ABSTRACT
Tissue regeneration and neovascularisation in cases of major bone loss is a challenge in maxillofacial surgery. The hypothesis of the present study is that the addition of resorbable bioactive ceramic Silica Calcium Phosphate Cement (SCPC) to Declluraized Muscle Scaffold (DSM) can expedite bone formation and maturation. Two surgical defect models were created in 18 nude transgenic mice. Group 1(n = 6), with a 2-mm decortication calvarial defect, was treated with a DSM/SCPC sheet over the corticated bone as an onlay then seeded with human Mesenchymal Stromal Cells hMSC in situ. In Group 2 (n = 6), a critical size (4 mm) calvarial defect was made and grafted with DSM/SCPC/in situ human bone marrow stromal cells (hMSCs). The control groups included Group 3 (n = 3) animals, with a 2-mm decortication defect treated with an onlay DSM sheet, and Group 4 (n = 3) animals, treated with critical size defect grafted with plain DSM. After 8 weeks, bone regeneration in various groups was evaluated using histology, immunohistochemistry and histomorphometry. New bone formation and maturation was superior in groups treated with DSM/SCPC/hMSC. The DMS/SCPC scaffold has the ability to augment and induce bone regeneration and neovascularisation in cases of major bone resorption and critical size defects.
Subject(s)
Bone Regeneration/drug effects , Ceramics/therapeutic use , Decellularized Extracellular Matrix/therapeutic use , Muscles/chemistry , Prosthesis Implantation , Animals , Biocompatible Materials/chemistry , Biocompatible Materials/therapeutic use , Bone Substitutes/chemistry , Bone Substitutes/therapeutic use , Calcium Phosphates/chemistry , Calcium Phosphates/pharmacology , Cells, Cultured , Ceramics/chemistry , Decellularized Extracellular Matrix/chemistry , Humans , Mesenchymal Stem Cells/drug effects , Mesenchymal Stem Cells/physiology , Mice , Mice, Nude , Mice, Transgenic , Osteogenesis/drug effects , Prosthesis Implantation/instrumentation , Prosthesis Implantation/methods , Skull/drug effects , Skull/pathology , Skull/physiopathology , Tissue Engineering/methodsABSTRACT
Hypoxia may lead to inflammatory responses by numerous signaling pathways. This investigation intended to inspect the defensive role of Quercetin (Quer) and/ or Melatonin (Mel) against reno toxicity induced by Sodium nitrite (Sod ntr). Sod ntr injection significantly decreased blood hemoglobin concentration (Hb) with a concurrent increase in serum tumor necrosis factor- α, interleukin-6, C-reactive protein, creatinine, and urea levels. Over protein-expression of vascular endothelial growth factor and heat shock, protein-70 and mRNA of HIF-1α were also observed. Pretreatment of the Sod ntr- injected rats with the aforementioned antioxidants; either alone or together significantly improved such parameters. Histopathological examination reinforced the previous results. It was concluded that the combined administration of Quer and Mel may be useful as a potential therapy against renal injury induced by Sod ntr. HIF-1α and HSP-70 are implicated in the induction of hypoxia and its treatment.
ABSTRACT
OBJECTIVE: To determine tendon stump changes following unrepaired Achilles tendon lacerations in an animal model. STUDY DESIGN: An experimental study. PLACE AND DURATION OF STUDY: King Saud University, Riyadh, Saudi Arabia, from October 2013 to January 2014. METHODOLOGY: Arabbit model was developed and studied tendon retraction and histological changes in the proximal and distal stumps following transection of the Achilles tendon. RESULTS: Over a period of 12 weeks, retraction of the distal tendon stump was minimal (2 - 3 mm). In contrast, retraction of the proximal tendon stump peaked to reach 6 mm at 4 weeks post-injury and plateaued to reach 7 - 8 mm at the 12-week interval. CONCLUSION: Following complete transection of the Achilles tendon, tendon retraction correlated with the density of myofibroblast expression within the tendon stump. Further research is needed to investigate the pathophysiology of these findings.
Subject(s)
Achilles Tendon/injuries , Achilles Tendon/pathology , Lacerations/etiology , Tendon Injuries/pathology , Achilles Tendon/surgery , Animals , Rabbits , Tendon Injuries/surgeryABSTRACT
OBJECTIVE: To investigate whether ruboxistaurin (a selective PKC-ß inhibitor) mediates renoprotective effect via interference with TGF-ß1/Smad-GRAP cross-signalling. METHOD: Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (55 mg/kg). Then, the diabetic rats were treated with ruboxistaurin (10 mg/kg, p.o) for 6 weeks. Valsartan (15 mg/kg, p.o) was used as a positive control. After 6 weeks of treatment, diabetic nephropathy biomarkers were assessed. TGF-ß1, Smad2, and Smad3 mRNA and protein levels were detected using qPCR and western blot analysis. KEY FINDINGS: Data showed that serum creatinine, kidney/body weight ratio and urinary albumin excretion significantly increased in diabetic rats. These changes were significantly attenuated by treatment with ruboxistaurin. A significant up-regulation of TGF-ß1, Smad2 and Smad3 mRNA expression was observed in diabetic rats, which was alleviated by administration of ruboxistaurin. Furthermore, immunoblotting showed a significant improvement in protein levels of TGF-ß1 (P < 0.01), Smad2/3 (P < 0.01) and p-Smad3 (P < 0.001) in diabetic rats treated with ruboxistaurin compared to untreated. Importantly, the reduction in GRAP protein expression in diabetic kidney was prevented by treatment with ruboxistaurin. CONCLUSION: These data suggest that the renoprotective effect of ruboxistaurin is possibly due to down-regulation of TGF-ß1/Smad pathway and normalization of GRAP protein expression.
