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Bone healing

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 nal
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 broblasts
are other sources of precursor cells.

1 Phases of fracture healing

There are three major phases of fracture healing ,[3] two
of which can be further sub-divided to make a total of ve
1. Reactive Phase
i. Fracture and inammatory phase
ii. Granulation tissue formation
2. Reparative Phase
Bone healing of a fracture by forming a callus as shown by Xray.

iii. Cartilage Callus formation

iv. Lamellar bone deposition
3. Remodeling Phase

Bone healing, or fracture healing, is a proliferative

physiological process in which the body facilitates the repair of a bone fracture.

v. Remodeling to original bone contour

Generally bone fracture treatment consists of a doctor reducing (pushing) displaced bones back into place via re- 1.1 Reactive
location with or without anaesthetic, stabilizing their position, and then waiting for the bones natural healing pro- After fracture, the rst change seen by light and electron
microscope is the presence of blood cells within the tiscess to occur.
sues adjacent to the injury site. Soon after fracture, the
Adequate nutrient intake has been found to signicantly blood vessels constrict, stopping any further bleeding.[4]
aect the integrity of the fracture repair.[1] Recently, Within a few hours after fracture, the extravascular blood
speed and quality of fracture healing process and osteo- cells form a blood clot, known as a hematoma. All of the
genesis has been shown to greatly improve when fracture cells within the blood clot degenerate and die.[5] Some
area is suitably exposed to external static magnetic eld, of the cells outside of the blood clot, but adjacent to the
which seems to stimulate physiological processes behind injury site, also degenerate and die.[6] Within this same
most stages of osteogenesis [2]
area, the broblasts survive and replicate. They form a
The process of the entire regeneration of the bone can loose aggregate of cells, interspersed with small blood
depend on the angle of dislocation or fracture. While the vessels, known as granulation tissue.[7]




3. Fibrous Union: Improper immobilization

Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal (clos- 1.5 Gallery
est) to the fracture gap develop into chondroblasts which
Collagen bers of woven bone
form hyaline cartilage. The periosteal cells distal to (further from) the fracture gap develop into osteoblasts which
Osteoclast displaying many nuclei within its
form woven bone. The broblasts within the granulation
foamy cytoplasm.
tissue develop into chondroblasts which also form hya Osteoblasts forming compact bone, containing two
line cartilage.[8] These two new tissues grow in size unosteocytes, within a resorption pit in trabecular
til 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.[9] Eventually, the fracture gap is bridged by the
hyaline cartilage and woven bone, restoring some of its 2 See also
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 ossication 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.[10] Eventually, all of the
woven bone and cartilage of the original fracture callus is
replaced by trabecular bone, restoring most of the bones
original strength.



The remodeling process substitutes the trabecular bone

with compact bone. The trabecular bone is rst resorbed
by osteoclasts, creating a shallow resorption pit known as
a Howships lacuna. Then osteoblasts deposit compact
bone within the resorption pit. Eventually, the fracture
callus is remodelled into a new shape which closely duplicates the bones original shape and strength. The remodeling phase takes 3 to 5 years depending on factors such
as age or general condition.[7] This process can be enhanced by certain synthetic injectable biomaterials, such
as cerament, which are osteoconductive and actively promote bone healing.[11]


Complications of Fracture Healing

The main complications include: these

1. Delayed Union: Poor blood supply or infection.
2. Non-Union: Bone loss or wound contamination.

CNT Network Bio-Stress Sensors

3 Footnotes
[1] Susan E. Brown, PhD. How to Speed Fracture Healing.
Center for Better Bones. While no scientist has yet conducted a clinical trial using all 20 key nutrients for fracture
healing, several studies have found multi-nutrient therapy
to reduce complication and accelerate fracture healing.
[2] Singh,P., YashRoy,R.C. and Hoque, M. (2006)
Augmented bone-matrix formation and osteogenesis under magnetic eld stimulation in vivo XRD,
TEM and SEM investigations.
Indian Journal of
Biochemistry and Biophysics, vol. 43, pp. 167-172.
[3] Iain H. Kalfas, MD (2001). Principles of Bone Healing.
[4] Brighton and Hunt (1997), p. 248: The extravascular
blood cells are identied as erythrocytes, platelets and
[5] Brighton and Hunt (1991), p. 837: The cells within the
clot are identied.
[6] Brighton and Hunt (1997)
[7] Ham and Harris
[8] Brighton and Hunt (1997), p. 248: Two light micrographs
showing the cells of the woven bone and hyaline cartilage.
[9] Brighton and Hunt (1986), p. 704: Two light micrographs
of a typical fracture callus: one showing the tissues and the
other showing the cells.
[10] Brighton and Hunt (1986); Brighton and Hunt (1997);
Ham and Harris
[11] Hatten Jr., H.P. and Voor, J. (2012): Bone Healing Using a Bi-Phasic Ceramic Bone Substitute Demonstrated
in Human Vertebroplasty and with Histology in a Rabbit
Cancellous Bone Defect Model. Interventional Neuroradiology, vol. 18, pp. 105-113.

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 calcication, 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


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