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Objective Evaluation of the ability of autogenous Platelet Rich Fibrin (PRF) and Zinc Oxide Nanoparticles (ZnONPs) to repair critical-sized ulnar defects in rabbits based on radiographic assessment. Design Randomized controlled study. Animals Twenty-four healthy male white New Zealand rabbits with an age of 6.0 ± 0.3 months and weight of 2.5 ± 0.29 Kg were used. Procedures A 12 mm defect was created in the diaphysis of the right ulnae in allrabbits,then the rabbits were randomly allocated into three groups (8 each): Control group, (the defect left for healing without grafts), platelets rich fibrin group (PRF group, the defect filled with PRF) and combination group (PRF/ZnONPs group, the defect filled with both PRF and ZnONPs). Healing capacity between the groups was evaluated by immediate postoperative radiographic assessment and subsequently at the first and the second postoperative months. Results Statistical analysis showed significant differences in the radiographic healing score between the groups (P = 0.000) at all-time points (P = 0.000- 0.003) during the study. Rabbits in the combination group showed the highest radiographic healing scores followed by the PRF group meanwhile, the Control group showed minimal radiographic healing scores. Conclusion and Clinical Relevance The addition of ZnONPs to PRF can accelerate the healing of ulnar critical-size defects in rabbits.
Background: Oral ingestion of zinc oxide nanoparticles (ZnONPs) may lead to serious liver injury. Vitamin E (VE) is an important antioxidant factor that can reduce such damage. Aim: This study aimed to evaluate the possible changes that could take place in the liver of adult male albino rats after oral ingestion of ZnONPs and elucidate the potential protective role of VE against such damage. Material and Methods: Forty eight male albino rats were divided into four groups of 12 animals each. Group (1) served as control group and received normal saline. Group (2) “VE-treated” received 100 mg/kg/day of VE dissolved in normal saline by oral gavage for 21 days. Group (3) “ZnONPs-treated” received a daily dose of ZnONPs dispersed in the fresh sterilized physiological saline solution 1mg/kg for 5 constitutive days. Group (4) “concomitant ZnONPs and VE-treated” was pretreated with VE 100 mg/kg/day for 14 days followed by the same dose of ZnONPs as in group (3) for 5 days. The extent of hepatic damage was evaluated by histological and immunohistochemical examination of liver samples and serological analysis of liver enzymes. Results: Body weights and liver weights showed very highly significant decrease (P <0.001) in the ZnONPs-treated group. The histological results in ZnONPs-treated group revealed congested dilated central veins and blood sinusoids, loss of normal arrangement of hepatocytes and most of hepatocytes showed marked vacuolated cytoplasm with darkly stained nuclei. Portal area affection was in the form of congested dilated portal veins with bile duct hyperplasia and cellular infiltration. There was an increase in the mount of blue stained collagen fibers around central veins together with strong positive reaction for Caspase 3 in ZnONPs-treated group. Similarly biochemical analysis indicated that the levels of serum aminotransferase (AST &ALT) significantly increased in ZnONPs-treated group when compared with other groups. Rats pretreated with VE showed improvement of the histological findings and biochemical parameters. Conclusion: Ingestion of ZnONPs could be associated with serious liver affection and pretreatment with VE is suggested to induce some improvement of such deleterious changes.