Journal
PAIN RESEARCH AND TREATMENT
Volume 2012, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2012/127636
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Funding
- National Chiropractic Mutual Insurance Company [17]
- NIH [R01AR053220]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR053220] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX002647] Funding Source: NIH RePORTER
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Objective. To develop a novel animal model of persisting lumbar facet joint pain. Methods. Sprague Dawley rats were anaesthetized and the right lumbar (L5/L6) facet joint was exposed and compressed to similar to 1mm with modified clamps applied for three minutes; sham-operated and naive animals were used as control groups. After five days, animals were tested for hind-paw sensitivity using von Frey filaments and axial deep tissue sensitivity by algometer on assigned days up to 28 days. Animals were sacrificed at selected times for histological and biochemical analysis. Results. Histological sections revealed site-specific loss of cartilage in model animals only. Tactile hypersensitivity was observed for the ipsi-and contralateral paws lasting 28 days. The threshold at which deep tissue pressure just elicited vocalization was obtained at three lumbar levels; sensitivity at L1 > L3/ 4 > L6. Biochemical analyses revealed increases in proinflammatory cytokines, especially TNF-alpha,IL-1 alpha, and IL-1 beta. Conclusions. These data suggest that compression of a facet joint induces a novel model of local cartilage loss accompanied by increased sensitivity tomechanical stimuli and by increases in inflammatory mediators. This new model may be useful for studies on mechanisms and treatment of lumbar facet joint pain and osteoarthritis.
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