scholarly journals The Wonder Tool Platelet Rich Plasma in Cosmetic Dermatology, Trichology and Hair Transplant

Author(s):  
Garg Suruchi ◽  
Manchanda Shweta ◽  
Garg Chandi
2020 ◽  
Vol 3 (1) ◽  
pp. 27-33
Author(s):  
Patrycja Przybylska ◽  
Teresa Matthews‑Brzozowska

Androgenetic alopecia is a common condition, accounting for about 95% of all male hair loss. Standard therapeutic solutions recommend the use of minoxidil, finasteride, spironolactone, nutritional supplementation, phototherapy and hair transplant surgery. An increasingly popular alternative method that has been used in the case report is platelet rich plasma (PRP) mesotherapy characterized by autologous character, minimal invasiveness and no serious side effects. A series of 3 treatments was performed at 3-week intervals. The effects of using medical photographic documentation after completing a series of treatments.


Author(s):  
Safi Abbas Rizvi

<p>Platelet rich plasma (PRP) is a promising treatment choice for patients with thinning hair. Despite excellent clinical safety and low cost, its clinical standing is still weak. The effectiveness of this method depends on its dosage, number of sessions, their intervals and technique of injection incorporated. PRP can produce particularly some phenomenal effects when applied in cosmetic dermatology. The therapeutic value of PRP is equivalent to stem cells and considered as one of the promising therapeutic agents in regenerative medicine. Harvesting of PRP plays a significant role, which is obtained from the patient's blood after centrifugation of the sample i.e., the platelet concentrates above the baseline which is the plasma fraction of the autologous blood. There are many applications of PRP in the medical field and has an incredibly significant role in dermatologic conditions e.g., tissue regeneration, wound healing, scar revision, skin rejuvenation and alopecia. In this review, we will be analyzing the authenticity of the use of PRP in the treatment of alopecia. PRP, in current scenario, is considered as a novel treatment modality. The efficacy of PRP therapy carries some deficiencies, which include lacking standard in preparation and concentration of platelets in PRP.</p><p><strong> </strong></p>


Author(s):  
D. C. Brindley ◽  
M. McGill

Morphological and cytochemical studies of platelets have reported a surface coat, or glycocalyx, external to the plasma membrane (1). Biochemical analyses have likewise confirmed the highly adsorptive properties of platelets as transporters of coagulation factors (2). However, visualization of the platelet membrane by conventional EM procedures does not reflect this special relationship between the platelet and its plasma environment. By the routine method of alcohol-propylene oxide dehydration for Epon embedding, the lipid bilayer nature of the platelet membrane appears similar to other blood cells (Fig. 1). A new rapid embedding technique using dimethoxypropane (DMP) as dehydrating agent (13) has permitted ultrastructural analyses of the surface features of the platelet-plasma interface.Aliquots of human or rabbit platelet-rich plasma (PRP) were added to equal volumes of 6% glutaraldehyde in Millonig's buffer at 37° for 45 minutes, rinsed in buffer and postfixed in 1% osmium in Millonig's buffer for 45 minutes.


1998 ◽  
Vol 79 (01) ◽  
pp. 177-185 ◽  
Author(s):  
Ashia Siddiqua ◽  
Michael Wilkinson ◽  
Vijay Kakkar ◽  
Yatin Patel ◽  
Salman Rahman ◽  
...  

SummaryWe report the characterization of a monoclonal antibody (MAb) PM6/13 which recognises glycoprotein IIIa (GPIIIa) on platelet membranes and in functional studies inhibits platelet aggregation induced by all agonists examined. In platelet-rich plasma, inhibition of aggregation induced by ADP or low concentrations of collagen was accompanied by inhibition of 5-hydroxytryptamine secretion. EC50 values were 10 and 9 [H9262]g/ml antibody against ADP and collagen induced responses respectively. In washed platelets treated with the cyclooxygenase inhibitor, indomethacin, PM6/13 inhibited platelet aggregation induced by thrombin (0.2 U/ml), collagen (10 [H9262]g/ml) and U46619 (3 [H9262]M) with EC50 = 4, 8 and 4 [H9262]g/ml respectively, without affecting [14C]5-hydroxytryptamine secretion or [3H]arachidonate release in appropriately labelled cells. Studies in Fura 2-labelled platelets revealed that elevation of intracellular calcium by ADP, thrombin or U46619 was unaffected by PM6/13 suggesting that the epitope recognised by the antibody did not influence Ca2+ regulation. In agreement with the results from the platelet aggregation studies, PM6/13 was found to potently inhibit binding of 125I-fibrinogen to ADP activated platelets. Binding of this ligand was also inhibited by two other MAbs tested, namely SZ-21 (also to GPIIIa) and PM6/248 (to the GPIIb-IIIa complex). However when tested against binding of 125I-fibronectin to thrombin stimulated platelets, PM6/13 was ineffective in contrast with SZ-21 and PM6/248, that were both potent inhibitors. This suggested that the epitopes recognised by PM6/13 and SZ-21 on GPIIIa were distinct. Studies employing proteolytic dissection of 125I-labelled GPIIIa by trypsin followed by immunoprecipitation with PM6/13 and analysis by SDS-PAGE, revealed the presence of four fragments at 70, 55, 30 and 28 kDa. PM6/13 did not recognize any protein bands on Western blots performed under reducing conditions. However Western blotting analysis with PM6/13 under non-reducing conditions revealed strong detection of the parent GP IIIa molecule, of trypsin treated samples revealed recognition of an 80 kDa fragment at 1 min, faint recognition of a 60 kDa fragment at 60 min and no recognition of any product at 18 h treatment. Under similar conditions, SZ-21 recognized fragments at 80, 75 and 55 kDa with the 55kDa species persisting even after 18 h trypsin treatment. These studies confirm the epitopes recognised by PM6/13 and SZ-21 to be distinct and that PM6/13 represents a useful tool to differentiate the characteristics of fibrinogen and fibronectin binding to the GPIIb-IIIa complex on activated platelets.


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