Restricted Research - Award List, Note/Discussion Page

Fiscal Year: 2018

1350  The University of Texas at Arlington  (74855)

Principal Investigator: Rhonda d Prisby

Total Amount of Contract, Award, or Gift (Annual before 2011): $ 250,000

Exceeds $250,000 (Is it flagged?): Yes

Start and End Dates: 6/30/17 - 6/29/20

Restricted Research: YES

Academic Discipline: Department of Kinesiology

Department, Center, School, or Institute: College of Nursing and Health Innovation

Title of Contract, Award, or Gift: Collaborative Research: Wireless Implantable Bone Intramedullary Fluid Modulator (WiBi FM) for the Treatment of Osteoporosis and Fracture Repair

Name of Granting or Contracting Agency/Entity: National Science Foundation (NSF)

CFDA: 47

Program Title: N/A


In collaboration with Jeong-Bong Lee at UT Dallas Research Program Goals: 1. Design/Fabrication of the WIBIM: We will design wireless implantable bone intramedullary fluid modulators (WIBIM) using extensive computer simulations using COMSOL. Then, we will fabricate the proposed implantable fluid modulator. 2. Reliability and accuracy of WIBIM: We will collect data on controlled alterations in bone intramedullary pressure in young and old male Fischer-344 rats and assess the reliability of WIBIM to accurately record these changes in pressure. Based upon the accuracy of the WIBIM at detecting intramedullary pressure, the signaling processes will be developed and refined. 3. Analysis of the effect of bone intramedullary fluid modulation: We will validate the effectiveness of the WIBIM by assessing bone microarchitecture, bone static and dynamic properties, and bone density in young and old male Fischer-344 rats. Significance of the Proposed Research Wolff’s Law best characterizes how bone adapts to functionally withstand its mechanical environment. Increased physical activity (i.e., bone mechanical loading) serves to augment bone mass, while reduced physical activity (e.g., sedentary lifestyle) serves to diminish bone mass. To date, the precise mechanism(s) by which mechanical loading imparts its stimulatory signal on bone cells (i.e., osteoblasts, osteoclasts, and osteocytes) to initiate bone remodeling remains unknown. However, alterations in bone intramedullary fluid flow and pressure can modulate bone cell activity. Skeletal tissue is a highly porous structure composed of a collagen-hydroxyapatite matrix and the lacunar-canalicular network. Bone interstitial fluid moves through the bone marrow and lacunar-canalicular network of bone, subjecting bone cells and bone marrow cells to interstitial fluid- and pressure-induced shear stress along their surface membranes. Shear stress stimulates the release of nitric oxide (NO) and prostaglandins (e.g., PGE2) by bone-derived cells and organ cultures. Nitric oxide is a osteoblast mitogen and inhibits osteoclastic degradation of bone and PGE2 enhances bone formation and reduces bone loss with immobilization. In fact, augmented flow-induced shear stress enhanced NO release from osteoblasts but mechanical strain did not elicit the same response. Further, when unloaded turkey ulnae were subjected to oscillatory fluid flow in the absence of bone matrix strain (i.e., mechanical loading), diaphyseal bone accrual resulted. Thus, alterations in bone intramedullary fluid flow and pressure in the absence of mechanical loading elicits the release of bone stimulating factors. Therefore, changes in intramedullary fluid flow and pressure may serve as the mechanism(s) by which mechanical loading initiates bone formation.

Discussion: No discussion notes


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