Cranioplasty, one of the oldest surgical procedures used to repair cranial defects, has undergone many revolutions over time to find the ideal material to improve patient prognosis. Cranioplasty offers cosmetic and protective benefits for patients with cranial defects. The first primitive cranioplasty procedures date back to 7000 bc and used metal and gourds to repair cranial defects. Cranioplasty was first documented by Fallopius who described repair using gold plates; the first bone graft was documented by van Meekeren. The first significant improvement for this procedure began with experimentation involving bone grafts in the late 19th century as a more natural approach for repairing cranial defects. The next impetus for advancement came because of wartime injuries incurred during World Wars I and II and involved experimentation with synthetic materials to counter the common complications associated with bone grafts. Methyl methacrylate, hydroxyapatite, ceramics, and polyetheretherketone implants among other materials have since been researched and used. Research now has shifted toward molecular biology to improve the ability of the patient to regenerate bone using bone growth factors. This paper reviews the evolution of materials used over time in addition to the various advantages and pitfalls associated with each change. It is important for neurosurgeons to be mindful of how these techniques have evolved in order to gain a better understanding of this procedure and how it has been adapted.

Glioblastoma multiforme (GBM) is a highly aggressive form of brain cancer associated with a very poor prognosis. Recently, the initiation and growth of GBM has been linked to brain tumor-initiating cells (BTICs), which are poorly differentiated and share features with neural stem cells (NSCs). Here we describe a kinome-wide RNA interference screen to identify factors that control the tumorigenicity of BTICs. We identified several genes whose silencing induces differentiation of BTICs derived from multiple GBM patients. In particular, knockdown of the adaptor protein TRRAP significantly increased differentiation of cultured BTICs, sensitized the cells to apoptotic stimuli, and negatively affected cell cycle progression. TRRAP knockdown also significantly suppressed tumor formation upon intracranial BTIC implantation into mice. Together, these findings support a critical role for TRRAP in maintaining a tumorigenic, stem cell-like state.