Paraspinal Muscle Passive Stiffness Remodels in Direct Response to Spine Stiffness: A Study Using the ENT1-Deficient Mouse

STUDY DESIGN.Basic science study of the relationship between the structural properties of the spine and its surrounding musculature. OBJECTIVE.To determine if an increase in spine stiffness causes an inverse compensatory change in the passive stiffness of the adjacent paraspinal muscles. SUMMARY OF BACKGROUND DATA.Intervertebral disc degeneration causes an increase in multifidus passive stiffness; this was hypothesized to compensate for a decrease in spine stiffness associated with disc degeneration. Mice lacking equilibrative nucleoside transporter 1 (ENT1) develop progressive ectopic calcification of the fibrous connective tissues of the spine, which affects the lumbar spine by 6 months of age and likely creates a mechanically stiffer spine. METHODS.Experiments were conducted on 4 groups of mice (n = 8 mice/group)wild-type (WT) and ENT1 knockout (KO) at 2 or 8 months of age. Lumbar spines were removed and tested in cyclic axial compression to determine neutral zone (NZ) length and stiffness. Single muscle fibres and bundles of fibres were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine related control) and tested to determine elastic modulus (passive stiffness). RESULTS.At 2 months of age, neither spine nor muscle stiffness was different between KO and WT. At 8 months of age, compared to WT the lumbar spines of ENT1 KO mice had a stiffer and shorter NZ, and the paraspinal muscle fibres were less stiff; however, fibre bundles were not different. Additionally, tibialis anterior was not different between KO and WT. CONCLUSIONS.This work has confirmed that calcification of spinal connective tissues in the ENT1 KO mouse results in a stiffened spine, while the concurrent decrease in muscle fibre elastic modulus in the adjacent paraspinal muscles suggests a direct compensatory relationship between the stiffness of the spine and the muscles that are attached to it.Level of EvidenceN/A