PEMF and Avascular Necrosis
Avascular necrosis (AVN), literally meaning "bone death”, is a pathologic process that results from interruption of blood supply to the bone. As result the bone dies and looses all strengths and ultimately cannot support the skeleton anymore. Avascular necrosis (AVN) is a rare and serious condition that affects bones, particularly around the joint. Due to its serious nature, treatments for AVN can be a frightening prospect in their own right. Each treatment comes with its own advantages and disadvantages. Knowing your options and understanding the topic can help you decide what is the best route for you. Your bones need to be oxygenated by your blood, just like any other part of your body. They have veins and arteries that connect them to your cardiovascular system, allowing the flow of blood. When that flow is interrupted or reduced, part of the bone may die. This is referred to as avascular necrosis. Avascular means that the bone has become disconnected from the vascular system. Necrosis refers to the death of cells in living tissue. AVN occurs most commonly at the end of bones, and at joints such as the hip and shoulders. When under the pressure that joints carry, the areas of dead bone can collapse. This can lead to serious arthritis and other problems.
Treatment for AVN revolves around returning blood flow to the affected area. Bone can repair itself if the damage is not too severe. Pain relievers are taken to manage the pain associated with AVN, which can be quite bad. Patients are advised to use the affected area sparingly, to keep pressure and weight off the recovering bone.
While avascular necrosis is a serious condition, plenty of treatment options exist. Alternative therapies can allow a recovery without an invasive, expensive, and time consuming surgery. When caught early, in particular, treatments that prevent further bone loss and promote the regrowth of damaged bone can lead to a full recovery. By choosing the right treatment option for you, you can continue to lead an active, healthy lifestyle.
PEMF Therapy can be a very effective non invasive/ non surgical treatment for this as it improves blood circulation and oxygenation in the effective area and helps the body to heal itself. The links below show you some of the clinical studies done on the same.
Treatment for AVN revolves around returning blood flow to the affected area. Bone can repair itself if the damage is not too severe. Pain relievers are taken to manage the pain associated with AVN, which can be quite bad. Patients are advised to use the affected area sparingly, to keep pressure and weight off the recovering bone.
While avascular necrosis is a serious condition, plenty of treatment options exist. Alternative therapies can allow a recovery without an invasive, expensive, and time consuming surgery. When caught early, in particular, treatments that prevent further bone loss and promote the regrowth of damaged bone can lead to a full recovery. By choosing the right treatment option for you, you can continue to lead an active, healthy lifestyle.
PEMF Therapy can be a very effective non invasive/ non surgical treatment for this as it improves blood circulation and oxygenation in the effective area and helps the body to heal itself. The links below show you some of the clinical studies done on the same.
Avascular necrosis of head of femur
Philippe Hernigou
Author information ► Copyright and License information ►
Osteonecrosis of the femoral head (ONFH) is a disabling condition that affects mainly younger subjects in the midst of their working lives; to this day, it has remained a devastating disease. It affects both hips in more than 60% of individuals and is being diagnosed with increasing frequency. Its treatment stands at the borderline between Medicine and Surgery and requires a thorough understanding of the pathogenesis, natural history, and treatment options as a function of the different disease stages, which are best assessed with further investigations. The management of hip osteonecrosis remains one of the more challenging problems facing the orthopaedic surgeons. Without definitive treatment, 70% to 80% of clinically diagnosed cases will progress, and will undergo arthroplasty. Our primary goal is to preserve rather than replace the femoral head and articular cartilage. There is no completely satisfactory method to accomplish this, although a number of approaches have been described. Opinions often vary as to their indications and effectiveness.
“Conservative” management with protected weight bearing is not effective. This treatment will allow progression of their condition in one or two years. Usually, the patients are kept off weight-bearing on the affected side; however, this treatment principle has several limitations: the lesion is frequently bilateral; it does not abolish the muscle tone around the joint, even when the patient is lying down. The use of two elbow crutches (as a substitute for axillary crutches) does not provide the required complete weight relief; and even if crutches afford some protection, there is still the question of how long the patients should be kept off weight-bearing.
Before the onset of femoral head collapse, nonoperative treatment includes the use of various electromagnetic, acoustic stimulation or pharmacologic agents. These are still in a stage of evaluation and development. Leo Massari et al have analysed the effects of stimulation with pulsed electromagnetic fields (PEMFs) on the treatment of avascular necrosis of the femoral head. Both hypothesized that the effect of PEMF stimulation may be to protect the articular cartilage from the catabolic effect of inflammation and subchondral bone-marrow edema.
Pain is the first symptom in osteonecrosis. Before collapse, pain may be in relation with bone marrow edema frequently seen on MRI in early stages of osteonecrosis. Roland Meizer has evaluated the efficacy of the vasoactive drug iloprost in the treatment of pain in bone marrow edema, which is sometimes a pre-condition of hip osteonecrosis and concluded that the use of parenteral iloprost might be a viable method for pain in this situation.
The repair of necrotic cancellous bone in osteonecrosis involves two different processes, which appear to occur independent of each other: cell proliferation and invasion of the femoral head by reparative tissue. Bone resorption is associated with the repair process and is in relation with osteoclasts. These cells are derived either from mesenchymal precursors or from blood monocytes. What causes a change in the mechanical properties of the femoral head as an organ, to make it deform and collapse, is the resorption due to osteoclasts involved in the reparative process. It would, therefore, make sense to stop the activity of these osteoclasts. Eli peled has evaluated the influence of alendronate treatment on the rat femoral head shape after 6 weeks of daily treatment, when compared with controls. Alendronate treatment prevented the distortion and destruction of the femoral head. Osteoclast inhibition might prolong the bone creeping substitution, which might reduce disability due to femoral head collapse.
Very early in the course of the disease, core decompression remains the most logical treatment modality if one accepts that the condition is a compartment syndrome with increased pressure inside the femoral head. Core decompression has been in use for a considerable time; the results reported by different authors vary no doubt because of different patient populations and different stages treated with core decompression. However, while fundamental research and clinical studies have shown that dead bone may be revascularized by living bone, the reparative osteogenic potential is slight in ONFH: because the number of bone progenitor cells in the uninvolved part of the femoral head and in the trochanteric region is less than in healthy subjects. It would, therefore, make sense not only to core, but to introduce new osteoprogentor cells. This can be done by placing a vascularized graft into the coring tract. Sudhir Babhulkar analyzed and reported a series of patients of osteonecrosis of femoral head treated by core decompression and vascular pedicle grafting of part of iliac crest based on deep circumflex iliac vessels. The core decompression and vascular pedicle grafting reduced the intraosseous tension to achieve early revascularization of ischemic femoral head. The high percentage of marrow and osteogenic cells survive within a vascularized pedicle graft, which helps in early vascularization and we have been able to achieve good outcome.
The same result may be produced more readily by harvesting bone marrow from the anterior iliac crests, concentrating the marrow thus obtained, and re-injecting it into the necrotic zones. Philippe Hernigou reported a series of patients operated on for early stages of osteonecrosis of the hip with autologous bone marrow. The aim was to increase the number of osteoprogenitor cells in the proximal femur to stimulate bone remodeling and creeping substitution. Hips with stage I osteonecrosis of the femoral head at the time of surgery demonstrated total resolution of osteonecrosis based on preoperative and postoperative MRI studies.
So, many different approaches have been described for the treatment of osteonecrosis. The decision as to which treatment to select will depend upon a number of factors, including a thorough clinical evaluation of the patient as well as the use of an effective method of staging to determine both the type and extent of the pathology present in the hip. Ramesh Kumar Sen described the different techniques that the surgeon may use according to the stage of the osteonecrosis.
We are pleased that it has been possible to devote this issue of the journal to the treatment of osteonecrosis of the femoral head. We have been fortunate in recruiting authors who have addressed their topics concisely and effectively. Our goal is to provide our readers with an informed and up-to-date overview of a challenging and poorly understood problem in order to assist them in the management of the patient with osteonecrosis of the hip. Challenges still lie ahead. In the coming years, we hope to conduct other studies on the development of animal models and on new therapeutic agents. Osteogenic and angiogenic stem cells or growth factors should improve the surgical techniques in the next years. We conclude by thanking the authors for their contribution to this special symposium. We also would like to express our sincere appreciation to the editor of the Indian Journal of Orthopaedics, for his support for this symposium.
Articles from Indian Journal of Orthopaedics are provided here courtesy of Medknow Publications
Source http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739493/
Philippe Hernigou
Author information ► Copyright and License information ►
Osteonecrosis of the femoral head (ONFH) is a disabling condition that affects mainly younger subjects in the midst of their working lives; to this day, it has remained a devastating disease. It affects both hips in more than 60% of individuals and is being diagnosed with increasing frequency. Its treatment stands at the borderline between Medicine and Surgery and requires a thorough understanding of the pathogenesis, natural history, and treatment options as a function of the different disease stages, which are best assessed with further investigations. The management of hip osteonecrosis remains one of the more challenging problems facing the orthopaedic surgeons. Without definitive treatment, 70% to 80% of clinically diagnosed cases will progress, and will undergo arthroplasty. Our primary goal is to preserve rather than replace the femoral head and articular cartilage. There is no completely satisfactory method to accomplish this, although a number of approaches have been described. Opinions often vary as to their indications and effectiveness.
“Conservative” management with protected weight bearing is not effective. This treatment will allow progression of their condition in one or two years. Usually, the patients are kept off weight-bearing on the affected side; however, this treatment principle has several limitations: the lesion is frequently bilateral; it does not abolish the muscle tone around the joint, even when the patient is lying down. The use of two elbow crutches (as a substitute for axillary crutches) does not provide the required complete weight relief; and even if crutches afford some protection, there is still the question of how long the patients should be kept off weight-bearing.
Before the onset of femoral head collapse, nonoperative treatment includes the use of various electromagnetic, acoustic stimulation or pharmacologic agents. These are still in a stage of evaluation and development. Leo Massari et al have analysed the effects of stimulation with pulsed electromagnetic fields (PEMFs) on the treatment of avascular necrosis of the femoral head. Both hypothesized that the effect of PEMF stimulation may be to protect the articular cartilage from the catabolic effect of inflammation and subchondral bone-marrow edema.
Pain is the first symptom in osteonecrosis. Before collapse, pain may be in relation with bone marrow edema frequently seen on MRI in early stages of osteonecrosis. Roland Meizer has evaluated the efficacy of the vasoactive drug iloprost in the treatment of pain in bone marrow edema, which is sometimes a pre-condition of hip osteonecrosis and concluded that the use of parenteral iloprost might be a viable method for pain in this situation.
The repair of necrotic cancellous bone in osteonecrosis involves two different processes, which appear to occur independent of each other: cell proliferation and invasion of the femoral head by reparative tissue. Bone resorption is associated with the repair process and is in relation with osteoclasts. These cells are derived either from mesenchymal precursors or from blood monocytes. What causes a change in the mechanical properties of the femoral head as an organ, to make it deform and collapse, is the resorption due to osteoclasts involved in the reparative process. It would, therefore, make sense to stop the activity of these osteoclasts. Eli peled has evaluated the influence of alendronate treatment on the rat femoral head shape after 6 weeks of daily treatment, when compared with controls. Alendronate treatment prevented the distortion and destruction of the femoral head. Osteoclast inhibition might prolong the bone creeping substitution, which might reduce disability due to femoral head collapse.
Very early in the course of the disease, core decompression remains the most logical treatment modality if one accepts that the condition is a compartment syndrome with increased pressure inside the femoral head. Core decompression has been in use for a considerable time; the results reported by different authors vary no doubt because of different patient populations and different stages treated with core decompression. However, while fundamental research and clinical studies have shown that dead bone may be revascularized by living bone, the reparative osteogenic potential is slight in ONFH: because the number of bone progenitor cells in the uninvolved part of the femoral head and in the trochanteric region is less than in healthy subjects. It would, therefore, make sense not only to core, but to introduce new osteoprogentor cells. This can be done by placing a vascularized graft into the coring tract. Sudhir Babhulkar analyzed and reported a series of patients of osteonecrosis of femoral head treated by core decompression and vascular pedicle grafting of part of iliac crest based on deep circumflex iliac vessels. The core decompression and vascular pedicle grafting reduced the intraosseous tension to achieve early revascularization of ischemic femoral head. The high percentage of marrow and osteogenic cells survive within a vascularized pedicle graft, which helps in early vascularization and we have been able to achieve good outcome.
The same result may be produced more readily by harvesting bone marrow from the anterior iliac crests, concentrating the marrow thus obtained, and re-injecting it into the necrotic zones. Philippe Hernigou reported a series of patients operated on for early stages of osteonecrosis of the hip with autologous bone marrow. The aim was to increase the number of osteoprogenitor cells in the proximal femur to stimulate bone remodeling and creeping substitution. Hips with stage I osteonecrosis of the femoral head at the time of surgery demonstrated total resolution of osteonecrosis based on preoperative and postoperative MRI studies.
So, many different approaches have been described for the treatment of osteonecrosis. The decision as to which treatment to select will depend upon a number of factors, including a thorough clinical evaluation of the patient as well as the use of an effective method of staging to determine both the type and extent of the pathology present in the hip. Ramesh Kumar Sen described the different techniques that the surgeon may use according to the stage of the osteonecrosis.
We are pleased that it has been possible to devote this issue of the journal to the treatment of osteonecrosis of the femoral head. We have been fortunate in recruiting authors who have addressed their topics concisely and effectively. Our goal is to provide our readers with an informed and up-to-date overview of a challenging and poorly understood problem in order to assist them in the management of the patient with osteonecrosis of the hip. Challenges still lie ahead. In the coming years, we hope to conduct other studies on the development of animal models and on new therapeutic agents. Osteogenic and angiogenic stem cells or growth factors should improve the surgical techniques in the next years. We conclude by thanking the authors for their contribution to this special symposium. We also would like to express our sincere appreciation to the editor of the Indian Journal of Orthopaedics, for his support for this symposium.
Articles from Indian Journal of Orthopaedics are provided here courtesy of Medknow Publications
Source http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739493/
Biophysical stimulation in osteonecrosis of the femoral head
Massari Leo, Fini Milena,1 Cadossi Ruggero,2 Setti Stefania,2 and Traina GianCarlo
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This article has been cited by other articles in PMC.
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Abstract
Osteonecrosis of the femoral head is the endpoint of a disease process that results from insufficient blood flow and bone-tissue necrosis, leading to joint instability, collapse of the femoral head, arthritis of the joint, and total hip replacement. Pain is the most frequent clinical symptom. Both bone tissue and cartilage suffer when osteonecrosis of the femoral head develops. Stimulation with pulsed electromagnetic fields (PEMFs) has been shown to be useful for enhancing bone repair and for exerting a chondroprotective effect on articular cartilage. Two Italian studies on the treatment of avascular necrosis of the femoral head with PEMFs were presented in this review. In the first study, 68 patients suffering from avascular necrosis of the femoral head were treated with PEMFs in combination with core decompression and autologous bone grafts. The second one is a retrospective analysis of the results of treatment with PEMFs of 76 hips in 66 patients with osteonecrosis of the femoral head. In both studies clinical information and diagnostic imaging were collected at the beginning of the treatment and at the time of follow up. Statistical analysis was performed using chi-square test. Both authors hypothesize that the short-term effect of PEMF stimulation may be to protect the articular cartilage from the catabolic effect of inflammation and subchondral bone-marrow edema. The long-term effect of PEMF stimulation may be to promote osteogenic activity at the necrotic area and prevent trabecular fracture and subchondral bone collapse. PEMF stimulation represents an important therapeutic opportunity to resolve the Ficat stage-I or II disease or at least to delay the time until joint replacement becomes necessary.
Keywords: Chondroprotective effect, osteonecrosis of the femoral head, pulsed electromagnetic fields
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IntroductionOsteonecrosis is a common disorder of bone circulation and it is particularly common in the femoral head; there are an estimated 20,000–30,000 new cases diagnosed annually.1 The syndrome may be minor, nonprogressive, asymptomatic, or it may result in the destruction of subchondral cortical bone leading to major problem for the hip.
There are two types of pathologic osteonecrotic disorders: medullary and corticocancellous involving the joint.2Medullary osteonecrosis is caused by interference in the blood supply to the medullary cavity, which results in the death of the cells of the trabecular bone. Corticocancellous osteonecrosis involving the joint is usually much more pernicious and causes much more patients distress; the vascular compromise usually occurs in the proximal femur, and both the trabecular and the subchondral bone die and the region does not calcify as in the medullary disease.
Pathogenesis of osteonecrosis refers to all the cellular events, reaction, and other pathological mechanisms occurring in the development and progression of the disease. There are many theories of the pathogenesis of osteonecrosis of the femoral head. Some authors postulated four possible structural or biological disorders by which the blood supply is interrupted: mechanical interruption, vascular thrombosis or embolism, external injury or pressure on a vascular wall, and venous occlusion. Most recently, some authors hypothesized that an impaired mesenchymal cellular differentiation may be a potential mechanism of action of the pathogenesis of osteonecrosis.3Arterial occlusion seems to be the main contributing factor. The two main pathologic mechanisms are thrombotic and embolic. Arterial thrombosis can occur in two different ways that can act synergistically. There may be a primary injury of the arterial wall or a primary coagulation disorder.4
Several authors have described a thrombosis caused by an injury of the endothelial layer by arteriosclerosis or other occlusive vascular disorders.5–7 In healthy subjects there is a controlled balance between thrombosis and/or hypofibrinolysis; the presence of hereditary or acquired thrombophilia and/or hypofibrinolysis can modify this balance leading to a thrombotic event.8
Another possible cause for avascular necrosis of the femoral head is the embolic disorder. An alteration of lipid metabolism causes an increase in circulating lipids due to a reduced lipolytic enzymatic activity. Circulating lipids accumulate in the liver causing fatty degeneration and adipose cyst formation. Rupture of the cysts or spontaneous diffusion of droplets from the liver leads to the formation of fat emboli in the bloodstream. From the pulmonary filter they can reach any other visceral site or bone. The subchondral region of the femoral head is an area of localization of fat emboli due to the small diameter and to terminal feature of arterial vessel at this level. Intraosseous fat emboli cause stasis through mechanical occlusion and also endothelial damage following their hydrolysis to free fatty acids. Another mechanism involved in the pathogenesis is an external compression of capillaries by the hypertrophy of marrow fat and cells with an increase of intramedullary pressure and reduction of blood flow.9,10
There are also some other disorders associated with osteonecrosis, such as AIDS, alcoholism, aging, corticosteroid administration, diabetes, fracture and dislocation, smoking status, obesity, and rheumatoid arthritis. Some authors currently believe that the most frequent cause is the use of corticosteroids, which induces a reduction in the concentration of a lipoproteic lipase, with a consequent increase in concentrations of fat.11
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Treatment Strategies and Clinical ResultsRetrospective clinical studies show that osteonecrosis of the femoral head in 80–90% of affected patients inevitably progresses to destroy the femur head, usually within 2–3 years of diagnosis.12 Osteonecrosis of the femoral head is a devastating disease that typically affects young patients (mean age, mid-thirties) and often leads to femoral head collapse if left untreated. Because these patients are young and relatively active, and because total hip arthroplasty has not always been associated with an optimal outcome in this patient population, various procedures for joint preservation in the early stages of the disease have been utilized, ranging from core decompression, percutaneous drilling, vascularized and nonvascularized bone-grafting, and osteotomies to hemiresurfacing. However, the success rate of these joint preserving operations are variable, and long- term success is not always reliable.13,14 In advanced osteonecrosis of the femoral head, total hip arthroplasty and metal-on-metal total hip resurfacing is necessary to provide joint functional recovery and pain relief. The National Health Insurance Bureau declared that the percentage of patients receiving total hip arthroplasty for nontraumatic osteonecrosis of the femoral head is more than 50% in Taiwan, Japan, and Korea; it is 2.2% in Sweden (85% for degenerative or traumatic arthritis), and 12% of 30,000 cases occur annually in the United States for nontraumatic osteonecrosis of the femoral head.15 The patients undergoing arthroplasty can be expected to require multiple future surgeries and should be well educated in this regards before surgery.
Alternative nonoperative treatments that conserve bone or that promote osteogenesis and angiogenesis as well as treatment that heal subchondral bone fractures should be taken into consideration. A treatment of the modern orthopedic surgery is represented by the regulation of skeletal repair by biophysical agents, including mechanical strain, ultrasound, and pulsed electromagnetic fields (PEMFs). Several double-blinded and controlled clinical trials have been conducted to demonstrate the clinical effectiveness of PEMFs to stimulate osteogenetic activity in fresh fractures, osteotomies, nonunions, spine fusion, and ultimately in the osteonecrosis of the femoral head in isolation or in combination with surgical techniques.16–21
In Italy, two different studies were conducted on the use of biophysical stimulation with PEMFs for the treatment of avascular necrosis of the femoral head.
In the first Italian study, 68 patients suffering from avascular necrosis of the femoral head were treated with PEMFs for 8 hours per day for six months, in combination with core decompression and autologous bone grafts, obtained from proximal metaphysis area and femoral neck.22 The pulse generator (SPT BIOSTIM; IGEA, Carpi, Italy [Figure 1]) supplied the coil with single-voltage pulses at 75 Hz, with each pulse of 1.3 ms. Patients were classified according the Steinberg staging by standard radiographs [Table 1]; magnetic resonance images and scintigrams were acquired to confirm the diagnosis. The average age was 44 years. The etiology of the necrosis was primary (n=34); corticosteroid therapy (n=17); and secondary to trauma (n=5). The mean duration of follow-up was 5.8 years (3 months to 11 years). To evaluate the bone grafts integration, instrumental evaluations (Rx and RMN) were performed at each follow-up: 1, 3, 6, 12, and 24 months from surgery. Then, radiographic evaluations were conducted each year and magnetic resonance every two or three years as requested by the surgeon.
Figure 1
Left: Clinical pulsed electromagnetic field generator; Right: Schematic representation of treatment modality
Table 1
Avascular necrosis staging
In 81% of patients with Steinberg stage -II, no pain and limping was detected and good radiographic results were reported. In patients with Steinberg stage -III, the success rate was reduced to 70%, and in patients with stage -IV, the good clinical and radiographic results were 53% and 27%, respectively. Total hip arthroplasty was necessary only in two patients (bilaterally in one patient with Steinberg stage -III and in one hip with Steinberg stage -IV).
The second Italian study is a retrospective review of 66 consecutive patients (76 hips) who received PEMFs (SPT BIOSTIM; IGEA, Carpi, Italy) for the treatment of Ficat stage-I, II, or III osteonecrosis of the femoral head.23 In this study, there were no identifiable associated risk factors in 51 patients (77%), whereas a predisposing factor could be identified in 15 patients (23%). The primary endpoint analyzed in this study was the avoidance of hip surgery, and the secondary endpoint was limiting the radiographic progression of osteonecrosis of the femoral head. Treatment with PEMFs was started at the time of the initial diagnosis and the patients were instructed to use the stimulator for 8 hours per day for six months. The mean duration of treatment was 5 ± 2 months. At the time of final follow-up, (a mean of 28 months), PEMFs preserved 50 (94%) of the 53 Ficat stage-I or -II hips [Figure 2]; the authors found 15 of the 76 hips (20%) had progression of osteonecrosis of the femoral head that led to the onset of a severe degenerative osteoarthritis and required surgery. Of these 15 hips, 12 had Ficat stage-III disease at the beginning of treatment, whereas the remaining three hips had Ficat stage-II disease at the beginning of treatment. All the patients reported with pain at the start of the treatment were pain free after 60 days of stimulation in 35 patients (53%) and pain was of moderate intensity in 17 patients (26%).
Figure 2
MRI of right hip (a) of 17 year old female shows edema with ficat stage II osteonecrosis shows bone edema. (b) MRI of the same hip after 6 months of stimulation and at the end of the treatment shows decreased bone edema and the patient had no pain.
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DiscussionBassett.24 (1989) was the first to propose PEMFs in treating 118 patients with avascular necrosis of the femur head, Steinberg assessed the possibility of employing electrical stimulation by faradic systems (implanted electrodes) and, subsequently, the feasibility of using capacitive systems.25,26 In both studies the stimulation was performed in combination with core decompression (CD); although the results obtained were good, it was not possible to demonstrate any statistically significant advantage of the combined treatment as against treatment with CD alone. Aaron performed a series of clinical studies aimed to evaluate the treatment of AVN with CD and PEMFs, whether used separately or in association; 657 hips underwent treatment.27 The hips have been studied with a follow-up of 36 months. The results of the stimulation with PEMFs were compared with those obtained by CD and CD + PEMFs in stage -II and stage -III hips. In stage -II, PEMFs and PEMFs + CD gave better results than CD alone. From the radiographic point of view, however, CD + PEMFs gave better results than PEMFs alone and CD. In the clinical outcomes, that PEMFs and CD + PEMFs gave greater probability of survival than CD alone.
The Italian experiences exhibits the typical features and shortcoming of not controlled study but the findings reported here confirm those previously obtained by other authors.28,29 The results of the studies suggest that an early instrumental diagnosis at the onset of the disorder and the immediate use of PEMFs enables better clinical results. The authors observed that the lesions in early stage respond well to treatment with PEMFs and, in the majority of cases, as far as Ficat II, are capable of preventing the progression of the disease. Ficat stage -III does not constitute a real indication for this treatment and must always be carefully assessed, the treatment eventually being advised for the younger patients. Idiopathic lesions seem more sensitive to PEMF therapy as compared with secondary forms, because the therapies responsible of the disease cannot be interrupted. The weight bearing does not influence the evolution of lesion. This observation is unexpected, but it has also been highlighted in other studies. The relief from pain accompanied by recovery of the joint function is important, as observed in the majority of the patients within 45 days from beginning of treatment. It is likely that this effect is mediated by the antiinflammatory action of the PEMFs that enables resolution of the joint edema. With regard to this, both authors concluded that in the presence of avascular necrosis of the femoral head we can distinguish two different aspects: one concerning the cartilage and one concerning the subchondral bone tissue.
The initial stages of the disease are dominated by the ischemic and inflammatory component; the latter is responsible for the joint pain, edema, and degradation of the cartilage. In 2002, some authors have demonstrated that the positive strong antiinflammatory effects of PEMFs causes an increase of adenylyl cyclase activity and a reduction of superoxide anion production, as a result of upregulation of the A2A receptors located on the neutrophil surface.30 Recently, this antiinflammatory action has been demonstrated on the sinoviocytes and chondrocytes.31 The binding plays a fundamental role on the inflammatory response and promotes new vessel formation and limits the extension of the necrotic area, resulting from ischemia. This effect is of extreme importance because of the role of the synovial membrane on the revascularization and resorption of necrotic bone. Moreover, biophysical stimulation is able to inhibit the catabolic effects of the inflammatory cytokines on the joint cartilage32and to stimulate the synthesis of proteoglycans and the local production of BMPs, TGF-α, and IGF-I;33 PEMFs exert a chondroprotective effect in vivo on osteoarthritis,34 which may play a fundamental role in the treatment of early stages of osteonecrosis of the femoral head by limiting the damage induced by inflammation and preserving cartilage and subchondral bone exerting a short term effects.
Regarding the bone tissue, in the long term, the main problem to resolve is the avascular deficit, the first step to get to the necrosis and the recovery of the ischemic bone tissue. In this condition, the PEMF has effects firstly on angiogenesis and then on osteogenesis. In association with core decompression, biophysical stimulation enhances the osteointegration of autologous bone grafts,35 stimulates the local production of growth factors, and favors the osteogenic activity of osteoblasts reducing the bone reabsorption by interfering with the activation of the parathyroid hormone receptor, thus decreasing the recruitment and differentiation of osteoclasts.36–38
In conclusion, both authors suggest that the treatment with PEMFs by now represents one of the conservative therapies used in the first stages of avascular necrosis of the femoral head at Ficat 0, I, II or Steinberg II and III but require from patients time of treatment, care, and precision to ensure the success expected by physicians and patients. The stimulation with PEMFs may be a good opportunity to resolve the disease or at least to delay the time until joint replacement becomes necessary.
Source : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739500/
Massari Leo, Fini Milena,1 Cadossi Ruggero,2 Setti Stefania,2 and Traina GianCarlo
Author information ► Copyright and License information ►
This article has been cited by other articles in PMC.
Go to:
Abstract
Osteonecrosis of the femoral head is the endpoint of a disease process that results from insufficient blood flow and bone-tissue necrosis, leading to joint instability, collapse of the femoral head, arthritis of the joint, and total hip replacement. Pain is the most frequent clinical symptom. Both bone tissue and cartilage suffer when osteonecrosis of the femoral head develops. Stimulation with pulsed electromagnetic fields (PEMFs) has been shown to be useful for enhancing bone repair and for exerting a chondroprotective effect on articular cartilage. Two Italian studies on the treatment of avascular necrosis of the femoral head with PEMFs were presented in this review. In the first study, 68 patients suffering from avascular necrosis of the femoral head were treated with PEMFs in combination with core decompression and autologous bone grafts. The second one is a retrospective analysis of the results of treatment with PEMFs of 76 hips in 66 patients with osteonecrosis of the femoral head. In both studies clinical information and diagnostic imaging were collected at the beginning of the treatment and at the time of follow up. Statistical analysis was performed using chi-square test. Both authors hypothesize that the short-term effect of PEMF stimulation may be to protect the articular cartilage from the catabolic effect of inflammation and subchondral bone-marrow edema. The long-term effect of PEMF stimulation may be to promote osteogenic activity at the necrotic area and prevent trabecular fracture and subchondral bone collapse. PEMF stimulation represents an important therapeutic opportunity to resolve the Ficat stage-I or II disease or at least to delay the time until joint replacement becomes necessary.
Keywords: Chondroprotective effect, osteonecrosis of the femoral head, pulsed electromagnetic fields
Go to:
IntroductionOsteonecrosis is a common disorder of bone circulation and it is particularly common in the femoral head; there are an estimated 20,000–30,000 new cases diagnosed annually.1 The syndrome may be minor, nonprogressive, asymptomatic, or it may result in the destruction of subchondral cortical bone leading to major problem for the hip.
There are two types of pathologic osteonecrotic disorders: medullary and corticocancellous involving the joint.2Medullary osteonecrosis is caused by interference in the blood supply to the medullary cavity, which results in the death of the cells of the trabecular bone. Corticocancellous osteonecrosis involving the joint is usually much more pernicious and causes much more patients distress; the vascular compromise usually occurs in the proximal femur, and both the trabecular and the subchondral bone die and the region does not calcify as in the medullary disease.
Pathogenesis of osteonecrosis refers to all the cellular events, reaction, and other pathological mechanisms occurring in the development and progression of the disease. There are many theories of the pathogenesis of osteonecrosis of the femoral head. Some authors postulated four possible structural or biological disorders by which the blood supply is interrupted: mechanical interruption, vascular thrombosis or embolism, external injury or pressure on a vascular wall, and venous occlusion. Most recently, some authors hypothesized that an impaired mesenchymal cellular differentiation may be a potential mechanism of action of the pathogenesis of osteonecrosis.3Arterial occlusion seems to be the main contributing factor. The two main pathologic mechanisms are thrombotic and embolic. Arterial thrombosis can occur in two different ways that can act synergistically. There may be a primary injury of the arterial wall or a primary coagulation disorder.4
Several authors have described a thrombosis caused by an injury of the endothelial layer by arteriosclerosis or other occlusive vascular disorders.5–7 In healthy subjects there is a controlled balance between thrombosis and/or hypofibrinolysis; the presence of hereditary or acquired thrombophilia and/or hypofibrinolysis can modify this balance leading to a thrombotic event.8
Another possible cause for avascular necrosis of the femoral head is the embolic disorder. An alteration of lipid metabolism causes an increase in circulating lipids due to a reduced lipolytic enzymatic activity. Circulating lipids accumulate in the liver causing fatty degeneration and adipose cyst formation. Rupture of the cysts or spontaneous diffusion of droplets from the liver leads to the formation of fat emboli in the bloodstream. From the pulmonary filter they can reach any other visceral site or bone. The subchondral region of the femoral head is an area of localization of fat emboli due to the small diameter and to terminal feature of arterial vessel at this level. Intraosseous fat emboli cause stasis through mechanical occlusion and also endothelial damage following their hydrolysis to free fatty acids. Another mechanism involved in the pathogenesis is an external compression of capillaries by the hypertrophy of marrow fat and cells with an increase of intramedullary pressure and reduction of blood flow.9,10
There are also some other disorders associated with osteonecrosis, such as AIDS, alcoholism, aging, corticosteroid administration, diabetes, fracture and dislocation, smoking status, obesity, and rheumatoid arthritis. Some authors currently believe that the most frequent cause is the use of corticosteroids, which induces a reduction in the concentration of a lipoproteic lipase, with a consequent increase in concentrations of fat.11
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Treatment Strategies and Clinical ResultsRetrospective clinical studies show that osteonecrosis of the femoral head in 80–90% of affected patients inevitably progresses to destroy the femur head, usually within 2–3 years of diagnosis.12 Osteonecrosis of the femoral head is a devastating disease that typically affects young patients (mean age, mid-thirties) and often leads to femoral head collapse if left untreated. Because these patients are young and relatively active, and because total hip arthroplasty has not always been associated with an optimal outcome in this patient population, various procedures for joint preservation in the early stages of the disease have been utilized, ranging from core decompression, percutaneous drilling, vascularized and nonvascularized bone-grafting, and osteotomies to hemiresurfacing. However, the success rate of these joint preserving operations are variable, and long- term success is not always reliable.13,14 In advanced osteonecrosis of the femoral head, total hip arthroplasty and metal-on-metal total hip resurfacing is necessary to provide joint functional recovery and pain relief. The National Health Insurance Bureau declared that the percentage of patients receiving total hip arthroplasty for nontraumatic osteonecrosis of the femoral head is more than 50% in Taiwan, Japan, and Korea; it is 2.2% in Sweden (85% for degenerative or traumatic arthritis), and 12% of 30,000 cases occur annually in the United States for nontraumatic osteonecrosis of the femoral head.15 The patients undergoing arthroplasty can be expected to require multiple future surgeries and should be well educated in this regards before surgery.
Alternative nonoperative treatments that conserve bone or that promote osteogenesis and angiogenesis as well as treatment that heal subchondral bone fractures should be taken into consideration. A treatment of the modern orthopedic surgery is represented by the regulation of skeletal repair by biophysical agents, including mechanical strain, ultrasound, and pulsed electromagnetic fields (PEMFs). Several double-blinded and controlled clinical trials have been conducted to demonstrate the clinical effectiveness of PEMFs to stimulate osteogenetic activity in fresh fractures, osteotomies, nonunions, spine fusion, and ultimately in the osteonecrosis of the femoral head in isolation or in combination with surgical techniques.16–21
In Italy, two different studies were conducted on the use of biophysical stimulation with PEMFs for the treatment of avascular necrosis of the femoral head.
In the first Italian study, 68 patients suffering from avascular necrosis of the femoral head were treated with PEMFs for 8 hours per day for six months, in combination with core decompression and autologous bone grafts, obtained from proximal metaphysis area and femoral neck.22 The pulse generator (SPT BIOSTIM; IGEA, Carpi, Italy [Figure 1]) supplied the coil with single-voltage pulses at 75 Hz, with each pulse of 1.3 ms. Patients were classified according the Steinberg staging by standard radiographs [Table 1]; magnetic resonance images and scintigrams were acquired to confirm the diagnosis. The average age was 44 years. The etiology of the necrosis was primary (n=34); corticosteroid therapy (n=17); and secondary to trauma (n=5). The mean duration of follow-up was 5.8 years (3 months to 11 years). To evaluate the bone grafts integration, instrumental evaluations (Rx and RMN) were performed at each follow-up: 1, 3, 6, 12, and 24 months from surgery. Then, radiographic evaluations were conducted each year and magnetic resonance every two or three years as requested by the surgeon.
Figure 1
Left: Clinical pulsed electromagnetic field generator; Right: Schematic representation of treatment modality
Table 1
Avascular necrosis staging
In 81% of patients with Steinberg stage -II, no pain and limping was detected and good radiographic results were reported. In patients with Steinberg stage -III, the success rate was reduced to 70%, and in patients with stage -IV, the good clinical and radiographic results were 53% and 27%, respectively. Total hip arthroplasty was necessary only in two patients (bilaterally in one patient with Steinberg stage -III and in one hip with Steinberg stage -IV).
The second Italian study is a retrospective review of 66 consecutive patients (76 hips) who received PEMFs (SPT BIOSTIM; IGEA, Carpi, Italy) for the treatment of Ficat stage-I, II, or III osteonecrosis of the femoral head.23 In this study, there were no identifiable associated risk factors in 51 patients (77%), whereas a predisposing factor could be identified in 15 patients (23%). The primary endpoint analyzed in this study was the avoidance of hip surgery, and the secondary endpoint was limiting the radiographic progression of osteonecrosis of the femoral head. Treatment with PEMFs was started at the time of the initial diagnosis and the patients were instructed to use the stimulator for 8 hours per day for six months. The mean duration of treatment was 5 ± 2 months. At the time of final follow-up, (a mean of 28 months), PEMFs preserved 50 (94%) of the 53 Ficat stage-I or -II hips [Figure 2]; the authors found 15 of the 76 hips (20%) had progression of osteonecrosis of the femoral head that led to the onset of a severe degenerative osteoarthritis and required surgery. Of these 15 hips, 12 had Ficat stage-III disease at the beginning of treatment, whereas the remaining three hips had Ficat stage-II disease at the beginning of treatment. All the patients reported with pain at the start of the treatment were pain free after 60 days of stimulation in 35 patients (53%) and pain was of moderate intensity in 17 patients (26%).
Figure 2
MRI of right hip (a) of 17 year old female shows edema with ficat stage II osteonecrosis shows bone edema. (b) MRI of the same hip after 6 months of stimulation and at the end of the treatment shows decreased bone edema and the patient had no pain.
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DiscussionBassett.24 (1989) was the first to propose PEMFs in treating 118 patients with avascular necrosis of the femur head, Steinberg assessed the possibility of employing electrical stimulation by faradic systems (implanted electrodes) and, subsequently, the feasibility of using capacitive systems.25,26 In both studies the stimulation was performed in combination with core decompression (CD); although the results obtained were good, it was not possible to demonstrate any statistically significant advantage of the combined treatment as against treatment with CD alone. Aaron performed a series of clinical studies aimed to evaluate the treatment of AVN with CD and PEMFs, whether used separately or in association; 657 hips underwent treatment.27 The hips have been studied with a follow-up of 36 months. The results of the stimulation with PEMFs were compared with those obtained by CD and CD + PEMFs in stage -II and stage -III hips. In stage -II, PEMFs and PEMFs + CD gave better results than CD alone. From the radiographic point of view, however, CD + PEMFs gave better results than PEMFs alone and CD. In the clinical outcomes, that PEMFs and CD + PEMFs gave greater probability of survival than CD alone.
The Italian experiences exhibits the typical features and shortcoming of not controlled study but the findings reported here confirm those previously obtained by other authors.28,29 The results of the studies suggest that an early instrumental diagnosis at the onset of the disorder and the immediate use of PEMFs enables better clinical results. The authors observed that the lesions in early stage respond well to treatment with PEMFs and, in the majority of cases, as far as Ficat II, are capable of preventing the progression of the disease. Ficat stage -III does not constitute a real indication for this treatment and must always be carefully assessed, the treatment eventually being advised for the younger patients. Idiopathic lesions seem more sensitive to PEMF therapy as compared with secondary forms, because the therapies responsible of the disease cannot be interrupted. The weight bearing does not influence the evolution of lesion. This observation is unexpected, but it has also been highlighted in other studies. The relief from pain accompanied by recovery of the joint function is important, as observed in the majority of the patients within 45 days from beginning of treatment. It is likely that this effect is mediated by the antiinflammatory action of the PEMFs that enables resolution of the joint edema. With regard to this, both authors concluded that in the presence of avascular necrosis of the femoral head we can distinguish two different aspects: one concerning the cartilage and one concerning the subchondral bone tissue.
The initial stages of the disease are dominated by the ischemic and inflammatory component; the latter is responsible for the joint pain, edema, and degradation of the cartilage. In 2002, some authors have demonstrated that the positive strong antiinflammatory effects of PEMFs causes an increase of adenylyl cyclase activity and a reduction of superoxide anion production, as a result of upregulation of the A2A receptors located on the neutrophil surface.30 Recently, this antiinflammatory action has been demonstrated on the sinoviocytes and chondrocytes.31 The binding plays a fundamental role on the inflammatory response and promotes new vessel formation and limits the extension of the necrotic area, resulting from ischemia. This effect is of extreme importance because of the role of the synovial membrane on the revascularization and resorption of necrotic bone. Moreover, biophysical stimulation is able to inhibit the catabolic effects of the inflammatory cytokines on the joint cartilage32and to stimulate the synthesis of proteoglycans and the local production of BMPs, TGF-α, and IGF-I;33 PEMFs exert a chondroprotective effect in vivo on osteoarthritis,34 which may play a fundamental role in the treatment of early stages of osteonecrosis of the femoral head by limiting the damage induced by inflammation and preserving cartilage and subchondral bone exerting a short term effects.
Regarding the bone tissue, in the long term, the main problem to resolve is the avascular deficit, the first step to get to the necrosis and the recovery of the ischemic bone tissue. In this condition, the PEMF has effects firstly on angiogenesis and then on osteogenesis. In association with core decompression, biophysical stimulation enhances the osteointegration of autologous bone grafts,35 stimulates the local production of growth factors, and favors the osteogenic activity of osteoblasts reducing the bone reabsorption by interfering with the activation of the parathyroid hormone receptor, thus decreasing the recruitment and differentiation of osteoclasts.36–38
In conclusion, both authors suggest that the treatment with PEMFs by now represents one of the conservative therapies used in the first stages of avascular necrosis of the femoral head at Ficat 0, I, II or Steinberg II and III but require from patients time of treatment, care, and precision to ensure the success expected by physicians and patients. The stimulation with PEMFs may be a good opportunity to resolve the disease or at least to delay the time until joint replacement becomes necessary.
Source : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739500/