Anabolic Fluid Flow as Dependent on It Dose and Frequency in Bone Formation and Inhibition of Bone Loss

Author(s):  
Yi-Xian Qin ◽  
Tamara Kaplan ◽  
Hoyan Lam

Anabolic response of bone to interstitial fluid flow is strongly dependent on the dynamic components of the fluid pressure, implying that fluid flow is a critical regulatory component to bone mass and morphology. While the fluid stimulus can be potentially applied for therapeutic in promoting turnover, the hypothesis of fluid induced bone adaptation was evaluated in an avian ulna model using varied flow rates and magnitudes. Total of 12 one-year old male avian animals was used in this study. A sinusoidal fluid pressure was applied to the experimental ulna 10 min/day for 4 weeks. Three experimental groups of loading were performed at 1 and 30 Hz of fluid loading. The results reveal an increase of 22.7%±7.2 in trabecular volume for group of 30 Hz, 76mmHg loading, while it had only 0.5 % increase at 1Hz, 76 mmHg loading. Under physiologic fluid pressure, a higher flow rate of stimuli generates much higher remodeling response than a lower rate of loading. This implies that bone turnover may be sensitive to the dynamic components of fluid flow, thereby initiating the adaptive response.

2001 ◽  
Author(s):  
Yixian Qin ◽  
Anita Saldanha ◽  
Tamara Kaplan

Abstract Load-generated intracortical fluid flow is proposed to be an important mediator for regulating bone mass and morphology [1]. Although the mechanism of cellular response to induced flow parameters, i.e., fluid pressure, pressure gradient, velocity, and fluid shear stress, are not yet clear, interstitial fluid flow driven by loading may be necessary to explain the adaptive response of bone, which is either coupled with load-induced strain magnitude or independent with matrix strain per se [2]. It has been demonstrated that load-induced intracortical fluid flow is contributed by both bone matrix deformation and induced intramedullary (IM) pressure [3]. To examine the hypothesis of fluid flow generated adaptation, it is necessary to test the mechanism under the circumstances of solely fluid induced bone adaptation in the absence of matrix deformation. While our previous data has demonstrated that bone fluid flow and its associated streaming potential product can be influenced by the dynamic IM pressure quantitatively [4], the objective of this study was to evaluate fluid induced bone adaptation in an avian ulna model using oscillatory IM fluid pressure loading in the absence of bone matrix strain. The potential fluid pathway was measured in the model.


Author(s):  
Qiuyun Wang ◽  
Shaopeng Pei ◽  
X. Lucas Lu ◽  
Liyun Wang ◽  
Qianhong Wu

2018 ◽  
Vol 29 (16) ◽  
pp. 1927-1940 ◽  
Author(s):  
Ran Li ◽  
Jean Carlos Serrano ◽  
Hao Xing ◽  
Tara A. Lee ◽  
Hesham Azizgolshani ◽  
...  

Tumor tissues are characterized by an elevated interstitial fluid flow from the tumor to the surrounding stroma. Macrophages in the tumor microenvironment are key contributors to tumor progression. While it is well established that chemical stimuli within the tumor tissues can alter macrophage behaviors, the effects of mechanical stimuli, especially the flow of interstitial fluid in the tumor microenvironment, on macrophage phenotypes have not been explored. Here, we used three-dimensional biomimetic models to reveal that macrophages can sense and respond to pathophysiological levels of interstitial fluid flow reported in tumors (∼3 µm/s). Specifically, interstitial flow (IF) polarizes macrophages toward an M2-like phenotype via integrin/Src-mediated mechanotransduction pathways involving STAT3/6. Consistent with this flow-induced M2 polarization, macrophages treated with IF migrate faster and have an enhanced ability to promote cancer cell migration. Moreover, IF directs macrophages to migrate against the flow. Since IF emanates from the tumor to the surrounding stromal tissues, our results suggest that IF could not only induce M2 polarization of macrophages but also recruit these M2 macrophages toward the tumor masses, contributing to cancer cell invasion and tumor progression. Collectively, our study reveals that IF could be a critical regulator of tumor immune environment.


2012 ◽  
Vol 12 (3) ◽  
pp. 533-553 ◽  
Author(s):  
Vittorio Sansalone ◽  
Joanna Kaiser ◽  
Salah Naili ◽  
Thibault Lemaire

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