Intratendon Delivery of Leukocyte-Poor Platelet-Rich Plasma Improves Healing Compared With Leukocyte-Rich Platelet-Rich Plasma in a Rabbit Achilles Tendinopathy Model

Intratendon Delivery of Leukocyte-Poor Platelet-Rich Plasma Improves Healing Compared With Leukocyte-Rich Platelet-Rich Plasma in a Rabbit Achilles Tendinopathy Model
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在兔跟腱病模型中,与富含白细胞的富含血小板的血浆相比,肌腱内输送缺乏白细胞的富含血小板的血浆可改善愈合

DOI:
10.1177/0363546517694357
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发表时间:
2017-07-01
影响因子:
4.8
通讯作者:
Ouyang, Hongwei
Ouyang, Hongwei
中科院分区:
医学1区
文献类型:
--
作者:
Yan, Ruijian;Gu, Yanjia;Ouyang, Hongwei

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背景:慢性肌腱病是一种常见的临床问题,既影响运动员,也影响不活跃的中年患者。尽管有研究表明,不同的富含血小板血浆(PRP)制剂在体外可以发挥不同的治疗作用,但在体内肌腱病条件下,白细胞在PRP中的作用尚未明确。目的:比较低白细胞PRP(LP-PRP)和富白细胞PRP(LR-PRP)在兔慢性肌腱病模型中的作用。研究设计:对照实验室研究。方法:跟腱局部注射胶原酶4周后,随机给予(1)L 200μLP-PRP(n=8),(2)200μL LR-PRP(n=8),(3)200μL生理盐水(n=8)治疗。在治疗后4周通过磁共振成像(MRI)、细胞因子定量、实时聚合酶链式反应基因表达分析、组织学和透射电子显微镜(TEM)评估愈合结果。结果:T2标测显示LR-PRP组和生理盐水组的T2信号强度均高于LP-PRP组。组织学上,LP-PRP组的总体评分明显好于LR-PRP组(P=.001)和生理盐水组(P&t;.001)。此外,透射电子显微镜显示,LP-PRP组的胶原纤维直径大于LR-PRP组(P<.001)。酶联免疫吸附试验显示,LP-PRP组分解代谢细胞因子IL-6水平显著低于LR-PRP组(P=.001)和生理盐水组(P=.021)。与生理盐水组相比,LP-PRP组I型胶原表达显著增加(P=0.004),而LR-PRP组则无明显变化。与生理盐水组相比,LP-PRP组和LR-PRP组的基质金属蛋白酶(MMP1)-1和MMP3的表达水平均显著降低。但仅LP-PRP组TIMP-1的表达显著高于生理盐水组(P=0.024)。结论:与LR-PRP相比,LP-PRP能促进肌腱愈合,是临床治疗肌腱病的较佳选择。临床意义:PRP广泛应用于慢性肌腱病的临床治疗。然而,临床结果并不明确。了解白细胞在体内对PRP介导的组织愈合的影响,有助于更好地临床治疗慢性肌腱病。需要进一步的研究才能将我们的发现转化为临床环境。
Background: Chronic tendinopathy is a commonly occurring clinical problem that affects both athletes and inactive middle-aged patients. Although some studies have shown that different platelet-rich plasma (PRP) preparations could exert various therapeutic effects in vitro, the role of leukocytes in PRP has not yet been defined under tendinopathy conditions in vivo. Purpose: This study compared the effects of the intratendon delivery of leukocyte-poor PRP (Lp-PRP) versus leukocyte-rich PRP (Lr-PRP) in a rabbit chronic tendinopathy model in vivo. Study Design: Controlled laboratory study. Methods: Four weeks after a local injection of collagenase in the Achilles tendon, the following treatments were randomly administered on the lesions: injections of (1) 200 μL of Lp-PRP (n = 8), (2) 200 μL of Lr-PRP (n = 8), or (3) 200 μL of saline (n = 8). Healing outcomes were assessed at 4 weeks after therapy with magnetic resonance imaging (MRI), cytokine quantification, real-time polymerase chain reaction analysis of gene expression, histology, and transmission electron microscopy (TEM). Results: MRI revealed that the Lr-PRP and saline groups displayed higher signal intensities compared with the Lp-PRP group with T2 mapping. Histologically, the Lp-PRP group displayed significantly better general scores compared with the Lr-PRP (P = .001) and saline (P < .001) groups. Additionally, TEM showed that the Lp-PRP group had larger collagen fibril diameters than the Lr-PRP group (P < .001). Enzyme-linked immunosorbent assay showed a significantly lower level of catabolic cytokine IL-6 in the Lp-PRP group compared with the Lr-PRP (P = .001) and saline (P = .021) groups. The Lp-PRP group displayed significantly increased expression of collagen I compared with the saline group (P = .004) but not the Lr-PRP group. Both the Lp-PRP and Lr-PRP groups exhibited significantly lower matrix metalloproteinase (MMP)–1 and MMP-3 expression levels compared with the saline group. However, only the Lp-PRP group displayed significantly higher expression of TIMP-1 than the saline group (P = .024). Conclusion: Compared with Lr-PRP, Lp-PRP improves tendon healing and is a preferable option for the clinical treatment of tendinopathy. Clinical Relevance: PRP is widely used in the clinical management of chronic tendinopathy. However, the clinical results are ambiguous. It is imperative to understand the influence of leukocytes on PRP-mediated tissue healing in vivo, which could facilitate the better clinical management of chronic tendinopathy. Further studies are needed to translate our findings to the clinical setting.