Callus hardening is the fourth phase of the five-phase secondary fracture healing process. Osteoblasts form a callus of connective tissue to bridge fracture gaps, which they mineralize with calcium to harden it. In fracture healing disorders, this process is impaired and the bone lacks stability.
What is callus hardening?
Callus hardening is the fourth phase of the five-phase secondary fracture healing process. A fracture occurs when a bone is completely severed after direct or indirect force. The elasticity or strength of the bone is exceeded by the impact, causing the bone to give way. Thus, two or more fractures are formed. A primary or direct fracture is when the bone breaks while retaining the periosteum. The fracture ends usually remain in contact and fracture healing leaves no visible scars. If there is a fracture gap of less than one millimeter, capillary-rich connective tissue fills the gap and is restructured step by step into a fully load-bearing bone. This is not possible with a secondary or indirect fracture. The fracture fragments are no longer in contact with each other in this type of fracture. A wide fracture gap lies between them. Fracture healing of a secondary fracture occurs in five phases. The injury phase, the inflammation phase and the granulation phase are followed by the callus hardening phase. The last phase corresponds to a remodeling phase and rounds off the other four steps. During callus hardening, scar tissue forms on the bone. This scar tissue hardens and thus serves to bridge the fracture gap.
Function and task
Callus hardening, by firmly bridging a fracture gap, allows bone fractures, with widely spaced fracture ends, to heal. Together with the four other phases of secondary fracture healing, it ensures the maintenance of a stable skeletal system. In the human organism, the so-called osteoblasts are responsible for the formation of new bone tissue. They develop from undifferentiated cells of the embryonic connective tissue (mesenchyme). By attaching themselves to bone in the form of skin layers, they indirectly create an initial basis for the formation of new bone substance. This base is also called bone matrix and consists mainly of type 1 collagen, calcium phosphates and calcium carbonates. These substances are released by the osteoblasts into the interstitial (interstitial) space. In the process, the cells transform into osteocytes capable of division. The framework of these cells mineralizes and becomes filled with calcium. The osteocyte network thus consolidated is incorporated into the new bone. Thus, osteoblasts are also involved in callus formation. A hematoma forms between the fracture sites. Subsequently, connective tissue forms at the fracture site. This connective tissue corresponds to the soft callus. The fracture callus is built by osteoblasts and is visible on radiographs about three months after the fracture. The radiologically visible callus formation only takes place when the fracture ends do not fully fit together. Indeed, only in this case are the osteoblasts forced to overbuild a gap. The osteoblasts build a thickening of the fracture site with the callus of connective tissue. This thickening is mineralized during callus hardening, giving it a load-bearing shape. During mineralization, osteoblasts fill the soft callus with calcium until it forms a stable bridge. Callus formation and its hardening take a total of three to four months. Over the next months to years, the thickening of the fracture changes. Osteoclasts reduce the extra substance to normal bone thickness. Boils are thus able to regenerate completely after a fracture.
Diseases and ailments
Various complications can occur during secondary fracture healing. For example, excessive callus formation may occur. If thickening at the fracture sites is conspicuously severe, this may indicate delayed fracture healing due to inadequate immobilization. In extreme cases, this phenomenon develops into pseudarthrosis. In the case of fractures near or directly in the joint, excessive callus hardening may also result in restricted movement, causing a contracture. Sometimes this also leads to compression of nerves and vessels.Surgical intervention is sometimes necessary for complications of this type. Complications during fracture healing can also be due to fracture healing disorders. For a secondary fracture to heal undisturbed, certain physiological conditions must be met. For example, the fracture area must be adequately supplied with nutrient-rich and oxygen-saturated blood and ideally be surrounded by soft tissue. The bone fragments must be brought into their original anatomical position and be in as close contact with each other as possible. If the bones are too far apart, they can move extensively and cause the connective tissue callus to tear before hardening. Poor stability, lack of immobilization and wide spacing are the most common causes of fracture healing problems. Smoking or malnutrition and underlying diseases such as diabetes and osteoporosis can also impair fracture healing by interfering with blood flow. Equally counterproductive to fracture healing are infections in the bone or soft tissues near the fracture. Genetic ossification disorders can also cause a bone healing disorder, such as brittle bone disease and all its related disorders. In some circumstances, medications also have a negative effect on healing. Examples of drugs of this type include cortisone and the cytostatic drugs used in cancer therapy.
