Bone healing

  Bone healing or fracture healing is a proliferative physiological process, in which the body facilitates repair of bone fractures.

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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 is relevant to the extent of the injury, and usual margins of two to three weeks are given for the reparation of the majority of upper bodily fractures; anywhere above four weeks given for lower bodily injury.

The process of the entire regeneration of the bone can depend upon the angle of dislocation or fracture, and dislocated bones are generally pushed back into place via relocation with or without anaesthetic. While the bone formation usually spans the entire duration of the healing process, in some instances, bone marrow within the fracture having 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 the primary 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 secondary 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. Callus formation
  • iv. Lamellar bone deposition
• 3. Remodeling Phase
  • v. Remodeling to original bone contour

Reactive

After fracture, the first change seen by light and electron microscopy is the presence of blood cells within the tissues which are adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding.^[1] Within a few hours after fracture, the extravascular blood cells, known as a "hematoma", form a blood clot. All of the cells within the blood clot degenerate and die.^[2] Some of the cells outside of the blood clot, but adjacent to the injury site, also degenerate and die.^[3] 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.^[4]

Reparative

Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal to the fracture gap develop into chondroblasts and form hyaline cartilage. The periosteal cells distal to the fracture gap develop into osteoblasts and form woven bone. The fibroblasts within the granulation tissue also develop into chondroblasts and form hyaline cartilage.^[5] These two new tissues grow in size until they unite with their counterparts from other pieces of the fracture. This process forms the fracture callus.^[6] 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, "vascular channels" with many accompanying osteoblasts penetrate the mineralized matrix. 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.^[7] Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabecular bone, restoring much, if not all, of the bone's original strength.

Remodeling

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.^[8]

Other forms and complications

Inadequate healing or formation

Inadequate bone healing is known as an "incomplete" form of bone healing, in which the regeneration of bone through natural processes is impeded due to other factors, such as malnutrition or immune disorders, which may prevent the reparation of bone due to the lack of nutrient intake, such as that seen in the case of osteomalacia and osteoporosis.

Similarly, factors such as the intake of carcinogens, such as nicotine or exposure to radiation may lead to the malformation or incomplete healing of bones, which can further facilitate the formation of newer fractures, due to the already weakened site of injury being more easily affected by impact or strain, as well pseudarthrosis, undesired mobility in what appears to have become a new joint.

Medical treatments

In terms of medical treatments and procedures, several options are available which facilitate faster reparation of bone if the specific patient has an aforementioned bone disorder. The use of Bone morphogenetic proteins is incurred in small amounts, and is also used in clinical practice, alongside immobilising surgical procedures involving vertebroplasty or percutaneous kyphoplasty in the case of bone malformation, and stimulate the growth of bone in areas which require "strengthening", such as in the case of spinal fusion.

Osseointegration

Osseointegration is the pattern of growth exhibited by bone tissue during assimilation of surgically-implanted devices, prostheses or bone grafts to be used as either replacement parts (e.g., hip) or as anchors (e.g., endosseous dental implants).

References

• 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

Notes

External links

• Long bone fracture and healing