Introduction

It has been well established that the skeleton, just like the muscular apparatus, responds to changes in applied mechanical stress by changing its mass. This phenomenon was first described by Wolff some hundred years ago in his book Das Gesetz der Transformation der Knochen (Wolff, 1986). Wolff was struck by gross changes in trabecular organisation of bones as a result of dramatic changes of their mechanical environment, as for instance occurs after maladjustment of the bone ends after a fracture. Wolff's Law, which is in fact not a law but the description of a biological phenomenon, states that bones adapt their tissue density and architecture to the functional demands of their mechanical environment, to obtain maximal strength with minimal tissue mass. Increased stress leads to denser bone, as in the dominant arm of professional tennis players (Montoye, Smith & Fardon, 1980), while stress reduction, as for instance after long-term bed rest, reduces bone density (Whedon & Heaney, 1993).

While these phenomena are quite apparent at the anatomical and tissue level, it is not well known how they are achieved at the cellular and molecular level. How skeletal cells react to mechanical stress in terms of cell proliferation and matrix metabolism, and what intermediate molecules are involved, are still matters of debate. Even the nature of the final physical stimulus which acts on the cell to modulate its behaviour has not been unequivocally determined.