This growth within a tissue is called interstitial growth. Most of the chondrocytes in the zone of calcified matrix , the zone closest to the diaphysis, are dead because the matrix around them has calcified, restricting nutrient diffusion. Capillaries and osteoblasts from the diaphysis penetrate this zone, and the osteoblasts secrete bone tissue on the remaining calcified cartilage. Thus, the zone of calcified matrix connects the epiphyseal plate to the diaphysis.
A bone grows in length when osseous tissue is added to the diaphysis. Bones continue to grow in length until early adulthood. The rate of growth is controlled by hormones, which will be discussed later. When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces all the cartilage, longitudinal growth stops. All that remains of the epiphyseal plate is the ossified epiphyseal line Figure 6. While bones are increasing in length, they are also increasing in diameter; growth in diameter can continue even after longitudinal growth ceases.
This growth by adding to the free surface of bone is called appositional growth. Appositional growth can occur at the endosteum or peristeum where osteoclasts resorb old bone that lines the medullary cavity, while osteoblasts produce new bone tissue.
The erosion of old bone along the medullary cavity and the deposition of new bone beneath the periosteum not only increase the diameter of the diaphysis but also increase the diameter of the medullary cavity. However, in adult life, bone undergoes constant remodeling, in which resorption of old or damaged bone takes place on the same surface where osteoblasts lay new bone to replace that which is resorbed.
Injury, exercise, and other activities lead to remodeling. Those influences are discussed later in the chapter, but even without injury or exercise, about 5 to 10 percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone. The severity of the disease can range from mild to severe. Those with the most severe forms of the disease sustain many more fractures than those with a mild form.
Frequent and multiple fractures typically lead to bone deformities and short stature. Bowing of the long bones and curvature of the spine are also common in people afflicted with OI. Curvature of the spine makes breathing difficult because the lungs are compressed. Because collagen is such an important structural protein in many parts of the body, people with OI may also experience fragile skin, weak muscles, loose joints, easy bruising, frequent nosebleeds, brittle teeth, blue sclera, and hearing loss.
There is no known cure for OI. Treatment focuses on helping the person retain as much independence as possible while minimizing fractures and maximizing mobility. Toward that end, safe exercises, like swimming, in which the body is less likely to experience collisions or compressive forces, are recommended.
Braces to support legs, ankles, knees, and wrists are used as needed. Canes, walkers, or wheelchairs can also help compensate for weaknesses. When bones do break, casts, splints, or wraps are used. In some cases, metal rods may be surgically implanted into the long bones of the arms and legs. Research is currently being conducted on using bisphosphonates to treat OI. Smoking and being overweight are especially risky in people with OI, since smoking is known to weaken bones, and extra body weight puts additional stress on the bones.
All bone formation is a replacement process. During development, tissues are replaced by bone during the ossification process. In intramembranous ossification, bone develops directly from sheets of mesenchymal connective tissue. In endochondral ossification, bone develops by replacing hyaline cartilage.
Activity in the epiphyseal plate enables bones to grow in length this is interstitial growth. Appositional growth allows bones to grow in diameter. Remodeling occurs as bone is resorbed and replaced by new bone. Considering how a long bone develops, what are the similarities and differences between a primary and a secondary ossification center? The periosteum continues its development and the division of cells chondrocytes continues as well, thereby increasing matrix production this helps produce more length of bone.
The stage of endochondral ossification. The following stages are: a Mesenchymal cells differentiate into chondrocytes. Perichondrium transforms into periosteum. Periosteal collar develops. Primary ossification center develops. During endochondral bone formation, mesenchymal tissue firstly differentiates into cartilage tissue. Endochondral bone formation is morphogenetic adaptation normal organ development which produces continuous bone in certain areas that are prominently stressed.
Therefore, this endochondral bone formation can be found in the bones associated with joint movements and some parts of the skull base.
In hypertrophic cartilage cells, the matrix calcifies and the cells undergo degeneration. In cranial synchondrosis, there is proliferation in the formation of bones on both sides of the bone plate, this is distinguished by the formation of long bone epiphyses which only occurs on one side only [ 2 , 14 ].
As the cartilage grows, capillaries penetrate it. This penetration initiates the transformation of the perichondrium into the bone-producing periosteum. Here, the osteoblasts form a periosteal collar of compact bone around the cartilage of the diaphysis. By the second or third month of fetal life, bone cell development and ossification ramps up and creates the primary ossification center , a region deep in the periosteal collar where ossification begins [ 4 , 10 ].
While these deep changes occur, chondrocytes and cartilage continue to grow at the ends of the bone the future epiphyses , which increase the bone length and at the same time bone also replaces cartilage in the diaphysis.
By the time the fetal skeleton is fully formed, cartilage only remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate, the latter of which is responsible for the longitudinal growth of bones.
After birth, this same sequence of events matrix mineralization, death of chondrocytes, invasion of blood vessels from the periosteum, and seeding with osteogenic cells that become osteoblasts occur in the epiphyseal regions, and each of these centers of activity is referred to as a secondary ossification center [ 4 , 8 , 10 ]. There are four important things about cartilage in endochondral bone formation: Cartilage has a rigid and firm structure, but not usually calcified nature, giving three basic functions of growth a its flexibility can support an appropriate network structure nose , b pressure tolerance in a particular place where compression occurs, c the location of growth in conjunction with enlarging bone synchondrosis of the skull base and condyle cartilage.
Cartilage grows in two adjacent places by the activity of the chondrogenic membrane and grows in the tissues chondrocyte cell division and the addition of its intercellular matrix. Bone tissue is not the same as cartilage in terms of its tension adaptation and cannot grow directly in areas of high compression because its growth depends on the vascularization of bone formation covering the membrane.
Cartilage growth arises where linear growth is required toward the pressure direction, which allows the bone to lengthen to the area of strength and has not yet grown elsewhere by membrane ossification in conjunction with all periosteal and endosteal surfaces.
Membrane disorders or vascular supply problem of these essential membranes can directly result in bone cell death and ultimately bone damage. Calcified bones are generally hard and relatively inflexible and sensitive to pressure [ 12 ].
Cranial synchondrosis e. Chondrogenesis is mainly influenced by genetic factors, similar to facial mesenchymal growth during initial embryogenesis to the differentiation phase of cartilage and cranial bone tissue.
This process is only slightly affected by local epigenetic and environmental factors. This can explain the fact that the cranial base is more resistant to deformation than desmocranium. Local epigenetic and environmental factors cannot trigger or inhibit the amount of cartilage formation. Both of these have little effect on the shape and direction of endochondral ossification. This has been analyzed especially during mandibular condyle growth.
Local epigenetics and environmental factors only affect the shape and direction of cartilage formation during endochondral ossification Considering the fact that condyle cartilage is a secondary cartilage, it is assumed that local factors provide a greater influence on the growth of mandibular condyle. Chondrogenesis is the process by which cartilage is formed from condensed mesenchyme tissue, which differentiates into chondrocytes and begins secreting the molecules that form the extracellular matrix [ 5 , 14 ].
The statement below is five steps of chondrogenesis [ 8 , 14 ]: Chondroblasts produce a matrix: the extracellular matrix produced by cartilage cells, which is firm but flexible and capable of providing a rigid support. Cells become embed in a matrix: when the chondroblast changes to be completely embed in its own matrix material, cartilage cells turn into chondrocytes. The new chondroblasts are distinguished from the membrane surface perichondrium , this will result in the addition of cartilage size cartilage can increase in size through apposition growth.
Chondrocytes enlarge, divide and produce a matrix. Cell growth continues and produces a matrix, which causes an increase in the size of cartilage mass from within. Growth that causes size increase from the inside is called interstitial growth.
The matrix remains uncalcified: cartilage matrix is rich of chondroitin sulfate which is associated with non-collagen proteins. Nutrition and metabolic waste are discharged directly through the soft matrix to and from the cell. The membrane covers the surface but is not essential: cartilage has a closed membrane vascularization called perichondrium, but cartilage can exist without any of these.
This property makes cartilage able to grow and adapt where it needs pressure in the joints , so that cartilage can receive pressure.
Endochondral ossification begins with characteristic changes in cartilage bone cells hypertrophic cartilage and the environment of the intercellular matrix calcium laying , the formation which is called as primary spongiosa. Blood vessels and mesenchymal tissues then penetrate into this area from the perichondrium. The binding tissue cells then differentiate into osteoblasts and cells. Chondroblasts erode cartilage in a cave-like pattern cavity.
The remnants of mineralized cartilage the central part of laying the lamellar bone layer. The osteoid layer is deposited on the calcified spicules remaining from the cartilage and then mineralized to form spongiosa bone, with fine reticular structures that resemble nets that possess cartilage fragments between the spicular bones.
Spongy bones can turn into compact bones by filling empty cavities. Both endochondral and perichondral bone growth both take place toward epiphyses and joints. In the bone lengthening process during endochondral ossification depends on the growth of epiphyseal cartilage. When the epiphyseal line has been closed, the bone will not increase in length. Unlike bone, cartilage bone growth is based on apposition and interstitial growth.
In areas where cartilage bone is covered by bone, various variations of zone characteristics, based on the developmental stages of each individual, can differentiate which then continuously merge with each other during the conversion process.
Environmental influences co: mechanism of orthopedic functional tools have a strong effect on condylar cartilage because the bone is located more superficially [ 5 ]. Cartilage bone height development occurs during the third month of intra uterine life. Cartilage plate extends from the nasal bone capsule posteriorly to the foramen magnum at the base of the skull.
It should be noted that cartilages which close to avascular tissue have internal cells obtained from the diffusion process from the outermost layer.
This means that the cartilage must be flatter. In the early stages of development, the size of a very small embryo can form a chondroskeleton easily in which the further growth preparation occurs without internal blood supply [ 1 ].
During the fourth month in the uterus, the development of vascular elements to various points of the chondrocranium and other parts of the early cartilage skeleton becomes an ossification center, where the cartilage changes into an ossification center, and bone forms around the cartilage.
Cartilage continues to grow rapidly but it is replaced by bone, resulting in the rapid increase of bone amount. Finally, the old chondrocranium amount will decrease in the area of cartilage and large portions of bone, assumed to be typical in ethmoid, sphenoid, and basioccipital bones.
The cartilage growth in relation to skeletal bone is similar as the growth of the limbs [ 1 , 3 ]. Longitudinal bone growth is accompanied by remodeling which includes appositional growth to thicken the bone. This process consists of bone formation and reabsorption. Bone growth stops around the age of 21 for males and the age of 18 for females when the epiphyses and diaphysis have fused epiphyseal plate closure. Normal bone growth is dependent on proper dietary intake of protein, minerals and vitamins.
A deficiency of vitamin D prevents calcium absorption from the GI tract resulting in rickets children or osteomalacia adults. Osteoid is produced but calcium salts are not deposited, so bones soften and weaken. At the length of the long bones, the reinforcement plane appears in the middle and at the end of the bone, finally produces the central axis that is called the diaphysis and the bony cap at the end of the bone is called the epiphysis.
Between epiphyses and diaphysis is a calcified area that is not calcified called the epiphyseal plate. Epiphyseal plate of the long bone cartilage is a major center for growth, and in fact, this cartilage is responsible for almost all the long growths of the bones. This is a layer of hyaline cartilage where ossification occurs in immature bones. On the epiphyseal side of the epiphyseal plate, the cartilage is formed. On the diaphyseal side, cartilage is ossified, and the diaphysis then grows in length.
The epiphyseal plate is composed of five zones of cells and activity [ 3 , 4 ]. Near the outer end of each epiphyseal plate is the active zone dividing the cartilage cells. Some of them, pushed toward diaphysis with proliferative activity, develop hypertrophy, secrete an extracellular matrix, and finally the matrix begins to fill with minerals and then is quickly replaced by bone.
As long as cartilage cells multiply growth will continue. Finally, toward the end of the normal growth period, the rate of maturation exceeds the proliferation level, the latter of the cartilage is replaced by bone, and the epiphyseal plate disappears. At that time, bone growth is complete, except for surface changes in thickness, which can be produced by the periosteum [ 4 ].
Bones continue to grow in length until early adulthood. The lengthening is stopped in the end of adolescence which chondrocytes stop mitosis and plate thins out and replaced by bone, then diaphysis and epiphyses fuse to be one bone Figure 7.
The rate of growth is controlled by hormones. When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces the cartilage, longitudinal growth stops. All that remains of the epiphyseal plate is the epiphyseal line. Epiphyseal plate closure will occur in year old females or year old males. Oppositional bone growth and remodeling. The epiphyseal plate is responsible for longitudinal bone growth. The cartilage found in the epiphyseal gap has a defined hierarchical structure, directly beneath the secondary ossification center of the epiphysis.
By close examination of the epiphyseal plate, it appears to be divided into five zones starting from the epiphysis side Figure 8 [ 4 ]: The resting zone: it contains hyaline cartilage with few chondrocytes, which means no morphological changes in the cells.
The proliferative zone: chondrocytes with a higher number of cells divide rapidly and form columns of stacked cells parallel to the long axis of the bone.
The hypertrophic cartilage zone: it contains large chondrocytes with cells increasing in volume and modifying the matrix, effectively elongating bone whose cytoplasm has accumulated glycogen. The resorbed matrix is reduced to thin septa between the chondrocytes.
The calcified cartilage zone: chondrocytes undergo apoptosis, the thin septa of cartilage matrix become calcified. The ossification zone: endochondral bone tissue appears.
Blood capillaries and osteoprogenitor cells from the periosteum invade the cavities left by the chondrocytes. The osteoprogenitor cells form osteoblasts, which deposit bone matrix over the three-dimensional calcified cartilage matrix. Epiphyseal plate growth. Five zones of epiphyseal growth plate includes: 1. The key difference between interstitial and appositional growth is that interstitial growth is the longitudinal growth of bone which increases the length of the bone while appositional growth is the bone growth which increases the diameter of the bone.
Bones can grow. They can increase in length as well as in diameter or thickness. Moreover, they are highly active organs which can repair themselves when injured. Bones are formed from cartilages. We call this process ossification. Soft cartilages gradually turn into hard bones. Overview and Key Difference 2. What is Interstitial Growth 3. What is Appositional Growth 4. Similarities Between Interstitial and Appositional Growth 5. Interstitial growth is a bone growth which results in the lengthening of the bone.
This growth occurs within the lacunae. It happens due to the cell division in the proliferative zone and the maturation of cells in the zone of maturation. Cartilage lengthens and is replaced by bone tissue during interstitial growth.
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