de Mos Marieke, van der Windt Anna E, Jahr Holger, van Schie Hans T M, Weinans Harrie, Verhaar Jan A N, van Osch Gerjo J V M
Department of Orthopaedics, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
Am J Sports Med. 2008 Jun;36(6):1171-8. doi: 10.1177/0363546508314430. Epub 2008 Mar 7.
Autologous platelet-rich plasma (PRP) application appears to improve tendon healing in traumatic tendon injuries, but basic knowledge of how PRP promotes tendon repair is needed.
Platelet-rich plasma has a positive effect on cell proliferation and collagen production and induces the production of matrix-degrading enzymes and endogenous growth factors by human tenocytes.
Controlled laboratory study.
Human tenocytes were cultured 14 days in 2% fetal calf serum medium complemented with 0%, 10%, or 20% vol/vol platelet-rich clot releasate ([PRCR] the active releasate of PRP) or platelet-poor clot releasate (PPCR). At day 4, 7, and 14, cell amount, total collagen, and gene expression of collagen I alpha 1 (COL1) and III alpha 1 (COL3), matrix metalloproteinases ([MMPs] MMP1, MMP3, and MMP13), vascular endothelial-derived growth factor (VEGF)-A, and transforming growth factor (TGF)-beta1 were analyzed.
Platelet numbers in PRP increased to 2.55 times baseline. Growth-factor concentrations of VEGF and platelet-derived growth factor (PDGF)-BB were higher in PRCR than PPCR. Both PRCR and PPCR increased cell number and total collagen, whereas they decreased gene expression of COL1 and COL3 without affecting the COL3/COL1 ratio. PRCR, but not PPCR, showed upregulation of MMP1 and MMP3 expression. Matrix metalloproteinase 13 expression was not altered by either treatment. PRCR increased VEGF-A expression at all time points and TGF-beta1 expression at day 4.
In human tenocyte cultures, PRCR, but also PPCR, stimulates cell proliferation and total collagen production. PRCR, but not PPCR, slightly increases the expression of matrix-degrading enzymes and endogenous growth factors.
In vivo use of PRP, but also of PPP to a certain extent, in tendon injuries might accelerate the catabolic demarcation of traumatically injured tendon matrices and promote angiogenesis and formation of a fibrovascular callus. Whether this will also be beneficial for degenerative tendinopathies remains to be elucidated.
自体富血小板血浆(PRP)的应用似乎可改善创伤性肌腱损伤的肌腱愈合,但需要了解PRP促进肌腱修复的基本知识。
富血小板血浆对细胞增殖和胶原蛋白生成具有积极作用,并可诱导人肌腱细胞产生基质降解酶和内源性生长因子。
对照实验室研究。
将人肌腱细胞在补充有0%、10%或20%体积/体积富血小板凝块释放物([PRCR],PRP的活性释放物)或贫血小板凝块释放物(PPCR)的2%胎牛血清培养基中培养14天。在第4天、第7天和第14天,分析细胞数量、总胶原蛋白以及胶原蛋白Iα1(COL1)和IIIα1(COL3)、基质金属蛋白酶([MMPs] MMP1、MMP3和MMP13)、血管内皮生长因子(VEGF)-A和转化生长因子(TGF)-β1的基因表达。
PRP中的血小板数量增加至基线的2.55倍。PRCR中VEGF和血小板衍生生长因子(PDGF)-BB的生长因子浓度高于PPCR。PRCR和PPCR均增加了细胞数量和总胶原蛋白,而它们降低了COL1和COL3的基因表达,且不影响COL3/COL1比值。PRCR而非PPCR显示MMP1和MMP3表达上调。两种处理均未改变基质金属蛋白酶13的表达。PRCR在所有时间点均增加VEGF-A表达,在第4天增加TGF-β1表达。
在人肌腱细胞培养中,PRCR以及PPCR均可刺激细胞增殖和总胶原蛋白生成。PRCR而非PPCR可轻微增加基质降解酶和内源性生长因子的表达。
在肌腱损伤中体内使用PRP以及在一定程度上使用PPP,可能会加速创伤性损伤肌腱基质的分解代谢分界,并促进血管生成和纤维血管性骨痂的形成。这是否对退行性肌腱病也有益仍有待阐明。