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The intravertebral pressure can be further subdivided into (a) the pressure required to inﬁltrate the trabecular cavities with cement, and (b) the shell pressure as hydrostatic resistance caused by the displacement of the bone marrow out of the vertebra into the adjacent structure. The hydrostatic resistance strongly depends on the trabecular structure and on the porosity of the vertebral shell. The revised mathematical representation is as follows: Pinj = Pextra + Pinf + Pkomp (II) where Pinf = inﬁltration pressure and Pkomp = shell pressure.
It has been suggested that cements could be adapted to more closely resemble the properties of bone as a possible solution to the risk of adjacent vertebral fractures. Young’s modulus and the ultimate strength can be decreased from normal cement values to match those of bone. Using computational models, Wilcox  and Sun and Liebschner  have both demonstrated that the excess loading on adjacent vertebrae can be altered through the use of less-stiff materials. The cement’s porosity can be increased by altering its composition through the addition of soluble ﬁllers or other materials not currently in use.
The augmentation creates a pillar of cement that reduces ﬂexibility of the endplate by inhibiting endplate bulge, thereby reducing ﬂexibility of the entire motion segment. This decreased ﬂexibility may cause loading to be redistributed, thereby increasing loading on adjacent vertebrae. These computational results thereby conﬁrm part (b) of the biomechanical hypothesis; that is, the rigid pillar effect of the cement creates increased loading in adjacent vertebrae. Results obtained in the multisegment model suggest a mechanism responsible for the change in biomechanical loading leading to adjacent vertebral fractures: the pillar effect, outlined in the following steps: 1.