Hip vessel examination provides key information on many hip-related pediatric diseases, and it has an important role in the evaluation of femoral head (FH) blood supply and diagnosis of avascular necrosis (AVN). The aim of this study was to investigate the feasibility of MR-enhanced high-resolution three-dimensional water-selective cartilage (3D-WATSc) sequence in visualizing the vessels of the hip joint in children.

Children with hip disease were randomly enrolled prospectively at our hospital from January 2021 to August 2022. We performed our institution's hip MRI protocol and enhanced high-resolution 3D-WATSc sequence. The 3D-WATSc images were reconstructed and analyzed, and images of the normal hip were categorized into grades 0-3. The abnormal hip images were compared with those of the normal side using the χ2 test.

Twenty-four patients with unilateral hip abnormalities were included in this study. The cartilaginous vascular canal and ossification centre vessels of normal FHs were observed in 18 patients (75%) and met the grade 3 standard. An abnormal cartilaginous canal was observed in 16 patients (67%); meanwhile, 18 patients (75%) had abnormal extrachondral vessels. Comparison of high-resolution 3D-WATSc images with those of the normal side provided effective abnormal vascular information in 95.8% of patients.

Enhanced high-resolution 3D-WATSc can visualize the blood vessels of the hip in children. This may provide a new method for the vascular study of various pediatric hip diseases.

Legg-Calvé-Perthes disease is a self-limiting disorder that develops in children following interruption of the blood supply to the capital femoral epiphysis. This review outlines the current knowledge on the epidemiology, natural evolution, clinical spectrum, and management of the disease.

The literature pertaining to these aspects of the disease were studied and summarized in this review.

Epidemiological studies suggest that environmental factors contribute to the causation of the disease. Incidence rates monitored over time indicate that the incidence of Legg-Calvé-Perthes disease is declining. The natural evolution followed on sequential plain radiographs enables division of the disease into Stages Ia, Ib, IIa, IIb, IIIa, IIIb, and IV. Reversible deformation of the capital occurs in Stages Ia-IIa simply on standing while irreversible deformation may occur in Stages IIb and IIIa. Treatment of Legg-Calvé-Perthes disease in Stages Ia-IIa aims to prevent the femoral head from getting deformed by containment and avoidance of weight-bearing. In Stages IIb and IIIa, treatment aims to remedy the effects of early irreversible deformation of the femoral head. In Stage IIIb and IV, treatment is directed to correcting the altered shape of the femoral head. The impression that these treatment methods are helpful is based on poor quality evidence.

There is an urgent need to undertake Level I studies to establish the efficacy of currently treatment.

level V.

The cause of Legg-Calvé-Perthes disease (LCPD) remains unknown. We propose a new hypothesis that the iliopsoas muscle and/or tendon affects the progression of ischemic necrosis of the femoral head as an anatomical factor. The purpose of this study was to test this hypothesis by measuring the psoas major tendon angle (PMTA) and cross-sectional area (CSA) of the iliopsoas muscle on MRI. We selected three predetermined axial MRI scans at the level of the psoas major tendon origin, the femoral head, and the lesser trochanter. We calculated the proximal, distal, and combined PMTA and compared these angles between the LCPD group and the transient synovitis (TS) group as a control. Our results revealed that the proximal PMTAs of the LCPD-affected sides were significantly greater than in the TS controls (P < 0.05), while there were no significant differences in the proximal PMTA, combined PMTA, and CSA. This result indicates that the psoas major tendon of the patient with LCPD curves sharply on the anterior capsule of the hip joint more than in the control group patients. This sudden curve of the psoas major tendon may be involved in the development of LCPD. We measured PMTAs in patients with LCPD. Our findings suggested that the running curve of the psoas major tendon is an anatomical factor that influences the development of mechanically-induced ischemia in LCPD.

The etiology and underlying pathogenic mechanisms of Legg-Calve-Perthes disease (LCPD) still remain unclear. A disruption of blood supply to the femoral head, producing ischemic necrosis, appears to be the critical pathological event. The lncRNAs play crucial roles in many biological processes and are dysregulated in various human diseases. However, its expression profiles and the potential regulatory roles in the development of LCPD have not been investigated.

In this study, differentially expressed lncRNA and mRNA of Legg-Calve-Perthes disease patients were profiled. Several GO terms and pathways that play important roles in the regulation of vascular structure, function or coagulation were selected for further analysis. The lncRNA -mRNA interacting networks in LCPD tissues were constructed to identify novel potential targets for further investigation.

The microarray analysis revealed that 149 lncRNAs and 37 mRNAs were up-regulated, and 64 lncRNAs and 250 mRNAs were down-regulated in LCPD tissues. After filtering, we finally found 14 mRNAs and constructed an mRNA-lncRNA interacting network. Through the analysis of the interaction network, we finally found 13 differentially expressed lncRNAs, which may be implicated in the pathogenesis of LCPD. These mRNAs/lncRNAs were further validated with qRT-PCR.

The findings of this study established a co-expression network of disease-related lncRNAs and mRNAs which screened out from the concerned G.O. terms and Pathways, which may provide new sights for future studies on molecular mechanisms of LCPD.

The etiology of Legg-Calvé-Perthes disease (LCPD) remains unknown; however, interruption of medial circumflex femoral artery (MCFA) supply to the femoral head is the key pathogenic factor. The main purpose of this study is to determine the feasibility of using magnetic resonance angiography (MRA) to evaluate the course of the MCFA in the normal and affected hips of patients with unilateral LCPD.

We analyzed 24 patients with unilateral LCPD using a time-resolved imaging of contrast kinetics magnetic resonance angiography (TRICKS-MRA). The course of the MCFA was divided into 4 segments in the coronal plane and in 3 segments in the axial plane, based on its location with respect to the femoral neck. The visibility of each segment was studied in the normal and affected sides. The segments were defined as not visible when no contrast was seen within the vessel lumen or visible when the lumen was partially or completely visualized with contrast. The statistical analysis was done using the χ2 test.

TRICKS-MRA provided well-defined images of the first 2 segments of the MCFA on both the normal and affected sides of patients with LCPD (P=1). In half of the patients, the third segment was also visible using TRICKS-MRA on both sides (P=1). The fourth segment of the MCFA, which was the ascending lateral epiphyseal segment, was not visible on either side (P=0.49). No significant difference was found between the normal and affected hips in terms of visibility of the 4 segments of the MCFA using TRICKS-MRA. Anastomosis of the MCFA with the inferior gluteal artery was found in 3 hips (2 hips with LCPD and 1 normal hip).

TRICKS-MRA provides well-defined images of the arterial supply to the proximal femoral epiphysis in children with LCPD, presenting a noninvasive and radiation-free alternative to conventional angiography. However, the TRICKS-MRA method used did not allow visualization of the ascending lateral epiphyseal segment of MCFA in the affected and the contralateral normal side. We believe that further advancement of this noninvasive imaging technique may open new opportunities for research aimed at evaluating the vascular supply of the femoral head in children.

Level IV-case-control study.

Legg-Calvé-Perthes disease is a childhood hip condition in which the blood supply to the capital femoral epiphysis is interrupted, causing osteonecrosis and chondronecrosis that lead to progressive deformity of the femoral head and secondary degenerative osteoarthritis in later life. The etiology of Legg-Calvé-Perthes disease remains unclear, with both biological and mechanical factors playing important roles in the pathogenesis of the condition. The treatment of Legg-Calvé-Perthes disease remains controversial but is dependent on several salient factors, including the age at clinical onset, the extent of epiphyseal involvement, the stage of the disease, and the degree of femoral head deformity. The literature supports operative containment treatment in the early stage of disease. Such treatment has led to improved femoral head sphericity with better patient outcomes in multicenter prospective cohort studies. The number of hips that need to be treated operatively in order to achieve a modest treatment effect remains high. Multicenter prospective cohort studies have shown that 6 to 7 patients need to be managed to create 1 spherical femoral head that would not have otherwise occurred.

Legg-Calvé-Perthes' (Perthes') disease is a developmental disease of the hip joint that may result in numerous short and long term problems. The etiology of the disease remains largely unknown, but the mechanism is believed to be vascular and/or biomechanical in nature. There are several anatomical characteristics that tend to be prevalent in children with Perthes' disease, namely: skeletal immaturity, reduced height, and rostral sparing. We present an overview of the literature, summarizing the current understanding of the pathogenesis, particularly related to how the formation of the vasculature to the femoral epiphysis places children aged 5-8 at a higher risk for Perthes' disease, how skeletal immaturity and rostral sparing could increase the probability of developing Perthes' disease, and how animal models have aided our understanding of the disease. In doing so, we also explore why Perthes' disease is correlated to latitude, with populations at higher latitudes having higher incidence rates than populations closer to the Equator. Finally, we present five hypotheses detailing how Perthes' disease could have a biomechanical cause. Clin. Anat. 29:759-772, 2016. © 2016 Wiley Periodicals, Inc.

Current radiographic prognosticators of the outcome of Perthes disease can only be applied after femoral head deformity has occurred. Quantification of femoral head perfusion using the gadolinium-enhanced subtraction magnetic resonance imaging (MRI) technique may serve as an early prognosticator of outcome. The purposes of this study were 2-fold: (1) to develop a reliable method to quantify femoral head perfusion using this MRI technique; and (2) to determine whether the perfusion at early stages of Perthes disease correlates with radiographic deformity after a 2-year follow-up.

A total of 20 patients meeting the following inclusion criteria were studied: radiographs and MRI obtained of femoral heads predeformity, age between 5 and 13 years, and unilateral disease. MR perfusion index, a measure of perfusion in the epiphysis, was obtained using digital image analysis of subtraction gadolinium-enhanced MRI. Intraobserver and interobserver agreement of this index was assessed by 2 independent observers. MR perfusion index was correlated with a radiographic deformity index (a measure of femoral head deformity) obtained after a minimum of 2 years.

The intraobserver agreement assessed by the intraclass correlation coefficient was 0.96 for observer 1 and 0.97 for observer 2. The interobserver agreement of the MR perfusion index was 0.90 for trials 1 and 2. MR perfusion index in the early stages of Perthes disease was highly variable, ranging from 0 to 0.70. After a minimum of 2 years following MRI acquisition, radiographs were obtained and evaluated using the deformity index, a continuous measure of femoral head deformity, by 2 blinded observers. Deformity index at 2-year follow-up showed moderate correlation with predeformity MR perfusion index (r=-0.56, P=0.01, R=0.31). In those patients who were treated nonoperatively, the correlation was stronger (r=-0.79, P=0.006, R=0.63).

MR perfusion index obtained from gadolinium-enhanced subtraction MR images showed a high interobserver agreement. MR perfusion index is highly variable at early stages of Perthes disease, and a lower MR perfusion index correlated with greater radiographic deformity at the 2-year follow-up. This pilot study shows the promise of predeformity MR perfusion index as a possible early prognosticator of outcome in Perthes disease.

Prognostic level II.

The evidence supporting continued use of shelf acetabuloplasty in Legg-Calvé-Perthes disease (LCPD) is not well-defined, and there is controversy regarding the long-term benefits related to clinical and functional improvement.

Our goals were to determine whether shelf arthroplasty for LCPD (1) prevents the onset of early osteoarthritis; (2) improves pain, ROM, activity, and functional outcomes; (3) maintains or improves femoral head containment, sphericity, and congruency; (4) changes the acetabular index; and (5) is associated with a low rate of complications.

We performed a systematic review of the medical literature from 1966 to 2009 using the search terms Perthes, shelf procedure, and acetabuloplasty. We excluded reports using multiple/combined treatment methods and those not clearly stratifying outcomes. Thirteen studies met the criteria. There were no Level I studies, one Level II prognostic study, five Level III therapeutic studies, and seven Level IV studies. Mean followup ranged from 2.6 to 17.9 years.

Only one study reported progression to early osteoarthritis in one patient. We found no evidence for improvement in ROM and continued pain relief at long-term followup. Mean decrease in lateral subluxation ratio was 13% to 30%, demonstrating an improvement in femoral head containment. Mean acetabular cover percentage improved 16% to 38%, and mean acetabular and center-edge angles improved 4° to 14° and 8° to 33°, respectively. There were no reports of any major complications after the procedure.

While radiographic measurements indicate improved coverage of the femoral head after shelf acetabuloplasty for LCPD, available evidence does not document the procedure prevents early onset of osteoarthritis or improves long-term function.

Legg-Calvé-Perthes disease consists of idiopathic osteonecrosis of the femoral head, causing proximal femoral growth deformity. Recent advances in surgical technique have permitted safe surgical dislocation of the hip, allowing for correction of femoracetabular impingement. The purpose of this study was to characterize the location and number of lateral epiphyseal arteries supplying the femoral head in children with healed Legg-Calvé-Perthes disease.

This retrospective study included nineteen children (twenty-two hips) with a diagnosis of Legg-Calvé-Perthes disease (the LCPD group) and a matched control group of seventeen children (twenty hips) with developmental hip dysplasia. All patients underwent high-resolution contrast-enhanced magnetic resonance imaging (MRI) to visualize the path of the medial femoral circumflex artery and the lateral epiphyseal artery branches supplying the femoral head.

All patients in the LCPD group were classified as having Waldenström grade-4 disease. Their average age at the time of MRI was fifteen years (range, eleven to eighteen years). The lateral epiphyseal arteries reliably inserted on the posterior-superior aspect of the femoral neck from a superior-anterior to a superior-posterior position in both groups. An average of 2.63 (standard deviation [SD], 1.47) retinacular vessels were visualized in the LCPD group, compared with 5.20 (SD, 1.06) retinacular vessels in the dysplasia group (p &lt; 0.0001).

The lateral epiphyseal arteries of the femoral head reliably insert in a narrow anatomic window on the femoral neck. Reperfusion of the medial femoral circumflex artery does occur in patients with Legg-Calvé-Perthes disease; however, the overall number of vessels is decreased as compared with that in patients with developmental hip dysplasia.

Legg-Calvé-Perthes disease is a juvenile form of idiopathic osteonecrosis of the femoral head that can lead to permanent femoral head deformity and premature osteoarthritis. According to two recent multicenter, prospective cohort studies, current nonoperative and operative treatments have modest success rates of producing a good outcome with a spherical femoral head in older children with Legg-Calvé-Perthes disease. Experimental studies have revealed that the immature femoral head is mechanically weakened following ischemic necrosis. Increased bone resorption and delayed new bone formation, in combination with continued mechanical loading of the hip, contribute to the pathogenesis of the femoral head deformity. Biological treatment strategies to improve the healing process by decreasing bone resorption and stimulating bone formation appear promising in nonhuman preclinical studies.

Since the original reports of Legg-Calvé-Perthes disease (LCPD), much research effort has been undertaken to improve understanding of this idiopathic hip disorder. This article focuses on the current knowledge of the pathophysiology, classifications, and natural history of LCPD. Although the cause of LCPD remains largely unknown, some insight has been gained on its pathophysiology through experimental studies using animal models of ischemic necrosis. The few available clinical studies on the natural history of LCPD suggest that femoral head deformity is well tolerated in short and intermediate terms, but 50% of patients develop disabling arthritis in the sixth decade of life.

We hypothesized that patients with Legg-Calvé-Perthes disease (LCPD) might have higher risks of cardiovascular and blood diseases.

A total of 3141 patients, 2 to 15 years of age, with LCPD diagnosed between 1965 and 2005 were identified with the Swedish Inpatient Register. A total of 15 595 individuals without LCPD were selected randomly from among the Swedish general population, with matching according to year of birth, age, gender, and region of residence. Cox proportional-hazard regression analyses, with adjustment for socioeconomic index, were used to estimate relative risks. The patients also were compared with their same-gender siblings.

Patients with LCPD had a hazard ratio (HR) of 1.70 (95% confidence interval [CI]: 1.39-2.09) for cardiovascular diseases, compared with individuals without LCPD. The point estimate was slightly higher among subjects >30 years of age at the follow-up (HR: 2.10 [95% CI: 1.52-2.91]). There were statistically significantly higher risks for blood diseases, including anemias and coagulation defects (HR: 1.41 [95% CI: 1.07-1.86]), which were more pronounced among subjects >30 years of age at the follow-up (HR: 2.70 [95% CI: 1.50-4.84]). Patients also had statistically significantly higher risks of hypertensive disease (HR: 2.97 [95% CI: 1.87-4.72]) and nutritional anemia (HR: 2.92 [95% CI: 1.58-5.40]). Analyses using siblings as the comparison group showed consistent results for cardiovascular diseases.

The results are consistent with the hypothesis that an insufficient blood supply to the femoral head, attributable to vascular pathologic conditions, is involved in the pathogenesis of LCPD.

The precise pathogenetic basis of Legg-Calve-Perthes disease (LCPD) is currently unknown. Hemostatic abnormalities, i.e., hypercoagulability and/or hypofibrinolysis, were proposed in the genesis of the LCPD. Deficiency of tissue factor pathway inhibitor (TFPI), a critical natural anticoagulant molecule, may lead to a prothrombotic state in a wide variety of conditions. The aim of this study is to assess the circulating TFPI pool in the LCPD. Group I consisted of 44 patients with LCPD and group II comprised 38 healthy children. Median (IQR) TPFI concentration was significantly higher in the group I (p < .0001). Enhanced TFPI response could be regarded as a compensatory defense mechanism against ongoing local microvascular events of occlusion and revascularization of LCPD. TFPI molecule may be an important link between the crossroads of the LCPD genesis and pathogenetic microvascular changes in the disease course. Further investigations are needed to shed light on the endothelial anticoagulant kinetics, the unique microvascular compromise, and the self-limiting nature of the disease.

Femoral head deformity is the most serious sequela of ischemic necrosis of the immature femoral head. The purpose of this study was to determine if a highly potent antiresorptive agent, ibandronate, can inhibit bone resorption during the repair of the infarcted femoral head and thus alter the repair process. We hypothesized that preservation of the trabecular framework by inhibiting osteoclastic bone resorption would minimize the development of deformity in a piglet model of ischemic necrosis. The effect of ibandronate on long-bone growth was also assessed.

Ischemic necrosis of the right femoral head was produced in twenty-four piglets by placing a ligature tightly around the femoral neck. The animals were divided into three groups according to whether they received saline solution, prophylactic treatment, or post-ischemia treatment. The contralateral, untreated femoral heads from the animals that had received saline solution served as the normal control group. At eight weeks, the femoral heads were assessed for deformity with radiography and for trabecular bone indices with histomorphometry. Also, the length of femur from the untreated side was measured on the radiographs and compared among the groups.

Radiographic assessment showed that the epiphyseal quotient, determined by dividing the maximum height of the osseous epiphysis by the maximum diameter, was better preserved in the prophylactic (p < 0.001) and post-ischemia (p = 0.02) treatment groups than in the group treated with saline solution. Histomorphometric assessment also showed that the trabecular bone indices were better preserved in the prophylactic and the post-ischemia treatment groups than in the group treated with saline solution (p < 0.01). The mean femoral length on the untreated side of the animals treated with ibandronate was reduced compared with the length on the untreated side of the animals that had received saline solution (p </= 0.01).

Ibandronate preserves the trabecular structure of the osseous epiphysis and prevents femoral head deformity during the early phase of repair of ischemic necrosis in the piglet model.

We evaluated the Doppler sonography of small feeding arteries to the femoral head in children.

In a prospective study of 224 hips in 112 patients (mean age, 5 years 11 months), the anterior ascending cervical arteries of the hip were identified with color Doppler sonography. Subsequently, we measured the resistive index (RI) with pulsed Doppler sonography.

In 61% (137/224) of hips, a Doppler signal could be obtained. In asymptomatic hips (n = 64), the mean RI was 0.58. In symptomatic hips, the definitive diagnoses and mean values of RI included transient synovitis (n = 31) and 0.92, Perthes' disease (n = 9) and 0.67, and miscellaneous (n = 5) and 0.68. In 28 symptomatic hips, no definite diagnosis could be determined and the complaints spontaneously disappeared during follow-up (mean RI, 0.57). We found no statistically significant difference in the RI of symptomatic versus asymptomatic hips, except in patients with transient synovitis (p < 0.001). In 11 hips with transient synovitis that were reexamined after 4-6 weeks, the RI returned to normal (0.57). The RI in symptomatic hips showed a positive correlation with the amount of effusion (r = 0.69, p < 0.001). In symptomatic and asymptomatic hips, we found no correlation with age (p = 0.9 and 0.1, respectively).

The deep capsular vessels of the hip joint can be evaluated on Doppler sonography in more than 60% of hips. Also, the RI is age independent and correlates with the amount of effusion.

Cylindrical biopsy specimens from the proximal femoral metaphysis were obtained in conjunction with surgery in 22 patients with Legg-Calvé-Perthes disease. The histopathological examination revealed fat necrosis, vascular proliferation, and focal fibrosis indicating previous episodes of ischemia. There was no correlation between the histopathological findings and the corresponding magnetic resonance images.

The concentrations of proteoglycan fragments and stromelysin were analyzed in joint aspirates in 19 children with Legg-Calvé-Perthes disease. We found increased levels of proteoglycan fragments and stromelysin consistent with the presence of synovitis, an important clinical and possibly also prognostic factor in these children.

39 children with Legg-Calvé-Perthes Disease (LCPD) and with a radiographically unsatisfactory development were examined with sonography regarding synovitis and with intracapsular pressure recording and aspiration performed 15 (2-36) months after the onset of symptoms. The mean anterior sonographic capsular distension was 3.0 (1.0-7.0) mm greater than that of the contralateral, asymptomatic hip. The mean intracapsular pressure was 4.5 (0-11.5) kPa with the hips in extension and neutral rotation, 9.7 (1.3-27.3) kPa with the hips in extension and inward rotation and 0.9 (-0.8-4.7) kPa in 45 degrees of flexion. We conclude that these children have synovitis as diagnosed sonographically. This synovitis is probably symptomatically and prognostically important in LCPD due to increased intracapsular pressure, with pain, a decreased range of motion and, potential joint contracture.

The onset of Legg-Calvé-Perthes (LCP) disease, avascular necrosis of the proximal femoral epiphysis, frequently is clinically undetectable for months before presentation. This traditional X-ray methods of diagnosis are insensitive for the diagnosis of early LCP as well as nonspecific for the diagnosis of advanced LCP. The X-ray may remain normal for weeks to months after the onset of LCP, and other disorders (steroid osteopathy, epiphyseal dysplasia) simulate the X-ray appearance of LCP during its later stages. Localization of bone-avid radiopharmaceuticals depends principally on bone perfusion and metabolism. Bone scintigraphy is a highly sensitive and specific means of detecting changes in bone perfusion. An understanding of the vascular anatomy of the pediatric hip and its revascularization mechanisms is essential for correlating the scintigraphic findings with the stages of healing in this disorder. Revascularization of bone can occur by recanalization of existing vessels or by neovascularization through the development of new vessels. Recanalization is a rapidly occurring process (minutes to weeks), whereas neovascularization is a prolonged process (months to years). The recanalization process has a characteristic scintigraphic pattern beginning with the visualization of a "lateral column" and is associated with a good prognosis for eventual outcome in LCP. Neovascularization also has a characteristic scintigraphic appearance ("base filling" and "mushrooming"), which is associated with a poorer prognosis because of the prolonged interval required for healing, which places the femoral head at risk for complications such as fracture, collapse, and extrusion. The scintigraphic staging classification presented here, when correlated with a modified Waldenstrom X-ray staging, readily differentiates three mechanisms of revascularization. The A (allright) track scintigraphic pattern represents the recanalization process, a process of short duration and good prognosis. The B (bad) track scintigraphic pattern represents the process of neovascularization, a process of long duration and poorer prognosis. A third process also is described in which complications of the healing process (collapse, extrusion), particularly during the reabsorptive phases of bone reconstitution when the bone is weakened, can cause conversion from track A to track B. Bone scintigraphy is useful in LCP for its ability to detect the disorder in its initial stages, thus allowing earlier treatment, and to provide prognostic information that may affect therapy.

Fourteen consecutive children with symptoms of transient synovitis of the hip were examined with sonography regarding intracapsular effusion, with scintimetry regarding blood-flow in the proximal femoral epiphysis (PFE) and with intracapsular pressure recording and aspiration. All patients had an intracapsular effusion. Intracapsular pressure was found to depend on the position of the hip. The mean pressure with hips in extension and inward rotation was 22.6 kPa (170 mm Hg) whereas in 45 degrees of flexion it was 2.3 kPa. In two cases scintimetry demonstrated reduced blood flow to the PFE; after aspiration, isotope uptake returned to normal, indicating that increased intracapsular pressure has a harmful effect on circulation to the PFE. Children with transient synovitis should be treated with the hips in 45 degrees of flexion to reduce intracapsular pressure. Forcing the hip in extension causes a risk of ischaemia of the PFE.

One hundred and thirty three children were studied (a total of 218 scintigrams) after IV injection of 100 microCi/kg 99Tc-MDP. Of 64 pathological hips (6 being bilateral), 52 were judged typically abnormal, 8 without initial radiological evidence. Of the rest, 8 were considered doubtful and 4 normal. No scan was considered typical of Perthes' disease in other hip disorders. The resulting figure of the sensitivity was 94%, for specificity 97%, for positive predictive value 97%, and for negative predictive value 95%. It is more difficult to assess the value of bone scintigraphy in the follow up of these patients. The disappearance of uptake defect in the femoral head may be a good index and occurs earlier than the normalization of the radiographs. On the other hand, the significance of the neighbouring region of increased uptake is difficult to assess although related to revascularization and reconstruction. The evolution of the disease does not seem to be correlated with the localization and the intensity of these regions in a straightforward manner.