OBJECTIVETo investigate the changes in brain injury after the induction chemotherapy in children with acute lymphoblastic leukemia (ALL) by cranial MRI.

METHODSThe clinical data and cranial MRI results of 62 children with ALL who were hospitalized from March 2014 to June 2015 were analyzed retrospectively.

RESULTSBefore chemotherapy, MRI showed bone marrow infiltration of the skull in 33 patients (53%); the children with WBC<20×10(9)/Lhad a significantly lower incidence rate of bone marrow infiltration of the skull than those with WBC≥20×10(9)/L (16 patients/42% vs 17 patients/71%; P<0.05), and the high-risk group had a significantly higher incidence rate of bone marrow infiltration of the skull than the non-high-risk group (71% vs 44%; P<0.05). Before chemotherapy, there were 4 cases (7%) of brain atrophy, and 2 cases (3%) of abnormal signals in the sensory conduction bundle. MRI reexamination in 28 patients after 3 months of chemotherapy showed 3 new cases (11%) of brain atrophy and 1 aggravated case of brain atrophy.

CONCLUSIONSThe children with ALL have bone marrow infiltration of the skull, brain atrophy, and abnormal signals in the sensory conduction bundle before chemotherapy, especially bone marrow infiltration of the skull, and some changes in brain injury disappear after treatment.

Adolescent ; Bone Marrow ; pathology ; Brain ; drug effects ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Induction Chemotherapy ; adverse effects ; Infant ; Magnetic Resonance Imaging ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; pathology ; Retrospective Studies ; Skull ; pathology

OBJECTIVETo observe the effect of a new biomaterial in promoting the bone regeneration for repairing critical-size cranial defects in SD rats.

METHODSCritical-size cranial defects were induced in 3-month-old male Sprague-Dawley rats and repaired with the implants of calcium phosphate from growth factor enhanced matrix 21 (CaPfromGEM21, control), CaPfromGEM21 preloaded with 10 ng bone morphogenetic protein-2 (BMP-2), CaPfromGEM21 preloaded with 100 ng BMP-2, CaPfromGEM21 preloaded with 0.3 µg platelet-derived growth factor-BB (PDGF-BB), or CaPfromGEM21 preloaded with 3 µg PDGF-BB. The defects were examined 6 weeks after the surgery with X-ray, micro-CT, HE staining and quantitative assessments.

RESULTSX-ray showed defect repair in all the groups. The fracture line became obscure, and the defects were almost fully repaired by the regenerated bone tissues in PDGF-BB group. Micro-CT demonstarted new bone formation in the defects. The new bone volume was significantly greater in PDGF-BB groups than in BMP-2 groups (P<0.05). HE staining revealed the presence of new bones in the defects and new vessels in and around the new bones without inflammatory cells. The new bone area fraction was significantly greater in 10 ng BMP-2 group and 0.3 µg PDGF-BB group than in the control group (P<0.05), and the new vessel density was similar in the all the 4 cytokine-preloaded groups and all significantly greater than that in the blank and CaPfromGEM21 control group (P<0.05).

CONCLUSIONCaPfromGem21 combined with BMP-2 or PDGF-BB has good biocompatibility and can better promote bone regeneration for repairing bone defects.

Animals ; Biocompatible Materials ; Bone Morphogenetic Protein 2 ; pharmacology ; Bone Regeneration ; drug effects ; Calcium Phosphates ; pharmacology ; Male ; Prostheses and Implants ; Proto-Oncogene Proteins c-sis ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Skull ; pathology ; Wound Healing

Tumor necrosis factor-alpha (TNF-alpha) and inflammatory cytokines released from activated macrophages in response to particulate debris greatly impact periprosthetic bone loss and consequent implant failure. In the present study, we found that a major polyphenolic component of green tea, (-)-epigallocatechin gallate (EGCG), inhibited Ti particle-induced TNF-alpha release in macrophages in vitro and calvarial osteolysis in vivo. The Ti stimulation of macrophages released TNF-alpha in a dose- and time-dependent manner, and EGCG substantially suppressed Ti particle-induced TNF-alpha release. Analysis of signaling pathway showed that EGCG inhibited the Ti-induced c-Jun N-terminus kinase (JNK) activation and inhibitory kappaB (IkappaB) degradation, and consequently the Ti-induced transcriptional activation of AP-1 and NF-kappaB. In a mouse calvarial osteolysis model, EGCG inhibited Ti particle-induced osteolysis in vivo by suppressing TNF-alpha expression and osteoclast formation. Therefore, EGCG may be a potential candidate compound for osteolysis prevention and treatment as well as aseptic loosening after total replacement arthroplasty.
Animals ; Catechin/*analogs & derivatives/pharmacology ; Cell Line ; Implants, Experimental ; Macrophages/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 8/metabolism ; NF-kappa B/metabolism ; Osteolysis/chemically induced/*metabolism/prevention & control ; Particulate Matter/*adverse effects ; Prosthesis Failure ; Signal Transduction/drug effects ; Skull/*drug effects/pathology ; Titanium/*adverse effects ; Transcription Factor AP-1/metabolism ; Tumor Necrosis Factor-alpha/*metabolism

OBJECTIVETo evaluate the effect of endothelial progenitor cells (EPCs) mobilization on the healing of calvarial defect in diabetic mice.

METHODS55 type II adult male diabetic mice were included in this study. They were randomly divided into three groups: the non-operative group (n = 5), the experimental group (n = 25) and the control group (n = 25). Two circular bony defects, 3 mm in diameter, were created on the parietal bones of the diabetic mice. Intraperitoneal AMD3100 (10 mg/kg; n = 25) or sterile saline (control group) was administered daily beginning at post-operative day 3 and continuing for 15 days. 5 mice were sacrificed in each group at non-operation, post-operative week 1,2,4, 8,12. Circulation EPC level was measured at pre-operation, post-operative day 7 and day 14. Bony regeneration was assessed with micro-CT at post-operative week 4, 8 and 12. HE staining was performed on all the decalcified bone samples. Immunofluorescent CD31 and osteocalcin staining was performed on calvarial defects at weeks 1, 2, and 4 to assess the vascularity and osteoblast density, respectively.

RESULTSThe mobilization of EPC in diabetic mice almost disappeared one week after trauma, while AMD3100 could dramatically increase the circulation EPC level for a long time after trauma. Compared to control group, the healing percentage of bony defect in the diabetic mice treated with AMD3100 was obviously increased at post-operative week 8 (50.5% vs. 34.8%) and week 12 (50.9% vs. 40.2%). Calvarial defects of AMD3100-treated mice harvested at 1, 2, and 4 weeks demonstrated increased vascularity and osteoblast density, compared to the controls. The difference was most marked in postoperative week 2 (vascularity: 6.11% vs. 2.47%; osteoblast density 2.81% vs. 1.22%, P < 0.01).

CONCLUSIONAMD3100 can improve the healing of calvarial defect in diabetic mice by increasing the vascularity and osteoblast density at the regeneration area.

Animals ; Bone Regeneration ; Diabetes Mellitus, Experimental ; Endothelial Cells ; cytology ; drug effects ; Endothelium, Vascular ; cytology ; Heterocyclic Compounds ; pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Osteoblasts ; cytology ; Parietal Bone ; Skull ; pathology ; Stem Cells ; cytology ; drug effects ; Wound Healing