Abstract
Used in conjunction with the words “endoprosthesis” and “bone-implant interface”, fluid flow is usually referred to as a potential mechanism for loosening and implant failure. Paradoxically, recent studies have shown the importance of fluid flow in augmenting molecular transport through the osteocytic syncytium. This transport is essential for maintenance of cellular nutrition as well as communication between osteocytes, osteoblasts and osteoclasts, which are interconnected biochemically by interstitial fluid in bone. In the absence of loading, larger sized molecules are not transported efficiently through bone tissue in vivo [1]. The efficacy of load-induced fluid flow, resulting from normal physiological loading of bone, has been proven for the transport of small (300-400 Da, on the order of smaller amino acids) and larger (1800 Da, on the order of small proteins) molecular weight tracers through bone [2]. Nonetheless, using a similar model to study perfusion and fluid flow in the vicinity of endoprosthetic
Recent studies have shown that the distinct porosities within bone tissue act as molecular sieves in situ [4] and that molecules on the order of cytokines and serum derived proteins can not be transported through the lacunocanalicular system without interstitial fluid flow resulting from physiological mechanical loads. These data as a whole suggest that fluid flow regimes in a physiological range are essential for osteocyte viability and function. In order to insure implant stability, health of the tissue at the interface must be insured. Hence, fluid flow in a physiological range could be considered essential for implant stability. These issues will be discussed in light of recent developments in endoprosthetic technology and the design of future generations of implants.
The abstracts were prepared by Nico Verdonschot. Correspondence should be addressed to him at Orthopaedic Research Laboratory, University Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
