Search Results (270)

Background/Objectives: Type 2 diabetes mellitus (T2DM) is associated with progressive hepatic alterations, including steatosis and fibrosis, which may affect liver mechanical properties. Shear wave elastography (SWE) is a non-invasive imaging technique that enables quantitative assessment of tissue stiffness; however, its application in diabetic animal models remains limited. This study aimed to evaluate liver elasticity using SWE in a high-fat diet (HFD) and streptozotocin (STZ)-induced rat model of T2DM, using histopathological examination as the reference standard. Methods: Twenty-four rats were randomly allocated to either a control group (n = 12) or a diabetic group (n = 12). Diabetes was induced using HFD feeding followed by low-dose STZ administration. Liver elasticity was assessed in vivo using SWE at two examination sessions. Shear wave velocity measurements were obtained from eight liver regions of interest and expressed in meters per second (m/s). Following euthanasia, liver tissues were subjected to histopathological evaluation using hematoxylin and eosin, Masson’s trichrome, and periodic acid–Schiff staining. Results: Diabetic rats demonstrated marked histopathological alterations, including macrovesicular and microvesicular steatosis, hepatocellular vacuolization, increased collagen deposition, and glycogen depletion. Collagen deposition was significantly greater in diabetic animals, while glycogen content was significantly reduced (3.70 ± 1.05 vs. 26.87 ± 2.87; p < 0.05). SWE revealed consistently higher liver shear wave velocities in diabetic rats compared with controls at both examination sessions. Although liver stiffness increased over time in both groups, these changes did not reach statistical significance. Conclusions: HFD/STZ-induced diabetes was associated with increased liver stiffness and histopathological evidence of hepatic injury and fibrosis. SWE may represent a feasible non-invasive approach for assessing diabetes-related changes in liver mechanical properties. Full article

Background: Coronary artery bypass grafting (CABG) is the standard revascularization procedure, and the left internal mammary artery (LIMA) is the most widely used conduit owing to its long-term patency and favorable impact on survival. Although fibrosis and calcification are comparatively infrequent in internal mammary artery (IMA) grafts, progressive remodeling may still compromise patency. Tumor necrosis factor-α (TNF-α) is a pro-inflammatory cytokine implicated in vascular remodeling and calcification, whereas L-arginine, a precursor of nitric oxide, may exert vasoprotective effects. Aim: To investigate the effects of ex vivo TNF-α and combined TNF-α plus L-arginine treatment on the morphology, calcification, elemental composition, and biomechanical properties of human LIMA grafts. Patients and Methods: LIMA graft segments from 18 male CABG patients were allocated to one control group (G0) and two ex vivo treatment groups. Grafts were assessed using hematoxylin and eosin and Masson’s Trichrome staining under brightfield microscopy, using Alizarin Red S fluorescence staining to measure calcification, and by scanning electron microscopy with energy-dispersive spectroscopy (SEM/EDS) to assess ultrastructure and elemental composition. Scanning acoustic microscopy (SAM) was used to derive acoustic impedance as a label-free index of tissue stiffness. Results: TNF-α treatment was associated with increased acoustic impedance, consistent with graft stiffening, together with greater calcification signatures, whereas combined TNF-α and L-arginine treatment shifted impedance toward control-like values and showed more organized tissue architectures with reduced calcification. Conclusions: In this preliminary ex vivo model, L-arginine attenuated TNF-α-associated remodeling and stiffening of LIMA grafts, suggesting a potential role in supporting graft durability; larger, statistically powered studies with molecular validation are required to confirm these findings. Full article

Background: Diabetic cardiomyopathy (DCM) is characterized by myocardial inflammation, apoptosis, and fibrosis that contribute to ventricular remodeling and dysfunction. We investigated the effects of 5-methoxytryptophan (5-MTP) on histopathological and molecular markers of myocardial remodeling in a rat model of DCM. Methods: Forty-eight Sprague–Dawley rats with DCM induced by a high-fat high-fructose diet and low-dose streptozotocin (25 mg/kg) were randomized to control or 5-MTP treatment (25, 50, or 100 mg/kg) and evaluated after 8, 16, and 32 days. Histopathological assessment using hematoxylin–eosin and Masson’s trichrome staining, along with immunohistochemical analysis of inflammatory, apoptotic, and fibrotic markers, was performed. Results: Myocardial inflammatory histopathological scores did not differ significantly among groups. Myocardial fibrosis assessed by Masson’s trichrome staining was significantly reduced at day 16 (p = 0.020), with all 5-MTP doses demonstrating lower fibrosis scores than DCM controls. Collagen I expression did not differ significantly. Caspase-3 expression was significantly reduced in all treatment groups at day 16 (p = 0.029), with persistent reduction at day 32 only in the 100 mg/kg group (p = 0.004). Early molecular modulation was observed through reduced TGF-β expression at day 8 in the 25 mg/kg and 50 mg/kg groups, followed by reduced SMAD3 expression at day 16 in the 25 mg/kg and 100 mg/kg groups. At day 16, AKT expression increased in the 25 mg/kg group, while cytoplasmic NF-κB expression decreased in the 25 mg/kg and 100 mg/kg groups. Conclusion: 5-MTP demonstrated time-dependent changes in molecular and histopathological markers associated with myocardial remodeling in experimental DCM. Full article

Background/Objectives: Silicosis is a progressive occupational lung disease characterized by persistent inflammation and irreversible pulmonary fibrosis. Reliable circulating biomarkers for the early detection of fibrotic remodeling and monitoring of disease progression remain limited. Prolidase, a key enzyme involved in collagen turnover and extracellular matrix remodeling, has emerged as a potential biomarker in fibrotic disorders. Therefore, this study aimed to evaluate the potential role of serum prolidase as a biomarker for fibrotic remodeling and treatment monitoring in an experimental rat model of silicosis. Methods: Male Wistar rats were divided into three groups: control, silicosis, and silicosis plus nintedanib. Silicosis was induced by intratracheal crystalline silica instillation. Nintedanib was administered by gastric gavage at 50 mg/kg/day from day 10 to day 30. Lung tissues were evaluated histopathologically using hematoxylin and eosin and Masson’s trichrome staining. Serum prolidase, fibroblast growth factor-2 (FGF-2), platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF-β) levels were measured by enzyme-linked immunosorbent assay (ELISA). Results: Histopathological injury scores were significantly increased in the silicosis group and were attenuated by nintedanib treatment. Serum prolidase levels were significantly higher in both silica-exposed groups than in controls (p = 0.017), but did not differ significantly between untreated and nintedanib-treated animals. TGF-β, FGF-2, and PDGF levels were also significantly elevated following silica exposure. Serum prolidase showed a strong positive correlation with TGF-β (r = 0.69, p < 0.001). ROC analysis demonstrated good diagnostic performance for prolidase (AUC = 0.877), while the combined Prolidase + TGF-β model further improved discrimination (AUC = 0.969). The internally validated multivariable biomarker panel maintained high diagnostic accuracy after leave-one-out cross-validation (LOOCV) (AUC = 0.892). Conclusions: Serum prolidase may serve as a potential circulating biomarker of silica-associated fibrotic remodeling. Although nintedanib improved histopathological lung injury, persistently elevated prolidase levels suggest ongoing extracellular matrix remodeling rather than short-term treatment response. Further longitudinal experimental and clinical studies are warranted to validate its diagnostic and prognostic utility. Full article

Nano-engineering strategies have been increasingly applied to enhance the biological performance of calcium silicate-based materials; however, the optimal concentration of nano-hydroxyapatite (HANP) remains unclear. This study evaluated the bone-healing response to different concentrations of HANP incorporated into mineral trioxide aggregate (MTA) and bioceramic (BC) sealers in an experimental rabbit model. Thirty adult New Zealand white rabbits were allocated into two experimental groups according to sealer type: HANP-modified MTA and HANP-modified BC (n = 15 each). Two standardized circular intrabony defects were created bilaterally in the maxillary diastema of each rabbit. In the MTA group, the right-side defects were filled with 2% and 4% HANP-modified MTA, while the left-side defect received 6% HANP-modified MTA, and the adjacent defect was left untreated as a control. The same protocol was followed for the BC group using corresponding HANP concentrations. Five rabbits per group were sacrificed at 2, 4, and 8 weeks postoperatively for histopathological hematoxylin and eosin (H&E) and Masson trichrome staining. The results demonstrated significant differences among groups at all time points, with 4% HANP showing the most favorable biological response, including reduced inflammatory cell infiltration, increased new bone formation, and improved collagen organization compared with lower and higher concentrations. Pairwise comparisons at matched HANP concentrations revealed no statistically significant differences between HANP-modified MTA and BC groups. These findings indicate that HANP incorporation enhances the biological performance of calcium silicate-based sealers in a concentration-dependent manner, with 4% representing the most favorable response among the concentrations evaluated for promoting bone regeneration. Full article

In spinal pathology, lumbar disc herniation (LDH) is typically contrasted with lumbar spinal stenosis (LSS) based on either its pathophysiology (structural compression vs. dynamic/vascular/degenerative changes) or its clinical presentation (acute radiculopathy vs. chronic claudication). We compared the ligamentum flavum (LF) tissue, primary LF cells, and serum cytokine profiles using human cytokine antibody arrays and Western blotting between patients with LDH (n = 17) and LSS (n = 23). LF specimens underwent hematoxylin–eosin, Masson’s trichrome, and immunohistochemical staining. Compared with LSS, LDH specimens showed relatively preserved LF architecture and higher tissue levels of IL-7, IL-10, eotaxin-3, HGF, and TGF-β2, suggesting an earlier immune-regulatory and reparative phase. In contrast, LSS specimens showed fragmented elastic fibers, increased collagen accumulation, and significantly elevated OPG in primary LF cell cultures. Serum cytokine profiles did not differ significantly between groups. These findings suggest that LDH-associated LF changes may involve immunoregulatory and repair-related cytokine expression, whereas LSS represents a more fibrotic, OPG-enriched remodeling phenotype. TGF-β2, eotaxin-3, and the RANKL/OPG pathway merit further evaluation as stage-specific biomarkers. Full article

Background/Objectives: Severe mitral regurgitation (MR) is associated with chronic atrial stretch, chamber enlargement, pulmonary pressure elevation, and atrial fibrosis, yet the relationship between tissue inflammatory/profibrotic signaling, histologically quantified fibrosis, and echocardiographic remodeling remains incompletely characterized. This study aimed to compare biatrial tissue remodeling in patients with severe MR undergoing mitral valve surgery with a practical non-valvular surgical comparator group undergoing isolated coronary artery bypass grafting (CABG). Methods: This single-center, observational, cross-sectional comparative study included 36 elective cardiac-surgery patients: 22 with severe MR and 14 undergoing isolated CABG without significant valvular disease. Left- and right-atrial tissue samples were collected intraoperatively. IL-6, TNF-α, and TGF-β expression was assessed by quantitative real-time PCR using pooled atrial samples stratified by atrial side and study group, whereas atrial fibrosis was quantified histologically on individual tissue specimens using Masson’s trichrome staining and digital image analysis. Clinical, laboratory, and echocardiographic parameters were compared between groups, and exploratory associations were assessed with cautious interpretation. Results: Compared with the CABG comparator group, patients with severe MR showed a pooled molecular profile compatible with higher aggregate atrial expression of IL-6, TNF-α, and TGF-β; because qPCR was performed on pooled tissue preparations, these molecular findings were interpreted descriptively and were not used for patient-level inferential statistics. Histologically quantified fibrosis was significantly increased in severe MR in both the left atrium (29.69 ± 12.26% vs. 12.17 ± 4.56%, p < 0.0001) and the right atrium (25.25 ± 11.33% vs. 9.01 ± 4.46%, p < 0.0001). The MR group also showed more pronounced echocardiographic remodeling, including larger estimated left atrial volume, higher pulmonary artery systolic pressure, and greater right ventricular diameter. Exploratory individual-level analyses were restricted to histological fibrosis and echocardiographic variables. Conclusions: Severe MR was associated with marked echocardiographic remodeling and significantly greater histologically quantified biatrial fibrosis compared with a CABG surgical comparator group. Pooled qPCR findings support an aggregate inflammatory/profibrotic signal, but they should be interpreted descriptively because individual-level molecular variability could not be assessed. These findings are hypothesis-generating and do not establish causality. Full article

Background: Branched-chain amino acids (BCAAs) regulate muscle protein metabolism, yet the systematic characterization of their dose-dependent morphological effects on exercised skeletal muscle remains limited. This study investigated the dose–response relationship between BCAA supplementation and skeletal muscle adaptations in exercise-trained mice. Methods: Seventy male Kunming mice were randomly assigned to seven groups (n = 10): a background group (no exercise), a control group (exercise + saline), and five exercise groups receiving BCAAs at 1–5 g/kg/day via intragastric gavage. Mice in the exercise groups performed 45 min of swimming daily (6 days/week) for 50 days. Gastrocnemius muscles were processed using hematoxylin–eosin staining, Masson trichrome staining, Gomori aldehyde fuchsin staining, and transmission electron microscopy. Data were analyzed using one-way ANOVA with Dunnett’s post hoc test. Results: BCAA supplementation increased gastrocnemius wet weight-to-body weight ratios and promoted denser fiber packing in a dose-dependent manner up to 3–4 g/kg/day. Deep-staining fiber proportion (putatively type II-like) increased progressively with BCAA concentration, plateauing at doses ≥ 3 g/kg/day, while elastic fiber content continued to rise through 5 g/kg/day. Mitochondrial size decreased as mitochondrial number increased; membrane and cristae thickness peaked at 3 g/kg/day. Sarcomere length, myofibril diameter, sarcoplasmic reticulum size, and transverse tubule diameter exhibited increasing trends. Conclusions: These findings establish a parameter-specific dose–response framework for BCAA-induced muscle remodeling. A supplemental dose of 3 g/kg/day above background dietary intake represents an effective threshold for maximizing indices of hypertrophic gains and mitochondrial structural maturation potentially indicative of functional enhancement. Higher doses (≥4 g/kg/day) elicited additional benefits in fiber density, mitochondrial proliferation, and elastic fiber content. Supplemental BCAA dosing strategies above constant background intake should be tailored to target specific structural outcomes, with functional validation required to confirm physiological relevance. Full article

Background: Tranilast is an anti-inflammatory and antifibrotic agent known to inhibit TGF-β-mediated fibroblast activation and matrix overproduction. Although its therapeutic potential has been explored in several fibrotic and inflammatory conditions, its effects on tendon healing remain unknown. This study aimed to evaluate the histopathological and biomechanical impact of tranilast in a rat Achilles tendon repair model. Methods: Thirty-two male Sprague–Dawley rats were randomly assigned to four subgroups, control (C-15, C-30) and tranilast-treated (TR-15, TR-30), and sacrificed on postoperative day 15 or 30. Tranilast (30 mg/kg/day) or placebo was administered intraperitoneally. Tendons were subjected to biomechanical testing (maximum load to failure) and histological evaluation using Bonar and Movin scoring systems on Hematoxylin + Eosin (HE)-, Masson Trichrome (MT)- and Alcian Blue (AB)-stained slides. Additional analyses included Sirius Red histochemistry with assessment of collagen type I/III intensity and polarization ratio, as well as H-scores for collagen I and III. Results: Tranilast produced marked improvements in histopathological healing. Both TR-15 and TR-30 exhibited significantly lower Bonar and Movin scores compared with controls, with reductions in tenocyte degeneration, ground-substance accumulation, collagen disorganization, vascularity, and hyalinization (all p < 0.01). However, biomechanical strength did not differ significantly among the groups (p = 0.3948). Sirius Red analysis and collagen I/III H-scores revealed no significant differences in collagen composition or polarization ratio. Histological improvements were therefore not accompanied by measurable changes in collagen subtype distribution or maximum load to failure. Conclusions: Tranilast was associated with favorable histopathological changes during Achilles tendon healing, including improvements in cellular morphology, matrix organization, and overall Bonar and Movin scores. However, these findings were not accompanied by significant differences in collagen composition or biomechanical strength within the 30-day observation period. Further long-term and mechanistic studies are warranted to determine whether these histopathological changes translate into functional improvements in tendon biomechanics. Accordingly, the present findings should be considered preliminary and exploratory. Full article

Background: Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia resulting from impaired insulin secretion or action. Persistent hyperglycemia contributes to the development of micro- and macrovascular complications, particularly affecting the kidneys and leading to diabetic nephropathy through mechanisms involving oxidative stress, fibrosis and apoptosis. Purpose: This study aimed to investigate the protective effects of hesperidin and carvacrol, individually and in combination, on streptozotocin-induced diabetic nephropathy in a Type 1 diabetes rat model. Study design: An experimental in vivo animal study was conducted using a streptozotocin-induced Type 1 diabetic rat model. Methods: Sixty adult Wistar Albino rats were randomly divided into six groups (n = 10): Control, Diabetes, Vehicle, Diabetes + Carvacrol, Diabetes + Hesperidin, and Diabetes + Hesperidin + Carvacrol. Following a 6-week (42-day) experimental period, systemic necropsy was performed. Renal tissues were evaluated histopathologically using Periodic Acid–Schiff, Masson’s trichrome, and Best Carmine staining. Immunohistochemical analyses were conducted to assess Bcl-2, Bax, Caspase-3, Caspase-9 expression, and apoptotic cell death using the TUNEL assay. Results: Histopathological analysis demonstrated significant differences in tubular dilatation, intracellular vacuolization, and mesangial matrix expansion among groups (p < 0.05), whereas tubular atrophy, hyaline accumulation, mononuclear cell infiltration, and the number of sclerotic glomeruli were not significantly different (p > 0.05). Treatment with hesperidin and carvacrol significantly attenuated renal injury and fibrosis in diabetic rats (p < 0.001). Diabetic kidneys exhibited increased immunopositivity for Bax, Caspase-3, and Caspase-9 and decreased Bcl-2 expression (p < 0.001). Combined hesperidin and carvacrol treatment markedly reduced apoptotic cell numbers compared with the untreated diabetic group (p < 0.001). Conclusions: The combined administration of hesperidin and carvacrol exerts protective effects against diabetic nephropathy, potentially through modulation of the Bcl-2/Bax-mediated apoptotic pathway and attenuation of renal fibrosis. Full article

Introduction: The 3 Rs principle advocates developing alternative, biologically relevant models. Thus, 3D fish liver in vitro models have been increasingly used for ecotoxicological studies. We previously optimized spheroids from the rainbow trout non-tumoral liver cell line RTL-W1 and employed them to assess the effects of aquatic pollutants. Although they demonstrated potential for assessing ecotoxicological effects, further optimization is warranted to enhance their physiological relevance. Incorporating an extracellular matrix (ECM), such as collagen, has been shown to be a promising strategy to improve spheroids’ structural organization and functionality. Objective: This study aimed to optimize 3D culturing conditions of RTL-W1 spheroids by evaluating the effects of collagen supplementation on viability, morphology, and functional response. Methodology: Spheroids from the RTL-W1 cell line (60,000 cells per well) were cultured in 96-well ultra-low attachment (ULA) plates at 18 °C. After spheroids’ formation, rat tail collagen was supplemented at concentrations of 15 (C15), 30 (C30), and 60 (C60) µg/mL at culture days 7, 8, and 9. Spheroids were collected at two sampling days (10 and 14). Viability was assessed using alamarBlue and lactate dehydrogenase (LDH) assays, while morphology was assessed by optical microscopy. Collagen penetration was evaluated using Masson’s trichrome staining technique. Protein expression of cytochrome P450(CYP)1A was assessed by quantifying immunocytochemistry staining using an anti-CYP1A antibody. Results: On day 10, LDH leakage decreased in C15 and C60, compared with the control, whilst C15 spheroids showed lower absorbance levels in the alamarBlue assay. On day 14, LDH showed no significant differences; however, C30 and C60 had higher alamarBlue absorbance, indicating greater metabolic capacity. Spheroid morphology appeared intact in all conditions. Masson trichrome revealed collagen fibrils at the periphery of the spheroids, especially in C30 and C60, indicating that spheroids incorporated collagen. CYP1A immunostain was present in all conditions, localized in the spheroids’ border, and tended to be higher when supplementation occurred in earlier days. Conclusions: Our results suggest that RTL-W1 spheroids interacted with the collagen matrix and appeared to functionally improve. Data suggest that incorporating ECM may increase the complexity and physiological relevance of RTL-W1 spheroids, thereby better supporting mechanistic and ecotoxicological applications. Full article

Background: The formation of wounds or scars often compromises skin anatomy and function, necessitating effective management to restore tissue integrity. Current interventions, including wound debridement, hyperbaric oxygen therapy, antibiotics, wound dressings, and surgical procedures, can be effective but are sometimes limited by high costs and the increasing prevalence of drug resistance. These challenges highlight the need for innovative, cost-effective, and therapeutic alternatives. Method. Our earlier studies assessed the wound closure of wounded human-equivalent epidermal full-thickness skin model (HEFT-SM) with a limited number of Phytoceutical^® retinol micellar formulations for a six-day treatment and found that the retinol micellar formulation accelerated wound closure significantly. In this work, three different types of Phytoceutical^® retinoid formulations, namely 0.3% retinol, 0.3% retinaldehyde, and 0.03% retinoic acid on the early-stage wound healing efficacy and its collagen structure were studied. Haematoxylin and eosin (H&E) staining analysis was used to assess the wound repair of the 3 mm punch wound after two days and the wound healing efficacy defined as the wound diameter contraction in percentage was assessed. The collagen matrix was examined through the use of Masson’s trichrome staining and confocal laser scanning microscopy (CLSM) for both qualitative and spatial assessment. Results. All formulations promoted wound contraction, with efficacy ranging from 15 ± 1% to 35 ± 2% after two days. The 0.3% retinol micelles showed the highest activity (35 ± 2%), followed by retinaldehyde (32 ± 3%) and retinoic acid (15 ± 1%). In addition, all treatments appeared to stimulate collagen architectural changes suggestive of remodelling activity. Conclusions. The enhanced wound healing observed may be attributed to increased cellular proliferation and migration within the wound microenvironment, supporting epidermal differentiation and tissue stratification. Furthermore, this work showed that combination of Masson’s trichrome staining and confocal laser scanning microscopy (CLSM) is a novel approach for qualitative and spatial assessment of collagen structure. Full article

Background: Acrylamide (ACR), a toxic compound formed during high-temperature cooking of carbohydrate-rich foods, is known to induce multi-organ toxicity, including oxidative and inflammatory lung injury. N-Acetylcysteine (NAC), a precursor of glutathione (GSH), possesses potent antioxidant and anti-inflammatory properties that may counteract ACR-induced pulmonary damage. This study investigated the protective effects of NAC against ACR-mediated lung toxicity, with an emphasis on the GSK-3β/Nrf2/NF-κB signaling axis. Methods: Forty male Wistar rats were allocated into four groups: control, NAC (250 mg/kg/day), ACR (50 mg/kg/day), and NAC + ACR. After 11 days of treatment, lung tissues were examined histopathologically using H&E, PAS, and Masson’s trichrome stains. Oxidative stress biomarkers (MDA, SOD, GPx, CAT, GSH) were quantified biochemically. Immunohistochemistry and qRT PCR assessed expression of Nrf2, NF-κB, IL-1β, and Caspase 3, while ELISA measured TNF α, IL-6, Bax, Bcl 2, and GSK 3β. Results: ACR exposure resulted in severe lung injury characterized by alveolar wall edema, epithelial hyperplasia, leukocytic infiltration, goblet cell hyperplasia, and peribronchiolar collagen deposition. These pathological changes were accompanied by a marked increase in MDA, NF-κB, IL-1β, TNF α, IL-6, Bax, Caspase 3, and GSK 3β, together with significant reductions in antioxidant enzymes and Nrf2/HO 1/NQO1 expression. NAC co-administration significantly ameliorated ACR-induced lung damage, restoring normal histological architecture, reducing fibrosis, and normalizing goblet cell activity. NAC also reversed oxidative stress, enhanced Nrf2 and downstream antioxidant responses, suppressed NF-κB-mediated inflammation, and mitigated apoptosis. Notably, NAC downregulated ACR-induced GSK 3β activation, thereby contributing to balanced redox and inflammatory signaling. Conclusions: NAC confers significant protection against ACR-induced pulmonary toxicity through its antioxidant, anti-inflammatory, and anti-apoptotic activities. These effects are mediated, at least in part, by modulation of the GSK 3β/Nrf2/NF-κB pathway. NAC demonstrates promising therapeutic potential for preventing chemically induced lung injury. Full article

Background: The socket preservation technique involves filling the bone defect that occurs after a tooth is extracted with bone substitute material. This procedure helps to minimize bone resorption of the alveolar ridge following extraction. Various bone substitute biomaterials can be used for augmentation, including autogenous, allogeneic, and xenogeneic options. This study aimed to assess changes in alveolar ridge dimensions and variations in radiographic bone density in sockets grafted with two distinct biomaterials. Furthermore, bone biopsies collected from the grafted sites were subjected to histological analysis. Methods: Forty generally healthy patients were enrolled in the study and split into four equal groups. The first and third groups underwent first or second maxillary premolar extraction and received treatment with an allogeneic material (BIOBank®, Biobank, Paris, France), while the second and fourth groups underwent first or second mandibular molar extraction and were treated with a xenogeneic material (Geistlich Bio-Oss®, Geistlich Pharma AG, Wolhusen, Switzerland). Following tooth extraction, the appropriate biomaterial was inserted into the socket. It was covered with a collagen membrane (Geistlich Bio-Gide®, Geistlich Pharma AG, Wolhusen, Switzerland) and stabilized with sutures, which were removed seven to ten days after the procedure. Micro-CBCT scans were conducted to evaluate the dimensions of the alveolar ridge and the radiographic density of the grafted socket at 7–10 days and 6 months after the procedure. A bone trepanobiopsy was performed concurrently with implant placement six months after socket preservation. The obtained biopsy was analyzed histologically using hematoxylin and eosin (H&E) and Masson’s trichrome staining. Results: There was no statistically significant difference in alveolar ridge height or width preservation between allogeneic and xenogeneic biomaterials. After six months of healing, sockets grafted with both materials exhibited greater radiographic bone density, with significantly greater density observed in the xenograft group. Conclusions: The findings of this study suggest that the two biomaterials are comparable in their effectiveness at maintaining the dimensions of the alveolar ridge. However, the quality of the newly formed bone may differ depending on the type of biomaterial used. Full article

Dermal senescence is associated with reduced fibroblast activity, decreased extracellular matrix synthesis, and impaired tissue repair. Commercial injectable formulations containing poly-L-lactic acid (PLLA), hyaluronic acid (HA), and polydeoxyribonucleotide (PDRN)-associated compounds have been proposed for dermal remodeling approaches and modulate tissue-response pathways; however, comparative studies evaluating commercially available formulations under standardized experimental conditions remain limited. This study aimed to characterize the morphology of formulations containing PLLA, HA, and PDRN, used alone or in combination, by environmental scanning electron microscopy (ESEM), and to investigate formulation-associated histological and collagen-related molecular responses in a murine model. Formulations containing PLLA, HA, HA + PDRN, and PLLA, HA and PDRN were administered into the dorsal subcutaneous tissue of 14 Mus musculus mice (Swiss strain). After 30 days, tissue response was assessed by ultrasound, histological analysis with Masson’s trichrome staining, and RT-qPCR quantification of collagen-related gene expression. ESEM analysis revealed distinct morphological characteristics among the biomaterials, and the combined PLLA, HA and PDRN formulation exhibited a more complex and integrated multiphase structure. Histological analysis showed preserved tissue architecture in all groups, with no evidence of marked inflammatory response or structural disruption. RT-qPCR demonstrated significantly higher COL1A1 expression in the PLLA-only and PLLA, HA, and PDRN groups compared with controls (p < 0.05), whereas no significant differences were observed for COL2A1 or COL3A1. These findings indicate that PLLA-containing formulations were associated with selective COL1A1 upregulation under the evaluated conditions, suggesting formulation-associated collagen-related molecular responses in this short-term model. Full article