Femoral head necrosis can lead to progressive damage to the hip joint. The cause of femoral head necrosis is not known, but possible risk factors include: hormone use, alcoholism, trauma, and abnormal coagulation. The size and location of the femoral head necrosis site are predictive factors for disease progression and can be accurately assessed by MRI. The efficacy of medical drugs and biophysical therapies in the treatment of femoral head necrosis is not conclusive and more research is needed in the long term. Surgery is the gold standard in the treatment of femoral head necrosis, and the choice of surgical option depends on individual patient factors and the characteristics of the lesion. In young patients without femoral head collapse, the femoral head can be preserved and treated by decompression of the femoral head alone, or by decompression of the femoral head combined with bone grafting with vascular tips, bone morphogenetic protein, stem cells, or circumferential osteotomy. In case of femoral head collapse, hip arthroplasty is the best treatment option.
Femoral head necrosis usually affects people in the 30-50 years age group. The literature reports that in the United States, the annual per capita incidence is between 20,000 and 30,000, with approximately 5-12% of hip replacement patients diagnosed with femoral head necrosis. Although clinical studies have demonstrated a high number of risk factors for femoral head necrosis, the exact clinicopathological course of the disease remains unclear. The disease continues to progress and can lead to collapse of the femoral head and destruction of the hip joint.
Several non-surgical treatment modalities are available clinically, but surgical treatment remains the cornerstone of femoral head necrosis treatment. There is still much controversy about the best surgical approach to preserve the femoral head; and, in some patients, the disease has the potential to continue to progress and the preserved femoral head may eventually collapse.
Etiology and pathology
Although several risk factors for femoral head necrosis have been identified, their specific etiology and pathological processes remain unclear (Table 1). Cell death is the ultimate outcome of most lesions, and factors contributing to cell death include: ischemia, direct cytotoxicity, and abnormal stem cell differentiation (Table 2).
Pathological causes of femoral head necrosis
Ischemia: Ischemia can be caused by vascular destruction, compression, contracture or vascular blockage. Rupture of the vascular network around the femoral head can lead to traumatic femoral head necrosis, which is prone to develop later in approximately 15-50% of patients with displaced femoral neck fractures and 10%-25% of patients with hip dislocations. Fatty infiltration in the bone marrow cavity (hormone use or alcoholism) or increased pressure in the hip joint can lead to vascular compression. Vascular contracture of the femoral epiphyseal artery can be exacerbated by hormone use. Intravascular obstruction can be due to blood clots, fat or gas embolism, or sickle cell aggregation.
The end result of multiple hematologic disorders is a tendency to intravascular thrombosis or a decreased ability to dissolve thrombi. (3/36,8%) than in normal patients.
Researchers are now more interested in the genetic factors of femoral head necrosis. However, it is still clinically unclear which genes can cause femoral head necrosis.
Direct cytotoxicity and abnormal stem cell differentiation
Direct cellular injury can occur by radiation, chemotherapy, or oxidative stress. a study by Lee et al. found that patients with femoral head necrosis had fewer mesenchymal stem cells of proximal femoral origin than patients with osteoarthritis.
Multifactorial process
However, it is interesting to note that not every patient with osteonecrosis of the femoral head is exposed to risk factors for the development of the disease. Furthermore, only a small percentage of patients exposed to risk factors developed osteonecrosis of the femoral head, and a study by Lieberman et al. found that only some of the patients exposed to high-dose hormone therapy developed osteonecrosis of the femoral head. The above facts suggest that the development of femoral head necrosis may be the result of multifactorial effects.
Diagnosis and evaluation
Early diagnosis of osteonecrosis of the femoral head can provide a longer time window for the treatment of the disease and allow patients to achieve a better functional prognosis. Patients with earlier exposure to risk factors for osteonecrosis of the femoral head need to be highly suspicious of the disease.
Clinical manifestations
Early stages of femoral head necrosis may be asymptomatic clinically. If the disease progresses and symptoms develop, the most common presentation is pain in the groin area, which may radiate to the ipsilateral hip or knee. The patient’s earlier medical history can provide assistance in the diagnosis. Physical examination may reveal a normal hip joint on the affected side, or limited motor function and pain on movement, especially limited internal rotation of the affected limb with induced pain. Restricted internal rotation of the affected limb is often indicative of femoral head collapse.
Diagnostic imaging
The basic imaging tools for the diagnosis of femoral head necrosis are anteroposterior and lateral X-rays and MRI. imaging X-rays can be normal in the early stages of femoral head necrosis, and in the later stages can show typical changes such as cystic degeneration of the femoral head and marginal osteosclerosis. the bimonthly sign on X-rays is a peeling and calcification of the cartilage within the femoral head from the subchondral bone and often indicates a poor functional prognosis (Figure 1A). Early changes in the flattening of the femoral head are milder and may be visible on X-rays in only one phase (Figure 1B). Progressive flattening of the femoral head and degenerative changes in the hip joint are seen in the mid to late stages of femoral head necrosis.
Figure 1: Crescent sign in lateral view of the left hip (A) and orthopantomogram of the left hip with arrows showing collapse and flattening of the femoral head
The accuracy and specificity of MRI in the diagnosis of femoral head necrosis are very high, up to 99%, and it is the gold standard for the diagnosis of femoral head necrosis. single line sign on T1 phase indicates the osteonecrosis interface, while double line sign on T2 phase indicates vascularized granulation tissue proliferation at the necrotic bone interface (Figure 2). Figure 2: Coronal MRIT1 phase of the right hip, with a single low-signal area shown by the arrow suggesting an area of osteonecrosis
Femoral head necrosis needs to be differentiated from transientosteoporosis of the hip (TOH). These disorders usually affect pregnant women and men aged 50-60 years and present with severe pain in the groin region and an antalgic gait, with bone marrow edema visible on MRI and signal extending to the femoral neck and femoral epiphysis. A key point in the differential diagnosis of the two diseases is that TOH is a self-limiting disease and the disease resolves spontaneously after a period of time.
Typology and staging of osteonecrosis of the femoral head
There are a number of ways to staging femoral head necrosis (Table 3). The University of Pennsylvania Femoral Head Necrosis Staging System incorporates the extent, location, and degree of femoral head necrosis on MRI as an evaluation index, which is a positive guide.
Table 3: Femoral head necrosis staging and staging methods
FicatandArlet staging staging
Stage I normal
Stage II osteosclerosis or cystic lesion
A No crescentic sign
B subchondral collapse (crescentic sign) without involvement of the femoral head
Stage III collapsed or compressed femoral head
Stage IV osteoarthritis, reduction of joint space with joint collapse
Steinberg staging (University of Pennsylvania staging)
Stage O suspected femoral head necrosis, normal radiographs, bone scan and MRI or non-diagnostic
Stage I normal radiographs, abnormal bone scan and/or MRI
I-A mild, MRI femoral head lesion extent less than 15%
I-B moderate, MRI femoral head lesion range 15-30%
I-C severe, MRI femoral head lesion greater than 30%
Stage II x-ray shows abnormalities such as cystic and sclerotic changes in the femoral head
II-A mild, X-ray femoral head lesion range less than 15%.
Ⅱ-B moderate, the extent of femoral head lesion on X-ray is 15-30%.
Ⅱ-C severe, the extent of femoral head lesion on X-ray is greater than 30%.
Stage III subchondral fracture produces crescentic sign, which appears as a small translucent line 1-2L below the plane of cartilage on X-ray, extending to the whole extent of necrosis.
In III-A mild, the subchondral collapse (crescent sign) occupies less than 15% of the articular surface.
III-B moderate, subchondral collapse (crescent sign) occupies 15-30% of the articular surface.
III-C severe, subchondral collapse (crescentic sign) accounting for more than 30% of the articular surface.
Stage IV femoral head articular surface collapse.
IV-A mild, joint surface collapse less than 15% or compression less than 2L.
IV-B moderate, joint surface collapse of 15-30% or compression of 2-4L.
Ⅳ-C severe, joint surface collapse1 greater than 30% or compression greater than 4L.
Stage V narrowing of the hip joint space and/or changes in acetabular cartilage.
Stage VI further degenerative changes in the femoral head and hip joint with gradual loss of joint space and significant deformation of the articular surface.
Natural history and predictors of prognosis
Symptomatic femoral head necrosis may show continuous progression. Predictors of progression include the extent of the necrotic lesion of the femoral head, the location of the necrotic lesion on the femoral head, and the degree of edema on MRI of the proximal femoral bone marrow.
The extent of femoral head necrosis is a predictor of femoral head collapse. The size of the necrotic area can be assessed by MRI in axial or sagittal view (modified Kerboul method, Figure 3).
Figure 3: Modified Kerboul’s method of measuring the extent of femoral head necrosis. The sum of the angular size consisting of the necrotic area of the femoral head in the median coronal (A) and median sagittal (B) positions and the circular position of the femoral head is the size of the femoral head necrosis. The calculation was based on an article by Ha et al. published in JBJSam, 2006, Vol. 88.
Ha et al. performed an imaging analysis of 37 patients with femoral head necrosis that was about to collapse and found that 23 patients (62%) had clinical symptoms and were followed up according to the method of treatment (conservative and femoral head decompression) received by the patient, with the endpoint event being the patient’s femoral head collapsing or no collapse of the femoral head found at least 5 years after follow-up. The femoral head collapsed in 4 patients with a joint necrosis angle of less than 190 degrees, while 4/8 patients with a joint necrosis angle of 190-240 degrees had femoral head collapse; 25 patients with a joint necrosis angle of more than 240 degrees had femoral head collapse. In contrast, the treatment modality (conservative or femoral decompression) had no significant effect on whether the femoral head collapsed.
In a minimum 5-year follow-up study of 35 patients with 54 cases of femoral head necrosis without collapse, Nishii et al. found that patients with more extensive femoral head necrosis (more than 2/3 of the femoral head in the weight-bearing area) had a significantly higher probability of femoral head collapse and progression of femoral head collapse (collapse greater than 2 mm) compared to patients with smaller areas of femoral head necrosis. Interestingly, in 8/9 patients with a femoral head necrosis area smaller than 2/3 of the weight-bearing surface of the femur, clinical symptoms were found to improve over the course of follow-up, with no significant progression of femoral head necrosis.
Proximal femoral bone marrow edema is a risk factor for femoral head collapse. a study by Ito et al. of 83 asymptomatic or only mildly symptomatic patients diagnosed with femoral head necrosis on MRI at follow-up found that 36 (43%) patients eventually developed clinical symptoms and femoral head collapse, and a correlation analysis found that the presence of bone marrow edema signal on the first MRI at diagnosis of femoral head necrosis The correlation analysis revealed a significant correlation between the presence of bone marrow edema signal on the first MRI for the diagnosis of femoral head necrosis and the progress of femoral head collapse.
All 21 patients with edema signal changes on first MRI eventually developed clinical symptoms or femoral head collapse, whereas the corresponding proportion of patients without bone marrow edema signal who developed clinical symptoms or femoral head collapse was only 24% (15/62 patients).
In a prospective study of 40 patients with asymptomatic osteonecrosis (lesions less than 10% of the femoral head), the authors followed all patients for a minimum of 10 years and found that 35/40 patients eventually developed clinical symptoms, and 29/40 of these patients developed femoral head collapse.
However, a minimum 5-year follow-up study by Nam et al. found that 43/105 (41%) patients were clinically asymptomatic, while only 62/105 (59%) patients developed pain and femoral head collapse. The probability of femoral head collapse was 83% for lesions of different sizes at the first visit, respectively for small lesions (<30% >50%).
Both studies found that in patients with femoral head necrosis, the onset of painful symptoms preceded femoral head collapse. A systematic evaluation of conservatively treated patients found that at a mean follow-up of 53 months, only 28% of patients were free of imaging progression and only 33% of patients ultimately did not require surgical treatment.
Treatment options
1. Non-surgical treatment
Non-surgical treatments for femoral head necrosis such as observation and weight bearing under protection are of very limited use to patients. The only exception is that for small lesions with asymptomatic femoral head necrosis, follow-up until clinical symptoms appear can be considered.
Biophysical and pharmacological therapies
Biophysical therapies such as extracorporeal shock waves and electrical pulses have been used in the treatment of osteonecrosis of the femoral head, but the results reported in the literature are variable and of limited significance. In a randomized study completed by Wang et al. comparing the effectiveness of extracorporeal shock wave and femoral decompression in the treatment of osteonecrosis, there was a significant improvement in pain and hip Harris scores in the extracorporeal shock wave group at a mean follow-up of 25 months.
Pharmacological measures such as anticoagulation, lipid-lowering drugs, bisphosphonates, growth factors, antioxidants, vasoactive drugs, and hormones have been used in the treatment of osteonecrosis of the femoral head. However, there are only very limited reports in the clinical literature describing the effectiveness of these drugs in the treatment of osteonecrosis of the femoral head.
Enoxaparin may be helpful in patients with coagulation-related problems, but not in patients with other causes of femoral head necrosis.
Two clinical studies have evaluated the efficacy of allen phosphate in the treatment of early femoral head necrosis, with mixed findings. lai et al. followed treated patients for 24 months and found that allen phosphate significantly reduced disease progression and femoral head collapse (collapse rate of 2/29, 7%), compared with a 76% collapse rate in the control group (19/25 cases). However, the study by Chen et al. found that neither the use of allen phosphate nor the use of allen phosphate changed the final clinical functional prognosis of the patients’ disease.
Given the lack of high-level clinical evidence supporting pharmacological treatment of femoral head necrosis, more recent studies are needed at a later stage.
2. Surgical treatment
Surgical treatment of femoral head necrosis can be broadly divided into two categories: head-preserving surgery to preserve the femoral head and hip arthroplasty. Head preservation surgery includes: femoral head decompression; femoral head decompression + fibular bone graft with vascularized tip, fibular bone graft without vascularized tip, intra-femoral injection of stem cells, biological cofactors, or tantalum metal rods; circumferential osteotomy. Hip replacements include: total hip replacement and hip surface replacement.
2.1 Decompression of the femoral head
Femoral decompression therapy is used more often in patients with early-stage femoral head necrosis. The basic principle is to reduce femoral head pressure, restore blood flow, and improve pain symptoms by opening a channel in the femoral head. Femoral decompression can be obtained by opening a single large aperture in the femoral head or by opening multiple small aperture channels (Figure 4).
Figure 4: Small lesion of necrosis in the right femoral head at coronal T1 phase MRI (A) with femoral decompression (B,C,D). Decompression and bone grafting was performed in the femoral head after completion of lesion scraping.
Israelite et al. found that only 38% of patients eventually required THA in a 2-year follow-up study of 276 cases of hip osteonecrosis after decompression of the femoral head. In the pre-collapse period, decompression of the femoral head was better in small lesions (<15%) (only 14% of patients required femoral head replacement), whereas a higher proportion of patients with both moderate and large lesions eventually required THA (48% and 42%, respectively). The patients had a good functional prognosis at final imaging follow-up.
2.2 Femoral head decompression + avascular fibular implant, intra-femoral stem cell injection, and biological cofactors
Femoral decompression combined with other adjunctive measures such as allograft or autologous bone blocks can provide support for the necrotic lesion and prevent collapse. Phemister technique, electric bulb technique, and open-window technique can be used to achieve bone grafting. Based on recent findings, stem cells or BMPs are also being used to treat femoral head necrosis.
Lieberman et al. treated 15, 17 patients with femoral head necrosis of the hip with femoral decompression + fibular block-supported bone grafting + BMP with a mean follow-up of 53 months and found that 14/15 patients with Ficat-Aelet stage IIA had pain relief and no visible disease progression on imaging.
Hernigou et al. evaluated the efficacy of femoral decompression + concentrated autologous bone marrow in 116 patients with 189 hip osteonecrosis with a mean follow-up of 5 years and found that only 9/145 Steinberg stage I/II patients required THA, whereas a significantly higher proportion of patients in stages III and IV required THA treatment (25/44, 57%).
In patients with hormone- and alcohol-related osteonecrosis, the number of progenitor cells obtained from the femoral head was significantly reduced, and the failure rate of these regimens was significantly higher in these patients.
A recent small prospective study found that postoperative pain and disease progression were significantly better in patients with femoral head decompression + autologous bone marrow implantation compared to femoral head decompression alone at 5 years of follow-up, with progression occurring in 3/13 patients in the bone marrow injection group compared to 8/11 patients in the femoral head decompression alone group. However, it is worth noting that there was no significant difference between the two groups in the proportion of patients who eventually received THA treatment (2/13 versus 3/11, respectively).
Based on the above study facts, future developments in basic and translational medicine may make the treatment modality of femoral decompression + autologous bone graft + biologic osteogenic factor the best strategy for the treatment of femoral head necrosis.
2.3 Bone graft with vascularized tip combined with femoral decompression
The purpose of using a vascularized bone graft into the femoral head is to provide subchondral bone support and to increase the blood supply to the femoral head (Figure 5). A study comparing femoral bone grafting with and without a vascularized tip found that bone grafting with a vascularized tip significantly improved femoral head collapse at the end of the 7-year follow-up.
Figure 5: Method of using a fibular implant block with a vascularized tip. The fibula is inserted into the decompression hole and fixed using a Kirschner pin, and the vessels on the implant block are anastomosed to the lateral rotor femoral artery vein, respectively.
Soucacos et al. reported that in patients with Steinberg II osteonecrosis, treated with a vascularized implant, the percentage of progression of osteonecrosis visible on imaging was only 5% after a mean follow-up of 4.7 years, whereas in patients with Steinberg III and above, the percentage increased sharply to 44%. collapsed femoral head and found that approximately 64.5% of patients did not require THA treatment at the end of the final 5-year follow-up despite more advanced disease. Unfortunately, there is no clinical level I study evidence comparing the effectiveness of implant blocks without and with a vascularized tip for the treatment of femoral head necrosis.
There is more clinical literature on the effectiveness of implants with vascularized tips in the treatment of osteonecrosis of the femoral head. yooo et al. reported a mean follow-up of 13.9 years after treatment, with 13/124 patients requiring THA. there was no significant difference in the clinical prognosis of osteonecrosis of the femoral head in Ficat-Arlet stage II or III. The clinical functional prognosis of the hip depended on the age of the patient, the size of the femoral head necrosis and the site of necrosis. edward et al. found an overall hip survival rate of 60% after a mean of 14.4 years and a mean hip haris score of 89 in 65 patients with Ficat-Arlet stage I or II.
A forceful implant block with a vascularized tip is technically demanding, requires extensive experience, and is prone to donor-site related complications. Usually this technique is used in patients with femoral head necrosis without femoral head collapse.
2.4 Tantalum rod placement
Tantalum rods were earlier used in femoral decompression as a substitute for bone graft blocks. The main purpose of its application was to provide structural support to the necrotic area and enhance bone ingrowth. a 24-month follow-up study by Veillete et al. of patients treated with the above protocol found that approximately 16/58 patients developed disease progression, 9 of whom required arthroplasty. Another study of 113 cases of femoral head necrosis treated with tantalum rods done by Tanzer et al. found a failure rate of about 15% with a mean time to failure of 13.4 months. Histological analysis of the failed removed tantalum rods revealed a lack of bone ingrowth within the metal rods and inadequate subchondral bone support of the femoral head. Based on the above research evidence, this paper does not recommend this technique for clinical use as a routine procedure unless supported by future high-quality research evidence.
2.5 Circumferential osteotomy
The basic principle of circumferential osteotomy for femoral head necrosis is to reduce the mechanical forces acting on the lesion by converting the weight-bearing area of the necrotic femoral head into a non-weight-bearing area through osteotomy. There are two main types of circumferential osteotomies used in clinical practice: circumferential osteotomy via the intertrochanteric space (anterior or posterior) and intertrochanteric osteotomy with internal or external rotation.
Sugioka et al. reported a success rate of 93% (43/46 cases) for posterior intertrochanteric osteotomy for femoral head necrosis at 12 years, but these results have not been replicated in studies in the United States and Europe, and therefore the use of internal or external rotor osteotomy is currently preferred in the United States and Europe. Mont et al. reported a success rate of over 70% (28/37 cases) for the treatment of femoral head necrosis.
The success rate of osteotomy for osteonecrosis depends on the size of the osteonecrotic lesion and requires a detailed preoperative evaluation to determine if there is sufficient healthy area for weight bearing after osteotomy. When the weight-bearing area of the transferred femur after osteotomy reaches or exceeds 1/3 of the weight-bearing area of the acetabulum, and when the joint angle of femoral osteonecrosis is less than 200 degrees, the above-mentioned surgical approach can achieve better clinical results. It should be noted that the osteotomy treatment requires high technical requirements, and if the treatment fails later, it is difficult to perform THA treatment again.
2.6 Total hip arthroplasty (THA)
The indications for total hip replacement are: femoral head collapse after femoral head necrosis; or femoral head necrosis although not collapsed, but the area is too large to perform head preservation surgery. At this time, the application of total hip replacement can significantly relieve pain and promote the functional recovery of patients.
One of the main problems of total hip replacement for the treatment of femoral head necrosis is the longevity of the total hip prosthesis. Compared to patients with osteoarthritis of the hip, patients with femoral head necrosis are younger and more mobile, and Ortiguera et al. reported that patients treated with total hip replacement for femoral head necrosis had a higher probability of prosthetic dislocation at 17.8 years of follow-up than patients with osteoarthritis. The reason for this may be that patients with femoral head necrosis have better preoperative hip mobility. In addition, the investigators found that a higher percentage of patients younger than 50 years of age required hip revision later in life than patients with osteoarthritis in the same age group.
Over the past 15 years, THA surgery outcomes have consistently improved. Arthroplasty can be accomplished by implanting a biologic total hip prosthesis in the majority of patients with osteonecrosis of the femoral head. Recent studies have found that the mid-term clinical prognosis of patients with osteonecrosis treated with a biologic total hip replacement is better than that of a cemented total hip (Table 4).
Table 4: Reported clinical outcomes in patients with osteonecrosis of the femoral head with biologic total hip replacement.
In a 15-year follow-up of patients younger than 50 years with osteonecrosis of the femoral head, Kim et al. found that no biologic femoral stems required revision and only 14% of uncemented acetabulums required revision due to aseptic loosening. similar conclusions were reached in the study by Bedard et al. and they found that a lower percentage required revision.
When preparing the acetabular side of the femoral head for total hip replacement, the surgeon needs to be aware that the pelvic bone density on the acetabular side may be very low at this time due to hormone use, lack of weight bearing, or underlying disease; in addition, subchondral osteosclerosis, which is common in arthritis, is not common in the acetabulum of patients with femoral head osteonecrosis. This means that the surgeon is reminded that special care needs to be taken when grinding out the acetabulum. At the same time, special attention needs to be paid when treating patients with total hip replacement, whether such patients have been treated with head-preserving surgery, and patients who have been treated with osteotomy need to be carefully questioned and preoperative imaging films analyzed in detail to determine the best surgical plan.
2.7 Hip surface replacement
Hip surface replacement can preserve most of the femoral head bone and does not interfere with the operation of total hip replacement at a later stage. Therefore, its can be a treatment measure for young patients with good bone quality before the femoral head collapses.
However, femoral neck fractures may complicate this procedure, and the results of surgical treatment vary from person to person. A follow-up analysis of 550 patients with surface replacement found that 71 patients who had surface replacement for femoral head necrosis had a femoral tibial incidence of 2.5%, and that obesity, females, and femoral neck or head cysts were significantly associated with the occurrence of femoral neck fractures. However, wear of the metal interface of the surface replacement prosthesis and reduced quality of the femoral head limit the use of surface replacement prostheses in patients with femoral head necrosis.
Treatment options
Based on the evidence from the above studies, it is difficult to recommend an optimal treatment option for patients with femoral head necrosis that is about to collapse. In addition, the inconsistency of staging and staging criteria for femoral head necrosis used in current clinical applications makes comparison between treatments in different studies difficult. Some studies suggest that if the femoral head has collapsed necrosis, then the clinical outcome of performing head preservation therapy is very unpredictable.
Given the lack of high-level Class I clinical evidence, it is not possible to recommend a gold standard treatment protocol for patients with femoral head necrosis. However, based on the evidence from the above studies, we can make the following recommendations.
1. head-preserving treatment options should be preferred for patients with symptomatic femoral head necrosis with only a small lesion and no femoral head collapse, or in the phase of imminent femoral head collapse.
2. for young patients with symptomatic femoral head necrosis with a large necrotic lesion, without femoral head collapse, or in the stage of imminent femoral head collapse, the head-preserving surgical option may be preferred; for elderly patients, THA is preferred.
3. For most patients with femoral head necrosis and femoral head collapse, head-preserving surgery is not effective, and THA should be the first choice of treatment at this time.
Summary
Femoral head necrosis usually affects patients between the ages of 30 and 50, and progressive disease progression can lead to femoral head collapse and degenerative changes in the hip joint. Risk factors for the development of osteonecrosis include: hormone use, excessive alcohol intake, trauma, and abnormal coagulation. The diagnosis of osteonecrosis is based on imaging X-rays and MRI, and the patient’s age, size and location of the osteonecrosis should be taken into account when deciding on a treatment plan. Drug and biophysical treatment of osteonecrosis requires more research in the later stages. Surgical treatment options include head-conserving surgery, which is indicated for younger patients without femoral head collapse, and THA, which can provide significant pain relief and functional improvement if femoral head collapse is present.