Explain the mechanism of fracture repair from a histology point of view.?

Question

Please include details such as cell types involved, what happens after what & why, etc.

Links to diagrams/pictures, quality sites appreciated.

I believe that's a picture of bone development. We just did that part in class. Bone growth is a different process. The picture is labelled wrong.

In any case, that is not a picture of fracture repair.

P.S. My previous blurb Re link to picture was regarding Emerson's link.

Answer 1

fracture healing

Once a fracture has occurred, almost immediately changes occur to the bone and surrounding tissue. Blood vessels clot, the normal vascular architecture of the bone marrow is lost as the cells within the marrow begin to reorganize. Within 24 hours these cells will transform into polymorphic cells with an osteoblastic phenotype and begin laying down bone.

At this point there are two types of bone healing, primary cortical healing and secondary fracture healing.


Primary cortical healing
(also called direct bone healing) represents an attempt by the cortex to directly reestablish cortical continuity. This type of healing requires absolute rigid stabilization (i.e. with a metal plate) after anatomic reduction of the fracture ends. Regions where the cortical ends are in contact stabilize the other regions where small gaps are found. Within the gaps, blood vessels will infiltrate and mesenchymal cells will follow close behind to begin laying down bone after differentiating into osteoblasts. The edges of the bones on either side of the gaps become necrotic and begin to resorb. Osteoclasts at the tip of cutting cones then begin to bridge the gaps and replace the tiny callus between the bones with new osteons . This process is called “gap healing”. The same process simultaneously occurs at regions where the cortices are in direct contact . When healing is complete there is no callus formation and the fracture has been replaced with new bridging osteons.


Secondary fracture healing (also called indirect bone healing) involves a completely different process that relies heavily on the periosteum for healing. With the loss of the endochondral blood supply, the periosteum rapidly becomes the primary blood supply to the surrounding bone. Osteoprogenitor cells within the periosteum are mobilized and begin to form bone by processes analogous to intramembranous ossification and endochondral bone formation. Peripheral to the site of the fracture intramembranous ossification takes place to form hard callus. Cartilage is not made before the matrix is solidified and structural proteins are employed from the beginning. The hard callus has an increased diameter when compared with the normal cortex, which helps reduce the strain on the fracture site. At the fracture site, bone is formed by endochondral ossification that requires the formation of a cartilage precursor. Eventually the cartilage is replaced by much the same mechanism as described in the chapter above . This process is enhanced by motion at the fracture site and inhibited by rigid fixation. Intramedullary nailing of fractures provides some relative fixation at a fracture site without eliminating all motion, as in rigid fixation with a plate. The IM nail is a powerful tool because it allows the process of secondary ossification to occur at a fracture site while keeping the bones aligned. Often a substantial callus can be seen at fracture sites that have been treated with an IM nail.

Answer 2

Osteoblasts are the bone forming cells while Osteoclasts are bone adsorption cells. Active Osteoblasts are situated on the perimysium of the bone. They produce alkaline phosphatase, an enzyme that catalyzes bone growth.

Depending on the type of facture, for instance a commuted fracture, the Osteoclasts will dissolve bone debris. The process releases calcium into the systemic circulation. These two processes together form what's called Bone Turnover or Remodeling.

Here is an image of this process:

http://en.wikipedia.org/wiki/Image:Illu_bone_growth.jpg