Intervertebral disk disease has multiple radiological expressions and is probably multifactorial, although being generally considered univocal. Mechanical factors have been the best studied etiological factors and appear to be capable of starting and aggravating the different components of disk degeneration. This process also depends on genetic influences such as a collagen type IX mutation, a polymorphism in the aggrecan gene and a polymorphism in the vitamin D receptor gene. Intervertebral disk cells produce numerous cytokines with catabolic and anabolic activity. One of the elements of disk degeneration could be the unbalance between catabolic/inflammatory cytokines (IL1, TNF alpha...) and anabolical/antiinflamatory cytokines (IL 10, IL1 Ra, growth factors...). The main driver force of disk matrix destruction is the unbalance between metaloproteases (collagenases, stromelysines and gelatinases) and its natural inhibitors. It is this process that characterizes the active disk disease. It implies a reduction in the radiological intervertebral space in a few months and a vertebral plate oedema sign in MRI, around degenerated disks. This is clinically manifested as pseudo-inflammatory pain, with increased severity during the morning. These periods of active disk disease respond to non steroidal anti-inflammatory drugs and to steroids, particularly when locally administered. The evidence of the existence of an active disk disease has not only clinical and management pertinence but also scientific, as it allows to better understand the process of disk destruction.