Bone infarction, also known as avascular necrosis (AVN) or osteonecrosis, is defined by the death of bone tissue. This cellular death occurs when the blood supply to a section of bone is temporarily or permanently interrupted. Without a steady flow of blood, bone cells cannot receive the oxygen and nutrients needed for survival. The condition can lead to tiny fractures within the bone structure, potentially causing the entire bone to collapse over time.
Understanding the Mechanism of Bone Death
The core problem in bone infarction is ischemia, which is the lack of adequate blood flow to the bone tissue. This interruption quickly leads to the death of specialized bone cells, particularly osteocytes and bone marrow cells. When these cells die, the structural integrity of the bone is compromised because the constant process of bone breakdown and renewal is halted.
Cellular death is most often seen in the epiphyses, the ends of the long bones that form the joints. Areas like the femoral head in the hip, the humeral head in the shoulder, and the bones of the knee are particularly vulnerable. These sites have a naturally limited blood supply, meaning they lack extensive collateral circulation to compensate for a blockage.
The lack of blood flow prevents the body’s repair mechanisms from working, causing the affected area to weaken and collapse. In the hip, this process can lead to the flattening of the femoral head, which severely disrupts joint movement. This structural damage often results in the rapid development of severe osteoarthritis in the adjacent joint.
Primary Causes and Risk Factors
Bone infarction is categorized by its origin: traumatic or non-traumatic. Traumatic causes involve an acute injury that directly damages the blood vessels supplying the bone. A severe fracture or joint dislocation, especially in the hip, can physically sever or compress the blood vessels, immediately cutting off circulation.
Non-traumatic causes are more numerous and involve underlying medical conditions or lifestyle factors that compromise the blood vessels from within. The most common non-traumatic cause is the use of high-dose glucocorticoids (steroids), which increases the fat content in the blood. These fatty deposits (lipids) can then block the small blood vessels that nourish the bone.
Excessive alcohol consumption also contributes to the formation of fatty emboli that obstruct blood flow. Certain medical conditions alter blood composition or circulation, significantly increasing risk.
Medical Conditions and Risk Factors
- Sickle cell disease, where abnormally shaped red blood cells clog small vessels.
- Gaucher disease, which involves the buildup of fatty substances.
- Systemic conditions like lupus and clotting disorders that impair circulation.
- Decompression sickness (“the bends”), which causes nitrogen bubbles to form in the bloodstream and block small arteries.
Recognizing the Signs and Confirmation
In its earliest stages, bone infarction may cause no symptoms, making detection challenging. As the condition progresses and the bone structure weakens, the primary symptom is pain localized to the affected joint. This pain is often mild initially but worsens when placing weight on the joint, such as walking or standing.
As the damage advances, the pain may become constant, persisting even during rest. Avascular necrosis of the hip often presents as pain in the groin, thigh, or buttock, and can lead to a noticeable limp or limited range of motion. These physical limitations occur as the damaged bone loses the smooth, spherical shape necessary for proper joint function.
Confirming a diagnosis requires medical imaging, as a physical exam alone cannot detect internal bone death. Early on, standard X-rays may appear normal because the bone has not yet structurally collapsed. Magnetic Resonance Imaging (MRI) is the most sensitive tool for early diagnosis, capable of detecting changes in the bone marrow before structural damage is visible.
Computed Tomography (CT) scans and bone scans may also be used to stage the disease and assess the extent of the damage. Early detection is a significant factor in treatment planning, as interventions performed before the bone collapses have a higher chance of preserving the joint. The presence of a subchondral fracture, sometimes called the “crescent sign,” on imaging indicates the bone is on the verge of collapse.
Therapeutic Approaches
Treatment for bone infarction depends heavily on the stage of the disease at diagnosis. Non-surgical approaches are usually reserved for the earliest stages or for managing symptoms. These methods include limiting weight-bearing on the affected joint, often using crutches, to prevent further structural damage.
Medication options involve nonsteroidal anti-inflammatory drugs (NSAIDs) to manage pain and inflammation. In some cases, drugs that reduce blood cholesterol or thin the blood may be prescribed to address underlying causes of vascular obstruction. Physical therapy can also be used to maintain the range of motion and strength in the surrounding muscles.
For more advanced stages, or when non-surgical methods fail, surgical intervention is necessary.
Joint-Preserving Surgery
A procedure called core decompression is a common technique used before the bone has collapsed. This surgery involves drilling small channels into the dead bone area to relieve internal pressure and stimulate the formation of new blood vessels and bone tissue.
Joint Replacement
In cases where the bone has already collapsed or the joint has developed severe arthritis, the definitive treatment is total joint replacement (arthroplasty). This involves removing the damaged bone and cartilage and replacing the joint surfaces with metal, plastic, or ceramic components. For hip involvement, total hip replacement is a successful procedure that restores function and alleviates chronic pain.