The inflammatory phase is one of the five phases in secondary fracture healing. It cleanses the fracture site of bacteria and calls upon immune cells to mediate bone reconstruction. An inadequate inflammatory phase delays fracture healing and can thus cause pseudarthrosis.
What is the inflammatory phase?
The inflammatory phase begins immediately after the actual fracture and is also called the inflammatory phase. A fracture is a break in the bone. Medicine distinguishes between indirect and direct fractures. In direct fractures, the fracture fragments are still in contact with each other or are at least no more than a millimeter apart. They fit together fully and can thus grow back together as part of primary fracture healing. In indirect fractures, fracture healing is secondary rather than primary. The bone fragments do not fully fit together. The fracture gap between the fracture pieces is more than one millimeter. This gap is bridged and mineralized during healing so that the bone forms a whole again. The callus between the fracture pieces is radiologically visible after healing. The inflammatory phase is one of five phases of secondary fracture healing. The other four phases are the injury phase, the granulation phase, the callus hardening phase, and the remodeling phase. The inflammatory phase begins immediately after the actual fracture and is also called the inflammatory phase. Various immune cells are involved in the phase, such as white blood cells, mast cells, and phagocytes in particular, which clear out the fracture site.
Function and task
The inflammatory phase clears out the fracture site and surrounding tissue so that osteoblasts and osteoclasts can work together to rebuild bone. The fracture phase that precedes it lasts only a few seconds. Immediately after a fracture occurs, the one to seven day inflammatory phase occurs. With each fracture, blood vessels in the bone and adjacent soft tissues are destroyed. The periosteum (the bone skin) and the surrounding muscles are also damaged and bleed into the fracture area. This causes a hematoma to form. In addition to the vessels, the canaliculi of the bone fragments are damaged. The interrupted blood supply and the canaliculi lesions disconnect the osteocytes from the supply, causing them to die. As they die, the osteocytes release lysosomal enzymes that degenerate the organic matrix and necrotize the fracture ends. The resulting tissue debris triggers immunologic inflammation. Acute-phase proteins migrate into the fracture site, such as interleukin-1 or -6. These proteins activate the proteolytic enzyme cascade, enhancing the inflammatory response and blood flow. The migrated platelets provide stability to the fracture hematoma and release the so-called platelet-derived-growth-factor and transforming-growth-factor-ß. This release brings reparative cells on the scene. Mediation of granulocytes, macrophages, endothelial cells, lymphocytes, osteoblasts, and fibroblasts occurs. Many inflammatory mediators cause endothelial cells to produce leukocyte-specific adhesion molecules. These molecules mediate the attachment of leukocytes to vessel walls. The leukocytes thus migrate into the wound tissue and fight invading bacteria. They release cytokines that initiate proliferation and differentiation of hematopoietic cells in the fracture area. Monocytes also migrate into the fracture area, where they become macrophages that remove cellular detritus and bacteria and create hypoxic conditions. Angiogenesis-stimulating factors are released. The fracture hematoma of the inflammatory phase is the main cytokine source in the early healing phase and at the same time connects the fracture ends through fibrin threads. The immunological inflammation prepares the remodeling by gathering all necessary cells around the fracture site and cleansing it from harmful and disturbing substances. The increased blood supply during this phase reaches six times normal after about two weeks, although the inflammatory phase has long since subsided by then.
Diseases and complaints
If the inflammatory phase is absent after a fracture, there is probably an immunologic deficiency. Such a condition can have serious consequences. The affected area is not cleared of bacteria and infections can set in.Fracture healing is delayed to a greater or lesser extent as part of this. The physician speaks of delayed wound healing if no ossification of the fracture site has taken place after 20 weeks. In addition to immunological dysfunctions, poor blood circulation, for example, can also cause an insufficient inflammatory response. For example, liver disease, malignancies or vascular disease, obesity, and diabetes mellitus can lead to an ineffective inflammatory phase after fractures. If the fracture heals only with a severe delay due to an immunologically diminished response, pseudarthrosis may develop. In addition to chronic swelling, this results in reduced load-bearing capacity of the affected bone. Functional and movement impairments result. In extreme cases, after disturbances of the inflammatory phase, the fracture does not heal at all or heals only incompletely. If infection of the fracture site occurs, this has serious consequences. The affected person is weakened and his organism gets out of balance. An insufficient defense reaction enables the bacteria to spread. Via the bloodstream, they can thus infect vital organs and trigger generalized sepsis, which can be life-threatening. To prevent this, surgical intervention may be necessary. However, in a healthy person of normal weight, infection as a result of a fracture is extremely rare. Delay in fracture healing is a much more common phenomenon and is exacerbated by inadequate immobilization of the affected bone.
