This systematic review evaluated the effects of functional additives on fluoride release, fluoride recharge/re-release, and selected mechanical, physical, and biological properties of orthodontic glass ionomer cements (GICs) and glass ionomer-based adhesives. The review followed PRISMA guidelines. The protocol was retrospectively registered in the Open Science Framework. PubMed, Scopus, Web of Science, Embase, and WorldCat were searched for in vitro studies investigating modified orthodontic GICs and reporting fluoride-related or clinically relevant material properties. The final literature search was conducted on 30 April 2026. After screening 87 records, 23 studies were included in the qualitative synthesis. Owing to substantial methodological and outcome heterogeneity among the included studies, no meta-analysis was performed, and the findings were synthesized narratively. Risk of bias was assessed using the QUIN Tool; 20 studies were classified as having a medium risk of bias and three as having a low risk, while none were classified as having a high risk. The effects of additives on fluoride release varied according to additive type and concentration, material composition, storage conditions, pH, and evaluation period. Increases in fluoride release were reported in studies evaluating materials containing nCaF₂, TMPnano, nanofluorapatite or nanofluorohydroxyapatite, hydroxyapatite, nanochitosan, SNP/ZnONP, and ZnSO₄. Several additives maintained or improved mechanical performance, whereas higher concentrations of some agents adversely affected bond strength, microhardness, or material stability. Antibacterial and antibiofilm activity was most evident for CHX, DMAHDM, MDPB, propolis, silibinin, nanosilver, and zinc-containing systems. Limited evidence also suggested potential benefits regarding enamel protection and cytocompatibility. Functional additives may enhance the preventive potential of orthodontic GIC-based materials, particularly through improved fluoride release and antibacterial activity. However, further standardized long-term and clinical studies are required before clinical recommendations can be made.

Background: Electronic cigarettes (e-cigarettes) are now the most widely used inhalational nicotine product among adolescents and young adults. Although marketed as safer than combustible tobacco, accumulating evidence indicates that vaping injures the vascular endothelium and elevates cardiovascular disease (CVD) risk. Aim: This review synthesizes current evidence on how e-cigarette aerosol affects endothelial function and the resulting cardiovascular consequences, with attention to mechanism, population outcomes, and special populations. Material and methods: PubMed, MEDLINE, Google Scholar, JEHS, and Quality in Sport were searched for peer-reviewed publications between 2015 and 2026, combining "e-cigarette" or "vaping" with terms for endothelial function, flow-mediated dilation, and cardiovascular outcomes. Results: E-cigarette aerosol carries nicotine, propylene glycol and vegetable glycerin thermolysis products, flavorings, and metals leached from heating coils. Acute use raises pulse-wave velocity by approximately 0.26 m/s and heart rate by about 5 beats/min. Chronic users show flow-mediated dilation reduced to roughly 5% versus 11% in non-users. Mechanisms include eNOS uncoupling, NADPH-oxidase activation, formaldehyde-driven TRPA1 signaling, flavoring-induced inflammation, and increased platelet reactivity. Daily vaping was associated with self-reported myocardial infarction in NHIS data (OR 1.79, 95% CI 1.20–2.66); dual use carried higher CVD odds than exclusive smoking (OR 2.56, 95% CI 2.11–3.11). Conclusions: E-cigarettes are not cardiovascularly neutral. They impair endothelial function through multiple, partially nicotine-independent pathways and are associated with adverse cardiovascular outcomes, particularly in dual users and youth.

Objective: The aim of this systematic review was to evaluate the in vitro effects of LED-based photobiomodulation on fibroblasts and osteoblasts, with particular focus on cellular processes involved in soft- and hard-tissue regeneration. Methods: A comprehensive electronic search was conducted on 3 April 2026 in PubMed, Scopus, Web of Science, Embase, and WorldCat according to PRISMA guidelines. The analyzed outcomes included cell viability, proliferation, migration, collagen synthesis, oxidative stress, mitochondrial activity, and selected regeneration-related processes. A total of 745 records were initially identified, and 32 studies met the inclusion criteria and were included in the qualitative synthesis. Results: The biological effects of LED-PBM depended strongly on irradiation parameters, including wavelength, fluence, irradiance, exposure time, treatment schedule, and the initial condition of the cells. Most included studies focused on fibroblast models. Red and near-infrared light showed the most consistent beneficial effects, particularly by supporting fibroblast viability, proliferation, migration, mitochondrial activity, ATP production, collagen-related responses, and oxidative stress modulation. In osteoblast-related models, LED irradiation showed potential to influence cell number, metabolic activity, maturation markers, and mineralization-related outcomes; however, the number of studies was limited. Blue light demonstrated dose-dependent effects, with higher fluences reducing fibroblast metabolic activity, proliferation, or viability. Green light improved fibroblast proliferation and migration in one model but was associated with increased cell death in osteoblast-like cells. Conclusion: LED-PBM may positively modulate cellular processes involved in soft- and hard-tissue regeneration in vitro. However, the observed effects are strongly parameter-dependent, and further standardized studies are required to define optimal irradiation protocols and validate their potential clinical relevance.

Background: Osteoporosis is the most prevalent metabolic bone disease, affecting roughly 200 million women worldwide and accounting for about 9 million osteoporotic fractures annually. Age, sex, and genetics shape baseline risk, but modifiable lifestyle behaviors explain a large share of the variance in bone mineral density (BMD) and fracture incidence. Aim: This narrative review synthesizes current evidence on how physical activity, diet, tobacco, alcohol, caffeine, body weight, sleep, and stress influence osteoporosis risk, with clinical implications. Material and methods: PubMed, Google Scholar, the Journal of Education, Health and Sport, Quality in Sport, and the Cochrane Library were searched for peer-reviewed publications from 1995 to 2026. Search terms combined "osteoporosis," "BMD," and "fracture" with each lifestyle factor of interest. Inclusion was restricted to original research, meta-analyses, systematic reviews, and authoritative guidelines. Results: High-intensity resistance and impact training increased lumbar spine BMD by 2.9% and femoral neck BMD by 0.3% in osteopenic postmenopausal women. Calcium plus vitamin D supplementation reduced hip fracture risk by 30%. Vegan diets were associated with 43% higher total-fracture risk and a 2.3-fold higher hip-fracture risk. Current smoking nearly doubled lifetime hip-fracture risk. Heavy alcohol intake raised hip-fracture risk by 59%; light intake was neutral. Short sleep (≤5 h) and chronic psychological stress were associated with lower BMD across multiple skeletal sites. Conclusions: Lifestyle behaviors are the principal modifiable determinants of osteoporosis risk. Integrated programs combining weight-bearing exercise, adequate calcium and vitamin D, and avoidance of tobacco and excess alcohol offer the greatest fracture-prevention potential.

Background: Social media use is near-universal among adolescents and young adults, with up to 95% of those aged 13–17 reporting active use and more than one third using it "almost constantly." Anxiety and depression indicators have risen sharply in this age band since the early 2010s, raising concern about a causal contribution. Aim: This narrative review synthesizes correlational, longitudinal, and experimental evidence linking social media overuse to anxiety and depression, with attention to mediators, vulnerable populations, and intervention efficacy. Material and methods: PubMed, MEDLINE, Google Scholar, the Journal of Education, Health and Sport (JEHS), and Quality in Sport (QS) were searched for peer-reviewed publications from 2014 to 2026, supplemented by World Health Organization and U.S. Surgeon General reports. Inclusion was restricted to original research, meta-analyses, systematic reviews, and randomized trials. Results: Pooled estimates indicate that depression risk rises by 13% per additional hour of daily use, and adolescents using platforms more than three hours daily approximately double their risk of poor mental health outcomes. Effects are larger in girls than boys and are mediated principally by sleep displacement, upward social comparison, fear of missing out, and cyberbullying. Randomized trials show that limiting use to roughly 30 minutes daily, or abstaining for one week, produces measurable reductions in depressive and anxious symptoms. Critical reanalyses caution that aggregate effect sizes are small in absolute terms, with platform use explaining roughly 0.4% of adolescent well-being variance. Conclusions: Social media overuse is consistently associated with higher anxiety and depression risk, with the strongest signal in adolescent girls and in patterns marked by passive nighttime browsing. Time-limiting and abstinence interventions are promising and warrant integration into preventive mental-health care.

Background. Alzheimer's disease (AD) accounts for 60–70% of the over 57 million dementia cases worldwide and is projected to nearly triple by 2050. Neuropathology precedes symptoms by roughly two decades, and the approval of anti-amyloid therapies has made biomarker-confirmed early diagnosis a clinical priority. Aim. This narrative review synthesizes evidence on cerebrospinal fluid (CSF), blood, neuroimaging, genetic, retinal, and emerging molecular biomarkers for early detection of AD, framed within the 2024 revised NIA-AA biological criteria. Material and methods. PubMed, MEDLINE, Google Scholar, the Journal of Education, Health and Sport, and Quality in Sport were searched for studies and consensus documents published between 2014 and 2026. Six mandatory references were integrated with seventeen additional peer-reviewed sources. Results. CSF Aβ42/40, total tau, and p-tau181 remain reference-standard markers. Plasma p-tau217 has emerged as the leading minimally invasive biomarker, with areas under the curve of 0.92–0.96 against amyloid PET. Serum neurofilament light and glial fibrillary acidic protein support staging and differential diagnosis. Amyloid and tau PET enable in vivo Braak staging; structural MRI tracks hippocampal atrophy. APOE ε4 genotyping has regained clinical relevance in the anti-amyloid era. Optical coherence tomography, metabolomics, microRNAs, and AI-driven multimodal models expand the diagnostic frontier. Conclusions. AD can now be detected biologically before symptoms become disabling. Translating plasma assays and AI-supported imaging into routine practice is the central challenge of the coming decade.