Nonossifying fibromas are very common benign, eccentric, cortically based lesions with an incidence as high as 40 % in boys and 20 % in girls. Most are asymptomatic. They belong to a continuum with fibrous cortical defects and are differentiated by size (fibrous cortical defects are smaller, less than 2 cm). These cortical lucencies are found close to the physis in younger children but appear to move toward the diaphysis with progressive bone growth (Fig. 13.7). Epiphyseal involvement has not been reported. They are not usually encountered before 18 months, peak at 5 or 6 years of age, and are rarely evident in adults. Lesions are commonly on the dorsal and medial aspect of the bone and may be bilateral. The vast majority occur in the lower extremity, and 82 % occur around the knee. They may be found simultaneously in the femur, tibia, and fibula.

These benign lesions probably originate at sites of tendinous or ligamentous insertion into the physeal perichondrium [3]. The traction force can be estimated by drawing a line toward the joint, along the long axis of the lucency. A defect in the dorsal medial femur thus results from traction by the adductor magnus muscle or medial gastrocnemius head; a defect in the dorsal medial tibia is due to pull from the semimembranosus muscle.

With longitudinal growth, the lesions appear to migrate away from the joint. Although initially ovoid and only faintly demarcated, they often become polycystic, with well-defined sclerotic margins and slight expansion of their thin cortical rim. During maturation the central lucency fills with sclerotic bone, beginning at the diaphyseal end. Once sclerosis is complete, the defect remodels to normal bone and usually disappears.

Radiographs are usually sufficient for diagnosis. Additional imaging should be performed only if the lesion is painful (in the absence of fracture). MRI shows lesions are initially low to intermediate on T1-weighted (T1-W) sequences and may initially demonstrate increased signal on T2-weighted (T2-W) images. As they involute, they become hypointense on all sequences (Fig. 13.8) [4]. The central tissue shows mild enhancement after gadolinium administration [3].

Stress fractures have been reported in association with nonossifying fibromas and fibrous cortical defects [5] (Figs. 13.9 and 13.10). Fractures are more likely with larger lesions that occupy more than half of the bone width, extending into the marrow cavity (Fig. 13.11).

Differential diagnoses include fibrous dysplasia, eosinophilic granuloma, and simple bone cysts. However, radiographic evaluation should show that benign cortical lesions are limited to the cortex, excluding these other diagnoses. In some cases, it may be difficult to completely exclude potentially intracortical lesions such as Brodie abscess or periosteal chondroma. Multiple nonossifying fibromas/fibrous cortical defects occur in neurofibromatosis and Jaffe-Campanacci syndrome [6]. (See Chap. 21 for further discussion.)

A hyperintense band of tissue is common along the subperiostium at the posterior aspect of the distal femoral metaphysis as well as along the posterior aspect of the proximal tibial metaphysis. This band, composed of loose fibrovascular connective tissue, is more prominent on the femur than on the tibia. It is seen only in skeletally immature patients and on proton density (PD), T2-W, and inversion recovery (IR) sequences (Fig. 13.12); it is not evident on T1-W images. The tissue probably contributes to dynamic bone modeling that accompanies skeletal growth [7].

Cortical desmoids occur at the posteromedial metaphysis of the distal femur, at the insertion site of the medial head of the gastrocnemius muscle. This cortical roughening is common between ages 10 and 15, occurring in about 11 % of boys and 3 % of girls [8]. The lesion is benign, self-limited, and usually asymptomatic, although there may be associated pain [9].

Etiology is uncertain. The lesion may represent a remodeling response to chronic or acute traction injury. It has also been theorized to result from chronic tension at the attachment of the medial head of the gastrocnemius or the adductor magnus aponeurosis, leading to the term “tug lesion.” Very rapid growth may contribute as well. Subperiosteal connective tissue and osteoclasts within a cortical erosion have been identified at the attachment of the adductor magnus muscle [10]. Lesion shape may differ depending on the orientation of mechanical traction [9].

At MRI, these lesions appear as T1-hypointense and T2-hyperintense cortical scalloping, with a dark rim of bony sclerosis along the attachment of the medial head of the gastrocnemius muscle (Fig. 13.16) [9]. If there has been acute trauma, marrow and intratendinous edema may be evident.

Although the appearance may resemble periosteal reaction with bony erosion, cortical desmoids should not be mistaken for a malignant or inflammatory process. If a pathological process is suspected, nuclear scintigraphy will not necessarily help differentiate, especially if the appearance is caused by a minor avulsion that might also generate increased radiotracer uptake. MRI may help confirm the benign nature of this lesion. Cortical desmoids are differentiated from nonossifying fibromas/fibrous cortical defects because the latter appear to migrate as the patient grows and also erode the cortex from within the bone, whereas cortical desmoids do not change position and do disrupt the outer surface [4].

The tibial tuberosity forms from an anteroinferior cartilaginous extension of the tibial epiphysis. Before ossification of the tuberosity begins, it can appear as a large, abruptly scalloped defect, which can be smooth or show mild undulation (Fig. 13.17). It may mimic an erosive lesion or a buckle fracture (Fig. 13.18) [11]. Ossification begins as a distal extension of the primary epiphysis. However, a separate center occasionally develops and grows concentrically, eventually uniting with the more proximal portion of the epiphysis. The tuberosity fuses with the adjacent bone by age 15 in girls and age 19 in boys.

In most cases, the developing center is either multicentric or irregular. Lack of soft tissue swelling and clinical complaints help differentiate it from an avulsion fracture or Osgood-Schlatter disease (Fig. 13.19).

Growth recovery lines appear as discrete horizontal lines of sclerosis parallel to the growth plate, developing after temporary growth cessation. They are quite common in both femoral and tibial metaphyses and are often present simultaneously at multiple metaphyses that significantly contribute to bone growth. They usually extend in a continuous line across the metaphysis and gradually remodel, apparently moving toward the diaphysis with continued growth (Fig. 13.20). While it seems logical that growth arrest lines would occur more often in children with frequent severe illnesses, in fact they are also common in healthy children or in those who have suffered the usual minor childhood illnesses. Persistence into early adulthood indicates a previous vigorous recovery response rather than chronic illness. Focal deformity of a growth arrest line can provide important information about adjacent growth arrest following physeal injury, before development of bony bridging or angular deformity.

The fabella is an ovoid, occasionally multipartite, sesamoid bone in the lateral gastrocnemius muscle belly (the tendinous portion of this muscle is distal) (Figs. 13.21 and 13.22). It is found in about 12 % of the population and is bilateral in more than half [12]. Although the fabella is almost always of no clinical significance, teens occasionally complain of pain with full extension as well as local tenderness, and this may be relieved by excision of the fabella [13].

The anterior surface of the bony patella has many vascular foramina and vertical striations. These appear on radiographs as lucencies or thin anterior fissures (Fig. 13.23) and on MRI as channels that parallel the long axis of the patella, generally with high signal on T2-W images (Fig. 13.24). The posterior surface of the patella has two facets, separated by a median ridge (Fig. 13.25). At birth the lateral facet is already larger than the medial, and it ultimately becomes 40 % longer. The lateral facet is less steeply angled. The angle between the two facets averages 130°. The upper two-thirds of the posterior surface is covered with articular cartilage (Fig. 13.26), and—as the thickest cartilage in the mature body—it may be up to 5 mm deep in the adult.

The shape of the patella, the shape of the femoral condyles posterior to the patella, and the configuration of the proximal tibia affect the likelihood of developing patellar derangement. The patella lies in a sulcus that is a superior extension of the intercondylar notch. The sulcus is formed by the anterior contours of adjacent portions of the medial and lateral femoral condyles. The lateral surface of the sulcus projects more anteriorly than does the medial, restricting lateral patellar subluxation. (The force vectors of the quadriceps muscles apply both a major component of longitudinal force on the patella and a smaller component of lateral force: this lateral force may contribute to patellar subluxation.) Thus, the lateral facet of the femoral trochlea plays an important role in helping to stabilize the patellofemoral articulation. A shallow sulcus, as seen in children with longitudinal deficiency of the fibula, can contribute to instability.

Another important factor in evaluating patellar stability is alignment of the patella with respect to the tibial tuberosity. This can be assessed in several ways. The Q angle is calculated on MRI from the midline of the quadriceps as it inserts into the patella to the patellar tendon as it aligns with the tibial tuberosity. Alternatively, the tibial tuberosity to trochlear groove (TT-TG) distance measures the space between the midpoint of the tibial tuberosity and the deepest part of the trochlear groove (described in detail in section below on developmental patellar instability and dislocation).

The suprapatellar pouch is usually an extension of the knee joint and very rarely a bursa that does not communicate with the joint. There is a small amount of fat anterior to this pouch, posterior and superior to the patella, and a larger amount of fat posterior to it, anterior to the femur. On a lateral knee radiograph, the pouch appears as soft tissue density outlined by fat. A joint effusion is present if the soft tissue between these two fat pads exceeds 10 mm in thickness (Fig. 13.27). If this distance is between 5 and 10 mm and the margins of the recess are fuzzy, an effusion is suggested.

The patella serves many functions: it decreases friction from the quadriceps around the femoral trochlea, transmits the vectors of the quadriceps system into one patellar tendon, protects against dislocation of the tendon from within the sulcus, and shields knee cartilage from injury.

Ossification variants are common. The ossified patella may be granular or nodular; it may have zones of sclerosis and lucency. Anterior lucencies as well as transverse and vertical anterior surface ridges are particularly common. Vertical fissures (larger than the thin branching fissures discussed above (see Figs. 13.23 and 13.24)) are most common (Fig. 13.28). Most variants are isolated, but they may mimic findings in multiple epiphyseal dysplasia or be confused with a patellar sleeve fracture.

A bipartite patella is the most common variation in patellar ossification, estimated to occur in 1–6 % of the population, and is slightly more likely to be unilateral than bilateral. The patella may form from multiple ossification centers, and if they fail to fuse a bi- (or tri-) partite patella results. The extra center is usually superolateral (Fig. 13.29), but in 20 % it is lateral and in 5 % at the lower pole (Fig. 13.30). There may be pain and increased mobility at the cartilaginous interspace adjacent to an accessory center.

It is possible that some bipartite patellae result from stress fracture rather than developmental variation [14]. In addition, several pathological entities mimic the inferior accessory center at the lower pole. It may be confused with a traumatic patellar sleeve fracture (Figs. 13.31 and 13.32) a hyperflexion injury involving both cartilage and bone. If this fracture affects an incompletely ossified patella, it may be subtle, involving only the cartilaginous portion of the lower pole. In the setting of fracture, the patella is often high riding, with a small fragment avulsed from the inferior pole. Radiography underestimates the extent of cartilaginous involvement, and MRI is often necessary [15].

Another differential consideration is Sinding-Larsen-Johansson disease. This is most common in children between the ages of 10 and 14 and presents with restricted knee motion as well as localized tenderness and soft tissue swelling over the lower patella. As with Osgood-Schlatter avulsion, this is neither a “disease,” osteochondritis, inflammation, nor avascular necrosis but is almost certainly traumatic. Radiographic findings of Sinding-Larsen-Johansson include an accessory ossification center or avulsed fragments at the lower border of the patella, with associated soft tissue swelling (Fig. 13.33). The appearance on both radiographs and MRI is essentially indistinguishable from patellar sleeve fracture, and differentiation relies on clinical history and examination.

Cerebral palsy is also associated with avulsion fractures of the lower pole of the patella, resembling an inferior patellar ossification center. There may be one or several fragments, separated from or adjacent to the patella. In spastic ambulatory children with cerebral palsy and flexion contractures, the patella may be high, elongated, and crescent shaped (see Chap. 24). The appearance probably reflects recurrent mechanical overload of the knee extensor mechanism with healed, subclinical avulsion fractures or ligamentous micro-tears. Ultrasound (US) can demonstrate patellar tendon thickening and local edema, probably due to contusion over (or avulsion of) an accessory center, a fracture-avulsion of the lower patella, or simply contusion of the patellar ligament with ligamentous ossification.