Deposited bone takes how long to harden

Provide structural support for the body Provide protection of vital organs Provide an environment for marrow where blood cells are produced Act as a storage area for minerals such as calcium.

Bones are made of two tissue types:. Compact bone: also known as cortical bone, this hard-outer layer is strong and dense Cancellous bone: also known as trabecular bone, this spongy inner layer network of trabeculae is lighter and less dense than cortical bone.

Bones are composed of:. Osteoblasts and Osteocytes: these are bone forming cells Osteoclasts: these are bone resorbing cells Osteoid: this is the non-mineral, organic part of the bone matrix made of collagen and non-collagenous proteins Inorganic mineral salts deposited within the matrix.

Bone Cells. Cells in our bones are responsible for bone formation, resorption, maintenance and re- modelling: Osteoblasts: These cells are derived from mesenchymal stem cells and are responsible for bone matrix synthesis and its subsequent mineralization.

In the adult skeleton, the majority of bone surfaces that are not undergoing formation or resorption i. Osteocytes: These cells are osteoblasts that become incorporated within the newly formed osteoid, which eventually becomes calcified bone.

Osteocytes situated deep in bone matrix maintain contact with newly incorporated osteocytes in osteoid, and with osteoblasts and bone lining cells on the bone surfaces, through an extensive network of cell processes canaliculi. They are thought to be ideally situated to respond to changes in physical forces upon bone and to transduce messages to cells on the bone surface, directing them to initiate formation or resorption responses.

Most experts recommend at least 1, milligrams of calcium and to 1, international units of vitamin D a day. Your health care provider may recommend a supplement to give you the calcium and vitamin D you need. Some recommendations call for much higher doses of vitamin D, but many experts feel that high doses of vitamin D are not safe for everyone.

In addition, very high amounts calcium in your diet can lead to health problems such as constipation, kidney stones, and kidney damage. If you are concerned about bone health, be sure to discuss with your provider whether supplements of calcium and Vitamin D are a good choice for you. People who have gut-related diseases inflammatory bowel disease, gastric bypass surgery , parathyroid gland disease, or are taking certain medications may need different recommendations for calcium and vitamin D supplementation.

Talk to your provider if you are unsure about how much calcium and vitamin D to take. Follow a diet that provides the proper amount of calcium, vitamin D, and protein. These nutrients will not completely stop bone loss, but they will help ensure that your body has the materials it needs to build bones.

Remaining fit and active can also protect bones and keep them stronger. Avoiding smoking also protects bones and keeps them stronger. Bone strength and calcium; Osteoporosis - calcium and bones; Osteopenia - calcium and bones; Bone thinning - calcium and bones; Low bone density - calcium and bones. Clinical practice: postmenopausal osteoporosis. Bone spurs usually occur in response to a particular stress at the site of the spur.

The body will lay down bone if a tendon, ligament or tissue becomes tight and puts increased tension at the attachment site. A heel spur in the foot is an example of a traction spur.

If a joint becomes loose or unstable such as the spine, the body will develop spurs in an attempt to create stability of the joint complex. The pain is often coming from the muscle, tendon, nerve or ligament around the spur. Some studies reveal that older people are more likely to display bone spurs, however spurs can occur in young athletically active people secondary to the athletic stress placed on the soft tissues attaching to the spur site.

Bone spurs are commonly associated with the following conditions osteoarthritis, spinal stenosis, spondylosis or plantar fasciitis. In comparison to traction bone spurs, calcium deposits are small, dense areas of calcium that can form after a bone or tissue is stressed or damaged. When an injury or stress occurs, calcium travels through the bloodstream to the injured area to help repair damage.

In some cases, the damaged area may receive more calcium than is needed. In other cases the microcirculation of the tissue is congested due to the injury. This will allow calcium to get into the tissue but the exiting circulation is restricted and therefore the excess calcium cannot get out. 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.

When bones are increasing in length, they are also increasing in diameter; diameter growth can continue even after longitudinal growth stops. This is called appositional growth. The bone is absorbed on the endosteal surface and added to the periosteal surface. Osteoblasts and osteoclasts play an essential role in appositional bone growth where osteoblasts secrete a bone matrix to the external bone surface from diaphysis, while osteoclasts on the diaphysis endosteal surface remove bone from the internal surface of diaphysis.

The more bone around the medullary cavity is destroyed, the more yellow marrow moves into empty space and fills space. Osteoclasts resorb the old bone lining the medullary cavity, while osteoblasts through intramembrane ossification produce new bone tissue beneath the periosteum. Periosteum on the bone surface also plays an important role in increasing thickness and in reshaping the external contour.

The erosion of old bone along the medullary cavity and new bone deposition under the periosteum not only increases the diameter of the diaphysis but also increases the diameter of the medullary cavity. This process is called modeling Figure 9 [ 3 , 4 , 15 ].