A unique feature of the immature skeleton is the presence of cartilaginous structures in the extremities of the long bones, namely, the epiphyseal cartilage and the physis (also referred to as primary physis, growth cartilage, or growth plate), which involute with skeletal maturation and are no longer present in the adult organism. These cartilages act together as a functional unit responsible for the longitudinal growth of the bone. On the other hand, the articular cartilage protects and nourishes the subchondral bone of the joint surfaces, and, unlike the physis and the epiphyseal cartilage, it does not ­disappear, remaining throughout the life course. Radiographs are insensitive to demonstrate these cartilages (Fig. 2.1), and computed tomography and ultrasonography are also limited in their evaluation. Because of its characteristics (see Chap. 1), magnetic resonance imaging (MRI) is the preferred imaging method for assessment of most structures of the immature bone (Fig. 2.2).

The immature epiphysis is situated between the joint ­cavity and the physis. During the early stages of development, the epiphyses are entirely cartilaginous, serving as precursors for the ossified ends of the long bones. The ­cartilaginous ­epiphysis usually display low signal intensity on T1-weighted images (T1-WI) and intermediate to high signal intensity in ­fluid-sensitive sequences. Transformation of cartilage into bone begins in the inner portion of the epiphysis, the ­so-called secondary ossification center (the primary ossification centers form the diaphyses of the tubular bones during ­intrauterine life). Ossification may occur in a single center (like in the proximal or distal femoral epiphyses – Fig. 2.3) or, less often, via multiple secondary ossification centers that later coalesce (such as in the distal humerus – Fig. 2.4). The secondary ossification center is surrounded by a specialized structure, the secondary physis, responsible for the endochondral ossification and ­structurally similar to the primary physis, appearing as a thin layer of high signal ­intensity on fluid-sensitive sequences (Figs. 2.5 and 2.6). The ossification center, which is round when it first appears, changes to a hemispheric configuration over time: it increases in size and molds to the contour of the epiphysis in which it is settled, at the same time as there is thinning of the epiphyseal cartilage (Fig. 2.7). The ­epiphyseal cartilage is ­homogeneous ­throughout the first year of life, but, as ­skeleton maturation takes place, focal areas of high signal intensity on T2-WI appear, more evident in the posterior aspect of the femoral condyles. Such areas are more common in preadolescent males and are typically not associated with abnormalities of the subchondral bone, being deprived of significance and representing the earliest stages of endochondral ossification (Figs. 2.3, 2.4, and 2.6). They are initially focal and heterogeneous, becoming more extensive and uniform with time (Fig. 2.8). As the child begins to walk, the weight-bearing portions of the epiphyseal cartilages present a decrease in their signal intensity on T2-WI, more evident in the knees and the hips, also deprived of importance (Figs. 2.6 and 2.8). Irregularity of the secondary ossification centers at the bone/cartilage junction is a normal finding, mostly seen during growth spurts (Fig. 2.9). Accessory ossification centers may also be present, usually adjoining the posterior aspect of the secondary ossification center of the distal femur, not associated with bone marrow edema or abnormalities of the overlying cartilage. The ­articular cartilage is hardly discernible on T1-WI, appearing as a thin layer of high signal intensity surrounding the immature epiphysis on T2-WI (Figs. 2.5, 2.6, 2.7, and 2.10).