Background/Objectives: Salivary adenoid cystic carcinoma (ACC) is a rare but aggressive neoplasm that predominantly arises from the salivary glands, accounting for a significant proportion of salivary gland cancers. The aim of this literature review is to illustrate the current insights on ACC with regards to related genes and molecular pathways by analyzing original research articles from the period 2015–2025. Methods: An electronic search of literature was performed between January and February 2025 to identify all articles investigating the current insights on salivary gland adenoid cystic carcinoma and its related genes and molecular pathways. The search was conducted using MEDLINE (National Library of Medicine)-PubMed with restrictions concerning the date of publication. In particular, we focused on the period 2015–2025 using the following keywords: Salivary gland adenoid cystic carcinoma AND genes AND molecular pathways. This was followed by a manual search, and references were used to identify relevant articles. Results: In total, 41 articles were identified through the keywords. After the implementation of the time frame 2015–2025, 31 articles remained. Subsequently, by reading the titles and abstracts and thereby excluding non-original research articles and articles written in a language other than English, 23 articles remained. Conclusions: These studies identified 23 relevant genes or pathways whose analysis yielded the most recent data regarding their function. The classification of ACC is multifaceted, encompassing distinct histological subtypes that are crucial for determining prognosis and treatment approaches. Current oncological practices classify ACC based on these histological features alongside emerging genetic and molecular markers that promise to enhance our understanding of the disease’s biology. Diagnostic strategies have evolved, leveraging techniques such as biopsy and molecular diagnostics, which have significantly improved the detection and characterization of ACC. Regarding treatment, the management of ACC remains a challenge due to its propensity for local invasion and metastasis, with surgery, radiation, and chemotherapy being the mainstays of therapy. The development of targeted therapies based on ACC’s molecular profile will allow for a better prognosis and an enhanced quality of life of patients.

Background: Oral Submucous Fibrosis (OSMF) is a chronic, progressive condition characterized by the fibrosis of the oral mucosa, often associated with the habitual consumption of areca nut and tobacco, leading to significant morbidity. Despite its prevalent occurrence in many parts of the world, the underlying genetic and molecular mechanisms remain poorly understood, highlighting a critical need for research into its molecular genomics. The aim of this literature review is to investigate the molecular genomics of Oral Submucous Fibrosis by analyzing the relevant literature of the past decade. Methods: The search was conducted using MEDLINE (National Library of Medicine)-PubMed, focusing on the period 2015–2025 using the following keywords: Molecular Genomics AND Oral Submucous Fibrosis. This was followed by a manual search, and references were used to identify relevant articles. Results: A total of 12 articles were included in our review according to our inclusion criteria, which illustrated the importance of TGF-β, Wnt inhibitory factor-1, CypA, Hsp-70 1B, Calreticulin, Lumican, Enolase 1, MMP-2, IGF-1R, XIST, Epigallocatechin-3-gallate, Von Hippel-Lindau, and MUC1 and 4. Conclusions: Understanding the molecular pathogenesis of OSMF involves examining the molecular interactions and the roles of specific proteins. Advanced genomic technologies have opened new frontiers in the study of OSMF. As research in OSMF continues to evolve, emerging interdisciplinary approaches may provide therapeutic strategies, aiming to improve management outcomes for the patients.

Background/Objectives: Ameloblastoma is a benign odontogenic neoplasm characterized by locally aggressive behavior and frequent recurrences despite surgical treatment. It originates from odontogenic epithelium, including the cell rests of the dental lamina, remnants of the enamel organ, epithelial cell rests of Malassez, or the basal cell layer of the oral mucosa. Investigation of the etiopathogenesis of ameloblastoma has gained critical relevance due to the need for extensive surgical procedures, high recurrence rates, and its malignant potential. Accordingly, the aim of the present narrative review is to summarize current evidence regarding key aspects of ameloblastoma etiopathogenesis, with emphasis on signaling pathways, mutations, epigenetics, and epithelial–stromal interactions. Methods: An extensive literature search was conducted using the PubMed, Scopus, and Google Scholar databases, employing the keywords: “etiology”, “pathogenesis”, “molecular”, “biomarkers”, “cellular”, “epigenetic”, “mutation”, “pathway”, and “ameloblastoma”. In vitro studies, clinical studies, case reports, and narrative and systematic reviews published in English were included, without restriction on publication year. Results: Current evidence indicates that ameloblastoma pathogenesis is driven by dysregulation of multiple signaling pathways, particularly the MAPK and Sonic Hedgehog pathways, through recurrent activating BRAF and SMO mutations. In addition, alterations affecting the WNT/β-Catenin and PI3K/AKT signaling cascades, epigenetic modifications, and epithelial–stromal interactions, contribute to tumor behavior. Conclusions: Despite significant advances, genotype–phenotype correlations, mutation frequencies and coexistence, clonality, and other associations remain incompletely understood. Larger tumor cohorts and robust meta-analyses are required to clarify these associations and to leverage the development of personalized therapeutic strategies.

Background: Among the various forms of root resorption, External Apical Root Resorption (EARR) has garnered particular attention due to its prevalence and potential complications associated with orthodontic interventions. Methods: An electronic search of literature was performed between September 2024 and December 2024 to identify all articles investigating the Role of Genetic Polymorphisms in External Apical Root Resorption Among Orthodontic Patients: Implications for Treatment Outcomes. The search was conducted using MEDLINE (National Library of Medicine)-PubMed with restrictions concerning the date of publication. In particular, we focused on the period 2014–2024 using the following keywords: gene polymorphisms AND orthodontic treatment AND apical root resorption OR external apical root resorption. This was followed by a manual search, and references were used to identify relevant articles. Results: The review showed that certain variations of the following genes may be positively associated with OIEARR: Osteopontin gene, P2RX7, IL-1β, IL-6, IL1RN, OPG, RANK, STAG2, RP1-30E17.2, SSP1, SFRP2, TNFSF11, TNFRSF11A, TNFRSF11B, VDR, CYP27B1, ACT3N, TSC2, WNT3A, LRP1, LRP6. Conversely, the IRAK1 gene has a protective function against the development of OIEARR. Conclusions: Despite these advancements, it is still not feasible to establish new guidelines and clinical protocols based on the existing research findings. The integration of genetic considerations into orthodontic practice has the potential to revolutionize treatment strategies, ensuring that they are not only effective but also respectful of each patient’s unique biological landscape.

Background/Objectives: Artificial intelligence (AI) has emerged as a transformative tool in oral medicine, where it holds significant promise for enhancing the diagnosis, treatment, and management of oral cancer. Our team aimed to develop a new tool, capable of diagnosing oral cancer utilizing the capabilities of AI. Methods: The task we aim to solve from computer vision’s perspective is an object detection task. Under this context, a detection is essentially a bounding box drawn around an oral lesion accompanied by the disease’s description. To solve the task at hand, we collected and annotated a wide set of images which were used for training our model. Specifically, we used 205 images of Oral Squamous Cell Carcinoma (OSCC). Following common practice, 80% of the total images were allocated for training, 10% for validation, and 10% for testing. The training set was used to optimize the model’s parameters across multiple iterations. The validation set served to prevent overfitting during training and to guide hyperparameter tuning. Lastly, the test set was used for evaluation of data that had not been previously seen by the model and had not influenced any decisions regarding its architecture or hyperparameters. Moreover, during evaluation, we supplemented the test set by adding 100 images of healthy mucosa to examine whether the model generated false positives on healthy tissue. To broaden the dataset’s coverage, we generated synthetic images by applying data augmentation techniques such as random rotation, scale and noise injection. The model’s architecture was based on YOLO11, which is a widely spread neural network architecture known for its balance between efficiency and performance, used in object detection tasks. Results: The model’s detections were accompanied by a confidence measure, which was used to filter out those with low confidence, and one could choose a lower threshold for maximizing precision or a higher threshold for maximizing recall. Among images that correspond to oral cancer (oral squamous cell carcinoma), the model achieved 59% precision and 41% recall on the validation set and 56% precision and 42% recall on the test set. The limitations of this study include the single institutional design and the relatively small sample size. The number of images used for model training was relatively small (205 images of oral squamous cell carcinoma), which may limit the generalizability of the findings. The main limitation is that the model distinguishes oral squamous cell carcinoma from healthy mucosa. In routine clinical practice, however, the diagnostic challenge is to differentiate oral cancer from a variety of benign and potentially malignant disorders that may present with similar clinical features. The inclusion of other oral lesions is planned in future studies. Conclusions: The efficiency of our AI application may be considered as encouraging, taking the pilot nature of the study into consideration. More clinical photos and better training of the model may lead to better precision and recall, enabling its inclusion in standard clinical practice. Larger multicenter datasets will be required for clinical implementation. AI-driven tools can assist in risk stratification, helping clinicians determine the best treatment plans by analyzing patient data and predicting the likelihood of recurrence or metastasis. AI’s potential extends beyond diagnosis and treatment; it also contributes to monitoring patient outcomes. As research and technology evolve, AI’s role in oral cancer is likely to become increasingly indispensable.

Background: Oral lichen planus (OLP) is a chronic inflammatory mucocutaneous disorder that is well documented in adults but remains relatively uncommon in the pediatric population. Due to its rarity, knowledge regarding its epidemiology, etiology, clinical behavior, diagnosis, and management in children remains limited. Objective: To review the current literature regarding epidemiology, pathogenesis, clinical presentation, diagnosis, histopathological characteristics, treatment, and outcomes of OLP in pediatric patients. Materials and Methods: An electronic search of the literature was conducted in the PubMed, Scopus, and Cochrane Library databases to identify OLP-associated case reports in the pediatric population. The search was limited to English-written publications of the past decade. The initial PubMed search yielded 228 publications. Following restriction to studies published between 2016 and 2026, 97 records remained. Limiting the search to English-language publications resulted in 95 studies. Screening for patients younger than 18 years identified 51 potentially relevant publications. After title, abstract, and full-text review, 10 studies fulfilled the inclusion criteria. To ensure comprehensive literature coverage, supplementary searches were subsequently conducted in the Scopus and Cochrane Library databases, identifying three additional eligible studies after excluding the duplicates. Consequently, a total of 13 studies were included in the final review. Results: Pediatric OLP is considerably less common than adult disease. The available evidence suggests an immune-mediated pathogenesis, although the exact mechanism remains unclear. Clinical presentations include reticular, erosive, plaque-like, linear, and severe mucocutaneous forms, with the reticular subtype being the most frequently reported. Histopathological findings consistently demonstrate basal cell degeneration and a dense subepithelial lymphocytic infiltrate. Topical corticosteroids remain the most commonly prescribed treatment and are generally associated with favorable clinical outcomes. Conclusions: Although relatively uncommon, OLP should be considered in the differential diagnosis of persistent oral white lesions in children. Early diagnosis and appropriate management are essential for symptom control and prevention of complications. Additional research is needed to better understand disease pathogenesis and establish evidence-based treatment protocols for pediatric patients.