Bone adaptation

Figure Bl.12.16. HETCOR NMR spectra from (a) bnishite and (b) bone. (Adapted from [48] with...

Although many experiments have been performed, quantitative relationships between mechanical loads and bone adaptation do not yet exist. In vivo strain gauge studies have found a remarkable similarity of peak surface strains -2000 p.e at the midshaft of different bones across different animals at maximum activity. Measuring strains in adaptation studies would allow us to relate in vivo load changes to altered surface strains to adapted bone mass and strength. 

Fig. 1.6 (A and B) Scanning electron micro- implantation in the bone marrow showing for-graphs of the porous hydroxyapatite-collagen mation of new bone (white asterisk) attached nanocomposite scaffolds at different magnifi- directly to the nanocomposite (asterisk). Arrows cations. Arrowheads in B indicate the hydroxy- indicate cuboidal osteoblasts on the surface of apatite nanocrystals on the collagen fibrils. new bone. Adapted from [94], reproduced by Histology at (C) 1 week and (D) 4 weeks after permission of Wiley-VCH.

Figure 10.1 Gross structural features of human compact bone. (Adapted from Gartner and Hiatt, 1994 Graphic 4.1.)...

McLeod, K.J., Rubin, C.T., et.al.(1998) Skeletal cell stresses and bone adaptation. American Journal of Medical Science 316 176-183... 

Fig. 23a, b HETCOR NMR of bovine cortical bone (adapted from [28]) a a 2D spec-... 

Bones adapt to handle the workload to which they are subjected. Long-term exercise (hkely many years) during youth increases peak BMD. Physical activity, especially aerobics, weight... 

Normal bone loading exists in a physiological range of mechanical strain, where the Mechanostat will not activate and therefore will not trigger bone geometric adaptation. Two set-points, an upper strain level and a lower strain level, bound this physiological range and control the type of bone adaptation needed. 

The set-point concept of the Mechanostat allows this theory to describe bone adaptation from agents (hormones, diseases, drugs) that produce no mechanical stimulus. These agents can alter the location of one or both set-points, causing the Mechanostat to activate, although the bone experiences physiologically normal mechanical strain. 

In this phase, the newly formed bone adapts to its function of load bearing, and unwanted bone is removed. Dead bone that may be relevant to the structure of the limb is revitalized by recanalization with Haversian systems or replaced by creeping substitution, gradually recovering the electrical characteristics of the region. 

Cortical tissue is the dense part of bone. As a living entity, this material is able to maintain and adapt its stracture to external physical stimuli [1], The seat of bone remodeling mechanisms corresponds to cyhndrical stractuial elements called osteons. Each osteon is surrounded by a thin layer (cement line) and is centered on Haversian canal which runs primarily in the bone longitudinal axis. The Haversian canals contain the vasculature, the nerves and interstitial fluid. There are also Volkmann canals which are similar to Haversian canals except that they run along the transverse direction of the bone. At a smaller scale, other extravascular pores exist in the solid matrix of the bone forming the la-cuno-canalicular system. This porous network irrigates the mechano-sensitive osteocytes which are believed to play an important role in bone adaptation as stated in recent experimental studies [2,3,4]. 

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