We used (31)P and (13)C solid-state nuclear magnetic resonance (NMR) spectroscopy to detect and analyze the major organic and inorganic components (collagen type I and bioapatite) in natural rabbit bone and beta-tricalcium phosphate implants loaded with osteogenically differentiated mesenchymal stem cells. High-resolution solid-state NMR spectra were obtained using the magic-angle spinning (MAS) technique. The (31)P NMR spectra of bone specimens showed a single line characteristic of bone calcium phosphate. (13)C cross-polarization (CP) MAS NMR spectra of bone exhibited the characteristic signatures of collagen type I with good resolution for all major amino acids in collagen. Quantitative measurements of (13)C-(1)H dipolar couplings indicated that the collagen segments are very rigid, undergoing only small amplitude fluctuations with correlation times in the nanosecond range. In contrast, directly polarized (13)C MAS NMR spectra of rabbit bone were dominated by signals of highly mobile triglycerides. These quantitative investigations of natural bone may provide the basis for a quality control of various osteoinductive bone substitutes. We studied the formation of extracellular bone matrix in artificial mesenchymal stem cell-loaded beta-tricalcium phosphate matrices that were implanted into the femoral condyle of rabbits. The NMR spectra of these bone grafts were acquired 3 months after implantation. In the (31)P NMR spectra, beta-tricalcium phosphate and bone calcium phosphate could be distinguished quantitatively, allowing recording of the formation of the natural bone matrix. Further, (13)C CPMAS allowed detection of collagen type I that had been produced in the implants. Comparison with the spectroscopic data from natural bone allowed assessment of the quality of the bone substitute material.
Preservation and repair of the hip joint capsule causes an 88-%-reduction of the dislocation rate in primary THA in this large series including 1972 cases, operated via the Bauer or the anterolateral approach. Several authors reported comparable results after THA using similar techniques of soft tissue and capsular repair through the posterior or posterolateral approach. Sparing and reconstructing the hip joint capsule therefore seems to reduce the dislocation rate after primary THA by one order of magnitude regardless of the surgical approach and, especially, if the acetabular origin is preserved. Capsule-related specific complications such as an increased revision rate, malfunction or pain were neither recorded in our study nor by others. Thus, careful preservation and reconstruction of the hip joint capsule may be expressly recommended in primary THA.
Due to their different clinical presentations periprosthetic fractures need to be managed individually and in most cases operatively. Internal fixation with a plate proved to give the best functional results for stable stem implants. Loosening stems have to be replaced by revision implants with long stems for intramedullary fixation. Alternative osteosynthetic techniques and additive minimal osteosynthesis can be favoured in special cases. Modular prostheses for bone replacement are reserved for fractures with extensive bone loss.
Hereditary multiple exostosis (HME), a disorder inherited in an autosomal dominant manner, is characterized by multiple projections of bone, mainly at the extremities. The risk of malignant transformation of the exostoses is estimated to be up to 2%. The most common underlying cause of the disease involves mutations in either the EXT1 or the EXT2 gene. We report on the clinical and molecular findings in a family affected with HME.A mother and her three children from different partnerships, all clinically diagnosed with HME, were referred for genetic counseling. Subsequently, molecular analysis of the EXT1 gene was performed according to standard procedures. We identified a mutation in the EXT1 gene in all four affected family members (delA in codon 133). This mutation has not been previously described and is suggested to cause the disease in this family. Identification of disease causing mutations in patients with HME and their relatives can help to improve the clinical management of tumor prevention, early tumor detection, and orthopedic therapy.
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