Pathomechanisms of injured-nerve pain have not been fully elucidated. Radicular pain and chronic constriction injury models have been established; however, producing these models is complicated. A sciatic nervepinch injury is easy to produce but the reliability of this model for evaluating pain behavior has not been examined. The current study evaluated pain-related behavior and change in pain markers in the dorsal root ganglion (DRG) of rats in a simple, sciatic nerve-pinch injury model. In the model, the sciatic nerve was pinched for 2 s using forceps (n = 20), but not injured in sham-operated animals (n = 20). Mechanical and thermal hyperalgesia were measured every second day for 2 weeks using von Frey filaments and a Hargreaves device. Calcitonin gene-related peptide (CGRP), activating transcription factor-3 (ATF-3), phosphorylated p38 mitogen activated protein (Map) kinase (p-p38), and nuclear factor-kappa B (NF-jB; p65) expression in L5 DRGs were examined at 4 and 7 days after surgery using immunohistochemistry. The proportion of neurons immunoreactive for these markers was compared between the two groups. Mechanical (during 8 days) and thermal hyperalgesia (during 6 days) were found in the pinch group rats, but not in the sham-operated animals (p \ 0.05); however, hyperalgesia was not significant from days 10 to 14. CGRP, ATF-3, p-p38, and NF-jB expression in L5 DRGs was upregulated in the nerveinjured rats compared with the sham-operated rats (p \ 0.01). Our results indicate that a simple sciatic nerve pinch produced pain-related behavior. Upregulation of the pain-marker expression in the nerve-injury model suggested it could be used as a model of pain. However, it was not considered as suitable for long-term studies.
Purpose
To determine if impregnating a suture with a cross-linking agent, f 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride (EDC), improved suture pull-out strength and cell viability.
Methods
Canine flexor digitorum profundus tendons were cut in canine zone D, and a single suture loop was placed in each end, with sutures soaked in either saline or in an EDC solution with a concentration of 1%, 10%, or 50%. Suture pull-out strength, stiffness, and elongation to failure was determined by pulling the loop until failure. Cytotoxicity of the EDC treatment was evaluated by suspending treated sutures over cultured tenocytes.
Results
Mechanical properties for the EDC-treated side were improved over controls when treated with the 10% and 50% EDC solutions. The ratio of dead to live cells was significantly increased at all distances from the suture for the 50%-EDC-treated group.
Conclusions
Suture treated with a 10% EDC solution provided the best combination of mechanical reinforcement and limited toxicity.
Clinical Relevance
Sutures so treated may improve the ability of a tendon repair to sustain early mobilization.
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