Although it is clear that the IDET* procedure owes its therapeutic effects to the controlled application of heat to disc tissue, the actual mechanism of action (MOA) is still a subject of research. A likely explanation is that the MOA is multifactorial, a combination of several heat-related effects. Those most often cited in the literature include the following:

• Destruction of pain receptors in the outer layers of the disc, reducing or eliminating the patient’s capacity to feel discogenic pain.
• Modification (denaturation) of collagen in the fibers that make up the anulus fibrosus. Denaturation of collagen is thought to shrink disc tissue, which may help seal minute tears and fissures in the anulus, and stiffen the disc, which may help increase spinal stability.
• Cauterization and subsequent disintegration of vascular ingrowth (i.e., granulation tissue) that forms like scar tissue in anular tears and fissures.

Anular Collagen Response to Heat Distribiution

The anulus fibrosis is composed primarily of type 1 collagen—a triple helix molecule with heat-sensitive bonds held in extended conformation under tension. At the levels of heat generated by IDET* (~60° C), hydrogen bonds in the molecule begin to break, and the fibers shrink.

Other major determinants of successful outcomes appear to be proper patient selection and catheter placement. For further information about the patient selection process, see Who is the IDET Procedure for?