It occurs if a fracture is adequately "fixed" through reduction, immobilization, and rehabilitation. Primary bone healing is the reestablishment of the cortex without the formation of a callus. This process takes place in the flat bones of the skull. The second type of ossification also occurs in the fetus this is intramembranous ossification this is the process by which mesenchymal tissue (primitive connective tissue) is converted directly to the bone, which no cartilage intermediate. This process is also the key to the formation of long bones in the fetus, in which the bony skeleton replaces the hyaline cartilage model. As described above, this occurs during the formation of bony callus, in which the newly formed collagen-rich cartilaginous callus gets replaced by immature bone. Īn important point to expand on is endochondral ossification, which is the name given for the process of conversion of cartilage to bone. The process of bone remodeling lasts for many months, ultimately resulting in the regeneration of the normal bone structure. Substantial remodeling of the vasculature occurs alongside these changes. The center of the callus is ultimately replaced by compact bone, while the callus edges become replaced by lamellar bone. With the continued migration of osteoblasts and osteoclasts, the hard callus undergoes repeated remodeling - termed 'coupled remodeling.' This 'coupled remodeling' is a balance of resorption by osteoclasts and new bone formation by osteoblasts. At the end of this phase, a hard, calcified callus of immature bone forms.īone Remodelling (Day 18 onwards, lasting months to years) The newly formed blood vessels continue to proliferate, allowing further migration of mesenchymal stem cells. Subperiosteally, woven bone continues to be laid down. As a result, the cartilaginous callus is resorbed and begins to calcify.
RANK-L is expressed, stimulating further differentiation of chondroblasts, chondroclasts, osteoblasts, and osteoclasts. The cartilaginous callus begins to undergo endochondral ossification. At the same time, adjacent to the periosteal layers, a layer of woven bone is laid down by the osteoprogenitor cells. As a result, chondrogenesis begins to occur, laying down a collagen-rich fibrocartilaginous network spanning the fracture ends, with a surrounding hyaline cartilage sleeve. Further mesenchymal stem cells are recruited to the area and begin to differentiate (driven by BMPs) to fibroblasts, chondroblasts, and osteoblasts.
The release of VEGF leads to angiogenesis at the site, and within the hematoma, fibrin-rich granulation tissue begins to develop. These cells act together to remove damaged, necrotic tissue and secrete cytokines like vascular endothelial growth factor (VEGF) to stimulate healing at the site.įibrocartilaginous Callus Formation (Days 5 to 11) These cytokines act to stimulate essential cellular biology at the site, attracting macrophages, monocytes, and lymphocytes. The injury to bone results in the secretion of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), bone morphogenetic proteins (BMPs), and interleukins (IL-1, IL-6, IL-11, IL-23). The hematoma clots and forms the temporary frame for subsequent healing. The blood vessels supplying the bone and periosteum are ruptured during the fracture, causing a hematoma to form around the fracture site. This stage begins immediately following the fracture. However, these stages have considerable overlap.
This process can be broken down into four stages.
The mechanism of fracture healing is an intricate and fluent process.
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