Ambulatory level and asymmetrical weight bearing after stroke affects bone loss in the upper and lower part of the femoral neck differently: bone adaptation after decreased mechanical loading

Bone ◽  
2000 ◽  
Vol 27 (5) ◽  
pp. 701-707 ◽  
Author(s):  
L. Jørgensen ◽  
N.J. Crabtree ◽  
J. Reeve ◽  
B.K. Jacobsen
2021 ◽  
Vol 12 ◽  
Author(s):  
Priyanka Garg ◽  
Maura Strigini ◽  
Laura Peurière ◽  
Laurence Vico ◽  
Donata Iandolo

Bone adaptation to spaceflight results in bone loss at weight bearing sites following the absence of the stimulus represented by ground force. The rodent hindlimb unloading model was designed to mimic the loss of mechanical loading experienced by astronauts in spaceflight to better understand the mechanisms causing this disuse-induced bone loss. The model has also been largely adopted to study disuse osteopenia and therefore to test drugs for its treatment. Loss of trabecular and cortical bone is observed in long bones of hindlimbs in tail-suspended rodents. Over the years, osteocytes have been shown to play a key role in sensing mechanical stress/stimulus via the ECM-integrin-cytoskeletal axis and to respond to it by regulating different cytokines such as SOST and RANKL. Colder experimental environments (~20–22°C) below thermoneutral temperatures (~28–32°C) exacerbate bone loss. Hence, it is important to consider the role of environmental temperatures on the experimental outcomes. We provide insights into the cellular and molecular pathways that have been shown to play a role in the hindlimb unloading and recommendations to minimize the effects of conditions that we refer to as confounding factors.


2006 ◽  
Vol 31 (6) ◽  
pp. 655-660 ◽  
Author(s):  
Ronald Zernicke ◽  
Christopher MacKay ◽  
Caeley Lorincz

Exercise-induced mechanical loading can have potent effects on skeletal form and health. Both intrinsic and extrinsic factors contribute to bone structure and function. Mechanical simuli (e.g., strain magnitude, frequency, rate, and gradients, as well as fluid flow and shear stress) have potent influences on bone-cell cytoskeleton and associated signalling pathways. Although the immature skeleton may be more able to benefit from exercise, a skeletally mature population can also benefit from exercise programs aimed at increasing the functional loads to which the skeleton is exposed. The definitive explanation of mechanical-loading and (or) bone-cell mechanotransductive phenomena, however, remains elusive. Here, we briefly review the structural and anatomical foundation for bone adaptation, focusing on mechanical loading effects on bone, linked to the roles of integrins, cytoskeleton, membrane channels, and auto- and paracrine factors in bone modeling and remodeling.


2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Yi-Xian Qin ◽  
Minyi Hu

While mechanotransductive signal is proven essential for tissue regeneration, it is critical to determine specific cellular responses to such mechanical signals and the underlying mechanism. Dynamic fluid flow induced by mechanical loading has been shown to have the potential to regulate bone adaptation and mitigate bone loss. Mechanotransduction pathways are of great interests in elucidating how mechanical signals produce such observed effects, including reduced bone loss, increased bone formation, and osteogenic cell differentiation. The objective of this review is to develop a molecular understanding of the mechanotransduction processes in tissue regeneration, which may provide new insights into bone physiology. We discussed the potential for mechanical loading to induce dynamic bone fluid flow, regulation of bone adaptation, and optimization of stimulation parameters in various loading regimens. The potential for mechanical loading to regulate microcirculation is also discussed. Particularly, attention is allotted to the potential cellular and molecular pathways in response to loading, including osteocytes associated with Wnt signaling, elevation of marrow stem cells, and suppression of adipotic cells, as well as the roles of LRP5 and microRNA. These data and discussions highlight the complex yet highly coordinated process of mechanotransduction in bone tissue regeneration.


2018 ◽  
Vol 3 (82) ◽  
Author(s):  
Rita Gruodytė ◽  
Toivo Jürimäe

Research background and hypothesis. Jumping ability correlates well with different bone values. The skeletal benefits of high-impact weight-bearing exercise have been shown to be greater when training is started prior to menarche. We hypothesized that significant differences would be apparent in the relationships between bone values and jumping height in favor of the girls’ prior menarche compared to post-menarcheal group. Research aim. The aim of the study was to investigate the relationships between jumping height and bone mineral density (BMD) in pre-menarcheal and post-menarcheal physically active girls. Research  methods.  In  total,  113  adolescent  girls  from  different  competitive  extramural  athletic  programs participated in this study. Femoral neck and lumbar spine BMD were measured. The heights of vertical jumps (i. e. countermovement jump (CMJ) and rebound jumps for 15 (RJ  15 s) and 30 (RJ  30 s) seconds) were obtained.Research results. After adjusting for major confounders (i. e. age, height, and body mass), the height of rebound jumps correlated only with femoral neck BMD and only in pre-menarcheal group (r = 0.37–0.46; p < 0.05). No correlations were found between BMD variables and jumping height in post-menarcheal girls. The height of CMJ did not correlate with measured BMD variables in the studied groups.Discussion and conclusions. Early puberty is an opportune period to increase bone adaptation to mechanical loading due to the velocity of bone growth and endocrine changes at this time. We suggest that powerful repetitive vertical jumping may be more beneficial to bone health compared to single jumping activities in physically active girls prior to menarche rather than after it.Keywords: bone health, vertical jumps, puberty.


2013 ◽  
Vol 46 (13) ◽  
pp. 2179-2185 ◽  
Author(s):  
M.M. Machado ◽  
P.R. Fernandes ◽  
G. Cardadeiro ◽  
F. Baptista

2012 ◽  
Vol 303 (11) ◽  
pp. E1354-E1362 ◽  
Author(s):  
Mohammad Shahnazari ◽  
Pam Kurimoto ◽  
Benjamin M. Boudignon ◽  
Benjamin E. Orwoll ◽  
Daniel D. Bikle ◽  
...  

Loss of skeletal weight bearing or skeletal unloading as occurs during spaceflight inhibits bone formation and stimulates bone resorption. These are associated with a decline in the osteoblast (Ob.S/BS) and an increase in the osteoclast (Oc.S/BS) bone surfaces. To determine the temporal relationship between changes in the bone cells and their marrow precursor pools during sustained unloading, and whether genetic background influences these relationships, we used the hindlimb unloading model to induce bone loss in two strains of mice known to respond to load and having significantly different cancellous bone volumes (C57BL/6 and DBA/2 male mice). Skeletal unloading caused a progressive decline in bone volume that was accompanied by strain-specific changes in Ob.S/BS and Oc.S/BS. These were associated with a sustained reduction in the osteoprogenitor population and a dramatic but transient increase in the osteoclast precursor pool size in both strains. The results reveal that bone adaptation to skeletal unloading involves similar rapid changes in the osteoblast and osteoclast progenitor populations in both strains of mice but striking differences in Oc.S/BS dynamics, BFR, and cancellous bone structure. These strain-specific differences suggest that genetics plays an important role in determining the osteoblast and osteoclast populations on the bone surface and the dynamics of bone loss in response to skeletal unloading.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ariane Zamarioli ◽  
Zachery R. Campbell ◽  
Kevin A. Maupin ◽  
Paul J. Childress ◽  
Joao P. B. Ximenez ◽  
...  

AbstractWith increased human presence in space, bone loss and fractures will occur. Thrombopoietin (TPO) is a recently patented bone healing agent. Here, we investigated the systemic effects of TPO on mice subjected to spaceflight and sustaining a bone fracture. Forty, 9-week-old, male, C57BL/6 J were divided into 4 groups: (1) Saline+Earth; (2) TPO + Earth; (3) Saline+Flight; and (4) TPO + Flight (n = 10/group). Saline- and TPO-treated mice underwent a femoral defect surgery, and 20 mice were housed in space (“Flight”) and 20 mice on Earth for approximately 4 weeks. With the exception of the calvarium and incisor, positive changes were observed in TPO-treated, spaceflight bones, suggesting TPO may improve osteogenesis in the absence of mechanical loading. Thus, TPO, may serve as a new bone healing agent, and may also improve some skeletal properties of astronauts, which might be extrapolated for patients on Earth with restraint mobilization and/or are incapable of bearing weight on their bones.


Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Malika A Swar ◽  
Marwan Bukhari

Abstract Background/Aims  Osteoporosis (OP) is an extra-articular manifestation of rheumatoid arthritis (RA) that leads to increased fracture susceptibility due to a variety of reasons including immobility and cytokine driven bone loss. Bone loss in other populations has well documented risk factors. It is unknown whether bone loss in RA predominantly affects the femoral neck or the spine. This study aimed to identify independent predictors of low bone mineral density (BMD) in patients RA at the lumbar spine and the femoral neck. Methods  This was a retrospective observational cohort study using patients with Rheumatoid arthritis attending for a regional dual X-ray absorptiometry (DEXA) scan at the Royal Lancaster Infirmary between 2004 and 2014. BMD in L1-L4 in the spine and in the femoral neck were recorded. The risk factors investigated were steroid use, family history of osteoporosis, smoking, alcohol abuse, BMI, gender, previous fragility fracture, number of FRAX(tm) risk factors and age. Univariate and Multivariate regression analysis models were fitted to explore bone loss at these sites using BMD in g/cm2 as a dependant variable. . Results  1,527 patients were included in the analysis, 1,207 (79%) were female. Mean age was 64.34 years (SD11.6). mean BMI was 27.32kg/cm2 (SD 5.570) 858 (56.2%) had some steroid exposure . 169(11.1%) had family history of osteoporosis. fragility fracture history found in 406 (26.6%). 621 (40.7%) were current or ex smokers . There was a median of 3 OP risk factors (IQR 1,3) The performance of the models is shown in table one below. Different risk factors appeared to influence the BMD at different sites and the cumulative risk factors influenced BMD in the spine. None of the traditional risk factors predicted poor bone loss well in this cohort. P129 Table 1:result of the regression modelsCharacteristicB femoral neck95% CIpB spine95%CIpAge at scan-0.004-0.005,-0.003&lt;0.01-0.0005-0.002,0.00050.292Sex-0.094-0.113,-0.075&lt;0.01-0.101-0.129,-0.072&lt;0.01BMI (mg/m2)0.0080.008,0.0101&lt;0.010.01130.019,0.013&lt;0.01Fragility fracture-0.024-0.055,0.0060.12-0.0138-0.060,0.0320.559Smoking0.007-0.022,0.0350.650.0286-0.015,0.0720.20Alcohol0.011-0.033,0.0 5560.620.0544-0.013,0.1120.11Family history of OP0.012-0.021,0.0450.470.0158-0.034,0.0650.53Number of risk factors-0.015-0.039,0.0080.21-0.039-0.075,-0.0030.03steroids0.004-0.023,0.0320.030.027-0.015,0.0690.21 Conclusion  This study has shown that predictors of low BMD in the spine and hip are different and less influential than expected in this cohort with RA . As the FRAX(tm) tool only uses the femoral neck, this might underestimate the fracture risk in this population. Further work looking at individual areas is ongoing. Disclosure  M.A. Swar: None. M. Bukhari: None.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Lei Qin ◽  
Xuekun Fu ◽  
Jing Ma ◽  
Manxia Lin ◽  
Peijun Zhang ◽  
...  

AbstractOsteocytes act as mechanosensors in bone; however, the underlying mechanism remains poorly understood. Here we report that deleting Kindlin-2 in osteocytes causes severe osteopenia and mechanical property defects in weight-bearing long bones, but not in non-weight-bearing calvariae. Kindlin-2 loss in osteocytes impairs skeletal responses to mechanical stimulation in long bones. Control and cKO mice display similar bone loss induced by unloading. However, unlike control mice, cKO mice fail to restore lost bone after reloading. Osteocyte Kindlin-2 deletion impairs focal adhesion (FA) formation, cytoskeleton organization and cell orientation in vitro and in bone. Fluid shear stress dose-dependently increases Kindlin-2 expression and decreases that of Sclerostin by downregulating Smad2/3 in osteocytes; this latter response is abolished by Kindlin-2 ablation. Kindlin-2-deficient osteocytes express abundant Sclerostin, contributing to bone loss in cKO mice. Collectively, we demonstrate an indispensable novel role of Kindlin-2 in maintaining skeletal responses to mechanical stimulation by inhibiting Sclerostin expression during osteocyte mechanotransduction.


2001 ◽  
Vol 4 (2) ◽  
pp. 263-269 ◽  
Author(s):  
Gordon Turner-Walker ◽  
Unni Syversen ◽  
Simon Mays

The application of medical scanning technologies to archaeological skeletons provides novel insights into the history and potential causes of osteoporosis. The present study investigated bone mineral density (BMD) in medieval skeletons from England and Norway. Comparisons between the two adult populations found no statistically significant differences. This compares with a modern fracture incidence for the femoral neck in women from Norway that is almost three times that in the UK. The pattern of age-related bone loss in medieval men was similar to that seen in men today. In contrast, the pattern in medieval women differed from that of modern young women. On average, medieval women experienced a decrease in BMD at the femoral neck of approximately 23 per cent between the ages of 22 and 35. These losses were partially recovered by age 45, after which BMD values show a decline consistent with post-menopausal bone loss in modern western women. A possible explanation of the rapid decline in BMD in young medieval women is bone loss in connection with pregnancy and lactation in circumstances of insufficient nutrition.


Sign in / Sign up

Export Citation Format

Share Document