Every one of the long skeletal bones in the body has a growth plate that governs its rate of the bone growth and development. This growth plate, or physis, is located near the end of each long bone, adjoining the head of the bone, called the epiphysis. The release of growth hormone, somatotropin, interacts with the cells of the growth plate during periods of cellular creation. As a child grows, the growth plates harden by a process known as ossification of the bone cells, eventually disappearing when the body reaches maturity. Thus, growth plate injuries are, by definition, damage sustained by a child or an adolescent.
Bones such as the tibia and fibula (lower leg), the radius (forearm), and the femur (thigh) are structures that commonly sustain growth plate damage. The growth plate in a child or adolescent is often softer than the supporting ligaments and connective tissues, because bones form more slowly, rendering the growth plate more vulnerable to fracture.
The period in physical development when the bones are at the greatest risk of a growth plate injury is near the end of puberty. Growth plate injuries are twice as likely to occur in boys as in girls, due primarily to the fact that girls reach physical maturation approximately two years earlier than boys, coupled with the greater degree of participation of boys in physically riskier activities. Approximately 30% to 40% of all growth plate injuries in both sexes occur in the competitive sport environment. A further 20% of growth plate damage occurs in recreational sports such as skateboarding.
These injuries regularly occur as a result of both direct trauma as well as through overuse or repetitive strain being placed upon a bone, such as the throwing shoulder or elbow of a youth baseball pitcher. The long bones of the fingers (phalanges), the radius, and the tibia/fibula structure are the most common sports-related growth plate fractures.
Fracture of the growth plate is the most common type of injury sustained to this portion of the bone. Diagnosis and treatment of such an injury are complicated by the speedy recuperative powers of children; damage to the growth plate can go undetected and quickly heal in a fashion in which the bone is misaligned.
A system of growth plate fracture classification was first devised in the 1960s, known as the Salter-Harris system, with five progressively more serious fractures described. In recent years, the Peterson classification system was developed, adding a sixth category of fracture. The categories and the general treatment methods range from Type I to Type VI.
Type I is a fracture of the bone above the growth plate, with a line extending into the growth plate. These fractures are treated by immobilizing the bone in a cast. Type II is a fracture of the bone in part of the growth plate, and a crack of the bone shaft. This is the most common type of growth plate fracture, typically requiring a cast; the fracture may also require surgery, often to insert a pin, or similar device, to stabilize the structure as it heals. Type III is a complete fracture of the growth plate. This injury will require surgical repair. Type IV is a fracture that results in a breaking off of the end of the bone (epiphysis). This injury will also require surgical repair. Type V is a fracture of the bone shaft, growth plate, and the end of the bone. This injury presents a significant risk of permanently arresting development of the bone, due to the potential future inability of the growth plate to function. Surgical repair is required. Finally, type VI is a fracture of the bone that is sufficiently traumatic to result in portions of the bone being removed, as might occur in a serious motor vehicle collision or gunshot wound absorbed by the bone. Surgical repair and reconstruction are necessary with this type of injury.
A common injury that occurs in young athletes that is very similar to a damaged growth plate is the patellar tendon ailment known as Osgood-Sclatter disease (OSD). Occurring primarily in adolescent boys, OSD is the result of a lesion that grows on the surface of the tibia, in the area of the epiphysis. This lesion creates an irritation on the tendon that connects the tibia to the patella (knee cap). The rapid bone growth is genetic in origin; when coupled with the stresses of running and jumping, OSD can cause significant pain to a young athlete; swelling and a lack of flexibility in the knee joint are common symptoms. OSD usually resolves itself when the person reaches physical maturity, but the condition will require attention, including rest, ice, stretching exercises, and efforts to ensure that the quadriceps is strong and balanced in relation to the lower leg.
The other mechanisms of injury that create potential risks to the growth plate include situations of child abuse, such as the repeated shaking of a child; exposure to extreme cold and resultant frostbite to bones such as the fingers; radiation as used in childhood chemotherapy; and inherited musculoskeletal disorders.