Abstract

BackgroundJoints withstand huge forces, but little is known about subchondral pressures and perfusion during loading. We developed an in vitro calf foot model to explore intraosseous pressure (IOP) and subchondral perfusion during weight bearing.MethodsFreshly culled calf forefeet were perfused with serum. IOP was measured at three sites in the foot using intraosseous needles, pressure transducers, and digital recorders. IOP was measured during perfusion, with and without a tourniquet and with differing weights, including static loading and dynamic loading to resemble walking.ResultsIOP varied with perfusion pressure. Static loading increased subchondral IOP whether the bone was non-perfused, perfused, or perfused with a proximal venous tourniquet (p < 0.0001). Under all perfusion states, IOP was proportional to the load (R2 = 0.984). Subchondral IOP often exceeded perfusion pressure. On removal of a load, IOP fell to below the pre-load value. Repetitive loading led to a falling IOP whether the foot was perfused or not.ConclusionSuperimposed on a variable background IOP, increased perfusion and physiological loading caused a significant increase in subchondral IOP. Force was thereby transmitted through subchondral bone partly by hydraulic pressure. A falling IOP with repeat loading suggests that there is an intraosseous one-way valve. This offers a new understanding of subchondral perfusion physiology.

Highlights

  • Intraosseous pressure (IOP) has been studied by authors interested in bone circulation, bone diseases, and bone pain for more than 70 years [1,2,3,4]

  • Simkin suggested that trabeculae and fat act together to cushion the effects of weight bearing in the subchondral region [19]

  • The skeleton is clearly designed for weight bearing, the possibility that intraosseous pressure (IOP) changes during weight bearing has not been explored

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Summary

Introduction

Intraosseous pressure (IOP) has been studied by authors interested in bone circulation, bone diseases, and bone pain for more than 70 years [1,2,3,4]. There has been limited progress in understanding IOP and subchondral bone perfusion physiology since Azuma reported IOP fluctuation in a rabbit model in 1964 [10]. IOP has often been found to be raised in bone diseases such as osteonecrosis and after steroid use. Ficat developed a technique for the “functional exploration” of bone in patients with early osteonecrosis [14]. Joints withstand huge forces, but little is known about subchondral pressures and perfusion during loading. We developed an in vitro calf foot model to explore intraosseous pressure (IOP) and subchondral perfusion during weight bearing

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