The causes of intervertebral disc (IVD) ruptures continue to elude both biomechanists and clinicians. It is widely accepted that unique traumatic high‐load impacts are unlikely to lead to isolated IVD herniation. Therefore, a suggested mechanism for disc rupture is an accumulation of microtrauma within the IVD tissue. Microtrauma development can be related to tissue fatigue caused by repetitive (physiological) load application, as shown, for example, in [1]. However, the impact of long‐term biological influence on microtrauma, such as changes in the tissue quality due to cellular activity, has not yet been extensively addressed. A persistent catabolic shift of cellular activity possibly leads to a reduction of the tissue’s capability to resist loads. Mechanobiological investigations showed that loads acting on the tissue impact cellular predisposition and therefore influence tissue maintenance (e.g. [2]). Loads can be sensed by cells in a direct or an indirect manner. Direct mechanotransduction refers to loads transmitted over the extracellular matrix (ECM) directly on the cell’s membrane, whereas indirect mechanotransduction refers to alteration in the ECM compaction, changes in solute transport to the cells and the effect of this on cell behaviour [3]. We assume that the latter is of special interest with regard to IVD microtrauma emergence because nutrition of Nucleus Pulposus (NP) and inner Annulus Fibrosus (AF) cells is diffusion‐dependent. The objective of this project is to find crucial mechanisms at the tissue and cellular levels that lead to microtrauma within the IVD. This short paper presents the first results to address the influence of indirect mechanotransduction on the predisposition of NP cells to develop catabolic activity and contribute locally to IVD tissue damage.

Comunicació presentada a: IRCOBI Conference 2018, celebrada a Atenes, Grècia, del 12 al 14 de setembre de 2018.