Can platelet-rich plasma enhance tendon repair? A cell culture study.
BACKGROUND
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.


OBJECTIVE
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.


METHODS
Controlled laboratory study.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.


CONCLUSIONS
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.
de Mos
Marieke
M
Department of Orthopaedics, Erasmus MC University Medical Center, Rotterdam, the Netherlands. m.demos@erasmusmc.nl
van der Windt
Anna E
AE
Jahr
Holger
H
van Schie
Hans T M
HT
Weinans
Harrie
H
Verhaar
Jan A N
JA
van Osch
Gerjo J V M
GJ
D049109:Cell Proliferation; D002478:Cells, Cultured; D024042:Collagen Type I / Q000096:biosynthesis* / Q000235:genetics; D024061:Collagen Type III / Q000096:biosynthesis* / Q000235:genetics; D004247:DNA / Q000032:analysis; D015870:Gene Expression; D006801:Humans; D020782:Matrix Metalloproteinases / Q000096:biosynthesis; D053657:Platelet-Rich Plasma; D013710:Tendons / Q000166:cytology* / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis; D014945:Wound Healing / Q000502:physiology*
D024042:Collagen Type I; D024061:Collagen Type III; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; D004247:DNA; D020782:Matrix Metalloproteinases