Numerical exploration of collagen type I and type II changes within lumbar intervertebral disc

Abstract

Intervertebral disc (IVD) degeneration is one of the main causes of low back pain syndrome, which affects between 80% and 85% of the general population at least once in their lives, generating large economic costs. Disc degeneration might be related to a deficit in metabolite transport. As a consequence, cells start a series of catabolic cascades that degrades the extracellular matrix; which compromises the ability of the disc to resist compressive loads. As an attempt to recover this resistance, during degeneration, collagen starts to proliferate and grow. Such changes in collagen are hard to study experimentally. Finite element (FE) models of the IVD rise as a tool to explore mechanics and metabolic transport of the disc, however, none of such models include the expression of collagen I and II. The aim of this project is to evaluate the expression

of type I and II collagen during disc degeneration through 3D FE models. A mechano- transport 3D model of L4-L5 IVD was used and collagen expression rates for both type

I and II were included. Two tissue conditions were evaluated: a) healthy (GI) disc, and b) degenerated one (GIII) during one day of physiological load and three days of nutrient transport. Results have shown that there is an activation in the expression of collagen in both GI and GIII. In the case of GI, this activation is too low to affect the ECM. Interestingly, there is a considerable activation of collagen expression in the case of GIII. Therefore, results point that this activity might facilitate the generation of fibrotic tissue in later stages of disc degeneration. This study represents an advance for the future development of personalized therapies aimed to slowing the fibrillation of disc tissue. Further studies would be necessary to develop novel therapies to treat patients with low back pain.