Avascular Necrosis Specialist

Are you or someone you love suffering from Avascular Necrosis of your hip or knee and looking for an avascular necrosis specialist?


Avascular necrosis or osteonecrosis of the femoral head means that the bone in the femoral head has died due to interruption in the blood supply. There are series of events that lead to interruption in the blood supply of the femoral head that leads to death of the bone cells, fracture and collapse of the femoral head.

Avascular necrosis of the femoral head typically affects young active people and unless treated the course is relentless leading to arthritis of the hip. Although the exact pathophysiology is not very clear, there are many risk factors that can lead to osteonecrosis of the femoral head.

Dr. Karkare was on a recent WCBS 12 segment about Avascular Necrosis with Dr. Max Gomez:

In the United States the main risk factors are alcohol intake and corticosteroid therapy. The vast majority of cause of necrosis of the femoral head remains idiopathic, which means the exact cause of avascular necrosis is unknown in a particular patient. Most studies have shown that the risk factors precipitate avascular necrosis in genetically predetermined individuals. Along with numerous metabolic factors and mechanical stresses, this eventually leads to collapse of the hip and arthritis.

The symptoms of avascular necrosis are pain at rest, pain at night. As the arthritis progresses, pain progresses and is associated with stiffness, difficulty walking, difficulty going up and down stairs, difficulty squatting, difficulty sitting cross-legged. The lack of blood supply along with increased pressure inside the bone along with increased stresses on the joint are responsible for these symptoms.

The risk factors for avascular necrosis of the femoral head are chronic corticosteroid use, chronic and excessive alcohol consumption, numerous coagulative disorders, several hemoglobinopathies, numerous autoimmune diseases, smoking, hyperlipidemia, Gauchers disease. Additional risk factors include myeloproliferative disorders, sickle cell disease, radiation to the hip. Numerous surgical factors also increase risk of avascular necrosis. These include history of surgery to the hip joint that can compromise the blood supply to the hip including femoral neck fracture surgery including surgery for cam and pincer lesion, surgical hip dislocation, etc.

The risk factors that lead to avascular necrosis of the femoral head can be classified as “direct” factors and “indirect” factors. They can also be classified as factors that are “constant” versus factor that “isolated”. Factors related to an isolated incident are fracture of the femoral head and hip dislocation. Additionally slipped capital femoral epiphysis that has been treated surgically or surgery that has been done on the femoral head for rotational osteotomy or for cam lesion can be classified into single isolated event.

I would like to classify causes compromising the blood supply of the femoral head as those related to a “single event” versus a “constant” circumstance. I do this because the prognosis can be better estimated based on differentiation in this manner. As an example, if there is a dislocation of the native hip and the hip is relocated and if the patient has not developed avascular necrosis of the hip in several years after this event, it is unlikely that the patient will develop avascular necrosis of the hip. On the contrary, if the patient has a myeloproliferative disorder, does heavy intake of alcohol or is constantly using corticosteroids, the hip is constantly getting insults that interrupt the blood supply and the prognosis is going to be guarded.

Numerous classification systems have been proposed for avascular necrosis of the femoral head including Ficat and Arlet, Steinberg classification, Association Research Circulatory Osseous (ARCO) classification, etc.

I use the Ficat and Arlet classification system which is the most commonly used system. It has good interobserver reliability.

  • Stage 0 is the stage where the radiographs are normal.
  • Stage 1 is minor osteopenia.
  • Stage 2 is sclerosis or cystic lesions. Stage 2A implies there is no crescent sign. Stage 2B is crescent sign without flattening of the femoral head.
  • Stage 3 involves flattening of the femoral head. Stage 4 involves arthritis of the hip involving the acetabulum.

The Steinberg Staging System is based on involvement of the femoral head.

  • Stage 0 involves normal radiograph, bone scan and MRI.
  • Stage 1 is classified into stage 1A, B, and C.
  • Stage 1 has normal MRI
  • Stage 1A has less than 15% involvement of the femoral head.
  • Stage 1B has 15% to 30% involvement of the femoral head
  • Stage 1C has significant involvement of the femoral head on MRI or on bone scan.
  • Stage 2 implies cystic and sclerotic changes in the femoral head
  • Stage 2A involves less than 15% of the femoral head
  • Stage B involves 15% to 30% of the femoral head
  • Stage 2C involves more than 30% of the femoral head.
  • Stage 3 implies subchondral collapse and crescent sign without flattening of the femoral head
  • Stage 3A involves less than 15% of the femoral head, stage 3B involves 15% to 30% of the femoral head and stage 3C involves more than 30% of the femoral head.
  • Stage 4 involves flattening of the femoral head with femoral head collapse. Again, it is described as mild, moderate and severe depending upon the involvement of the femoral head.
  • Stage 4A – Less than 15% of the femoral head is stage 4A,
  • Stage 4B – 15% to 30% of the femoral head is stage 4B
  • Stage 4C – More than 30% involvement of the femoral head is stage 4C.
  • Stage 5 is joint space narrowing and acetabular changes classified as A, B and C as mild, moderate and severe.
  • Stage 6 is advanced degenerative disease.

Most cases of avascular necrosis progress to advanced deterioration of the necrosis, collapse, and arthritis. Spontaneous disappearance of avascular necrosis is extremely rare. Some cases progress slower than others.

There is not a single uniform algorithm that is agreed among orthopedic surgeons to treat avascular necrosis since there is lack of level 1 evidence in literature. Level 1 evidence implies that studies have been done which are double blind studies comparing one treatment protocol to the other. It is a “double blind randomized prospective level 1” study.

My evaluation starts with the patient’s symptoms. The examination findings are normal in the initial stages, but in the advanced stages there is restriction of range of motion which is accompanied with pain.

I take anteroposterior and frog leg lateral x-rays of the hip as a starting point. In the initial stages, MRI is the goal standard for diagnosis as well as classifying the severity of avascular necrosis. On MRI we look at the T1-weighted images and T2-weighted images. The T1-weighted images show a single-density line and the T2-weighted images show high-intensity signal representing the necrotic bone and normal bone. There is also hypervascular granulation tissue seen on the MRI. Subchondral insufficiency fractures of the femoral head can also be seen on the MRI.


The treatment of avascular necrosis depends on the grade of avascular necrosis. Evaluation starts with physical examination of the patient, getting accurate symptoms, looking for relevant signs in the hip joint on examination and on radiological investigations that include x-ray and MRI. Certain physicians use invasive investigations like bone marrow pressure, core biopsy and venography, but I feel that invasive investigations are unnecessary.

I start investigations with plain x-rays. I evaluate the MRI when patient is in initial stages of the disorder. CT is an additional tool to look at the sphericity of the femoral head, however, it involves more radiation and I rarely use it.

Medical treatment involves bisphosphonates, anabolic bone agents, lipid lowering agents, vasoactive agents such as prostacyclin, anticoagulents such as enoxaparin, etc. Most of the medications are used for treatment of the other medical conditions associated with avascular necrosis. Medications are the good adjuvant therapy when surgery is needed. Additional biophysical treatments include electromagnetic therapy, hyperbaric oxygen (HBO), extracorporeal shockwave therapy (ESWT) but the results have not been strongly supported by literature.

Among the surgical procedures, total hip replacement is the most common method for treatment of femoral heads that have suffered with collapse and core decompression is the most common method of treating femoral head avascular necrosis without a collapse.

When the joint has collapsed, certain physicians do hemiarthroplasty or arthrodesis in which the joint is fused. However, I feel that for a surgeon, who is comfortable doing total joint replacement surgery, total joint replacement surgery should be treatment of choice for replacement as against partial hip replacement or hip fusion.

Core decompression is performed for decompressing the femoral head pressure and to bring in more vasculature. It is done with the hope to decrease pain and delay the deterioration of the joint. Delaying the progression of osteonecrosis will delay the need for joint replacement surgery.

There are numerous bone grafting procedures including “vascularized” and “non-vascularized” grafts that have been used for treatment of femoral head osteonecrosis. The graft can be from the patient’s bone, from a cadaver or it could be artificial bone substitute material. Free vascular grafting has been tried with the hope of restoring the vasculature as well as providing some structural integrity.

Tantalum implants have been combined with core decompression with the hope of maintaining the structural integrity. I do not use them because of the concerns of metal debris in a joint when total hip arthroplasty becomes necessary. Additionally, total hip arthroplasty will be a more involved procedure in the presence of tantalum implants.

I like to use some sort of biological agents with core decompression with the hope of improving the results. I use osteogenic mesenchymal cells with osteoinductive agents. Bone morphogenetic proteins improve the results of core decompression.

The technique of core decompression depends largely on the surgeon. I like to have a core tract through which I can introduce biological agents to improve the osteonecrotic lesion. The osteonecrotic lesion is evaluated on the MRI and extrapolated on the Xray. The tip of the drill is directed towards the lesion where the core decompression is intended to be performed.

I aspirate stem cells from the iliac crest, spin them down and use the concentrated stem cells to inject into the osteonecrotic lesion. There are some concerns with the “amount of dosage” of mesenchymal cells that are obtained. The dose is variable because the amount of stem cells depend upon the characteristics of the individual.

Older patients who have significant fibrosis in iliac crest, patients who are smokers have less stem cells than patients who are younger without any medical comorbidities. Under any circumstance, I maximize the dose of mesenchymal cells that can be injected into the defect and that is achieved by maximizing the stem cells that can be obtained from the patient.

There are osteotomies that have been described to delay the need for total joint arthroplasty. The most commonly described osteotomy is a transtrochanteric rotational osteotomy by Sugioka, in which the defective part of the femoral head is rotated and placed in a non-weight bearing portion.

The results of this procedure have not been replicated well. Additionally, when a total hip arthroplasty is done, the procedure becomes more complicated. I therefore do not do any osteotomies for avascular necrosis of the femoral head.

Total hip arthroplasty remains in the goal standard for treatment of advanced osteonecrosis that has been associated with arthritis. It is critically important to realize that there have been numerous studies that have shown poor results of total hip replacement for avascular necrosis of the femoral head. The failure rate has been significantly more for total hip replacements done for avascular necrosis than total hip replacements done for the garden variety of arthritis.

It is important to use the latest materials and surgical techniques in these patients to optimize results of total hip arthroplasty when a total hip arthroplasty is required for avascular necrosis of the femoral head.

Femoral stem for primary hip replacement

The image above shows a femoral stem with a wedge tapered porous-coated design used for primary uncemented hip replacement. The porous coating aids in biological fixation by promoting bone on-growth over the implant surface.

Acetabular shell with a multi-hole option

The acetabular shell lines the prepared acetabular cavity during a total hip replacement and hosts the polyethylene liner. The prosthetic head rotates on the polyethylene liner.

Avascular Necrosis Case Studies

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Why choose Dr. Karkare?Avascular Necrosis

Dr. Karkare is a leading orthopedic surgeon in New York City with multiple locations on Long Island. He provides patients with the most effective and advanced treatments for avascular necrosis.

His extensive experience and in-depth knowledge of bone and joint health issues mean he is uniquely positioned to help patients understand the cause of their condition while creating customized solutions based on each patient’s unique needs and health profiles.

If you’ve been experiencing any type of joint or bone pain or weakness, the first step is to evacuate toward ensuring you get the best and most appropriate care for complete recovery and optimum health.

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