Nonunion is one of the most troublesome complications to treat
in orthopaedics. Former authors believed that atrophic nonunion
occurred as a result of lack of mesenchymal stem cells (MSCs). We
evaluated the number and viability of MSCs in site of atrophic nonunion compared
with those in iliac crest. We enrolled five patients with neglected atrophic nonunions of
long bones confirmed by clinical examinations and plain radiographs
into this study. As much as 10 ml bone marrow aspirate was obtained
from both the nonunion site and the iliac crest and cultured for
three weeks. Cell numbers were counted using a haemocytometer and
vitality of the cells was determined by trypan blue staining. The
cells were confirmed as MSCs by evaluating their expression marker
(CD 105, CD 73, HLA-DR, CD 34, CD 45, CD 14, and CD 19). Cells number and
viability were compared between the nonunion and iliac creat sites.Objectives
Methods
The biomembrane (induced membrane) formed around polymethylmethacrylate (PMMA) spacers has value in clinical applications for bone defect reconstruction. Few studies have evaluated its cellular, molecular or stem cell features. Our objective was to characterise induced membrane morphology, molecular features and osteogenic stem cell characteristics. Following Institutional Review Board approval, biomembrane specimens were obtained from 12 patient surgeries for management of segmental bony defects (mean patient age 40.7 years, standard deviation 14.4). Biomembranes from nine tibias and three femurs were processed for morphologic, molecular or stem cell analyses. Gene expression was determined using the Affymetrix GeneChip Operating Software (GCOS). Molecular analyses compared biomembrane gene expression patterns with a mineralising osteoblast culture, and gene expression in specimens with longer spacer duration (> 12 weeks) with specimens with shorter durations. Statistical analyses used the unpaired student Objectives
Methods
Heterotopic ossification (HO) is perhaps the
single most significant obstacle to independence, functional mobility, and
return to duty for combat-injured veterans of Operation Enduring
Freedom and Operation Iraqi Freedom. Recent research into the cause(s)
of HO has been driven by a markedly higher prevalence seen in these
wounded warriors than encountered in previous wars or following
civilian trauma. To that end, research in both civilian and military
laboratories continues to shed light onto the complex mechanisms
behind HO formation, including systemic and wound specific factors,
cell lineage, and neurogenic inflammation. Of particular interest,
non-invasive