thumbnail|200px|right|Bone healing of a fracture by forming a callus as shown by [[X-ray.]]
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. 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.
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.
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 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.
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.
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 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.
Repair
thumb|Radiolucency around a 12-day-old [[scaphoid fracture that was initially barely visible.]]
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 through bone resorption of calcified cartilage and recruitment of bone cells and osteoclasts.
- 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. 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
- 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.
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| Resolution of soft tissues || 7–10 days (or 2–21 days)
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| Gap widening || 4–6 weeks (56%)
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| Periosteal reaction || 7 days – 7 weeks
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| Marginal sclerosis || 4–6 weeks (85%)
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| First callus || 4–7 weeks (100%)
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| Radiodensity of callus > cortex || 13 weeks (90%)
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| Bridging callus || 2.6 – 13 weeks
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| Periosteal incorporation || 14 weeks
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| Remodeling || 9 weeks (50%)
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Footnotes
References
- 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