Bone healing is a proliferative physiological process in which the body
facilitates the repair of a bone fracture.
1-Generally bone fracture treatment consists
of a doctor reducing (pushing) displaced bones back into place via relocation
with or without anaesthetic, stabilizing their position to aid union, and then
waiting for the bone's natural healing process to occur.
2-Adequate nutrient
intake has been found to significantly affect the integrity of the fracture
repair. Age, Bone type, drug therapy and pre existing bone pathology are
factors which affect healing. The role of bone healing is to produce new bone
without a scar as seen in other tissues which would be a structural weakness or
deformity.
3-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.
4-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.
There
are three major phases of fracture healing
1. Reactive
phase
Fracture and inflammatory phase
Granulation
tissue formation
2. Reparative
phase
Cartilage callus formation
Lamellar bone deposition
3. Remodeling
phase
. 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 adjacent
to the injury site. Soon after fracture, the blood vessels constrict, stopping
any further bleeding. Within a few hours after fracture, the extra vascular
blood cells form a blood clot, known as a hematoma. These cells release cytokines
and increase blood capillary permeability. 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. This
tissue reduces strain across the fracture site. Osteoclasts move in to reabsorb
dead bone ends and other necrotic tissue are removed.
Reparative
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.[12] 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.
Remodelling
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. This process can be enhanced by certain synthetic injectable
biomaterials, such as cerament, which are
osteoconductive and actively promote bone healing.
Obstructions to Bone Healing
1. Poor blood supply which leads to the death of the
osteocytes. Bone cell death is also dependent on degree of fracture and
disruption to the Haversian system.
2. Condition of the soft tissues. Soft tissue in between bone
ends restrict healing.
3. Nutrition and drug therapy. Poor general health reduces
healing rate. Drugs that impair the inflammatory response impede healing also.
4. Infection. Diverts the inflammatory response away from
healing towards fighting of the infection.
5. Age. Young bone unites more rapidly than adult bone.
6. Pre existing Bone malignancy.
7. Fracture healing is determined by mechanical factors and
obstructions to healing include the bone not aligned and too much or little
movement. Excess mobility can disrupt the bridging callus interfering with
union. Slight biomechanical motion is also seen to improve callus formation