LAUSR

The case presented here is a very interesting one as the authors and the expert commentator appropriately point out in their respective articles [1, 2]. Both are food-for-thought in a longstanding discussion about the biomechanical and the biological components of DDD aetiology as well as about the therapeutic options available. I would like to ask the authors, however, what additional data they have that leads them to interpret their observations as anything biologically ‘‘active’’ beyond the simple effect of the mechanical unloading of the—previously loaded—remaining posterior nucleus, visualized by MRI? Putzier et al. have described the protective effects of dynamic stabilization on disc survival after microdiscectomy [3]. Talking about dynamic stabilization—the interpretation of image 6a as the ‘‘progression of bony union’’ touches me as a bit far-fetched. Seeing only minute, reactive calcifications in the outermost annulus at 9 months after stand-alone cage implantation with zero visible disc space bridging in the radiographs could just as well represent a stable pseudarthrosis.