After their job is accomplished, the osteoclast undergo apoptosis. This process proceed to the reversal stage, during which coupling signals are sent to attract osteoblast into resorptive sites. Resorption is then turned off and the formation stage follows. The osteoclasts synthesize bone matrix and facilitate its mineralization. Calcium and phosphate ion are deposited into the matrix, leading to hardening of the bone.
The growth hormone also achieves the growth discs: the growth hormone stimulates the cartilage cells to produce growth factors. The cartilage cells then divide themselves. The new cartilage cells push out the ends of the bone, so the bone at the ends becomes longer, bit by bit. The growth process summarized: The pituitary gland is a growth hormone. The growth hormone stimulates cells to produce growth factor (IGF-I).
Third, hard callus forms when osteoblasts produce trabeculae and the callus is replaced by this bone. Bone will continue to grow and thicken. Finally, remodeling is the final phase of fracture repair. During the final phase osteoclasts remove excess bony material from both exterior and interior surfaces. Compact bone is now replaced by primary bone.
This accordance is one of the most important features of skeletal muscles. Muscle mass is the primary indicator of muscle strength and it is not stable. There is continuous process that includes the balance between protein synthesis and catabolism, which determines hypertrophy or atrophy (Blaauw et al., 2013). Increase in muscle proteins during muscle hypertrophy occurs because of either increasing RNA and protein synthesis by existing nuclei or preserving of the same level RNA and protein synthesis from each nuclei and new myonuclei addition to fibers. Because mature muscle fiber myonuclei cannot divide, source of new myonuclei added to fiber is the external of the fiber.
• Osteoclasts are used to break done bone matrix and prevent a build up of too much of it and also helps bones to maintain a proper shape. These two cells found the in bones also deposits or removes minerals from the bones, and also help control the amount of these minerals in the blood. Osteosarcoma is the most common type of cancer that develops in bone ("Osteosarcoma | Osteosarcoma Causes, Treatment, Cure, Symptoms, Prevention | Modasta", 2017). The cells that are involved in causing this type of cancer are like the osteoblasts in normal bone, the cells that form this cancer make bone matrix. Therefore, the bone matrix of an osteosarcoma is not as strong as that of normal bones because most of osteosarcomas happen in children and young adults.
P4 – Describe the three structures of the skeletal muscle (Epimysium, Perimysium and Endomysium) There are three structures of the skeletal muscle: Epimysium is a thick layer of irregular connective tissue that pulls the entire muscle as well as protecting the muscle from friction that may be caused by other muscles and bones surrounding them. Also, it is the fibrous tissue which covers and surrounds skeletal muscles. The Epimysium carries on past the end of bones in order to create muscle tendons. Perimysium surrounds a bundle of muscle fibres, it is a casing of connective tissue. Endomysium is found within a muscle and it contains nerves and capillaries.
The continuum model contain three distinct stages- reactive, disrepair and degenerative tendinopathies. The progression through each stage will inhibit the pathological areas ability to recover. Progression through the stages is dependent on load and internal factors such as genetics and other predisposed pathological illnesses such as including adiposity, cholesterol, insulin resistance, diabetes and menopause (cook and Bass et al 2007). Reactive tendinopathy is a short term response to acute overload and will lead to a inflammatory response. Proteoglycan contents within the extracellular matrix are increased however collagen will only undergo a small amount of change.
The FGFR3 protein spans across the cell membrane resulting in one end inside the cell and the other outside the cell allowing the protein to interact with growth factors outside the cell and receive signals for growth and development. The FGFR3 protein in the bone cells help control bone growth through a process previously mentioned called ossification, where cartilage is transformed into bone using calcium. When growth factors bind to the FGFR3, the protein is activated and FGFR3 is able to regulate ossification. When the Gly380Arg mutation occurs, it results in the FGFR3 protein being absent or damaged therefore preventing it from interacting with external growth factors causing the loss of control of ossification. This causes problems during bone development where cartilage fails to turn into bone.
Many concerns have centered in on the possible links between repeated concussions and chronic traumatic encephalopathy or CPE. Chronic traumatic encephalopathy is a serious, degenerative brain disease that affects a person’s ability to think. Chronic traumatic encephalopathy involves the progressive brain damage, particularly in the frontal region of the brain, which controls many functions including people’s judgement, emotion, impulsive control, social behavior and their memory. A signature feature of the disease is abnormal deposits of a protein called tau that accumulates around small blood vessels in brain crevices. Researchers believe that multiple blows to the head may dislodge the tau protein from the cell structure and cause it to form in clumps inside nerve cells.
Located underneath the lamina, mono-nucleated cells are stimulated as the muscle tissue is damaged. The stimulation causes the cells to divide and proceed to fuse with already present muscle fibres in order to repair and regenerate the damaged fibres. Muscle fibres use hypertrophy to lay down new protein and enlarge as they are unable to divide