Histopathological, immunohistochemical, and biomechanical effects of splenectomy on Achilles tendon healing in rats
Gulec, M. Akif
Eker, A. Akdogan
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CitationYuksel, S., Gulec, M. A., Gultekin, Z., Caglar, A., Beytemur, O., Alagoz, E., … Karaoz, E. (2019). Histopathological, immunohistochemical, and biomechanical effects of splenectomy on Achilles tendon healing in rats. CONNECTIVE TISSUE RESEARCH, 60(2), 200–208. https://doi.org/10.1080/03008207.2018.1483361
Purpose: This study aimed to assess Achilles tendon repair in rats following splenectomy to simulate patients with musculoskeletal system injury who had splenectomy after spleen injury, a situation often seen in orthopedics and traumatology practice. Materials and Methods: The study included 32 male Sprague-Dawley rats (10 months old; average weight, 394.5 +/- 28.3 g). The rats were fed with standard rodent food ad libitum at 22 degrees C in a dark environment for 12 h. They were divided into two groups, namely the splenectomy (total splenectomy and Achilles tendon repair) and control groups (only Achilles tendon repair; n = 16). Four weeks after the surgery, the rats were euthanized, and their Achilles tendons were examined histopathologically, immunohistochemically, and biomechanically. Results: In the splenectomy group, proinflammatory cytokines, such as interleukin-1 beta, tumor necrosis factor-alpha, and interferon-gamma, showed significantly lower values than those in the control group (p <0.01); moreover, the levels of anti-inflammatory cytokines like vascular endothelial growth factor, transforming growth factor-beta 1, interleukin-2, interleukin-10, and hepatocyte growth factor were significantly higher than in the control group (p < 0.001). The average ultimate tensile strengths were 2.58 +/- 0.5 in the splenectomy and 2.78 +/- 0.3 in the control group (p = 0.043). The average values were 0.33 +/- 0.5 in the splenectomy and 0.44 +/- 0.1 in the control group (p = 0.021). Conclusion: Splenectomy may positively influence Achilles tendon healing through modification of the proinflammatory/anti-inflammatory ratio in favor of anti-inflammatory cytokines by causing a decrease in spleen-originated inflammatory cells.