Late postoperative infection following spinal instrumentation: stainless steel versus titanium implants.

Late postoperative infection following instrumented spinal surgery is a clinical entity that has emerged in recent years. The extended surface of the spinal instrumentation in combination with hematogenous seeding or intraoperative inoculation is the main predisposing factor. In order to investigate the contribution of the instrumentation material (stainless steel versus titanium implants) and mechanical loosening, two groups of patients are presented. The first group includes 50 idiopathic scoliotic patients who were treated with first-generation posterior stainless steel spinal segmental multihook instrumentation [Texas Scottish Rite Hospital (TSRH) instrumentation system], and the second group includes 45 similar patients who were treated with newer titanium implants (MOSS MIAMI, XIA, and CD). Follow-up ranged from 3 to 13 years. Six patients from the first group and one patient from the second group presented with late infections 1 to 7 years postoperatively. Common intraoperative findings were excessive inflammatory tissue and some degree of instrumentation loosening and corrosion (stainless steel). Removal of instrumentation in combination with appropriate antibiotics was an effective treatment. Further study with long-term follow-up is necessary in order to understand the exact incidence and pathology of such infections.

Human osteoblasts express functional CXC chemokine receptors 3 and 5: activation by their ligands, CXCL10 and CXCL13, significantly induces alkaline phosphatase and beta-N-acetylhexosaminidase release.

Osteoblasts (OBs) contribute to the maintenance of bone homeostasis and their activity can be influenced by immune cells localized in bone lacunae. We investigated the expression of the chemokine receptors in isolated human OBs by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry, and report a novel finding, namely, that OBs express high levels of CXC chemokine receptor 3 (CXCR3) and 5 (CXCR5). Functional assays to evaluate CXCR3 and CXCR5 demonstrated that their ligands-CXCL10 and CXCL13, respectively-significantly induce the release of beta-N-acetylhexosaminidase, an enzyme involved in endochondral ossification and bone remodeling able to degrade important extracellular matrix components. Alkaline phosphatase activity, a useful index of matrix formation was also up-regulated by CXCL10 and CXCL13. However, OB activation by these ligands does not affect OB proliferation. Both Bordetella pertussis toxin and neutralizing anti-CXCR3/anti-CXCR5 monoclonal antibodies block CXCL10 and CXCL13 induction, respectively. We also demonstrated the expression of CXCL10 and CXCL13 in human bone tissue biopsies. These results indicate that both CXCR3/CXCL10 and CXCR5/CXCL13 receptor-ligand pairs may play an important role in OB activity through the specific up-regulation of two enzymes, which are involved in the bone remodeling process. Moreover, our data suggest that OBs may play a role in the modulation of bone formation through the combined action of these two enzymes.