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Platelet Rich Plasma

STEM CELL is the future and PRP is the gateway


Skin aging is a natural part of getting older.  The loss and dysfunction of fibroblasts - the cells that produce collagen and the matrix of our skin, results in the loss of collagen, thinning of the skin and wrinkling.  


We can counter this by exploiting the natural healing and repair mechanism that occurs with an injury.  When an injury occurs, our body calls in platelets and these become activated releasing growth factors, stimulating fibroblasts and recruiting stem cells to repair the injury.  In the process, a remodeling and renewal of the skin occurs.  Platelets are also an immune system cell, controlling inflammation and the activity of the T-lymphocytes, providing a local anti-inflammatory effect in the tissues.  


PRP (platelet rich plasma) is produced when your blood is drawn (via regular IV blood draw) into a special tube Regen-PRP which is then centrifuged to concentrate the platelets.  To use, we draw up only the golden PRP leaving behind the red blood cells.  This is colloquially called “liquid gold” for its golden color.  This liquid contains growth factors which are involved in activation, proliferation, and differentiation of fibroblasts, keratinocytes, and stem cells.  It is involved in remodeling of the extracellular matrix ECM, melanogenesis and immunomodulation.  It also has the ability to restore cell-cell communication and rebalance the immune response.  This is the power of PRP:  Collectively, these signals help stimulate mesenchymal stem cell (MSC) migration and differentiation at the site of injection.  


Platelet activation occurs when PRP is injected into the patient’s tissues.  Platelets are activated by contact with extracellular matrix protein (e.g. collagen) at the injection site.  


Intradermal injections of PRP results in overall improvement in skin texture, elasticity, tone, with improvement in pigmentation, scarring, wrinkles and inflammation.  


Histological examinations of the skin from patients treated with PRP have shown changes to the epidermis and dermis with increased thickness, better organization of collagen fibers, and restoration of the skin architecture.


For the best treatment and to prevent diffusion of PRP and ensure a sustained and localized action, we recommend PRF (platelet rich fibrin):  2  vials of PRP  and 1 vial of RegenATS (autologous-thrombin serum) for a total of three vials.  RegenATS system is designed to separate the enzymes of the coagulation cascade from the patient's serum.  This produces a serum containing activated thrombin which converts plasma fibrinogen to fibrin  monomers which will polymerize and form the clot.  Mixing the product of the RegenATS with PRP allows the physiological formation of a fibrin clot in which platelets will secrete growth factors slowly and in a controlled manner.   The fibrin scaffold guides clot formation, serves as a supportive template for tissue regeneration, and sustains growth factors and stem cells. 


Other systems may produce an injectable PRF liquid that is much smaller in volume and is often red and cloudy in color due to contamination with red blood cells and granulocytes (a type of white blood cell) which greatly affects the therapeutic effect of PRP.  Monocytes are preserved as the presence of monocytes have non-specific immunomodulatory activity and are also a source of certain growth factors. 


Why is this? 

Red blood cells trapped in the fibrin clot must be eliminated and their degradation releases free radicals and oxidative stress and components such as heme from hemoglobin are inflammatory.  

White blood cells are a double edged sword.  While  granulocytes can secrete a large amount of growth factors that stimulate angiogenesis and new collagen deposition, they are the quintessential pro-inflammatory cell.  They are full of potent destructive enzymes such as peroxidases, proteases and collagenases that are crucial for fighting bacterial infection.  It has been demonstrated in neutrophil (the main granulocyte) depleted mice that the absence of neutrophils does not affect cutaneous healing, and might even accelerate it.  


PRF = PRP + ATS (anti-thrombin serum):  offers all the clinical benefits of PRP as well as a naturally forming fibrin scaffold that guides clot formation, serves as a supportive template for tissue regeneration, and  sustains growth factors and stem cells.  PRF confines growth factor secretion to the clotting site. In tissue repair, recruited fibroblasts reorganize this fibrin matrix and initiate collagen synthesis.  Thus, the combined effects of growth factor secretion and fibroblast recruitment in PRF work synergistically to promote collagenesis and tissue regeneration. Injury-induced growth factor signaling recruits


PRP contains these main platelet released growth factors:

PDGF (platelet derived growth factor):  Cell growth, new generation and repair of blood vessels, collagen production

VEGF (vascular endothelial growth factor): Promotion of angiogenesis, promotion of wound healing.

EGF (endothelial growth factor): Promotion of epithelial cell growth, angiogenesis, promotion of wound healing.

FGF (fibroblast growth factor):  Growth factor present in the epithelialization phase of wound healing.  Keratinocytes cover the wound, forming the epithelium.

TGF-B (transforming growth factor beta): Growth and neogenesis of epithelial cells and vascular endothelial cells, promotion of wound healing

IGF (insulin growth factor):  Cell growth regulation

CTGF (connective tissue growth factor): Promotes angiogenesis, cartilage regeneration, and platelet adhesion.

KGF (keratinocyte growth factor):  Growth and new keratinocytes generation.



Anti-aging:  Activation of fibroblasts, endothelial cells, and stem cells that can result in increased production of collagen, elastin, improved vascularization and improved fat volume.  PRP can also increase the production of hyaluronic acid.  


Acne scars:  PRP increases the ECM through activation of fibroblasts and scar remodeling. 


Scar improvement:  In scars, there is an imbalance of collagen breakdown and collagen generation.  PRP restores balance between MMP (matrix metalloproteinases - enzymes involved in selective degradation of collagen) and TIMP (tissue inhibitor metalolloproteinases - enzymes involved in preventing excessive tissue degradation) and allows scar tissue to be remodeled. 


Vulvar lichen sclerosis:  This condition is thought to be due to two things:  1) an  imbalance in removal of damaged tissue and regeneration with scarring  and 2) an autoimmune response that targets extracellular matrix ECM resulting in inflammation.  PRP helps to restore the balance of MMP and TIMP to induce tissue remodeling and repair of damaged skin and also modulates autoimmunity.  


Lichen Planopilaris: Similar to vulvar lichen sclerosis, this condition is thought to be due to two things:  1) an  imbalance in removal of damaged tissue and regeneration with scarring  and 2) an autoimmune response that targets extracellular matrix ECM resulting in inflammation.  PRP helps to restore the balance of MMP and TIMP to induce tissue remodeling and repair of damaged skin and also modulates autoimmunity.  


Hair Growth: PRP contains many growth factors such as VEGF, PDGF, HGF, IGF1 that are known to influence the hair growth cycle and is thought to function by initiation/ extension of the anagen phase and promoting vascularization. 


Melasma: Melasma is a complex disorder and thought to be more than just a pigmentation disorder which makes sense because we know sun protection and bleaching agents alone does not fix the problem. It is now thought to have alterations on the molecular level of the Wnt pathway and TGFB.  Melasma lesions have reduced expression of TGFB.  PRP contains growth factors that can modulate the signaling pathways associated with melasma.   Cayirli et al 2004 reported that end the end of three sessions with 15-day intervals, there was >80% reduction in epidermal hyperpigmentation and in the follow-up period of 6months, there was no recurrence of melasma.  


Vitiligo: TGFB has been implicated due to its ability to decrease melanin synthesis. PRP is thought to modulate the signaling pathways and also modulate autoimmunity. 


RegenPRP: Standardized PRP for skin, hair and genitourinary disorders.  Antoin Turzi & Regn Lab team.  Biobridge foundation Editions. 

Boer HD, Verseyden C, Ulfman L, et al. Fibrin and activated platelets cooperatively guide stem cells to a vascular injury and promote differentiation towards an endothelial cell phenotype. Arterioscler Thromb Vasc Biol 2006;26(7):1653–9.  (activated platelets recruit stem cells) 

Ponte AL, Marais E, Gallay N, et al. The in vitro migration capacity of human bone marrow mesenchymal stem cells: comparison of chemokine and growth factor chemotactic activities. Stem Cells 2007;25(7):1737–45.

Jenkins G 2002 Molecular mechanisms of skin ageing. Mech Ageing Dev 123, 801-810.  (Anti ageing effects via activation of fibroblasts.)

Dovi et al 2003; Dovi et 2004 Accelerated wound closure in neutrophil-depleted mice.  J of leukocyte biology 73, 448-455. 

Dovi et 2004 Neutrophil function in the healing wound; adding insult to injury?  Thomb Haemost 92, 275-280 (Neutrophils are not necessary for wound healing)

de Oliverira GAP et al 2012 Metalloproteinases 2 and 9 and their tissue inhibitors 1 and 2 are increased in vulvar lichen sclerosus. Eur J Obstet Gynecol Reprod Bio 161, 91-101.  (Balance of MMP and TIMP is altered in aged skin, acne, and lichen sclerosus)

Chan I et al 2004 Characterization of IgG autoantibodies to ECM 1 in lichen sclerosus.  Clin Exp Dermatol 29, 499-504. 

Erickson BA et al 2016 Understanding the relationship between chronic systemic disease and lichen sclerosus urethral strictures.  J Urol 195. 363-368. (Autoimmune responses that target ECM may be contributing factors in vulvar lichen sclerosus.)

Cheng M et al 2012 Effects of age and platelet rich plasma on ACL cell viability and collagen gene expression.  J Orthop Res 30, 79-85. (PRP increases production of collagen)

Abuaf OK et al 2016 Histologic evidence of new collagen formulation using PRP in skin rejuvenation:  A prospective controlled clinical study.  Ann Dermatol 28, 718-724.

Charles-de-Sa L et al, 2018 Effect of use of PRP in skin with intrinsic aging process. Aesthet Surg J 38, 321-328. 

Diaz-Ley B et al, 2015 Benefits of plasma rich growth factors in skin photodamage: clinical response and histological  assessment. Dermal Ther 28, 258-263.

Draelos ZD et al 2019 Pilot study.  Autologous PRP used in a topical cream for facial rejuvenation.  J of Cosmetic dermatology.

Min S et al 2018 Combination of PRP in fractional CO2 laser treatment increased clinical efficacy of  acne scar by enhancement of collagen production and modulation of laser induced inflammation.  Lasers in surgery and medicine 50, 302-310.

Na JJ et al 2011 Rapid healing and reduced erythema after ablative fractional carbon dioxide laser resurfacing combined with the application of autologous PRP.  Dermatol Surg 37, 463-468. (Histologic examinations of skin treated w/ PRP show changes in epi and dermis with increased skin thickness, better organization of collagen fibers and restoration of sin architecture. )

Carlavan I et 2018 Atrophic scar formation in patients with acne involves long acting immune responses with plasma cells and alteration of sebaceous glands.  The British J of Dermatology 179, 906-917. 

Holland DB et al 2004 Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar.  The British J of Dermatology 150, 72-81. (Acne patients prone to scarring express differences in expression of MMP and TIMP which affect remodeling of the ECM as well as pro and antiinflammatory cytokines.)

Lee WJ  et al 2013  Serial sections of atrophic acne scars help in the interpretation of microscopic findings and the selection of good therapeutic modalities.  J Eur Acad Dermatol Venereol 27, 643-646.  (A prolonged inflammatory response is associated with decreased collagen deposition.) 

Girijala RL et al 2018 PRP for androgenic alopecia treatment:  a comprehensive review. Dermatol Online J 24, 1-13. 

Gupta AK and Carveil 2016 A mechanistic model of PRP treatment for AGA.  Dermatol Surg 42, 1335-1339. 

(PRP contains growth factors known to influence hair growth cycle.) 

Kim DS et al 2004 TGFB1 decreases melanin synthesis via delayed extracellular signal-regulated kinase activation.  Int J Biochem Cell Biol 36, 1482-1491. (TGFB involved in regulation of melanin synthesis.)

Hofny ERM et al 2019b Increased expression of TGF-beta protein in the lesional skins of melasma patients following treatment with PRP.  J Cosmet Laser Ther, 1-8. (Melasma lesions have reduced expression of TGFB compared to normal ones. )

Cayirli M. et al 2014 Regression of melasma with PRP treatment. Ann Dermatol 26, 401-402. 


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