The epiphyseal growth plate (physis) is a specialized area of tissue found near the ends of the long bones in children and adolescents. It is the sole engine responsible for the longitudinal growth of the skeleton, allowing bones like the femur, tibia, and humerus to increase in length. This cartilaginous structure drives skeletal elongation, which determines a person’s final height. The growth plate’s continuous activity ensures that long bones grow proportionally until skeletal maturity is reached.
What the Growth Plate Is and Where It Is Found
The growth plate is strategically positioned within a long bone, separating the epiphysis (the rounded end) from the metaphysis (the wider part of the shaft). This structure is not made of hard bone tissue, but rather hyaline cartilage, a flexible material. Because the growth plate is made of cartilage, it is notably weaker than the surrounding bone, making it a common site for injury in growing individuals. Its precise location means that forces causing a ligament tear or fracture in an adult often result in a separation or break through the growth plate in a child.
How Bones Lengthen: The Zones of Ossification
Longitudinal bone growth occurs through endochondral ossification, where bone is formed by replacing a cartilage model. This mechanism is organized into five distinct layers, or zones, within the growth plate, each performing a specific function to facilitate lengthening. The process involves the continuous conversion of cartilage into bone tissue.
Zone of Reserve and Proliferation
The zone of reserve is the layer closest to the epiphysis and contains quiescent chondrocytes (cartilage cells) that serve as progenitor cells for the entire plate. Adjacent to this is the zone of proliferation, where chondrocytes rapidly divide through mitosis and align themselves into distinct vertical columns. This rapid cell division physically pushes the epiphysis and diaphysis apart, increasing the bone’s length.
Zone of Hypertrophy and Calcification
The newly formed cells then enter the zone of hypertrophy, where they cease dividing and dramatically increase in size, growing up to five times their original volume. These enlarged cells begin preparing the surrounding matrix for mineralization. As the chondrocytes swell, they restrict their own nutrient supply and eventually enter the zone of calcification, where they die.
Zone of Ossification
These dead, hypertrophic chondrocytes leave behind a framework of calcified cartilage matrix. In the zone of ossification, blood vessels from the diaphysis invade the empty spaces, carrying osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells). The osteoblasts adhere to the calcified matrix scaffold and secrete new bone tissue, permanently replacing the temporary cartilage structure and resulting in a longer, mature bone segment.
When Growth Stops: Understanding Plate Closure
The growth plates do not remain active indefinitely. This process, known as epiphyseal closure or growth plate fusion, occurs during adolescence and is primarily driven by hormonal changes associated with puberty. Increasing levels of sex steroids, particularly estrogen, trigger the final stages of longitudinal growth and accelerate the maturation of the growth plate. This hormonal action leads to a decrease in the proliferative capacity of the chondrocytes.
The continuous replacement of cartilage by bone eventually bridges the epiphysis and the diaphysis, leaving no remaining cartilage to facilitate further lengthening. Plate closure typically occurs earlier in females (ages 13–15) than in males (ages 15–17). Once the cartilage is completely replaced by bone, the former location of the growth plate is visible on X-rays as a thin, bony line called the epiphyseal line.
Common Injuries and Growth Disorders
Because the cartilaginous growth plate is structurally weaker than the ligaments or the bone shaft, injuries to this area are common in children and are classified using the Salter-Harris system. A growth plate fracture (physeal fracture) is a break that runs through the plate and risks growth disturbance. The prognosis depends on the injury type; Type I and II are the most common and generally have a better outcome.
Fractures that crush the plate (Type V) or involve the joint surface (Type IV) have a poorer prognosis because they can damage the resting and proliferative zones. Damage to these germinal layers can lead to premature fusion, causing a growth arrest or an angular deformity.
Systemic disorders can also affect the growth plate’s function. Achondroplasia, a common form of dwarfism, is characterized by a disruption in chondrocyte proliferation and maturation, leading to significantly shortened long bones. Conversely, Rickets, often caused by a Vitamin D deficiency, results in a failure of the cartilage matrix to properly calcify and mineralize.