Background: Amelogenesis imperfecta affecting enamel formation is frequently associated with a variety of malocclusions and eruption disturbances. Orthodontic treatment is crucial in comprehensive patient management. Previous studies have shown that orthodontic treatment becomes more challenging in patients with AI as the defective enamel affects the bracket bonding, retention of appliances and treatment mechanics and often needs modified bonding protocols, pre-treatment restorative build-ups, skeletal anchorage and general multidisciplinary management. There is no evidence of the ideal orthodontic treatment yet; available evidence only consists of case reports and small observational studies that address specific aspects with no established consensus. Therefore, this narrative review aimed to critically examine the contemporaneous evidence on orthodontic assessment and treatment planning in AI patients, drawing on studies identified through a structured literature search. Materials and Methods: An electronic search of the literature was conducted in the PubMed, Scopus, and ScienceDirect databases. Out of 640 records that were initially identified, 11 studies met the inclusion criteria for qualitative synthesis. Results: Bonding issues resulting from enamel defects tend to be identified as a significant clinical challenge necessitating modified orthodontic techniques. The included studies demonstrated that by using individualized treatment planning, modified bonding procedures, fixed appliances, expansion procedures, skeletal anchorage and combined orthognathic surgery in some cases within the multidisciplinary treatment approach, there can be successful orthodontic management for these patients. Conclusions: Vital steps such as early diagnosis, careful treatment planning, and coordination with restorative and prosthodontic treatment were associated with better functional and esthetic outcomes. Consequently, even though there is limited evidence, the available literature supports a customized interdisciplinary approach as the most predictable and effective strategy for managing orthodontic problems in patients with AI, while emphasizing that case reports and small observational studies are the main sources of current findings.

Background/Objectives: Bullous pemphigoid (BP) in children is a rare autoimmune subepidermal blistering condition that shows significant clinical variability depending on age. This narrative review summarizes the available literature on the epidemiology, etiology, clinical manifestations, diagnosis, management, outcomes, and future perspectives of pediatric BP. Methods: A search of the PubMed/MEDLINE and Scopus databases from their inception to July 2026 was conducted for English-language articles on BP in patients younger than 18 years old. After record screening and full-text assessment, 55 publications were selected and narratively synthesized. Results: Infants with BP frequently present with acral and palmoplantar blistering, whereas older children and adolescents show more heterogeneous clinical manifestations. BP180 is the principal autoantigen, although antigenic heterogeneity has been reported. Diagnosis requires integration of clinical, histopathological, and immunopathological findings. Linear IgG and/or C3 deposition along the basement membrane zone on direct immunofluorescence (DIF) is an important but non-specific finding. Salt-split skin testing and antigen-specific serology may assist in distinguishing BP from other autoimmune subepidermal blistering diseases. Corticosteroids are the most frequently reported initial treatment, while dapsone and other steroid-sparing agents have been used in selected patients. Intravenous immunoglobulin (IVIG), immunosuppressants, and targeted therapies have primarily been reported in refractory cases, with evidence derived predominantly from case reports and small series. Conclusions: The prognosis reported in the pediatric literature is generally favorable, although there are some reports of resistant or recurrent cases. However, relapse rates in the long-term are not known. There is a need for multicenter prospective trials and standardization of outcomes.

Oral cavity and maxillofacial aspergillosis can take one of four clinically different forms: primary invasive aspergillosis of the oral cavity, invasive aspergillosis of the paranasal sinuses with secondary involvement of the oral cavity, chronic granulomatous invasive fungal rhinosinusitis, and non-invasive maxillary sinus fungus ball. The basis of this narrative review was a structured search of PubMed, Scopus, Cochrane CENTRAL and ClinicalTrials.gov databases. Each of the statements will be identified according to whether it is supported by direct evidence on oral or maxillofacial conditions, or whether it is an extrapolation from invasive fungal rhinosinusitis of mixed fungal aetiology or from invasive aspergillosis occurring at other sites. Direct evidence on primary invasive oral aspergillosis is restricted to small case series from a single centre involving 12–16 patients and individual case reports. Violaceous gingival margin and spontaneous pain progressing to a necrotic ulcer should be suspicious in patients with leukaemia and neutropenia; diagnosis relies on histopathology and culture. Local control in the case series was achieved mostly via haematological remission. Pooled mortality rate of about 31% is derived from acute invasive fungal rhinosinusitis of mixed aetiology and does not apply to the disease of the mouth. Antifungal treatment strategy is based on guidelines and clinical trials of invasive aspergillosis and mucormycosis. Liposomal amphotericin B is used until the exclusion of Mucorales, and either voriconazole or isavuconazole after confirmation of Aspergillus infection, in combination with debridement whenever possible. The fungus ball is related to endodontic and other dental procedures in case–control studies and is removed endoscopically without antifungals. There are no registered clinical trials for oral or sinonasal aspergillosis.

Background: Effective management of peri-implant disease relies primarily on mechanical removal of the bacterial biofilm. However, achieving adequate surface decontamination can be challenging due to complex implant-surface morphology and restricted access to deep peri-implant pockets. This has prompted the use of adjunctive antimicrobial agents to complement mechanical therapy and improve therapeutic outcomes. Objective: To investigate whether the adjunctive use of antimicrobial strategies improves clinical, microbiological, and radiographic outcomes in patients with peri-implant mucositis and peri-implantitis. Materials and Methods: A structured narrative review was conducted using PubMed/MEDLINE and Scopus in July 2026. No database filters concerning language, human participants or study design were applied. During the screening process, only randomized controlled clinical trials involving human participants and available as English-language full texts were selected. Eligible interventions included locally or systemically administered antibiotics, antiseptics, antimicrobial drug-delivery systems, antimicrobial photodynamic therapy (aPDT), ozone-based therapies, and microbiome-modulating adjuncts. Conventional laser therapy was not classified as an eligible antimicrobial intervention. The database searches retrieved 462 records, including 252 from PubMed and 210 from Scopus. Following duplicate removal and eligibility assessment, 100 publications representing 93 independent clinical trials were included. Results: adjunctive antimicrobial efficacy was highly variable and appeared to depend on disease severity, debridement strategy, antimicrobial agent, delivery modality, and follow-up period. Repeated or sustained local antimicrobial delivery was associated with modest, short-term benefits in several studies, whereas chlorhexidine (CHX) generally provided limited additional benefit over mechanical therapy. Evidence for systemic antibiotics remained inconsistent and insufficient to support routine use, while aPDT offered potential benefits that varied according to treatment protocol. Ozone therapy, herbal agents, and novel drug-delivery systems yielded encouraging preliminary results, although evidence remains scarce. Moreover, reductions in bleeding and probing depth (PD) did not reliably correspond to superior microbiological outcomes, radiographic bone gain, or complete disease resolution. Conclusions: Mechanical debridement (MD) and effective plaque control remain central to peri-implant disease management. Some adjunctive interventions produced modest short-term improvements in individual studies; however, the available evidence does not demonstrate durable disease control or support routine use. Therapeutic decisions should be tailored to disease severity, patient and implant characteristics, and the balance between potential benefits and antimicrobial-associated risks. Further well-designed and adequately powered randomized controlled trials with extended follow-up periods are needed to establish more definitive recommendations.

Background: N6-methyladenosine (m6A) is the most abundant mRNA internal modification in eukaryotes and regulates inflammatory and regenerative processes. Many studies relate the dysregulation of m6A-related pathways to periodontal inflammation, imbalance in cell homeostasis, impaired tissue regeneration, and remodeling of the alveolar bone. However, the mechanisms of the relationship between the m6A pathway and periodontitis have not been elucidated clearly yet. Objective: The objective of the current narrative review is to integrate the information related to the role of m6A RNA modification in the pathogenesis of periodontitis by focusing on inflammatory signaling, osteoimmune regulation, periodontal cell activity, bone remodeling, and its possible applications as a diagnosis and treatment approach. Methods: A literature search was conducted in PubMed to identify original research studies investigating the role of m6A RNA methylation and its regulators in periodontitis and periodontal tissues/cells. Out of 49 publications reviewed, 34 original research articles fulfilled the predetermined inclusion criteria. Results: The current literature suggests that N6-methyladenosine (m6A) modification is involved in various interconnected biological processes contributing to the development of periodontitis, including inflammatory responses, inflammasome activation and pyroptosis, osteoimmune reactions by macrophages, osteogenic differentiation, osteoclast formation, cellular senescence, and periodontal cells homeostasis. METTL3 has been reported to be the most widely investigated regulator, but its roles are not consistently harmful or beneficial. Depending on the RNA target, cellular environment, and state of inflammation, some of the m6A-associated pathways have been linked to periodontal inflammation and alveolar bone resorption, while others were linked to osteogenesis and regeneration. Several studies have highlighted the possibility of therapeutic interference in pathways leading to the formation of m6A, while human transcriptomic and gingival/salivary studies suggested that m6A could be used as a biomarker. Conclusions: The m6A modification of RNA is an emerging epitranscriptomic effect relating periodontal inflammation, immune responses, cellular differentiation, and bone remodeling. Even though target molecules and signaling pathways have been experimentally identified as points of potential therapeutic interference, the available evidence remains predominantly preclinical. Future work is expected to validate the diagnostic and therapeutic involvement of the m6A modification in periodontitis.

Background: Oral leukoplakia is a clinically important oral potentially malignant disorder with variable risk of progression to oral squamous cell carcinoma. Histopathological grading of oral epithelial dysplasia remains the primary method for risk assessment; however, its predictive accuracy is limited by sampling variability, lesion heterogeneity, and interobserver variation. DNA aneuploidy and abnormal DNA ploidy status have therefore been investigated as objective biomarkers of genomic instability and potential predictors of malignant transformation. Aim: This narrative review evaluates whether DNA aneuploidy or abnormal DNA ploidy status predicts malignant transformation of oral leukoplakia to oral squamous cell carcinoma compared with diploid DNA status, and whether DNA ploidy should be interpreted as a stand-alone prognostic marker or as part of combined risk-assessment models. Materials and Methods: A structured PubMed/MEDLINE search (last performed on 12 July 2026) identified 162 records using terms related to oral leukoplakia, oral potentially malignant disorders, DNA ploidy, DNA aneuploidy, cytometry, malignant transformation, and oral squamous cell carcinoma. After screening and full-text eligibility assessment, 45 studies were included and organised according to their evidential role as core prognostic studies, PVL-specific subgroup evidence, and supporting/background evidence addressing diagnostic relevance, dysplasia correlation, treatment monitoring, genomic instability, and methodological development. Results: Most core prognostic studies showed that DNA aneuploidy, abnormal DNA content, or chromosomal instability was associated with increased malignant transformation risk compared with diploid or non-aneuploid status. Several studies reported higher transformation rates, hazard ratios, or improved prediction when DNA ploidy was combined with dysplasia grading, lesion site, clinical heterogeneity, or other biomarkers. However, predictive performance varied across studies, and DNA ploidy alone often showed modest sensitivity, specificity, or positive predictive value. Diploid or non-aneuploid status appeared more useful for identifying lower-risk lesions, although it did not completely exclude malignant transformation. PVL evidence suggested frequent aneuploidy and aggressive genomic behaviour, but DNA ploidy appeared less reliable for discriminating risk within PVL. Conclusions: DNA aneuploidy and abnormal DNA ploidy status are meaningful markers of genomic instability and are associated with increased malignant transformation risk in oral leukoplakia. However, when used alone, DNA ploidy often shows only modest predictive performance, and prediction improves consistently when it is combined with dysplasia grading and other clinicopathological factors. Their strongest clinical value is therefore as adjunctive biomarkers within combined clinicopathological and molecular risk models, rather than as stand-alone replacements for histopathological assessment; routine clinical implementation is not yet supported by the current evidence.