Body processes

Inflammatory phase – function, task and diseases

Inflammatory phase

The inflammatory phase is one of the five phases in secondary fracture healing . It cleans bacteria from the fracture site and activates immune cells that mediate the reconstruction of the bone . An insufficient inflammatory phase delays fracture healing and can thus cause pseudarthrosis .

What is the inflammatory phase?

A fracture is a broken bone . Medicine distinguishes between indirect and direct fractures. In direct fractures, the fragments are still in contact with each other, or at least are no more than a millimeter apart. They fit together perfectly and can thus grow together again as part of the primary fracture healing.

In the case of indirect bone fractures, fracture healing is not primary but secondary. The broken bones don’t fit together perfectly. The fracture gap between the fragments is more than one millimeter. This gap is bridged and mineralized during healing , allowing the bone to form a whole again. The callus between the fragments 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, above all white blood cells , mast cells and phagocytes , which clear out the fracture site.

Function & task

The inflammatory phase clears out the fracture site and surrounding tissue to allow osteoblasts and osteoclasts to work together to rebuild bone. The phase of the fracture that precedes it lasts only a few seconds. Immediately after the occurrence of a fracture, the one to seven-day inflammatory phase occurs.With every fracture, blood vessels in the bone and in the adjacent soft tissues are destroyed. The periosteum (the periosteum ) 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 disrupted blood supply and canicular lesions cut off the supply to the osteocytes, causing them to die. As the osteocytes die, they release lysosomal enzymes that degenerate the organic matrix and necrotize the fracture ends. The resulting tissue debris triggers an immunological inflammation .

Acute phase proteins migrate into the fracture area, such as interleukin-1 or -6. These proteins activate the proteolytic enzyme cascade, increasing the inflammatory response and blood flow . The immigrated platelets give the fracture hematoma stability and release the so-called plateled-derived growth factor and the transforming growth factor ß. This delivery brings reparative cells into play. There is a mediation of granulocytes , macrophages, endothelial cells, lymphocytes , osteoblasts and fibroblasts .

Many inflammatory mediators cause the endothelial cells to form leukocyte-specific adhesion molecules. These molecules mediate the attachment of leukocytes to vessel walls. The leukocytes 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 to the fracture site and become macrophages there, removing cellular debris and bacteria and creating hypoxic conditions. Angiogenesis stimulating factors are released. The fracture hematoma of the inflammatory phase is the most important source of cytokines in the early healing phase and at the same time connects the broken ends of the fracture with fibrin threads .

The immunological inflammation prepares the remodeling by gathering all the necessary cells around the fracture site and cleaning them from harmful and disruptive substances. The increased blood supply during this phase reaches six times the normal value after around two weeks, although the inflammatory phase has long since subsided.

Diseases & Ailments

If the inflammatory phase does not occur after a fracture, then there is probably an immunological deficiency. Such a situation can have serious consequences. The affected area is not cleared of bacteria and infection can set in. The healing of the fracture is delayed to a greater or lesser extent as a result. The doctor speaks of delayed wound healing if no ossification of the fracture site has taken place after 20 weeks.In addition to reduced immunological functions, poor blood circulation can also cause an insufficient inflammatory reaction. Liver diseases , malignancies or vascular diseases, obesity and diabetes mellitus can lead to an ineffective inflammatory phase after fractures.

If the fracture heals only with a long delay due to an immunologically reduced reaction, a non-union can develop. In addition to chronic swelling, the affected bone also has a reduced load-bearing capacity. Functional and movement impairments result. In extreme cases, after disturbances in the inflammatory phase, the fracture does not heal at all or only heals incompletely.

If infection occurs at the fracture site, the consequences are serious. The affected person is weakened and his body is out of balance. A defense reaction that is too weak enables the bacteria to spread. They can infect vital organs via the bloodstream and trigger generalized sepsis , which can be life-threatening. Surgical intervention may be necessary to prevent this.

In a healthy person of normal weight, however, infection as a result of a fracture is extremely rare. The delay in fracture healing is a far more common phenomenon and is exacerbated by insufficient immobilization of the affected bone.

Lisa Newlon
 | Website

Hello! I am Lisa Newlon, and I am a medical writer and researcher with over 10 years of experience in the healthcare industry. I have a Master’s degree in Medicine, and my deep understanding of medical terminology, practices, and procedures has made me a trusted source of information in the medical world.