Biomechanical and Molecular Regulation of Bone Remodeling

Abstract

Bone is a dynamic tissue that is constantly renewed. The cell populations that participate in this process--the osteoblasts and osteoclasts--are derived from different progenitor pools that are under distinct molecular control mechanisms. Together, these cells form temporary anatomical structures, called basic multicellular units, that execute bone remodeling. A number of stimuli affect bone turnover, including hormones, cytokines, and mechanical stimuli. All of these factors affect the amount and quality of the tissue produced. Mechanical loading is a particularly potent stimulus for bone cells, which improves bone strength and inhibits bone loss with age. Like other materials, bone accumulates damage from loading, but, unlike engineering materials, bone is capable of self-repair. The molecular mechanisms by which bone adapts to loading and repairs damage are starting to become clear. Many of these processes have implications for bone health, disease, and the feasibility of living in weightless environments (e.g., spaceflight).

Biomechanics of phalangeal curvature

“…Biewener et al (1986: 393) note that "the state of strain within and along the bone's length likely represents an important stimulus for adjustments in bone mass and shape during postnatal growth." These data and others (e.g., Rubin and Lanyon, 1985b;Rohling et al, 2006) suggest that the biomechanical consequences of using the hands and feet in arboreal and terrestrial settings influence phalangeal development.…”

Bone morphology allows estimation of loading history in a murine model of bone adaptation

“…If this indeed is an important factor, better results would be expected for bone in older subjects that might be more adapted to their loading history. But also in fully grown bone, other factors of biological nature like calcium homeostasis or sex hormones could be physiologically more important than a bone structure perfectly adapted to its loading regime (Beaupre et al 1990;Frost 1987;Harada and Rodan 2003;Manolagas 2000;Robling et al 2006).…”

“…We assume that bone adapts to its internal architecture in order to achieve a uniform tissue loading that we quantified as SED. Several other candidates for the mechanical signal have been proposed, such as fluid flow shear stress (Burger and Klein-Nulend 1999;Burra and Jiang 2009;Rath et al 2010) or micro-damage (Mori and Burr 1993;Robling et al 2006). However, earlier studies have demonstrated that the choice of the mechanical signal is not very critical since most of these signals are highly correlated (Ruimerman et al 2005).…”

Exercise loading history and femoral neck strength in a sideways fall: A three-dimensional finite element modeling study

“…Therefore, to comply with valid QCT-based proximal femur FE modeling studies, we adopted similar BCs and loading conditions [22,28]. In the present study, however, trabecular bone was modeled as a non-porous homogeneous structure in contrast to its actual non-uniform structure [63], which could cause < 10% error in the maximum stress reported in the literature [19]. However, according to Koivumäki et al, inclusion of the trabecular bone in the sideways falling FE models may not play a crucial role, and the proximal femoral strength can be…”