Remodeling of bone

Once the skeleton is formed, continual remodelling of bone tissue maintains structural integrity and creates more orderly tissue structures. Remodelling involves coupled resorption and formation on all bone surfaces in a well-defined sequence of events. The remodelling sequence has been described as activation of the surface, resorption by osteoclasts, reversal, formation by osteoblasts, and return to quiescence of the surface. In... 

Calcium is the major mineral component of bone and normal repair and remodelling of bone is reliant on an adequate supply of this mineral. Calcium uptake in the gut, loss through the kidneys and turnover within the body are controlled by hormones, notably PTH and 1,25 dihydroxy cholecalciferol (1,25 DHCC or 1,25 dihydroxy vitamin D3 or calcitriol). Refer to Figure 8.12 for a summary of the involvement of PTH and vitamin D3 in controlling plasma calcium concentration. These two major hormones have complementary actions to raise plasma calcium concentration by promoting uptake in the gut, reabsorption in the nephron and bone resorption. Other hormones such as thyroxine, sex steroids and glucocorticoids (e.g. cortisol) influence the distribution of calcium. 

Calcium and phosphate, the major mineral constituents of bone, are also two of the most important minerals for general cellular function. Accordingly, the body has evolved a complex set of mechanisms by which calcium and phosphate homeostasis are carefully maintained (Figure 42-1). Approximately 98% of the 1-2 kg of calcium and 85% of the 1 kg of phosphorus in the human adult are found in bone, the principal reservoir for these minerals. These functions are dynamic, with constant remodeling of bone and ready exchange of bone mineral with that in the extracellular fluid. Bone also serves as the principal structural support for the body and provides the space for hematopoiesis. Thus, abnormalities in bone mineral homeostasis can lead not only to a wide variety of cellular dysfunctions (eg, tetany, coma, muscle weakness) but also to disturbances in structural support of the body (eg, osteoporosis with fractures) and loss of hematopoietic capacity (eg, infantile osteopetrosis). 

Whalen JP, O Donohue N, Krook L, et al. 1973. Pathogenesis of abnormal remodeling of bones Effects of yellow phosphorus in the growing rat. Anat Rec 177 15-22. 

Modulates cell proliferation, differentiation, matrix synthesis, apoptosis initiates, promotes, and regulates the development, growth, and remodeling of bone and cartilage Induces bone and cartilage formation plays an important role in cardiac morphogenesis... 

The remodeling of bone structure results from the activities of osteoblasts and osteoclasts, which provide constant deposition and re-adsorption of bone matrix, respectively. This occurs through a phenomenon known as Wolffs Law in response to the application of weight bearing loads, often through daily routines such as walking or exercising, osteoblasts and osteoclasts will remodel bone structure [18,19],... 

Jowsey, J. (1971) The internal remodeling of bones, in The Biochemistry and Physiology of Bone III Development and Growth (ed. G.H. Bourne), Academic Press, New York, pp. 201-238. 

A more positive control of calcium ion concentration is brought about by the cell-mediated resorption or deposition of stable bone material. These adjustments are slower, but quantitatively greater, than the simple exchange reaction. They take place with great precision with regard to the sites in the bone where resorption and deposition occur, their timing and the constancy of plasma ion concentration achieved. The process thus provides for both the continuous remodelling of bone and for the calcium-phosphorus homoeostasis of the blood and tissue fluids. The former depends on the position on the bone surface of various stimulated cells and the latter on the net result of stimulation of cells in bone, intestine and kidney by parathyroid hormone, calcitonin and vitamin D. The mode of action of these substances and the interplay of their various effects are complex. 

The amplitude of static (constant) magnetic can be a cause of changing the internal remodeling of bone. In order to investigate this effect, various values of amplitude were applied to the model and the model was run under these conditions. The amplitude values were chosen to be v /= -1, -0.5, 0, 0.5, 1 Amperes (A). The result of this simulation is shown in Fig. 4. 

Bone consists of three kinds of cells osteoblasts, osteoclasts, and osteocytes. Osteoblasts are derived from mesoderm-specific progenitor cells and synthesize ECM associated with bone. Osteocytes are osteoblasts that become embedded within the bone matrix. Osteoclasts (from hematopoietic lineage) degrade bone matrix using a combination of proteases and are instrumental in resorption of bone and regulation of Ca + balance in serum. The antagonistic activity of osteoblasts and osteoclasts is critical in the remodeling of bone tissue. 

Cell activity, of the bone tissue in particular, is closely connected to mechanical stimuli. This effect is now well established, based on observations that in the absence of mechanical stress the remodeling of bones tends to slow down. The implant integration in the bone tissue depends also on biomechanical factors. Besides, since the Young s modulus of ceramics is generally much higher than that of the bone tissue, the implant can cause mechanical stresses at the bone interface. Moreover, it produces a modification of the lines of force (stress shielding) which can result in bone defects close to the implant. This phenomenon is sometimes visible in x-rays and manifests itself by a diminution of the bone density near the implant related to the lack of mechanical stimulation of the tissue. 

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