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Necrotic Bone (necrotic + bone)
Selected AbstractsTreatment results of bisphosphonate-related osteonecrosis of the jaws,HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 9 2008Arno Wutzl MD Abstract Background. Osteonecrosis of the jaws occurs after the administration of bisphosphonates. An unequivocal treatment strategy is yet to be devised. We assess the treatment of patients with bisphosphonate-related osteonecrosis of the jaws (BRONJ). Methods. The investigators studied a prospective cohort of 58 patients 6 months after surgical treatment of BRONJ. Outcome variables were the status of the mucosa, the visual analog score of pain, and prosthetic rehabilitation. Preoperative staging results were compared with the postoperative outcome and statistically evaluated. Results. Of 58 patients, 41 surgically treated patients could be followed up after a mean period of 189 (±23) days. Twenty-four (58.5%) were free of pain and had an intact mucosa. A statistically significant improvement was registered between preoperative and postoperative staging (p <.01); 11 of 12 patients who had been treated with a flap procedure for soft tissue closure had an intact mucosa. Conclusions. This is the first prospective study to report the outcome of treatment in a cohort of patients with BRONJ. Minimal resection of necrotic bone and local soft tissue closure might be a feasible treatment strategy in patients with established BRONJ. © 2008 Wiley Periodicals, Inc. Head Neck 2008 [source] Cell-based immunotherapy with mesenchymal stem cells cures bisphosphonate-related osteonecrosis of the jaw,like disease in miceJOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2010Takashi Kikuiri Abstract Patients on high-dose bisphosphonate and immunosuppressive therapy have an increased risk of bisphosphonate-related osteonecrosis of the jaw (BRONJ); despite the disease severity, its pathophysiology remains unknown, and appropriate therapy is not established. Here we have developed a mouse model of BRONJ-like disease that recapitulates major clinical and radiographic manifestations of the human disease, including characteristic features of an open alveolar socket, exposed necrotic bone or sequestra, increased inflammatory infiltrates, osseous sclerosis, and radiopaque alveolar bone. We show that administration of zoledronate, a potent aminobisphosphonate, and dexamethasone, an immunosuppressant drug, causes BRONJ-like disease in mice in part by suppressing the adaptive regulatory T cells, Tregs, and activating the inflammatory T-helper-producing interleukin 17 cells, Th17. Most interestingly, we demonstrate that systemic infusion with mesenchymal stem cells (MSCs) prevents and cures BRONJ-like disease possibly via induction of peripheral tolerance, shown as an inhibition of Th17 and increase in Treg cells. The suppressed Tregs/Th17 ratio in zoledronate- and dexamethasone-treated mice is restored in mice undergoing salvage therapy with Tregs. These findings provide evidence of an immunity-based mechanism of BRONJ-like disease and support the rationale for in vivo immunomodulatory therapy using Tregs or MSCs to treat BRONJ. © 2010 American Society for Bone and Mineral Research [source] Quantitative mouse model of implant-associated osteomyelitis and the kinetics of microbial growth, osteolysis, and humoral immunity,JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2008Dan Li Abstract Although osteomyelitis (OM) remains a serious problem in orthopedics, progress has been limited by the absence of an in vivo model that can quantify the bacterial load, metabolic activity of the bacteria over time, immunity, and osteolysis. To overcome these obstacles, we developed a murine model of implant-associated OM in which a stainless steel pin is coated with Staphylococcus aureus and implanted transcortically through the tibial metaphysis. X-ray and micro-CT demonstrated concomitant osteolysis and reactive bone formation, which was evident by day 7. Histology confirmed all the hallmarks of implant-associated OM, namely: osteolysis, sequestrum formation, and involucrum of Gram-positive bacteria inside a biofilm within necrotic bone. Serology revealed that mice mount a protective humoral response that commences with an IgM response after 1 week, and converts to a specific IgG2b response against specific S. aureus proteins by day 11 postinfection. Real-time quantitative PCR (RTQ-PCR) for the S. aureus specific nuc gene determined that the peak bacterial load occurs 11 days postinfection. This coincidence of decreasing bacterial load with the generation of specific antibodies is suggestive of protective humoral immunity. Longitudinal in vivo bioluminescent imaging (BLI) of luxA-E transformed S. aureus (Xen29) combined with nuc RTQ-PCR demonstrated the exponential growth phase of the bacteria immediately following infection that peaks on day 4, and is followed by the biofilm growth phase at a significantly lower metabolic rate (p,<,0.05). Collectively, these studies demonstrate the first quantitative model of implant-associated OM that defines the kinetics of microbial growth, osteolysis, and humoral immunity following infection. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J. Orthop Res 26:96,105, 2008 [source] Dental management of patients at risk of osteochemonecrosis of the jaws: a critical reviewORAL DISEASES, Issue 8 2009S Fedele Osteonecrosis of the jaw bones is a complication of bisphosphonate (BP) drug usage characterised by trans-mucosal exposure of necrotic bone, often followed by infection and pain. Osteonecrosis is observed in cancer patients on high-potency intravenous BP more frequently than in osteoporotic individuals using low-potency oral BP. The management of osteonecrosis caused by BP is often unsatisfactory and control of risk factors is considered the most effective means of prevention. Surgical manipulation and dental infection of the jawbone are the major risk factors, hence it is suggested that careful management of oral health and relevant dental procedures may decrease the risk of osteonecrosis in individuals on BP. Recommendations for dentists and oral surgeons have been suggested by different groups of clinicians but they are often controversial and there is no clear evidence for their efficacy in reducing the likelihood of osteonecrosis development. This report critically reviews current dental recommendations for individuals using BP with the aim of helping the reader to transfer them into practice as part of pragmatic and non-detrimental clinical decisions making. [source] Avascular necrosis of the femoral head in a patient with Fabry's disease: Identification of ceramide trihexoside in the bone by delayed-extraction matrix-assisted laser desorption ionization,time-of-flight mass spectrometryARTHRITIS & RHEUMATISM, Issue 7 2002Hiroshi Horiuchi Fabry's disease is a lipid storage disease caused by an X-linked hereditary deficiency of ,-galactosidase. The enzymatic defect causes progressive deposition of ceramide trihexoside (CTH) in various tissues, leading to renal failure, premature myocardial infarction, and stroke, with a high rate of mortality in younger patients. Among the complications associated with Fabry's disease, a few cases involving avascular necrosis (AVN) of the femoral head have been reported. However, direct evidence of deposition of CTH in bone marrow in the femoral head has not been demonstrated. This report describes a 58-year-old man who underwent total hip arthroplasty for femoral head AVN associated with Fabry's disease. The accumulation of CTH was examined by chemical analysis of the sphingolipid extracted from the femoral head, using delayed-extraction matrix-assisted laser desorption ionization,time-of-flight mass spectrometry. This is the first report confirming the presence of CTH in the sphingolipid fraction from normal and necrotic bone of a patient with Fabry's disease. [source] | ||||||||||