Unlike most connective tissues, cartilage is avascular, meaning that it has no blood vessels supplying nutrients and removing metabolic wastes. All of these functions are carried on by diffusion through the matrix from vessels in the surrounding perichondrium , a membrane that covers the cartilage, a. As more and more matrix is produced, the cartilaginous model grow in size. Blood vessels in the perichondrium bring osteoblasts to the edges of the structure and these arriving osteoblasts deposit bone in a ring around the diaphysis — this is called a bone collar Figure 6.
The bony edges of the developing structure prevent nutrients from diffusing into the center of the hyaline cartilage. This results in chondrocyte death and disintegration in the center of the structure. Without cartilage inhibiting blood vessel invasion, blood vessels penetrate the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which will become osteoblasts.
These enlarging spaces eventually combine to become the medullary cavity. Bone is now deposited within the structure creating the primary ossification center Figure 6. This continued growth is accompanied by remodeling inside the medullary cavity osteoclasts were also brought with invading blood vessels and overall lengthening of the structure Figure 6.
By the time the fetal skeleton is fully formed, cartilage remains at the epiphyses and at the joint surface as articular cartilage. 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 occurs in the epiphyseal regions, and each of these centers of activity is referred to as a secondary ossification center Figure 6. Throughout childhood and adolescence, there remains a thin plate of hyaline cartilage between the diaphysis and epiphysis known as the growth or epiphyseal plate Figure 6.
Eventually, this hyaline cartilage will be removed and replaced by bone to become the epiphyseal line. The epiphyseal plate is the area of elongation in a long bone. It includes a layer of hyaline cartilage where ossification can continue to occur in immature bones. We can divide the epiphyseal plate into a diaphyseal side closer to the diaphysis and an epiphyseal side closer to the epiphysis. On the epiphyseal side of the epiphyseal plate, hyaline cartilage cells are active and are dividing and producing hyaline cartilage matrix.
On the diaphyseal side of the growth plate, cartilage calcifies and dies, then is replaced by bone figure 6. As cartilage grows, the entire structure grows in length and then is turned into bone.
Once cartilage cannot grow further, the structure cannot elongate more. The epiphyseal plate is composed of five zones of cells and activity Figure 6. The reserve zone is the region closest to the epiphyseal end of the plate and contains small chondrocytes within the matrix.
These chondrocytes do not participate in bone growth but secure the epiphyseal plate to the overlying osseous tissue of the epiphysis. The proliferative zone is the next layer toward the diaphysis and contains stacks of slightly larger chondrocytes.
It makes new chondrocytes via mitosis to replace those that die at the diaphyseal end of the plate. Chondrocytes in the next layer, the zone of maturation and hypertrophy , are older and larger than those in the proliferative zone. The more mature cells are situated closer to the diaphyseal end of the plate.
The longitudinal growth of bone is a result of cellular division in the proliferative zone and the maturation of cells in the zone of maturation and hypertrophy. Osteoblasts are bone-forming cells, osteocytes are mature bone cells and osteoclasts break down and reabsorb bone. Intramembranous ossification involves the replacement of sheet-like connective tissue membranes with bony tissue. Bones formed in this manner are called intramembranous bones.
They include certain flat bones of the skull and some of the irregular bones. The future bones are first formed as connective tissue membranes. Osteoblasts migrate to the membranes and deposit bony matrix around themselves. When the osteoblasts are surrounded by matrix they are called osteocytes. Endochondral ossification involves the replacement of hyaline cartilage with bony tissue.
Most of the bones of the skeleton are formed in this manner. These bones are called endochondral bones. 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.
The cells, which are pushed from the epiphysis, mature and are destroyed by calcification. This process replaces cartilage with bone on the diaphyseal side of the plate, resulting in a lengthening of the bone. Long bones stop growing at around the age of 18 in females and the age of 21 in males in a process called epiphyseal plate closure. During this process, cartilage cells stop dividing and all of the cartilage is replaced by bone.
The epiphyseal plate fades, leaving a structure called the epiphyseal line or epiphyseal remnant, and the epiphysis and diaphysis fuse. Appositional growth is the increase in the diameter of bones by the addition of bony tissue at the surface of bones. Osteoblasts at the bone surface secrete bone matrix, and osteoclasts on the inner surface break down bone.
The osteoblasts differentiate into osteocytes. A balance between these two processes allows the bone to thicken without becoming too heavy. Bone renewal continues after birth into adulthood. Bone remodeling is the replacement of old bone tissue by new bone tissue.
It involves the processes of bone deposition by osteoblasts and bone resorption by osteoclasts. Normal bone growth requires vitamins D, C, and A, plus minerals such as calcium, phosphorous, and magnesium. Hormones such as parathyroid hormone, growth hormone, and calcitonin are also required for proper bone growth and maintenance.
Bone turnover rates are quite high, with five to seven percent of bone mass being recycled every week. Differences in turnover rate exist in different areas of the skeleton and in different areas of a bone.
For example, the bone in the head of the femur may be fully replaced every six months, whereas the bone along the shaft is altered much more slowly. Figure 2. After this bone is set, a callus will knit the two ends together. Bone remodeling allows bones to adapt to stresses by becoming thicker and stronger when subjected to stress.
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