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• W2949623312 abstract "A high number of fractures fails to heal adequately in the elderly population as a result of inadequate fixation, insufficient blood supply or infection, all of which impede bone regeneration. Several methods have been developed to accelerate and improve bone healing. Autogenous bone is ideal for this purpose but is limited in supply and associated with donor site morbidity. Devitalized allograft bone is more plentiful but has poor osteoinductive capability and also carries the risk of infection. The use of bone morphogenetic proteins to augment healing of large defects is associated with serious side effects, including osteosarcoma, marrow fibrosis and ectopic bone formation. While each approach has advantages and disadvantages there is a pressing need to develop more effective adjunct therapies. Consistent with the notion that a more complete understanding of the processes of inflammation and immunity during bone healing is necessary to improve therapeutic modalities accelerating fracture repair, this thesis investigates the influence of systemic inflammation and mast cell deficiency on bone healing. A murine model was designed to investigate the osseous regeneration of a large-sized femoral defect. Systemic inflammation induced by the injection bacterial surface proteins for one week significantly impaired the repair of this defect. Increased inflammation resulted in decreased bone anabolic processes and an altered activity of macrophages. Moreover, the formation of new vessels was compromised in the absence of any changes of the local vascular endothelial growth factor concentrations. The same large-sized bone defect was then used to compare bone healing in wild type and mast cell deficient mice with c-kit loss of function. Mast cell deficient mice displayed reduced bone healing in association with decreased vessel formation and an excessive expression of catabolic cells. Modulation of the immune response is a promising approach to improve and increase the speed and quality of the fracture repair process. However, further preclinical studies are necessary to understand the key processes of inflammation and immunity more rigorously before clinical trials are warranted.%%%%Un nombre eleve de fractures ne guerissent pas de maniere optimale dans la population âgee en raison de la mobilite des fragments due a une fixation inadequate, d'un apport sanguin insuffisant ou d'une infection ; ce qui empechent la bonne regeneration osseuse. Plusieurs methodes ont ete developpees pour accelerer et ameliorer ce processus. Les autogreffes osseuses ont prouve leur efficacite, mais sont limitees et associees a la morbidite du site operatoire. Les allogreffes osseuses devitalisees sont plus disponibles, mais ont une faible capacite osteo-inductrice et entraine egalement un risque infectieux. Par ailleurs, l'utilisation de proteines osseuses morphogenetiques dans le but d'ameliorer la cicatrisation des pertes de substances osseuse importantes est associee a des effets secondaires graves comprenant : les osteosarcomes, la fibrose de…" @default.
• W2949623312 created "2019-06-27" @default.
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• W2949623312 date "2017-01-01" @default.
• W2949623312 modified "2023-09-24" @default.
• W2949623312 title "Preclinical assessment of the influence of inflammation on bone regeneration" @default.
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