Avascular necrosis

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Avascular necrosis
Other namesOsteonecrosis, [1] bone infarction, [2] aseptic necrosis, [1] ischemic bone necrosis [1]
Head of femur avascular necrosis.jpg
Femoral head showing a flap of cartilage due to avascular necrosis (osteochondritis dissecans). Specimen removed during total hip replacement surgery.
Specialty Orthopedics
Symptoms Joint pain, decreased ability to move [1]
Complications Osteoarthritis [1]
Usual onsetGradual [1]
Risk factors Bone fractures, joint dislocations, high dose steroids [1]
Diagnostic method Medical imaging, biopsy [1]
Differential diagnosis Osteopetrosis, rheumatoid arthritis, Legg–Calvé–Perthes syndrome, sickle cell disease [3]
TreatmentMedication, not walking on the affected leg, stretching, surgery [1]
Frequency~15,000 per year (US) [4]

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. [1] Early on, there may be no symptoms. [1] Gradually joint pain may develop, which may limit the person's ability to move. [1] Complications may include collapse of the bone or nearby joint surface. [1]

Contents

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. [1] The condition may also occur without any clear reason. [1] The most commonly affected bone is the femur (thigh bone). [1] Other relatively common sites include the upper arm bone, knee, shoulder, and ankle. [1] Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI. [1] Rarely biopsy may be used. [1]

Treatments may include medication, not walking on the affected leg, stretching, and surgery. [1] Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. [1]

About 15,000 cases occur per year in the United States. [4] People 30 to 50 years old are most commonly affected. [3] Males are more commonly affected than females. [4]

Signs and symptoms

In many cases, there is pain and discomfort in a joint which increases over time. It can affect any bone, and for in about half of affected people, multiple sites are damaged. [5]

Avascular necrosis most commonly affects the ends of long bones, such as the femur. Other common sites include the humerus (upper arm), [6] [7] knees, [8] [9] shoulders, [6] [7] ankles and the jaw. [10]

Causes

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. [1] Other risk factors include radiation therapy, chemotherapy, and organ transplantation. [1] Osteonecrosis is also associated with cancer, lupus, sickle cell disease, [11] HIV infection, Gaucher's disease, and Caisson disease (dysbaric osteonecrosis). [1] [12] Bisphosphonates are associated with osteonecrosis of the mandible (jawbone). [13] The condition may also occur without any clear reason. [1]

Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood. [14] [15]

In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome, [16] and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation. [17]

Pathophysiology

The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. [2] Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days. [2]

Upon reperfusion, repair of bone occurs in two phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. [2] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. [2] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue. [2]

Diagnosis

Front X-ray of right knee of an adolescent (epiphyseal plates are open): arrows point to avascular necrosis and developing osteochondritis dissecans in the outer medial condyle of femur OCD Knee WalterReed-1.jpg
Front X-ray of right knee of an adolescent (epiphyseal plates are open): arrows point to avascular necrosis and developing osteochondritis dissecans in the outer medial condyle of femur

In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools. [18] [19]

X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. [2] The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts. [2] Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.[ citation needed ]

Types

When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböck's disease, which affects the lunate bone in the wrist. [21]

Treatment

A variety of methods may be used to treat [5] the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and the life spans of the hip joints (often around 20 to 30 years [22] ). THRs are an effective means of treatment in the older population; however, in younger people, they may wear out before the end of a person's life. [22]

Other techniques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. [23] Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN. [24]

Core decompression

Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head. [25] A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease. [11]

Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique. [26] [27]

Prognosis

The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth. [23] Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals. [23] In the course of avascular necrosis, however, the healing process is usually ineffective and the bone tissues break down faster than the body can repair them. If left untreated, the disease progresses, the bone collapses, [28] and the joint surface breaks down, leading to pain and arthritis. [1]

Epidemiology

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year.[ citation needed ]

Society and culture

Cases of avascular necrosis have been identified in a few high-profile athletes. It abruptly ended the career of American football running-back Bo Jackson in 1991. Doctors discovered Jackson to have lost all of the cartilage supporting his hip while he was undergoing tests following a hip-injury he had on the field during a 1991 NFL Playoff game. [29] Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade to the Green Bay Packers in 1992. [30] However, Favre would go on to have a long career at the Packers.[ citation needed ]

Another high-profile athlete was American road racing cyclist Floyd Landis, [31] winner of the 2006 Tour de France, the title being subsequently stripped from his record by cycling's governing bodies after his blood samples tested positive for banned substances. [32] During that tour, Landis was allowed cortisone shots to help manage his ailment, despite cortisone also being a banned substance in professional cycling at the time. [33]

Rafael Nadal successfully continued his tennis career after having surgery for Mueller–Weiss syndrome (osteonecrosis of the navicular.) [34]

See also

Related Research Articles

<span class="mw-page-title-main">Legg–Calvé–Perthes disease</span> Osteochondrosis that results in death and fracture located in hip joint

Legg–Calvé–Perthes disease (LCPD) is a childhood hip disorder initiated by a disruption of blood flow to the head of the femur. Due to the lack of blood flow, the bone dies and stops growing. Over time, healing occurs by new blood vessels infiltrating the dead bone and removing the necrotic bone which leads to a loss of bone mass and a weakening of the femoral head.

<span class="mw-page-title-main">Phossy jaw</span> Disease caused by phosphorus exposure

Phossy jaw, formally known as phosphorus necrosis of the jaw, was an occupational disease affecting those who worked with white phosphorus without proper safeguards. It is also likely to occur as the result of use of chemical weapons that contain white phosphorus. It was most commonly seen in workers in the matchstick industry in the 19th and early 20th centuries. It was caused by white phosphorus vapor, which destroys the bones of the jaw. Modern occupational hygiene practices have since eliminated the working conditions that caused this disease.

<span class="mw-page-title-main">Bisphosphonate</span> Pharmaceutical drugs for preventing bone loss

Bisphosphonates are a class of drugs that prevent the loss of bone density, used to treat osteoporosis and similar diseases. They are the most commonly prescribed drugs used to treat osteoporosis. They are called bisphosphonates because they have two phosphonate groups. They are thus also called diphosphonates.

<span class="mw-page-title-main">Alendronic acid</span> Chemical compound

Alendronic acid, sold under the brand name Fosamax among others, is a bisphosphonate medication used to treat osteoporosis and Paget's disease of bone. It is taken by mouth. Use is often recommended together with vitamin D, calcium supplementation, and lifestyle changes.

Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen (N2) embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers. Although the definitive pathologic process is poorly understood, there are several hypotheses:

<span class="mw-page-title-main">Slipped capital femoral epiphysis</span> Medical condition

Slipped capital femoral epiphysis is a medical term referring to a fracture through the growth plate (physis), which results in slippage of the overlying end of the femur (metaphysis).

<span class="mw-page-title-main">Osteochondritis dissecans</span> Ischemic bone disease

Osteochondritis dissecans is a joint disorder primarily of the subchondral bone in which cracks form in the articular cartilage and the underlying subchondral bone. OCD usually causes pain during and after sports. In later stages of the disorder there will be swelling of the affected joint which catches and locks during movement. Physical examination in the early stages does only show pain as symptom, in later stages there could be an effusion, tenderness, and a crackling sound with joint movement.

<span class="mw-page-title-main">Transient synovitis</span> Medical condition

Transient synovitis of hip is a self-limiting condition in which there is an inflammation of the inner lining of the capsule of the hip joint. The term irritable hip refers to the syndrome of acute hip pain, joint stiffness, limp or non-weightbearing, indicative of an underlying condition such as transient synovitis or orthopedic infections. In everyday clinical practice however, irritable hip is commonly used as a synonym for transient synovitis. It should not be confused with sciatica, a condition describing hip and lower back pain much more common to adults than transient synovitis but with similar signs and symptoms.

<span class="mw-page-title-main">Ibandronic acid</span> Chemical compound

Ibandronic acid is a bisphosphonate medication used in the prevention and treatment of osteoporosis and metastasis-associated skeletal fractures in people with cancer. It may also be used to treat hypercalcemia. It is typically formulated as its sodium salt ibandronate sodium.

<span class="mw-page-title-main">Osteonecrosis of the jaw</span> Medical condition

Osteonecrosis of the jaw (ONJ) is a severe bone disease (osteonecrosis) that affects the jaws. Various forms of ONJ have been described since 1861, and a number of causes have been suggested in the literature.

<span class="mw-page-title-main">Crescent sign</span>

In radiology, the crescent sign is a finding on conventional radiographs that is associated with avascular necrosis. It usually occurs later in the disease, in stage III of the four-stage Ficat classification system. It appears as a curved subchondral radiolucent line that is often found on the proximal femoral or humeral head. Usually, this sign indicates a high likelihood of collapse of the affected bone. The crescent sign may be best seen in an abducted (frog-legged) position.

<span class="mw-page-title-main">Hip dysplasia</span> Joint abnormality

Hip dysplasia is an abnormality of the hip joint where the socket portion does not fully cover the ball portion, resulting in an increased risk for joint dislocation. Hip dysplasia may occur at birth or develop in early life. Regardless, it does not typically produce symptoms in babies less than a year old. Occasionally one leg may be shorter than the other. The left hip is more often affected than the right. Complications without treatment can include arthritis, limping, and low back pain. Females are affected more often than males. Risk factors for hip dysplasia include female sex, family history, certain swaddling practices, and breech presentation whether an infant is delivered vaginally or by cesarean section. If one identical twin is affected, there is a 40% risk the other will also be affected. Screening all babies for the condition by physical examination is recommended. Ultrasonography may also be useful.

<span class="mw-page-title-main">Medication-related osteonecrosis of the jaw</span> Medical condition

Medication-related osteonecrosis of the jaw is progressive death of the jawbone in a person exposed to a medication known to increase the risk of disease, in the absence of a previous radiation treatment. It may lead to surgical complication in the form of impaired wound healing following oral and maxillofacial surgery, periodontal surgery, or endodontic therapy.

<span class="mw-page-title-main">Spontaneous osteonecrosis of the knee</span> Medical condition

Spontaneous osteonecrosis of the knee is the result of vascular arterial insufficiency to the medial femoral condyle of the knee resulting in necrosis and destruction of bone. It is often unilateral and can be associated with a meniscal tear.

<span class="mw-page-title-main">Femoroacetabular impingement</span> Medical condition

Femoroacetabular impingement (FAI) is a condition involving one or more anatomical abnormalities of the hip joint, which is a ball and socket joint. It is a common cause of hip pain and discomfort in young and middle-aged adults. It occurs when the ball shaped femoral head contacts the acetabulum abnormally or does not permit a normal range of motion in the acetabular socket. Damage can occur to the articular cartilage, or labral cartilage, or both. The condition may be symptomatic or asymptomatic. It may cause osteoarthritis of the hip. Treatment options range from conservative management to surgery.

<span class="mw-page-title-main">Chandler's disease</span> Medical condition

Chandler's disease, also known as idiopathic avascular osteonecrosis of the femoral head, is a rare condition in which the bone cells in the head of the femur (FH) die due to lack of blood. This disease is caused when blood flow is reduced to the part of a bone near a joint. It is specifically unique because the femoral head is for some reason the only affected part of the body and rarely travels down to the main part of the femur. In 1948, F. A. Chandler did a multi-case review and first released his interpretations as Coronary Disease of the Hip. This term is now considered incorrect as it improperly describes the actual disease.

<span class="mw-page-title-main">Hip pain</span>

Pain in the hip is the experience of pain in the muscles or joints in the hip/ pelvic region, a condition commonly arising from any of a number of factors. Sometimes it is closely associated with lower back pain.

<span class="mw-page-title-main">Phemister graft</span>

A Phemister graft is a type of bone graft which uses bone tissue harvested from the patient to treat slow-healing, or delayed union bone fractures. Thus, it is a form of autotransplantation. Typically, the tissue used in the graft is cancellous bone harvested from the patient's Iliac crest and laid in strips across the fracture site. The use of the patient's living bone stimulates osteogenesis, the growth of bones.

Dieterich's disease, also known as avascular necrosis of the metacarpal head, is an extremely rare condition characterized by temporary or permanent loss of blood supply to the metacarpal head of the metacarpal bone, resulting in loss of bone tissue. The five metacarpal bones are long bones located between the carpals of the wrist and phalanges of the fingers. Collectively, the metacarpals are referred to as the "metacarpus."

<span class="mw-page-title-main">Trabecular oedema</span> Medical condition

Trabecular edema, also known as bone marrow edema (BME), is a traditional term describing the interstitial fluid accumulation at the trabecular bone marrow. The term was first used in 1988, referring to the changes in the bone marrow due to inflammation. Bone marrow edema was later renamed to bone marrow lesion (BML), as later studies show that the increased fluid content in the trabecular bone was more likely caused by inflammatory responses instead of fluid influx. Hence, this narrows down the condition to the damage at the articular surface of the trabecular bones. Despite so, the terms BME and BML are still used interchangeably in radiology.

References

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