Epiphyseal plate

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Epiphyseal plate
Tib fib growth plates.jpg
Radiogram of distal tibia (left) and fibula (right) showing two epiphyseal plates
Hypertrophic Zone of Epiphyseal Plate.jpg
Light micrograph of an undecalcified epiphyseal plate that is displaying the hypertrophic zone with its typical chondrocytes, 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

The epiphyseal plate, epiphysial plate, physis, or growth plate is a hyaline cartilage plate in the metaphysis at each end of a long bone. It is the part of a long bone where new bone growth takes place; that is, the whole bone is alive, with maintenance remodeling throughout its existing bone tissue, but the growth plate is the place where the long bone grows longer (adds length).

Contents

The plate is only found in children and adolescents; in adults, who have stopped growing, the plate is replaced by an epiphyseal line. This replacement is known as epiphyseal closure or growth 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]

Structure

Development

Endochondral ossification is responsible for the initial bone development from cartilage in utero and infants and the longitudinal growth of long bones in the epiphyseal plate. The plate's chondrocytes are under constant division by mitosis. These daughter cells stack facing the epiphysis while the older cells are pushed towards the diaphysis. 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 increased apoptosis of chondrocytes in the epiphyseal plate. [6] Depletion of chondrocytes due to apoptosis leads to less ossification 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]

Histology

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 reserveQuiescent chondrocytes are found at the epiphyseal end
Zone of proliferationChondrocytes undergo rapid mitosis under influence of growth hormone
Zone of maturation and hypertrophyChondrocytes stop mitosis, and begin to hypertrophy by accumulating glycogen, lipids, and alkaline phosphatase
Zone of calcificationChondrocytes undergo apoptosis. Cartilagenous matrix begins to calcify.
Zone of ossificationOsteoclasts and osteoblasts from the diaphyseal side break down the calcified cartilage and replace with mineralized bone tissue.
Masson Goldner trichrome stain of rabbit epiphysial plate Proximal tibia Masson Goldner Trikrom rabbit 600x growth zone.jpg
Masson Goldner trichrome stain of rabbit epiphysial plate

Clinical significance

Defects in the development and continued division of epiphyseal plates can lead to growth disorders collectively known as osteochondrodysplasia. The most common defect is achondroplasia, where there is a defect in cartilage formation. Achondroplasia is the most common cause of dwarfism or short 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 the tibia, 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 as Blount's disease, rickets, arthrogryposis multiplex congenita and osteochondrodysplasias among others. [13] [14] [15] This applies to bone and joint deformities in the coronal – medial/lateral – plane or genu varum/genu valgum plane [14] and in the sagittal – anterior/posterior – plane or knee flexion deformity/genu recurvatum plane. [15]

Other animals

John Hunter studied growing chickens. He observed bones grew at the ends and thus demonstrated the existence of the epiphyseal plates. Hunter is considered the "father of the growth plate". [16]

See also

Related Research Articles

<span class="mw-page-title-main">Knee</span> Leg joint in primates

In humans and other primates, the knee joins the thigh with the leg and consists of two joints: one between the femur and tibia, and one between the femur and patella. It is the largest joint in the human body. The knee is a modified hinge joint, which permits flexion and extension as well as slight internal and external rotation. The knee is vulnerable to injury and to the development of osteoarthritis.

<span class="mw-page-title-main">Epiphysis</span> End of a long bone that ossifies from a secondary center

An epiphysis is one of the rounded ends or tips of a long bone that ossify from a secondary center of ossification. Between the epiphysis and diaphysis lies the metaphysis, including the epiphyseal plate. At the joint, the epiphysis is covered with articular cartilage; below that covering is a zone similar to the epiphyseal plate, known as subchondral bone. In evolution, reptiles do not have epiphyses and diaphyses, being restricted to mammals.

An osteotomy is a surgical operation whereby a bone is cut to shorten or lengthen it or to change its alignment. It is sometimes performed to correct a hallux valgus, or to straighten a bone that has healed crookedly following a fracture. It is also used to correct a coxa vara, genu valgum, and genu varum. The operation is done under a general anaesthetic.

<span class="mw-page-title-main">Genu valgum</span> Medical condition known as knock-knee

Genu valgum, commonly called "knock-knee", is a condition in which the knees angle in and touch each other when the legs are straightened. Individuals with severe valgus deformities are typically unable to touch their feet together while simultaneously straightening the legs. The term originates from the Latin genu, 'knee', and valgus which means "bent outwards", but is also used to describe the distal portion of the knee joint which bends outwards and thus the proximal portion seems to be bent inwards.

<span class="mw-page-title-main">Genu varum</span> Varus deformity marked by (outward) bowing at the knee

Genu varum is a varus deformity marked by (outward) bowing at the knee, which means that the lower leg is angled inward (medially) in relation to the thigh's axis, giving the limb overall the appearance of an archer's bow. Usually medial angulation of both lower limb bones is involved.

<span class="mw-page-title-main">Hereditary multiple exostoses</span> Rare skeletal disorder

Hereditary multiple osteochondromas (HMO), also known as hereditary multiple exostoses, is a disorder characterized by the development of multiple benign osteocartilaginous masses (exostoses) in relation to the ends of long bones of the lower limbs such as the femurs and tibias and of the upper limbs such as the humeri and forearm bones. They are also known as osteochondromas. Additional sites of occurrence include on flat bones such as the pelvic bone and scapula. The distribution and number of these exostoses show a wide diversity among affected individuals. Exostoses usually present during childhood. The vast majority of affected individuals become clinically manifest by the time they reach adolescence. A small percentage of affected individuals are at risk for development of sarcomas as a result of malignant transformation. The incidence of hereditary multiple exostoses is around 1 in 50,000 individuals. Hereditary multiple osteochondromas is the preferred term used by the World Health Organization.

<span class="mw-page-title-main">Endochondral ossification</span> Cartilaginous bone development that forms the long bones

Endochondral ossification is one of the two essential pathways by which bone tissue is produced during fetal development of the mammalian skeletal system, the other pathway being intramembranous ossification. Both endochondral and intramembranous processes initiate from a precursor mesenchymal tissue, but their transformations into bone are different. In intramembranous ossification, mesenchymal tissue is directly converted into bone. On the other hand, endochondral ossification starts with mesenchymal tissue turning into an intermediate cartilage stage, which is eventually substituted by bone.

<span class="mw-page-title-main">Ossification</span> Development process in bones

Ossification in bone remodeling is the process of laying down new bone material by cells named osteoblasts. It is synonymous with bone tissue formation. There are two processes resulting in the formation of normal, healthy bone tissue: Intramembranous ossification is the direct laying down of bone into the primitive connective tissue (mesenchyme), while endochondral ossification involves cartilage as a precursor.

<span class="mw-page-title-main">Proximal femoral focal deficiency</span> Medical condition

Proximal femoral focal deficiency (PFFD), also known as Congenital Femoral Deficiency (CFD), is a rare, non-hereditary birth defect that affects the pelvis, particularly the hip bone, and the proximal femur. The disorder may affect one side or both, with the hip being deformed and the leg shortened.

<span class="mw-page-title-main">Osteochondroma</span> Medical condition

Osteochondromas are the most common benign tumors of the bones. The tumors take the form of cartilage-capped bony projections or outgrowth on the surface of bones exostoses. It is characterized as a type of overgrowth that can occur in any bone where cartilage forms bone. Tumors most commonly affect long bones about the knee and in the forearm. Additionally, flat bones such as the pelvis and scapula may be affected. Hereditary multiple exostoses usually present during childhood. Yet, the vast majority of affected individuals become clinically manifest by the time they reach adolescence. Osteochondromas occur in 3% of the general population and represent 35% of all benign tumors and 8% of all bone tumors. The majority of these tumors are solitary non-hereditary lesions and approximately 15% of osteochondromas occur as hereditary multiple exostoses preferably known as hereditary multiple osteochondromas (HMOs). Osteochondromas do not result from injury and the exact cause remains unknown. Recent research has indicated that multiple osteochondromas is an autosomal dominant inherited disease. Germ line mutations in EXT1 and EXT2 genes located on chromosomes 8 and 11 have been associated with the cause of the disease. The treatment choice for osteochondroma is surgical removal of solitary lesion or partial excision of the outgrowth, when symptoms cause motion limitations or nerve and blood vessel impingements. In hereditary multiple exostoses the indications of surgery are based upon multiple factors that are taken collectively, namely: patient's age, tumor location and number, accompanying symptomatology, esthetic concerns, family history and underlying gene mutation. A variety of surgical procedures have been employed to remedy hereditary multiple exostoses such as osteochondroma excision, bone lengthening, corrective osteotomy and hemiepiphysiodesis. Sometimes a combination of the previous procedures is used. The indicators of surgical success in regard to disease and patient characteristics are greatly disputable. Because most studies of hereditary multiple exostoses are retrospective and of limited sample size with missing data, the best evidence for each of the currently practiced surgical procedures is lacking.

<span class="mw-page-title-main">Osteochondritis dissecans</span> Ischemic bone disease

Osteochondritis dissecans is a joint disorder primarily of the subchondral bone in which cracks form in the articular cartilage and the underlying subchondral bone. OCD usually causes pain during and after sports. In later stages of the disorder there will be swelling of the affected joint which catches and locks during movement. Physical examination in the early stages does only show pain as symptom, in later stages there could be an effusion, tenderness, and a crackling sound with joint movement.

An osteochondrodysplasia, or skeletal dysplasia, is a disorder of the development of bone and cartilage. Osteochondrodysplasias are rare diseases. About 1 in 5,000 babies are born with some type of skeletal dysplasia. Nonetheless, if taken collectively, genetic skeletal dysplasias or osteochondrodysplasias comprise a recognizable group of genetically determined disorders with generalized skeletal affection. These disorders lead to disproportionate short stature and bone abnormalities, particularly in the arms, legs, and spine. Skeletal dysplasia can result in marked functional limitation and even mortality.

<span class="mw-page-title-main">Salter–Harris fracture</span> Medical condition

A Salter–Harris fracture is a fracture that involves the epiphyseal plate of a bone, specifically the zone of provisional calcification. It is thus a form of child bone fracture. It is a common injury found in children, occurring in 15% of childhood long bone fractures. This type of fracture and its classification system is named for Robert B. Salter and William H. Harris who created and published this classification system in the Journal of Bone and Joint Surgery in 1963.

<span class="mw-page-title-main">Multiple epiphyseal dysplasia</span> Rare genetic disorder

Multiple epiphyseal dysplasia (MED), also known as Fairbank's disease, is a rare genetic disorder that affects the growing ends of bones. Long bones normally elongate by expansion of cartilage in the growth plate near their ends. As it expands outward from the growth plate, the cartilage mineralizes and hardens to become bone (ossification). In MED, this process is defective.

<span class="mw-page-title-main">Pseudoachondroplasia</span> Inherited disorder of bone growth

Pseudoachondroplasia is an inherited disorder of bone growth. It is a genetic autosomal dominant disorder. It is generally not discovered until 2–3 years of age, since growth is normal at first. Pseudoachondroplasia is usually first detected by a drop of linear growth in contrast to peers, a waddling gait or arising lower limb deformities.

<span class="mw-page-title-main">Blount's disease</span> Medical condition

Blount's disease is a growth disorder of the tibia which causes the lower leg to angle inward, resembling a bowleg. It is also known as "tibia vara".

<span class="mw-page-title-main">Boomerang dysplasia</span> Medical condition

Boomerang dysplasia is a lethal form of osteochondrodysplasia known for a characteristic congenital feature in which bones of the arms and legs are malformed into the shape of a boomerang. Death usually occurs in early infancy due to complications arising from overwhelming systemic bone malformations.

Epiphysiodesis is a pediatric orthopedic surgery procedure that aims at altering or stopping the bone growth naturally occurring through the growth plate also known as the physeal plate. There are two types of epiphysiodesis: temporary hemiepiphysiodesis and permanent epiphysiodesis. Temporary hemiepiphysiodesis is also known as guided growth surgery or growth modulation surgery. Temporary hemiepiphysiodesis is reversible i.e. the metal implants used to achieve epiphysiodesis can be removed after the desired correction is achieved and the growth plate can thus resume its normal growth and function. In contrast, permanent epiphysiodesis is irreversible and the growth plate function cannot be restored after surgery. Both temporary hemiepiphysiodesis and permanent epiphysiodesis are used to treat a diverse array of pediatric orthopedic disorders but the exact indications for each procedure are different.

<span class="mw-page-title-main">Fibrochondrogenesis</span> Medical condition

Fibrochondrogenesis is a rare autosomal recessive form of osteochondrodysplasia, causing abnormal fibrous development of cartilage and related tissues.

<span class="mw-page-title-main">Index of trauma and orthopaedics articles</span>

Orthopedic surgery is the branch of surgery concerned with conditions involving the musculoskeletal system. Orthopedic surgeons use both surgical and nonsurgical means to treat musculoskeletal injuries, sports injuries, degenerative diseases, infections, bone tumours, and congenital limb deformities. Trauma surgery and traumatology is a sub-specialty dealing with the operative management of fractures, major trauma and the multiply-injured patient.

References

  1. Crowder, C; Austin, D (September 2005). "Age ranges of epiphyseal fusion in the distal tibia and fibula of contemporary males and females". Journal of Forensic Sciences. 50 (5): 1001–7. doi:10.1520/JFS2004542. PMID   16225203. 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
  2. Barrell, Amanda. "At what age do girls stop growing?". MedicalNewsToday. Retrieved 9 June 2020.
  3. Jarret, Robert R. "Puberty: Tanner Stages – Boys". Pediatric HOUSECALLS. Retrieved 9 June 2020.
  4. Jarret, Robert R. "Puberty: Tanner Stages – Girls". Pediatric HOUSECALLS. Retrieved 9 June 2020.
  5. "When do most males' growth plates close?". Zoodoc. Retrieved 9 June 2020.
  6. Zhong, M; Carney, DH; Boyan, BD; Schwartz, Z (January 2011). "17β-Estradiol regulates rat growth plate chondrocyte apoptosis through a mitochondrial pathway not involving nitric oxide or MAPKs". Endocrinology. 152 (1): 82–92. doi: 10.1210/en.2010-0509 . PMID   21068162.
  7. "Skeletal System / Bone Development and Growth". Archived from the original on 2008-07-09. Retrieved 2008-07-10.
  8. Ovalle, William K.; Nahirney, Patrick C. (2007). Netter's essential histology : with Student consult online access (1st ed.). Philadelphia, Pa.: Elsevier Saunders. ISBN   9781929007868.
  9. El-Sobky, TamerA; Shawky, RabahM; Sakr, HossamM; Elsayed, SolafM; Elsayed, NermineS; Ragheb, ShaimaaG; Gamal, Radwa (2017). "A systematized approach to radiographic assessment of commonly seen genetic bone diseases in children: A pictorial review". Journal of Musculoskeletal Surgery and Research. 1 (2): 25. doi: 10.4103/jmsr.jmsr_28_17 . S2CID   79825711.
  10. E.L.-Sobky, Tamer A.; Samir, Shady; Atiyya, Ahmed Naeem; Mahmoud, Shady; Aly, Ahmad S.; Soliman, Ramy (2018). "Current paediatric orthopaedic practice in hereditary multiple osteochondromas of the forearm: a systematic review". SICOT-J. 4: 10. doi:10.1051/sicotj/2018002. PMC   5863686 . PMID   29565244.
  11. Duque Orozco, Maria del Pilar; Abousamra, Oussama; Rogers, Kenneth J.; Thacker, Mihir M. (July 2018). "Radiographic Analysis of the Pediatric Hip Patients With Hereditary Multiple Exostoses (HME)". Journal of Pediatric Orthopaedics. 38 (6): 305–311. doi:10.1097/BPO.0000000000000815. PMID   27328120. S2CID   23800752.
  12. Mirghasemi, Alireza; Mohamadi, Amin; Ara, Ali Majles; Gabaran, Narges Rahimi; Sadat, Mir Mostafa (November 2009). "Completely displaced S-1/S-2 growth plate fracture in an adolescent: case report and review of literature". Journal of Orthopaedic Trauma. 23 (10): 734–738. doi:10.1097/BOT.0b013e3181a23d8b. ISSN   1531-2291. PMID   19858983. S2CID   6651435.
  13. Journeau, P (2020). "Update on guided growth concepts around the knee in children". Orthop Traumatol Surg Res. S1877-0568 (19): S171–S180. doi: 10.1016/j.otsr.2019.04.025 . PMID   31669550.
  14. 1 2 EL-Sobky, TA; Samir, S; Baraka, MM; Fayyad, TA; Mahran, MA; Aly, AS; Amen, J; Mahmoud, S (1 January 2020). "Growth modulation for knee coronal plane deformities in children with nutritional rickets: A prospective series with treatment algorithm". JAAOS: Global Research and Reviews. 4 (1): e19.00009. doi: 10.5435/JAAOSGlobal-D-19-00009 . PMC   7028784 . PMID   32159063.
  15. 1 2 Trofimova, SI; Buklaev, DS; Petrova, EV; Mulevanova, SA (2016). "Guided growth for correction of knee flexion contracture in patients with arthrogryposis: preliminary results". Pediatric Traumatology, Orthopaedics and Reconstructive Surgery. 4 (4): 64–70. doi: 10.17816/PTORS4464-70 .
  16. "Growth Plate (Physeal) Fractures". EMedicine.com. Retrieved 2008-01-15.