How The Strength And Bmd Is Maintained

| - osteoblasts begin to replace the fibrocartilage splint with spongy and compact bone, forming a bulge that is initially wider than the original bony shaft

The 2 types of cells are dependent on each other for production and linked in the process of bone remodeling. Osteoblasts not only secrete and mineralize osteoid but also appear to control the bone resorption carried out by osteoclasts. Osteocytes, which are terminally differentiated osteoblasts embedded in mineralized bone, direct the timing and location of bone remodeling. In osteoporosis, the coupling mechanism between osteoclasts and osteoblasts is thought to be unable to keep up with the constant microtrauma to trabecular bone. Osteoclasts require weeks to resorb bone, whereas osteoblasts need months to produce new bone. Therefore, any process that increases the rate of bone remodeling results in net bone loss over

The skeletal system supports the body shape and helps in movement. Skeletons are a dynamic tissue, constantly rebuild and reabsorb throughout lifetime (Karsenty and Wagner, 2002). Bone formation (osteogenesis), growth and remodeling are highly dependent on new blood vessel formations (angiogenesis) (Brandi and Collin-Osdoby, 2006). Notably, angiogenesis plays a major role in fracture healing and repair. Moreover imbalance of the vasculature leads to progression of numerous bone diseases (osteoporosis, osteonecrosis, rheumatoid arthritis, bone cancer and metastasis)(Carulli et al., 2013). In angiogenesis, avascular region of the tissue is hypoxic and secretes angiogenic factors to induce the new blood vessel formation form existing ones (Potente et al., 2011). The inner layer of blood vessel is covered by endothelial cells (ECs) and shielded by perivascular cells (pericytes and smooth muscle cells) and outer layer is directly connected to the vascular beads (Carmeliet and Jain, 2011). Further, the vessel formation, architecture and function are varying in organ specific manner (Rocha and Adams, 2009). Signal from perivascular

Bone at the tissue level undergoes remodeling: it is continuously being resorbed and rebuilt (or formed). A negative balance between bone resorption and formation, frequently due to excessive resorption, is the basis of many bone diseases.

The word Osteoporosis literally means “porous bone” (Martini, Nath, & Bartholomew, 2014). When looked at closely with the use of a microscope, a bone that has not lost an adequate amount of bone mass as it does in Osteoporosis, resembles a honey comb (What is Osteoporosis and What Causes it?, 2016). Once osteoporosis takes place and the bone loses mass or density, the holes and spaces in the honeycomb become much larger than they would be in healthy bone (What is Osteoporosis and What Causes it?, 2016). In the femur, osteoporotic changes would appear as a diminishing of the outer layer of compact bone around the epiphyses and diminishing of the bony collar around the diaphysis (Osteoporosis, 2014). There would likewise be loss of cancellous

Osteoblasts helpt the ossification of the bones and more in particularly the lengthening of the bones. Ossification is a development process taking place between 0 and 20 years to gradually harden and lengthen the bones. Young children have more flexible cartilage. Osteoblasts absorb calcium from the blood and lay it down as small plates in the cartilage in both directions. This causes the bone to

Subsequently following in bone deformation past the yield point and consequently, inflammation that results in apoptosis of osteocytes and loss of homeostasis of the bone matrix (see fig 5). Bone then hypermineralises (>66% mineral) and considering that bone is characteristically an inflexible structure with a low strain tolerance to rupture ~4% cortical bone and 5% in cancellous bone (Mc Nally, 2014).

Successful bone grafts includes osteo-conduction (growth of the natural bone), osteo-induction (enhancing undistinguishable cells toturn into active osteoblasts), and osteo-genesis (cells of living bone in the graft material give bone makeover). Osteo-genesis happens with auto-graft only. (5)

The function of all three help is to maintain calcium homeostasis and provide enough calcium to effectively maintain bone strength. In an depth analysis on bone and bone structure; the dynamics of calcium homeostasis are simplified; “When blood calcium levels decrease below normal, calcium is released from the bones so that there will be an adequate supply for metabolic needs. When blood calcium levels are increased, the excess calcium is stored in the bone matrix. The dynamic process of releasing and storing calcium goes on almost continuously, and is carried out by different bone cells” (Gray-Wilson & Wilkin, 2016, p. 9). Osteoblasts assist this calcium homeostasis by forming into osteocytes when trapped in the bone matrix, and cause the under stimulation of the production of osteoid. With less focus on the production osteoid, attention is directed to the production of calcium and the directing of calcium into the blood where it is transported to provide for numerous functions in various other systems of the body. When calcium levels begin to decrease again, the cycle begins anew when osteoclasts break down the bone matrix to dissolve calcium

Cancellous bone is more active and is broken down and regenerated more quickly than compact bone. Because of this, cancellous bone is more likely to be affected when the break down and regeneration of bone are out of balance in osteoporosis. The cells that are responsible for the BMD to stay constant is osteoblasts and osteoclasts. The function of osteoblasts is that it produces new bone matrix in a process called ossification while osteoclasts are cells that remove and recycle bone matrix. For a normal bone, there is a balance between the action of osteoblasts and osteoclasts but in osteoporotic bone, the activity of the osteoclasts in removing bone matrix is faster than the osteoblasts can form a new bone matrix. This results in a net bone lose. Osteoporosis can also lead to thinning of both the compact bone and cancellous bone which makes bone more fragile to

The biological process of osseointegration following the creation of an osteotomy site includes blood clot formation and the release of growth factors (BMP’s, VEGF etc.); this is followed by new blood vessel formation (Angiogenesis). The presence of a fibrin scaffold between the osteotomy site and the surface of the implant serves as a transition between the bone marrow (where the osteoprogenitor cells are located) and the surface of the implant, which is a very important factor in the migration of osteoprogenitor cells into the bone-implant interface zone. When the cells get there, they begin the deposition of lamellar bone and then the formation of a more mature bone on the surface of the implant to achieve a good osseointegration. The reason

Bone repair happens when there is an existing fracture in a bone. The first process in bone repair is when a clotting process begins in the fractured area of the bone in which it forms the hematoma or a blood filled swelling. This connects the bone’s blood vessels together after it had been destroyed by the fracture. The next process is when the break is splintered by the fibrocartilage callus made by fibrous tissue and cartilage which was formed by the action of fibroblasts. After that, the fibrocartilage callus was converted to a bony callus made up of a spongy bone. The final process of bone repair is when the bony callus was remodeled by the action of both osteoblast and osteoclast.

Last, but not least, the ability of bone to change its structure and adapt to mechanical loads implies that mechanical forces can regulate bone resorption and formation: increased loads should increase formation and decrease resorption whereas unloading should have the opposite effect. Indeed, immobilization stimulates resorption and suppresses formation (for review, see ref, providing a clear example of “uncoupling” between the two processes. The mechanism for these effects has not been elucidated fully, but, here again, osteoblast lineage cells, osteocytes, and lining cells were proposed to mediate the mechanical signals because their location is best suited to perceive

thesis project. A description of the biology of bone will be provided first and its focus

This paper summarizes the process and implications of bone remodeling as proposed by Svetalana V. Komarova, Robert J. Smith, S. Jeffrey Dixon, Stephan M Sims, and Lindi M. Wahl. Bone remodeling in the human body is an intricate process where osteoclasts resorb existing mineralized tissue and osteoblasts form new bone. Bone remodeling involves various interactions between different cells in the osteoclasts and osteoblasts. A problem occurs when these interactions are disturbed and can lead to numerous different bone disorders such as osteoporosis, osteoarthritis, or Paget’s disease. Manipulating Frost’s mechanostat theory, a theory that describes bone biology, and its corresponding biomechanical mathematical models of bone, Komoarova, Smith, Dixon, Sims, and Wahl were able to form their own model that allowed them to analyze how a change in interactions between cells can affect the bone remodeling process.