Trabecular Bone Score Significantly Influences Treatment Decisions in Secondary Osteoporosis.

The trabecular bone score (TBS) can be determined in addition to the Dual Energy X-ray Absorptiometry (DXA) for bone mineral density (BMD) measurement to diagnose, evaluate, and stratify bone loss and decide on appropriate treatment in patients at risk. Especially in patients with secondary osteoporosis, TBS detects restricted bone quality. To investigate the influence of an additional evaluation of TBS on patients' treatment strategy decisions, we enrolled 292 patients, with a high proportion of patients with secondary osteoporosis, from one outpatient unit over one year. Patients eligible for BMD measurement had the option to opt-in for TBS measurement. We analyzed demographic data, leading diagnoses, bone metabolism parameters, and results of BMD and TBS measurements. More than 90% of patients consented to TBS measurement. TBS measurement influenced the decision in approximately 40% of patients with a treatment indication for anti-osteoporotic drugs. We demonstrate that depending on the underlying disease/risk spectrum, 21-25.5% of patients had an unremarkable BMD measurement with poor bone quality shown in the TBS measurement. In patients with secondary osteoporosis, the use of TBS supplementary to DXA seems useful to better assess fracture risk and, thus, to initiate therapy for osteoporosis in these patients in time.

Cytokine expression in human osteoblasts after antiseptic treatment: a comparative study between polyhexanide and chlorhexidine.

PURPOSE/AIM OF THE STUDY: Chlorhexidine and polyhexanide are frequently used antiseptics in clinical practice and have a broad antimicrobial range. Both antiseptics are helpful medical agents for septic wound treatment with a high potential for defeating joint infections. Their effect on human osteoblasts has, so far, not been sufficiently evaluated. The aim of this study was to investigate the activating potential of polyhexanide and chlorhexidine on inflammatory cytokines/chemokines in human osteoblasts in vitro. MATERIALS AND METHODS: Human osteoblasts were isolated and cultivated in vitro and then treated separately with 0.1% and 2% chlorhexidine and 0.04% polyhexanide as commonly applied concentrations in clinical practice. Detection of cell structure and cell morphology was performed by light microscopic inspection. Cytokine and chemokine secretion was determined by using a multiplex suspension array. RESULTS: Cell shrinking, defective cell membrane, and the loss of cell adhesion indicated cell damage of human osteoblasts after treatment with both antiseptics was evaluated by using light microscopy. Polyhexanide, but not chlorhexidine, caused human osteoblasts to secrete various interleukins (1ß, 6, and 7), interferon γ, tumor necrosis factor α, vascular endothelial growth factor, eotaxin, fibroblast growth factor basic, and granulocyte macrophage colony-stimulating factor as quantified by multiplex suspension array. CONCLUSIONS: Both antiseptics induced morphological cell damage at an optimum exposure between 1 and 10 min. But only polyhexanide mediated a pronounced secretion of inflammatory cytokines and chemokines in human osteoblasts. Therefore, we recommend a preferred usage of chlorhexidine in septic surgery to avoid the induction of an inflammatory reaction.

Human immune cells' behavior and survival under bioenergetically restricted conditions in an in vitro fracture hematoma model.

The initial inflammatory phase of bone fracture healing represents a critical step for the outcome of the healing process. However, both the mechanisms initiating this inflammatory phase and the function of immune cells present at the fracture site are poorly understood. In order to study the early events within a fracture hematoma, we established an in vitro fracture hematoma model: we cultured hematomas forming during an osteotomy (artificial bone fracture) of the femur during total hip arthroplasty (THA) in vitro under bioenergetically controlled conditions. This model allowed us to monitor immune cell populations, cell survival and cytokine expression during the early phase following a fracture. Moreover, this model enabled us to change the bioenergetical conditions in order to mimic the in vivo situation, which is assumed to be characterized by hypoxia and restricted amounts of nutrients. Using this model, we found that immune cells adapt to hypoxia via the expression of angiogenic factors, chemoattractants and pro-inflammatory molecules. In addition, combined restriction of oxygen and nutrient supply enhanced the selective survival of lymphocytes in comparison with that of myeloid derived cells (i.e., neutrophils). Of note, non-restricted bioenergetical conditions did not show any similar effects regarding cytokine expression and/or different survival rates of immune cell subsets. In conclusion, we found that the bioenergetical conditions are among the crucial factors inducing the initial inflammatory phase of fracture healing and are thus a critical step for influencing survival and function of immune cells in the early fracture hematoma.