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Research progress in mechanism of traumatic brain injury affecting speed of fracture healing / 中华创伤杂志(英文版)
Chinese Journal of Traumatology ; (6): 376-380, 2007.
Article Dans Anglais | WPRIM | ID: wpr-236746
ABSTRACT
In patients who have sustained traumatic brain injury with associated extremity fracture, there is often a clinical perception that the rate of new bone formation around the fracture site increases.(1) An overgrowth of callus is observed and ectopic ossification even occurs in the muscle,(2) but the mechanism remains unclear. Whether this rapidly-formed new bone is fracture callus or a variant of heterotopic ossification, a common complication of traumatic brain injury, is the subject of some debates.(3) It is generally believed that the process of fracture healing is a recapitulation of normal embryonic osteogenesis,(4) i.e. ,a series of changes in the intracellular and extracellular matrix, which start from the injury of cells, blood vessels and bone matrix to a complete reconstruction of the bone.(5) It is a complex process influenced by multi-level and multi-route regulations of the general and local environments in the body, and many growth factors participate in this process, which is the base of bone healing;(6) whatever methods are used to promote bone healing, they are based on accelerating the changes of growth factors.(7) So it is worth making a thorough study on the mechanism, by which traumatic brain injury influences the expression levels of growth factors and consequently affects the speed of bone healing.
Sujets)
Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Sujet Principal: Physiologie / Encéphale / Lésions encéphaliques / Expression des gènes / Facteur de croissance fibroblastique de type 2 / Protéines oncogènes v-fos / Protéine oncogène p65(gag-jun) / Consolidation de fracture / Facteur de croissance endothéliale vasculaire de type A / Métabolisme Limites du sujet: Animaux / Humains langue: Anglais Texte intégral: Chinese Journal of Traumatology Année: 2007 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Sujet Principal: Physiologie / Encéphale / Lésions encéphaliques / Expression des gènes / Facteur de croissance fibroblastique de type 2 / Protéines oncogènes v-fos / Protéine oncogène p65(gag-jun) / Consolidation de fracture / Facteur de croissance endothéliale vasculaire de type A / Métabolisme Limites du sujet: Animaux / Humains langue: Anglais Texte intégral: Chinese Journal of Traumatology Année: 2007 Type: Article