Ceramic bone scaffolds with both microporosity (<50µm) and macroporosity (>100µm) are known to enhance bone formation. Including microporosity in a scaffold increases bone volume and distribution. The integration of the bone with the scaffold is also improved as both cells and mineralized bone have been observed inside micropores. However, until now, a mechanism to explain the increased bone formation and the presence of cells has not been proven.

In this dissertation I present the first mechanism that explains enhanced bone formation and integration in micorporous hydroxyapatite (HA) scaffolds. Microporous scaffolds can “self load” cells and molecules upon implantation via micropore-induced capillary forces. The localization and entrapment of cells within the micropores forms a reservoir of cells that not only can begin the process of bone formation but can also signal other cells to further enhance the regeneration process. I also demonstrate that micropore-induced capillary forces can be altered by changing parameters in the microstructure – namely pore size, pore fraction, and pore-interconnection size – and that the microstructure can be used to control the release rate of an incorporated drug or protein. The identification of these parameters and their influence on capillary force and controlled release lays the foundation for optimization of microstructure in bone scaffold design. The work in this dissertation can be applied to many types of tissue engineering as well as to microfluidic processes such as cell sorting. By proving and exploring the effects of microstructure and capillary forces in porous scaffolds, this work enables researchers to identify ideal microstructures for cell penetration and drug release that will result in faster and more complete healing of tissue defects.