History and Development of Prostate Cryoablation

Abstract

Cryoablation is one of several therapeutic interventions that can result in thermal tissue destruction. This technique has well- documented scientific evidence supporting its efficacy as a treatment modality in the treatment of both benign and malignant diseases [1–3]. The operative mechanism produced by freezing is the extraction of heat from the targeted tissue that initiates a series of destructive events. The severity of the freezing process has long been recognized to result in a tissue response varying from inflammation to total destruction. Histologically freezing produces an area of central necrosis with a surrounding peripheral rim in which cell death is apparent [4, 5]. Successful tissue destruction resulting from cryoablation is founded on two scientific principles; first the cellular response to freezing itself and second to operative procedural factors. Freezing tissue induces cell death by setting off a cascade of events that include freeze rupture, necrosis and apoptosis. As ice forms in the targeted tissue, water is extracted from the extracellular space forming pure crystalline ice leaving behind hyperosmotic fluid in the extracellular compartment. As a consequence of this physical event, intracellular water moves to the extracellular space followed by cell shrinkage and damage to the intracellular matrix including proteins resulting from the increased salinity. In an anatomic constrained structure such as the prostate which is not totally encapsulated the expanding ice front and the spear-like ice crystals destroy both prostate cells and the capillary endothelial lining, the latter impairing the vascular tree after thawing [6]. In addition to the physical rupture of targeted tissue cells from the intracellular ice crystal formation apoptosis has been linked to thermal injury [7]. Hollister et al. have reported that after a freezing insult, prostate cancer cells die at temperatures consistent with the freeze-zone margin [8]. Induction of the apoptotic event is said to be associated with an intrinsic mitochondria induced mechanism characterized by the upregulation of cellular Bax, the pro-apoptotic protein [9]. More recently, prostate cancer cell apoptotic induction has been reported to be facilitated through an extrinsic pathway involving the interaction of tumor necrosis factor-related apoptosis-inducing ligand with its ligand in the plasma membrane [10].