Oral Surgery Oral Medicine Oral Pathology Oral Radiology最新文献

Introduction

Squamous Cell Carcinoma (SCC) is the most common malignant tumor in the oral cavity and has been reported to be more common in older men. It has been associated with smoking, smokeless tobacco and alcohol. Recent studies have posited an increase in incidence of oral SCC in younger populations. The objective of this study is to examine incidence of oral SCC in different age groups, stratified by sex and site.

Materials and Methods

Demographic information was collected by searching the Oral Pathology Laboratory, Inc/ NYPQ database from 2003-2023. Data was collected for all SCCs and separated into 5 year age brackets (<45, <40, <35 and <30) and by decade (2003-2010, 2011-2020 and 2021-2023) This was further subcategorized by location and by gender.

Results

The incidence of SCC decreased in the <40 and <45 yo age brackets from 2003-2023 by 1.1% and 1.54%, respectively. The incidence of SCC increased in the <30 and <35 yo age brackets from 2003-2023 by 0.7% and 0.4%, respectively. While the incidence of SCC amongst females decreased from 2003-2023, the incidence of SCC on the tongue in females in the <40, <35 and <30 yo age brackets increased from 2003-2023 by 17.1%, 20% and 33.3%, respectively. For men, the incidence of SCC varied over the years and across age brackets, with the highest incidence occurring in 2011-2020. The incidence of tongue SCC in men increased as age decreased. From 2003 to 2023, its incidence increased in all age groups except the <30 age group where it decreased by 16.9%.

Conclusion

This study shows a slight increasing trend in SCC in all patients <35. There's a marked increase in females with SCC of the tongue. Further demographic information is needed to better understand the etiology of these trends.

Introduction

Oral squamous cell carcinoma (OSCC) shows a limited response to current systemic treatments, and this resistance could be associated with cancer stem cells (CSC). NFκB is an activated pathway in several malignancies, including head and neck cancer. Here we evaluated the role of NFκB inhibitor on the behavior of CSC derived from OSCC.

Material and methods

Emetine was used as an NFκB inhibitor. CSC presence was assessed by tumorspheres, and the emetine IC₅₀ was determined in this specific cell population. Also, the CSC was quantified by the enzymatic activity of aldehyde dehydrogenases (ALDH) using flow cytometry. Immunofluorescence staining for phosphorylated protein p65 was used to identify the NFκB levels of tumor cells. Finally, OSCC cells were sensitized with emetine for 24 hours followed by administration of cisplatin (IC₅₀).

Results

The IC₅₀ of emetine in CSC OSCC was 0.5μM. We then treated the OSCC cells with the emetine IC₅₀, which showed a significant reduction of the ALDH population, while the NFκB pathway was inhibited. Further, emetine sensitized OSCC cells to cisplatin, resulting in a reduction of the IC₅₀ from 3.9μM to 1.3μM for SCC9.

Conclusion

Our results suggested that CSCs play an important role in tumor resistance to chemotherapy and highlight the disruption of these cells by the NFκB inhibition as a promisor target therapy.

This study presents a series of six cases involving patients who underwent previous cancer treatments and utilized bisphosphonates, monoclonal antibodies, and high-dose corticosteroids, subsequently experiencing osteonecrosis in the oral cavity. The associated challenges included pain, recurrent infections, diminished quality of life—especially in terms of food intake—and social discomfort due to characteristic lesion odor. Medication-associated osteonecrosis (OAM) is identified as an injury leading to the temporary or permanent loss of blood supply to bones, with diverse causal factors. Patients underwent thorough anamnesis, substantiating medication use via medical prescriptions, clinical examinations by qualified Dental Surgeons, and imaging assessments including panoramic radiography, periapical radiographs during follow-up, and, in specific cases, computed tomography. The treatment involved weekly monitoring, adjusting consultation frequencies as the condition stabilized, and implementing Sonodynamic Therapy (SDT). SDT, an innovative approach, utilizes low-frequency, high-intensity ultrasound to stimulate sonosensitizers, inducing the formation of reactive oxygen species (ROS). A non-invasive treatment, SDT offers site-specific cytotoxicity by generating ROS in response to sonic/ultrasonic sources, potentially treating bacterial infections. All six patients treated with SDT experienced improved quality of life, as documented through visual evidence. The adaptability of SDT to equipment emitting sonic/ultrasonic waves envisions broader applications, particularly in resource-limited regions, rendering it a potentially accessible method for both professionals and patients. This research underscores the promising outcomes of SDT in managing medication-associated osteonecrosis, paving the way for further exploration and potential integration into broader clinical practices.

Introduction

Idiopathic gingival papillokeratosis with crypt formation (IGPCF) is an uncommon condition of unknown etiology, characterized by keratotic plaques in the upper labial attached gingiva of young patients. No treatment is required, although periodic follow-up is recommended as some lesions persist. Despite the limited number of published cases, the diagnosis of IGPCF is highly suggestive based on the distinctive clinical features, and biopsy is usually unnecessary. We aim to report seven additional patients with IGPCF from Brazil and the United States.

Material and Methods

Seven IGPCF cases were retrieved from the archives of the Oral Pathology Laboratories from the Federal University of Rio de Janeiro, Brazil, and Texas A&M University, USA, between 2017 and 2023.

Results

Six patients were male, and one patient was female, with an average age of 15.8 years (ranging from 12 to 21). All patients presented with asymptomatic bilateral papillary white plaques located exclusively in the attached anterior gingiva with a duration ranging from 4 to 12 months. Six cases presented in the maxillary labial gingiva, whereas a single case was located in the mandibular labial gingiva. Clinically, the lesions appeared as well-demarcated symmetric white plaques with an irregular surface, stopping abruptly at the mucogingival junction. Incisional biopsies were performed on six patients with exuberant lesions, while an exclusively clinical diagnosis was established in a single patient with discrete plaques. Microscopic analysis revealed gingival mucosa showing overlying parakeratosis with papillary architecture and multifocal epithelial crypt-like invaginations with parakeratin plugging. Mild pseudoepitheliomatous hyperplasia was noticed, with no signs of epithelial atypia.

Conclusion

Clinicians should be aware of IGPCF and differentiate it from other papillary keratotic oral lesions. Reporting additional cases may provide further characterization of this unusual entity and improve understanding as it relates to etiology and prognosis.

Introduction

Nodular hidradenomas are benign adnexal neoplasms presenting as solitary asymptomatic intradermal nodules, often on facial skin. Tumors are covered by normal skin, but superficial ulcers may occur. Hidradenomas often exhibit cuboidal cells with pink cytoplasm, but clear cell, squamoid, plasmacytoid, and mucinous variants have been described. Malignant counterpart of hidradenoma exists. There is morphologic and molecular overlap between cutaneous adnexal tumors and salivary gland tumors, for example, hidradenoma and mucoepidermoid carcinoma (MEC).

Case Findings

A 64-year-old male patient presented with a submental subcutaneous mass for six months. A fine needle aspiration (FNA) was performed, based on the clinical suspicion for a granulomatous process and to rule out malignancy. FNA cytology was interpreted as positive for malignant cells, suspicious for squamous cell carcinoma (SCC). Constituent cells were p40 positive and negative for p16, androgen receptor (AR), and CD163. AFB staining negative for acid fast bacilli. Excision of the lesion was performed.

Results

Microscopic examination reveals a fragmented epithelioid tumor with squamoid, clear cell, glandular, and papillary features favoring a benign adnexal skin tumor. The proliferative index was < 5%. Included in the differential diagnosis was MEC. Positive MAML2 gene rearrangement was identified on fluorescent in-situ hybridization (FISH). Upon consultation with dermatopathology, a diagnosis of benign nodular hidradenoma was rendered.

Conclusions

Clinical presentation, discussed with the surgeon, excluded association with salivary glands, emphasizing the subcutaneous location. Although there is morphologic and molecular overlap between nodular hidradenoma and MEC, clinical location supports the final diagnosis of a benign adnexal tumor, specifically benign nodular hidradenoma. In addition, MAML2 interrogation can help distinguish hidradenoma from other sweat gland neoplasms.

Introduction

Different markers, such as p53, CK13, CK17, and Ki67, have been used to assist in the histopathologic grading of oral epithelial dysplasia (OED). This study aims to evaluate the correlation between these markers and histopathologic grading.

Materials and Methods

This retrospective study included 65 OED cases: 15 with mild dysplasia, 31 with moderate dysplasia, and 19 with severe dysplasia. Patient age, gender, lesion location, histopathologic grading, and expression patterns of p53, CK13, CK17, and Ki67 immunohistochemical studies were reviewed and analyzed.

Results

In our cases, half of the mild dysplasia and all of the moderate and severe dysplasia cases showed a reverse CK13/CK17 staining pattern. An increased number of Ki67-positive cells, located upward, were frequently associated with moderate and severe dysplasia cases. However, mutated p53 staining patterns were correlated with severe dysplasia (16/19; 84.2%). All our mild dysplasia cases showed a wild-type p53 staining pattern, and fewer than one-third (7/31; 22.6%) of moderate dysplasia cases revealed a mutated p53 staining pattern. The staining patterns were not associated with patient age and gender. Lesions at the ventral and lateral border of the tongue and soft palate were mainly associated with a mutated p53 staining pattern (12/14; 85.7% and 3/3; 100%, respectively). Only 17.5% (7/40) of the lesions on the buccal mucosa were associated with mutated p53.

Conclusions

The alteration in the CK13/17 staining pattern can be used to detect differentiation changes in early OED. Mutation of p53 is most likely a later event and is associated with more advanced OED.

Introduction

The cellular spindled histiocytic pseudotumor is a rare, benign, and reactive mass-producing lesion that clinically and histopathologically mimics spindle cell neoplasms. There is only one previous report of twenty cases, all arising in the breast in association with fat necrosis. This is the first description of oral involvement.

Materials and Method

A 70-year-old male presented with a few month history of a painful swelling of the anterior maxilla. Teeth 8 and 9 were extracted approximately three years ago. A CBCT showed a mass partially covered by a thin rim of bone. Clinical suspicion for a neoplastic process was high and an incisional biopsy was submitted for histopathological evaluation.

Results

The lesion consisted of cohesive and compact fascicles of spindle cells with scattered lymphocytes. One focus of necrotic bone and degenerating fat was seen. Two pieces of likely graft foreign material were embedded among lesional cells towards one margin of the submitted tissue. Lesional cells were seen infiltrating surrounding skeletal muscle fibers. Mitotic figures were not obvious. Lesional cells expressed CD68 and CD163 strongly but were negative to AE1/AE3, S100, SMA, desmin, CD34 and CD21. A working diagnosis of reactive proliferation with features like a cellular spindled histiocytic pseudotumor was given. Thorough curettage and follow-up were recommended. Following a thorough curettage, healing was uneventful with no recorded recurrence.

Conclusions

The cellular spindled histiocytic pseudotumor is an exaggerated reactive response to degenerating fat and foreign material. The clinical and histopathological presentation is worrisome for benign and malignant spindle cell tumors. Incisional biopsies may not show degenerating fat or other foreign material. This is the first report of oral involvement. Awareness of this entity will prevent misadventures in its diagnosis and management.

Lesions of Myofibroblastic origin are very rare to occur in the tongue, sometimes they have an aggressive presentation that could be easily misdiagnosed as malignancy. There is not a clear etiology, however trauma and infection are suggested factors. Histologically, myofibroblastic and inflammatory cells are present.

Here we present a case report of a 46-year-old Caucasian female that presented with approximately three year-history of laceration of dorsum tongue that was recently further traumatized by biting it. The clinical exam revealed a traumatic raised nodular lesion on the right side towards the mid-line of dorsum tongue.

The histological findings revealed a poorly demarcated mass of atypical proliferating spindle cells, infiltrating into the muscle fibers and extending to the base of the specimen. Desmin and Myogenin, were focally positive in regenerating/degenerating muscle cells. MSA was diffusely positive in the spindle cells. Within the submucosa there was a proliferation of actin positive myofibroblasts with associated inflamed granulation tissue containing scattered acute and chronic inflammatory cells. CK (AE1/AE3), CD31, S-100, and HMB45 were negative for the spindle cells. CD31 highlighted the small blood vessels in the granulation tissue. Perivascular necrosis was noted. Ki-67 showed high proliferative index (>25%). Factor XIIIa highlighted fibroblasts and MyoD1 showed scattered positivity.

The final diagnosis was in favor of a benign reactive myofibroblastic proliferation.

Myofibroblastic proliferation lesion is a challenging diagnosis because of the clinical appearance and the histological features mimicking malignancy. For this reason, it is imperative to have an accurate diagnosis to prevent unnecessary radical treatment.

Introduction

WHO grading of oral epithelial dysplasia (OED) is employed by pathologists to aid in prognostication and treatment planning. However, considerable inter-observer variability exists. Recently, p53 abnormal OED has been proposed as a unique entity with an increased risk of malignant transformation. Subsequently, a pattern-based approach to p53/p16 immunohistochemistry (IHC) interpretation has been developed to classify OED into Human Papillomavirus (HPV)-associated, p53 wild-type (conventional), and p53 abnormal OED. In this study, the grading (three-tiered and two-tiered) and classification of OED were compared using hematoxylin and eosin-stained sections (H&E) with and without p53/p16 IHC.

Materials and Methods

Formalin-fixed, paraffin-embedded oral biopsy specimens with targeted Next-Generation Sequencing results and/or high-risk HPV in situ hybridization results were collected from 51 patients. Inter-observer variability among 18 pathologists was determined using Fleiss’ kappa (κ).

Results

93% of HPV-associated OED and 77% of p53 abnormal OED were successfully identified using p53/p16 IHC. In contrast, 55% of HPV-associated OED and 37% of p53 abnormal OED were identified using H&E. 19% of p53 abnormal OED were initially interpreted as “reactive, no dysplasia” using H&E; this decreased to 10% following reviewing of p53/p16 IHC. There is excellent agreement beyond chance and fair to good agreement beyond chance for the classification of OED using p53/p16 IHC (overall, κ = 0.61, HPV-associated OED, κ = 0.92; p53 abnormal OED, κ = 0.56). Both the three-tiered and two-tiered dysplasia grading systems demonstrate poor agreement beyond chance in H&E (κ = 0.35 and 0.39; p < 0.0001) and p53/p16 IHC (κ = 0.33 and 0.37; p < 0.0001).

Conclusions

A panel of p53/p16 IHC can improve both diagnostic accuracy and inter-observer agreement in the diagnosis of OED. p53 abnormal OED cannot be reliably identified on H&E alone, and the histologic spectrum of HPV-associated dysplasia is broader than currently appreciated.

Introduction

Acute Myeloid Leukemia (AML), a malignant neoplasm characterized by the rapid proliferation of abnormal cells in the bone marrow, often manifests oral signs such as gingival bleeding and purple-colored gum hyperplasia. This clinical case underscores the pivotal role of dentists in diagnosing AML, shedding light on the nuanced presentation of hematological diseases in the oral cavity.

Case Report

A 57-year-old Caucasian female with a history of fibromyalgia and current use of Fluoxetine and Amitriptyline presented with a chief complaint of gum pain and bleeding persisting for 60 days. Clinical examination revealed distinctive purple hemorrhagic gingival hyperplasia, prompting a comprehensive evaluation. Initial investigations, including a full blood count, clotting profile, and HIV serology (suspected Kaposi's sarcoma), returned within normal parameters. Recognizing the potential severity of the oral manifestation, the patient was promptly referred for oncology-hematology assessment. Given the suspicion of an underlying hematologic condition, an incisional biopsy was performed, revealing a diagnosis of Acute Myeloid Leukemia. This diagnosis, unexpected in the absence of abnormal laboratory findings, underscores the imperative role of dental professionals in early detection and referral.

Conclusion

This case serves as a compelling example highlighting the significance of dental professionals in identifying potentially life-threatening oral lesions, even when routine laboratory tests appear normal. The timely and astute recognition of aberrant oral presentations can expedite referral to specialized medical care, significantly influencing patient outcomes. In essence, the presented case reinforces the critical collaboration between dentists and oncology-hematology specialists, emphasizing the need for a comprehensive understanding of oral manifestations of systemic diseases. This interdisciplinary approach contributes not only to the prompt diagnosis of potentially severe conditions like AML but also to the overall well-being of the patient.