title: Degenerative anular changes induced by puncture are associated with insufficiency of disc biomechanical function.
abstract: METHODS
  In vivo experiments to examine physiologic consequences and in vitro tests to determine immediate biomechanical effects of anular injury by needle puncture.
  
  
  OBJECTIVE
  To determine whether a relationship exists between induction of degenerative changes in anulus fibrosus (AF) and compromised disc biomechanical function according to injury size.
  
  
  BACKGROUND
  Various studies in intervertebral disc mechanics, degeneration, and regeneration involve the creation of a defect in the anulus fibrosus (AF). However, the impact of the puncture, itself, on biomechanical function and disc health are not understood.
  
  
  METHODS
  For in vivo experiments, rat caudal discs subjected to percutaneous anular punctures using different gauge size hypodermic needles (18, 22, 26 g) and nonpunctured controls were examined histologically up to 4 weeks postsurgery. For in vitro biomechanical testing, healthy motion segments were isolated and their creep compression response assessed immediately after needle puncture.
  
  
  RESULTS
  We found that needle size-dependence of creep compression behavior paralleled the size-dependence of degenerative changes in the AF. Specifically, 18-g punctures resulted in inward bulging of the AF, lamellar disorganization, and cellular changes. These changes were not seen in 22- and 26-g punctured discs. Biomechanical tests showed that only 18-g needle punctures led to significant changes in disc mechanics. Importantly, a statistically significant association was found between needle sizes that caused biomechanical changes and induction of degenerative changes in the AF.
  
  
  CONCLUSIONS
  Our findings suggest that injury sizes large enough to disrupt biomechanical function are needed to drive degenerative changes in rat caudal disc AF. Based on the data, we believe that small anular defects become sealed, allowing the disc to function normally and the AF to heal. Larger defects appear to require longer wound closure times, and may prolong the duration of impaired disc function.
authors.affiliation: Fischell Department of Bioengineering, Orthopaedic Mechanobiology Laboratory, University of Maryland, College Park, MD 20742, USA. hsieh@umd.edu
authors.forename: Adam H
authors.initials: AH
authors.lastname: Hsieh
authors.forename: David
authors.initials: D
authors.lastname: Hwang
authors.forename: David A
authors.initials: DA
authors.lastname: Ryan
authors.forename: Anike K
authors.initials: AK
authors.lastname: Freeman
authors.forename: Hyunchul
authors.initials: H
authors.lastname: Kim
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena / Q000502:physiology; D004195:Disease Models, Animal; D018450:Disease Progression; D051445:Fibrocartilage / Q000293:injuries / Q000473:pathology* / Q000503:physiopathology*; D007403:Intervertebral Disc / Q000293:injuries / Q000473:pathology* / Q000503:physiopathology*; D007405:Intervertebral Disc Displacement / Q000473:pathology* / Q000503:physiopathology*; D009339:Needles / Q000009:adverse effects; D016059:Range of Motion, Articular / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology; D013314:Stress, Mechanical; D016474:Weight-Bearing / Q000502:physiology; D014945:Wound Healing / Q000502:physiology