• Bmc Musculoskel Dis · Dec 2020

    Parecoxib alleviates the inflammatory effect of leukocyte-rich platelet-rich plasma in normal rabbit tendons.

    • Ming Zhou, Ning Wang, Gang Wang, Zishan Jia, and Xiaolei Qi.
    • Department of Rehabilitation Medicine, First Medical Center of Chinese PLA General Hospital, 28 Fuxing Road, Beijing, 100853, People's Republic of China.
    • Bmc Musculoskel Dis. 2020 Dec 10; 21 (1): 831.

    BackgroundPlatelet-rich plasma (PRP) is widely used to treat tendon injuries. Its therapeutic effect varies depending on the different cell components, and white blood cells (WBCs) may play an important role in this phenomenon. The purpose of this study was to evaluate how PRP with different concentrations of WBCs affect normal rabbit tendon and assess whether non-steroidal anti-inflammatory drugs (NSAIDs) can suppress the catabolic effects of WBCs.MethodsSixteen adult New Zealand White rabbits were used. Blood samples were collected from each rabbit, and PRP was extracted following two different protocols to obtain leukocyte-poor PRP (LP-PRP) and leukocyte-rich PRP (LR-PRP). LP-PRP or LR-PRP was injected into the patellar tendon of each rabbit, while normal saline (NS) was injected as control. In LR-PRP + NSAID group, Parecoxib was administered after LR-PRP injection. For each group, 2 rabbits were euthanatized at day 5 and 14. The patellar tendons were collected and stained with hematoxylin and eosin. A semi-quantitative approach was used to assess the inflammatory response and tendon destruction based on the evaluation of the WBCs, vascularization, fiber structure, and fibrosis.ResultsThe LR-PRP group exhibited a higher total tendon score than the LP-PRP group at day 5 after PRP injection, but there was no significant difference between the two groups at day 14. For the NSAID group, the tendon score was lower than that of the LR-PRP group both at day 5 and 14.ConclusionLR-PRP can promote a higher inflammatory response than LP-PRP in the normal rabbit patellar tendon, and this effect can be suppressed by NSAIDs.

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