INTRODUCTION
Platelet-rich plasma (PRP) is an autologous blood product consisting of platelet-derived growth factors and concentrated platelets 1.6 to 8-fold times physiologic levels. Platelets may be “activated†to release growth-factor (GF)-rich granules using calcium-based compounds, thrombin, and components of extracellular matrix.1 Due to PRP’s purported regenerative, anti-inflammatory and anti-bacterial properties, it is utilized for various medical conditions. In dermatology, PRP is promising for skin rejuvenation, chronic ulcers, and alopecia.
The Mechanism of PRP for Hair Regrowth
The exact mechanism for PRP-induced hair regrowth is unknown. Platelet-derived GFs include platelet-derived growth factor (PDGF), transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF), epithelial growth factor (EGF), and insulin-like growth factor (IGF). It is unclear whether platelet activation is required, or if the injection process is enough for GF release as both preparations result in therapeutic response.
GFs bind receptors on hair follicle bulge stem cells – PDGF causes keratinocyte proliferation and prolongs the anagen phase in mouse models, IGF-1 prevents induction of the catagen phase, fibroblast growth factor (FGF) promotes dermal papilla cell (DPC) proliferation and hair shaft elongation, while VEGF is implicated in hair follicle revascularization.2-5 Although it was hypothesized that PRP’s effects are dependent on GF plasma concentration,5,8 clinically significant results despite low GF concentrations contradict this theory.9 For instance, a clinical trial demonstrated that although two, commercially available, calcium-activated PRP kits had similar GF concentrations, one kit resulted in superior hair growth.1
Calcium chloride-activated PRP causes upregulation of mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling, as well as downregulation of glycogen synthase kinase-3 and Wnt pathways, all playing a role in hair growth.6,7 PRP increases expression of type I collagen and matrix metalloproteinase 1 mRNA in dermal fibroblasts. Upregulation of Bcl-2, an anti-apoptotic protein, allows for differentiation of hair follicle stem cells, while β-catenin and FGF-7 in dermal fibroblasts prolongs the anagen phase, and Ki-67 results in epidermal cell proliferation.10 PRP also contains fibrin, fibronectin, thrombin, vitronectin and cytokines [interferon (IFN)-α, interleukins (ILs)-4, 5, 13, 17, tumor necrosis factor (TNF)]; their role in hair regeneration is unknown.3
The Mechanism of PRP for Hair Regrowth
The exact mechanism for PRP-induced hair regrowth is unknown. Platelet-derived GFs include platelet-derived growth factor (PDGF), transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF), epithelial growth factor (EGF), and insulin-like growth factor (IGF). It is unclear whether platelet activation is required, or if the injection process is enough for GF release as both preparations result in therapeutic response.
GFs bind receptors on hair follicle bulge stem cells – PDGF causes keratinocyte proliferation and prolongs the anagen phase in mouse models, IGF-1 prevents induction of the catagen phase, fibroblast growth factor (FGF) promotes dermal papilla cell (DPC) proliferation and hair shaft elongation, while VEGF is implicated in hair follicle revascularization.2-5 Although it was hypothesized that PRP’s effects are dependent on GF plasma concentration,5,8 clinically significant results despite low GF concentrations contradict this theory.9 For instance, a clinical trial demonstrated that although two, commercially available, calcium-activated PRP kits had similar GF concentrations, one kit resulted in superior hair growth.1
Calcium chloride-activated PRP causes upregulation of mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling, as well as downregulation of glycogen synthase kinase-3 and Wnt pathways, all playing a role in hair growth.6,7 PRP increases expression of type I collagen and matrix metalloproteinase 1 mRNA in dermal fibroblasts. Upregulation of Bcl-2, an anti-apoptotic protein, allows for differentiation of hair follicle stem cells, while β-catenin and FGF-7 in dermal fibroblasts prolongs the anagen phase, and Ki-67 results in epidermal cell proliferation.10 PRP also contains fibrin, fibronectin, thrombin, vitronectin and cytokines [interferon (IFN)-α, interleukins (ILs)-4, 5, 13, 17, tumor necrosis factor (TNF)]; their role in hair regeneration is unknown.3
