of TMJ chondrosarcoma cases reported from a single institution and to review the literature about chondrosarcoma involving the TMJ. METHODS: Ten TMJ chondrosarcoma patients at Seoul National University Dental Hospital were included in this study. Radiographic features, surgical approaches, histopathologic subtypes, and treatment modalities were evaluated. All case reports of TMJ chondrosarcoma published in English from 1954 to 2021 were collected under PRISMA guidelines and comprehensively reviewed. RESULTS: The lesions were surgically resected in all 10 patients with efforts to preserve facial nerve function. Wide excision including margins of normal tissue was performed to ensure adequate resection margins. All TMJs were reconstructed with a metal condyle except one, which was reconstructed with vascularized costal bone. At last follow-up, all patients were still alive, and there had been no recurrence. Among 47 cases (patients from the literature and our cases), recurrence was specified in 43 and occurred in four (9.5%). CONCLUSIONS: For surgical management of TMJ chondrosarcoma, wide excision must consider preservation of the facial nerve. Reconstruction using a metal condyle prosthesis and a vascularized free flap is reliable. A more conservative surgical approach correlates with a favorable prognosis for facial nerve recovery. Nevertheless, wide excision is imperative to prevent tumor recurrence. In cases in which the glenoid fossa is unaffected by the tumor, it is deemed unnecessary to reconstruct the glenoid fossa within an oncological setting.
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Neoplasias Ósseas , Condrossarcoma , Retalhos de Tecido Biológico , Humanos , Recidiva Local de Neoplasia/cirurgia , Condrossarcoma/cirurgia , Margens de Excisão , Neoplasias Ósseas/cirurgiaRESUMO
Although several types of odontogenic tumors share the same mutations in MAPK pathway genes, their effects on MAPK activation remain unclarified. This study aimed to evaluate the associations between these mutations and ERK phosphorylation in ameloblastoma and mixed odontogenic tumors (MOTs) and to analyze the expression pattern of phosphorylated ERK (p-ERK) for determining the involvement of MAPK activation in the development and progression of odontogenic tumors. Forty-three odontogenic tumors consisting of 18 ameloblastomas and 25 MOTs were analyzed for BRAF, KRAS, and NRAS mutations by Sanger sequencing. The expressions of BRAFV600E protein and p-ERK were detected by immunohistochemistry. The associations between mutation status and p-ERK expression were statistically analyzed. The effect of BRAFV600E inhibition on MAPK activation was investigated in ameloblastoma cells. In benign MOTs, BRAFV600E mutations were neither expressed at the protein level nor associated with p-ERK expression. In contrast, BRAFV600E -mutant ameloblastic fibrosarcoma showed co-expression of BRAF V600E protein and p-ERK, especially in the sarcomatous component. In ameloblastoma, p-ERK was predominantly expressed in the tumor periphery showing a significant correlation with BRAFV600E mutations, and in vitro BRAFV600E inhibition decreased ERK phosphorylation. KRASG12C mutations, previously unidentified in odontogenic tumors, were detected in one case each of benign MOT and ameloblastoma; only the latter was high-p-ERK. In conclusion, unlike in benign MOTs, BRAFV600E and KRASG12C mutations lead to MAPK activation in ameloblastoma, suggesting their role as therapeutic targets. p-ERK intratumoral heterogeneity indicates that MAPK pathway activation may be associated with sarcomatous proliferation of ameloblastic fibrosarcoma and infiltrative behavior of ameloblastoma.
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Ameloblastoma , Fibrossarcoma , Tumores Odontogênicos , Proteínas Proto-Oncogênicas B-raf , Proteínas Proto-Oncogênicas p21(ras) , Ameloblastoma/genética , Ameloblastoma/patologia , Fibrossarcoma/genética , Fibrossarcoma/patologia , Humanos , Mutação , Tumores Odontogênicos/genética , Tumores Odontogênicos/patologia , Proteínas Proto-Oncogênicas B-raf/genética , Proteínas Proto-Oncogênicas p21(ras)/genéticaRESUMO
BACKGROUND: Primary intraosseous carcinoma (PIOC) is a rare malignant odontogenic tumor that predominantly occurs in males older than 50 years. PIOC can be misdiagnosed as odontogenic cyst because it occasionally shows a well-defined border on radiography. In this study, related literatures of pediatric and adolescent PIOC cases were analyzed under strict PRISMA guidelines along with an adolescent case who was provisionally misdiagnosed as an odontogenic cyst. METHODS: All case reports for PIOC published in English from 1966 to 2021 were collected. Cases under the age of 20 were classified as pediatric and adolescent populations in this study. A total of 12 pediatric and adolescent cases including 11 PIOCs from the literature and one new case of a 14-year-old female were analyzed. Clinical and radiographic features, diagnosis and treatment approaches, and prognosis were investigated. RESULTS: Ages ranged from 4 to 18 years. The female to male ratio was 1.4:1. Seven cases occurred in the mandible. Swelling was observed in 11 patients. The radiologic borders were well-defined in six cases and corticated in four cases. Tooth displacement and root resorption were observed in four and six cases, respectively. The provisional diagnosis for seven patients was odontogenic cyst and enucleation was performed in six cases including the new case. During the follow-up period, local recurrence occurred in three patients. The pediatric and adolescent PIOC cases with local recurrence showed poor prognosis. The locally recurred lesion in the new case did not decrease in size despite concurrent chemo-radiation therapy. CONCLUSIONS: Three-dimensional imaging modalities and incisional biopsy with multiple specimens are necessary to rule out PIOC in the lesions with atypical radiographic findings. PIOC should be diagnosed differentially from odontogenic cyst even in pediatric and adolescent populations to properly manage the disease with poor prognosis.
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Carcinoma de Células Escamosas , Neoplasias de Cabeça e Pescoço , Cistos Odontogênicos , Tumores Odontogênicos , Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , MandíbulaRESUMO
ABSTRACT: Odontogenic keratocyst (OKC) arising from purely soft tissue other than the mucosa covering the jawbone is rare. A 57- year-old Korean female patient presented with a lump on her right cheek, which had been suspected as a fibrotic mass on the buccinator muscle by the local clinic. Magnetic resonance imaging showed an ovoid mass in the buccal space just before the right ramus with an enhancing component in the marginal area, and the interior of the mass revealed a fluid signal. Histopathologically, the lesion showed the typical features of OKC and the cyst wall contained some daughter cysts and the minor salivary gland, muscle, and fat tissues. The authors report a very unique case of OKC arising in the masseter muscle.
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Cistos Odontogênicos , Tumores Odontogênicos , Bochecha/patologia , Feminino , Humanos , Imageamento por Ressonância Magnética , Músculo Masseter/diagnóstico por imagem , Músculo Masseter/patologia , Pessoa de Meia-Idade , Cistos Odontogênicos/diagnóstico por imagem , Cistos Odontogênicos/patologia , Cistos Odontogênicos/cirurgia , Tumores Odontogênicos/patologiaRESUMO
ABSTRACT: The latissimus dorsi free flap (LDFF), that provides long vascular pedicle with rich vascularization and adequate bulk for maxillofacial defect coverage, is utilized in microvascular surgery for maxilla-mandibular reconstruction with high success rate, less morbidity, and ability to provide facial symmetry. In addition, it can reduce the risk of adjuvant therapies, such as radiotherapy. Seroma formation at the donor site following LDFF harvest has been reported as a common postoperative sequela. On the other hand, chronic expanding hematoma (CEH) in an LDFF donor site is a rare postoperative complication. in this case report, the authors describe a rare occurrence of a solidified CEH on an LDFF donor site in a male patient 17âyears after mandible reconstruction surgery. For treatment, the patient underwent mass resection with drain placement and quilting suture, resulting in reduction of the hematoma and faster healing.
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Mamoplastia , Músculos Superficiais do Dorso , Hematoma/complicações , Hematoma/cirurgia , Humanos , Masculino , Mamoplastia/efeitos adversos , Mamoplastia/métodos , Estudos Retrospectivos , Seroma/etiologia , Músculos Superficiais do Dorso/transplante , Retalhos Cirúrgicos , Técnicas de Sutura/efeitos adversosRESUMO
BACKGROUND: Although immunohistochemistry (IHC) along with molecular tests has been investigated in ameloblastoma for BRAF V600E detection, VE1 IHC has not been studied in odontogenic carcinomas (OCs) and benign mixed epithelial and mesenchymal odontogenic tumours (BMOTs). Here, we performed BRAF V600E mutation analysis, examined the expression pattern of VE1 IHC, and comparatively evaluated the performance of two VE1 antibodies in ameloblastomas, OCs and BMOTs. METHODS: BRAF V600E detection was performed using Sanger sequencing in a total of 47 odontogenic tumours: 28 ameloblastomas, 6 OCs and 13 BMOTs. VE1 IHC was conducted using two different antibodies (IHC-A and IHC-V), and their performance was analysed by calculating the sensitivity and specificity compared with sequencing. RESULTS: BRAF V600E mutations were identified in 24/28 (85.7%) ameloblastomas, 2/5 (40.0%) ameloblastic carcinomas (ACs), 3/7 (42.9%) ameloblastic fibromas and 1/2 (50.0%) ameloblastic fibro-odontomas. In the presence of the mutation, VE1 showed diffuse cytoplasmic staining in ameloblastomas and ACs, whereas all BMOTs were negative for VE1. IHC-A and IHC-V yielded a sensitivity of 76.7% and 60.0%, respectively, although both antibodies showed 100% specificity. CONCLUSION: OCs and BMOTs have BRAF V600E mutations in common at lower frequencies than ameloblastoma. Diffuse VE1 cytoplasmic staining in AC suggests the utility of MAPK-targeted therapy as selectively applied in ameloblastoma, and consistent VE1 false-negative expression in BMOTs requires further investigation. Considering the high specificity but low sensitivity of VE1 IHC, molecular tests should be performed to determine the presence of BRAF V600E mutations in odontogenic tumours.
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Ameloblastoma , Biomarcadores Tumorais , Imuno-Histoquímica , Proteínas Proto-Oncogênicas B-raf , Ameloblastoma/genética , Anticorpos Monoclonais , Biomarcadores Tumorais/análise , Humanos , Mutação , Proteínas Proto-Oncogênicas B-raf/genética , Sensibilidade e EspecificidadeRESUMO
BACKGROUND: The aims of this study were to evaluate expression of Twist and Snail in tumor and stromal cells of epithelial odontogenic tumors and to analyze relationships between Twist and Snail expression and between tumor and stromal expression. METHODS: Immunohistochemistry was performed using Twist and Snail antibodies in 60 ameloblastomas (AMs; 20 solid/multicystic, 20 unicystic, and 20 recurrent), six ameloblastic carcinomas (ACs), 10 adenomatoid odontogenic tumors (AOTs), and six calcifying epithelial odontogenic tumors (CEOTs). RESULTS: A higher rate of tumor cells strongly positive for Twist was observed in AC compared to the other tumors (P = 0.019). The rate of tumor cells strongly positive for Snail tended to be higher in AC than in AM (P = 0.060). AM and AC showed a higher rate of Twist-positive stromal cells than AOT and CEOT (P < 0.001). Tumor cells of recurrent AM showed stronger expression of Twist (P < 0.001) and Snail (P = 0.001) compared to AM without recurrence. A moderate positive correlation was observed between tumor expression of Twist and Snail (r = 0.376, P = 0.001) and between tumor and stromal expression of Snail (r = 0.334, P = 0.002). CONCLUSIONS: Twist and Snail may affect the epithelial-mesenchymal transition in AC and be involved in recurrence of AM. Stromal Twist expression may be associated with aggressive clinical behavior of epithelial odontogenic tumors. A Twist-Snail pathway may participate in the development and progression of odontogenic tumors, and tumor-stroma interaction in odontogenic tumors may be mediated by Snail.
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Ameloblastoma/metabolismo , Transição Epitelial-Mesenquimal/fisiologia , Tumores Odontogênicos/metabolismo , Neoplasias Cutâneas/metabolismo , Fatores de Transcrição da Família Snail/metabolismo , Proteína 1 Relacionada a Twist/metabolismo , Humanos , Imuno-HistoquímicaRESUMO
Odontogenic ameloblast-associated protein (ODAM) contributes to cell adhesion. In human cancer, ODAM is down-regulated, and the overexpression of ODAM results in a favourable prognosis; however, the molecular mechanisms underlying ODAM-mediated inhibition of cancer invasion and metastasis remain unclear. Here, we identify a critical role for ODAM in inducing cancer cell adhesion. ODAM induced RhoA activity and the expression of downstream factors, including Rho-associated kinase (ROCK). ODAM-mediated RhoA signalling resulted in actin filament rearrangement by activating PTEN and inhibiting the phosphorylation of AKT. When ODAM is overexpressed in MCF7 breast cancer cells and AGS gastric cancer cells that activate RhoA at high levels, it decreases motility, increases adhesion and inhibits the metastasis of MCF7 cells. Conversely, depletion of ODAM in cancer cells inhibits Rho GTPase activation, resulting in increased cancer migration and invasion. These results suggest that ODAM expression in cells maintains their adhesion, resulting in the prevention of their metastasis via the regulation of RhoA signalling in breast cancer cells. SIGNIFICANCE Breast cancer represents the first most frequent cancer, and the ratio of mortality is high in women. Of utmost importance for reducing risk by breast cancer are their anti-invasion mechanisms, particularly in the non-invasive cancer cells because metastasis is the principal cause of death among cancer patients. ODAM induced RhoA activity. ODAM-mediated RhoA signalling resulted in actin filament rearrangement, increased cell adhesion and inhibited the migration/invasion of MCF7 cells. These results suggest that ODAM expression maintains their adhesion, resulting in the prevention of their metastasis via the regulation of RhoA signalling in breast cancer cells.
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Adenocarcinoma/patologia , Neoplasias da Mama/patologia , Proteínas de Transporte/metabolismo , Adesão Celular , Transdução de Sinais , Proteína rhoA de Ligação ao GTP/metabolismo , Adenocarcinoma/metabolismo , Amiloide , Animais , Neoplasias da Mama/metabolismo , Carcinogênese , Proteínas de Transporte/genética , Linhagem Celular Tumoral , Feminino , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Células MCF-7 , Camundongos , Camundongos Endogâmicos BALB C , Invasividade Neoplásica , Proteínas de Neoplasias , PTEN Fosfo-Hidrolase/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismoRESUMO
Sialadenoma papilliferum-like intraductal papillary tumour (SP-IPT) is a recently described salivary gland tumour that shows identical morphology to sialadenoma papilliferum (SP) except for the lack of an exophytic papillary component. However, the immunohistochemical phenotypes and molecular profiles of SP-IPT remain unclear. This study aims to report new cases of SP-IPT and to determine its cellular differentiation and molecular basis. After histopathological review, four cases of SP-IPT were retrieved. Immunohistochemical staining was performed to analyse the expression patterns of cytokeratin 7 (CK7), p63, smooth muscle actin (SMA), vimentin, S100, mammaglobin, androgen receptor, SOX10, BRAF V600E-mutated protein, and phosphorylated ERK. Sanger sequencing was performed to determine the mutation status of the BRAF, KRAS, NRAS, and HRAS genes. All four cases affected the posterior mandible with a mean age of 62 years and a male-to-female ratio of 3:1. Histologically, all cases consisted of multiple tubular and cystic structures with varying sizes and shapes. The tubulocystic components were lined by a double or few-layered epithelium frequently showing a micropapillary pattern. The outer layer consisted of a rim of myoepithelial cells, which were CK7+/p63+/SMA+/vimentin+/S100+/SOX10+. The inner ductal cells were CK7+/S100+/SOX10+, consistent with intercalated duct differentiation. All cases harboured BRAF V600E mutations, but no other mutations were detected. The BRAF V600E-mutated protein and phosphorylated ERK were expressed in both ductal and myoepithelial cells. These findings demonstrate the immunohistochemical and molecular similarities between SP-IPT and SP and the role and extent of MAPK pathway activation in the pathogenesis of SP-IPT.
Assuntos
Neoplasias Epiteliais e Glandulares , Neoplasias das Glândulas Salivares , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Vimentina , Proteínas Proto-Oncogênicas B-raf/genética , Neoplasias das Glândulas Salivares/genética , Neoplasias das Glândulas Salivares/patologia , Células Epiteliais/patologia , Diferenciação CelularRESUMO
Adenomatoid odontogenic tumor (AOT) is a rare, asymptomatic, slow-growing benign tumor that can be divided into three variants: follicular, extrafollicular, and peripheral. By treating AOT using an enucleation and curettage approach, recurrence can be avoided. We report a case of a 24-year-old female who presented with a lump in the right mandibular premolar area along with diastema between displaced teeth #43 and #44 and was diagnosed with extrafollicular AOT. The patient was managed with enucleation-curettage surgery without additional bone graft procedure along with routine follow-up. A successful outcome without recurrence was achieved, and diastema closure with repositioning of the displaced teeth did not require orthodontic treatment. AOT should be managed via enucleation and curettage to obtain successful outcomes without recurrence. Spontaneous bone regeneration following enucleation can be achieved without guided bone regeneration. Also, diastema closure and repositioning of displaced teeth can occur without orthodontic interventions through physiologic drift.
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BACKGROUND: Surgical ciliated cysts, also known as postoperative maxillary cysts or implantation cysts, occur mainly in the posterior maxilla after radical maxillary sinus surgery; they rarely develop in the mandible. They are thought to occur when the sinonasal epithelium is infiltrated by a surgical instrument during surgery or as a result of transplantation of bone or cartilage with respiratory epithelium attached. CASE PRESENTATION: We report a case in which a surgical ciliated cyst developed in the anterior part of the mandible, presumably as a result of bimaxillary orthognathic surgery and genioplasty performed 24 years earlier. We then review the few similar cases reported in the literature. CONCLUSION: Surgical ciliated cysts in the mandible are extremely rare, but they could occur after simultaneous surgery on the maxilla and mandible, even decades later. To prevent surgical ciliated cysts in the mandible, we recommend that the surgical instruments, especially the saw blade used during bimaxillary surgery, be new or cleaned and that previously placed plates and screws be removed at an appropriate time.
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Several cases of intraosseous mandibular tumors have been reported under the name "tubulopapillary hidradenoma-like tumor of the mandible (TPHLTM)." However, the intraosseous occurrence of sweat gland tumors needs to be reappraised. The aim of this review was to propose a new name for these tumors to reflect the possible tumor origin. In view of the incidence and the tissue of origin, TPHLTM is more likely to be a salivary gland tumor than a sweat gland tumor. Among salivary gland tumors, a recently described salivary neoplasm called "sialadenoma papilliferum-like intraductal papillary tumor (SP-IPT)" seems to be histologically and genetically identical to tubulopapillary hidradenoma. Therefore, we proposed that the term TPHLTM be replaced by "SP-IPT of the mandible," which better explains its origin and could help in clarifying the nature of SP-IPT.
Assuntos
Acrospiroma , Adenoma de Glândula Sudorípara , Neoplasias das Glândulas Salivares , Neoplasias das Glândulas Sudoríparas , Acrospiroma/patologia , Adenoma de Glândula Sudorípara/patologia , Humanos , Mandíbula/patologia , Neoplasias das Glândulas Salivares/patologia , Neoplasias das Glândulas Sudoríparas/patologiaRESUMO
The specific muscular structure of the tongue greatly affects margin shrinkage and tumor invasion, making the optimal surgical margin controversial. This study investigated surgical margin correlated prognosis of TSCC (tongue squamous cell carcinoma) according to margin location and its value, and the histopathologic factors which are suggestive of tumor invasion. And we would like to propose defining of the surgical margin for TSCC via prognosis according to location and margin values. We reviewed 45 patients diagnosed with TSCC who visited Seoul National University Dental Hospital (SNUDH) (Seoul, Republic of Korea) from 2010 to 2019, who were managed by a single surgical team. Patient clinical and pathological data of patients were retrospectively reviewed, and in 36 out of 45 patients, the pathologic parameters including the worst pattern of invasion (WPOI) and tumor budding were investigated via diagnostic histopathology slide reading. When standardized with as 0.25 cm anterior margins, as 0.35 cm deep margin, there was no significant difference in disease specific survival (DSS) or loco-regional recurrence-free survival (LRFS). Additionally, there was a non-significant difference in DSS and LRFS at the nearest margin of 0.35 cm (PDSS=0.276, PLRFS=0.162). Aggressive WPOI and high tumor budding showed lower survival and recurrence-free survival, and there were significant differences in close margin and involved margin frequencies. In TSCC, the value and location of the surgical margin did not have a significant relationship with prognosis, but WPOI and tumor budding suggesting the pattern of muscle invasion affected survival and recurrence-free survival. WPOI and tumor budding should be considered when setting an optimal surgical margin.
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OBJECTIVES: The objective of this study was to demonstrate the clinical, radiologic, and histologic features of orthokeratinized odontogenic cyst (OOC); determine the characteristics of multiple OOCs; and present rare but significant manifestations of OOC. STUDY DESIGN: A clinical, radiologic, and histopathologic study of 65 primary and 2 recurrent OOC cases was performed retrospectively along with a comprehensive literature review. RESULTS: OOCs shared similar radiologic findings with odontogenic keratocyst, yet some showed features that have not been previously described: root resorption and radiopaque foci. Histologic review revealed a unique histiocytic lining and some findings suggestive of the multipotentiality of the odontogenic epithelium. The analysis of patients with multiple OOCs demonstrated that multiple OOCs occurred synchronously with a marked predilection for young male adults. Two unusual cases were also identified: an OOC combined with a BRAFV600E ameloblastoma and a recurrent OOC with malignant transformation. CONCLUSIONS: This largest series presents previously unreported radiographic and histopathologic features that can be seen in OOC. Multiple OOCs have clinical characteristics distinct from those of solitary cases. The first reported OOC associated with ameloblastoma suggests the involvement of oncogenic mutations in odontogenic tumorigenesis. Although OOC shows a low recurrence rate, the possibility of malignant transformation of recurrent OOCs should be emphasized.
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Ameloblastoma , Cistos Odontogênicos , Tumores Odontogênicos , Adulto , Ameloblastoma/diagnóstico por imagem , Transformação Celular Neoplásica , Humanos , Masculino , Cistos Odontogênicos/diagnóstico por imagem , Cistos Odontogênicos/patologia , Tumores Odontogênicos/diagnóstico por imagem , Estudos RetrospectivosRESUMO
BACKGROUND: Multiple calcifying hyperplastic dental follicles (MCHDF) is a rare disorder that is characterized by multiple impacted teeth and enlarged dental follicles that include calcifications. The current lack of information characterizing MCHDF impedes clinicians from making prompt differential diagnoses. We describe five cases of MCHDF and analyze their clinical and histopathological features in an effort to compare MCHDF with hyperplastic dental follicles (HDF) of singly impacted teeth. METHODS: Our five cases of MCHDF were examined and clinically/histologically compared with data from 50 singly impacted teeth with HDFs. RESULTS: The five patients described in this study were all male. The pattern of impaction varied, but every second molar was impacted in all the patients. Alterations in the number of teeth, such as supernumerary or congenitally missing teeth were observed. Upon microscopic examination, most of the calcifications consisted of basophilic droplets that were fused to one another, and were surrounded by whirling spindle cells. Another type of calcification that was observed less frequently resembled woven bone. These features were consistent with three previously reported cases and observed in HDFs of 20 singly impacted teeth. While the average period of impaction and the time to reach some level of calcification in MCHDFs was shorter than in single calcifying HDFs, the calcification was more generalized in MCHDFs. CONCLUSIONS: This study indicates that MCHDF is a separate pathologic entity with exclusive male predilection and earlier calcifications, different to HDF. Further studies are needed to understand the etiology of MCHDFs to provide various options for treatment, and to clarify the mechanisms of eruption.
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Calcinose/diagnóstico , Saco Dentário/patologia , Dente Impactado/diagnóstico , Adolescente , Adulto , Anodontia/diagnóstico , Calcinose/patologia , Criança , Cisto Dentígero/diagnóstico , Diagnóstico Diferencial , Feminino , Humanos , Hiperplasia , Incisivo/anormalidades , Masculino , Pessoa de Meia-Idade , Dente Molar/patologia , Estudos Retrospectivos , Fatores Sexuais , Fatores de Tempo , Dente Impactado/patologia , Dente Supranumerário/diagnóstico , Adulto JovemRESUMO
SUMMARY: As one of the suprahyoid muscles, the digastric muscle is characterized by two separate bellies of different embryologic origins. The origin of the anterior belly is the digastric fossa, while the origin of the posterior belly is the mastoid notch. They share a common insertion: the intermediate tendon. When the digastric muscle contracts, the hyoid bone is raised. Opening of the jaw and swallowing of food boli are associated with digastric muscle activity. This review discusses the general anatomic features of the digastric muscle and its variation, primary functions, and clinical implications focused on surgical reconstruction and rejuvenation.
Como uno de los músculos suprahioideos, el músculo digástrico se caracteriza por dos vientres separados, de diferentes orígenes embriológicos. El origen del vientre anterior es la fosa digástrica, mientras que el origen del vientre posterior es la incisura mastoidea. Comparten una inserción común, El tendón intermedio. Cuando el músculo digástrico se contrae, el hueso hioides se eleva. La apertura de la mandíbula y la deglución del bolo alimenticio se asocian con la actividad del músculo digástrico. Esta revisión analiza las características anatómicas generales del músculo digástrico y su variación, funciones primarias e implicaciones clínicas centradas en la reconstrucción y el rejuvenecimiento quirúrgico.
Assuntos
Humanos , Músculos do Pescoço/anatomia & histologia , Músculos do Pescoço/fisiologiaRESUMO
OBJECTIVES: The staging significance of bone invasion is controversial in oral squamous cell carcinoma (OSCC) cases with tumors measuring 4cm or less according to the American Joint Committee on Cancer (AJCC). Our aim was to retrospectively examine a large group of patients with OSCC to determine the staging significance of bone invasion. MATERIALS AND METHODS: Three hundred and twenty-three patients with primary OSCC were classified based on tumor size. Bone invasion was categorized as absent, one side bone, and both buccal and lingual bones, and analyzed for association with disease progression. Regional lymph node metastasis (N), perineural invasion, vascular invasion, surgical margin involvement, and adjuvant treatment were also analyzed. RESULTS: In all OSCC cases, bone invasion (p=0.007) with stage N, perineural invasion, and surgical margin involvement were significant independent prognostic factors of disease progression. However, in OSCC cases with tumors measuring 4cm or less, bone invasion was not significantly associated with disease progression. Nevertheless, invasion of both buccal and lingual bones was significantly associated with disease progression (p=0.03). In multivariate analysis, both buccal and lingual bone invasion (p=0.04; hazard ratio=3.4; 95% confidence interval, 1.0-11.0), stage N2, and perineural invasion were also independent prognostic factors. CONCLUSION: Although OSCC bone invasion was an independent prognostic factor, bone invasion in small OSCC was not. However, small OSCC with both buccal and lingual bone invasion had a significantly worse prognosis. The AJCC T system is of limited prognostic value for small OSCC with bone invasion. But other elements should be examined before a modification can be accepted.