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Vasculature deprivation-induced osteonecrosis of rats’ femoral heads associated with the formation of deep surface depressions

  • J. Bejar
  • J. H. BossEmail author
Original Article
  • 110 Downloads

Abstract

An impeded blood flow through the femoral head is incriminated in the etiopathogenesis of osteonecrosis of the femoral head. The disorder is either primary (idiopathic avascular osteonecrosis) or secondary to one condition or another, such as corticosteroid medication, fracture of the neck, coagulation defects, physical or thermal damage, storage disorders, alcoholism, and infectious, autoimmune as also marrow infiltrating diseases. In the wake of the necrosis, several mediators are released in increased amounts, prime among which is the vascular endothelial growth factor. The intermediates recruit endothelial progenitor cells, macrophages, osteoclasts, fibroblasts, and osteoblasts, which, pervading throughout the necrotic areas, initiate the reparative processes. The dead, soft, and hard tissular debris is substituted by fibrous — later on by hematopoietic-fatty tissue — and bone. The newly formed, appositional and intramembranous bone is deficient in its mechanical properties. The ordinary load-carrying functions suffice to deform these weakened femoral heads so that osteoarthritic changes develop. Considering contemporary assumptions of the causes of osteonecrosis, oxygenation, revascularization, and core decompression are the realistic therapeutic interventions. Necrosis of rats’ femoral heads is studied as a model of osteonecrosis in both adults and children. In view of rodents’ lifelong persisting physeal cartilage, vascular deprivation-induced osteonecrosis in rats mimics children’s Perthes disease. The experimental model, which is well suited to test treatment modalities, has been used to investigate the effects of exposure to hyperbaric oxygen with and without non-weight bearing, medication of enoxaparin, and creation of an intraosseous conduit on the remodeling of the avascular necrotic femoral head. Intriguingly, the shape of treated rats’ femoral heads is disfigured to a greater degree than that of untreated animals. This is most likely due to the reduced yield strength and elastic modulus as well as the raised strain-to-failure of the recently formed bone making up the post-necrotic femoral heads. It follows that expedited osteogenesis is, counter intuition, detrimental to maintaining the hemispherical shape of the femoral head, and thus to an articulation with congruent load-bearing surfaces. If this is indeed the case, the remodeling of the necrotic femoral head should be delayed, rather than sped up, as the present day paradigm would have it. Bearing in mind that the dead osseous structures keep their mechanical attributes for quite a while, a slowed down new bone formation would favor the gradual replacement of the necrotic by living bone. Therefore, management of the adult patients with osteonecrosis and children with Perthes disease should focus on a slowly progressive substitution so that the decline of the bone’s mechanical properties is kept to a minimum. One viable therapeutic mode is a medication of inhibitors of the vascular endothelial growth factor.

Keywords

Femoral head Vascular deprivation-induced osteonecrosis Vascular deprivation-induced articular surface depression Drilling of articular surface of femoral head Rat 

Mots clés

Tête fémorale Ostéonécrose par privation vasculaire Rat 

Dévascularisation: ostéonécrose induite de la tête fémorale de rats

Résumé

Une gêne du flux sanguin à travers la tête fémorale est impliquée dans la pathogenèse de l’ostéonécrose de la tête fémorale. Le trouble est soit primitif (ostéonécrose avasculaire idiopathique), soit secondaire à l’une ou l’autre condition suivante, à savoir, corticothérapie, fracture du col, troubles de la coagulation, dommages thermiques ou physiques, obésité, alcoolisme, infections, troubles immunitaires et affections de la moelle osseuse. Lors du déclenchement de la nécrose différents médiateurs sont largués dans des proportions variables, dont le plus important est le facteur de croissance endothélial. Les intermédiaires recrutent les cellules endothéliales souches, les macrophages, ostéoclastes, fibroblastes et ostéoblastes qui en envahissant la zone de nécrose, initient le processus de reconstruction. Les débris nécrosés de tissus mous et osseux sont remplacés par du tissu fibreux, puis graisseux et hématopoïétique et enfin par de l’os. L’os néoformé, os d’apposition et membraneux est dépourvu de propriétés mécaniques. Les contraintes ordinaires liées au poids suffisent à déformer cette tête fémorale de faible consistance, de telle sorte que se développent des modifications ostéoarthosiques. En considérant les actuelles théories de l’étiopathogénie de l’ostéonécrose, l’oxygénation, la revascularisation et la décompression centrale sont des gestes réalistes. La nécrose des têtes fémorales de rats a été étudiée comme un modèle de l’ostéonécrose aussi bien des adultes que des enfants. La persistance durant toute leur vie du cartilage de conjugaison épiphysaire chez les rongeurs, fait que l’ostéonécrose induite par privation vasculaire imite la maladie de Legg- Perthes des enfants. Le modèle expérimental, conçu pour diverses modalités de traitement, a été utilisé pour étudier les effets de l’exposition à l’oxygénothérapie hyperbare, avec et sans contrainte de poids, à la médication par enoxaparine et la création d’un tunnel intra-osseux. Curieusement les têtes fémorales des rats traités sont déformées de façon plus importante que celles des animaux non-traités. Ceci est dû à la diminution du module élastique et à la moindre résistance de l’os néoformé dans les têtes fémorales réossifiées. Il en résulte que, contrairement à ce que l’on peut penser, l’ostéogenèse active se fait au détriment du maintient de la sphéricité et de la congruence des surfaces articulaires portantes. Si tel est le cas, le remodelage de la tête fémorale devrait pouvoir être ralenti et non-accéléré, comme on le pense actuellement. En gardant à l’esprit que les structures osseuses nécrosées gardent leurs propriétés mécaniques durant un certain temps, une néoformation osseuse lente sera à même de remplacer progressivement l’os nécrosé par de l’os vivant. C’est pourquoi, le traitement de l’ostéonécrose de l’adulte et celle des enfants ayant la maladie de Legg-Perthes devrait être centrée sur une lente et progressive substitution de telle sorte que la diminution des propriétés mécanique se fasse a minima. Une méthode utilisable est celle des médications inhibant le facteur de croissance de l’endothélium vasculaire.

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Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  1. 1.The Department of Pathology, Bnai-Zion Medical Center, the Bruce Rappaport Faculty of Medicine, TechnionIsrael Institute of TechnologyHaifaIsrael

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