Background Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with limited prognostic biomarkers, in which metabolic reprogramming contributes to tumor progression. Amino acid transporters of the solute carrier family have emerged as key regulators of cancer biology; however, the role of solute carrier family 7 member 3 (SLC7A3), a cationic amino acid transporter involved in arginine uptake, remains poorly characterized in OSCC.Methods SLC7A3 expression was evaluated using RNA expression data from the Cancer Genome Atlas OSCC cohort (TCGA-OSCC), and protein levels were assessed by immunohistochemistry in a tissue microarray comprising 67 OSCC samples matched with normal oral tissue and 18 metastatic lymph nodes. Associations with clinicopathological features and survival were analyzed using chi-squared tests, Kaplan-Meier curves, and Cox regression. Functional assays, including cell cycle, apoptosis, migration, and invasion analyses, were performed in HSC3 cells following SLC7A3 knockdown.Results In TCGA-OSCC, SLC7A3 mRNA levels were significantly lower in tumors than in nontumor tissues (p = 0.017), with no association with disease-specific or disease-free survival. At the protein level, SLC7A3 was significantly upregulated in tumors (p = 0.007), and high expression was associated with early clinical stage (p = 0.007) and improved disease-specific survival, remaining significant in multivariate Cox analysis (HR: 0.18, 95% CI: 0.07-0.50, p = 0.001). Functionally, SLC7A3 knockdown did not alter cell cycle distribution or apoptosis but significantly increased OSCC cell migration and invasion.Conclusion High SLC7A3 protein levels were associated with OSCC cell migration and invasion and improved disease-specific survival, suggesting its potential as an indicator of tumor aggressiveness and a promising prognostic potential.
Background The expanding use of glucagon-like peptide-1 receptor agonists and the dual incretin agonist tirzepatide for Type 2 diabetes mellitus and obesity has drawn attention to potential oral and salivary adverse effects. This short communication summarizes the available evidence, discusses potential mechanisms, and highlights implications for oral medicine practice.Methods A narrative synthesis of published case reports, pharmacovigilance findings, and indirect experimental evidence was undertaken to discuss reported manifestations, biological plausibility, and existing knowledge gaps.Results Reported manifestations include xerostomia, hyposalivation, dysgeusia, oral mucosal discomfort, burning sensations, and throat-related symptoms. Proposed mechanisms include modulation of cyclic adenosine monophosphate-dependent signaling in salivary acinar cells, altered autonomic regulation of salivary secretion, and dehydration secondary to gastrointestinal adverse events. Reduced salivary protection combined with gastric acid exposure from reflux or vomiting may increase susceptibility to dental erosion, although a direct association with these therapies has not been established. Sporadic immune-mediated mucocutaneous reactions and facial soft-tissue changes associated with rapid weight loss have also been described. Evidence remains limited and largely indirect.Conclusion Potential oral and salivary adverse effects warrant clinical awareness, careful medication history-taking, assessment of salivary function, and individualized preventive care. Systematic reporting and focused clinical and experimental studies are needed to clarify causality, frequency, and underlying mechanisms.
ABSTRACT Background Oral squamous cell carcinoma (OSCC) remains a clinically challenging malignancy characterized by marked biological heterogeneity, high recurrence rates, and limited progress in survival outcomes. MicroRNAs (miRNAs) have emerged as key post‐transcriptional regulators involved in carcinogenesis and cancer progression, yet their expression patterns within phenotypically distinct tumor cell subpopulations, particularly CD44 + cancer stem cells‐like (CSC‐like), remain insufficiently characterized. Objective This study investigated the expression of five candidate miRNAs (hsa‐miR‐26a‐5p, hsa‐miR‐31‐5p, hsa‐miR‐133a‐5p, hsa‐miR‐491‐3p, and hsa‐miR‐532‐3p) in OSCC on multiple levels: public dataset analysis, whole‐tissue expression profiling, and evaluation within sorted CD44 + and CD44 − primary cell populations. Results TCGA‐HNSC dataset analysis revealed upregulation of hsa‐miR‐31‐5p and hsa‐miR‐532‐3p ( p < 0.0001), alongside downregulation of hsa‐miR‐26a‐5p and hsa‐miR‐133a‐5p in tumor tissue ( p < 0.0001, p = 0.0015, respectively), whereas hsa‐miR‐491‐3p showed no significant difference ( p = 0.925). In our OSCC cohort ( n = 20 OSCC, n = 10 controls), hsa‐miR‐31‐5p was significantly upregulated ( p = 0.0086), while hsa‐miR‐26a‐5p, hsa‐miR‐133a‐5p, and hsa‐miR‐491‐3p were markedly downregulated in tumor samples compared with normal mucosa ( p = 0.0363, p = 0.0029, p < 0.0001, respectively). Although hsa‐miR‐532‐3p exhibited an upward trend, this change did not reach statistical significance. CD44 expression was significantly higher in OSCC tissues, particularly in advanced TNM stages ( p = 0.0319), confirming its association with tumor aggressiveness. To explore miRNA dysregulation within CD44‐defined subpopulations, CD44 + and CD44 − cells were isolated from primary OSCC cultures ( n = 5 primary cultures). hsa‐miR‐133a‐5p, hsa‐miR‐491‐3p, and hsa‐miR‐532‐3p were significantly less expressed in CD44 + cells than in CD44 − cells ( p = 0.0142, p = 0.0015 and p = 0.0002), indicating that their downregulation characterizes the CD44 + ‐enriched fraction. These findings suggest that the tumor‐suppressive miRNAs hsa‐miR‐133a‐5p, hsa‐miR‐491‐3p, and hsa‐miR‐532‐3p are selectively dysregulated within CSC‐like cells, potentially contributing to stemness‐associated signaling and therapy resistance. Conclusion Overall, this study integrates bioinformatic, tissue‐level, and cell‐specific analyses to identify miRNAs implicated in CSC‐like biology in OSCC, highlighting their potential as biomarkers and targets for therapeutic strategies aimed at eradicating chemotherapy‐resistant CSC‐like populations.
ABSTRACT Purpose Familial florid cemento‐osseous dysplasia (FFCOD) is a rare fibro‐osseous jaw disorder characterized by multifocal lesions and familial aggregation. This systematic review aimed to synthesize the evidence on the demographic, clinical, radiographic, histopathological, genetic, therapeutic, and follow‐up characteristics of FFCOD. Methods A systematic review was conducted in accordance with PRISMA 2020 guidelines and registered in PROSPERO (CRD420261295922). Searches were performed in PubMed, Embase, Scopus, Web of Science, Cochrane Library, SciELO, LIVIVO, ProQuest, OpenGrey, IBICT/BDTD, Google Scholar, and reference lists through April 2025. Studies following the current World Health Organization (WHO) diagnostic criteria were eligible. Two independent reviewers performed study selection, data extraction, and risk‐of‐bias assessment using the Joanna Briggs Institute critical appraisal tool for case reports. Results Eight studies comprising 25 affected individuals were included. Females accounted for 60.0% of cases, and the mean age was 34.8 ± 19.9 years. Multifocal involvement of both jaws (48.0%) and all four quadrants (32.0%) was common. All included cases exhibited a mixed radiolucent‐radiopaque appearance (100.0%), while bone expansion was the most frequent clinical manifestation (33.3%). Histopathological examination consistently demonstrated fibrocellular stroma associated with cemento‐ and/or bone‐like mineralized material. Molecular analysis was reported in one study and identified an ANO5 missense variant. Osteomyelitis, osteonecrosis, and bone exposure/sequestration were the most frequently reported complications. Conclusion FFCOD demonstrates consistent clinicopathological characteristics, including multifocal jaw involvement, bone expansion, and a mixed radiolucent‐radiopaque appearance. Although many individuals remain asymptomatic, infectious and necrotic complications may occur, emphasizing the importance of early recognition, careful treatment planning, and long‐term clinical and radiographic follow‐up.
Objective This cross-sectional study aimed to comprehensively evaluate clinical forms, anatomical location, symptoms, systemic comorbidities, and potentially relevant factors in patients with oral lichen planus (OLP).Methods Seventy-two patients with histopathologically confirmed OLP were included. Awareness of the disease, clinical forms, lesion location, and symptoms and their relationships were investigated. Smoking and alcohol consumption, and the presence of adjacent prosthetic or restorative materials were evaluated as potentially relevant factors. The prevalence of systemic diseases was assessed.Results The reticular form was the most frequent clinical presentation, followed by plaque-like and erosive forms. Lesions were most commonly localized on the buccal mucosa, followed by the tongue and the gingiva. The reticular form was most frequently observed on the buccal mucosa and tongue (p = 0.001). The combination of the reticular and erosive forms was most frequently observed on the buccal mucosa (p = 0.001), whereas the combination of the reticular and plaque-like forms was more commonly observed on the buccal mucosa and tongue. The erosive form was associated with more prominent symptoms (p = 0.003, p = 0.001). The most frequent systemic comorbidities were hypertension, diabetes, and hypothyroidism. No significant differences were observed in systemic diseases, symptoms, or relevant factors between sexes.Conclusions Clinical forms of OLP may coexist within the same patient and, in some cases, within the same lesion. The most common combination was the coexistence of the reticular form with plaque-like or erosive forms. The erosive form is symptomatic. Systemic comorbidities were also commonly observed among patients with OLP, warranting attention during clinical evaluation.
