An apophysis is an ossification center that – unlike the epiphysis – does not contribute to longitudinal bone growth; instead, it serves as an insertion site for tendons, being especially subjected to traction forces and anomalous stress. In addition, the apophyseal physes are inherently weaker and more vulnerable to traumatic lesions than the adjacent bones and tendons. These lesions may be represented by acute apophyseal avulsions at the level of the growth plate, or by chronic apophysitis, which is an inflammatory process typical of skeletally immature athletes related to excessive traction and microavulsions at the bone/cartilage interface. The latter is commonly found during growth spurts, and it may be considered a non-displaced transphyseal stress fracture (Salter-Harris type I – see Chap. 9). Patients with chronic apophysitis present insidious local pain that worsens with physical activity, as well as tenderness and soft-tissue swelling over the inflamed apophysis.

In acute avulsion fractures, radiographs show a bone fragment with incompletely corticated borders in the soft tissues adjacent to the expected apophyseal site, with no need for additional investigation, even though magnetic resonance imaging (MRI) allows for a more precise and detailed assessment (Fig. 10.1). Radiographs are often normal in patients with early-stage apophysitis, while those with chronic apophysitis often exhibit apophyseal fragmentation and enlargement, physeal widening, and periosteal reaction (Fig. 10.2), which are also well demonstrated on computed tomography (CT) (Fig. 10.3). It is important to have in mind that irregularity and fragmentation may also be found in normal apophyses as a developmental variant, which is deprived of significance if there are no clinical manifestations. On ultrasound (US), chronically inflamed apophyses usually present increased size and heterogeneous vascularity; there may be swelling of the adjacent soft tissues as well, and the tendon may appear thickened, hypervascular, and hyperechogenic. Magnetic resonance imaging (MRI) is the most sensitive and specific method for evaluation of chronic apophysitis, showing an edematous apophysis of increased size that often presents post-gadolinium enhancement; edematous changes are also found in the adjacent bone marrow, in the physis, and in the surrounding soft tissues (Figs. 10.4 and 10.5). Physeal widening may be subtle or marked, and even apophyseal avulsion is found in severe cases (Figs. 10.4, 10.6, and 10.7). Chronic apophysitis may present a misleading appearance on imaging and simulate an aggressive process, with mass effect, marked periosteal reaction and exuberant bone neoformation, in addition to significant bone marrow edema and soft-tissue swelling (Fig. 10.4). Correlation between clinical data and imaging findings is crucial in order to avoid unnecessary biopsies, as that the histopathological picture may lead to an erroneous diagnosis of sarcoma.

Several apophyses may be affected in the pelvis and in the hips, such as the iliac crest, the anterior superior and anterior inferior iliac spines, the ischial tuberosity, and the greater trochanter. Apophysitis of anterior inferior iliac spine is more prevalent in countries where soccer is more popular, resulting from excessive traction exerted by the tendon of the direct head of the rectus femoris. Apophysitis around the hip typically does not affect individuals under age 13, given that the apophyseal ossification centers usually appear between 13 and 15 years of age and fuse between 16 and 18. Inclusion of both hips in the field of view is recommended for CT and MRI coronal and axial images, as comparative analysis of the apophyses maximizes the diagnostic capabilities of these methods (Figs. 10.1, 10.2, 10.3, 10.4, 10.6, and 10.7). Old healed lesions frequently lead to deformity of the affected apophysis, which displays ­density/signal intensity similar to those of the normal bone (Fig. 10.8).

Osgood-Schlatter disease (OSD) is a traction apophysitis of the insertion of the patellar tendon in the tibial tubercle. It is more frequent in male athletes between 10 and 15 years of age, occurring bilaterally in 20–30 % of the cases. In addition to the above-mentioned classic radiographic findings (Fig. 10.9), heterotopic intratendinous ossification is also common, as well as fluid distension of the deep infrapatellar bursa (Figs. 10.5, 10.10, and 10.11). Residual bone deformity and/or persistence of an intratendinous ossicle in the distal portion of the patellar tendon can be found after healing and may cause chronic pain (Fig. 10.12).

Sinding-Larsen-Johansson disease (SLJD) is a reaction to traction at the inferior pole of the patella, more common in males between 9 and 12 years old, mainly those involved in jumping, gymnastics, and kicking sports. Strictly speaking, the inferior patellar pole is not an apophysis; nonetheless, the etiology and the inflammatory response to traction are identical to those seen in classic apophysitis. Imaging findings include bone fragmentation and inflammation in the inferior pole of the patella, occasionally associated with ossification of the proximal portion of the patellar tendon (Figs. 10.13, 10.14, and 10.15). Tendinopathy/partial tear of the patellar tendon (Fig. 10.16) and patellar fractures are the main differential diagnosis.

Sever’s disease is the inflammation of the calcaneal apophysis, adjacent to the insertion of the Achilles tendon. It is more common in males with less than 11 years of age, occurring bilaterally in up to 60 % of the patients. Pain worsens with physical activity and can be reproduced upon latero-lateral compression of the heel. As stated above, even though the classic findings of apophyseal fragmentation and sclerosis are present, the same findings may be found in normal individuals; additionally, recent works indicate that radiographs are not necessary in the workup as they have no real influence in the diagnosis or in therapeutic decision making. Similarly, bone marrow edema pattern may be found in the calcaneal apophysis of symptomatic and asymptomatic children on MRI. Therefore, there is no characteristic imaging pattern for this disease and the diagnosis is primarily a clinical one.