Oral diseases最新文献

Background: Identification of healthy bone margins is a critical step in the surgical resective treatment of medication-related osteonecrosis of the jaw (MRONJ). Fluorescence-guided surgery (FGS) has been proposed as a method to identify resection margins and improve clinical outcomes. The purpose of this review was to systematically evaluate the success rate of FGS.

Materials and methods: The Cochrane Central Register, PubMed, Scopus and Web of Science databases were searched. Success was defined as the absence of exposed necrotic bone with full mucosal coverage and no signs of MRONJ recurrence, assessed at overall follow-up. The risk of bias was evaluated using the Newcastle-Ottawa Scale, the Moga Index and the GRADE approach. The PRISMA protocol was followed to evaluate and present the results.

Results: Nine studies met the inclusion criteria, comprising a total of 285 patients. Of the 314 lesions treated with FGS, 285 achieved complete healing during a mean follow-up of 13.0 months, with an overall success rate of 88.54%. The fluorescence modalities used included autofluorescence, tetracycline-induced fluorescence and near-infrared fluorescence imaging with indocyanine green.

Conclusion: Fluorescence-guided surgery appears to be a promising adjunctive tool for the surgical management of MRONJ, contributing to high success rates.

Background: Oral leukoplakia (OLK) lacks effective chemopreventive treatments. Thalidomide, with anti-angiogenic, anti-inflammatory, and immunomodulatory effects, may influence OLK progression. This study assessed feasibility and preliminary biological effects of low-dose thalidomide on dysplasia and microvasculature.

Methods: A retrospective analysis was conducted on patients with OLK treated with thalidomide 50 mg/day for ≥ 30 days (2020-2024). The primary endpoint was change in dysplasia grade on paired biopsies. The secondary endpoint was change in intrapapillary capillary loop (IPCL) patterns on narrow-band imaging (NBI). Lesion size was also recorded. Adverse events (AEs) were graded using CTCAE.

Results: Twenty-eight patients were included, most with moderate to severe dysplasia. No patient showed ≥ 50% lesion size reduction, and all maintained stable clinical size. Among 13 patients with paired biopsies, 38.5% showed histological improvement, while 30.8% showed progression. In 25 patients with NBI, 52.0% had improved IPCL patterns, while 32.0% remained stable, and 16.0% worsened. AEs were reported in 32.1%, most commonly peripheral neuropathy (14.3%), with no treatment discontinuations.

Conclusions: Low-dose thalidomide was feasible and well tolerated, showing biological activity by modulating dysplasia and IPCL patterns, despite minimal change in lesion size. These results support further prospective trials to confirm efficacy and refine treatment protocols.

Objectives: Endothelial dysfunction is a key contributor to periodontal disease and apical periodontitis. However, the role of macrophages in mediating endothelial function via exosomes in these inflammatory diseases remains elusive.

Materials and methods: Exosomes isolated from Porphyromonas gingivalis (P.g)-infected THP-1-derived macrophages (P.g-Exos) and uninfected macrophages (Con-Exos) were verified and their effects on human umbilical vein endothelial cells (HUVECs) were investigated. The expression of TNF-α and IL-6 in HUVECs was tested by quantitative real time PCR (qRT-PCR) and ELISA. A fluorescein isothiocyanate (FITC)-dextran leakage assay and a THP-1 monocyte adhesion assay were used to explore vascular permeability and cellular adhesion. The migration and angiogenic capacity were evaluated using transwell, cell scratch, and tube-forming assays. HUVECs were pretreated with SC79 (Akt activator) to explore the mechanism.

Results: P.g stimulation increased the release of exosomes from macrophages. P.g-Exos inhibited HUVECs' migration and tube formation capabilities while increasing vascular permeability, promoting leukocyte adhesion and releasing proinflammatory factors. Importantly, P.g-Exos induced endothelial dysfunction partially via the Akt/mTOR pathway suppression.

Conclusions: Summarily, this study reveals that the exosomes derived from inflammatory macrophages mediate HUVECs dysfunction partially via the Akt/mTOR pathway, providing novel insights into potential treatments for oral inflammatory diseases.

Objective: The oral cavity represents a key but underexplored interface between host immunity and microbial communities. The aim of this systematic review was to synthesize current literature on oral microbiota alterations in systemic autoimmune diseases.

Methods: PubMed and Web of Science databases were searched for human studies published between January 2000 and April 2025. Eligible observational studies compared adults with diagnoses of systemic autoimmune diseases to controls and characterized oral microbiota diversity and/or composition using sequencing-based methods. Different oral habitats were analyzed (saliva, dental plaque, oral mucosa, gingival crevicular fluid).

Results: 42 studies met inclusion criteria: 19 on rheumatoid arthritis, 18 on primary Sjögren's syndrome, 5 on systemic lupus erythematosus, and 1 on anti-neutrophil cytoplasmic autoantibody-associated vasculitis. 16S rRNA gene sequencing predominated and only 3 studies used shotgun metagenomics, among which one also profiled the oral virome. Across systemic autoimmune diseases, dysbiosis was characterized by enrichment of anaerobic genera (Prevotella, Veillonella) and depletion of commensals (Neisseria, Haemophilus), with distinct β-diversity separation from controls. Periodontal disease and reduced salivary secretion significantly modulated microbial communities but did not fully explain disease-associated alterations.

Conclusion: The oral microbiome exhibited shared dysbiotic signatures. However, methodological and clinical heterogeneity limited direct comparison between studies.

Objective: The study investigated the biological roles of LINC01106 in oral squamous cell carcinoma (OSCC) progression.

Methods and methods: RT-qPCR quantified LINC01106 levels in OSCC tissues and cell lines. Cell proliferation, migration, and invasion assays evaluated its function, while luciferase reporter assays and Western blot confirmed the regulatory axis.

Results: Elevated LINC01106 expression in OSCC tissues and cell lines correlated with poor prognosis. Multivariate Cox analysis identified high LINC01106 as an independent adverse prognostic factor for overall survival (OS). LINC01106 silencing suppressed proliferation, migration, and invasion of OSCC cells and reduced xenograft growth. Mechanistically, LINC01106 sponged miR-449a to up-regulate MYC; inhibition of miR-449a or MYC re-expression rescued the malignant phenotype after LINC01106 knockdown.

Conclusion: LINC01106 exerts oncogenic effects via the miR-449a/MYC axis and may serve as a therapeutic target in OSCC.