INTRODUCTIONThis study evaluated the effect of autologous bone marrow derived adult Mesenchymal Stem Cells (MSCs) on the biological healing of weight bearing diaphyseal bone allograft in the tibia of adult rabbits.

MATERIALS AND METHODSForty Adult New Zealand White Rabbits divided into 3 groups (Autograft, Allograft or Allograft impregnated with MSCs) with 12 rabbits in each group were used for the study. A 1.5 cm of cortical bone segment was excised from the rabbit's right tibia. The segment was replaced by an Autograft, Allograft or Allograft loaded with MSCs, depending on which group the rabbit was assigned. Internal fixation was performed using a 9-hole Mini-compression Plate and Cerclage Wires. Rabbits were sacrificed at end of observation periods of 12, 16 and 24 weeks. Specimens procured were assessed clinically and radiologically and fixed in 10% buffered formalin. For each specimen, 5 μm undecalcified sections were cut and stained with Von Kossa and Toluidine Blue stains. Histomorphometery was then performed.

RESULTSOur study showed that addition of autologous MSCs to diaphyseal allograft segments enhances and accelerates not just the union at host graft junctions and also the biological incorporation of the allograft segment as shown by Resorption Index, New-Bone Formation Index and Osteocyte Index.

CONCLUSIONSThe addition of autologous MSCs to deep frozen cortical allograft segments improved the host - allograft union rate and biological incorporation of diaphyseal allografts as shown by resorption activity, new bone formation and osteocyte cell counts.

Animals ; Disease Models, Animal ; Male ; Mesenchymal Stem Cell Transplantation ; methods ; Mesenchymal Stromal Cells ; Rabbits ; Tibia ; abnormalities ; Transplantation, Homologous ; Wound Healing

Background: and Purpose High-grade carotid artery stenosis may alter hemodynamics in the ipsilateral hemisphere, but consequences of this effect are poorly understood. Cortical thinning is associated with cognitive impairment in dementia, head trauma, demyelination, and stroke. We hypothesized that hemodynamic impairment, as represented by a relative time-to-peak (TTP) delay on MRI in the hemisphere ipsilateral to the stenosis, would be associated with relative cortical thinning in that hemisphere. Methods: We used baseline MRI data from the NINDS-funded Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis–Hemodynamics (CREST-H) study. Dynamic contrast susceptibility MR perfusion-weighted images were post-processed with quantitative perfusion maps using deconvolution of tissue and arterial signals. The protocol derived a hemispheric TTP delay, calculated by subtraction of voxel values in the hemisphere ipsilateral minus those contralateral to the stenosis. Results: Among 110 consecutive patients enrolled in CREST-H to date, 45 (41%) had TTP delay of at least 0.5 seconds and 9 (8.3%) subjects had TTP delay of at least 2.0 seconds, the maximum delay measured. For every 0.25-second increase in TTP delay above 0.5 seconds, there was a 0.006-mm (6 micron) increase in cortical thickness asymmetry. Across the range of hemodynamic impairment, TTP delay independently predicted relative cortical thinning on the side of stenosis, adjusting for age, sex, hypertension, hemisphere, smoking history, low-density lipoprotein cholesterol, and preexisting infarction (P=0.032). Conclusions Our findings suggest that hemodynamic impairment from high-grade asymptomatic carotid stenosis may structurally alter the cortex supplied by the stenotic carotid artery.