H-1 NMR investigation of changes in the metabolic profile of synovial fluid in bilateral canine osteoarthritis with unilateral joint denervation

Citation
Az. Damyanovich et al., H-1 NMR investigation of changes in the metabolic profile of synovial fluid in bilateral canine osteoarthritis with unilateral joint denervation, OSTEO CART, 7(2), 1999, pp. 165-172
Citations number
27
Categorie Soggetti
Rheumatology,"da verificare
Journal title
OSTEOARTHRITIS AND CARTILAGE
ISSN journal
10634584 → ACNP
Volume
7
Issue
2
Year of publication
1999
Pages
165 - 172
Database
ISI
SICI code
1063-4584(199903)7:2<165:HNIOCI>2.0.ZU;2-B
Abstract
Objective: High resolution H-1-nuclear magnetic resonance (NMR) techniques have been used to compare the effects of unilateral knee-joint denervation on the biochemical profiles of synovial fluid in a bilateral canine model o f osteoarthritis. Method: Paired synovial fluid samples were obtained from seven dogs all of which had previously undergone bilateral anterior cruciate ligament transec tion, unilateral knee denervation and contralateral sham nerve exposure. Al l synovial fluid samples were then analyzed using 500 MHz H-1-CPMG spin-ech o NMR Spectroscopy to assess differences in endogenous metabolite levels be tween the paired fluids. Results: The results indicate statistically significant increases in glycer ol, hydroxybutyrate, glutamine/glutamate, creatinine/creatine, acetate and N-acetyl-glycoprotein concentrations in synovial fluids from denervated wit h respect to control knees. Furthermore, significant trends towards elevate d lactate, alanine and pyruvate levels in the denervated knee fluids are co nsistent with our previous findings comparing NMR spectroscopy metabolic pr ofiles of normal and osteoarthritic canine synovial fluids. Conclusion: This study lends support to the principle of neurogenic acceler ation of OA in that the observed differences in metabolite concentrations f ound in the denervated knee fluids seem to correlate with metabolic changes resulting from aggravation of the OA process caused by joint denervation.