title: Response of knee ligaments to prolotherapy in a rat injury model.
abstract: BACKGROUND
  Prolotherapy is an alternative therapy for chronic musculoskeletal injury including joint laxity. The commonly used injectant, D-glucose (dextrose), is hypothesized to improve ligament mechanics and decrease pain through an inflammatory mechanism. No study has investigated the mechanical effects of prolotherapy on stretch-injured ligaments.
  
  
  OBJECTIVE
  Dextrose injections will enlarge cross-sectional area, decrease laxity, strengthen, and stiffen stretch-injured medial collateral ligaments (MCLs) compared with controls. Dextrose prolotherapy will increase collagen fibril diameter and density of stretch-injured MCLs.
  
  
  METHODS
  Controlled laboratory study.
  
  
  METHODS
  Twenty-four rats were bilaterally MCL stretch-injured, and the induced laxity was measured. After 2 weeks, 32 MCLs were injected twice, 1 week apart, with either dextrose or saline control; 16 MCLs received no injection. Seven uninjured rats (14 MCLs) were additional controls. Two weeks after the second injection, ligament laxity, mechanical properties (n = 8), and collagen fibril diameter and density (n = 3) were assessed.
  
  
  RESULTS
  The injury model created consistent ligament laxity (P < .05) that was not altered by dextrose injections. Cross-sectional area of dextrose-injected MCLs was increased 30% and 90% compared with saline and uninjured controls, respectively (P < .05). Collagen fibril diameter and density were decreased in injured ligaments compared with uninjured controls (P < .05), but collagen fibril characteristics were not different between injured groups.
  
  
  CONCLUSIONS
  Dextrose injections increased the cross-sectional area of MCLs compared with saline-injected and uninjured controls. Dextrose injections did not alter other measured properties in this model.
  
  
  CONCLUSIONS
  Our results suggest that clinical improvement from prolotherapy may not result from direct effects on ligament biomechanics.
authors.affiliation: Department of Biomedical Engineering, University of Wisconsin, Madison, Wisconsin, USA.
authors.forename: Kristina T
authors.initials: KT
authors.lastname: Jensen
authors.forename: David P
authors.initials: DP
authors.lastname: Rabago
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Best
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Patterson
authors.forename: Ray
authors.initials: R
authors.lastname: Vanderby
mesh_terms: D000818:Animals; D018771:Arthralgia / Q000517:prevention & control; D001696:Biomechanical Phenomena; D000529:Complementary Therapies / Q000379:methods*; D005947:Glucose / Q000008:administration & dosage*; D007249:Inflammation / Q000139:chemically induced; D007270:Injections, Intra-Articular; D007593:Joint Instability / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D017888:Medial Collateral Ligament, Knee / Q000293:injuries* / Q000503:physiopathology / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012597:Sclerosing Solutions / Q000008:administration & dosage*
chemical_list: D012597:Sclerosing Solutions; D005947:Glucose