Search Wikipedia

Bone healing
Article Talk

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

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.

Adequate nutrient intake has been found to significantly affect the

integrity of the fracture repair.[1] Age, bone type, drug therapy and
pre-existing bone pathology are factors that 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.[2]

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 remodelling phase.[citation needed]
Bone healing of a fracture by
While immobilization and surgery may facilitate healing, a fracture forming a callus as shown by X-ray.
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 that develop into chondroblasts and osteoblasts that
are essential to the healing of bone. Other sources of precursor cells are the bone marrow (when
present), endosteum, small blood vessels, and fibroblasts.[3]

Contents

Primary healing
Contact healing

Gap healing

Secondary healing
Reaction

Repair

Remodelling

Obstructions

Complications

Gallery

Radiologic timeline in young children

Footnotes

References

Primary healing

Primary healing (also known as direct healing) requires a correct anatomical reduction which is stable,
without any gap formation. Such healing requires only the remodeling of lamellar bone, the Haversian
canals and the blood vessels without callus formation. This process may take a few months to a few
years.[4]

Contact healing

When the gap between the bone ends is less than 0.01 mm, and interfragmentary strain is less than
2%, contact healing can occur. In this case, cutting cones, which consists of osteoclasts, form across
the fracture lines, generating cavities at a rate of 50–100 µm/day. Osteoblasts fill up the cavities with
the Haversian system. This causes the formation of lamellar bone that orients longitudinally along the
long axis of the bone. Blood vessels form that penetrate the Haversian system. Remodelling of lamellar
bone results in healing without callus formation.[4]

Gap healing

If the fracture gap is 800 µm to 1 mm, the fracture is filled by osteoblasts and then by lamellar bone
oriented perpendicular to the axis of the bone. This initial process takes three to eight weeks.
Perpendicular orientation of lamellar bone is weak, thus a secondary osteonal reconstruction is
required to re-orient the lamellar bone longitudinally.[4]

Secondary healing

Secondary healing (also known as indirect fracture healing) is the most common form of bone healing.
It usually consists of only endochondral ossification. Sometimes, intramembranous ossification occurs
together with endochondral ossification. Intramembranous ossification, mediated by the periosteal
layer of bone, occurs with the formation of callus. For endochondral ossification, deposition of bone
only occurs after the mineralised cartilage.[citation needed] This process of healing occurs when the
fracture is treated conservatively using orthopaedic cast or immobilisation, external fixation, or
internal fixation.[4]

Reaction

After bone fracture, blood cells accumulate adjacent to the injury site. Soon after fracture, blood
vessels constrict, stopping further bleeding. Within a few hours, the extravascular blood cells form a
clot called a hematoma[5] that acts as a template for callus formation. These cells, including
macrophages, release inflammatory mediators such as cytokines (tumor necrosis factor alpha (TNFα),
interleukin-1 family (IL-1), interleukin 6 (IL-6), 11 (IL-11), and 18 (IL-18)) and increase blood capillary
permeability. Inflammation peaks by 24 hours and completes by seven days. Through tumor necrosis
factor receptor 1 (TNFR1) and tumor necrosis factor receptor 2, TNFα mediates the differentiation of
mesenchymal stem cell (originated from the bone marrow) into osteoblast and chondrocytes. Stromal
cell-derived factor 1 (SDF-1) and CXCR4 mediate recruitment of mesenchymal stem cells. IL-1 and IL-6
are the most important cytokines for bone healing. IL-1 promotes formation of callus and of blood
vessels. IL-6 promotes differentiation of osteoblasts and osteoclasts.[4] All cells within the blood clot
degenerate and die. Within this area, the fibroblasts replicate. Within 7–14 days, they form a loose
aggregate of cells, interspersed with small blood vessels, known as granulation tissue.[citation needed]
Osteoclasts move in to reabsorb dead bone ends, and other necrotic tissue is removed.[6]

Repair

Seven to nine days after fracture, the cells of the periosteum

replicate and transform. The periosteal cells proximal to (on the
near side of) the fracture gap develop into chondroblasts, which
form hyaline cartilage. The periosteal cells distal to (at the far end
of) the fracture gap develop into osteoblasts, which form woven
bone[citation needed] through bone resorption of calcified cartilage
and recruitment of bone cells and osteoclasts.[4] The fibroblasts
within the granulation tissue develop into chondroblasts which
also form hyaline cartilage. These two new tissues grow in size Radiolucency around a 12-day-old
until they unite with each other. These processes culminate in a scaphoid fracture that was initially
barely visible.[7]
new mass of heterogeneous tissue known as a fracture
callus[citation needed] Callus formation peaks at day 14 of fracture.[4] Eventually, the fracture gap is
bridged[citation needed]

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 woven bone happens before
substitution of hyaline cartilage. The lamellar bone begins forming soon after the collagen matrix of
either tissue becomes mineralized[citation needed] At this stage, the process is induced by IL-1 and
TNFα.[4] The mineralized matrix is penetrated by 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[citation needed]

Remodelling

Remodeling begins as early as three to four weeks after fracture and may take 3 to 5 years to
complete.[4] The 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. This
process can be achieved by the formation of electrical polarity during partial weight bearing a long
bone;[citation needed] where electropositive convex surface and electronegative concave surface
activates osteoclasts and osteoblasts respectively.[4] This process can be enhanced by certain
synthetic injectable biomaterials, such as Cerament, which are osteoconductive and promote bone
healing[citation needed]

Obstructions
1. Poor blood supply which leads to the death of the osteocytes.
Bone cell death also depends on degree of fracture and
disruption to the Haversian system.

2. Condition of the soft tissues. Soft tissue between bone ends

restricts healing.

3. Nutrition and drug therapy. Poor general health reduces healing

rate. Drugs that impair the inflammatory response impede
healing also.
Femur (top) healed while improperly
4. Infection. Diverts the inflammatory response away from healing aligned
towards fighting off the infection.

5. Age. Young bone unites more rapidly than adult bone.

6. Pre-existing bone malignancy.

7. Mechanical factors such as the bone not being aligned, and too much or too little movement. Excess
mobility can disrupt the bridging callus, interfering with union; but slight biomechanical motion is seen
to improve callus formation.[6]

Complications

Complications of fracture healing include:

1. Infection: this is the most common complication of fractures and predominantly occurs in open
fractures. Post-traumatic wound infection is the most common cause of chronic osteomyelitis in
patients. Osteomyelitis can also occur following surgical fixation of a fracture.[8]

2. Non-union: no progression of healing within six months of a fracture occurring. The fracture pieces
remain separated and can be caused by infection and/or lack of blood supply (Ischaemia) to the
bone.[9] There are two types of non-union, atrophic and hypertrophic. Hypertrophic involves the
formation of excess callus leading to bone ends appearing sclerotic causing a radiological "Elephants
Foot" appearance[6] due to excessive fracture ends mobility but adequate blood supply.[4] Atrophic
non-union results in re-absorption and rounding of bone ends[6] due to inadequate blood supply and
excessive mobility of the bone ends.[4]

3. Mal-union: healing occurs but the healed bone has 'angular deformity, translation, or rotational
alignment that requires surgical correction'. This is most common in long bones such as the femur.[10]

4. Delayed union: healing times vary depending on the location of a fracture and the age of a patient.
Delayed union is characterised by 'persistence of the fracture line and a scarcity or absence of callus
formation' on x-ray. Healing is still occurring but at a much slower rate than normal.[9]

Gallery

Collagen fibers of woven Osteoclast displaying Light micrograph of

bone many nuclei within its decalcified cancellous
"foamy" cytoplasm. bone displaying
osteoblasts forming new
bone tissue, containing
two osteocytes, within a
resorption pit.

Radiologic timeline in young children

On medical imaging, secondary bone healing displays the following features over time in young
children:

Features and when they appear (and percentage of

individuals having the feature in that period or at that time
point)[11]
Resolution of soft tissues 7–10 days (or 2–21 days)

Gap widening 4–6 weeks (56%)

Periosteal reaction 7 days – 7 weeks

Marginal sclerosis 4–6 weeks (85%)

First callus 4–7 weeks (100%)

Radiodensity of callus > cortex 13 weeks (90%)

Bridging callus 2.6 – 13 weeks

Periosteal incorporation 14 weeks

Remodeling 9 weeks (50%)

Footnotes

1. ^ Karpouzos, A.; Diamantis, E.; Farmaki, P.;

Savvanis, S.; Troupis, T. (2017). "Nutritional
Aspects of Bone Health and Fracture Healing"
Journal of Osteoporosis. 2017: 1–10.
doi:10.1155/2017/4218472 . PMC 5804294
PMID 29464131 . 9. ^ a
2. ^ Gomez-Barrena E, Rosset P, Lozano D, Stanovici
J, Ermthaller C, Gerbhard F. Bone fracture healing:
Cell therapy in delayed unions and nonunions.
Bone. 2015;70:93–101.
3. ^ Ferretti C, Mattioli-Belmonte M. Periosteum
derived stem cells for regenerative medicine
proposals: Boosting current knowledge. World
Journal of Stem Cells. 2014;6(3):266-277.
doi:10.4252/wjsc.v6.i3.266.
4. ^ a b c d e f g h i j k l
Richard, Marsell; Thomas A,
Einhorn (1 June 2012). "The biology of fracture
healing" . Injury. 42 (6): 551–555.
doi:10.1016/j.injury.2011.03.031 . PMC 3105171
PMID 21489527 .
5. ^ "Overview of Bone Fractures" . The Lecturio
Medical Concept Library. Retrieved 26 August 2021.
6. ^ a b c d
Nyary Tamas, Scamell BE. (2015).
Principles of bone and joint injuries and their
healing. Surgery(Oxford). 33 (1), p 7-14.
7. ^ Jarraya, Mohamed; Hayashi, Daichi; Roemer,
Frank W.; Crema, Michel D.; Diaz, Luis; Conlin,
Jane; Marra, Monica D.; Jomaah, Nabil; Guermazi,
Ali (2013). "Radiographically Occult and Subtle
Fractures: A Pictorial Review" . Radiology
Research and Practice. 2013: 1–10.
doi:10.1155/2013/370169 . ISSN 2090-1941
PMC 3613077 . PMID 23577253 . CC-BY 3.0
8. ^ Rowbotham, Emma; Barron, Dominic (2009).
"Radiology of fracture complications". Orthopaedics
.
and Trauma. 23 (1): 52–60.
doi:10.1016/j.mporth.2008.12.008 .
.
b
Jahagirdar, Rajeev; Scammell, Brigitte E
(2008). "Principles of fracture healing and
disorders of bone union". Surgery. 27 (2): 63–69.
doi:10.1016/j.mpsur.2008.12.011 .
10. ^ Chen, Andrew T; Vallier, Heather A (2016).
"Noncontiguous and open fractures of the lower
extremity: Epidemiology, complications, and
unplanned procedures". Injury. 47 (3): 742–747.
doi:10.1016/j.injury.2015.12.013 .
PMID 26776462 .
11. ^ Unless otherwise specified in boxes, reference is:
- Prosser, Ingrid; Lawson, Zoe; Evans, Alison;
Harrison, Sara; Morris, Sue; Maguire, Sabine; Kemp,
Alison M. (2012). "A Timetable for the Radiologic
.
Features of Fracture Healing in Young Children" .
American Journal of Roentgenology. 198 (5): 1014–
1020. doi:10.2214/AJR.11.6734 . ISSN 0361-
803X . PMID 22528890 .
- Data is taken from scientific studies, notably Islam
et al. where data is contradictory to radiology
textbooks:
Islam, Omar; Soboleski, Don; Symons, S.; Davidson,
L. K.; Ashworth, M. A.; Babyn, Paul (2000).
"Development and Duration of Radiographic Signs
of Bone Healing in Children". American Journal of
Roentgenology. 175 (1): 75–78.
doi:10.2214/ajr.175.1.1750075 . ISSN 0361-
803X . PMID 10882250 .
.

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

Last edited on 25 December 2023, at 02:45

Content is available under CC BY-SA 4.0 unless otherwise noted.

Terms of Use • Privacy policy • Desktop

: