Bone Remodeling Essay

An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as OSTEOPOROSIS.

Osteoporosis develops when the remodeling cycle, which is when the disruption of the bone resorption and bone formation occurs. The imbalance of the remodeling cycle causes osteoporosis. Hormones, cytokines, and paracrine stromal-cell interactions affect the osteoclast’s processes, which includes proliferation, maturation, fusion and activation. The osteoclasts are controlled by the interaction between several interleukins, tumor necrosis factor, transforming growth factor-beta, prostaglandin E2 and hormones. The glucocorticoid-induced osteoporosis is related to increased destruction of osteocytes. Glucocorticoid increase receptor activator of nuclear factor ligand (RANKL) effect and inhibit osteoprotegerin (OPG) production through

What are the roles of osteoclasts in bone formation? Osteoclasts are large cells that function to reabsorb, or to digest bone tissue. They digest bone tissue from the inner sides of bones thus enlarging the inner bone cavity so that the bone does not become overly thick and heavy.

The continuous high levels of PTH stimulate bone resorption by osteoclasts, but do so indirectly. The PTH will bind to the receptors located on the osteoblast, which then signal bone marrow-derived osteoclast precursors to differentiate into osteoclasts. This is done through the activity of RANKL binding to RANK. When stimulated by PTH, the osteoblasts up-regulate expression of RANKL which binds to RANK and activates osteoclast production. This process will result in high bone turnover and ultimately, bone resorption. Overall, there will be more activity in the resorption phase of the bone remodeling cycle.

According to Judith (2010), Osteoporosis is a loss of the reabsorption in the bones by way of calcium, plasma, and phosphate. Estrogen production helps bones metabolism by stimulating osteoblastic activity and limiting osteoclastic effects of the parathyroid hormone. It develops when the new formation of bones fall behind in the reabsorption process (Judith, 2010). In simpler terms, it’s a loss of bone mass due to a metabolic bone disorder affected by the rate of bone resorption advances while the rate of the bone formation reduces. According to Judith (2010), the bones end up losing calcium, phosphates and end up brittle making them prone to fractures and further complications (P . 236).

Throughout life the skeletal system is constantly changing. Bone modeling, formation and growth of bones, occurs from birth to early adulthood resulting in increase in skeletal mass and changes in skeletal form. Naturally the peak bone mass is achieved in the third decade of life, meaning the bones are at their strongest state in human development. Bone remodeling, a response to micro trauma and stress on the bone, is a dynamic process that also occurs through life. Bone is composed of collagen type 1, a protein, minerals such as calcium and phosphate and bone forming cells (osteoblasts and osteocytes) as wells as bone resorbing cells known as osteoclasts. Calcium is a main contributor of bone strength. In fact 99% of calcium is stored in bones and teeth with one percent remaining in the blood. The process of bone remodeling is activated by stressors such as weight bearing and is necessary to maintain bone mass in an adult. It’s a dynamic process in which bone resorption is always

PTH is released in response to low blood calcium levels. It increases calcium levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which are cells that cause bone to be reabsorbed, releasing calcium from bone into the blood. PTH also inhibits osteoblasts, cells which deposit bone, reducing calcium deposition in bone. In the intestines, PTH increases dietary calcium absorption and in the kidneys, PTH stimulates reabsorption of the calcium. While PTH acts directly on the kidneys to increase calcium reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels. Levels of estrogen peak during puberty and decrease with age. Until about age 30, a person normally builds more bone than he or she loses. After age 35, bone breakdown overtakes bone buildup, which causes a gradual loss of bone mass. Once this loss of bone reaches a certain point, a person has osteoporosis. In osteoporosis, bone tissue becomes brittle, thin, and spongy. Bones break easily, and the spine sometimes begins to crumble and

Introduction: Osteoporosis is a disease that disproportionately affects postmenopausal women. It is an important disease for public health to address as it greatly contributes to frailty and risk of injury, largely due to fractures, and the associated burdens on the health care system. Literally translating to “porous bones”, osteoporosis occurs when bones lose their density, and the inner bone matrix becomes much more brittle (Figure 1).1,2 Health adult bones are in a constantly dynamic state, with living cells that multiply to grow and repair bones as we age. Bones structurally consist of a hard, calcified outer layer, and an inner matrix made of collagen and non-collagen proteins.3 Healthy bone mass, and the structure of this inner matrix, is maintained through processes called resorption and remodeling.1 Resorption occurs as some cells dissolve bone matrix for the body to reabsorb and reuse the minerals, and remodeling occurs simultaneously as other cells deposit new bone matrix proteins to replace the dissolved minerals. Each remodeling activity is associated with a slight net loss in bone mass, and as such, healthy adults achieve peak bone density in their early 20s, and bone density gradually declines thereafter.1,4

The process of aging presents a plethora of health complications that must be understood and dealt with in an effective manner so as to sustain a positive quality of life for the increasing numbers of aging individuals within the world’s populations. These complications and conditions are quite varied in their severity and commonality. Osteoporosis, unfortunately, is both highly detrimental and exceedingly common, despite the many efforts made to prevent it. It is a disease of the bone, reducing bone qualities such as mass and density in such a way as to make the daily activities of life both risky and difficult. I will examine the exact pathophysiology of this disease later in this paper, but for the time being, let it

First of all, sex hormones play a crucial role in osteoporosis. For instance, when females' monthly periods stop, their estrogen levels will drop. Moreover, their bone density will decrease because estrogen (females' hormone) is important to maintain their bone healthy (3). Like females, the level of Testosterone hormone in males impacts the bones health. Second, lack of the calcium and vitamin D in people's daily meals. Calcium and vitamin D are both essential items to support the bone structure. Since the bones consist of calcium and without vitamin D the absorption of calcium will be less than the normal

There are numerous factors that contribute to the development of this horrible disease, but the most important factor is vitamin D deficiency. When the minerals in osteoid crystallize, they require adequate concentration of calcium and phosphate. When the concentration is not at the correct level, ossification does not proceed normally (Huether & McCance, 2008). Vitamin D regulates the absorption of calcium from the intestine. When there is a lack of vitamin D, the concentration of calcium begins to fall (Huether & McCance, 2008). The body begins to regulate this calcium drop by increases the amount of PTH synthesis and secretion (Huether & McCance, 2008). An increase of PTH causes a clearance of phosphate and without the correct levels of phosphate mineralization of the bones cannot proceed in the correct manor (Huether & McCance, 2008). The abnormality of bone growth can occur in spongy and compact bone (Mayo

Osteoporosis is defined by the World Health Organization as “a systemic skeletal disease characterized by low bone mass and microarchitecture deterioration of bone tissue with consequential increase in bone fragility and susceptibility to fracture” This condition is a result of an imbalance in the normal processes of “ bone formation” and “bone reabsorption” which work together to maintain bone strength.” (Leyland, S. 2013) The purpose of this paper is to educate the reader about bone and joint health and how it effects the elderly population. The topic of this paper is osteoporosis.

Although common, osteoporosis in a disease that can be prevented to an extent with modified lifestyle choices including nutrition and exercise. When considering bone health, the

Menopause comes a drop in defensive estrogen creation. For these females, hormone therapy is a treatment alternative. In any case, it is not commonly utilized as a first line of safeguarding. Particular Estrogen Receptor Modulators re-make the bone-protecting impact of estrogen. Thyrocalcitonin is a hormone made by the thyroid gland. The gland controls calcium levels in the body. Synthetic thyrocalcitonin, or calcitonin, is utilized to treat spinal osteoporosis in patients who cannot take bisphosphonates. It can likewise ease pain in a few patients with spinal fractures. The medication is accessible by nasal spray or injection. Parathyroid Hormone (PTH) controls calcium and phosphate levels in the bone. Medicines with a synthetic PTH like teriparatide can really advance new bone development. The medication is given by everyday infusion in mix with calcium and vitamin D supplements. This medication is extremely costly. As Williams state, “It is for the most part saved for patients with serious osteoporosis who have poor resistance for different medications”

This paper will discuss the composition and cells of bone, different types and organization of bone, bone remodeling, bone development in children, and bone fractures