Synovial Fluid Interleukin 6, Tumor Necrosis Factor, and Nitric Oxide Values in Dogs with Osteoarthritis Secondary to Cranial Cruciate Ligament Rupture
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Objective: To measure and compare values of interleukin 6 (IL-6), tumor necrosis factor (TNF), and nitric oxide (NO) metabolites in synovial fluid from canine joints with osteoarthritis (OA) secondary to naturally acquired cranial cruciate ligament (CCL) rupture and experimental CCL transection.
Animals: 57 dogs (clinical group) with OA secondary to CCL rupture; 5 dogs (experimental group) with OA secondary to CCL transection; 19 control dogs with normal joints.
Procedure: Joints were radiographed and graded for seventy of OA. Synovial fluid was collected from dogs: at surgery from the clinical group, at 90 days after surgery from the experimental group, and at necropsy from the control group. Activities of IL-6 and TNF, as well as concentration of the NO metabolites (NO2-/NO3-) were measured, and results were reported as mean +/- SEM.
Results: IL-6 activity in dogs of the clinical (290 +/- 40 U/ml) and experimental (494 +/- 165 U/ml) groups was greater than that in control dogs (6 +/- 1.6 U/ml; P < 0.05). The TNF values in dogs of the clinical (3.0 +/- 0.5 pg/ml) and experimental (2.0 +/- 0.9 pg/ml) groups were lower than those in control dogs (8.6 +/- 2.3 pg/ml; P < 0.05). The IL-6 values were negatively associated with radiographic score of OA and were positively associated with age (R2 = 26.5%, P < 0.05).
Conclusion: Dogs with OA secondary to naturally acquired CCL rupture and experimental CCL transection had significantly different alterations in synovial fluid IL-6 and TNF values. The decrease in IL-6 activity with advancing OA was independent of the increase in IL-6 activity with aging.
Clinical Relevance: IL-6 and TNF may be involved in pathogenesis of OA secondary to naturally acquired and experimentally induced CCL rupture.
Etiopathogenesis of Canine Cruciate Ligament Disease: A Scoping Review.
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