What is the mechanism of action (MOA) of platelet-rich plasma (PRP) in hair loss?

Mechanism of Action of Platelet-Rich Plasma in Hair Loss

PRP promotes hair growth primarily by increasing proliferative activity of hair follicle cells, enhancing perifollicular vascularization, and accelerating the transition from telogen (resting) to anagen (growth) phase through concentrated growth factors released from platelets. 1, 2

Cellular and Molecular Mechanisms

Growth Factor Release and Follicular Stimulation

• Growth factors contained in platelet alpha-granules bind to the bulge area of hair follicles, which houses stem cells critical for hair regeneration 3
• PRP increases proliferative activity of hair follicle cells, as demonstrated by elevated Ki67+ keratinocytes in the epidermis and follicular bulge cells 1, 4
• Transforming growth factor beta (TGF-β) promotes extracellular matrix remodeling around hair follicles, creating a favorable microenvironment for growth 2
• Plasma proteins, particularly fibrin, act as a scaffold for sustained growth factor release rather than a single burst effect 2

Dermal Papilla Cell Activation

• PRP induces proliferation of dermal papilla cells, which are the command center for hair follicle cycling and growth 2
• Increased vascularization of perifollicular tissue provides enhanced nutrient and oxygen delivery to actively growing follicles 2

Hair Cycle Modulation

• PRP accelerates the telogen-to-anagen transition, shifting more follicles into active growth phase 2
• The percentage of anagen hairs increases significantly (p = 0.0016) compared to controls 1
• Studies demonstrate increased number of basal keratinocytes and improved epidermal thickness at the follicular level 1, 4

Histological Evidence

Microscopic Changes

• Scalp biopsies show increased epidermal thickness after PRP treatment compared to baseline 1
• Immunohistology reveals elevated β-catenin, CD34, and Ki67 antibodies, indicating enhanced proliferative activity of hair follicle cells 1
• Decreased Dkk-1 antibodies suggest reduced inhibition of Wnt signaling, which is crucial for hair follicle development 1
• Slight increase in small blood vessels around hair follicles supports the vascularization mechanism 4

Concentration-Dependent Effects

Platelet Threshold Requirements

• Higher platelet concentrations (1 to 1.5 million platelets per microliter) correlate with greater efficacy in terms of hair density, follicle diameter, and terminal hair density 1, 2
• Low platelet concentration is a common cause of treatment failure, along with inadequate injection volume and insufficient treatment frequency 1, 2

Growth Factor Paradox

• Interestingly, no direct correlation exists between individual growth factor levels (PDGF, EGF, VEGF) and clinical outcomes 1, suggesting the mechanism involves synergistic effects of multiple factors rather than any single growth factor
• Activated versus non-activated PRP shows no difference in efficacy for androgenetic alopecia, indicating that activation may not be necessary 1

Clinical Translation of Mechanism

Measurable Outcomes

• Hair density increases by 45.9 hairs per cm² on average after treatment series 1, 4
• Mean hair count increases by 33.6 hairs in treated areas compared to baseline 1, 4
• Terminal/vellus hair ratio improves, indicating conversion of miniaturized hairs to terminal hairs 1
• Hair shaft diameter increases, reflecting healthier, thicker hair production 1

Important Caveats

• Individual genetic factors significantly influence response to PRP therapy, explaining variable outcomes between patients 1, 2
• Some studies report no significant effects, likely attributable to suboptimal platelet concentration, inadequate volume, or insufficient treatment frequency 1
• The mechanism does not appear to involve permanent follicular rescue—relapse occurs 12-16 months after treatment cessation in some patients, requiring re-treatment 4