Investigation of the regulation of bone mass by mechanical loading: from quantitative cytochemistry to gene array

2003 ◽  
Vol 21 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Tim M. Skerry ◽  
Larry J. Suva
Keyword(s):  
Bone Mass ◽  
Mechanical Loading ◽  
Gene Array ◽  
Quantitative Cytochemistry

Aging and the Osteogenic Response to Mechanical Loading

2001 ◽  
Vol 11 (s1) ◽  
pp. S137-S142 ◽  
Author(s):  
Wendy M. Kohrt
Keyword(s):  
Growth Factors ◽  
Bone Mass ◽  
Mechanical Loading ◽  
Bone Cells ◽  
Weight Bearing ◽  
Bone Modeling ◽  
Mineral Density ◽  
Increase Bone Mass ◽  
Age Related ◽  
Osteogenic Response

The osteogenic response to mechanical stress is blunted with aging. It has been postulated that this decline in responsiveness is related to (a) a limited ability to engender the strain necessary to reach the bone modeling threshold, due to decreased muscle mass and strength, and/or (b) a decline in certain hormones or growth factors that may interact with mechanical signals to change the sensitivity of bone cells to strain. There is reason to believe that both of these factors contribute to the reduced ability to increase bone mass through exercise with advancing age. Weight-bearing endurance exercise and resistance exercise have both been found to increase bone mass in older women and men. However, exercise training studies involving older individuals have generally resulted in increased bone mineral density only when the exercise is quite vigorous. There is also evidence that the osteogenic response to mechanical loading is enhanced by estrogens. Whether age-related changes in other factors (e.g., other hormones, growth factors, cytokines) also contribute to the reduced responsiveness of the aged skeleton to mechanical loading remains to be investigated.

scholarly journals Absence of mechanical loading in utero influences bone mass and architecture but not innervation in Myod-Myf5-deficient mice

2007 ◽  
Vol 210 (3) ◽  
pp. 259-271 ◽  
Author(s):  
Cédric Gomez ◽  
Valentin David ◽  
Nicola M. Peet ◽  
Laurence Vico ◽  
Chantal Chenu ◽  
...  
Keyword(s):  
Bone Mass ◽  
Mechanical Loading ◽  
In Utero ◽  
Deficient Mice

Regulation of bone mass by mechanical loading: Microarchitecture and genetics

2005 ◽  
Vol 3 (2) ◽  
pp. 46-51 ◽  
Author(s):  
Larry J. Suva ◽  
Dana Gaddy ◽  
Daniel S. Perrien ◽  
Ruth L. Thomas ◽  
David M. Findlay
Keyword(s):  
Bone Mass ◽  
Mechanical Loading

scholarly journals NaQuinate selectively synergises with in vivo mechanical loading stimuli to enhance cortical bone mass and architectural modifications

Bone Reports ◽  
2021 ◽  
Vol 14 ◽  
pp. 100885
Author(s):  
Behzad Javaheri ◽  
Amy Lock ◽  
Mark Hopkinson ◽  
Samuel Monzem ◽  
Yu-Mei Chang ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Mechanical Loading ◽  
Cortical Bone Mass

scholarly journals Influence of mechanical loading and skeleton geometry in bone mass at the proximal femur in 10[ndash]12 years old children: a longitudinal study

2013 ◽  
Author(s):  
Graca Cardadeiro ◽  
Fatima Baptista ◽  
Nicolleta Rosati ◽  
Vera Zymbal ◽  
Lurdes Rebocho ◽  
...  
Keyword(s):  
Longitudinal Study ◽  
Bone Mass ◽  
Mechanical Loading ◽  
Proximal Femur

scholarly journals Applied mechanical loading to mouse hindlimb acutely increases skeletal perfusion and chronically enhanced vascular porosity

2020 ◽  
Vol 128 (4) ◽  
pp. 838-846
Author(s):  
Stephanie Gohin ◽  
Behzad Javaheri ◽  
Mark Hopkinson ◽  
Andrew Anthony Pitsillides ◽  
Timothy R. Arnett ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Mechanical Loading ◽  
Blood Supply ◽  
Axial Loading ◽  
Blood Perfusion ◽  
Doppler Imaging ◽  
Vascular Canal ◽  
Acute Responses ◽  
The Right

Blood supply is essential for osteogenesis, yet its relationship to load-related increases in bone mass is poorly defined. Herein, we aim to investigate the link between load-induced osteogenesis and the blood supply (bone perfusion and vascular porosity) using an established osteogenic noninvasive model of axial loading. Accordingly, 12 N mechanical loads were applied to the right tibiae of six male C57BL6 mice at 10–12 wk of age, 3 times/wk for 2 wk. Skeletal perfusion was measured acutely (postloading) and chronically in loaded and contralateral, nonloaded hindlimbs by laser-Doppler imaging. Vascular and lacunar porosity of the cortical bone and tibia load-related changes in trabecular and cortical bone was measured by nanoCT and micro-CT, respectively. We found that the mean skeletal perfusion (loaded: nonloaded limb ratio) increased by 56% immediately following the first loading episode (vs. baseline, P < 0.01), and a similar increase was observed after all loading episodes, demonstrating that these acute responses were conserved for 2 wk of loading. Loading failed, however, to engender any significant chronic changes in mean perfusion between the beginning and the end of the experiment. In contrast, 2 wk of loading engendered an increased vascular canal number in the tibial cortical compartment (midshaft) and, as expected, also increased trabecular and cortical bone volumes and modified tibial architecture in the loaded limb. Our results indicate that each episode of loading both generates acute enhancement in skeletal blood perfusion and also stimulates chronic vascular architectural changes in the bone cortices, which coincide with load-induced increases in bone mass. NEW & NOTEWORTHY This study investigated modifications to the blood supply (bone perfusion and intracortical vascular canals) in mechanoadaptive responses in C57BL6 mice. Each episode of mechanical loading acutely increases skeletal perfusion. Two weeks of mechanical loading increased bone mass and cortical vascular canal number, while there was no chronic increase in hindlimb perfusion. Our findings suggest that the blood supply may participate in the processes that govern load-induced bone formation.

scholarly journals Risedronate does not reduce mechanical loading-related increases in cortical and trabecular bone mass in mice

Bone ◽  
2011 ◽  
Vol 49 (1) ◽  
pp. 133-139 ◽  
Author(s):  
Toshihiro Sugiyama ◽  
Lee B. Meakin ◽  
Gabriel L. Galea ◽  
Brendan F. Jackson ◽  
Lance E. Lanyon ◽  
...  
Keyword(s):  
Bone Mass ◽  
Trabecular Bone ◽  
Mechanical Loading ◽  
Trabecular Bone Mass

scholarly journals Prevention of Bone Destruction by Mechanical Loading Is Not Enhanced by the Bruton’s Tyrosine Kinase Inhibitor CC-292 in Myeloma Bone Disease

2021 ◽  
Vol 22 (8) ◽  
pp. 3840
Author(s):  
Fani Ziouti ◽  
Maximilian Rummler ◽  
Beatrice Steyn ◽  
Tobias Thiele ◽  
Anne Seliger ◽  
...  
Keyword(s):  
Bone Mass ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Mechanical Loading ◽  
Bone Disease ◽  
Kinase Inhibitor ◽  
Bone Destruction ◽  
Bruton's Tyrosine Kinase ◽  
Myeloma Bone Disease ◽  
Physical Stimuli

Limiting bone resorption and regenerating bone tissue are treatment goals in myeloma bone disease (MMBD). Physical stimuli such as mechanical loading prevent bone destruction and enhance bone mass in the MOPC315.BM.Luc model of MMBD. It is unknown whether treatment with the Bruton’s tyrosine kinase inhibitor CC-292 (Spebrutinib), which regulates osteoclast differentiation and function, augments the anabolic effect of mechanical loading. CC-292 was administered alone and in combination with axial compressive tibial loading in the MOPC315.BM.Luc model for three weeks. However, neither CC-292 alone nor its use in combination with mechanical loading was more effective in reducing osteolytic bone disease or rescuing bone mass than mechanical stimuli alone, as evidenced by microCT and histomorphometric analysis. Further studies are needed to investigate novel anti-myeloma and anti-resorptive strategies in combination with physical stimuli to improve treatment of MMBD.

The Role of Integrins in Osteocyte Response to Mechanical Stimulus

2012 ◽  
Author(s):  
Matthew G. Haugh ◽  
Laoise M. McNamara
Keyword(s):  
Physical Activity ◽  
Bone Mass ◽  
Mechanical Strength ◽  
Mechanical Loading ◽  
Integrin Αvβ3 ◽  
Mechanical Stimulus ◽  
Mechanical Environment ◽  
Physiological Processes ◽  
Cell Processes

Bone is an exceptional material that is efficiently lightweight, possesses excellent mechanical strength and can also adapt itself in response to changes in physical activity by means of coordinated physiological processes known as modelling and remodelling. The response of bone to mechanical loading is thought to be regulated by mechanosensitive osteocyte cells that can direct the alteration of bone mass, by osteoblasts and osteoclasts, and thereby play an important role in optimizing bone strength. The mechanisms by which osteocytes sense their mechanical environment are not well understood. It has been proposed that integrin-based (αVβ3) attachments to ECM on osteocyte cell processes may facilitate mechanosensation in osteocytes [1,2]. While previous studies have shown that integrin beta;1 plays an important role in response to mechanical stimulus, the role of integrin αVβ3 in osteocyte mechanotransduction has yet to be investigated [3,4].

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