Generally bone fracture treatment consists of a doctor reducing (pushing) displaced bones back into place via relocation with or without anaesthetic, stabilizing their position, and then waiting for the bone's natural healing process to occur.
Physiology and process of healing
In the process of fracture healing, several phases of recovery facilitate the proliferation and protection of the areas surrounding fractures and dislocations. The length of the process depends on the extent of the injury, and usual margins of two to three weeks are given for the reparation of most upper bodily fractures; anywhere above four weeks given for lower bodily injury.
The process of the entire regeneration of the bone can depend on the angle of dislocation or fracture. While the bone formation usually spans the entire duration of the healing process, in some instances, bone marrow within the fracture has healed two or fewer weeks before the final remodeling phase.
While immobilization and surgery may facilitate healing, a fracture ultimately heals through physiological processes. The healing process is mainly determined by the periosteum (the connective tissue membrane covering the bone). The periosteum is one source of precursor cells which develop into chondroblasts and osteoblasts that are essential to the healing of bone. The bone marrow (when present), endosteum, small blood vessels, and fibroblasts are other sources of precursor cells.
Phases of fracture healing
There are three major phases of fracture healing, two of which can be further sub-divided to make a total of five phases;
- 1. Reactive Phase
- i. Fracture and inflammatory phase
- ii. Granulation tissue formation
- 2. Reparative Phase
- iii. Cartilage Callus formation
- iv. Lamellar bone deposition
- 3. Remodeling Phase
- v. Remodeling to original bone contour
After fracture, the first change seen by light and electron microscope is the presence of blood cells within the tissues adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding. Within a few hours after fracture, the extravascular blood cells form a blood clot, known as a hematoma. All of the cells within the blood clot degenerate and die. Some of the cells outside of the blood clot, but adjacent to the injury site, also degenerate and die. Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue.
Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal (closest) to the fracture gap develop into chondroblasts which form hyaline cartilage. The periosteal cells distal to (further from) the fracture gap develop into osteoblasts which form woven bone. The fibroblasts within the granulation tissue develop into chondroblasts which also form hyaline cartilage. These two new tissues grow in size until they unite with their counterparts from other parts of the fracture. These processes culminate in a new mass of heterogeneous tissue which is known as the fracture callus. Eventually, the fracture gap is bridged by the hyaline cartilage and woven bone, restoring some of its original strength.
The next phase is the replacement of the hyaline cartilage and woven bone with lamellar bone. The replacement process is known as endochondral ossification with respect to the hyaline cartilage and bony substitution with respect to the woven bone. Substitution of the woven bone with lamellar bone precedes the substitution of the hyaline cartilage with lamellar bone. The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized. At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts. The osteoblasts form new lamellar bone upon the recently exposed surface of the mineralized matrix. This new lamellar bone is in the form of trabecular bone. Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabecular bone, restoring most of the bone's original strength.
The remodeling process substitutes the trabecular bone with compact bone. The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a "Howship's lacuna". Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled into a new shape which closely duplicates the bone's original shape and strength. The remodeling phase takes 3 to 5 years depending on factors such as age or general condition.
Complications of Fracture Healing
The main complications include:
- Delayed Union: Poor blood supply or infection.
- Non-Union: Bone loss or wound contamination.
- Fibrous Union: Improper immobilization
- Brighton and Hunt (1997), p. 248: The extravascular blood cells are identified as erythrocytes, platelets and neutrophils.
- Brighton and Hunt (1991), p. 837: The cells within the clot are identified.
- Brighton and Hunt (1997)
- Ham and Harris
- Brighton and Hunt (1997), p. 248: Two light micrographs showing the cells of the woven bone and hyaline cartilage.
- Brighton and Hunt (1986), p. 704: Two light micrographs of a typical fracture callus: one showing the tissues and the other showing the cells.
- Brighton and Hunt (1986); Brighton and Hunt (1997); Ham and Harris
- Brighton, Carl T. and Robert M. Hunt (1986), "Histochemical localization of calcium in the fracture callus with potassium pyroantimonate: possible role of chondrocyte mitochondrial calcium in callus calcification", Journal of Bone and Joint Surgery, 68-A (5): 703-715
- Brighton, Carl T. and Robert M. Hunt (1991), "Early histologic and ultrastructural changes in medullary fracture callus", Journal of Bone and Joint Surgery, 73-A (6): 832-847
- Brighton, Carl T. and Robert M. Hunt (1997), "Early histologic and ultrastructural changes in microvessels of periosteal callus", Journal of Orthopaedic Trauma, 11 (4): 244-253
- Ham, Arthur W. and William R. Harris (1972), "Repair and transplantation of bone", The biochemistry and physiology of bone, New York: Academic Press, p. 337-399