Search Results (5,820)

Nickel (Ni) contamination threatens plant growth and ecosystem stability, and plant-growth-promoting rhizobacteria (PGPR) are sustainable bioremediation candidates. Here, we isolated and characterized a Ni-resistant PGPR strain, Microbacterium algeriense C14, from the rhizosphere of Zinnia elegans in Ni-contaminated soil. C14 exhibited exceptional Ni tolerance (up to 800 mg·L⁻¹), produced indole-3-acetic acid (IAA), and maintained pH homeostasis (8.3–8.7). XPS and XRD analyses confirmed a novel carboxylate-based precipitation mechanism: C14 secretes carboxyl-containing metabolites that coordinate with Ni²⁺ to form stable amorphous nickel–carboxylate complexes. Under Ni stress (50–600 mg·L⁻¹ for germination; 50–600 mg·kg⁻¹ soil for pot experiments), C14 inoculation increased the seed germination index by up to 47.3%, seedling root length by 36.9%, and mature plant aboveground fresh weight by 21.32%, while reducing plant Ni uptake by 38.7% (seedlings) and 49.9% (mature shoots). It also enhanced plant antioxidant-enzyme (SOD and POD) activities and soluble protein content, improved soil quality (pH +0.16–0.33 units, urease/acid phosphatase activities elevated), and reduced soil-available Ni by 23.7%. Additionally, C14 enriched Proteobacteria in the rhizosphere and modified microbial community structure. These results highlight M. algeriense C14 as a promising resource for Ni-contaminated soil remediation via integrated metal immobilization, growth promotion, and rhizosphere regulation. Full article

Clarifying the responses of microbial communities in distinct microhabitats like roots, the soil, and litter layers to secondary succession is critical for predicting the effects of global climate change on ecosystem functions. We investigated the microbial activities, compositions, and networks in these microhabitats of Fagus lucida forests ranging from 40 to 200 years. The results showed that soil physicochemical properties decreased with forest succession, except for NH₄⁺-N and available phosphorus, which decreased at the early stage. All vector angles of extracellular enzyme stoichiometry that were greater than 45° indicated that phosphorus was the key limiting element for microorganisms. The microbial community shifted from r- to K-strategists with forest succession, displaying the replacement of most bacterial phyla by Proteobacteria and Acidobacteriota, and an increase in the Acidobacteriota: Proteobacteria ratio, especially in the soil and litter layers. Soil properties, particularly NH₄⁺-N and pH, significantly affected the bacterial diversity and structure. Moreover, the bacterial network complexity increased with succession, particularly in the litter layer, and the topological properties of bacterial networks showed a stronger influence on microbial activities compared with those of fungal networks. The richness of keystone taxa in the litter layer was higher than in the soil layer and roots. However, the fungal community dominated by symbiotrophs showed lower sensitivity to soil nutrient changes and greater resilience to forest succession, displaying stable diversity and decreased network complexity, particularly in the roots. Ectomycorrhizal fungi (e.g., Russula) dominated the fungal guilds, and their abundance increased with forest succession, accompanied by a decrease in pathogenic fungi. Plant roots with significantly higher phosphatase activities played a stronger role than soils in structuring the litter microbial community, as reflected by similar carbon- and nitrogen-acquiring enzyme activities, microbial compositions, a greater share of taxa, and closer community distance. Our results revealed the increasingly important role of plant roots with forest succession in structuring the microbial community and nutrient cycling in the soil and litter layers. Full article

Osteoporosis is a major global health challenge, particularly among aging populations, underscoring the need for safe and effective nutritional interventions. Probiotics and their metabolites have emerged as promising candidates for modulating bone health via the gut-bone axis. In this study, we investigated the effects of a cell-free culture supernatant (CFS) from the food-grade bacterium Limosilactobacillus fermentum GBE18 on the proliferation, differentiation, and mineralization of MC3T3-E1 pre-osteoblasts. GBE18 CFS exhibited no cytotoxicity at concentrations ranging from 1% to 4% (v/v). Notably, 2% (v/v) CFS significantly enhanced alkaline phosphatase (ALP) activity and extracellular matrix mineralization (p < 0.05). Transcriptomic profiling revealed that differentially expressed genes were enriched in osteoblast-related processes and two key signaling pathways: Wnt/β-catenin and PI3K/Akt. Subsequent qRT-PCR and Western blot analyses confirmed the upregulation of critical regulators (Rspo2, Pdpk1, Malat1) and demonstrated coordinated activation of Akt phosphorylation, β-catenin stabilization, and Runx2 protein expression. Our findings indicate that GBE18 CFS promotes osteogenic differentiation through coordinated modulation of the PI3K/Akt and Wnt/β-catenin pathways. Consequently, this study provides mechanistic evidence supporting the potential application of L. fermentum GBE18-derived metabolites as functional food ingredients or dietary interventions for bone health and osteoporosis management. Full article

Oligodendroglial cells are the myelinating glial cells of the central nervous system (CNS), and their morphological differentiation is a prerequisite for efficient myelin formation, which is essential for proper neuronal function. While oligodendroglial morphological changes normally proceed through tightly regulated developmental transitions, disruption of the underlying molecular mechanisms can lead to aberrant cellular phenotypes characterized by either premature, insufficient, or excessive differentiation. Although the phosphatidylinositol 3-kinase (PI3K) and its downstream Akt kinase signaling are well established as major drivers of oligodendrocyte morphological differentiation, myelination, and CNS white matter formation, how its negative regulator, phosphatase and tensin homolog (PTEN), is involved in the regulation of oligodendroglial morphogenesis remains incompletely understood. Recent genetic studies have highlighted a spectrum of disorders caused by PTEN dysfunction, conceptually established but currently evolving as PTENopathy, which has been partially associated with white matter abnormalities. Here, we report that, in an experimental model using the FBD-102b cell line, a well-established model of oligodendroglial cell differentiation, chemical inhibition of PTEN enhances pronounced morphological changes characterized by widespread membranes, accompanied by increased expression of differentiation and/or myelin marker proteins. We then focused on Rho family small GTPases, central regulators of cell morphogenesis, and examined their potential involvement downstream of this signaling. Expression of the RhoG-binding domain (RBD) of engulfment and cell motility 1 (ELMO1) attenuated the increased morphological changes. Similarly, inhibition of downstream Akt signaling also reversed these changes. Taken together, these results provide insight into how balanced regulation between PTEN and downstream signaling molecules governs oligodendroglial cell differentiation and suggest that dysregulation of this signaling equilibrium may contribute to cellular phenotypes relevant to disease-associated cellular alterations. Full article

Background/Objectives: Chemically induced hepatotoxicity is widely used in experimental research to model liver disease pathophysiology and to support preclinical studies. Thioacetamide (TAA) is a well-established hepatotoxic agent in conventional laboratory rodents; however, its effects in synanthropic rats—characterized by genetic heterogeneity and chronic environmental exposure—remain poorly defined. This study aimed to establish and characterize a preclinical model of TAA-induced hepatotoxicity in synanthropic rats and to assess its relevance for experimental liver disease research. Methods: Female synanthropic rats representing four phenotypic variants (albino, mottled, black, and brown; total n = 132) were housed under controlled conditions and assigned to control or TAA-treated groups. TAA was administered intraperitoneally at doses ranging from 200 to 300 mg/kg. Clinical parameters, including body weight and vital signs, were periodically monitored. Hematological profiles and serum biochemical markers of liver function were analyzed. Hepatic injury was evaluated by histopathological examination using hematoxylin–eosin staining. Statistical analyses were performed using R software, with p ≤ 0.05 considered statistically significant. Results: TAA-treated rats developed consistent clinical manifestations of hepatotoxicity, including progressive weight loss and reduced activity. Biochemical analyses revealed significant increases in serum transaminases, gamma-glutamyl transferase, and alkaline phosphatase, accompanied by alterations in hematological parameters. Histological evaluation demonstrated dose-dependent liver injury characterized by centrilobular necrosis, inflammatory infiltration, hepatocellular degeneration, and architectural disruption across all synanthropic rat variants. Conclusions: Synanthropic rats exhibit reproducible biochemical, hematological, and histopathological features of TAA-induced liver injury comparable to those reported in conventional laboratory strains. This model represents a robust preclinical approach for studying chemically induced hepatotoxicity and may provide enhanced translational relevance due to its genetic and environmental heterogeneity. Full article

Bone morphogenetic protein-2 (BMP-2) and vascular endothelial growth factor (VEGF) play a pivotal role in promoting osteogenesis and angiogenesis that concurrently take place during bone regeneration. The rapid degradation and diffusion of these growth factors, combined with the potential side effects associated with their exogenous insertion, limit their applications. To overcome these shortcomings, we developed a controlled release system for BMP-2 and VEGF on microspheres comprising gelatin (Gel) and polyvinyl alcohol (PVA). We fabricated Gel–PVA microspheres using a constant Gel concentration of 10% w/v and a varied PVA concentration of 0, 5, and 10% w/v (Gel–PVA0%, Gel–PVA5%, and Gel–PVA10%, respectively). The microspheres were loaded with the model protein bovine serum albumin (BSA) first. The Gel–PVA10% microspheres demonstrated significantly higher loading capacity and encapsulation efficiency, as well as lower cumulative release rate, compared to the Gel–PVA5% ones when loaded with BSA. Thus, the microspheres with the Gel–PVA10% composition were selected for loading with BMP-2 and VEGF. Kinetic studies of BMP-2 and VEGF loaded into Gel–PVA10% microspheres indicated similar results to those with BSA. The microsphere concentration with the optimal cytocompatibility was 0.5 mg/mL, and it was applied for the assessment of the osteogenic differentiation using bone marrow-derived mesenchymal stem cells (MSCs), and for the angiogenic differentiation in Wharton jelly and adipose-derived MSCs. Alkaline phosphatase activity, collagen secretion, and calcium mineralization were significantly upregulated in the presence of BMP-2-loaded microspheres, while tubular formation and PECAM-1 secretion were significantly higher in VEGF-loaded microspheres compared to the unloaded control, demonstrating their effectiveness as drug delivery carriers. Full article

Glycation of superoxide dismutase 1 (SOD1) has been shown to modulate the cytosolic levels of phosphorylated TAR DNA-binding protein 43 (TDP-43), a hallmark of amyotrophic lateral sclerosis (ALS) pathology. In this study, we investigated the interaction between TDP-43 and SOD1 and assessed how methylglyoxal (MGO)-induced glycation and the ALS-associated G93A SOD1 mutation affect this interplay in H4 cells. MGO exposure reduced SOD1 activity and TDP-43 phosphorylation in cells expressing WT SOD1, but not in those expressing G93A SOD1. Both WT and mutant SOD1 interacted with TDP-43 in the nucleus and cytosol; however, cytosolic interactions were more prevalent in G93A-expressing cells. Although MGO did not significantly alter the overall interaction between TDP-43 and WT SOD1, it induced cytosolic inclusion formation at 0.4 mM, a concentration associated with reduced cell viability. These inclusions did not colocalize with stress granules, indicating alternative aggregation pathways. Treatment with cyclosporin A, which inhibits the phosphatase calcineurin, decreased both TDP-43–WT SOD1 inclusions and cytosolic interactions between TDP-43 and G93A SOD1. Together, these findings suggest that SOD1 damage, induced by glycation or ALS-linked mutation, may affect TDP-43 phosphorylation status and promote its cytosolic mislocalization and aggregation, providing new insights into ALS-associated proteinopathy. Full article

Background/Objectives: Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder for which there are limited pharmacotherapies. Sodium rutin (NaR), a soluble flavonoid derivative, has shown beneficial metabolic effects, but its role in NAFLD remains unclear. This study investigates whether NaR ameliorates high-fat diet (HFD)-induced NAFLD and insulin resistance through promoting hepatic lipophagy. Methods: Male mice aged 8 weeks old were fed a HFD for 12 weeks with/without NaR supplementation. Body weight was measured every week. After 12 weeks of treatment, GTT and ITT were performed to assess insulin resistance. Then, the tissues were collected and hepatic histology, serum biochemistry, and markers of autophagy and senescence were assessed. Results: NaR treatment significantly attenuated HFD-induced weight gain, reduced visceral fat and liver weights, and ameliorated hepatic steatosis and vacuolization. NaR improved serum lipid profiles; lowered alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase levels; and reduced hepatic cellular senescence. NaR enhanced hepatic autophagy, evidenced by decreased p62 levels, increased LC3-II/LC3-I ratio, and enhanced colocalization of lipid droplets with LC3 and LAMP1 in vivo and in vitro. These changes were accompanied by improved glucose tolerance and insulin sensitivity. Conclusions: NaR effectively alleviates HFD-induced NAFLD and insulin resistance by activating hepatic lipophagy. These findings support NaR as a promising multi-targeted therapeutic candidate for NAFLD. Full article

Background and Aim: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by immune dysregulation. Environmental factors, including infectious agents, have been proposed to influence disease activity in inflammatory bowel disease. Although Borrelia burgdorferi has been shown to exert complex immunomodulatory effects on host immune responses, its seroprevalence and potential association with disease activity in patients with ulcerative colitis have not been systematically investigated. This study aimed to evaluate the seroprevalence of Borrelia burgdorferi IgG antibodies in patients with ulcerative colitis and to assess the relationship between seropositivity and laboratory markers of disease activity. Methods: In this retrospective observational study, 100 patients with ulcerative colitis (59 males, 41 females; mean age 48.5 ± 17 years) who underwent Borrelia burgdorferi IgG serological testing due to musculoskeletal or neurological symptoms suggestive of possible Lyme disease between October 2020 and October 2024 were included. Demographic characteristics, hematological and biochemical parameters, and inflammatory markers were compared between seropositive and seronegative groups. Due to the retrospective design, validated clinical disease activity indices were not consistently available; therefore, disease activity was indirectly assessed using laboratory inflammatory markers. Results: Among patients with ulcerative colitis, 22% were seropositive for Borrelia burgdorferi IgG. Seropositive patients had significantly lower uric acid, alkaline phosphatase, and C-reactive protein levels compared to seronegative patients (p = 0.001, p = 0.023, and p = 0.020, respectively). Free T4 levels were significantly higher in the seropositive group (p = 0.049). In terms of erythrocyte indices, mean corpuscular volume and mean corpuscular hemoglobin were significantly higher, while RDW-CV values were significantly lower in seropositive patients (all p < 0.05). Conclusion:Borrelia burgdorferi IgG seropositivity in patients with ulcerative colitis was associated with lower laboratory markers of systemic inflammation and a more stable hematological profile. Although causality cannot be established, these findings may suggest a potential association between prior Borrelia exposure and a distinct inflammatory phenotype in UC; however, this relationship should be interpreted with caution. Further prospective and mechanistic studies are warranted to clarify the potential immunological interactions between environmental microbial exposure and inflammatory bowel disease activity. Full article

Continuous cropping obstacles in watermelon are closely linked to rhizosphere microbial imbalance, posing a major threat to the sustainability of the industry in Xinjiang. Exogenous additives are widely used to regulate soil health, yet comprehensive comparisons of their mechanisms and effects remain limited. In this study, a field experiment was conducted under continuous watermelon cropping conditions in Xinjiang to evaluate the impact of eight treatments, including chemical fertilizer (NPK) alone and its combination with organic fertilizer (NPKM), glucose (NPKG), oxalic acid (NPKOA), amino acids (NPKGA), citric acid (NPKCA), and acetic acid (NPKAA), with unfertilized soil as the control (CK). Treatment effects were assessed through soil physicochemical analysis, fruit quality evaluation, and high-throughput sequencing (16S rRNA and ITS). Among all treatments, NPKM showed the greatest improvement in soil fertility, increasing soil organic matter by 13.91%, total nitrogen by 23.08%, and single fruit weight by 35.75% compared to CK. NPKGA also enhanced fruit weight (+33.06% vs. CK) and increased catalase activity, while oxalic acid exhibited the strongest activation of alkaline phosphatase. Microbiome analysis revealed that NPKM and NPKAA significantly reshaped both bacterial and fungal community structures. NPKM enriched beneficial taxa such as unclassified Chitinophagaceae and Lophotrichus, whereas NPKCA enriched the biocontrol bacterium Pseudomonas chlororaphis. Soil organic matter and total nitrogen were identified as key environmental drivers, showing significant positive correlations with core bacterial genera (Dokdonella) and negative correlations with the pathogenic fungus Alternaria. Collectively, this study elucidates the distinct mechanisms of various additives by linking treatment-specific microbial shifts to key soil factors and crop performance, providing a theoretical and technical framework for mitigating watermelon continuous cropping obstacles through rhizosphere environmental regulation. Full article

Cyprinid herpesvirus 3 (CyHV-3) is a pathogen that causes high mortality in common carp (Cyprinus carpio) and koi. Common carp breeding lines with different genetic backgrounds exhibit different resistance levels to viral pathogens. This study aimed to determine the differences in CyHV-3 disease resistance performance between the hybrid offspring (Y × M and M × Y) of the mirror carp ‘Longke 11’ (resistant to CyHV-3) and Yellow River carp, as well as the self-crossed offspring (M and Y). The M, Y × M, M × Y and Y groups were infected with CyHV-3 by immersion. The order of mortality and the duration of death for the four groups of carp were as follows: Y group > Y × M group > M × Y group > M group. Throughout the entire infection stage, the mRNA expression levels of the viral factors thymidine kinase (TK) and open reading frame 72 (ORF72) in the four groups of carp tended to first increase but then decrease. The viral factor expression evaluated on days 30 and 31 post-infection (p.i.), which was the peak of infection mortality, was the highest in the Y group and the lowest in the M group, and compared with the Y × M group, the M × Y group had considerably lower viral gene expression (p < 0.05). The immune-related enzyme activity and content levels of the four carp groups matched the patterns of viral gene expression. On day 29 p.i., a time point with high mortality, the levels of alkaline phosphatase (AKP), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were significantly the lowest in the Y group and significantly the highest in the M group, while the Y × M group showed a significant decrease compared to the M × Y group (p < 0.05). Quantitative real-time (q-PCR) analysis revealed that interleukin-21 receptor (IL21R), interferon regulatory factor 9 (IRF9), interferon type I (IFN-I), interleukin-6 (IL-6) and microtubule-associated protein light chain 3 (LC3), exhibited an initial increase followed by a decrease among the four experimental groups of common carp. In the peak mortality period of carp in the four groups (30 days post-infection), the expression levels of IL21R, IRF9, LC3, and IFN-I were significantly the highest in the M group and significantly the lowest in the Y group, with the mRNA expression of these genes in the M × Y group being significantly higher than that in the Y × M group (p < 0.05). In contrast, IL-6 expression levels exhibited the opposite trend. In this study, the M group exhibited the greatest resistance to CyHV-3, followed by the M × Y group, whose resistance was greater than that of the Y × M group, with the Y group showing the lowest disease resistance. Our findings demonstrate that hybridization modulates resistance to CyHV-3. Furthermore, we identified conserved immune signatures common to both susceptible and resistant carp, including the activation of nonspecific immunity and the upregulation of immune-associated genes. Full article

Background/Objectives: Feeding with a ketogenic diet (KD), nutritionally devoid of carbohydrates, may be metabolically beneficial. The administration of a KD to mice after previous feeding with a high-fat, high-carbohydrate diet (HFD) induced weight loss, ketonemia, and glycemic normalization. Here, to compare organ-specific responses to KD, we analyzed lipogenic and gluconeogenic enzymes and genes in the liver and kidney of mice submitted to KD versus (i) HFD or (ii) a saccharose-enriched diet. Methods: Liver and kidney were from (i) mice fed a HFD followed by an 8-week switch to a chow diet (CD), KD continuation of HFD, and (ii) mice submitted to CD, KD, or a saccharose-enriched diet for 1 week. Protein expression levels were determined by Western blotting, and gene expression by qPCR. Hepatic lipid accumulation was visualized by red oil-O. Results: Switch to a KD led to a simultaneous decrease in lipogenic FASN (Fatty Acid Synthase), ACC (Acetyl-CoenzymeA Carboxylase), and its phosphorylated form (pACC-Ser79) in the liver and kidney. In parallel, we observed increased activating phosphorylation of AMPK, the kinase responsible for ACC phosphorylation. In the liver, but not in the kidney, the gluconeogenic rate-limiting enzyme G6Pase (Glucose 6-phosphatase) was repressed under a KD. The switch to a CD significantly reduced hepatic fat accumulation, while a switch to a KD did not allow a significant reversal of hepatic fat accumulation, suggesting resilience to hepatic fat loss under KD. Comparison of a KD versus saccharose-supplemented diet showed an opposite expression pattern of lipogenic enzymes. Conclusions: Administration of KD after previous HFD induced convergent repression of lipogenic enzymes in the liver and kidney, and specific repression of G6Pase in the liver, suggesting a role for kidney gluconeogenesis during KD. KD versus saccharose-supplemented diet had opposite effects on lipogenesis and glycemic control, but both induced loss of lean body mass. Full article

Tropical grasses are increasingly present in farming systems in Brazil. However, a national-scale assessment of this practice’s impact on soil health (SH) and soybean yield has been lacking. In this study, we conducted a meta-analysis of 55 studies published until February 2026, comprising field trials run in 33 locations in Brazil, aiming to assess the effects of deep-rooted tropical grasses as preceding crops on biological indicators of SH and soybean yield. Results showed that grasses (Urochloa spp. and Megathyrsus maximus) promote soybean yield by 15%, representing an average increase of 515 kg ha⁻¹ and an additional revenue of US$198 ha⁻¹. The analysis of forage grass species used, management system (single or intercropped), soybean cultivar (growth habit, life cycle, genetic modification), and edaphoclimatic controlling factors revealed positive effects of tropical grasses on soybean yield under all the study conditions and yield ranges. SH indicators also showed sizeable increment, notably the activity of arylsulfatase (+35%) and β-glucosidase (+31%), followed by acid phosphatase activity (+20%), microbial biomass carbon (+24%), and organic carbon (+11%). The results confirmed the beneficial effects of deep-rooted tropical grasses, highlighting their contribution to sustainable intensification in tropical farming systems due to their ability to enhance SH. This, in turn, leads to increased soybean yield under most agronomic and environmental conditions. Full article

The majority of terrestrial plant species establish below-ground interconnections via arbuscular mycorrhizal (AM) mycelium, thereby forming extensive common mycorrhizal networks (CMNs). CMNs serve as critical infrastructure for nutrient acquisition, mediating soil nutrient capture and distribution. In nitrogen-fixing plants, phosphorus (P) transport is particularly dependent on functional CMNs. The rapid expansion in graphene oxide (GO) production and its broad application have raised significant ecological concerns, particularly regarding its potential impacts on terrestrial ecosystems. Despite these concerns, the impact of GO on P transport dynamics within legume–arbuscular mycorrhizal fungi (AMF) symbioses remains critically scarce. This study established a symbiotic system using the model nitrogen-fixing legume Medicago sativa L. and AMF. This experimental system enabled a comprehensive assessment of GO effects on rhizosphere P mobilization, plant P acquisition, CMNs architecture, fungal community composition, and expression of key P transporter genes. Our results demonstrated that high GO concentrations significantly altered rhizosphere properties, increasing pH while reducing organic acid content and alkaline phosphatase activity. Furthermore, GO exposure significantly inhibited root growth, mycorrhizal colonization rates, and plant P acquisition efficiency. Additionally, GO exposure altered AMF community composition, reduced rhizosphere microbial diversity, and suppressed P metabolism gene expression. Specifically, 0.6% GO induced significant downregulation of MsCS and GigmPT by 83.5% and 62.3%, respectively. This indicates that GO impairs plant P uptake by disrupting the core pathway involving GigmPT and MsCS, triggering P stress in M. sativa. Collectively, these findings provide compelling evidence that GO exposure disrupts legume–AMF symbiotic integrity, ultimately impairing P transport efficiency. Full article

Background and Objectives: This study aimed to evaluate associations between dental caries, periodontal pockets, and radiologically detected periapical lesions in relation to serum levels of Dickkopf-1 (Dkk-1) and tartrate-resistant acid phosphatase 5B (TRAP-5B) in oncologic patients with ear, nose, and throat (ENT) cancer compared with healthy controls. Materials and Methods: The study included 63 subjects divided into a study group of 33 patients diagnosed with ENT cancer and a control group of 30 healthy individuals. Blood samples were collected to assess serum Dkk-1 levels using a sandwich enzyme immunoassay and TRAP-5B levels. Radiological dental evaluation included orthopantomography (OPT) and cone beam computed tomography (CBCT) to assess the number and depth of dental caries and the presence of periapical lesions. Periodontal pockets were recorded through clinical examination. Results: Serum biomarker analysis demonstrated significant differences between groups: TRAP-5B levels were significantly higher in patients with ENT cancer, whereas Dkk-1 concentrations were significantly lower compared with healthy controls (p < 0.001). OPT revealed up to eight carious lesions in both groups. The mean number of carious lesions was higher in healthy subjects (2.97 ± 2.48) than in patients with ENT cancer (2.06 ± 2.29). CBCT evaluation revealed 0–8 carious lesions in healthy individuals and 0–6 lesions in patients with ENT cancer, with a significantly higher mean number of lesions in the control group (2.97 ± 2.48 vs. 1.85 ± 1.89). Periodontal pockets were more frequent in patients with ENT cancer (0.67 ± 1.32) than in controls (0.37 ± 0.81). OPT evaluation also showed a higher mean number of periapical lesions in patients with ENT cancer (0.82 ± 1.29) compared with controls (0.37 ± 0.67). CBCT examination demonstrated that the mean number of periapical lesions in patients with ENT cancer was more than twice that of the control group, although this difference did not reach statistical significance. Conclusions: Patients with ENT cancer exhibited significantly altered systemic bone turnover biomarker profiles, characterized by increased TRAP-5B and decreased Dkk-1 levels. Clinically, these patients also presented a higher prevalence of periodontal pockets and periapical lesions, whereas carious lesions were more frequently detected in healthy individuals. The combined radiological and biochemical findings contribute to a better understanding of oral–systemic interactions in oncologic patients and highlight the importance of comprehensive dental evaluation prior to oncologic therapy. Full article