Diagnosis and management of growth plate injuries in the skeletally immature patient can be challenging. Inability to visualize the injury on a radiograph and incomplete understanding of normal bone development can contribute to diminished recognition of these injuries. Proper identification is a vital first step to prevent devastating outcomes in limb form and function. The goal of this review is to provide a thorough understanding of the physis and the types of physeal injuries, the keys to radiographic interpretation, and management strategies.
GROWTH PLATE ANATOMY
The skeleton of a 10-week-old fetus is 100% cartilage.1 At birth, bone mineralization is approximately 85% of adult composition,1 but a large portion of cartilage remains to allow for growth. Growth in long bones occurs through endochondral ossification, the process by which a cartilage progenitor is converted to bone. These precursors to bone, which reside between ossification centers in the diaphysis and distal ends of long bones, ultimately comprise the epiphyseal, or growth, plate.
By the time an infant is 3 months old, the first growth plate to form (the proximal humerus) can be well-visualized on radiographs of the upper extremity.2 Each plate is seen as a discrete linear lucency between the metaphysis (toward the shaft) and the epiphysis (toward the joint). Over time, bone growth is seen radiographically to progress from the metaphysis toward the epiphysis, but cell differentiation occurs in the opposite direction. Chondrocytes travel through four distinct layers of the growth plate until they mature and push the entire physis distally to continue longitudinal growth. The four layers of differentiation include: the resting zone, the proliferative zone, the hypertrophic zone, and the provisional calcification zone (Figure 1). Most of the growth plate is avascular, but the epiphyseal vascular system penetrates the resting zone and supplies the proliferative zone.3,4
PHYSIS PHYSIOLOGY
The resting zone is epicentral to the ossific nucleus and comprises a large extracellular matrix with inert chondrocytes dispersed randomly throughout. The matrix contains an array of proteoglycans and collagen fibrils that suppress the deposition of calcium.3,4
Chondrocytes migrate from the resting zone into the proliferative zone, where the cells begin to organize and condense tightly into longitudinal columns. Accelerated replication further reduces the matrix volume, leading to deformation and flattening of the cells. Hormones, growth factors, and rich vascularization to this area help to mediate the process.3,4
As the proliferative zone advances, the cell bed left behind continues to develop and is referred to as the hypertrophic zone. Here, the environment becomes progressively more hypoxic, forcing the cells into anaerobic metabolism and creating an imbalance in intracellular calcium concentrations. Calcium is released from the cells and saturates the extracellular matrix. Collagen and proteoglycans are now compelled to interact with calcium to form a crystalline structure and solid bone. The exact mechanism of bone formation is still debated.3,4
CLASSIFICATION OF INJURY
In 1963, Salter and Harris evaluated and categorized growth plate fractures.5 The Salter-Harris classification system groups fractures into five types based on the combined involvement of the ph ysis, metaphysis, or epiphysis and an increasing risk of circulatory disruption to the region of growth. Type I fractures involve the growth plate only. Type II and type III fractures represent injuries to the growth plate in addition to a fracture through the metaphysis or epiphysis, respectively. A longitudinal injury through all three structures (epiphysis, growth plate, metaphysis) constitutes a type IV fracture. The most severe type (Salter-Harris V) results from an impact-type injury, which causes compression and narrowing of the growth plate.5 This type is at the highest risk for premature closure. A schematic of the Salter-Harris classification is seen in Figure 2.
INJURY BY REGION
Most physeal injuries (76%) occur in the upper extremity.6 The distal radius, phalanges, and distal humerus are the most frequent locations of fractures with growth plate involvement.6 Understanding the potential for injury in each body region can be useful in diagnosis, since most patients offer nothing more specific than a complaint of joint pain following trauma.
Shoulder Injury to the proximal humeral epiphysis is relatively infrequent (about 2%-3% of all physeal fractures).6,7 Shoulder injuries are usually type I or type II fractures from a fall or direct trauma. Similar trauma can also result in a glenohumeral joint dislocation or acromioclavicular sprain, so the differential diagnosis should include these injuries. One retrospective series of 57 patients with proximal humeral epiphysis fractures found patients were aged 8 to 15 years at the time of injury. Growth arrest greater than 1 cm was observed in only one patient with a type I or II injury but increased to 8 cm with type III and IV fractures.7
Elbow The elbow has six ossification centers, making this joint susceptible to complex patterns of injury. Most fractures occur in the distal humerus and the proximal radius (7% and 4.5% of all physeal injuries, respectively).6 There are two age ranges during which elbow injuries peak. The first is between the ages of 2 and 8 years, and the second is between the ages of 11 and 15 years. Males account for about 90% of the injuries in the distal humerus.8 This may be a result of higher activity levels and later physeal closure in males than in females and a relative weakening of the physis at puberty.5,6 Type I and type II injuries are common prior to 4 years of age, but as the growth plate becomes more irregular, developing hills and valleys, with age, supracondylar or type IV condylar fractures become more likely. Lateral condyle fractures comprise 25% of all physeal injuries in the area surrounding the elbow.8