The utility of conservative treatment modalities in the management of osteonecrosis: a systematic review.
Introduction: Osteonecrosis is an ischemic pathologic process associated with a number of conditions affecting a range of age groups. The problem faced in the management of osteonecrosis is whether conservative treatment is a viable and effective option for patients. In this systematic review, we investigated the efficacy of various nonoperative treatment modalities for hip and knee osteonecrosis, including pharmacological management and biophysical modalities.
Methods: We identified 16 studies based on electronic searches through the PubMed, Embase, CINAHL Plus, and Cochrane databases from January 2001 to November 2015. The therapies we assessed for the conservative osteonecrosis management included bisphosphonates, prostaglandin agents, enoxaparin, statins, hyperbaric oxygen, extracorporeal shockwave therapy, and pulsed electromagnetic field therapy.
Results: Several studies have reported that early intervention (Fiscat stage I/II) osteonecrosis can be effectively managed conservatively. Pain levels and rate of bone necrosis was decreased with bisphosphonate use. Iloprost was seen to have improvement in pain, functional, and radiological outcomes. Progression of osteonecrosis was curbed with enoxaparin use. Statin use was seen to have protective effects on bone in patients taking high dose corticosteroids. The biophysical modalities (hyperbaric oxygen, extracorporeal shockwave therapy, and pulsed electromagnetic field therapy) all saw delay and partial reversal of disease progression.
Conclusion: Generally, stage I and II, prior to subchondral collapse, can be approached with both pharmacological and biophysical treatment modalities before more invasive measures, such as core decompression, are considered. At stage III and beyond, these conservative treatments are no longer viable treatment options. Further research must be performed to determine which modality carries the best cost to risk to benefit ratio in order to establish a standard of care for the treatment of osteonecrosis.
Osteonecrosis is an ischemic pathologic process associated with a number of conditions affecting patients over a range of age groups. Two common pathologies seen in orthopaedics are hip and knee osteonecrosis. The problem faced in the management of osteonecrosis is whether conservative treatment (Table 1) is a viable and effective option for patients.
Hip osteonecrosis is generally seen in younger patients, ages 20 to 40 years old. Currently, the incidence stands at 20,000 to 30,000 affected patients and contributes to 10% of annual total hip arthroplasty (THA) procedures in the USA. Although it is seen, spontaneous regression is rare, with a collapse rate of 67% in asymptomatic hips and 85% in symptomatic hips. (1,2) To date, the literature has not agreed on a uniform treatment algorithm.
Knee osteonecrosis is most commonly due to ischemia to the watershed areas of the medial femoral condyle. Spontaneous osteonecrosis of the knee typically affects an older patient population, ages 50 to 65, while secondary osteonecrosis is commonly seen in younger patients. Up to 4% patients can be found with post-arthroscopic knee osteonecrosis. (3)
Osteonecrosis essentially begins with various factors that lead to a disruption in blood flow to osteocytes. This ischemia causes bone necrosis, which in turn stimulates an inflammatory response. The inflammation is followed by the reabsorption and collapse of the affected areas. Two principal pathways exist in the pathology of osteonecrosis: the traumatic and atraumatic pathway.
The traumatic pathway begins with an inciting event resulting in the interruption of blood flow. Without timely correction, this initial insult may lead to critical ischemia and the resulting bone necrosis. (4)
The atraumatic pathway is caused by a variety of factors that may decrease blood flow. These include coagulopathy (antiphospholipid antibody, inherited thrombrophilia, hypofibrinolysis), glucocorticoids, alcohol, sickle cell crisis, decompression sickness, Gaucher's, and drugs, toxins, and radiation. The final common pathway of this inciting episode may stimulate adipocyte hypertrophy, endothelial damage, and thrombus formation leading to the critical ischemia. (4)
The classification of osteonecrosis is based upon radiographic and magnetic resonance imaging (MRI) findings. The Ficat and Arlet classification is divided from 0-normal radiographs to IV-femoral head collapse and osteoarthritis (Table 2). The Steinberg staging system expanded upon the Ficat and Arlet classification with more thorough categories and introduces mild, moderate, and severe subclassifications (Table 3). The Steinberg staging system is currently used to guide management, with stage I and II being handled more conservatively. At stage III and beyond, subchondral collapse occurs, and a more aggressive management strategy must be considered. The Association Research Circulation Osseous (ARCO) classification is a hip joint specific international standard that stages osteonecrotic changes, from 0 (no disease) to 5 (complete joint destruction), (Table 4).
Several conservative treatment modalities are available for the management of osteonecrosis that attempt to target different pathologic pathways; however, very little comparison data is available. (5) In this systematic review, we investigate the efficacy of various nonoperative treatment options for hip and knee osteonecrosis, including pharmacological management and biophysical modalities.
We performed a comprehensive electronic search through the PubMed, Embase, CINAHL Plus, and Cochrane databases for case-control, cohort studies (both prospective and retrospective), and clinical trials investigating the utility of various nonoperative osteonecrosis treatment modalities (Table 5). The studies reviewed had a minimum follow-up of 12 months and took place between January 2001 to November 2015 using combinations of the following keywords: "osteonecrosis management," "avascular necrosis management," "hip osteonecrosis," "hip avascular necrosis," "knee osteonecrosis," and "knee avascular necrosis." The inclusion criteria were English language studies that reported on hip and knee osteonecrosis management. The exclusion criteria included studies in other languages that were not focused on hip or knee osteonecrosis. The inclusion and exclusion criteria were applied to study titles and abstracts independently by three reviewers to identify potentially eligible studies; disagreements and final selections were made by a fourth reviewer. The therapies we assessed for the conservative osteonecrosis management included bisphosphonates, prostaglandin agents, enoxaparin, statins, hyperbaric oxygen, extracorporeal shockwave therapy, and pulsed electromagnetic field therapy.
Based on the inclusion and exclusion criteria, 16 studies were reviewed and identified based on the treatment and then stratified as hip, knee, or other. Five studies involved bisphosphonate treatment, four studies relating to hip and one relating to knee. Two Iloprost studies were identified with one specifically treating hip osteonecrosis and one study examining both hip and knee. One study investigated the role of enoxaparin in the treatment of hip osteonecrosis was reviewed. Two studies involving statin use were reviewed, both in the context of the development of any type of osteonecrosis. Two studies using hyperbaric oxygen to treat hip osteonecrosis were reviewed. Two studies using extracorporeal shockwave therapy to treat hip osteonecrosis were reviewed. Two studies using pulsed electromagnetic field therapy, one relating the treatment of hip and one relating to the treatment of knee osteonecrosis, were reviewed.
Agarwala and colleagues evaluated the efficacy of bisphosphonates in the treatment of avascular necrosis of the hip: 100 hip cohort was given 70 mg orally per week of alendronate and 500 to 1,000 mg calcium and 400 to 800 IU vitamin D3 and followed every 3 months for up to 1 year, then every 6 months thereafter. (6) Walking time, standing time, and pain were shown to have improved at all the time points. The intervention was most effective for early stages (Stages I and II). Of the 10 hips that underwent replacement during the follow-up period, 8 had advanced stages (Stages III and IV). (6) A similar study by the same investigators following the same methods analyzed 395 hips. At a 4-year follow-up, 92.2% of hips did not need surgery whereas 2% of stage I hips, 8% of stage II hips, and 33% of stage III hips needed arthroplasty. (7)
Lai and associates analyzed 40 patients with Steinberg stage II or III nontraumatic osteonecrosis. (8) Twenty patients (29 hips) received 70 mg alendronate weekly for 25 weeks, and 20 control patients (25 hips) received no drug or placebo, and radiographs were obtained every 10 weeks. On follow-up, only two of the 29 femoral heads in the alendronate group had collapsed, and one hip had undergone THA, in contrast to the control group where 19 of the 26 hips collapsed and 16 hips underwent THA.
Nishii and coworkers compared 14 patients (20 hips) receiving 5 mg alendronate daily to 8 patients (13 hips) as a control group. The alendronate group showed a reduced biochemical marker of bone reabsorption, lower frequency of collapse of the femoral head, and reported less pain, as compared to the control group. (9)
With regard to spontaneous osteonecrosis of the knee, ibandronate was used in a retrospective double-blind study conducted by Meier and associates. (10) Fourteen patients were treated with IV ibandronate and 16 patients received IV placebo for 3 months. All subjects received oral diclofenac with oral supplementation of calcium carbonate and vitamin D for 12 weeks. On follow-up at 48 weeks, the ibandronate treatment showed no significant beneficial effect of the NSAID therapy.
Disch and colleagues (11) used a 5-day IV iloprost course to treat 33 affected hip patients, 16 with isolated edema and 17 with necrosis, ARCO stages I to III. The Harris hip score (HHS), range of movement, the extent of the edema as measured by MRI, pain on a visual scale, and patient satisfaction was monitored and recorded. There was a significant improvement in these observations during the follow-up period. Regardless of the etiology, Disch and coworkers explained that iloprost may be a feasible conservative treatment option in order to reduce pain and promote early mobilization. (11)
Jager and colleagues (12) reported on 50 patients affected by bone marrow edema or avascular necrosis that were given iloprost. Significant improvement was seen in pain, functional, and radiological outcomes after administration. The mean pain level decreased from 5.36 on day 0 to 1.63 at 6 months, and both HHS and Knee Society Score (KSS) increased during follow-up. (12) Jager and colleagues also describes the complex intracellular interactions associated with iloprost, and it is easy to realize that we do not completely understand all the downstream pathways that can affect osteonecrosis. (12)
A prospective study was performed by Glueck and associates (13) to analyze the effects of enoxaparin on patients with hip osteonecrosis related to thrombophilia and hypofibrinolysis (Ficat stages I/II). (13) Twenty hips (13 patients) were treated with 60 mg of enoxaparin daily for 3 months. Fifteen hips (12 patients) with osteonecrosis from other causes were used as the control and did not receive the medication. At 2 years, only 1 hip of the enoxaparin group had progressed to necessitating a total hip arthroplasty, while 12 hips of the control group had progressed to needing replacement.
Enoxaparin may hence restrict the progression of hip osteonecrosis, reducing the incidence of total hip arthroplasty. However, more studies need to be performed to bolster the case for enoxaparin as a medical therapy for osteonecrosis.
High-dose steroid use is a known cause of osteonecrosis. Pritchett and coworkers (14) studied 284 patients on statins at the time they were started on high dose steroid therapy. MRI scans were used to verify if osteonecrosis had developed. After an average of 7.5 years of follow-up, only 1% of patients had developed osteonecrosis, in contrast to the 3% to 20% usually reported in patients taking high-dose steroids.
Another study analyzed whether statin usage reduces corticosteroid-related osteonecrosis in the renal transplant population. Ajman and colleagues (15) looked at 2,881 patients in the renal transplant database; of 338 patients on statins, 15 (4.4%) developed osteonecrosis, in contrast to 180 of 2,543 (7%) of patients who were not on statins.
These studies have provided evidence that statins may offer protection from osteonecrosis in patients taking high-dose steroids.
A double blind trial performed by Camopresi and coworkers (16) studied 19 patients with stage II hip osteonecrosis, comparing 6 weeks of compressed oxygen (HBO) to compressed air (HBA) treatment. Significant reduction in pain was observed after 20 HBO treatments. Range of motion improved significantly during HBO for all parameters between 20 to 30 treatments. All patients remained pain free at 7-year follow-up and none required THA.
Reis and associates (17) treated 12 patients (16 hips) with stage I femoral head osteonecrosis with HBO for 100 days, following up with an MRI at 2 years. At follow-up, 81% of hips had reversal of osteonecrosis.
Extra Corporeal Shock Wave (ECSW)
ECSW was compared to core decompression by Wang and colleagues (18) in a randomized control trial. Patients were identified as ARCO stage I to III, and 23 patients (29 hips) were placed in the ECSW group while 25 patients (28 hips) were placed in the core decompression group. Before the treatment both groups shared similar pain and HHS. At 25-month follow-up, the ECSW group showed significant improved in HHS and pain scores. Of the ECSW group, 5 of the 13 lesions designated as stage I or II showed regression on imaging, and two stage II and two stage III lesions had progressed. In the core decompression group, 4 lesions regressed and 15 progressed. ECSW was observed to be more effective than core decompression in stage I and II osteonecrosis. At stage III, regression had not occurred in either study group. (18)
Wang and coworkers (19) compared ECSW therapy to ECSW and alendronate in a 48 patient cohort. The ECSW only group contained 25 patients (30 hips), and the ECSW and alendronate (70 mg per week for 1 year) group contained 23 patients (30 hips). On follow-up, both groups showed significant improvements in pain and function; however, there was no significant difference between the two groups. ECSW alone shows a comparable result to ECSW and alendronate; both therapies proved to be effective treatments for osteonecrosis.
Pulsed Electromagnetic Field Therapy
In a retrospective analysis by Massari and associates, (20) 66 patients (76 hips) were treated with pulsed electromagnetic field stimulation of the femoral head for 8 hours per day for an average of 5 months. The pulsed electromagnetic field stimulation preserved 94% of Ficat stage I or stage II hips. Fifteen hips required THA, although 12 of these patients were Ficat stage III. Pain, which was present in all patients at the beginning of the treatment period, disappeared after 60 days in 53% of patients.
Marcheggiani Mucciolo and colleagues (21) followed 28 patients with MRI confirmed Koshino stage 1 spontaneous osteonecrosis of the knee who were treated with pulsed electromagnetic fields therapy for 6 hours per day for 90 days. It was observed that there was a significant reduction in knee pain and necrosis at 6-month follow-up, and 86% of knees were preserved from surgery at 23-month follow-up.
Pulsed electromagnetic field stimulation is a viable option for early stage osteonecrosis of both knee and hip.
As previously mentioned, atraumatic osteonecrosis of the hip traditionally affects younger patients, whereas osteonecrosis of the knee affects older patients. The atraumatic pathway is a complex interplay of multiple factors leading to bone death. These factors can be inhibited or reversed by the pharmacologic or biophysical management regimens investigated in this review.
With no uniform treatment algorithm in place, the management of osteonecrosis is difficult and open to interpretation. This may lead to poorer prognosis due to the time sensitive nature of osteonecrosis. Fiscat stages I and II may be effectively managed conservatively. When the severity progresses to stage IV or V, operative intervention is the only resolution. Surgery may be problematic in young patients, and the literature recommends delaying total joint replacement as long as possible to avoid the associated and downstream complications. We investigated the role of various pharmacologic and biophysical therapies in the treatment of hip and knee osteonecrosis.
Bisphosphonates principally function by inhibiting osteoclasts leading to decreased edema and remodeling in order to increase bone mineral density and delay collapse. (22) In the management of osteonecrosis, these medications have proven to be effective with improvements in walking time, standing time, pain, and delays in surgery; however, questions are raised regarding cost, length of therapy, combination therapy with vitamin D or calcium, and certain weightbearing protocols that must be taken into consideration before initiating a regimen. (7-10) Safety is always a concern with bisphosphonate use with adverse events being categorized by their frequency. (22) The most common side effects include gastrointestinal disturbance, acute phase response, renal impairment, hypocalcemia, atrial fibrillation, osteonecrosis of the jaw (ONJ), and atypical subtrochanteric femoral fractures (AFF). (22) Gastrointestinal irritation accounts for most of the adverse effects associated with bisphosphonate use, affecting some 20% to 30% of users and is a common reason for drug discontinuation. (22) The development of an acute phase response in the form of "flu-like" symptoms has also been demonstrated to be a relatively common side effect when compared to placebo. Forty-two percent of patients developed symptoms within the first 15 days of Zolendronate use, in contrast to 12% receiving placebo. (22) Subsequent doses were associated with decreasing severity. Caution must be taken in patients with known renal impairment. Although intravenous administration would not be common practice in this setting, a GFR less than 50 mL/min must be managed conservatively. (22) Caution must also be taken in patients with a predisposition for hypocalcemia, as bisphosphonates act as a trigger. (22) This is much more of a concern with IV administration. Atrial fibrillation is not considered a significant adverse effect of bisphosphonate use as it was only demonstrated in one of the two phase III trials with Zolendronate. For the management of hip or knee osteonecrosis, ONJ is not a significant concern, as it is seen only at higher doses and IV administration. (22) Although bisphosphonate use demonstrated reduction in the risk of classic subtrochanteric fractures, typical subtrochanteric fracture patterns have been seen in patient on long-term therapy. (22)
Iloprost is a vasoactive synthetic prostacyclin analog that functions to dilate arterial and venous vascular beds, reduce capillary permeability, and inhibit platelet aggregation. Recent studies have also shown evidence of pain reduction in treated patients. (11) The most common side effect profile includes severe headaches and nausea. Others side effects include flushing and hypotension, trismus and jaw pain, cough, and flu-like symptoms. Overall, the literature has shown the therapy to be effective with increased range of motion, decreased pain and improved HHS and KSS, and patient satisfaction.
A commonly used low-molecular weight heparin, enoxaparin has been shown to prevent the progression of Ficat stage I and II of osteonecrosis of the hip. (13) In younger patients especially, this is beneficial in delaying or preventing total hip arthroplasty. However, the literature is scarce, and further investigation is required to determine enoxaparin's role, including the associated risks and benefits in osteonecrosis management. The most common side effects of enoxaparin use include nausea, diarrhea, fever, mild swelling, bruising, and redness. (13)
Statins have been well documented for uses in cholesterol and heart disease management. For the treatment of osteonecrosis, statins increase expression of BMP-2 and decrease expression of the adipocyte gene, resulting in a reduction in intraosseous pressure. High dose steroid use predisposes patients to osteonecrosis. (14-16) The studies discussed have shown evidence that the incorporation of statin management in patients on high-dose steroid therapy may prevent the development of osteonecrosis altogether. (14-16) The most serious adverse reaction to statin therapy is life-threatening rhabdomyolysis, leading to muscle pain and liver and kidney failure, and possibly death.
Overall, the literature has demonstrated that pharmacologic treatment modalities generally reduce pain levels, improve Harris Hip and Knee Society Scores, and may delay or prevent surgical intervention. (6-14) Risk to benefit must be further investigated when beginning these pharmaceutical regimens.
Pressurized oxygen supplementation increases extracellular oxygen levels, reducing edema and reversing ischemia. (16,17) The studies reviewed showed that patients that underwent hyperbaric oxygen therapy had improved range of motion (ROM) and pain scores. (16,17) Patients treated at early stages of osteonecrosis showed evidence of reversal on MRI. Unfortunately, the most significant downfall with this option is the substantial cost of therapy. (17) Serious side effects have been observed with hyperbaric oxygen therapy. Seventeen percent of patients reported ear pain or discomfort, and otological trauma was verified in 3.8% of patients; however, other studies have shown the incidence of inner ear and lung pathology. (23) Careful pre-examination and intra-therapy monitoring is paramount.
Extra corporeal shock wave treatment upregulates VEGF and BMP-2 expression stimulating angiogenesis and osteogenesis in order to prevent osteonecrosis. Patients with stage I and II osteonecrosis have been observed to have improvements in HHS, hip and knee pain scores, and regression in hip and knee necrosis. (18,19) The side effect profile is relatively mild with the most common side effects being pain and localized swelling and redness. (24)
Similar to ECSW, pulsed electromagnetic field therapy uses upregulation of VEGF and BMP-2 to promote angiogenesis and osteogenesis. (20) For stage I and II osteonecrosis, pain was found to be the most significantly improved metric. (20,21) The KSS increased, the patient-reported outcome EQ-5D score improved, and MRI findings improved from baseline. (20,21) It is also noteworthy that a delay in arthroplasty was observed. (20,21) There have not been any adverse effects reported in the literature regarding this therapy.
Similar in efficacy but generally much more costly than pharmacologic agents, biophysical therapy has been shown to improve outcomes in the osteonecrosis population. Interestingly, not only has the development of osteonecrosis decrease, several studies have shown that reversal of bone necrosis may be evident.
As this systematic review has revealed, conservative management for both hip and knee osteonecrosis is reserved for Ficat stages I and II, and no significant data demonstrated efficacy in the later stages. Before more invasive procedures are considered, conservative management with pharmacologic or biophysical modalities should be considered and discussed with patients as a viable treatment option to potentially reverse or slow disease progression in patients with diagnosed Ficat stage I or II osteonecrosis of the hip or knee. However, treatment of stage III and beyond will only be achieved with joint arthroplasty. The side effect profile and administration cost must be further investigated in this patient population to effectively determine the value of these interventions.
Osteonecrosis of the hip and knee can be effectively treated with conservative management early in its prognostic course. Generally, Ficat and Arlet stage I and II, prior to subchondral collapse, may be approached with both pharmacological and biophysical treatment modalities before more invasive measures are considered. (6-21) At stage III and beyond, these conservative treatments are no longer viable options, and joint replacement surgery must be considered as the only definitive treatment.
Although these various conservative treatments are available, further research must be performed to determine which modality carries the best cost to risk to benefit ratio in order to establish a standard of care for the treatment of osteonecrosis.
None of the authors have a financial or proprietary interest in the subject matter or materials discussed, including, but not limited to, employment, consultancies, stock ownership, honoraria, and paid expert testimony.
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(5.) Rajpura, Wright AC, Board TN. Medical management of osteonecrosis of the hip: a review. Hip Int. 2011 Jul-Aug;21(4):385-92.
(6.) Agarwala S, Jain D, Joshi VR, Sule A. Efficacy of alendronate, a bisphosphonate, in the treatment of AVN of the hip. A prospective open-label study. Rheumatology (Oxford). 2005 Mar;44(3):352-9.
(7.) Agarwala S, Shah S, Joshi VR. The use of alendronate in the treatment of avascular necrosis of the femoral head: follow-up to eight years. J Bone Joint Surg Br. 2009 Aug;91(8):1013-8.
(8.) Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg Am. 2005 Oct;87(10):2155-9.
(9.) Nishii T, Sugano N, Miki H, et al. Does alendronate prevent collapse in osteonecrosis of the femoral head? Clin Orthop Relat Res. 2006 Feb;443:273-(9.)
(10.) Meier C, Kraenzlin C, Friederich NF, et al. Effect of ibandronate on spontaneous osteonecrosis of the knee: a randomized, double-blind, placebo-controlled trial. Osteoporos Int. 2014 Jan;25(1):359-66.
(11.) Disch AC, Matziolis G, Perka C. The management of necrosis-associated and idiopathic bone-marrow oedema of the proximal femur by intravenous iloprost. J Bone Joint Surg Br. 2005 Apr;87(4):560-4.
(12.) Jager M, Tillmann FP, Thornhill TS, et al. Rationale for prostaglandin I2 in bone marrow oedema--from theory to application. Arthritis Res Ther. 2008;10(5):R120.
(13.) Glueck CJ, Freiberg RA, Sieve L, Wang P. Enoxaparin prevents progression of stages I and II osteonecrosis of the hip. Clin Orthop Relat Res. 2005 Jun;(435):164-70.
(14.) Pritchett JW. Statin therapy decreases the risk of osteonecrosis in patients receiving steroids. Clin Orthop Relat Res. 2001 May;(386):173-8.
(15.) Ajmal M, Matas AJ, Kuskowski M, Cheng EY. Does statin usage reduce the risk of corticosteroid-related osteonecrosis in renal transplant population? Orthop Clin North Am. 2009 Apr;40(2):235-9.
(16.) Camporesi EM, Vezzani G, Bosco G, et al. Hyperbaric oxygen therapy in femoral head necrosis. J Arthroplasty. 2010 Sep;25(6 Suppl):118-23.
(17.) Reis ND, Schwartz O, Militianu D, et al. Hyperbaric oxygen therapy as a treatment for stage-I avascular necrosis of the femoral head. J Bone Joint Surg Br. 2003 Apr;85(3):371-5.
(18.) Wang CJ, Wang FS, Huang CC, et al. Treatment for osteonecrosis of the femoral head: comparison of extracorporeal shock waves with core decompression and bone-grafting. J Bone Joint Surg Am. 2005 Nov;87(11):2380-7.
(19.) Wang CJ, Wang FS, Yang KD, et al. Treatment of osteonecrosis of the hip: comparison of extracorporeal shockwave with shockwave and alendronate. Arch Orthop Trauma Surg. 2008 Sep;128(9):901-8.
(20.) Massari L, Fini M, Cadossi R, et al. Biophysical stimulation with pulsed electromagnetic fields in osteonecrosis of the femoral head. J Bone Joint Surg Am. 2006 Nov;88 Suppl 3:56-60.
(21.) Marcheggiani Muccioli GM, Grassi A, Setti S, et al. Conservative treatment of spontaneous osteonecrosis of the knee in the early stage: pulsed electromagnetic fields therapy. Eur J Radiol. 2013 Mar;82(3):530-7.
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(23.) Plafki C, Peters P, Almeling M, et al. Complications and side effects of hyperbaric oxygen therapy. Aviat Space Environ Med. 2000 Feb;71(2):119-24.
(24.) Haake M, Buch M, Schoellner C, et al. Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial. BMJ. 2003 Jul 12;327(7406):75.
Feroz Osmani, B.S., Savyasachi Thakkar, M.D., and Jonathan Vigdorchik, M.D.
Feroz Osmani, B.S., Savyasachi Thakkar, M.D., and Jonathan Vigdorchik, M.D., Department of Orthopaedic Surgery, NYU Hospital for Joint Diseases, New York, New York.
Correspondence: Feroz Osmani, B.S., Department of Orthopaedic Surgery, NYU Hospital for Joint Diseases, 301 East 17th Street, New York, New York, 10003; email@example.com.
Table 1 Conservative Treatments for the Management of Osteonecrosis Pharmacologic Treatments Biophysical Treatment Bisphosphonates Hyperbaric oxygen Prostaglandin agents Extracorporeal shockwave therapy Enoxaparin Pulsed electromagnetic field Statins Table 2 Ficat and Arlet Classification System Stage Features 0 Normal radiographs I I Slight abnormalities on x-ray; patchy and oblique areas with minor osteopenia observed II Sclerotic or cystic lesions seen IIa: No crescent sign IIb: Crescent sign without flattening of the femoral head III Flattening of the femoral head or collapse of the femoral head IV Osteoarthritis of the hip and femoral head collapse Jawad MU, Haleem AA, Scully SP. In brief: Ficat classification: avascular necrosis of the femoral head. Clin Orthop Relat Res. 2012;470(9):2636-9. Table 3 Steinberg Classification (Modification of the Ficat Classification System) Stage Features 0 Normal scans I Normal radiographs but abnormal bone scan or MRI Ia: Mild (< 15% of femoral head involved) Ib: Moderate (15%-30% of femoral head involved) Ic: Severe (> 30% of femoral head involved) II Cystic and sclerotic changes in the femoral head IIa: Mild (< 15% of femoral head involved) IIb: Moderate (15%-30% of femoral head involved) IIc: Severe (> 30% of femoral head involved) III Subchondral collapse without femoral head flattening IIIa: Mild (< 15% of femoral head involved) IIIb: Moderate (15%-30% of femoral head involved) IIIc: Severe (> 30% of femoral head involved) IV Femoral head flattening/collapse IVa: Mild (< 15% of femoral head involved) IVb: Moderate (15%-30% of femoral head involved) IVc: Severe (> 30% of femoral head involved) V Joint space narrowing and/or acetabular changes IIa: Mild IIb: Moderate IIc: Severe VI Advanced disease Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br. 1995;77(1):34-41. Table 4 Association Research Circulation Osseous (ARCO) International Classification System Stage Features 0 No changes I Normal x-rays and CT; lesion visible on MRI or scintigraphy II Sclerosis, osteolysis, or focal porosis observed III Crescent sign with or without flattening of articular head IV Osteoarthritis, acetabular changes, joint destruction ARCO (Association Research Circulation Osseous): Committee on terminology and classification. ARCO News. 1992;4:41-6. Table 5 List of Studies Reviewed 1. Agarwala S, Jain D, Joshi VR, Sule A. Efficacy of alendronate, a bisphosphonate, in the treatment of AVN of the hip. A prospective open-label study. Rheumatology (Oxford). 2005 Mar;44(3) :352-9. 2. Agarwala S, Shah S, Joshi VR. The use of alendronate in the treatment of avascular necrosis of the femoral head: follow-up to eight years. J Bone Joint Surg Br. 2009 Aug;91(8):1013-8. 3. Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg Am. 2005 Oct;87(10):2155-9. 4. Nishii T, Sugano N, Miki H, et al. Does alendronate prevent collapse in osteonecrosis of the femoral head? Clin Orthop Relat Res. 2006 Feb;443:273-9. 5. Meier C, Kraenzlin C, Friederich NF, et al. Effect of ibandronate on spontaneous osteonecrosis of the knee: a randomized, double-blind, placebo-controlled trial. Osteoporos Int. 2014 Jan;25(1):359-66. 6. Disch AC, Matziolis G, Perka C. The management of necrosis-associated and idiopathic bone-marrow oedema of the proximal femur by intravenous iloprost. J Bone Joint Surg Br. 2005 Apr;87(4) :560-4. 7. Jager M, Tillmann FP, Thornhill TS, et al. Rationale for prostaglandin I2 in bone marrow oedema--from theory to application. Arthritis Res Ther. 2008;10(5):R120. 8. Glueck CJ, Freiberg RA, Sieve L, Wang P. Enoxaparin prevents progression of stages I and II osteonecrosis of the hip. Clin Orthop Relat Res. 2005 Jun;(435):164-70. 9. Pritchett JW. Statin therapy decreases the risk of osteonecrosis in patients receiving steroids. Clin Orthop Relat Res. 2001 May;(386):173-8. 10. Ajmal M, Matas AJ, Kuskowski M, Cheng EY. Does statin usage reduce the risk of corticosteroid-related osteonecrosis in renal transplant population?. Orthop Clin North Am. 2009 Apr;40(2) :235-9. 11. Camporesi EM, Vezzani G, Bosco G, et al. Hyperbaric oxygen therapy in femoral head necrosis. J Arthroplasty. 2010 Sep;25(6 Suppl):118-23. 12. Reis ND, Schwartz O, Militianu D, et al. Hyperbaric oxygen therapy as a treatment for stage-I avascular necrosis of the femoral head. J Bone Joint Surg Br. 2003 Apr;85(3):371-5. 13. Wang CJ, Wang FS, Huang CC, et al. Treatment for osteonecrosis of the femoral head: comparison of extracorporeal shock waves with core decompression and bone-grafting. 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|Author:||Osmani, Feroz; Thakkar, Savyasachi; Vigdorchik, Jonathan|
|Publication:||Bulletin of the NYU Hospital for Joint Diseases|
|Date:||Jul 1, 2017|
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