At birth, bone is relatively less dense, less lamellar, and has increased porosity relative to a mature bone¹,²,³. With increasing age, adaptive changes occur that result in progressive formation of lamellar and osteon bone within the diaphysis compared to the spongy, trabecular bone of the metaphysis and epiphysis. Immature bone has a lower elastic modulus than mature bone. It bends to a greater extent when stressed and absorbs more energy before it breaks. These differences in architecture result in different healing patterns with buckle fractures in the softer spongy bone of the metaphysis and greenstick fractures and plastic deformation in the diaphysis of the long bones (Figure 2.1A-C).

One of the most distinguishing differences between the bones of a child and an adult is the presence of a thick and robust periosteum. This layer is strong but is easily lifted by hematoma or purulence and is less likely to rupture than in adults. This thick bridge adds stability to fractures, is instrumental in the remodeling and correction of longitudinal deformities (Figure 2.2A-C), and also accounts for the rapidity with which infant and toddler fractures heal relative to their adult counterparts (Figure 2.3). While periosteum is an important aid in fracture remodeling, it can also be a block to reduction. For instance, it can often be found in the fracture site on the tension side of a displaced epiphysis (eg, distal tibia) or through an apophyseal injury (tibial tubercle avulsion).

Growing bone is constantly changing due to the endochondral ossification process (Figure 2.4). The chondro-osseous epiphyses are variably radiolucent, especially in the very young, and can be difficult to interpret on plain radiographs. Similarly, the physis (growth plate) is constantly changing in appearance making interpretation of radiographs more challenging. Physeal injuries often need to be inferred on the basis of sound clinical judgment coupled with an accurate physical examination, rather than on the radiographic appearance. In cases where fractures are suspected, a contralateral radiograph can allow one to distinguish between subtle injury and normal developing bone. Of course, once periosteal new bone has appeared 10 days after the injury, the diagnosis can be confirmed in retrospect (Figure 2.5).

Normal infants can have joint contractures as a result of intrauterine positioning that will eventually stretch out. For instance, infants have 70° to 80° of passive and active hip external rotation, and this progressively resolves as they become ambulatory. It is well known that toddlers and young children are very flexible and with time, the joints become stiffer. Increased ligamentous laxity can be associated with hereditary diseases of connective tissue such as Ehlers-Danlos, Marfan, and Down syndromes. Nonsyndromic ligamentous laxity is often familial and is seen in 10% to 15% (this likely factors into many common conditions such as hip dysplasia, recurrent patellar subluxation, and flexible flat feet). Generalized ligamentous laxity can be established clinically based on the thumb-to-forearm distance, hyper extensibility of the long fingers, and hyper extensibility of the elbow and knee joints⁴ (Table 2.1; Figure 2.6).

The most distinct structural difference between young and mature bone is the presence of the physis or growth plate. The anatomy and function of the various layers and components of this structure are well defined (Figure 2.7). The zone of hypertrophy is where chondrocytes are undergoing enlargement

and programmed cell death (apoptosis). This region is very susceptible to shear forces and represents the weakest and most vulnerable area of the growth plate. Although deriving some mechanical protection from the perichondrial ring of Lacroix, the weakness of the hypertrophic zone is associated with, or affected by, many common childhood conditions as noted below.

Slipped capital epiphysis of the proximal femur likely represents an admixture of pubertal hormonal imbalance which may widen the growth plate and, coupled with increased shear forces, can overload the hypertrophic zone leading to gradual or abrupt slipping of the femoral head (Figure 2.8). In rickets, due to defective mineralization, the hypertrophic zone becomes disorganized and expanded (Figure 2.9). Skeletal dysplasias also affect this zone, leading to progressive deformity (Figure 2.10).

Another major difference in the growing skeleton is the presence of the apophysis, which is basically a growth plate under tension from the insertion of large tendons. These growth plates do not lengthen the bone much, yet can be a location of acute injury or chronic irritation. In adults, a rapid increase in tension at a tendon can lead to rupture while overuse can lead to painful mid-substance tendonitis. In children, similar acute stress on the strong tendon will lead to failure through the apophysis as opposed to adult tendon rupture. Chronic overuse can lead to clinical inflammation and pain at the insertion of the tendon and not along the tendon itself as seen in adults. With chronic apophysitis, radiographs will show fragmentation and irregular bone at the insertion site. Osgood-Schlatter disease of the tibial tubercle is an example of abnormal bone development due to repetitive traction through strong ligaments (Figure 2.11).

In acute trauma, it is important to remember that the tendon and ligaments are stronger than the bone and the growth plate. Suspicion of these growing conditions should direct the examination to bone rather than the ligaments. Many “ankle sprains,” “medial collateral ligament strains,” and other injuries in growing children are actually Salter-Harris type 1 fractures and not sprains at all. This can easily be differentiated on examination by accurately localizing the area of maximal tenderness to the bone and not the ligament.