Search Results (5,579)

Background/Objectives: Halitosis in geriatric patients is multifactorial, but the joint contribution of prosthetic rehabilitation type and polypharmacy after routine dental procedures has rarely been quantified. We investigated how prosthesis type, polypharmacy, and salivary function were associated with volatile sulfur compound (VSC) burden and self-perceived halitosis in elderly dental patients. Methods: This cross-sectional study enrolled 88 patients aged ≥65 years, four weeks after completing routine dental procedures. Participants were stratified into three groups: complete denture wearers (n = 30), partial removable denture wearers (n = 28), and fixed prostheses/implants (n = 30). We measured unstimulated salivary flow rate (uSFR), tongue coating index (TCI), denture biofilm index, total VSCs (Halimeter^®), organoleptic score (0–5), and self-perceived halitosis. Polypharmacy, comorbidities, and the Geriatric Oral Health Assessment Index (GOHAI) were recorded. Analyses included one- and two-way ANOVA, Spearman correlations, theory-informed multivariable linear and logistic regression, exploratory mediation analysis, and ROC curves. Results: Forty-two participants (47.7%) reported halitosis. Mean VSC differed across groups (complete dentures 278.2 ± 38.6 ppb; partial 211.2 ± 46.3 ppb; fixed 164.4 ± 43.9 ppb; ANOVA p < 0.001). uSFR correlated inversely with VSC (ρ = −0.61, p < 0.001) and TCI correlated positively (ρ = 0.56, p < 0.001). A significant prosthesis × polypharmacy interaction was observed (F = 3.74, p = 0.029, η²_p = 0.082): polypharmacy was associated with higher VSC most clearly among partial and fixed prostheses wearers, whereas complete denture wearers showed high VSC levels regardless of polypharmacy status. Exploratory mediation findings were consistent with partial indirect association, with 45.9% of the polypharmacy–VSC association statistically explained by reduced uSFR; however, the cross-sectional design precludes causal or temporal interpretation. The full multivariable model showed apparent discrimination for self-perceived halitosis (AUC = 0.92), while the simplified four-item chairside composite model showed AUC = 0.89; neither estimate was optimism-corrected or externally validated. Conclusions: In elderly post-procedure patients, complete denture wearing, polypharmacy, and salivary hypofunction were independently and jointly associated with higher halitosis burden. Reduced salivary flow was consistent with a partial indirect statistical pathway in the polypharmacy–VSC association, supporting hydration counseling and meticulous prosthesis hygiene as low-cost geriatric interventions. Sensitivity analyses excluding implant-supported restorations, participants with MMSE scores of 24–26, and expanded mediation models including TCI and biofilm/plaque did not materially change the main inference. Full article

Backgrounds: Carotid atherosclerotic plaques (CAPs) are a reliable marker of systemic atherosclerosis and a predictor of cardiovascular events. Despite advances in prevention, the prevalence of CAPs in high-income regions remains uncertain due to heterogeneity in imaging definitions, study designs, and populations. We strived to provide an updated meta-analysis of population-based studies conducted in Europe and North America between 2015 and 2025, estimating the prevalence of CAPs in general populations. Methods: Following the PRISMA 2020 guidelines, PubMed and Web of Science were searched for original studies. Eligible studies reported CAPs prevalence in adult general populations using ultrasonography, computed tomography angiography, and magnetic resonance imaging. Pooled prevalence was calculated using a random-effects meta-analysis of proportions, and heterogeneity was assessed using I² and τ² statistics. Subgroup and meta-regression analyses explored associations with age and comorbidities. Results: A total of 80 studies comprising 177,196 participants were included. The pooled prevalence of CAPs was 39.8% (95% CI 32.6–47.5%) under a random-effects model with substantial heterogeneity (I² = 99.6%). The prevalence of CAPs increased with age, exceeding 59% among individuals aged over 70 years. High-risk populations, particularly those with T2DM, exhibited a prevalence exceeding 50%. Conclusions: CAPs are present in approximately 40% of adults in Europe and North America, with prevalence strongly driven by age and comorbidities. Despite therapeutic advances, the prevalence of CAPs has not declined, reflecting the growing impact of population aging and comorbidities. Standardized imaging definitions, longitudinal outcome linkage, and pragmatic prevention strategies are needed to translate CAPs detection into reduced cardiovascular events. Full article

Background: Coronary bifurcation lesions represent one of the most technically demanding scenarios in coronary artery disease (CAD), associated with higher procedural complexity, restenosis, and periprocedural complications. Recent advances in coronary computed tomography angiography (CCTA) have markedly improved its ability to visualize complex coronary anatomy, assess plaque morphology, and guide revascularization. Objectives: This review summarizes (1) technological advances in CCTA over the last decade, (2) its role in evaluating bifurcation stenosis, (3) assessment of plaque morphology and distribution, (4) quantification of bifurcation geometry, and (5) emerging evidence supporting its application in revascularization planning and guidance. Findings: Modern wide-detector and dual-source CT systems, iterative and deep-learning reconstruction algorithms, and photon-counting CT (PCCT) have significantly improved temporal and spatial resolution, reduced blooming artifacts, and lowered radiation dose. CCTA now reliably quantifies bifurcation stenosis and plaque distribution, characterizes high-risk plaque features, and accurately measures bifurcation angles. The integration of CT-derived fractional flow reserve (FFR-CT) and artificial intelligence (AI)-based plaque quantification further strengthens its diagnostic and prognostic performance. CCTA-derived bifurcation scores and 3D modelling support procedural strategy selection, stent sizing, and side-branch (SB) protection. Conclusions: CCTA has evolved into a comprehensive tool for non-invasive diagnosis, physiological assessment, and pre-procedural planning of bifurcation disease. With the advent of PCCT and AI-enhanced quantitative tools, CCTA is poised to become a central component of revascularization decision-making in complex coronary bifurcations. Full article

Acute cardiovascular events driven by atherosclerosis primarily originate from thrombosis triggered by vulnerable plaque rupture or endothelial erosion. Endothelial barrier destabilization—characterized by glycocalyx impairment, intercellular junction disassembly, and abnormal cytoskeletal tension—is a core upstream pathological stage that promotes atherogenic lipoprotein leakage, inflammatory cell infiltration, and matrix degradation. Hemodynamics, primarily through wall shear stress (WSS), shape the spatial distribution and plaque phenotypes of atherosclerosis; notably, low or oscillatory shear stress is associated with, and in experimental systems can promote, pro-inflammatory, pro-oxidant and pro-permeability endothelial phenotypes that contribute to plaque initiation and vulnerability. Conversely, regular exercise training, as an intervention that modulates hemodynamics, is widely suggested to promote anti-inflammatory, antioxidant, and antithrombotic endothelial phenotypes by significantly increasing antegrade shear stress and reducing detrimental retrograde/oscillatory shear stress. With a central focus on the axis of “exercise-shear stress-glycocalyx-cytoskeleton/junction-permeability-plaque stability,” this review integrates evidence from in vitro flow chambers, animal models and human studies to critically discuss: (1) the spatiotemporal heterogeneity of WSS and its relationship with plaque vulnerability; (2) the composition, barrier function, and plasticity of the glycocalyx as the primary interface for shear stress; (3) the mechanosensory complexes at the glycocalyx and junctions that transduce shear stimuli to protective pathways such as Phosphoinositide 3-kinase (PI3K)-Akt-endothelial nitric oxide synthase (eNOS) and Krüppel-like factor 2 (KLF2), thereby stabilizing adherens/tight junctions; (4) how improved barrier homeostasis promotes the maintenance of the fibrous cap collagen scaffold by reducing lipoprotein leakage and dampening the inflammation–matrix metalloproteinase (MMP) axis. Finally, this review highlights the boundary conditions of the biological effects of shear stress: low/oscillatory shear stress is primarily associated with plaque initiation and susceptible sites, whereas focal, extremely high WSS in established stenotic lesions may contribute to late-stage high-risk remodeling. Therefore, the protective hemodynamic adaptations induced by exercise should not be simply equated with the pathologically high WSS found at stenotic sites. Full article

Carotid artery disease has traditionally been assessed according to luminal stenosis, although plaques with similar narrowing may differ substantially in biological activity and clinical risk. Intraplaque neovascularization is a key feature of plaque vulnerability, reflecting microvascular proliferation and its association with inflammation, hemorrhage, and structural destabilization. Dynamic contrast-enhanced ultrasound (DCE-US) offers a real-time, radiation-free method for evaluating intraplaque enhancement kinetics using strictly intravascular microbubble agents. However, its broader use in carotid plaque imaging remains limited by variability in acquisition protocols, contrast administration, signal processing, curve fitting, and parameter interpretation. This technical review clarifies the main analytical approaches used in carotid DCE-US, distinguishing bolus-based wash-in/wash-out analysis from destruction–replenishment modeling. Bolus analysis describes first-pass microbubble transit through the plaque microvasculature and commonly provides parameters such as peak intensity, wash-in slope, area under the curve, and time to peak. Destruction–replenishment analysis evaluates post-destruction refill under stable or quasi-stable contrast conditions and relies on model-based estimation of plateau intensity and the replenishment rate. Because these approaches interrogate different kinetic regimes, their outputs should not be considered interchangeable, even when similar terms are used across studies. Particular emphasis is placed on the operational meaning of quantitative and semi-quantitative parameters, the assumptions underlying curve modeling, and the methodological consequences of ROI placement, motion correction, acoustic settings, and fitting constraints. Rather than proposing a universal acquisition protocol, this article provides practical principles for acquisition, analysis, and reporting, helping radiologists, neuroradiologists, neurologists, and vascular imaging specialists understand the processing steps, algorithmic assumptions, and model-dependent choices underlying software-derived curves and parameters. By making this analytical layer more explicit, the review seeks to support a transparent, reproducible, and biologically coherent approach to quantitative carotid plaque characterization. Full article

Oral health has significant implications for pulmonary outcomes, particularly among individuals with dysphagia who are at risk for aspiration. Moreover, oral health and condition affect nutrition accessibility and status. Inadequate oral hygiene promotes bacterial colonization, plaque accumulation, and aspiration-related respiratory complications. This narrative review aimed to explore current evidence and expert perspectives across palliative medicine, pulmonary and critical care, and dentistry on the role of oral hygiene in supporting pulmonary health and maintaining opportunities for oral nutrition. A comprehensive literature search was conducted through the Texas Tech University Health Sciences Center digital library using Cochrane Library (Wiley), EBSCO Discovery, Embase, Ovid databases, PubMed, SCOPUS, ScienceDirect, Web of Science, and Google Scholar between 14 January 2026 and 1 April 2026. From 1287 identified records, 70 studies were selected to be highlighted in the manuscript after duplicate removal and eligibility screening. Relevant literature was reviewed to examine associations among dysphagia, oral health and condition, oral hygiene and care protocols, feeding route, salivary composition and function, and respiratory outcomes. Emphasis was placed on studies addressing pneumonia, oral versus tube feeding, and evidence-based oral care practices. Findings indicate that pneumonia, depression, and mortality rates are higher in patients receiving tube feeding compared to oral feeding. Evidence-based oral care practices inclusive of mechanical plaque disruption, oral cleansing products (Chlorhexidine, hydrogen peroxide, and sodium bicarbonate), and structured oral hygiene protocols can reduce pulmonary consequences of aspiration and support safer/least risk oral intake. Saliva plays a pivotal role in plaque breakdown, microbial defense, and host immunity; oral feeding helps to preserve salivary function. Results of this review highlight the importance of oral hygiene in both restorative and palliative care contexts. This review establishes a framework for embedding oral cleansing agents and protocols into a nutrition-focused health care infrastructure. Based on the literature analysis and inter- and multidisciplinary clinical expertise of the author group, the manuscript proposes consensus statements intended as expert guidance rather than formal clinical practice guidelines. Adherence to best practices in oral care can mitigate pulmonary consequences of aspiration amid dysphagia, make oral nutrition more accessible and comfortable, sustain opportunities for least risk oral feeding across diagnoses and health care settings, and improve quality of life for patients with dysphagia amid life-limiting illness. Full article

Background/Objectives: The management of moderate-to-severe psoriasis in patients with a recent history of internal malignancy is a clinical challenge, as systemic immunosuppressive therapies are often avoided because of concerns about cancer recurrence. While Psoralen and Ultraviolet A (PUVA) photochemotherapy remains a valuable non-immunosuppressive alternative, regional variations in therapeutic response are not well-characterized in this population. This study aimed to evaluate total and segmental Psoriasis Area and Severity Index (PASI) responses to PUVA in patients with chronic plaque psoriasis and recent internal organ malignancy. Methods: This prospective, single-center, real-world cohort study enrolled 20 adults with moderate-to-severe chronic plaque psoriasis and a recent (<5 years) diagnosis of internal organ malignancy in complete remission. Participants received oral PUVA three times weekly for up to 30 sessions. Primary and secondary outcomes included changes in total PASI, segmental PASI (head/neck, trunk, upper limbs, and lower limbs), and Dermatology Life Quality Index (DLQI) at baseline, completion of therapy, and 6 months post-treatment. Results: PUVA led to a significant reduction in mean total PASI from 18.6 ± 3.2 at baseline to 5.7 ± 6.0 at treatment completion (69% reduction; p < 0.001). However, regional responses differed significantly: the head and neck improved the most (80.4%), followed by the trunk (72.2%) and upper limbs (72.3%), while the lower limbs showed the weakest response (59.5%; p < 0.001). At baseline, trunk contributed the most to total PASI (38%), while post-treatment, lower-limb lesions accounted for approximately 47% of the remaining total disease burden, showing the highest contribution to total PASI of all body regions. At 6 months, the lower limbs remained the most affected area, with significantly lower improvement (52.9%) compared to other regions. Mean DLQI also improved significantly from 17.2 ± 2.8 to 5.6 ± 2.6 (p < 0.001). Conclusions: PUVA is an effective and safe treatment for patients with psoriasis and a recent history of malignancy. Nevertheless, lower-limb psoriasis is relatively recalcitrant and contributes disproportionately to residual disease burden and relapse. These findings support the use of regional PASI assessment to guide individualized management and clinical expectations in this complex patient group. Full article

Background:/ Over the past decade, increasing evidence has shifted attention from the brain to the gut microbiota (MB) as a source and site of systemic dissemination of amyloid-β (Aβ), an APP derivative responsible for plaque formation in the brains of Alzheimer’s disease (AD) patients. Furthermore, AD patients and APP/PS1 mice, a transgenic model of AD, exhibit dysbiosis. Objectives: Using APP/PS1 mice treated from 2 to 8 months of age, we studied ileal and colonic epithelial integrity, intestinal barrier (IB) integrity assessed through tight junction (TJ) protein expression, local immune system, the presence/increase in Aβ expression in enterocytes, and the protective effects of synbiotic treatment. Methods: The tissue was stained with Periodic Acid-Schiff and Alcian Blue to evaluate epithelial morphology and mucus production, and immunohistochemistry was performed to assess TJs, immune markers, and Aβ expression. Results: Our results demonstrate that colonic and ileal epithelium of 8-month-old APP/PS1 mice displays IB impairment in term of alterations of goblet cells staining and TJ protein expression and signs of immune involvement. The ileum was more severely affected, showing a reduced epithelial surface area, decreased lysozyme production, and fewer tuft cells. Long-term synbiotic treatment largely prevented APP/PS1 mouse changes and caused a significant increase in Aβ expression in all treated mice. Conclusions: These findings support the belief in early intestinal involvement in AD and highlight the potential of the microbiota as a target for early intervention aimed at modifying the progression to neurodegeneration. Increased epithelial Aβ labeling after treatment raises the possibility of intestinal management of Aβ, which requires further validation. Full article

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by amyloid-β (Aβ) and the accumulation of tau in the brain, which triggers robust innate immune responses. Growing evidence indicates that neuroinflammation contributes to AD progression by overactivating microglia through the release of cytokines and chemokines. In general, chemokines can disrupt neuronal communication and promote blood–brain barrier permeability. Peripheral immune cells are mobilized into the brain by a gradient of chemokines. These processes link peripheral immune responses with substantial T-cell infiltration into the CNS parenchyma, leptomeninges and cerebrospinal fluid of both AD mice and AD patients. This finding underscores the relevance of the adaptive immune system, particularly T and B cells, in AD neuropathology. T-cell infiltration into the brain can influence amyloid clearance through chemokine signalling. However, chemokines play a critical role in AD by either promoting or suppressing disease progression. The infiltration of peripheral T and B cells into the brain parenchyma can exacerbate neuronal loss, yet it may also exert neuroprotective effects. Despite the presence of CD4⁺ and CD8⁺ T cells in postmortem brains of AD patients, debate continues about their role in AD brains, in terms of whether they are protective or detrimental. Understanding the complex role of chemokines in controlling innate and adaptive immune responses by modulating neuron–glia interactions (involving astrocytes and microglia) may provide novel therapeutic approaches for AD. Targeting chemokine signalling or treating with drugs that can prevent the recruitment of immune cells may be promising strategies for treating AD neuropathology. Therapies that prevent the overactivation of T cells in the brain could lead to protective strategies against AD. In fact, regulatory T cells (Tregs) could delay the onset of cognitive symptoms, because they suppress inflammation and slow the accumulation of Aβ plaques and p-Tau in the brain. Complementary strategies, such as photobiomodulation, nanoparticle, and T-cell-based approaches, could mitigate AD progression in patients. Full article

Objectives: Alzheimer’s disease (AD) is associated with impaired adult hippocampal neurogenesis (AHN). This study aimed to establish an in vitro model of Aβ_1–42 oligomer-damaged neural stem cells (NSCs) and to employ the 5×FAD mouse model of AD in vivo, and to evaluate the therapeutic effects of brain-derived neurotrophic factor-loaded hyaluronic acid hydrogel (BDNF-HA gel) on AHN. Methods: In vitro, BDNF-HA gel was co-cultured with Aβ_1–42 oligomer-impaired NSC spheres and evaluate NSC proliferation, migration, and differentiation. In vivo, BDNF-HA gel was infused intracerebroventricularly into 5×FAD mice. Using BrdU labeling, immunofluorescence, anterograde transsynaptic viral tracing, and behavioral tests, we assessed the effects of BDNF-HA gel on adult neurogenesis, newborn neuron integration into memory circuits, and cognitive function. Results: In vitro, BDNF-HA gel attenuated Aβ_1–42-induced NSC apoptosis, restored proliferation and migration, promoted differentiation into neuroblasts, newborn neurons, and oligodendrocytes, and alleviated mitochondrial depolarization and loss of mitochondrial mass. In vivo, despite the absence of significant Aβ plaques reduction in 5×FAD mice, BDNF-HA gel markedly enhanced NSC proliferation and neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ). Behavioral tests further revealed significant improvements in object recognition, spatial working memory, and spatial reference memory. Conclusions: BDNF-HA gel can effectively counteract the toxic microenvironment induced by Aβ oligomers, promoting NSC proliferation, migration, and differentiation into neurons. Without altering the Aβ burden, it significantly enhances adult neurogenesis and rescues cognitive deficits in AD mice. Full article

Background/Objectives: Orthodontic treatment induces controlled mechanical forces that alter the periodontal environment, including changes in oral microbiota composition and activation of local inflammatory pathways. Despite the widespread and growing use of orthodontic appliances across all age groups, the magnitude, timing, and multi-domain biological impact of these changes have not been comprehensively quantified in a single systematic synthesis. This systematic review and meta-analysis aimed to synthesize the available evidence on periodontal clinical parameters, oral microbiota composition, and local inflammatory biomarkers associated with orthodontic treatment using fixed appliances and clear aligners, and to provide a structured, GRADE-rated evidence base for clinical practice. Methods: A systematic review and meta-analysis was conducted in accordance with PRISMA 2020 guidelines. PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to March 2026. Prospective cohort studies, longitudinal clinical studies, and randomized controlled trials evaluating periodontal parameters, oral microbiota, and inflammatory biomarkers during orthodontic treatment were included. Quantitative synthesis was performed using mean differences or standardized mean differences with 95% confidence intervals, primarily assessing within-group (pre–post) changes. Results: Eighteen studies (n = 812 patients; follow-up 3–12 months) met inclusion criteria. Fixed orthodontic appliances were consistently associated with transient increases in plaque index (MD 0.45, 95% CI 0.32–0.58; I² = 62%), gingival index (MD 0.38, 95% CI 0.25–0.51; I² = 55%), and bleeding on probing (MD 15.2%, 95% CI 10.1–20.3%; I² = 48%), particularly during early treatment phases. Microbiological analyses demonstrated within-group shifts toward increased prevalence of periodontopathogenic species (Streptococcus mutans OR 2.45, 95% CI 1.89–3.18; Porphyromonas spp. OR 2.14, 95% CI 1.67–2.75) in patients treated with fixed appliances. Local inflammatory responses were characterized by elevated IL-1β (MD 1.2, 95% CI 0.8–1.6) and IL-6 (MD 0.9, 95% CI 0.6–1.2) in gingival crevicular fluid. Certainty of evidence was rated moderate for plaque and gingival indices and low for microbiological and inflammatory outcomes (GRADE). Conclusions: Orthodontic treatment—particularly with fixed appliances—is associated with transient, reversible deterioration of periodontal indices, shifts toward a more dysbiotic oral microbiome, and elevation of local inflammatory mediators in gingival crevicular fluid during active treatment phases. These changes are manageable through structured preventive protocols and regular periodontal monitoring. Future prospective studies with concurrent control groups and standardized multi-domain outcome measures are needed to better define the magnitude and reversibility of these biological responses. PROSPERO: CRD420261336117. Full article

Periodontitis treatment remains challenging due to incomplete removal of plaque biofilms, increasing antibiotic resistance, and dysregulated host inflammatory responses. In this study, an MPB@ZnPc nanomaterial was constructed to achieve efficient antibacterial activity through the synergistic effects of photothermal therapy (PTT) and photodynamic therapy (PDT), while also exerting immunomodulatory functions under dark conditions. MPB@ZnPc (mesoporous Prussian blue @ zinc phthalocyanine) was synthesized using a polymer-templating method and systematically characterized. The results demonstrated that the nanomaterial exhibited excellent photothermal conversion efficiency and stability under near-infrared (NIR) irradiation. It also showed strong photocatalytic degradation performance toward methylene blue and rhodamine B, accompanied by substantial reactive oxygen species (ROS) generation. In vitro antibacterial assays revealed that MPB@ZnPc achieved significantly enhanced antibacterial efficacy compared with individual components, with bactericidal rates of 99.61 ± 0.52% against Porphyromonas gingivalis and 99.77 ± 0.32% against Fusobacterium nucleatum. The corresponding biofilm removal rates reached 93.60 ± 3.30% and 93.25 ± 3.30%, respectively. Under dark conditions, the nanomaterial exhibited good biocompatibility toward L929 cells and effectively inhibited lipopolysaccharide (LPS)-induced M1 polarization of macrophages, leading to reduced expression of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. Mechanistically, MPB@ZnPc suppressed the activation of the NF-κB signaling pathway. Overall, MPB@ZnPc provides a promising strategy for precise periodontitis treatment by integrating synergistic antibacterial activity with immunomodulatory effects. Full article

Background: Full-mouth disinfection (FMD) has been proposed as an effective non-surgical approach for the management of periodontitis; however, its clinical and microbiological outcomes in patients with depressive comorbidity remain insufficiently explored. Methods: This prospective study included 80 patients diagnosed with stage II periodontitis, allocated into two groups based on the presence or absence of depressive disorder. All participants underwent standardized FMD. Clinical parameters, including bleeding on probing and plaque index, together with subgingival bacterial load (total bacterial load, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia), were assessed at baseline and 12 weeks post-treatment using quantitative polymerase chain reaction. Microbiological data were log10-transformed prior to statistical analysis. Results: Significant reductions in both clinical and microbiological parameters were observed following treatment in both groups. Improvements in bleeding on probing and plaque index were accompanied by a marked decrease in total bacterial load and in the targeted periodontal pathogens. Patients with depressive disorder exhibited a higher baseline microbial burden; however, post-treatment reductions were comparable between groups. Moderate positive correlations were identified between total bacterial load and clinical parameters. Conclusions: FMD was associated with substantial short-term improvements in both clinical and microbiological outcomes in patients with stage II periodontitis. Depressive comorbidity did not appear to adversely influence treatment response. These findings support the role of biofilm control as a central component of periodontal therapy across different patient profiles. Full article

Systemic antibiotics are among the most widely prescribed therapeutic agents worldwide, and their effects on host–microbe equilibrium extend well beyond the infection for which they are intended. Periodontitis is conventionally framed as a biofilm-initiated, host-mediated inflammatory disease, although recent work has shifted this framework toward microbial homeostasis as a regulator of periodontal stability. We hypothesize that antibiotics are not direct etiologic agents of periodontitis but instead act as risk-modifying factors that lower the threshold at which plaque-mediated inflammation progresses to destructive disease. We propose that this effect may operate through several mechanisms: broad-spectrum or repeated exposure could deplete protective commensals and narrow microbial diversity, creating ecological space for opportunistic and pathogenic taxa; antibiotics may also alter host neutrophil function, cytokine profiles, and antimicrobial peptide regulation and may interfere with the osteoblastic and osteoclastic dynamics governing alveolar bone remodelling; and antibiotic-induced gut dysbiosis may propagate systemic inflammatory signals that further modulate periodontal susceptibility. To evaluate this hypothesis, we synthesize the available clinical, epidemiological, and experimental data across four converging axes—oral microbial ecology, immune regulation, alveolar bone remodelling, and the gut–oral axis—and identify the predictions the hypothesis generates and the evidence gaps it exposes. We emphasize that no clinical study has yet demonstrated a causal link between antibiotic exposure and periodontitis; the framework advanced here is therefore intended to inform antimicrobial stewardship in dentistry and to define a research agenda for determining whether antibiotic exposure constitutes a clinically meaningful modifier of periodontal disease susceptibility. Full article

Background: Carotid atherosclerosis is a recognised manifestation of systemic vascular disease, and its association with coronary artery disease (CAD) has been well described. However, previous studies have largely been conducted under conventional diagnostic conditions and have focused on carotid plaque, intima–media thickness, or simple present-versus-absent stenosis classifications, rather than duplex-derived haemodynamic markers across the spectrum of angiographic CAD burden. The COVID-19 pandemic and post-pandemic period changed referral patterns and created more variable cardiovascular presentations, including symptoms that could resemble or mask obstructive CAD. Therefore, we investigated whether the established association between carotid stenosis severity and CAD burden remains detectable in a diagnostically heterogeneous real-world cohort, and whether routinely available carotid duplex haemodynamic parameters provide a clinically relevant signal in this setting. Methods: This single-centre, cross-sectional study was performed as a carotid-focused secondary analysis of the BG Study cohort. We included 902 consecutive patients who underwent invasive coronary angiography between 2021 and 2023 and carotid duplex ultrasonography during the same hospitalisation. CAD burden was defined according to the number of major coronary vessels with ≥70% diameter stenosis and classified as no CAD, one-vessel, two-vessel, or three-vessel disease. Carotid duplex parameters included peak systolic velocities of the common, internal, and external carotid arteries, as well as ICA stenosis severity graded according to NASCET criteria. Associations with CAD burden were assessed using a staged statistical approach combining χ² tests, Kruskal–Wallis tests with post hoc pairwise comparisons, Spearman correlation, inverse probability weighting, and ordered logistic regression. Results: The prevalence of measured ICA stenosis of any grade and severe ICA stenosis increased with greater CAD burden (both p < 0.001). Median PSV values of the bilateral ICAs and ECAs differed significantly across CAD groups on global intergroup testing. Post hoc pairwise analyses showed that significant corrected differences were concentrated between patients without CAD and those with multivessel or three-vessel CAD, particularly for ICA stenosis measures and bilateral ECA PSV. Spearman analysis demonstrated weak but statistically significant correlations between carotid parameters and CAD burden (ρ = 0.085–0.134). After inverse probability weighting, covariate balance was achieved, with all post-IPW standardised mean differences being <0.01. In ordered logistic regression (OLR) analysis, patient-reported history of carotid stenosis (OR 2.25, 95% CI 1.38–3.67; p < 0.001), right external carotid artery PSV per 10 cm/s (OR 1.31, 95% CI 1.09–1.57; p = 0.004), left ICA PSV per 10 cm/s (OR 1.17, 95% CI 1.01–1.36; p = 0.034), and left ICA stenosis per 10% (OR 1.24, 95% CI 1.11–1.39; p < 0.001) were independently associated with higher CAD burden. Exploratory ratio-based analyses showed that the ECA/CCA PSV ratio was associated with CAD presence and higher CAD burden, whereas the ICA/CCA ratio showed weaker associations; neither ratio-based index outperformed absolute ECA PSV. Conclusions: In this carotid-focused secondary analysis of a pandemic-era angiography cohort, carotid stenosis severity and duplex-derived haemodynamic parameters were independently but modestly associated with increasing angiographic CAD burden. These findings support carotid duplex markers as adjunctive indicators of systemic atherosclerotic burden rather than standalone tools for CAD detection or treatment decision-making. Future validation in vascular surgery populations is warranted to determine whether routinely available carotid duplex parameters can contribute to targeted cardiovascular risk recognition before major vascular procedures. Full article