Bone Fracture Healing
1. What exactly (physics or physical parameters) causes an increase in volume of local tissue following an inflammation – associated with the initial anabolic phase of fracture healing?
2. What is the physics associated with the formation of hematoma which essentially acts as a temporary scaffold for stem cell differentiation into fibrous tissue, cartilage and bone?
3. What exactly controls the release of cytokinetic factors such as TNF-α, TFG-β, BMP, IL-1 β, IL-6, IL-7F & IL-23 during an inflammatory phase?
4. How exactly mechanical loads (strain or hydrostatic pressure) play a crucial role in bone fracture healing on top of the role played by the released cytokinetic factors?
5. How exactly the coupling effect between the biological factors and mechanical environment keep regulating the activities of MSC (mesenchymal stem cells) – in addition to the activities of chondrocytes, osteoblasts, fibroblasts and endothelial cells?
6. Where do we stand with reference to the understanding of the interaction between cellular activities and the mechanical environment?
7. During the reparative phase (following an inflammatory phase), what exactly dictates the formation of cartilaginous callus (soft callus) through the activities of skeletal and endothelial cells, which essentially bridge the gap between the bone fragments – before its progresses into hard callus?
8. What exactly decides the resulting mechanism (intramembranous ossification, where MSCs differentiate to osteoblasts and thereby creating bone tissue directly in an anabolic process; or, endochondral ossification where MSCs differentiate into chondrocytes, which essentially create a cartilage tissue usually associated with long bones; or, both) by which the bone should be formed?
9. During primary bone healing, what is the amount of strain generated, where the bony fragments remain tightly fixed under compression from implantation; and where, the healing remains directed by osteoclasts and osteoblasts activities in the absence of callus formation?
10. During secondary bone healing, do we still end up with significant strain resulting from the mobility associated with the fracture site?
During the formation of soft callus associated with the mobility of inter-fragments, whether the formation of secondary bone through both intramembranous and endochondral ossifications have an accumulated strain? How to have a control over the developed strain during the transition between anabolic phase and catabolic phase upon reduction in callus volume?
11. How exactly the coordination between osteoblast and osteoclast remains controlled as a function of strain during the bone remodeling phase?
And, how does the accumulated strain gets vanished during the reabsorption of callus tissues and during the formation of lamellar bone?
Afin de mieux comprendre votre problématique je conseille vivement la lecture de l article de Frost H.M. sur la théorie du Mécanostat. (Mécanisation déterminants of bonne modélisation.
Met. bone. Dis. Rel. Res.,4:217-229. 1982.
- Badges
- Science method