# Lower Limb Osteochondrosis and Apopbysitis in Young Athletes--A Comprehensive Review
## 6 Legg-Calve-Perthes Disease: Presentation, Diagnosis, and Management  
Legg-Calve-Perthes disease (LCPD) is a pediatric orthopedic condition marked by avascular necrosis of the femoral head, which can occur unilaterally or bilaterally [78]. It primarily affects children between the ages of 3 and 12 years, with the highest incidence occurring between the ages of 5 and 7 years. The disease has a marked male predilection, with males being three to five times more likely to develop LCPD than females [79]. Figure 4 illustrates the case of a young male patient diagnosed with LCPD. The two upper images show augmented vascular flow, indicating an active inflammatory state. The two lower images reveal the presence of inflammatory changes within the joint, characterized by a thickened, hypoechoic joint capsule and a collapsed femoral head. Several risk factors have been associated with the development of LCPD, including short stature, obesity, hyperactivity, low geographic birthplace, low birth weight, and prenatal or postnatal exposure to tobacco smoke [80]. The pathogenesis of LCPD is multifactorial and is based on a combination of environmental, metabolic, and genetic factors that impair the blood supply to the femoral head and lead to avascular necrosis and bone deformation [81; 82]. In the early stages of the disease, the impaired vascular supply to the femoral head makes the subchondoral bone susceptible to mechanical stress. The subchondoral bone pertains to the bony layer situated beneath the hyaline cartilage and cement line. This diminished structural integrity predisposes the femoral head to deformation, including flattening and widening, especially under the influence of weight-bearing forces [80]. These morphologic changes may progressively worsen under loading and contribute to the characteristic deformities observed in the early phase of LCPD [80; 83]. The diagnosis of LCPD is primarily made by clinical assessment and supported by imaging modalities such as X-ray, MRI, ultrasound, bone scintigraphy, and computed tomography (CT) [84]. Patients typically present with hip pain, which may radiate into the thigh or knee, and with limited internal rotation of the affected hip or leg length discrepancy, which is a notable clinical indicator [80]. A significant proportion of patients have a history of high-impact sports, which may exacerbate the onset of symptoms [79]. Radiographic assessment, particularly in the anterior or posterior view and in the lateral frog-leg view, may not provide clear results in the early stages of LCPD due to the subtlety of the initial changes. However, as the disease progresses, characteristic radiographic features, such as flattening and fragmentation of the femoral head, become evident [84]. MRI offers a higher sensitivity for early detection and often shows joint effusions and pathologic changes of the acetabular labrum and articular cartilage even before radiologic abnormalities occur [79]. MRI is recognized to help detect the earliest changes in the femoral head associated with LCPD, especially with optimal use of a contrast agent through dynamic imaging [84]. An ultrasound examination helps further in the detection of LCPD. Careful assessment of the proximal femoral epiphysis is essential to detect inflammatory conditions. If abnormalities are suspected, a comparison with the contralateral side is recommended. This is a reasonable assumption, as illustrated in Figure 5, which depicts the characteristics of hip arthritis in the context of LCPD. In addition, the process of ischemia with subsequent bone regeneration is divided into several different stages from a radiological point of view, including the necrosis phase (initial phase), fragmentation phase, reassification phase, and final phase (healing phase), which encompass the progression of the proximal head. Figure 4: Legg–Calvé-Perthes disease on the ultrasound image. (**a**) Inflammatory changes with joint capsule vascularization on Power Doppler ultrasound. (**b**) Joint capsule thickening to 8 mm with decreased echogenicity.