Background: To describe the severity and types of blast-related extremity injuries and the presence of accompanying vascular injuries (VI) and amputation, and to identify the associated factors affecting the treatment management and clinical course. Methods: The study included 101 patients with extremity injuries caused by a bomb explosion. The radiographs and computed tomography angiographies of the patients were evaluated in terms of injury patterns, presence of penetrating fragments and fractures, and localization (upper or lower extremity) and type (open or closed) of injury. The Gustilo-Anderson classification was used for open fractures. According to their severity, open fractures classified as types 1 and 2 were included in Group 1 and those classified as type 3A, 3B and 3C in Group 2. Results: As a result of blast exposure, 101 (57.7%) patients had extremity injuries, of which 76 (75.2%) presented with at least one fracture. Of the total of 103 fractures, nine (8.8%) were closed and 94 (91.2%) were open. Thirty-eight (40.4%) of the open fractures were located in the upper extremities, and 56 (59.6%) in the lower extremities and pelvis. Open fractures were most frequently localized in the femur (n = 20; 21.2%), followed by the tibia (n = 18; 19.1%). The majority of patients with open fractures were in Group 1 (71.4%). The duration of hospital stay was longer in Group 2 (12.1 ± 5.8 vs. 6.3 ± 6.7 days, p < 0.0001, respectively). Mortality among patients in Group 2 (45.0%) was significantly higher than in Group 1 (8.0%) (p < 0.0001). Similarly, the injury severity score (ISS) was higher in Group 2 (median 20 vs. 9, p < 0.0001). VI was present in 13 (12.9%) of all patients, and amputation in seven (7.9%). Conclusion: The presence of severe open fractures, VI, and high ISS score can be considered as important factors that increase morbidity and mortality. In extremity traumas, through the secondary blast mechanism, contaminated-fragmented tissue injuries occur. Therefore, we believe that it will be beneficial to apply damage control surgery in places with low socioeconomic level and poor hygienic conditions.

This study investigates whether intra-articular polyacrylamide hydrogel (iPAAG) provides superior outcomes compared to conventional injections, namely hyaluronic acid (HA) and corticosteroid, in managing knee osteoarthritis (KOA). This retrospective cohort study included primary KOA patients (Kellgren–Lawrence grade II–IV) treated between January 2023 and December 2024 with 1 of 3 intra-articular injections: iPAAG (6 mL Arthrosamid), HA (2 mL, 60 mg Artroaid), and Steroid (40 mg methylprednisolone acetate, Arhropan). Outcomes were assessed at baseline, 3, 6, and 12 months. Primary outcomes were the Visual Analog Scale (VAS) and Western Ontario and McMaster Universities Osteoarthritis Index. Clinically meaningful improvements were evaluated using minimal clinically important difference (MCID) and patient acceptable symptom state thresholds. A total of 150 patients (n = 50 per group) were included. The groups were comparable at baseline in median age (HA: 66; Steroid: 69.5; iPAAG: 69.5; P = .104), sex (female: 72%, 62%, 66%; P = .566), median body mass index (30.4, 30.6, 30.7 kg/m²; P = .716), and Kellgren–Lawrence distribution (P = .765). Baseline median VAS was 7, dropping to 3 in all groups at 3 months (P < .001). At 6 months, they rose to 4 (HA), 5 (Steroid), and 4 (iPAAG) (P < .001). By 12 months, VAS returned to baseline in HA and Steroid, while iPAAG remained slightly improved (P = .219). iPAAG outperformed Steroid at 6 months (P < .001), but not HA (P = 1.000). No significance at 12 months (P = .128). Baseline median Western Ontario and McMaster Universities Osteoarthritis Index scores were 49.5 (HA), 59.5 (Steroid), and 57 (iPAAG), improving at 3 months to 42.5, 48.5, and 45 (P < .001). At 6 months, scores were 45, 57, and 47.5 (P < .001). At 12 months, HA and Steroid returned to baseline, while iPAAG remained stable (P = .979). iPAAG was better than Steroid at 6 months (P = .008), but not HA (P = .066). Although overall differences at 12 months were significant (P = .044), pairwise comparisons were not. iPAAG showed the highest patient acceptable symptom state rates (72%, 54%, and 42% at 3, 6, and 12 months), and greatest minimal clinically important difference achievement at 3 and 6 months, though without significant intergroup differences (P > .05). iPAAG offers comparable short-term efficacy and modest advantage at 6 months. However, long-term superiority is limited. It may be a complementary option in individualized osteoarthritis management. Further prospective studies are needed to define its optimal use.

Background and Objectives: Osteoarthritis (OA) is a degenerative joint disease involving inflammation, oxidative stress, and extracellular matrix (ECM) degradation, leading to cartilage damage and joint dysfunction. This study aimed to evaluate the chondroprotective effects of intra-articular hydrolyzed collagen in a rat model of knee OA using a dual-compartment biochemical and histological approach. Materials and Methods: Twenty male Sprague-Dawley rats underwent ACL transection to induce osteoarthritis and were randomly assigned to receive intra-articular hydrolyzed collagen or saline once weekly for three weeks. At six weeks, knee joints were evaluated histologically using the Mankin score. Synovial fluid and cartilage homogenates were analyzed via enzyme-linked immunosorbent assay (ELISA) for cytokines, cartilage degradation markers, and oxidative stress indicators. Results: The collagen-treated group demonstrated significantly lower Mankin scores. Levels of pro-inflammatory cytokines, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), as well as cartilage degradation markers, matrix metalloproteinase-13 (MMP-13), C-terminal crosslinked telopeptide of type II collagen (CTX-II), and cartilage oligomeric matrix protein (COMP), were significantly reduced (p < 0.05). Additionally, oxidative stress indicators including inducible nitric oxide synthase (iNOS), total oxidant status (TOS), and oxidative stress index (OSI) were decreased, while total antioxidant status (TAS) was increased in both synovial fluid and cartilage homogenates (p < 0.05). Conclusions: Intra-articular hydrolyzed collagen reduced inflammation, oxidative stress, and extracellular matrix (ECM) degradation, indicating potential chondroprotective effects across both synovial and cartilage compartments.

Background and Objectives: Tendon healing is a multifactorial process influenced by inflammation and oxidative stress. Avocado–soybean unsaponifiables (ASU), recognized for their anti-inflammatory and antioxidant properties in osteoarthritis, have not yet been evaluated in tendon repair. This study aimed to investigate the effects of systemic ASU administration on histological, biomechanical, and biochemical parameters of tendon healing in a rat Achilles tendon injury model. Materials and Methods: Twenty male Wistar rats underwent bilateral Achilles tendon transection and repair. The ASU group received intraperitoneal ASU (300 mg/kg/day) for four weeks; controls received saline. Right tendons were analyzed histologically using a semiquantitative scoring system adapted from Curtis–DeLee, Bonar, and Modified Soslowsky criteria. Left tendons were tested biomechanically for maximum force, displacement, stress, stiffness, and energy parameters. Serum interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were measured by ELISA. Results: ASU markedly improved histological healing with better collagen alignment, reduced inflammation, and normalized tenocyte morphology (p < 0.001). Biomechanical strength increased, with higher maximum force (p = 0.002), displacement (p = 0.004), stress (p = 0.001), and total energy to failure (p = 0.001). Serum IL-1β, IL-6, and TNF-α levels were lower (p < 0.001), while TAS increased and TOS/OSI decreased (p < 0.001). Conclusions: Systemic ASU administration enhances tendon healing by improving tissue organization, increasing mechanical strength, and modulating systemic inflammation and oxidative stress. These findings suggest that ASU may serve as a safe, clinically relevant adjunct therapy to promote tendon regeneration.

Background/Objectives: Osteoarthritis (OA) is a multifactorial degenerative joint disease characterized by synovial inflammation, oxidative stress, and progressive cartilage degeneration. This study investigated whether intra-articular N-acetylcysteine (NAC) attenuates synovial inflammation and oxidative stress and whether these effects translate into structural cartilage protection. Methods: OA was induced in rats by anterior cruciate ligament transection (ACLT). NAC (5 mg/50 µL) was administered intra-articularly once weekly for three weeks post-ACLT. Inflammatory cytokines (IL-1β, IL-6, TNF-α), oxidative stress markers (iNOS, TAS, TOS, OSI), and cartilage degradation markers (MMP-13, COMP, CTX-II) were quantified in synovial fluid and cartilage homogenates using ELISA. Cartilage integrity was evaluated histologically using the modified Mankin scoring system. Results: Compared with controls, NAC significantly reduced synovial IL-1β, IL-6, TNF-α, MMP-13, and iNOS levels and improved the synovial redox profile by increasing TAS and reducing TOS and OSI (all p < 0.05). In contrast, NAC did not significantly alter cartilage homogenate levels of inflammatory cytokines, oxidative stress indices, or degradation markers (COMP, CTX-II, MMP-13). Histological analysis demonstrated persistent cartilage fissuring, hypocellularity, and proteoglycan loss in both groups (p > 0.05). Conclusions: Intra-articular NAC exerts potent anti-inflammatory and antioxidative effects within the synovial compartment but fails to prevent cartilage degeneration in the ACLT model. These findings indicate a compartment-specific therapeutic profile, suggesting that NAC may function as a symptom-modifying agent in synovitis-dominant OA rather than a structure-modifying therapy. Future studies should focus on optimized delivery systems or combination strategies targeting cartilage and subchondral bone to achieve disease modification.