Callus hardening

The Callus hardening is the fourth phase of the five-phase secondary fracture healing. Osteoblasts form a callus of connective tissue to bridge fracture gaps, which they mineralize with calcium and thus harden. In fracture healing disorders, this process is impaired and the bone lacks stability.

What is callus hardening?

A fracture occurs when a bone is completely severed after direct or indirect violence. The elasticity or strength of the bone is exceeded by the action, so that the bone gives way. This creates two or more fractions.

A primary or direct fracture is when the bone breaks while preserving the periosteum. The ends of the fracture usually remain in contact and the fracture healing does not leave any visible scars. If there is a fracture gap of less than a millimeter, capillary-rich connective tissue fills the gap and is gradually restructured into a fully resilient bone. This is not possible with a secondary or indirect break. In this type of fracture, the fragments are no longer in contact with one another. There is a wide crack between them.

The fracture healing of a secondary bone fracture proceeds in five phases. The phase of callus hardening follows the injury phase, the inflammation phase and the granulation phase. The last phase corresponds to a conversion phase and rounds off the other four steps. When callus hardening, scar tissue forms on the bone. This scar tissue hardens and thus serves to bridge the fracture gap.

Function & task

Callus hardening enables bone fractures with far apart fracture ends to heal through the firm bridging of a fracture gap. Together with the four other phases of secondary fracture healing, it ensures the maintenance of a stable skeletal system.

So-called osteoblasts are responsible for building new bone tissue in the human organism. They arise from undifferentiated cells of the embryonic connective tissue (mesenchyme). By attaching themselves to the bones like a layer of skin, they indirectly create an initial basis for building new bone substance. This base is also called the bone matrix and consists primarily of type 1 collagen, calcium phosphates and calcium carbonates.

These substances are released into the interstitial space by the osteoblasts. The cells are transformed into osteocytes that can divide.The framework from these cells mineralizes and is filled with calcium. The osteocyte network strengthened in this way is built into the new bone.

The osteoblasts are thus also involved in callus formation. A hematoma forms between the break points. Then connective tissue forms at the break point. This connective tissue corresponds to the soft callus. The fracture callus is built by osteoblasts and is visible on x-rays about three months after the fracture. The radiologically visible callus formation only takes place when the fracture ends do not fully fit together. Only in this case are the osteoblasts forced to build over a gap.

The osteoblasts build a thickening of the fracture site with the callus made of connective tissue. This thickening is mineralized during callus hardening and is given a resilient shape. During mineralization, the 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 few months to years, the thickening of the fracture site will change. Osteoclasts restore the multiple substance to the normal bone thickness. Boils are able to regenerate completely after a fracture.

Illnesses & ailments

Various complications can arise during secondary fracture healing. For example, excessive callus formation can occur. If the thickening at the fracture points is noticeably severe, this can be an indication of delayed fracture healing due to insufficient immobilization. In extreme cases, this phenomenon develops into pseudarthrosis.

In the case of fractures in the vicinity of the joint or directly in the joint, excessive callus hardening can also result in restricted movement, which causes a contracture. Sometimes this also results in compression of nerves and vessels. Surgical intervention is sometimes necessary for such complications.

Complications during fracture healing can also result from bone fracture healing disorders. In order for a secondary fracture to heal undisturbed, certain physiological requirements 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 as possible with one another. If the bones are too far apart, they can move around extensively and cause the connective tissue callus to tear before hardening. Poor stability, lack of immobilization and long distances are the most common causes of bone fracture healing disorders.

Smoking or malnutrition and underlying diseases such as diabetes and osteoporosis can also impair the healing of the fracture, as they disrupt the blood flow. Infections in the bone or in the soft tissues near the fracture are also counterproductive to fracture healing.

Genetic ossification disorders can also cause bone healing disorders, for example vitreous bone disease and all diseases related to it. Medicines may also have a negative effect on healing. Examples of drugs of this type are cortisone and the cytotoxic drugs used in cancer therapy.