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Avascular necrosis of the femoral head

116 citationsUpdated Sep 2026

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Overview

Osteonecrosis of the femoral head is a disabling pathology affecting a young population and represents the most important cause of total hip arthroplasty in this demographic [5]. The prognosis for patients can be significantly improved with early diagnosis and timely intervention [2]; however, nearly 80% of patients present with late-stage disease, indicating a narrow window of opportunity for hip preservation surgery before femoral head collapse [14]. While small, asymptomatic, medially-placed lesions of non-traumatic osteonecrosis may be treated with observation alone [7], larger lesions carry a 25% to 50% risk of progression [7]. Necrosis involving the anterior aspect of the femoral head is an important risk factor for collapse in JIC type C1 nontraumatic osteonecrosis [6]. Additionally, patients with nontraumatic osteonecrosis have a higher incidence and risk of major adverse cardiovascular and cerebrovascular events than the general population, with a greater than 1.3-fold risk [30].

In the context of trauma, avascular necrosis is the most common and most devastating complication associated with hip fractures in children [12]. Fracture displacement is the most important risk factor for avascular necrosis in pediatric hip fractures [12], with the presence of a type I or II fracture and age greater than 12 years also serving as risk factors [12]. Radiographic evidence of avascular necrosis in pediatric hip fractures can be seen as early as 2 months after injury and is generally present within 1 year, with a median time to presentation of 7.8 months [12]. Avascular necrosis is relatively uncommon in type 1 dislocations reduced within 6 hours [10], yet symptomatic avascular necrosis can develop 8 years post-injury despite no evidence at 3 years, implying a need for extended follow-up [10].

Management strategies vary based on disease stage and etiology. Joint-preserving procedures should be attempted in early-stage lesions to save the femoral head [23], with core decompression augmented with autologous bone marrow aspiration concentrate recommended for early stages (Ficat stages 0 through II) [4]. Core decompression and concentrated autologous bone marrow containing mononuclear cells may be the treatment of choice particularly in stages I–II nontraumatic osteonecrosis [13]. Arthroscopic management is viable and has significant advantages [15], while free vascularized fibular grafting is indicated for small osteonecrosis (less than 300 degrees of the femoral head) without preoperative collapse (Steinberg's stages I and II) [36]. Patients with postcollapse, predegenerative osteonecrosis appear to benefit from free vascularized fibular grafting, with good overall survival of the joint and significant improvement in the Harris hip score [28]. Femoral head-preserving surgery is not recommended for patients with type 3 osteonecrosis [64]. The results of intertrochanteric curved varus osteotomy for idiopathic osteonecrosis were successful if indicated for cases with an intact load-bearing area of more than 40% [73]. One in five patients require conversion to arthroplasty after non-vascularized bone grafts [80], and a previous joint-preserving procedure poses technical challenges for subsequent total hip reconstruction and might have a detrimental effect on the short-term clinical outcome [31]. Femoral head necrosis following renal transplantation and extension of the necrotic area into the femoral neck are contraindications for the thrust plate prosthesis [65]. The care of adults with osteonecrosis varies among American orthopaedic surgeons specializing in hip and knee surgery [27], and the management of pediatric osteonecrosis is complicated by a limited body of evidence and a lack of consensus on prevention or treatment of femoral head collapse [16]. Outcomes of total hip arthroplasty in the setting of osteonecrosis are excellent [23].

Anatomy & Pathophysiology

Vascular Anatomy

The primary blood supply to the femoral head in adults derives from cervical arteries originating from the extracapsular ring at the base of the femoral neck [101]. This ring is formed by contributions from the medial femoral circumflex artery (MFCA) posteriorly and the lateral femoral circumflex artery (LFCA) anteriorly [101]. The superior and posterior vessels, derived primarily from the MFCA, constitute the dominant blood supply to the femoral head [101]. The MFCA supplies the inferior retinacular branch, which runs along the ligament of Weitbrecht to supply the inferior medial portion of the femoral head [101]. A minor contribution arises from the foveal artery, a branch of the obturator artery within the ligamentum teres [101]. In approximately 75% of hips, the foveal artery makes a significant contribution to the epiphyseal portion of the femoral head vasculature [101].

In newborns, the main source of femoral head blood supply is derived from vessels arising from the medial and lateral circumflex femoral arteries [97]. In 79% of cases, these circumflex arteries are branches of the profunda femoris, while in 20% of patients, one or both arise from the femoral artery [97]. At about 3 years of age, the lateral circumflex artery regresses, and branches of the medial circumflex femoral artery become the main blood supply to the femoral epiphysis and proximal femoral physeal plate [97]. The deep branch of the MFCA is the most important source of femoral head blood supply [97]. It gives off the inferior retinacular artery, which runs toward the femoral head in the ligament of Weitbrecht [97]. The main terminal branch of the deep MFCA, often referred to as the superior retinacular artery, divides into two to four terminal branches [97]. These vessels course within fibrous extensions of the capsule wall known as the retinacula of Weitbrecht posterosuperiorly on the femoral neck [97]. They perforate the bone at a distance 2 to 4 mm lateral to the bone–cartilage junction of the head [97]. The lateral group of retinacular vessels is the largest contributor to femoral head blood supply [97]. A cadaveric MRI study estimated the contribution of the MFCA to femoral head perfusion at 82% and that of the LFCA at 18% [97]. The acetabular artery of the MFCA gives off the foveal or medial epiphyseal artery [97].

In children with slipped capital femoral epiphysis, the blood supply to the capital epiphysis is primarily by vessels arising from the lateral epiphyseal system entering the epiphysis at its outer posterior margin [131]. The ligamentum teres supplies the epiphysis in children, and in late adolescence, metaphyseal vessels that pierce the physis reappear [131].

Pathogenic Mechanisms

Osteonecrosis of the femoral head is defined as an end condition resulting from many possible pathogenic pathways [42]. No single pathophysiologic mechanism has been identified as the sole etiology for the development of osteonecrosis of the femoral head [11]. Proposed mechanisms include ischemia from various mechanisms, direct cellular toxicity, and alteration of differentiation of mesenchymal stem cells [42]. Most etiologic factors in atraumatic osteonecrosis are related to underlying pathologic conditions that alter blood flow, leading to cellular necrosis and ultimately to collapse of the femoral head [3].

Ischemic mechanisms include vascular disruption, vascular compression or constriction, and intravascular occlusion [134]. Vascular disruption causes include femoral head fracture, hip dislocation, and surgery [134]. Vascular compression or constriction can result from increased intraosseous pressure caused by marrow fatty infiltration, corticosteroids, alcohol, or vasoconstriction of arteries perfusing the femoral head [134]. Intravascular occlusion mechanisms include thrombosis, embolization of fat or air, and sickle cell occlusion [134]. Thrombophilia risk factors include low protein C and S, activated protein C resistance, factor V mutation, high homocysteine, and eNOS polymorphisms [134]. Hypofibrinolysis risk factors include high PAI activity, PAI-1 polymorphisms, and high lipoprotein(a) [134].

Direct cellular toxicity mechanisms include pharmacologic agents, irradiation, and oxidative stress [134]. Altered differentiation of mesenchymal stem cells is a proposed mechanism associated with corticosteroids and alcohol [134]. Direct damage to osteocytes may occur via toxin production, while indirect damage may result from disorders in fat metabolism or hypoxia [3].

The basic mechanism of osteonecrosis involves impaired circulation to a specific area that ultimately becomes necrotic [11]. The subchondral regions of bone are particularly prone to osteonecrosis due to the microarchitecture of blood vessels at these locations [79]. Arterioles in the subchondral region are isolated from the rest of the circulation by a cartilage boundary and lack collateral vessels [79]. Edema associated with cell death and the normal reparative process causes further damage by increasing local compartmental pressure and decreasing vascular ingress [79]. Repeated mechanical insult without the inherent healing mechanism of live bone results in propagated stress fractures and eventual femoral head collapse [79]. Femoral head collapse generally results in an anterolateral wedge-shaped area of necrosis with normal cartilage overlying the defect [79]. Large defects in the femoral head do not heal spontaneously [79]. Osteonecrosis of the femoral head is characterized by microfractures of the subchondral bone and subsequent collapse of the femoral head [157]. The failure of bone formation by osteoblasts to match bone resorption by osteoclasts is the main mechanism of avascular necrosis [178]. In osteonecrosis, dead trabecular bone replaces the cancellous bone of the normal femoral head [79]. The necrotic area can include the osteochondral plate below the cartilage [79]. Death of bone elements and marrow in the femoral head can result from interruption of the vascular supply due to cyclical insults or one large crisis [79]. A reduced head–neck offset may act as a mechanical co-factor in developing osteonecrosis of the femoral head [37]. Osteoarthritis in hips with osteonecrosis can be caused by elevated contact stress [184].

Traumatic Pathophysiology

In hip dislocations, the position of the hip can kink the vessels supplying the head, making collateral circulation important [101]. Injection studies of cadaveric hips after forceful dislocation and relocation demonstrated filling defects at the junction of the external iliac and common femoral arteries and at the circumflex vessels [101]. Changes in extraosseous blood supply after dislocation did not cause a consistent change in intraosseous supply to the head, presumably due to collateral circulation [101]. The cause of avascular injury in hip dislocation is multifactorial, involving damage to cervical vessels and contributions from the ligamentum teres at the time of injury [153]. An ischemic insult to the femoral head while it is dislocated affects outcome [153]. Studies in rabbits demonstrated that cervical vessels to the head are not normally disrupted by dislocation but do not provide adequate circulation due to spasm of larger vessels or the cervical vessels themselves [153]. Early reduction restored the vascular supply to the head better than late reduction, in some cases almost to the level of the contralateral hip [153]. The majority of avascular necrosis following hip dislocation is secondary to initial ischemia of the femoral head rather than torn vessels [153]. AVN is predominantly present after posterior dislocation and correlates with the time to reduction [153]. If the hip is reduced within 6 hours of dislocation, AVN rates are 0% to 10% [153]. Reduction after 12 hours increases the risk of AVN 5.6 times [153].

In children with hip fractures, AVN is thought to result from disruption or compromise of the blood supply of the femoral head at the time of initial trauma and potentially from the tamponade effect of hip hemarthrosis [12]. Fracture displacement is the most important risk factor for AVN in children with hip fractures [12]. The presence of a type I or II fracture and a fracture in an older child (>12 years) are risk factors for AVN in children [12]. Radiographic evidence of AVN in children can be seen as early as 2 months after injury and is generally present within 1 year [12]. The median time to presentation of AVN symptoms in children is 7.8 months [12]. Radiographs in children with AVN may demonstrate osteopenia of the femoral head, followed later by sclerosis, fragmentation, and often collapse and deformity [12].

In slipped capital femoral epiphysis, the lateral epiphyseal arteriolar system may be damaged directly by tearing of the periosteum during acute displacement, forcible reduction, or intraarticular surgery [131]. Intraarticular tamponade by traumatic effusion associated with acute displacement could theoretically cause loss of blood supply indirectly, although this mechanism has not been substantiated [131]. Multiple pins in the superior posterior quadrant of the femoral head may pose a risk of injury to the intraepiphyseal blood supply producing segmental AVN [131]. In SCFE, the affected epiphysis first fails to become osteopenic because the absence of blood supply prevents normal resorption of bone from disuse [131]. This abnormality in SCFE is evident as early as a few weeks after onset of the slip and almost all cases are evident within 1 year [131]. Resorption of necrotic bone with collapse of the affected portion of the epiphysis usually follows early radiographic changes in SCFE [131]. Two patterns of distribution are typically seen in SCFE-related AVN: total head necrosis and partial (or segmental) necrosis [131].

Type I AVN in children is characterized by severe diffuse necrosis totally involving the femoral head and the proximal fragment of the femoral neck [12]. Type I AVN results from interruption of the lateral epiphyseal and metaphyseal vessels and accounts for more than 50% of cases [12]. Type II AVN in children is characterized by more localized necrotic changes, often in the anterosuperior aspect of the femoral head, with little collapse [12]. Type II AVN is usually caused by interruption of the lateral epiphyseal vessels before entrance into the epiphysis and is seen in approximately 25% of cases [12]. Type III AVN in children is characterized by sclerosis from the fracture line of the femoral neck to the physis, with sparing of the femoral head [12]. Type III AVN accounts for 25% of cases and has the best results [12]. Assessment of preserved angles on plain radiographs is a simple method to quantify the extent of lateral and anterior necrosis of the femoral head [24].

Pediatric Pathophysiology (Legg-Calvé-Perthes Disease)

In Legg-Calvé-Perthes disease, the blood supply to the femoral head is interrupted, leading to devascularization of all or a portion of the femoral capital epiphysis with subsequent resorption of necrotic bone [131]. The condition is unlike typical Legg-Calvé-Perthes disease in that there is a single vascular insult and much less restorative capacity [131]. Studies of cartilage samples from patients with Legg-Calvé-Perthes disease showed that epiphyseal and physeal cartilage involvement is a pathologic feature of vascular disruption of the growing epiphysis [144]. A thick region of epiphyseal cartilage was found under the normal articular cartilage in the lateral portion of the femoral head and neck [144]. The fibrillar area of the epiphyseal cartilage showed increased amounts of proteoglycan, a reduction in structural glycoproteins, and collagen fibrils that differed in size from normal epiphyseal cartilage [144]. The border of the lateral physis contained profuse amounts of large lipid inclusions [144]. Investigators postulated that epiphyseal change is primary, whereas femoral head collapse and necrosis could be caused by deterioration and disarray of the matrix of the epiphyseal cartilage and subsequent abnormal ossification [144].

In a large animal model of ischemic osteonecrosis, cell death occurred in the deep layer of the epiphyseal cartilage following the induction of ischemia with subsequent degenerative changes in the cartilage matrix [144]. The viable, superficial region of the epiphyseal cartilage highly expressed hypoxia inducible factor-1, a master regulator of cell response to hypoxia [144]. Vascular endothelial growth factor (VEGF) and other proteins and cytokines such as interleukin-6 are released in response to hypoxic stress in the viable superficial region of the epiphyseal cartilage [144]. The deep layer of the epiphyseal cartilage can suffer ischemic damage at the time of epiphyseal AVN, and the viable superficial region can mount a repair response to the ischemic damage [144].

In Meyer dysplasia, radiographic changes are limited to specific segments of the femoral head, likely resulting from a minimal form of Legg-Calvé-Perthes disease where segmental patterns of blood supply dictate affected locations [78]. Bucholz-Ogden type IV avascular necrosis involves the medial head and metaphysis, producing early closure of the medial portion of the physis with resultant growth into a varus deformity [83]. Bucholz-Ogden type II avascular necrosis involves the lateral head and metaphysis, leading to caput valgus during adolescence [83]. Bucholz-Ogden type III avascular necrosis involves the whole head and metaphysis, resulting in a short femoral neck and high trochanter [83]. Kalamchi-MacEwen grade 1 avascular necrosis involves the head only with normal development [83]. Kalamchi-MacEwen grade 2 avascular necrosis involves the lateral head and metaphysis, leading to caput valgus during adolescence [83]. Kalamchi-MacEwen grade 3 avascular necrosis involves the central head and metaphysis [83]. Kalamchi-MacEwen grade 4 avascular necrosis involves the whole head, resulting in a short neck and high trochanter [83].

Closure of the lateral portion of the capital femoral growth plate during adolescence may be a manifestation of AVN, occurring in hips that have shown no early evidence of a vascular insult [148]. Progressive valgus tilting of the femoral head on the metaphysis occurs when the lateral portion of the growth plate closes early [148]. Relative overgrowth of the greater trochanter may occur if the disease has disrupted growth of the capital physis [47]. The shape of the femoral head may continue to evolve after healing, and only at the completion of skeletal growth is its permanent contour established [47]. If the disease has disrupted growth of the capital physis, gradual relative overgrowth of the greater trochanter may occur [47]. The more severe the disease, the longer the duration of each stage, particularly the reossification stage [47].

In Stulberg group V hips, there is collapse of the femoral head but the acetabular contour does not change, referred to as incongruous incongruity [20]. Stulberg group V hips are similar to those seen in adult AVN in which the central portion of the femoral head collapses without acetabular change [20]. Patients with Stulberg group III, IV, and V hips had evidence of arthritic changes at an average follow-up of 40 years [20]. Patients with Stulberg group I and II hips had a good long-term prognosis [20]. In Stulberg group IV hips, the femoral head is flattened, and the range of motion changes to match the cylindrical shape of the femoral head, resulting in an almost normal range of flexion and extension [20]. In Stulberg group IV hips, the hip rotates externally whenever the joint is flexed and resumes a neutral position with extension [20]. In Stulberg groups III and IV, the contour of the acetabulum matches that of the femoral head, referred to as congruous incongruity [20]. MRI is an accurate imaging modality for the early diagnosis of Legg-Calvé-Perthes disease and for visualizing the configuration of the femoral head and acetabulum [49]. Noncontrast MRI relies on signal changes from fat degradation in the necrotic

Classification

Reliability and Validity: The modified Ficat classification for osteonecrosis of the femoral head lacks acceptable interobserver reliability and intraobserver reproducibility, rendering it unsuitable for basing treatment protocols or determining outcomes [116]. Commonly used classification systems generally lack intraobserver and interobserver reliability and fail to fully incorporate advances in biology, biomechanics, and imaging [85]. In contrast, the 2021 Association Research Circulation Osseous (ARCO) classification is a highly reliable and valid method compared to previous systems and is recommended by ARCO as a unified classification for early-stage osteonecrosis of the femoral head [53]. By utilizing MRI, the 2021 ARCO classification serves as a reliable and valid tool for predicting the occurrence of collapse in patients with early-stage osteonecrosis of the femoral head [159]. A staging system was developed to revise the 1994 ARCO classification through an expert panel-based Delphi survey [130].

China-Japan Friendship Hospital (CJFH) Classification: The CJFH classification system is a simple and direct evaluation model for osteonecrosis of the femoral head that demonstrates substantial inter- and intraobserver reliability [163].

BRB Classification: The newly proposed BRB classification provides a systematic approach to assessing necrotic lesion severity in traumatic osteonecrosis of the femoral head and demonstrates a significant correlation with femoral head collapse risk [128].

Matrix Model: The matrix model, which combines ARCO staging, Japanese Investigation Committee (JIC) classification, and necrotic area, demonstrates strong predictive ability for femoral head collapse, with higher scores correlating to higher collapse rates [139].

Lesion Characteristics: The location of the necrotic lesion exerts a greater impact on femoral head collapse compared with the size of the lesion [41].

Stulberg Classification: The Stulberg classification categorizes the radiographic appearance of hips at skeletal maturity into five groups based on femoral head shape and acetabular fit [20]. * Group I: Completely normal femoral head shape [20]. * Group II: Spherical femoral head within 2 mm of a circle on both AP and frog-leg lateral radiographs [20]. * Group III: Ovoid femoral head that deviates from a circle by more than 2 mm [20]. * Group IV: Flattened femoral head with a flattened area greater than 1 cm in the weight-bearing area [20]. * Group V: Collapse of the femoral head without corresponding acetabular contour change [20].

Lateral Pillar Classification: The lateral pillar classification system is based on radiographic changes in the lateral portion of the femoral head during the fragmentation stage as seen on the AP view [87]. * Group A: Minimal density change in the lateral pillar with no loss of height [87]. * Group B: Lucency in the lateral segment with loss of height up to, but not exceeding, 50% of the original height [87]. * Group C: Collapse of the lateral pillar to less than half its original height [87].

This system has been reported to have greater interobserver reliability and to be a better predictor of final outcome compared with the Catterall classification system [87]. The Catterall and lateral pillar classification systems are best applied during the middle stage of fragmentation, as earlier application has been shown to lead to inaccurate assignment [87].

Pipkin Classification: The Pipkin classification describes femoral head fractures associated with posterior dislocations [18]. * Type I: Fracture line inferior to the fovea [18]. * Type II: Fracture fragment that includes the fovea [18]. * Type III: Associated femoral neck fracture [18]. * Type IV: Any pattern of femoral head fracture and an acetabular fracture [18].

Garden Classification: The Garden classification is commonly used to describe displacement in intracapsular hip fractures [18]. * Stage I: Incomplete impacted fracture, typically valgus [18]. * Stage II: Complete but undisplaced fracture [18]. * Stage III: Complete fracture with moderate displacement [18]. * Stage IV: Severely displaced fracture [18].

Clinical Presentation

Epidemiology and Demographics

Osteonecrosis of the femoral head affects approximately 10,000 to 20,000 new patients annually in the United States [3]. The estimated mean annual prevalence from 2002 to 2006 was 14,103 cases, corresponding to 28.91 cases per 100,000 persons [45]. The disease typically presents in patients in their late 30s and early 40s [3]. Etiology is linked to corticosteroid use, substance abuse, and various systemic medical conditions [3]. Approximately 10% to 20% of cases are classified as idiopathic due to the absence of a clearly identifiable risk factor [3].

Adult Symptomatology and Physical Examination

Patients with osteonecrosis of the femoral head commonly present with groin pain [12]. Some patients experience minimal pain despite significant radiographic deformity [81]. On physical examination, findings may include limited range of motion, particularly in abduction and internal rotation, and slight atrophy of the femoral muscles [82]. A reduced head–neck offset in nontraumatic osteonecrosis may act as a mechanical co-factor in disease development [37].

Pediatric Presentation: Legg-Calvé-Perthes Disease

Legg-Calvé-Perthes disease (LCPD) onset occurs between 2 and 12 years of age, with a peak incidence between 6 and 8 years [82]. The mean age at onset is 6 years, with 82% of patients between 4 and 9 years of age [82]. Boys are four times more likely to be affected than girls [82], with one source specifying a ratio of 3.7 times [82]. Bilateral disease occurs in 10% of patients [82].

Clinical Course and Staging: * Early Presentation: Children usually present with a limp, and some complain of pain in the hip, thigh, or knee [82]. Symptoms are frequently mild, causing considerable delay before medical consultation [82]. Children younger than 4 years are often asymptomatic and show no femoral head deformation [71]. * Increased Density Stage: Clinical findings include variable, often mild and intermittent limp and pain [71]. * Fragmentation Stage: Pain and limp may worsen, and range of motion may be lost [71]. * Reossification Stage: Limp and pain gradually resolve, and range of motion improves [71]. * Healed Stage: Patients may experience an occasional limp, occasional locking or popping, or develop impingement symptoms [71].

Most children experience moderate symptoms and endure 12 to 18 months of difficulty before gradual resolution and a return to normal physical activities [71]. The age at onset is the most consistently reported factor affecting disease course [71]. Patients with onset after age 12 have the worst prognosis [71]. Three patterns of femoral head necrosis are identified in late-onset cases: late-onset pattern, segmental collapse pattern, and destructive pattern [71]. The destructive pattern is characterized by severe head collapse without reossification, often resulting in severe symptoms and loss of function in late adolescence [71]. Meyer dysplasia is a variant where radiographic changes are limited to specific segments without head deformation; these heads gradually ossify and do not progress through standard stages of increased density, fragmentation, and healing [78]. A central notch in the femoral head, representing the fovea, is often mistaken for avascular change [78].

Pediatric Presentation: Post-Traumatic Avascular Necrosis

The median time to presentation for avascular necrosis (AVN) after pediatric hip fractures is 7.8 months [12]. Radiographic evidence can appear as early as 2 months post-injury and is generally present within 1 year [12]. However, AVN can develop 8 years post-injury despite no evidence at 3 years, implying a need for extended follow-up [10].

Risk Factors: * Fracture Characteristics: Fracture displacement is the most important risk factor for AVN following pediatric hip fractures [12]. The presence of a type I or II fracture is a risk factor [12]. * Patient Age: A fracture in an older child (>12 years) is a risk factor for AVN [12].

Incidence and Classification: Historically, the incidence of AVN after pediatric hip fractures was reported as 100%, 50%, 25%, and 15% for types I, II, III, and IV fractures, respectively, with an overall incidence of 43% [12]. A more recent literature review reported incidences of 38%, 28%, 18%, and 5% for types I, II, III, and IV fractures, respectively, with an overall rate of 29% [12].

Morphological Patterns: * Type I: Characterized by severe diffuse necrosis totally involving the femoral head and the proximal fragment of the femoral neck. It accounts for more than 50% of cases and has the worst prognosis [12]. * Type II: Characterized by more localized necrotic changes, often in the anterosuperior aspect of the femoral head, with little collapse. It is seen in approximately 25% of cases and has a better prognosis than type I [12]. * Type III: Characterized by sclerosis from the fracture line of the femoral neck to the physis, with sparing of the femoral head. It accounts for 25% of cases and has the best results [12].

AVN after pediatric femoral neck fractures shows a tendency toward extensive necrotic lesions, presumably resulting in rapid progression of femoral head collapse [22]. In general, AVN after hip fractures in children results in poor outcomes in up to 60% of cases [12].

Diagnostic Timing and Prognostic Factors

Most cases of osteonecrosis are diagnosed in an advanced stage, when minimally invasive surgical procedures are no longer helpful [3]. Key management recommendations require accurately staging the condition and determining when pain may be due to osteonecrosis [35]. Small, asymptomatic, medially-placed lesions may be treated with observation alone [7]. Larger lesions carry a 25% to 50% risk of progression [7].

Prognostic Indicators: * Necrosis Location: Necrosis involving the anterior aspect of the femoral head is an important risk factor for collapse [6]. * Collapse Mechanism: Collapse in nontraumatic osteonecrosis starts in the lateral column due to ischemia [29]. Preserving blood supply to the lateral column improves prognosis and delays collapse [29]. * Contralateral Involvement: Collapse progression on the symptomatic side is a poor prognostic factor for the natural history of contralateral osteonecrosis [26].

Systemic Associations: Femoral head necrosis is associated with coagulation malfunction, lipid metabolic abnormalities, and inflammation [66]. More extensive osteonecrosis may accompany steroid-associated osteonecrosis of the hip [67].

Investigations

MRI: Magnetic resonance imaging is the most sensitive test for confirming avascular necrosis and defining the extent of femoral head and neck involvement [12]. MRI demonstrated 100% accuracy in hips with histological proof of osteonecrosis and in those with medullary changes without necrotic bone [118]. In comparative studies, MRI showed higher diagnostic accuracy (97% to 99%) for early diagnosis than radiography (88% to 93%) or scintigraphy (88% to 91%) [49]. Gadolinium-enhanced subtraction MRI is more effective than noncontrast MRI in delineating epiphyseal necrosis early in the disease process [49]. In the initial stage of Legg-Calvé-Perthes disease, contrast-enhanced MRI provides clearer depiction of head involvement and higher interobserver agreement regarding the extent of involvement compared to non-contrast MRI [49]. Quantitative assessment of femoral head perfusion using perfusion MRI at the initial or early fragmentation stage predicts lateral pillar involvement and radiographic outcome at 2-year follow-up [49]. Diffusion and contrast-enhanced MRI in early Legg-Calvé-Perthes disease predict the risk of later femoral head deformity, with increased apparent diffusion coefficient in the metaphysis and decreased significant enhancement in the central epiphysis serving as significant prognostic indicators [49]. Perfusion MRI also provides quantitative information about hip synovitis by depicting synovial membrane hyperemia and thickening [49]. Subtraction MRI allows recognition of early reperfusion patterns, and contrast-enhanced MRI better delineates revascularization patterns in the femoral head than scintigraphy [49]. Biplanar MRI is as effective as arthrography in evaluating femoral head sphericity and containment [49]. Although MRI is essential for detecting pre-radiographic stage osteonecrosis of the femoral head (ONFH), less than half of these cases progress to stage 2 or higher [142]. Accurate evaluation of the posterior boundary of the necrotic lesion using the oblique axial plane is necessary for predicting prognosis and considering indications for anterior rotational osteotomy [70]. Volumetric measurements should be universally included in the assessment of patients with osteonecrosis of the femoral head [154].

Plain radiography: Standard anteroposterior and lateral radiographs are obtained at initial presentation and at three to six month intervals [61]. Radiographs are staged using the modified criteria of Ficat [61]. Radiographic evidence of avascular necrosis can appear as early as 2 months after injury and is generally present within 1 year [12]. The median time to presentation of symptoms is 7.8 months [12]. Radiographs may demonstrate osteopenia of the femoral head, followed later by sclerosis, fragmentation, and often collapse and deformity [12]. Hips with ONFH had a higher risk of disease progression with far more anterior necrotic lesions (type III) in the FL radiographs [147]. In the healed stage of Legg-Calvé-Perthes disease, no additional changes are noted in the density of the femoral head, but the shape may continue to evolve until the completion of skeletal growth [47]. After healing, the shape of the femoral head may vary from completely normal to extremely flat and aspherical [47].

CT: CT scan should be obtained to evaluate for loose bodies after reduction of a hip dislocation because it is more sensitive than plain radiographs [57]. CT scan was 87% sensitive for detecting intra-articular fragments [57]. In a series of 117 patients with simple dislocations, 12 patients (10%) had loose bodies present [57]. CT scan is more sensitive in detecting small intra-articular fragments, femoral head fractures, femoral head impaction injuries, acetabular fractures, and joint incongruity [122]. A difference as small as 0.5 mm in the distance from the anterior articular surface to the femoral head has been reported to indicate a subluxation of the hip [122].

Bone scan: Radioisotope scanning shows decreased uptake in the femoral head or neck (or both) and is useful in a hip that has stainless steel internal fixation [12]. SPECT/CT was useful in evaluating the perfusion status of the femoral head, showing high accuracy in predicting the occurrence of avascular necrosis [143]. Bone scintigraphy performed within three weeks after the operation can predict a satisfactory outcome of rotation of the femoral head, whereas conventional radiographs were not associated with the final result [168]. Studies evaluating single photon emission computed tomography and MRI following hip dislocation were unable to correlate findings with the risk for osteonecrosis [57].

Other Considerations: Positron emission tomography/computed tomography (PET/CT) at 6 weeks could detect recovery of vascularity and could predict the risk of vascular necrosis [102]. Dynamic MRI–positive enhancement integral color mapping (PEICM) preoperatively estimated femoral head perfusion by classifying it as normal, decreased, or completely absent [102]. The nonunion rate was zero in the normal perfusion group, 6.7% in the reduced perfusion group, and 50% in the absent perfusion group when using dynamic MRI-PEICM [102]. The Stulberg classification system classifies the radiographic appearance of hips at skeletal maturity into five groups based on femoral head shape and acetabular fit [20]. In Stulberg group I hips, the shape of the femoral head is completely normal [20]. In Stulberg group II hips, a spherical femoral head is present, but coxa magna, short neck, or steep acetabulum may also be present [20]. In Stulberg group III hips, the femoral head is more elliptical and deviates from a circle by more than 2 mm [20]. In Stulberg group IV hips, the femoral head is flattened, with a flattened area greater than 1 cm in the weight-bearing area [20]. In Stulberg group V hips, there is collapse of the femoral head but the acetabular contour does not change [20]. The Stulberg classification system was found to correlate with the development of arthritic changes in the hip joints at an average follow-up of 40 years [20]. Patients with Stulberg group I and II hips had a good long-term prognosis, whereas those with group III, IV, and V had evidence of arthritic changes [20]. The study demonstrates varying levels of reliability and diagnostic precision among different classification systems for femoral head avascular necrosis [32]. Collapse of the femoral head in nontraumatic osteonecrosis starts in the lateral column due to ischemia; preserving blood supply to the lateral column improves prognosis and delays collapse [29]. Small, asymptomatic, medially-placed lesions may be treated with observation alone while larger lesions have a 25% to 50% risk of progression [7]. AVN after pediatric femoral neck fracture showed a tendency toward extensive necrotic lesions, presumably resulting in a rapid progression of femoral head collapse [22]. Avascular necrosis of the femoral head is relatively uncommon in type 1 dislocations reduced within 6 hours, but symptomatic AVN can develop 8 years post-injury despite no evidence at 3 years [10]. Early MRI screening 3 months after renal transplantation is desirable to enable joint-preserving operations with a chance of success [152].

Treatment

General Principles and Prognosis

Osteonecrosis of the femoral head is the most important cause of total hip arthroplasty in young populations [5]. Effective management of nontraumatic osteonecrosis requires accurately staging the condition and determining when pain may be attributable to osteonecrosis [35].

Non-Operative

Small, asymptomatic, medially-placed lesions of the femoral head may be treated with observation alone [7]. Larger lesions carry a 25% to 50% risk of progression [7]. In children with Gaucher disease and osteonecrosis of the femoral head, symptomatic management with bed rest and analgesics followed by non-weight-bearing on the involved limb during the symptomatic stage is recommended, as no known treatment effectively prevents femoral head deformity [137]. For children with avascular necrosis following hip fractures, treatment should begin at the onset of symptoms and entail partial weight bearing or non-weight bearing until painful symptoms resolve [12].

Operative

Indications: Core decompression augmented with autologous bone marrow aspiration concentrate is recommended for early stages of avascular necrosis of the femoral head (Ficat stages 0 through II) [4]. Vascularized pedicle bone-grafting is sometimes indicated for avascular necrosis of the femoral head in an early stage before collapse [138]. Management of Ficat stage III and IV osteonecrosis of the hip remains controversial; the choice of option depends on patient age, the cause of osteonecrosis, the extent of femoral head involvement, and the condition of the acetabular articular cartilage [75]. Femoral head-preserving surgery is not recommended for patients with type 3 osteonecrosis of the femoral head [64].

Surgical Approach / Technique: Core decompression with multiple small-size holes is an effective method for treating early-stage avascular necrosis of the femoral head, particularly in those with pathological changes in the hip joint [141]. The success of arthroscopic core decompression depends on the amount of necrotic tissue remaining in the femoral head after the procedure [125]. Mid-term outcomes of arthroscopic-assisted core decompression for precollapse osteonecrosis of the femoral head have been reported with a minimum of 5-year follow-up [58]. A nomogram can divide precollapse nontraumatic osteonecrosis of the femoral head patients into prognosis groups following core decompression [51]. Combining core decompression with biotechnology could result in a novel long-lasting hip-preserving treatment option, provided therapeutic principles are correctly mastered and methods are oriented to different stages [21]. The combination of bone marrow-derived cell therapy with core decompression may be better for pain relief, function, and survival of joints for osteonecrosis of the femoral head than core decompression alone, though evidence remains limited and heterogeneous [111]. Implantation of autologous bone-marrow mononuclear cells appears to be a safe and effective treatment for early stages of osteonecrosis of the femoral head [121]. Drilling decompression with autologous bone marrow and allogeneic bone grafting is safe and effective for treating HIV-positive patients with early osteonecrosis of the femoral head and can effectively delay or postpone total hip replacement [123]. Treatment by cell transplantation and replacement could improve the armamentarium for osteonecrosis of the femoral head, particularly in the pre-collapse stage [132].

Implant Selection: Impaction bone allograft and fibular grafting for osteonecrosis of the femoral head have reported favourable medium-term results [19]. A vascularized pedicle iliac bone graft to treat avascular necrosis of the femoral head is considered promising for joint preservation [136]. Unilateral free vascularized fibula is effective for the treatment of bilateral osteonecrosis of the femoral head [140]. Patients with preoperative stage V osteonecrosis or corticosteroid use had worse outcomes after vascularized fibular grafting if they had a previous core decompression of the femoral head [145].

Other Considerations: The long-term effect of core decompression in the treatment of steroid-induced femoral head osteonecrosis is not satisfactory [48]. The prognosis of the femoral head did not improve significantly in the long term when core decompression was combined with β-tri-calcium phosphate grafts and platelet-rich plasma [39].

Arthroplasty: Studies of total joint arthroplasty, once femoral head collapse is present, have described excellent outcomes at greater than ten years of follow-up [11]. Total hip arthroplasty was a safe, effective treatment for young patients with osteonecrosis of the femoral head, with demonstrated efficacy over 120 months [55]. Cementless total hip arthroplasty in patients with osteonecrosis of the femoral head has satisfactory midterm clinical and radiographic outcomes, but the long-term effect should be further studied [46]. The results of hemiresurfacing and total resurfacing arthroplasty have been suboptimal, and these procedures have restricted indications in patients with osteonecrosis of the femoral head [11].

Pediatric and Specific Populations: In children with avascular necrosis following hip fractures, treatment has been relatively unsuccessful, and some investigators have suggested that treatment does not affect the natural history [12]. Operative treatment options for this population include intertrochanteric osteotomy (usually valgus) to place the viable head in the weight-bearing zone, capsulotomy, and arthrodesis [12]. In children with avascular necrosis following slipped capital femoral epiphysis, an intertrochanteric osteotomy may be performed to reposition the limb in a more functional arc of motion and to prevent impingement if the hip is in a poor functional position [81]. Vascularized fibular intertrochanteric osteotomy (VFITO) provides a good outcome at medium-term follow-up in adolescent patients with partial avascular necrosis of the femoral head after slipped capital femoral epiphysis [43]. For children with Legg-Calvé-Perthes disease, the best management in the early stages (stage 1 and 2) remains controversial because the results of treatment are less clear [172]. Multiple epiphyseal drilling or core decompression is considered for those with onset after the eleventh birthday if the head has not collapsed [172]. Trochanteric epiphysiodesis should be performed when major avascular necrosis is recognized and the ossific nucleus of the greater trochanter is present, and is most effective if performed when the child is approximately 5 years old [83]. Trochanteric advancement may be considered when an objectionable abductor limp results from trochanteric overgrowth, specifically when the greater trochanter has reached the level of the top of the femoral head, there is a congruous and concentric reduction of the hip, a Trendelenburg sign can be elicited, and the child is older than 8 years [83].

Complications

Natural History and Progression

Osteonecrosis of the femoral head is a progressive disease that typically leads to collapse of the femoral head and eventual deterioration of the hip joint [42]. Large defects in the necrotic area do not heal spontaneously [79]. More than one-third of patients with symptomatic osteonecrosis of the femoral head experienced accelerated collapse within 1 year [56]. Larger lesions carry a 25% to 50% risk of progression [7].

Post-Traumatic Complications

Avascular necrosis (AVN) of the femoral head is the most common and most devastating complication associated with hip fractures in children [12]. Fracture displacement is the most important risk factor for AVN in pediatric hip fractures [12]. The presence of a type I or II fracture is a risk factor for AVN in pediatric hip fractures [12]. A fracture in an older child (>12 years) is a risk factor for AVN in pediatric hip fractures [12].

The historical incidence of AVN for types I, II, III, and IV pediatric hip fractures was reported as 100%, 50%, 25%, and 15%, respectively, with an overall incidence of 43% [12]. A more recent literature review reported the incidence of AVN for types I, II, III, and IV pediatric hip fractures as 38%, 28%, 18%, and 5%, respectively, with an overall rate of 29% [12]. Type I AVN accounts for more than 50% of cases and has the worst prognosis [12]. Type II AVN is seen in approximately 25% of cases and has a better prognosis than type I AVN [12]. Type III AVN accounts for 25% of cases of AVN and has the best results [12]. AVN after hip fractures in children results in poor outcomes in up to 60% of cases [12].

Radiographic evidence of AVN after pediatric hip injury can be seen as early as 2 months after injury and is generally present within 1 year of injury [12]. The median time to presentation of AVN symptoms after pediatric hip injury is 7.8 months [12]. Complications following a femoral head fracture include osteonecrosis in approximately 20% of cases [18]. Symptomatic AVN can develop 8 years post-injury despite no evidence at 3 years, implying a need for extended follow-up [10].

Osteonecrosis of the femoral head, particularly involving the lateral head-neck junction, is a major risk factor for spontaneous femoral neck fracture [174]. Pathological fractures of the bilateral femoral neck can be caused by femoral head necrosis [40]. Avascular necrosis of the femoral head can develop after intramedullary fixation of a femoral fracture in an adolescent [44]. Two cases of post-traumatic avascular necrosis of the femoral head without obvious dislocation or fracture of the head or neck have been described [25].

Surgical and Treatment-Related Complications

Despite subjective success in 90% of patients without failure, femoral osteotomy and iliac graft vascularization could not restore normal hip anatomy, and arthritis progressed with time [69]. Structural bone-grafting failure may occur if risk factors persist or if the graft does not extend completely into the lesion [92]. The prognosis of the femoral head did not improve significantly in the long term with core decompression with β-tri-calcium phosphate grafts in combination with platelet-rich plasma [39].

Salvage total hip arthroplasty following failed internal fixation of intracapsular fractures is associated with a significantly higher overall complication rate than primary total hip arthroplasty [77]. Salvage total hip arthroplasty following failed internal fixation is associated with a significantly higher rate of dislocation, infection, and periprosthetic fracture than primary total hip arthroplasty [77]. Avascular necrosis was more common in the sliding hip screw group than in the cancellous screws group (9% vs. 5%) for low-energy hip fractures [77]. Open reduction of intracapsular fractures was associated with a 3.9% wound infection rate compared to 0.49% in the closed reduction group [77].

Systemic and Associated Conditions

Patients with nontraumatic osteonecrosis of the femoral head had a higher incidence and risk of major adverse cardiovascular and cerebrovascular events than the general population, with a greater than 1.3-fold risk [30]. Patients in the advanced stage of osteonecrosis must undergo total hip replacement at a young age, which carries a poor long-term prognosis [3].

Recovery

Prognosis and Natural History: Most cases of osteonecrosis are diagnosed in an advanced stage of disease, when minimally invasive surgical procedures are no longer helpful [3]. Patients in the advanced stage of the disease must undergo total hip replacement at a young age, which carries a poor long-term prognosis [3]. Nearly 80% of patients with osteonecrosis of the femoral head presented with late-stage disease, indicating a narrow window of opportunity for hip preservation surgery before femoral head collapse [14]. Preserving blood supply to the lateral column improves prognosis and delays collapse in nontraumatic osteonecrosis [29]. Acetabular coverage was not as strong an associated factor in the natural history of osteonecrosis as expected [56]. Collapse of the femoral head and the contralateral condition of osteonecrosis strongly affect patients' activities of daily life [162]. Avascular necrosis after pediatric femoral neck fracture showed a tendency toward extensive necrotic lesions, presumably resulting in a rapid progression of femoral head collapse [22].

Joint-Preserving Procedures: Joint-preserving procedures are indicated in the treatment of precollapse disease, with several studies showing successful outcomes at mid-term and long-term follow-up [11]. Platelet-rich plasma use after core decompression provides significant pain relief, better midterm functional outcome, retards progression, and enhances survivorship free from reoperation for hip arthroplasty and femoral head collapse in early stages of avascular necrosis compared to core decompression alone [89]. In patients with precollapse osteonecrosis of the femoral head, core decompression combined with allograft-bone threaded cage or mineralized collagen threaded scaffold demonstrated comparable long-term survivorship and functional outcomes [177]. The efficacy of core decompression combined with allograft-bone threaded cage or mineralized collagen threaded scaffold diminished in advanced stages of osteonecrosis [177]. Structural bone-grafting is effective for early atraumatic avascular necrosis, though failure may occur if risk factors persist or if the graft does not extend completely into the lesion [92]. Eighteen of 21 hips (86%) were clinically successful at latest followup with nonvascularized bone grafting for osteonecrosis of the femoral head [93]. The study reports favourable medium-term results of impaction bone allograft and fibular grafting for osteonecrosis of the femoral head [19]. VFITO provides a good outcome at medium-term follow-up in adolescent patients with partial avascular necrosis of the femoral head after slipped capital femoral epiphysis [43]. Valgus intertrochanteric osteotomy can improve the long-term function of the hip joint in adolescents with avascular necrosis of the femoral head after a femoral neck fracture, but cannot restore completely the original shape and structure of the femoral head [155]. Hormonal osteonecrosis of the femur, extent of necrosis, type C1 and type C2 in the Japanese Society for the Study of Femoral Osteonecrosis staging, and distance of the tip of the tantalum rod from the center of necrosis are risk factors for postoperative femoral head collapse in patients with Ficat I, II, and III stages of aseptic necrosis [90]. A nomogram could divide precollapse nontraumatic osteonecrosis of the femoral head patients into prognosis groups and performed well in internal validation for predicting collapse-free survival after core decompression [51].

Total Hip Arthroplasty: Reports since 1993 have suggested improved survivorship of total hip arthroplasty reconstructions for the treatment of osteonecrosis of the hip [176].

Pediatric and Specific Populations: In children less than one year old, premanipulation traction of twenty-one days or more substantially reduces the incidence of avascular necrosis [204]. Cases submitted to early reduction and internal fixation for femoral neck fractures had a reduced incidence in severity of avascular necrosis compared with those in whom operation was delayed [200].

Key Evidence

• [L4] The prognosis of patients with osteonecrosis of the femoral head can be significantly improved with early diagnosis and timely intervention. [2] (10.1302/2058-5241.4.180073)
• [L5] [3] (10.5435/00124635-199907000-00005)
• [Paper] The authors recommend this procedure for early stages of avascular necrosis (Ficat stages 0 through II) of the femoral head. [4] (10.1016/j.eats.2016.02.009)
• [L5] Osteonecrosis of the femoral head is a disabling pathology affecting a young population and is the most important cause of total hip arthroplasty in this group. [5] (10.1302/2058-5241.4.180036)
• [L3] Necrosis involving the anterior aspect of the femoral head is an important risk factor for collapse. [6] (10.1186/s12891-023-06890-0)
• [L2] The review provides an up-to-date, evidence-based guide to the management, both non-operative and operative, of non-traumatic osteonecrosis of the femoral head, emphasizing that small, asymptomatic, medially-placed lesions may be treated with observation alone while larger lesions have a 25% to 50% risk of progression. [7] (10.1302/0301-620x.99b10.bjj-2017-0233.r2)
• [L5] Avascular necrosis of the femoral head is relatively uncommon in type 1 dislocations reduced within 6 hours, but this case demonstrates symptomatic AVN developing 8 years post-injury despite no evidence at 3 years, implying a need for extended follow-up and reconsideration of medico-legal reporting timing. [10] (10.1016/j.injury.2006.11.004)
• [L5] [11] (10.2106/jbjs.o.00071)
• [L4] It may be the treatment of choice particularly in stages I–II nontraumatic osteonecrosis of the femoral head. [13] (10.1007/s00402-009-0939-0)
• [L3] Nearly 80% of the patients presented with late-stage ONFH, indicating a narrow window of opportunity for hip preservation surgery before femoral head collapse. [14] (10.1016/j.arth.2020.04.092)
• [L4] Arthroscopic management of avascular necrosis of the femoral head is viable and has significant advantages. [15] (10.1007/s00167-011-1587-9)
• [Paper] The management of pediatric ONFH is complicated by a limited body of evidence and a lack of consensus on prevention or treatment of femoral head collapse. [16] (10.2106/jbjs.rvw.25.00046)
• [L3] The study reports favourable medium-term results of impaction bone allograft and fibular grafting for osteonecrosis of the femoral head. [19] (10.1302/0301-620x.102b7.bjj-2019-1101.r2)
• [L2] Combining core decompression with biotechnology could result in a novel long-lasting hip-preserving treatment option, but only by correctly mastering therapeutic principles and adopting proper methods specifically oriented to different stages can the best therapeutic effect be achieved. [21] (10.1302/2058-5241.2.150006)
• [L4] AVN after PFNF showed a tendency toward extensive necrotic lesions, presumably resulting in a rapid progression of femoral head collapse. [22] (10.1186/s13018-020-02037-2)
• [L4] Joint-preserving procedures should be attempted in early-stage lesions to save the femoral head, while outcomes of total hip arthroplasty in the setting of osteonecrosis are excellent. [23] (10.2106/jbjs.19.01271)
• [L3] Assessment of preserved angles on plain radiographs is a simple method to quantify the extent of lateral and anterior necrosis of the femoral head. [24] (10.2106/jbjs.20.00507)
• [L4] Two cases of post-traumatic avascular necrosis of the femoral head without obvious dislocation or fracture of the head or neck are described. [25] (10.1016/s0020-1383(70)80004-3)
• [L3] Collapse progression on the symptomatic side is a poor prognostic factor for the natural history of contralateral osteonecrosis of the femoral head. [26] (10.1016/j.arth.2021.08.005)
• [L5] The care of adults with osteonecrosis of the femoral head varies among American orthopaedic surgeons specializing in hip and knee surgery. [27] (10.2106/jbjs.f.00302)
• [L4] Patients with postcollapse, predegenerative osteonecrosis of the femoral head appear to benefit from free vascularized fibular grafting, with good overall survival of the joint and significant improvement in the Harris hip score. [28] (10.2106/00004623-200306000-00001)
• [L4] Collapse of the femoral head in nontraumatic osteonecrosis starts in the lateral column due to ischemia; preserving blood supply to the lateral column improves prognosis and delays collapse. [29] (10.2106/jbjs.20.00490)
• [L2] Patients with nontraumatic osteonecrosis of the femoral head had a higher incidence and risk of major adverse cardiovascular and cerebrovascular events than the general population, with a greater than 1.3-fold risk. [30] (10.1007/s11999.0000000000000161)
• [L3] A previous joint-preserving procedure for osteonecrosis of the femoral head poses technical challenges for subsequent total hip reconstruction and might have a detrimental effect on the short-term clinical outcome. [31] (10.1016/j.arth.2007.05.026)
• [L3] The study demonstrates varying levels of reliability and diagnostic precision among different classification systems for femoral head avascular necrosis. [32] (10.1186/s12891-025-08398-1)
• [L1] Key recommendations of these guidelines require accurately staging ONFH and determining when pain may be due to ONFH. [35] (10.2106/jbjs.25.01616)
• [L4] Small osteonecrosis (less than 300 degrees of the femoral head) without preoperative collapse (Steinberg's stages I and II) is the major indication for free vascularized fibular grafting. [36] (10.1186/1471-2474-8-78)
• [L3] A reduced head–neck offset in patients with nontraumatic osteonecrosis of the femoral head may act as a mechanical (co-)factor in developing osteonecrosis of the femoral head. [37] (10.1007/s00402-013-1771-0)
• [L3] However, the prognosis of the femoral head did not improve significantly in the long term. [39] (10.1186/s12891-022-06120-z)
• [Case_report] This is the first report of pathological fractures of the bilateral femoral neck caused by femoral head necrosis, conforming to the histological characteristics of rapidly destructive hip disease. [40] (10.1186/s12891-023-06992-9)
• [L5] The location of the necrotic lesion exerts a greater impact on femoral head collapse compared with the size of the lesion. [41] (10.1186/s13018-025-05453-4)
• [L4] VFITO provides a good outcome at medium-term follow-up in adolescent patients with partial avascular necrosis of the femoral head after slipped capital femoral epiphysis. [43] (10.1007/s00402-010-1161-9)
• [Case_report] The report documents the danger of developing avascular necrosis of the femoral head after intramedullary fixation of a femoral fracture in an adolescent. [44] (10.2106/00004623-199411000-00014)
• [L3] The estimated mean annual prevalence of osteonecrosis of the femoral head from 2002 to 2006 was 14,103 cases, corresponding to 28.91 cases per 100,000 persons. [45] (10.1016/j.arth.2009.05.022)
• [L3] Cementless total hip arthroplasty in patients with osteonecrosis of the femoral head has satisfactory midterm clinical and radiographic outcomes, but the long-term effect should be further studied. [46] (10.1016/j.arth.2006.12.098)
• [L5] Thus, the long-term effect of core decompression in the treatment of steroid-induced femoral head osteonecrosis is not satisfactory. [48] (10.1186/1471-2474-13-142)
• [L3] The nomogram could divide precollapse nontraumatic osteonecrosis of the femoral head patients into prognosis groups and performed well in internal validation. [51] (10.1186/s13018-021-02664-3)
• [L3] The novel 2021 ARCO classification is a highly reliable and valid method compared to previous classifications and is recommended by ARCO as a unified classification for early-stage osteonecrosis of the femoral head. [53] (10.1016/j.arth.2022.02.009)
• [L3] THA was a safe, effective treatment for young ONFH patients, with demonstrated efficacy over 120 months. [55] (10.1016/j.arth.2025.05.106)
• [L5] More than one-third of patients with symptomatic osteonecrosis of the femoral head experienced accelerated collapse within 1 year, and acetabular coverage was not as strong an associated factor in the natural history of the disease as expected. [56] (10.1097/corr.0000000000002501)
• [L4] [58] (10.1186/s12891-019-2853-0)
• [L3] [61] (10.2106/00004623-198971050-00003)
• [L4] We do not recommend femoral head-preserving surgery for patients with type 3 ONFH. [64] (10.1186/s12891-023-06587-4)
• [Paper] Femoral head necrosis following renal transplantation and extension of the necrotic area into the femoral neck are contraindications for TPP. [65] (10.1007/s00402-002-0422-7)
• [L4] Femoral head necrosis is associated with a range of variables including coagulation malfunction, lipid metabolic abnormalities, and inflammation. [66] (10.1186/s13018-023-04235-0)
• [L4] More extensive osteonecrosis may accompany steroid-associated osteonecrosis of the hip. [67] (10.2106/00004623-200411000-00017)
• [L3] Despite subjective success in 90% of patients without failure, the surgery could not restore normal hip anatomy, and arthritis progressed with time. [69] (10.1097/01.blo.0000071756.07450.76)
• [L3] Accurate evaluation of the posterior boundary of the necrotic lesion using the oblique axial plane is necessary for predicting the prognosis of the femoral head and considering indications for anterior rotational osteotomy. [70] (10.2106/jbjs.20.00493)
• [L4] The results of CVO for idiopathic osteonecrosis of the femoral head were successful if the procedure was indicated for cases with an intact load-bearing area of more than 40%. [73] (10.1007/s00402-013-1919-y)
• [L5] Management of Ficat stage III and IV osteonecrosis of the hip remains controversial; the choice of option depends on patient age, the cause of osteonecrosis, the extent of femoral head involvement, and the condition of the acetabular articular cartilage. [75] (10.5435/00124635-200403000-00005)
• [L4] [79] (10.5435/00124635-199801000-00005)
• [L1] One in five patients require conversion to arthroplasty after non-vascularized bone grafts in patients with osteonecrosis of the femoral head. [80] (10.1186/s13018-023-03544-8)
• [L5] There remains plenty of room for improvement in the classification of ONFH, as commonly used classification systems lack intraobserver and interobserver reliability and do not fully incorporate advances in biology, biomechanics, and imaging. [85] (10.1097/01.blo.0000533640.75452.45)
• [L1] PRP use after CD provides significant pain relief, better midterm functional outcome, retards the progression, and enhances the survivorship free from reoperation for hip arthroplasty and femoral head collapse in early stages of avascular necrosis of hip than CD alone. [89] (10.1016/j.arth.2020.07.010)
• [L3] Hormonal osteonecrosis of the femur, extent of necrosis, type C1 and type C2 in the Japanese Society for the Study of Femoral Osteonecrosis staging, and distance of the tip of the tantalum rod from the center of necrosis are risk factors for postoperative femoral head collapse in patients with Ficat I, II, and III stages of aseptic necrosis of the femoral head. [90] (10.5435/jaaos-d-22-00198)
• [L4] The procedure is effective for early atraumatic avascular necrosis, though failure may occur if risk factors persist or if the graft does not extend completely into the lesion. [92] (10.2106/00004623-199173090-00011)
• [L4] Eighteen of 21 hips (86%) were clinically successful at latest followup. [93] (10.1097/01.blo.0000096826.67494.38)
• [L1] The combination of bone marrow-derived cell therapy with core decompression may be better for pain relief, function, and survival of joints for osteonecrosis of the femoral head than core decompression alone but remains limited and heterogeneous. [111] (10.1002/arj.70449)
• [L4] The modified Ficat classification for osteonecrosis of the femoral head does not have acceptable interobserver reliability and intraobserver reproducibility on which to base treatment protocols and determinations of outcome. [116] (10.2106/00004623-199611000-00010)
• [L3] Magnetic resonance imaging was accurate in all hips with histological proof of osteonecrosis and in those with medullary changes without necrotic bone. [118] (10.2106/00004623-198971050-00002)
• [L2] Implantation of autologous bone-marrow mononuclear cells appears to be a safe and effective treatment for early stages of osteonecrosis of the femoral head. [121] (10.2106/jbjs.d.02662)
• [L3] This method is safe and effective for treating HIV-positive patients with early osteonecrosis of the femoral head and can effectively delay or postpone total hip replacement. [123] (10.1186/s12891-023-07039-9)
• [L3] The success of ACD depends on the amount of necrotic tissue remaining in the femoral head after the procedure. [125] (10.1007/s00402-015-2287-6)
• [L3] The newly proposed BRB classification provides a systematic approach to assessing necrotic lesion severity in TONFH and demonstrates significant correlation with femoral head collapse risk. [128] (10.1016/j.arth.2025.06.030)
• [L5] A staging system has been developed to revise the 1994 ARCO classification for ONFH by an expert panel-based Delphi survey. [130] (10.1016/j.arth.2019.11.029)
• [L4] The treatment by cell transplantation and replacement could improve the armamentarium for osteonecrosis of the femoral head (ONFH), particularly in the pre-collapse stage. [132] (10.1007/s00264-010-1009-5)
• [L4] A vascularized pedicle iliac bone graft to treat avascular necrosis of the femoral head is considered promising for joint preservation. [136] (10.1007/s004020100263)
• [L4] The authors recommend symptomatic management with bed rest and analgesics followed by non-weight-bearing on the involved limb during the symptomatic stage of bone crisis, as no known treatment effectively prevents femoral head deformity. [137] (10.2106/00004623-199601000-00003)
• [L4] Vascularized PBG is sometimes indicated for ANFH in an early stage before collapse of the femoral head. [138] (10.1007/bf00390047)
• [L3] The matrix model, which combines ARCO staging, JIC classification, and necrotic area, demonstrated strong predictive ability for femoral head collapse, with higher scores correlating to higher collapse rates. [139] (10.1186/s13018-024-04587-1)
• [L4] Unilateral free vascularized fibula is effective for the treatment of bilateral osteonecrosis of the femoral head. [140] (10.1016/j.arth.2012.09.002)
• [L4] The core decompression with multiple small-size holes is an effective method for treating early-stage avascular necrosis of the femoral head, particularly in those with pathological changes in the hip joint. [141] (10.1186/s42836-023-00181-8)
• [L3] Although MRI is essential for detecting pre-radiographic stage ONFH, less than half of preradiographic ONFH cases progress to stage 2 or higher. [142] (10.1016/j.arth.2025.05.089)
• [L2] SPECT/CT was useful in evaluating the perfusion status of the femoral head, showing high accuracy in predicting the occurrence of avascular necrosis. [143] (10.1186/s12891-020-03538-1)
• [L3] However, patients with preoperative stage V osteonecrosis or corticosteroid use had worse outcomes after vascularized fibular grafting if they had a previous core decompression of the femoral head. [145] (10.1016/j.arth.2006.12.042)
• [L4] Hips with ONFH had higher risk of disease progression with far more anterior necrotic lesions (type III) in the FL radiographs. [147] (10.1002/jor.24825)
• [L3] Early MRI screening 3 months after renal transplantation is desirable to enable joint-preserving operations with a chance of success, as core decompression appears to be the therapy of choice during early stages of femoral head necrosis in these patients. [152] (10.1007/bf00426064)
• [L4] Volumetric measurements should be universally included in the assessment of patients with osteonecrosis of the femoral head. [154] (10.1016/j.arth.2019.05.039)
• [L4] VITO can improve the long-term function of the hip joint in adolescents with ANFH after a femoral neck fracture, but cannot restore completely the original shape and structure of the femoral head. [155] (10.1186/s12891-023-06598-1)
• [L4] [157] (10.3389/fgene.2022.1037190)
• [L3] The 2021 ARCO classification system, by using MRI, is a reliable and valid tool for predicting the occurrence of collapse in patients who have early-stage ONFH. [159] (10.1016/j.arth.2025.05.071)
• [Paper] Collapse of the femoral head and the contralateral condition of ONFH strongly affect patients' activities of daily life. [162] (10.1007/s00264-018-3867-1)
• [L4] The CJFH classification system is a simple and direct evaluation model for ONFH with substantial inter- and intraobserver reliability. [163] (10.2106/jbjs.20.00051)
• [L3] Bone scintigraphy performed within three weeks after the operation can predict a satisfactory outcome of rotation of the femoral head, whereas conventional radiographs were not associated with the final result. [168] (10.2106/00004623-200010000-00008)
• [L3] Osteonecrosis of the femoral head, particularly involving the lateral head-neck junction, was confirmed as a major risk factor for spontaneous femoral neck fracture. [174] (10.1186/s12891-023-07058-6)
• [L3] Previously, THA was believed to have poor survivorship and clinical results for the treatment of osteonecrosis of the hip, but reports since 1993 have suggested improved survivorship of these reconstructions. [176] (10.1007/s11999-013-3220-3)
• [L3] In patients with precollapse ONFH, CD combined with ATC or MCTS demonstrated comparable long-term survivorship and functional outcomes, though both their efficacy diminished in advanced stages. [177] (10.1016/j.arth.2025.05.003)
• [L5] [178] (10.1016/j.eats.2024.103233)
• [L5] Osteoarthritis in hips with osteonecrosis can be caused by elevated contact stress. [184] (10.1097/01.blo.0000203472.88926.c8)
• [L2] This study shows that those cases which were submitted to early reduction and internal fixation had a reduced incidence in severity of avascular necrosis compared with those in whom operation was delayed. [200] (10.1016/0020-1383(85)90162-7)
• [L4] In children less than one year old, premanipulation traction of twenty-one days or more substantially reduces the incidence of avascular necrosis. [204] (10.2106/00004623-197759030-00002)

See Also

• Total hip replacement

References

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