Previous work on drug release from nanotubes has concluded that the diffusion process depends significantly on the nanotube dimension in addition to factors like the molecular size and charge of the drug, drug solubility, pH, etc. The release kinetics within these structures consisting mostly of an initial burst release followed by a constant gradual zero-order kinetic mechanism[ ]. This initial burst release is undesirable and various strategies such as structural modification of the nanotube, reduction of pore size by polymer deposition, surface functionalization, etc., have been explored to limit it and extend the release time in zero-order release kinetics ]. The general outcome from previous findings revealed that an increase in tube dimensions translated to an extended-release time. However, increasing other morphological dimensions, such as the pore-diameter also increases the initial burst release, while a longer tube length with a smaller constant pore diameter minimizes the loading and release capacity ]. Attempts at reducing the diameter of the pore-openings via biopolymer deposition have also been investigated. While this approach may have significantly reduced the initial burst release and extended the release time [ , these deposited polymers are suspected to potentially degrade over time and may release their monomer in the body, leading to possible inflammation and subsequent implant failure[ ] Furthermore, coating with a polymer may change the surface roughness at the cell-implant interacting surface, in some cases lowering the interaction of the ECM due to suppression of the underlying nanostructural morphology, which has been proven to demonstrate improved biocompatibility ]. Hence, structural modification continues to remain the more straightforward, simple and effective approach to maximize host-cell response while also controlling the release properties from such nanotubular structures.