Oral Surgery Oral Medicine Oral Pathology Oral Radiology最新文献

Introduction

Ischemic fasciitis is a pseudosarcomatous proliferation of the subcutaneous tissue resulting in variably painful, non-ulcerated tumor-like masses. Most cases are seen overlying bony prominences of the pelvic and pectoral girdle in elderly patients who suffer from immobility due to debilitating conditions. Histopathologically similar lesions have not been reported in the oral cavity. This is the first report of two cases of ischemic fasciitis-like lesions affecting the dorsum of the tongue.

Materials and Method

Two elderly patients presented with a tumor-like mass of the dorsum of the tongue. One patient was otherwise healthy and the other had deep vein thrombosis and was on warfarin anticoagulant therapy. The submitted clinical diagnoses were squamous cell carcinoma and vascular malignancy in the first and second cases, respectively. The lesions were biopsied, and the processed and stained tissue were microscopically examined. Immunohistochemistry (IHC) stains including SMA, AE1/AE3 pankeratin, S100, p63, CD34, desmin and CD31 were used in only the first case.

Results

Surface epithelium was continuous with no dysplasia. The connective tissue deep to the epithelium, including the extrinsic skeletal muscle fibers of the tongue were replaced by a large central hypocellular zone of fibrinoid degeneration. This zone of fibrinoid degeneration was surrounded by a vascular granulation-type tissue containing atypical, plump myofibroblasts with dark smudged nuclei. Ganglion-like myofibroblasts were also seen. While SMA reactivity was focal, other IHC markers were negative.

Conclusion

A diagnosis of ischemic fasciitis-like degenerative, pseudosarcomatous process was given in both cases. Characteristic histopathological features were used to arrive at that working diagnosis. Excision is the preferred treatment, but incomplete removal may also result in healing. The prognosis is excellent.

Introduction

The legalization and increasing social acceptance of marijuana heightens the need for a better understanding of its potential role in the development of head and neck cancer (HNC). This study reviews the impact of marijuana use on HNC and explores the demographic and clinical characteristics and treatment outcomes of HNC in marijuana users.

Materials & Methods

An online search was conducted through the PubMed, MedLine, Cochrane Library, Web of Science, and Google Scholar databases. Exclusion criteria included abstracts, editorials, review articles, studies with insufficient information on marijuana use, and those in a non-English language. Inclusion criteria included original studies published up to 2023, marijuana use in any form, and studies focussing on oral, oropharyngeal, laryngeal, and nasopharyngeal cancers.

Results

Six case studies and fifteen case-control studies met our inclusion criteria. The case studies suggested a strong association of marijuana use with oral and oropharyngeal cancers. The patients’ ages ranged from 19 to 52 years. Thirteen were male, and six were female. About 47.3% of marijuana users had no history of tobacco use. Most were treated with radical neck dissection with radiation and chemotherapy. Four died of the disease, two were alive with the disease, and thirteen were disease-free at the time of follow-up. Six case-control studies reported a direct association of marijuana with HNC. Five studies reported marijuana as a strong risk factor for p16-positive oropharyngeal cancers and for nasopharyngeal cancer.

Conclusion

The increasing prevalence of marijuana use raises concerns about its potential role in HNC. There is limited data regarding the causal relationship between marijuana use and the development of HNC. As more states continue to allow marijuana for both medicinal and recreational usage, well-designed studies are warranted to understand the pathogenesis and potential sequelae of using this substance.

Neuroendocrine carcinomas (NEC) are extremely uncommon, representing 0.3% of head and neck cancers. Primary NEC arising in the oral and maxillofacial region are exceptionally rare, with <30 cases reported. Herein, we study the demographic, clinical, and pathologic features of these rare tumors, emphasizing the importance of accurate diagnosis at these sites.

Materials and Methods

A retrospective review was conducted on 12 cases of primary oral and maxillofacial NEC cases, excluding metastatic tumors and oropharynx, sinonasal, salivary, and middle ear origin cases.

Results

The cohort comprised 10 small-cell NEC (SCNEC), one large-cell NEC (LCNEC), and one mixed neuroendocrine non-neuroendocrine neoplasm (MiNEN). With a median age of 57 years and a male-to-female ratio of 5:1, the tumors were distributed in the oral tongue (n=4), maxillary sinus (n=2), upper alveolus (2), hard palate (2), mandible (1), and buccal mucosa (1). Most (63.6%) patients were diagnosed at an advanced stage including one presenting with bone metastasis. The average tumor size was 3.5 cm. Microscopy of SCNEC cases displayed solid sheets of round cells with hyperchromatic nuclei, and scant cytoplasm while LCNEC revealed large cells with vesicular nuclei and conspicuous nucleoli. One rare MiNEN case comprised mixed small cell carcinoma and salivary duct carcinoma arising in a background of pleomorphic adenoma. Overall, the mitotic rate was 15–65/2mm2. All cases were positive for synaptophysin, chromogranin, and INSM1; seven were diffuse p16 positive. Ki67 ranged from 65-90%. Lymph node metastatic rate was 63.6%. With a median follow-up of 23 months, two patients developed recurrence, and three developed distant metastases.

Conclusions

Oral and maxillofacial NEC is an extremely rare and aggressive malignancy that mimics diverse neoplasms common in the head and neck region. Herein, we expand the morphologic spectrum of these rare tumors and underscore the importance of their accurate diagnosis for optimal patient management.

Background

Langerhans cell histiocytosis (LCH) is a spectrum of rare histiocytic neoplasms characterized by clonal proliferation of Langerhans cell histiocytes along with eosinophils, lymphocytes, plasma cells, and multinucleated giant cells. Approximately 40-60% of all cases of LCH harbor mutations of BRAF and MAP2K1 genes with the timing of these mutations likely impacting the extent of the disease dissemination. Eosinophilic granuloma (EG) represents the mildest form of this spectrum presenting with solitary or multifocal bone lesions while sparing the visceral organs. Accounting for less than 1% of all osseous neoplasms, EG shows a predilection for the axial skeleton with 75% of the cases involving the mandible. While EG can arise across a broad age range, more than half of the cases are found in patients younger than the age of 15 years.

Case Summary

A 51 year-old female patient with a prior history of breast cancer presented to oral and maxillofacial surgeon with a complaint of left-sided mandibular paresthesia. While not appreciable in plain panoramic radiograph, computed tomography (CT) scan revealed an isolated, ill-defined and small radiolucent lesion in the left mandibular ramus. Surgical curettage and biopsy of the lesion revealed a dense mixed inflammatory infiltrate characterized by numerous eosinophils admixed with lymphocytes, plasma cells, scattered giant cells, and occasional histiocytic cells with reniform nuclei reminiscent of eosinophilic granuloma. Immunohistochemical studies confirmed immunoreactivity of these histiocytic cells with CD-1a, CD-207, and S-100 antibodies. Positron emission tomography (PET) scan and comprehensive physical exam ruled out involvement of the other organ systems. Subsequent post-operative follow-up revealed gradual reduction in the radiographic size and improvement in paresthesia.

Conclusion

This rare case suggests that the true spectrum of variations in LCH has yet to be fully appreciated and highlights the importance of utilization of three-dimensional imaging in diagnostic workup of gnathic pathologic lesions.

Introduction

Evaluation of p53 immunohistochemistry (IHC) in oral epithelial dysplasia (OED) has demonstrated a characteristic staining pattern in cases associated with high-risk human papillomavirus (HPV), identical to the pattern of expression reported in HPV associated dysplasia of the vulva. The accuracy of p53, in combination with p16, as a surrogate marker for HR HPV infection in OED, has not been extensively studied.

Materials & Methods

Expression of p53 was evaluated in 105 cases of HR HPV positive oral cavity OED, in which 104 cases were p16 positive and 1 case was p16 negative. HPV status was confirmed by RT-qPCR for E6 mRNA or RNA in situ hybridization (ISH). 7 cases of p16 positive oral cavity OED with abnormal p53 expression and/or TP53 mutation had negative HPV RNA ISH and were excluded.

Results

Our cohort included 96 males and 9 females, with a median age of 57 years (range 32-89). 93% of cases demonstrated classic HPV-associated basaloid morphology, and 7% of cases were keratinizing. The floor of mouth/ventral tongue were the most affected sites (61%), followed by the lateral tongue (18%) and gingiva (13%). 76% of cases demonstrated null-like/basal sparing pattern with p53 staining and 24% demonstrated a mid-epithelial/basal sparing pattern. 11 cases had an associated squamous cell carcinoma at the time of initial biopsy. A single case progressed to squamous cell carcinoma in an immunosuppressed patient, and 16 cases recurred. Of the cases with recurrence, 38% recurred more than once.

Conclusions

This study unequivocally demonstrates that p53 IHC, in combination with p16, can accurately identify HPV OED. Further, p53 can correctly identify p16 positive HR HPV negative p53 mutant OED with basaloid morphology. HPV OED can present with invasive SCC, but malignant progression in HPV OED is extremely rare.

Introduction

The ameloblastic fibromas is a rare mixed odontogenic tumor composed of epithelial and mesenchymal tissue. The lesion was first described by Krause in 1891. Ameloblastic fibroma usually occur in the first two decades of life with a slight female predilection and is frequently found in the posterior region of the mandible and is often associated with an unerupted tooth.

Materials and Methods

A 8 year old male with past medical history of asthma presented to the pediatric dental clinic. On routine examination a large unilocular radiolucency under tooth #T was noted. Patient was referred to the oral surgery clinic for evaluation where a panoramic radiograph was taken and tooth #29 was noted to be inferior displaced. Further imaging with CBCT showed a well circumscribed mandibular right lesion associated with impacted tooth #29, tooth #29 was displaced inferiorly and the lesion extended horizontally from primary tooth #S to mesial of root of tooth #30, there appeared to be resorption of roots of tooth #T, no obvious cortical perforation was noted. Clinical differential diagnosis included: dentigerous cyst, OKC, ameloblastoma, aneurysmal bone cyst, giant cell lesion.

After negative fine needle aspiration an incisional biopsy was conducted under IV sedation. The incisional biopsy of the cystic tissue lining was sent to pathology for interpretation.

Results

Based on histological analysis the entity was diagnosed as ameloblastic fibroma. Treatment for the lesion was extraction of teeth #29,30, excisional biopsy and enucleation and curettage. Final pathology result after excisional biopsy confirmed diagnosis of ameloblastic fibroma.

Conclusion

Ameloblastic fibroma is an uncommon mixed odontogenic tumor. Practitioner should be aware that ameloblastic fibromas do have the potential for recurrence and malignant transformation. Of concern is transformation to ameloblastic fibrosarcoma which have occurred in sites of previously diagnosed ameloblastic fibromas. Prolonged periods of follow-up are essential.

Introduction

Secreted Semaphorin-3F (SEMA3F) protein induces repulsion in Neuropilin-2 (NRP2)-expressing cells and guides nervous and circulatory system patterning during embryogenesis. <em>SEMA3F</em> is frequently deleted in human small cell lung cancer and is a potential tumor suppressor gene. SEMA3F is constitutively expressed in epithelial cells in the skin and oral cavity. Recent data from our group has identified NRP2 in CD4+ T cells.

Aims

Our goal is to investigate the role of endogenous in oral carcinogenesis, tumor progression, and tumor immunity.

Methods

NRP2 expression was evaluated in progressive stages of oral carcinogenesis. Cancer initiation and progression was analyzed histologically in novel transgenic mice with Sema3Fdeletion in adult keratinocytes before or after exposure to carcinogen compared to controls. Syngeneic oral cancer xenografts were implanted in Nrp2-knockout (KO) or wildtype mice. T cell trafficking in Sema3FKO, K14-Sema3FiKO, Nrp2-KO, and CD4-Nrp2-KO mice were compared to controls during antigen-induced hypersensitivity reactions..

Results

was not expressed in normal oral and skin epithelium but upregulated in late dysplasia during carcinogenesis in humans and mice. The majority of control (Sema3F-intact) mice (25/30) developed carcinoma in situ (CIS) or invasive oral squamous cell carcinoma (OSCC) while only 21.7% of K14-Sema3F-KO mice (5/23) developed CIS and none progressed to OSCC. Oral cancer xenografts showed increased CD4+ lymphocyte infiltration in Nrp2 compared to Nrp2 mice. Mice lacking epithelial Sema3F or Nrp2+ T cells showed enhanced and prolonged inflammation, tissue swelling, and T cell infiltration while control mice resolved quickly.

Conclusion

Sema3F is not a tumor suppressor in OSCC because the epithelium lacks Nrp2 expression and deletion of Sema3Freduced carcinogenesis. Cancerous and inflamed tissues lacking Sema3F or Nrp2 increased immune surveillance and lymphocyte recruitment abrogating cancer initiation and preventing oral cancer progression. The SEMA3F/NRP2 pathway suppresses host immunity and provides new targets for immunotherapy in oral cancer.

Introduction

the persistent issue in the diagnostic separation between OLP and OED is the considerable clinical and histologic overlap between the two entities. The differentiation is currently based on relatively subjective evaluation of the histological findings by the examining pathologist taking into account the clinical presentation. Although direct immunofluorescence studies can help diagnose OLP, DIF has to be correlated with the appropriate clinical presentation and permanent sections, as basement membrane fibrinogen deposition is not pathognomonic of OLP and has been described in OED specimens and other mimickers. Thus, discrimination of OED associated with chronic interface mucositis from OLP with reactive cellular atypia can be challenging, requiring subjective assessment of ostensibly objective morphologic features.

Materials and Methods

We performed bulk RNA sequencing on all the samples to evaluate genetic markers previously described in tumor-infiltrating immune cells and compare between groups. Gene ontology and enrichment analysis were performed to explore the function and product of differential gene expressions in both study groups. The p-value of <0.05 and fold change >1.3 was set for this purpose, utilizing the Gene Ontology knowledgebase by the Gene Ontology Consortium (release date 2023-01-05).

Results

Functional analysis revealed enrichment of immune signatures associated with immunosurveillance, lymphocyte infiltration, cytotoxic response, and surrogate markers of tumor-associated macrophages in high-grade OED. In OLP, our data revealed differential gene expression mainly related to cell regulation process, lymphocyte infiltration, and pathways related to T-cell regulation.

Conclusions

Immune reactivity is prominent in both epithelial and connective tissue components of OED and OLP. Nonetheless, our data suggests that the phenotype and genetic markers in the immune component are different. Further studies, including more cases and single-cell RNA sequencing, are necessary to substantiate these findings.

Introduction

Soft tissue myoepithelial carcinoma (MECA) represents an uncommon malignancy showing overlapping histomorphologic, immunophenotypic and genetic features with its salivary and cutaneous counterparts. Most MECAs harbor rearrangements. Genetic aberrations of TERT have only rarely been documented in soft tissue neoplasms, including myxoid and spindle cell liposarcoma and chordoma, but not MECA.

Material and methods

A 67-year-old male with a history of pancreatic neuroendocrine tumor metastatic to the liver and skeletal bones, presented with a large, bone-destructive, skull-base tumor of the left pterygopalatine fossa with extension into the orbit, optic canal, cavernous sinus and sinonasal cavity presumed to represent new metastases. An endoscopic biopsy was performed.

Results

Histopathologic examination disclosed an infiltrative malignant neoplasm composed of spindle cells arranged in short intersecting fascicles and immersed in a dense fibrocollagenous stroma. Lesional cells featured plump, ovoid or elongated, open-face nuclei with coarse chromatin, rich eosinophilic cytoplasm, and indistinct cell membrane borders. Nuclear pleomorphism and cytologic atypia were minimal, and mitoses were infrequent. By immunohistochemistry, the neoplastic cells were strongly and diffusely positive for CAM5.2 and SMA with focal reactivity for CK7, EMA, AE1/AE3, ERG and SATB2. Lesional cells were negative for p40, INSM1, S100, SOX10, GFAP, Desmin and STAT6. Ki-67 was approximately 30-45% by manual quantitation. SMARCB1 was retained. The overall histopathologic and immunophenotypic features were considered diagnostic of MECA. Genomic profiling of the tumor identified an intrachromosomal fusion and an inactivating mutation. The patient was treated with definitive chemoradiation and remains asymptomatic with significant tumor volume reduction 6 months post-treatment.

Conclusions

Herein, we report a unique case of a clinically aggressive skull-based MECA with novel gene fusion and expand the molecular landscape of non-rearranged MECA. The biologic significance of the above gene fusion remains, hitherto, unknown.