What Is An Epiphyseal Line

Fractures and Dislocations in Children

Frederick M. Azar Dr. , in Campbell's Operative Orthopaedics , 2021

Fractures of the Distal Femoral Physis

Fractures of the distal femoral physis are not equally mutual equally physeal injuries elsewhere, accounting for only 7% of physeal injuries of the lower extremity. At the distal femur, Salter-Harris type Two physeal fractures cause more than severe physeal arrests than in other parts of the skeleton. Occult Salter-Harris type V compression fractures with premature closure of the physis as well occur more frequently in this location.

Salter-Harris type I fractures of the distal femoral physis rarely need operative handling unless they are displaced. These fractures are caused more than often by motor vehicle accidents or by a varus or valgus strength encountered in able-bodied activities, and many are undisplaced (Fig. 36.152). Gentle stress radiographs may be helpful in differentiating a tear of a collateral ligament from a type I epiphyseal separation. Salter-Harris type Two fractures are most common and occur in older children. Displacement unremarkably is in the coronal plane, although it can be in the anteroposterior plane. Physeal arrest is more frequent later on this fracture than after type 2 fractures in many other locations.

In an experimental study in rabbits, Mäkelä et al. found that destruction of 7% of the cantankerous-sectional area of the distal femoral physis caused permanent growth disturbance and shortening of the femur. The portion of the physis beneath the metaphyseal fracture fasten (Thurston-Holland sign) usually is spared. If the metaphyseal fasten is medial, valgus deformity may occur because of lateral closure of the physis. If the spike is lateral, varus angulation may follow.

Salter-Harris type Iii fractures rarely occur. The corporeality of displacement is important because joint incongruity results if anatomic alignment is not restored and a bony span develops if the physis is non realigned exactly (Fig. 36.153A). A Salter-Harris type IV fracture is even more than uncommon. It likewise requires accurate reduction. The metaphyseal spike of bone that occurs with this type of fracture is worrisome because of the increased possibility of physeal arrest from bony bridge formation (Fig. 36.153B).

When belatedly premature physeal closure occurs, a retrospective diagnosis of a Salter-Harris type V compression injury is made. Whether this is a truthful compression injury, with premature closure uniformly across the distal femoral physis, was questioned by Peterson and Burkhart, who speculated whether this uniform premature physeal closure could exist caused by some other mechanism, such as prolonged immobilization or an undiscovered machinery.

An avulsion injury can occur at the edge of the physis, especially on the medial side. A small fragment, including a portion of the perichondrium and underlying bone, may be torn off the femur when the proximal attachment of a collateral ligament is avulsed. This uncommon injury, although causeless to be benign, can lead to localized premature physeal arrest. If physeal arrest from a bony bridge is located at the most peripheral edge of a physis, severe angular deformity can occur.

Growth Plate

Javad Parvizi Doctor, FRCS , ... Associate Editor, in High Yield Orthopaedics, 2010

Zone Dependent:

•: Epiphyseal Avenue: Supplies the reserve zone, the proliferative zone, and the 2 upper zones of the hypertrophic zone. Claret supply decreases from the reserve zone to the zone of degeneration.
•: Metaphyseal Artery: Supplies the secondary and main spongiosa with a rich claret supply.

Fig. 103-1. Types of growth plate injury (I to 5) every bit classified by Salter and Harris.
(From Salter RB, Harris WR: Injuries involving the epiphyseal plate. J Os Joint Surg [Am] 45:587, 1963.)

Fig. 103-2. The physics of the proximal humerus. Annotation that fractures through the growth plate frequently occur through the zone of hypertrophy and the zone of provisional calcification.
(From DeLee D, Drez D [eds]: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed. Philadelphia, Saunders, 2003.)

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Growth considerations in pediatric upper extremity trauma and reconstruction

James Chang MD , in Plastic Surgery: Book 6: Manus and Upper Extremity , 2018

Anatomy and physiology of the epiphyseal growth plate

The physis (likewise known as growth plate, epiphyseal plate, epiphyseal growth plate, epiphyseal cartilage) is a highly specialized and organized cartilaginous structure derived from the mesoderm. It develops in the bone bud, secondary to the primary ossification centers (metaphysis) and is responsible for longitudinal and circumferential bone growth . ^one The physis must be distinguished from the epiphysis, or secondary ossification center (Fig. 30.1).

The physis consists of proliferating chondrocytes surrounded by synthesized extracellular matrix. The extracellular matrix is composed of h2o, collagen fibrils (mainly types II, IX, Ten, and 11) and proteoglycans (aggrecan, decorin, annexin II, V, and VI) bundled to form a sort of sponge with very small pores. ² This system confers peculiar mechanical backdrop that allow the physis to be "hard" when an axial load is applied chop-chop (a jumping child) or "soft" when plain-featured slowly (when chondrocytes secrete new extracellular matrix). ^three

The physis is traditionally divided into horizontal zones of chondrocytes at different stages of maturation (come acrossFig. 30.1). The resting zone (reserve zone or germinal matrix), immediately adjacent to the epiphysis, contains small, uniform, irregularly scattered chondrocytes, besides referred to as stalk cells, with low rates of proliferation but rich in storage materials (lipids and cytoplasmic vacuoles) for later growth. ^4,five The resting zone is responsible for protein synthesis and for maintaining a germinal structure. Injury to this layer results in cessation of growth.

When chondrocytes enter into the proliferative zone they undergo rapid duplication, increase the synthesis of collagen, in particular types II and 11, ⁴ and get apartment and well organized into longitudinal columns. Mitotic activity is present simply at the base of these columns. This layer is responsible for longitudinal growth of the bone via agile cell division. These showtime two zones accept an abundant extracellular matrix that confers a great deal of mechanical strength, in particular in response to shear forces.

Farther morphological changes – maturation, degeneration, and conditional calcification – accept place in the transformation (or hypertrophic) zone, divided into upper and lower hypertrophic zones.

The presence of conditional calcification ^4–6 confers shear resistance to the lower hypertrophic zone. In contrast, the upper hypertrophic zone containing scant extracellular matrix is the weakest portion of the physis and it is here that most injury or alteration to the physis occurs. ^7–9

In continuity with the metaphysis is the zone of endochondral calcification where the mineralization process of the matrix becomes more intensive.

Disorders of Childhood Growth

Alexander A.L. Jorge , ... Jeffrey Businesswoman , in Sperling Pediatric Endocrinology (Fifth Edition), 2021

Disorders Involving Autocrine/Paracrine Factors

Growth plate chondrocytes secrete multiple factors that human activity locally in a paracrine manner on nearby chondrocytes and an autocrine manner on the secreting cell. These factors, many of which are polypeptides, serve to coordinate the proliferation and differentiation of cells in the different zones of the growth plate (encounter section on Autocrine/Paracrine Regulation of Linear Growth earlier). Consequently, mutations in genes that are involved in this local intercellular communication tin impair growth plate chondrogenesis, causing short stature, or sometimes heighten growth plate chondrogenesis, causing tall stature. If the aberrant growth plate chondrogenesis affects non simply bone length simply also bone shape, malformation ensues, and the condition is termed a chondrodysplasia. ⁵³ The give-and-take that follows provides some examples of growth disorders related to paracrine signaling defects, focusing particularly on those that can nowadays as isolated brusque stature without an obvious chondrodysplasia.

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Vascularized Os Grafting

Scott W. Wolfe MD , in Greenish's Operative Hand Surgery , 2017

Fibula With Physis.

Inclusion of the proximal growth plate to allow for growth of the transferred bone is a reasonable process when no other options be. In a leg with normal vascular beefcake, current opinion favors the use of the anterior tibial vascular pedicle, which will support the fibular caput and cervix with a food vessel supply, and a periosteal supply to the diaphysis. The technique of harvest is well described by Innocenti. ⁶¹ It is about used in the upper limb for restoration of growth following resection of the distal radius in children, ^3,60 just is as well useful with resection of the proximal humerus ⁹² or distal ulna. ³

A longitudinal incision centered between the tibialis inductive and extensor digitorum longus is prolonged proximally, post-obit the biceps femoris muscle. Dissection in the intermuscular plane betwixt these two muscles, starting distally, exposes the tibialis inductive neurovascular parcel and preserves the frail network of periosteal vessels supplying the diaphysis. During proximal dissection, many motor branches of the peroneal nerve cross the operating field, and they must be carefully preserved.

The common peroneal nerve is identified and protected at the level of the fibular neck. The origins of the extensor digitorum longus and peroneal muscles are incised and reflected laterally and inferiorly ii cm distal to the proximal fibular tip, leaving a muscular gage surrounding the fibular epiphysis. Once the vessels are isolated, the fibular head is released by sectionalization of the biceps femoris tendon and iliotibial band attachments and release of the lateral collateral ligament and tibiofibular joint capsule. The inductive tibial vessels may exist ligated at their origin to complete the harvest.

Skeletal Dysplasias

FREDERIC SHAPIRO , in Pediatric Orthopedic Deformities, 2001

4. VARIATIONS IN GROWTH PLATE THICKNESS

The growth plate can be the same thickness every bit normal, thicker than normal, or thinner than normal. In many skeletal dysplasias, there is no change in the thickness, as determined by qualitative assessments and on occasion by quantitative assessment. In those abnormalities associated with a defect of mineralization, the growth plate is thicker than normal with persistence of cartilage in the hypertrophic zone and next metaphysis in which mineralization commonly occurs. Thickened growth plates are the hallmark of rickets disorders, regardless of whether these are nutritional in nature or due to genetic disorders such as hypophosphatemic rickets. The physis can also be thicker in metaphyseal dysplasias, although they tend to be so in an irregular fashion with isolated areas of radiolucency in metaphyseal bone next to the physis. The majority of skeletal dysplasias that evidence changes in physeal thickness have thinner growth plates. This is particularly true in the lethal chondrodystrophies in which cartilage tissue itself is markedly poor in germination and in diastrophic dysplasia toward the end of the showtime decade when premature growth plate closure farther worsens prognosis.

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New Perspectives on Bone Morphogenetic Protein Signaling in Chondrogenic Differentiation During Skeletogenesis

Maiko Omi , Yuji Mishina , in Encyclopedia of Bone Biology, 2020

Signaling Pathways in Growth Plates

Growth plates formed at the ends of long bones play a major part in the longitudinal growth of the bones. The growth plates consist of singled-out chondrocyte prison cell layers such as resting, proliferative (or columnar), prehypertrophic, and hypertrophic zones (Kronenberg, 2003) (Fig. 1). Cells in the resting zone are quiescent, and they have stem cell characteristics (Ono et al., 2019; Mizuhashi et al., 2018). Once the chondrocytes start to proliferate, descendant cells form a columnar construction to constitute the proliferative zone (Romereim et al., 2014; Li et al., 2011; Moore and Jacobs, 2018). Afterwards, those cells differentiate into prehypertrophic chondrocytes to modify the cell'southward shape to go hypertrophic chondrocytes. A balance betwixt proliferation and differentiation is disquisitional to determine the height of the column and contributes to the growth of the long bone (Fig. 1). The height of the growth plates is tightly controlled by a feedback loop betwixt parathyroid hormone-related poly peptide (PTHrP) and Indian hedgehog (IHH) (Kronenberg, 2003). PTHrP produced at the resting zone suppresses the differentiation of chondrocytes while IHH produced at the prehypertrophic zone stimulates the differentiation of chondrocytes and positively regulates production of PTHrP. Fibroblast growth factor (FGF) signaling mediated past FGFR3 is a negative regulator for chondrocytic proliferation. Elongation of the long bones ceases when growth plates disappear during adolescence.

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The Growth Plate

Emmanouil Grigoriou , ... John P. Dormans , in Fetal and Neonatal Physiology (Fifth Edition), 2017

Summary

The growth plate is responsible for longitudinal bone growth by the mechanism of endochondral ossification. Limb development is initiated during the fourth calendar week of gestation and results in the formation of the limb bud. Three axes—the proximodistal, anteoposterior, and dorsoventral—are responsible for limb bud patterning. Endochondral os germination begins early on in the embryonic period when mesenchymal cells form condensations. These jail cell clusters differentiate into chondrocytes, which proliferate to course the growth plate or physis. This is a complex procedure that is regulated past a number of transcriptional factors and soluble mediators. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in the formation of cartilage that is subsequently invaded by blood vessels and bone cells that remodel the cartilage into bone tissue. A complex network of endocrine signals—including GH, IGF-I thyroid hormones, estrogen, androgen, and vitamin D—work seamlessly to regulate longitudinal bone growth. Their action might occur locally on the growth plate chondrocytes, or by modulation of other endocrine signals in the network. Many human being skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate, including achondroplasia, diastrophic dysplasia, and Jansen metaphyseal chondrodysplasia. The determinants of chondrocyte shape and the coordination of growth plate function with the development of joints, tendons and ligaments is currently nether report but our agreement of this still remains very preliminary.

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Physiology of Growth Hormone in Fetus and Child

Vijayarangan G. Kannian , Fiona J. Ryan , in Encyclopedia of Endocrine Diseases (2d Edition), 2019

Effects of GH and IGF-one on Tissues and Growth Plate

GH is the major growth factor in the linear growth of children. It mediates many of its biological actions via IGF-1, which acts on the epiphyseal plates of long bones also known every bit the growth plates. Chondrocytes in the growth plates which are regarded as stem cells, nether the influence of GH/IGF-1 and other growth factors, undergo cell proliferation and maturation that results in the linear growth of children.

Contempo studies has shown the role of suppressor of cytokine signaling ii (SOCS2) as a key modulator of GH at the growth plate. The SOCS proteins are a family unit of negative regulatory proteins that are expressed in response to activation of cytokine and growth factor signal cascades, specially those apply JAK/STAT signaling system (Greenhalgh et al., 2005).

Excess GH levels in pre-pubertal children where the epiphyses are yet to fuse results in uncontrolled linear growth, termed every bit gigantism. Whereas, acromegaly results in individuals whose epiphyses are fused with excess secretion of GH.

In addition to linear growth, GH too has other potent furnishings—including modulation glucose, lipids and nitrogen metabolism; promotion of lipolysis, increment amino acid uptake and protein synthesis and decrease in protein breakdown (Press, 1988).

Growth Plate

The growth plate, also known as the epiphyseal plate is a thin layer of cartilage that lies between the epiphyses and metaphyses, and is where the growth of long bones takes place. Such longitudinal bone growth occurs here through the mechanism of endochondral ossification, with germination of cartilage and and so remodeling into bone tissue ( Fig. 6).

The chondrocytes in the growth plates are surrounded by matrix consisting of proteoglycan aggregates and are divided into three zones, reserve/resting zone, proliferative zone and hypertrophic zone. The procedure starts with recruitment of chondrocytes in the stem prison cell zone, then actively proliferates by cell division and followed past differentiation, apoptosis and finally mineralization in the hypertrophic zone. Among other hormones, GH and IGF-i regulates this process.

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Knee 1

B.J. Manaster Md, PhD, FACR , ... David Chiliad. Disler MD, FACR , in Musculoskeletal Imaging (Fourth Edition), 2013

Physeal Injury

Growth plate injuries at the genu are uncommon, but they are highly associated with complications, peculiarly growth disturbance (run across Fig. 3-6). Proximal tibial epiphyseal fractures often occur in association with patellar tendon traction (see Fig. 12-17). In the distal femur, Salter-Harris II fractures predominate, occurring in lxx% of injuries; the next almost common design is Salter-Harris Three fractures, occurring in 15% of children. Most Salter-Harris Three fractures of the distal femur involve the medial femoral condyle and are caused by valgus stress. They are usually without deportation and are occult radiographically even so tin exist demonstrated at MRI. The knee is the nearly common site for Salter-Harris Five fractures, which occur at the proximal tibia and have a loftier frequency of localized growth plate arrest with angular deformity or limb shortening. Salter-Harris I fractures tin can be subtle, seen only every bit asymmetry of the physis (Fig. 12-20).

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