Bone healing

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

Contents 1 Physiology and process of healing 1.1 Phases of fracture healing 1.1.1 Reactive Phase 1.1.2 Reparative Phase 1.1.3 Remodeling Phase 2 Other forms and complications 2.1 Inadequate bone healing 3 Medical Treatments 3.1 Osseointegration 4 References 5 Notes 6 External links

[edit] 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.

[edit] Phases of fracture healing

There are three phases of fracture healing which are separated into 5 total phases;

1. Reactive Phase

2. • Fracture and inflammatory phase

   • Granulation tissue formation

3. Reparative Phase

4. • Callus formation

   • Lamellar bone deposition

5. Remodeling Phase

6. • Remodeling to original bone contour

[edit] Reactive Phase

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]

[edit] Reparative Phase

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][8][9] Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabeclular bone, restoring much, if not all, of the bone's original strength.

[edit] Remodeling Phase

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.^[10]

Treatment:

The treatment of a pathological fracture consists of; 1. Detecting the underlying cause of the fracture 2. Making an assessment of the capacity of the fracture to unite, based on the nature of the underlying disease.

A fracture in the bone affected by a generalized disease like Paget’s disease, osteogenesis imperfecta or osteoporosis is expected to unite with conventional methods of treatment. A fracture at the site of bone cyst or a benign tumor will also generally unite but the union may be delayed. Fractures occurring in osteomyelitic bones take a long time and sometimes fail to unite despite the best efforts. Fractures through metastatic bone lesions often do not unite at all, though the union may occur if the malignancy has been brought under control by chemotherapy or radiotherapy. With the availability of facilities for internal fixation, more and more pathological fractures are now being treated operatively with an aim to; 1. Enhance process of union by bone grafting. 2. Mobilize the patient by surgical stabilization of the fracture.

HEALING OF FRACTURES: Healing starts immediately after fracture has occurred and is a continuous process.

1. STAGE OF HAEMATOMA: As the result of the tearing of blood vessels at the time of the injury, a haematoma is formed at the fracture site .A very small portion of bone immediately adjacent to the fracture dies and is gradually absorbed. There is a proliferation of cells from the deep surface of periosteum adjacent to the fracture site. These cells are the precursors of the osteoblasts and form round each fragment of the bone. At the same time cells proliferate from the endosteum in each fragment and this tissue gradually forms a bridge between the bone ends. During this stage the haematoma is gradually absorbed.

2. STAGE OF SUB-PERIOSTEAL AND ENDOSTEAL PROLIFERATION: There is a proliferation of cells from the deep surface of the periosteum adjacent to the fracture site. These cells are the precursors of osteoblasts and form around each fragment of the bone. At the same time cells proliferate from the endosteum in each fragment and this tissue gradually forms a bridge between the bone ends. During this stage the haematoma is gradually absorbed.

3. STAGE OF CALLUS FORMATION: The proliferating cells mature as osteoblasts or in some cases as chondroblasts. Chondroblasts form cartilage and this is found in varying amounts at fracture site but is not essential to healing. The osteoblasts lay down an intercellular matrix of collagen and polysaccharides which then become impregnated with calcium salts thus forming the immature bone called callus or weaven bone. This is visible in X-Ray and gives evidence of healing.

4. STAGE OF CONSOLIDATION: Osteoblastic activity results in the change of primary callus to bone which has a lamellar structure and at the end of this stage, union is complete. This new bone forms a thickened mass at the fracture site and obliterates the medullary cavity. The amount of this new bone varies for a number of reasons. It tends to be more extensive if there has been a large haematoma or it has been impossible to obtain the exact position of the bone fragments.

5. STAGE OF REMODELLING: The lamellar structure is changed and the bone is strengthened along the line of stress. The surplus bone formed during healing is gradually removed and eventually the bone structure appears very similar to the original. In children, healing is usually very good and it is difficult to see the fracture site on a radiograph. In adults, there is a permanent area of thickening which might be felt or seen in the superficial bone.

[edit] Other forms and complications

[edit] Inadequate bone healing

Inadequate bone healing may predispose to further fractures at the same site, as well pseudarthrosis, undesired mobility in what appears to have become a new joint.

Many factors may contribute to lack of bone healing, including smoking (nicotine is known toxin for bones)[1]

[edit] Medical Treatments

Many treatments may be employed to stimulate bone healing. A few treatments include: - Bone morphogenetic proteins (BMP) are used to stimulate formation of new bone growth in areas such as with a spinal fusion. - Sex - During sexual intercourse and/or stimulation of the genitalia small amounts of BMP are released into the blood stream. - Electrical stimulation - either external or internal - may be used to stimulate bone growth and healing after a spinal fusion - Surgery to immobolize the bone may be used in certain instances to help a fracture heal. For example, with a spinal fracture, vertebroplasty or kyphoplasty may be used to immobolize a vertebra and create a better healing environment.

[edit] 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).

[edit] 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

[edit] Notes

[edit] External links

Article on Spine-health.com about bone healing.