| Epiphyseal plate | |
|---|---|
 | |
 Light micrograph of an undecalcified epiphyseal plate that is displaying the hypertrophic zone with its typicalchondrocytes,matrix and three zones: maturation (top), degenerative (middle) and provisional calcification (bottom). | |
| Details | |
| Identifiers | |
| Latin | lamina epiphysialis |
| MeSH | D006132 |
| TA98 | A02.0.00.020 |
| TA2 | 395 |
| FMA | 75427 |
| Anatomical terminology | |
Theepiphyseal plate,epiphysial plate,physis, orgrowth plate is ahyaline cartilage plate in themetaphysis at each end of along bone. It is the part of a long bone where new bone growth takes place; that is, the whole bone is alive, with maintenanceremodeling throughout its existingbone tissue, but the growth plate is the place where the long bone grows longer (adds length).
The plate is only found in children and adolescents; in adults, who have stopped growing, the plate is replaced by anepiphyseal line. This replacement is known asepiphyseal closure orgrowth plate fusion. Complete fusion can occur as early as 12 for girls (with the most common being 14–15 years for girls) and as early as 14 for boys (with the most common being 15–17 years for boys).[1][2][3][4][5]
Endochondral ossification is responsible for the initial bone development from cartilagein utero and infants and the longitudinal growth of long bones in the epiphyseal plate. The plate'schondrocytes are under constant division bymitosis. Thesedaughter cells stack facing theepiphysis while the older cells are pushed towards thediaphysis. As the older chondrocytes degenerate,osteoblasts ossify the remains to form new bone. In puberty increasing levels of estrogen, in both females and males, leads to increasedapoptosis of chondrocytes in the epiphyseal plate.[6] Depletion of chondrocytes due to apoptosis leads to lessossification and growth slows down and later stops when the entire cartilage have become replaced by bone, leaving only a thin epiphyseal scar which later disappears.[7]
The growth plate has a very specific morphology in having a zonal arrangement as follows:[8]
| Epiphyseal plate zone (from epiphysis to diaphysis) | Description |
|---|---|
| Zone of reserve | Quiescent chondrocytes are found at the epiphyseal end |
| Zone of proliferation | Chondrocytes undergo rapid mitosis under influence ofgrowth hormone |
| Zone of maturation and hypertrophy | Chondrocytes stop mitosis, and begin tohypertrophy by accumulating glycogen, lipids, andalkaline phosphatase |
| Zone of calcification | Chondrocytes undergoapoptosis. Cartilagenous matrix begins to calcify. |
| Zone of ossification | Osteoclasts and osteoblasts from the diaphyseal side break down the calcified cartilage and replace with mineralized bone tissue. |
Defects in the development and continued division of epiphyseal plates can lead to growth disorders collectively known asosteochondrodysplasia. The most common defect isachondroplasia, where there is a defect in cartilage formation. Achondroplasia is the most common cause ofdwarfism orshort stature and it also manifests in generalized deformities of bones and joints. However, various other types of osteochondrodysplasias can cause short stature and generalized deformities of bones and joints due to abnormal function of growth plate cartilage cells.[9]Hereditary multiple exostoses is a genetic condition that is caused by growth irregularities of the epiphyseal plates of the long bones of the upper[10] and lower limbs.[11] It usually results in limb deformities and a certain degree of functional limitations.
Salter–Harris fractures are fractures involving epiphyseal plates and hence tend to interfere with growth, height or physiologic functions.[12]
Osgood–Schlatter disease results from stress on the epiphyseal plate in thetibia, leading to excess bone growth and a painful lump at the knee.
There are important clinical implications of the growth plate physiology. For example guided growth surgery, also known as temporary hemiepiphysiodesis is used to achieve correction or straightening of the bone deformities in a variety of pediatric orthopedic disorders such asBlount's disease,rickets,arthrogryposis multiplex congenita andosteochondrodysplasias among others.[13][14][15] This applies to bone and joint deformities in thecoronal – medial/lateral – plane orgenu varum/genu valgum plane[14] and in thesagittal – anterior/posterior – plane or knee flexion deformity/genu recurvatum plane.[15]
John Hunter studied growing chickens, and observed that bones grew at the ends, demonstrating the existence of the epiphyseal plates. Hunter is often considered the "father of the growth plate" because of his early research on growth plates.[16]
complete fusion in females occurs as early as 12 years in the distal tibia and fibula. All females demonstrated complete fusion by 18 years with no significant differences between ancestral groups. Complete fusion in males occurs as early as 14 years in both epiphyses. All males demonstrated complete fusion by 19 years
