Hindawi Publishing Corporation
BioMed Research International
Volume 2014, Article ID 760709, 9 pages
http://dx.doi.org/10.1155/2014/760709

Clinical StudyThe Effect of Autologous Activated Platelet
Rich Plasma (AA-PRP) Injection on Pattern Hair Loss:
Clinical and Histomorphometric Evaluation
V. Cervelli,1 S. Garcovich,2 A. Bielli,3 G. Cervelli,4 B. C. Curcio,1 M. G. Scioli,3A. Orlandi,3 and P. Gentile1,5
1

Plastic and Reconstructive Surgery Department, University of Rome Tor Vergata, Via Montpellier, No. 1, 00173 Rome, Italy
Institute of Dermatology, Catholic University of the Sacred Heart, Rome, Italy
3
Institute of Anatomic Pathology, University of Rome Tor Vergata, Via Montpellier, No. 1, 00173 Rome, Italy
4
Science Education Department, University of Rome Tor Vergata, Via Montpellier, No. 1, 00173 Rome, Italy
5
San Salvatore in Lauro Place, No. 15, 00186 Rome, Italy
2

Correspondence should be addressed to P. Gentile; pietrogentile2004@libero.it
Received 28 November 2013; Revised 23 January 2014; Accepted 5 March 2014; Published 6 May 2014
Academic Editor: Garrett McGuinness
Copyright © 2014 V. Cervelli et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
To investigate the safety and clinical efficacy of AA-PRP injections for pattern hair loss. AA-PRP, prepared from a small volumeof blood, was injected on half of the selected patients’ scalps with pattern hair loss. The other half was treated with placebo. Threetreatments were given for each patient, with intervals of 1 month. The endpoints were hair re-growth, hair dystrophy as measured
by dermoscopy, burning or itching sensation, and cell proliferation as measured by Ki-67 evaluation. At the end of the 3 cycles oftreatment, the patients presented clinical improvement in the mean number of hairs, with a mean increase of 18.0 hairs in the target
area, and a mean increase in total hair density of 27.7 ( number of hairs/cm2 ) compared with baseline values. Microscopic evaluation
showed the increase of epidermis thickness and of the number of hair follicles two weeks after the last AA-PRP treatment compared
to baseline value (𝑃 < 0.05). We also observed an increase of Ki67+ keratinocytes of epidermis and of hair follicular bulge cells anda slight increase of small blood vessels around hair follicles in the treated skin compared to baseline (𝑃 < 0.05).

1. Introduction
Proponents of platelet-rich plasma (PRP) technology suggestthat its benefits include an increase in hard- and soft-tissue
wound healing. In addition, the role of PRP for the treatmentof pattern hair loss has been demonstrated in recent reports[1–4]. In particular, Rinaldi described the use of PRP in
alopecia areata (AA). This pilot study suggests that PRP may
serve as a safe and effective treatment option in AA andcalls for more extensive controlled studies with this method[4]. Uebel et al. showed that pretreatment of follicular units
with PRP before transplantation resulted in improved hair
growth and density [3]. Activated autologous PRP has beenreported to induce the proliferation of dermal papilla cells
by upregulating fibroblast growth factor 7 (FGF-7) and bcatenin as well as extracellular signal-related kinase (ERK)and Akt signalling [2]. Anagen-associated angiogenesis has
been suggested as one of the important factors in active
hair growth [5], due to the secretion of vascular endothelial
growth factor (VEGF) by the keratinocytes of the outerroot sheath and fibroblasts of the dermal papilla [5–7].
Increased secretion of VEGF influences growth of normal
and pathological dermal structures [8]. Tobin et al. reported
that the hair follicle mesenchyme exhibits significant haircycle-associated plasticity. Modulation of these cell interchanges is likely to be important during clinically importanthair follicle transformations, for example, vellus-to-terminal
and terminal-to-vellus transformations during androgenetic
alopecia [9]. Injection of PRP has been demonstrated to
improve cutaneous ischemic conditions and to increasevascular structures around hair follicles [1, 10]. Many of thecurrent treatment modalities for pattern hair loss have been

2

BioMed Research International
Table 1: Summary of patients’ characteristics.

Case

Age

The
Norwood-Hamilton
classification stage

Injection site

1
2
3
4
5
6
7
8
9
10

20
32
42
40
41
52
25
26
28
21

IIa
IIa
III
III vertex
IIaIV
III vertex
III
III
IIa

FrontalFrontalParietalParietal
FrontalParietal and vertex
ParietalParietal
FrontalFrontalshown to modulate angiogenesis and enhance blood flow [11].
The aim is to evaluate the effects of AA-PRP obtained froma small volume of blood on active hair growth. The data wereported proves the clinical efficacy of the treatment with
AA-PRP; moreover, patients’ satisfaction further confirms
the quality of the results. After studying this paper, thereader should be able to (1) prepare AA-PRP, (2) apply PRP
intraoperatively, (3) evaluate the clinical effect of AA-PRP on
hair growth, and (4) evaluate the histomorphometric effect of
AA-PRP on the proliferation of dermal papilla cells.

2. Material and Methods
2.1. Patients. A total of 10 male patients (age range: 22–60)
with male pattern hair loss (MPHL) were treated. The patientcharacteristics are summarized in Table 1. Patients, who hadreceived topical (such as minoxidil, prostaglandin, analogues,
retinoids, and corticosteroid) or systemic treatments for
MPHL (such as finasteride, dutasteride, and antiandrogens)in the previous 12 months were excluded. Patients witha propensity for keloids and patients who were immunosuppressed were also excluded. In addition, the numbersof platelets in PRP obtained from all participants weremicroscopically counted. This was a randomized, TrichoScan
evaluator blinded, placebo half-head group study.
The diagnosis of MPHL was established on the basis ofclinical and trichoscopic features (more than 20% variability
in hair diameter between affected and uninvolved areas),
while the extent and stage of MPHL were assessed according to the Norwood-Hamilton classification (as shown in
Table 1).
All patients provided written informed consent before
participating in the study, which was performed according to
the Declaration of Helsinki.
2.2. Treatment Protocol. AA-PRP was prepared from a small
volume of blood (18 cc) according to the method of CascadeSelphyl-Esforax system, with modifications [12–14]. Briefly,
to prepare PRP, blood was taken from a peripheral veinusing sodium citrate as an anticoagulant. The current systems

for preparing platelet concentrations use various centrifuges(however in this case we used 1100 g for 10 min). AA-PRP
was prepared in all cases with approval of the Transfusional Service. Although the method of preparation was notselective and may include leukocytes, the final aim is toobtain a platelet pellet. Growth factors are only secreted
once platelet activation begins, which in turn is stimulated
by Ca2+ . To optimize the secretion process, the optimum
concentration of Ca2+ was previously determined [12, 13].
Then, autologous-PRP not activated (A-PRP) obtained after
centrifugation (9 mL) was switched into 10-mL tubes containing Ca2+ extracted by Cascade-Selphyl-Esforax Kit. The
patients’ scalp affected by hair loss was divided in four
halves (Figure 8(a)) and cleansed with 70% alcohol, but local
anaesthesia was not injected on the treated areas. The AAPRP was injected on selected areas of the scalp at the amountof 0.1 mL/cm2 (Figure 3(d)). AA-PRP injections were injectedwith the AAPRP only on the frontal areas (Figures 1(b),9(b), and 10(b)); the parietal area was treated with placebo(Figure 8(b)). The scalps of patients affected by hair loss weredivided, respectively, into four parts: frontal, parietal, vertex,
and occipital parts. Patients with hair loss localized to thefrontal and parietal areas (Figures 1(a), 2(a), 9(a), and 10(a))
were injected with the AA-PRP only on the frontal areas(Figure 1(b)); the parietal area was treated with placebo basedon the injection of physiological solution. Patients with hairloss in the parietal and vertex parts (Figures 3(a) and 4(a))
were injected with the AA-PRP only in the parietal part of thescalp (Figure 4(b)); the vertex area was treated with placebo
based on the injection of physiological solution. In detail theauthors repeat the same numbers of injections in the half
treated with PRP and in the half treated with placebo. The
analysis of the areas of the scalp treated with PRP and placebo
was reported in Figures 8(a), 8(b), and 8(c).
2.3. Assessment Criteria. All patients were evaluated in fourstages: T0, beginning of study; T1 in 14 weeks; T2, 6 months;
and T3, 12 months. The effects of the treatment on hair growth
were assessed in all patients with the help of global photography, physician’s and patient’s global assessment scale, andstandardized phototrichograms.
Phototrichograms were performed in all patientsby a trained evaluator by means of FotoFinder-videoepiluminescence microscopy in combination with the
TrichoScan digital image analysis (Figure 7). TrichoScan
is a digital software-supported epiluminescence techniquefor measuring hair count (number of hairs/0.65 cm2 ), hairdensity (number of hairs/cm2 ), hair diameter, anagen/telogen
ratio, and vellus hair/terminal hair ratio. To determine thequality of hair leading to an increased hair density, it isimportant to differentiate the number of terminal and vellus
hairs. In TrichoScan all hairs with a diameter > 40 𝜇m
are categorized as terminal hair, and all hairs with lesser
diameter are categorized as vellus hair. In all patients, in boththe treatment and control half heads, two transitional areasof hair loss were defined and marked with a semipermanent
tattoo for the subsequent trichogram. In the target area
hairs were clipped and dyed with hair brown color for ten

BioMed Research International

3

(a)

(b)

Figure 1: A smoker 34-year-old male patient affected by hair loss. (a): preoperative situation of the frontal line. (b): postoperative situationof the frontal line after two weeks from the last treatment with increase of the hair count and hair density.

(a)

(b)

Figure 2: (a): preoperative situation of the scalp. (b): postoperative situation of the scalp two weeks from the last treatment. The picture showsa postoperative situation with increase of the hair count and hair density.

minutes in order to improve the hair contrast for the analytic
software. TrichoScan analysis. The evaluator of TrichoScan
analysis was blinded regarding the treatment and control
areas of the scalp and not involved in administration oftreatment.

Denmark), with positive and negative controls [16, 17]. The
percentage of Ki67+ cells in basal layer of epidermis, in outerroot sheath of hair follicles, and the number of vessels per
mm2 were calculated according to morphometric criteria[17].

2.4. Histological Evaluation. Incisional punch biopsies (3 mmin diameter) of the hair skin were obtained (Figure 3(c))
at baseline and after two months from the last AA-PRP
treatment and fixed in buffered formalin. Morphometricanalysis [15] was performed on Haematoxylin-Eosin-stained
paraffin serial sections (Figures 5 and 6) by evaluating the
thickness of epidermis and the number of follicles per mm2 ,according to the method [1]. About the orientation of skinbiopsies, all samples were cut perpendicularly at the surface
and embedded making attention to the correct orientation.

3. Results

2.5. Immunohistochemistry. Immunohistochemistry was
performed using mouse monoclonal anti-Ki67 (DakoCytomation, Denmark) and anti-CD31 (DakoCytomation,

3.1. Clinical Evaluation of AA-PRP Injection on Pattern Hair
Loss. The various hair growth parameters measured after
3 months of the first treatment were compared with thebaseline study before treatment (Figures 1(a), 2(a), 3(a), and4(a)) and between both treatment and control areas. Mean
total hair counts, hair density, and terminal and vellus hairdensities for the treatment and control areas are listed inTable 2. At baseline, there were no statistical differencesin hair count, hair density, and terminal and anagen hairdensities between the treatment and control area of the scalp.
The results of this study showed a significant increase in themean hair count for the treatment area after three months(3 months versus 0 month), with a mean increase of 18.0

4

BioMed Research International

(a)

(b)

(c)

(d)

Figure 3: A nonsmoker 52-year-old male patient affected by hair loss. (a): preoperative situation of the scalp with hair loss localized to thetemporal and nuchal areas. (b): intraoperative injection with the AA-PRP at 0.1 mL/cm2. (c): intraoperative incisional punch biopsies (3 mmin diameter) of the hair skin fixed in buffered formalin. (d): intraoperative study design.

(a)

(b)

Figure 4: A nonsmoker 52-year-old male patient affected by hair loss. (a): preoperative situation of the scalp with hair loss localized to theparietal and vertex areas. (b): postoperative situation of the scalp two weeks from the last treatment with increase of the hair count and hairdensity.

hairs in the target area compared to baseline, while thecontrol area showed a mean decrease of 2,0 hairs (control
versus treatment; 𝑃 < 0.0001). Accordingly, in the treatmentarea, a mean increase in total hair density of 27.7 (numberof hairs/cm2 ) compared to baseline was observed after 3
months and the control area displayed a mean decrease of
3.0 (number of hairs/cm2 ) in hair density at the same time(control versus treatment; 𝑃 < 0.0001). In addition, terminal
hair density improved significantly by 27.0 ± 15.3 (number ofhairs/cm2 ) in the treatment area (Figures 1(b), 2(b), and 4(b))
compared to baseline, while decreasing by 2.1±12.4 (numberof hairs/cm2 ) in the control area of the scalp (control versus
treatment; 𝑃 = 0.0003). There were no statistically significant
differences in vellus hair density between the study and thecontrol area after three months.
3.2. Histomorphometric Evaluation of AA-PRP Injection
on Pattern Hair Loss. Microscopic evaluation showed the5
PRP treatment

Baseline

Epidermal thickness (mm)

BioMed Research International
0.2
∗
0.1

0
Baseline
PRP treatment

(b)

(c)

Number of follicles (mm2 )

(a)

2
∗

1.5
1
0.5
0

Baseline
PRP treatment

(d)

(e)

(f)

Figure 5: PRP treatment increases the thickness of epidermis and the number of follicles of hair skin. (a) and (b): representative
microphotographs of hair skin epidermis at baseline (a) and after PRP treatment (b). (c): bar graph of epidermis thickness. (d) and (e):representative microphotographs of dermal hair follicles at baseline (d) and after PRP treatment (e). (f): bar graph of the number of hairfollicles/mm2 at baseline and after PRP treatment; ∗ indicates 𝑃 < 0.05. Original magnification: (a) and (b): 200x and (d) and (e): 100x.

Table 2: Relevant hair growth parameters assessed by TrichoScan
analysis for the treatment and control half-head areas at baseline andafter 14 weeks (T1).
Hair count (mean ± SD)
Baseline
T1
Hair density [1/cm2 ](mean ± SD)
Baseline
T1
Terminal hair density [1/cm2 ](mean ± SD)
Baseline
T1
Vellus hair density [1/cm2 ](mean ± SD)
Baseline
T1

Treatment area

Control area

103.6 ± 30.9
121.6 ± 34.1

111.3 ± 28.9
109.3 ± 28.2

159.4 ± 47.6
187.1 ± 52.5

171.2 ± 44.4
168.1 ± 43.3

142.7 ± 41.8
169.8 ± 47.0

152.7 ± 39.7
150.6 ± 41.7

14.8 ± 9.7
15.8 ± 8.5

16.9 ± 10.4
17.4 ± 13.9

increase of epidermis thickness (Figure 5(c); 𝑃 < 0.05)
in PRP-treated hair skin (Figure 5(b); 𝑃 < 0.05) after
three months from the AA-PRP treatment compared tobaseline value (Figure 5(a)). Two-week PRP treatment(Figure 5(e); 𝑃 < 0.05) was also accompanied by an increaseof the number of follicles (Figure 5(f); 𝑃 < 0.05) compared
to baseline value (Figure 5(d)). To better report the effectsof PRP, we investigated the proliferation of epidermal andhair follicular bulge cells (Figures 6(b) and 6(e); 𝑃 < 0.05).
After two weeks from the last treatment, we observed anincrease of Ki67+ basal keratinocytes of epidermis and ofhair follicular bulge cells (Figures 6(c) and 6(f); 𝑃 < 0.05)
compared to baseline (Figures 6(a) and 6(d)). PRP treatment(Figure 6(h); 𝑃 < 0.05) also associated with a slight increaseof small blood vessels around hair follicles in the skin treated(Figure 6(i); 𝑃 < 0.05) compared to baseline (Figure 6(g)).

4. Discussion
Current strategies for the treatment of pattern hair loss
are mainly focused on promoting cellular proliferation anddifferentiation during the hair growth cycle. It has been
postulated that minoxidil prolongs anagen and increases
hair follicle size through stimulation of potassium channels
and prostaglandin endoperoxide synthase-1, which increaselevel of prostaglandin E2 (PGE2) [11]. Minoxidil promotes
the survival of dermal papilla cells by increasing Bcl-2/Bax
ratio and by activating ERK and Akt [18]. Oral finasteridealso induces the prolongation of anagen hairs, which resultsin gradual thickening and elongation of the hairs [19]. In
addition, finasteride has been shown to reduce the pattern

6

BioMed Research International
PRP treatment

6

Ki67+ epidermal cells (%)

Baseline∗

420Baseline
PRP treatment

(b)

(c)

Ki67+ follicle cells (%)

(a)

6
∗
4
2
0
Baseline
PRP treatment

(e)

(f)

CD31+ vessels (mm2 )

(d)

3
∗

2
1
0

Baseline
PRP treatment
(g)

(h)

(i)

Figure 6: PRP treatment increases proliferation of epidermis basal cells and hair follicular bulge cells. (a) and (b): representative
microphotographs of Ki67+ proliferating cells by immunohistochemistry of hair skin epidermis at baseline (a) and after PRP treatment (b). (c):morphometric analysis of Ki67+ cells of hair skin epidermis at baseline and after PRP treatment. (d) and (e): representative microphotographsof Ki67+ proliferating cells by immunohistochemistry of hair follicles at baseline (d) and after PRP treatment (e). (f): morphometric analysisof the percentage of Ki67+ nuclei in hair follicles at baseline and after PRP treatment. (g) and (h): representative microphotographs of CD31+
small dermal vessels of hair skin at baseline (g) and after PRP treatment (h). (i): morphometric analysis of CD31+ small dermal vessels of hairskin at baseline and after PRP treatment; ∗ indicates 𝑃 < 0.05. Original magnification: (a) and (b): 200x and (d), (e), (g), and (h): 100x.

hair loss associated with increased expression of caspases andapoptosis inhibitors and therefore it is ultimately suggested
to activate anagen hair growth [20, 21]. Antiapoptotic effectsof activated PRP have been suggested as one of the major
contributing factors stimulating hair growth [2, 22]. PRPinduced activation of antiapoptotic regulators, such as the
Bcl-2 protein and Akt signalling, prolongs the survival ofdermal papilla cells during the hair cycle [2, 23]. In addition,
the upregulation of FGF-7/b-catenin signalling pathways
with PRP treatment is suggested to stimulate hair growthby inducing follicular stem cell differentiation as well as
prolonging the anagen phase of the hair growth cycle [2, 24].
Kang et al. [25] reported the clinical efficacy of injectionof CD34+ cell-containing PRP preparation for pattern hairloss. In this study, at three months after the first treatment, thepatients presented clinical improvement in the mean numberof hairs, 20.5 ± 17.0%, mean hair thickness, 31.3 ± 30.1%,
and mean two-point score, 84.4 ± 51.7%, compared withbaseline values. At 6 months, the patients presented clinicalimprovement in mean hair count, 29.2 ± 17.8%, mean hairthickness, 46.4 ± 37.5%, and mean two-point score, 121.3 ±
66.8%, compared with baseline.
In our study, AA-PRP was prepared from a small volumeof blood (18 cc) according to the method of Cascade-SelphylEsforax system [12, 13]. The authors suggested that a sufficientnumber of platelets could be obtained in all patients byusing an automated PRP preparation system. Giusti et al.
demonstrated that the optimal platelet concentration for theBioMed Research International

7

(a)

(b)

Figure 7: TrichoScan digital image analysis. (a) shows a preoperative hair count 154.5 hairs per cm2 and density 237.3 per cm2 . (b) shows apostoperative hair count 169,0 hairs per cm2 , and density 259.6 per cm2 .

(a)

(b)

(c)

Figure 8: Photos demonstrating the division of the scalp in four halves: frontal, parietal, vertex, and occipital (a). Patients with hair loss
localized to the frontal and parietal areas were injected with the AA-PRP only on the frontal areas (b); the parietal area was treated withplacebo based on the injection of physiological solution. Patients with hair loss in the parietal and vertex parts were injected with the AAPRP only in the parietal part of the scalp (c); the vertex area was treated with placebo based on the injection of physiological solution.

(a)

(b)

Figure 9: A nonsmoker 52-year-old male patient affected by hair loss. (a) Preoperative situation of the scalp with hair loss localized to theparietal and frontal areas. (b) Postoperative situation of the scalp two weeks from the last treatment with increase of the hair count and hairdensity.

8

BioMed Research International

(a)

(b)

Figure 10: A smoker 42-year-old male patient affected by hair loss. (a) Preoperative situation of the scalp with hair loss localized to the parietal
and frontal areas. (b) Postoperative situation of the scalp two weeks from the last treatment with increase of the hair count and hair density.

induction of angiogenesis in human endothelial cells was
1,500,000 platelets/𝜇L, whereas excessively high concentrations of platelets were suggested to decrease the angiogenic
potential [26]. In this study, a mean 1,484,555.6 platelets/𝜇L in
the PRP preparation could effectively stimulate follicular andperifollicular angiogenesis, which is suggested to be one of the
major factors in active hair growth [5, 11]. Our data suggestthat the injection of AA-PRP preparations has a positive
therapeutic effect on male and pattern hair loss without major
side effects.

Conflict of Interests
The authors declare that there is no conflict of interests
regarding the publication of this paper.

Authors’ Contribution
Pietro Gentile and Valerio Cervelli contributed to the following: conception and design, paper writing, and final approvalof the paper; Augusto Orlandi, Alessandra Bielli, and Maria
Giovanna Scioli contributed to the following: histomorphometric evaluation of AA-PRP injection on pattern hairloss and immunohistochemistry analysis; Simone Garcovich
contributed to the following: assessment criteria analysis
and TrichoScan evaluation; Beniamino Cristiano Curcio andGiulio Cervelli contributed to the following: English editing,collection and assembly of data, and data analysis.

References[3] C. O. Uebel, J. B. da Silva, D. Cantarelli, and P. Martins, “Therole of platelet plasma growth factors in male pattern baldness
surgery,” Plastic and Reconstructive Surgery, vol. 118, no. 6, pp.
1458–1466, 2006.
[4] A. Trink, E. Sorbellini, P. Bezzola et al., “A randomized,
double-blind, placebo- and active-controlled, half-head study
to evaluate the effects of platelet-rich plasma on alopecia areata,”
British Journal of Dermatology, vol. 169, no. 3, pp. 690–694, 2013.
[5] L. Mecklenburg, D. J. Tobin, S. Müller-Röver et al., “Active hair
growth (anagen) is associated with angiogenesis,” Journal of
Investigative Dermatology, vol. 114, no. 5, pp. 909–916, 2000.
[6] S. Lachgar, H. Moukadiri, F. Jonca et al., “Vascular endothelial
growth factor is an autocrine growth factor for hair dermal
papilla cells,” Journal of Investigative Dermatology, vol. 106, no.
1, pp. 17–23, 1996.
[7] U. Kozlowska, U. Blume-Peytavi, V. Kodelja et al., “Expressionof vascular endothelial growth factor (VEGF) in various compartments of the human hair follicle,” Archives of DermatologicalResearch, vol. 290, no. 12, pp. 661–668, 1998.
[8] V. Tarallo, L. Vesci, O. Capasso et al., “A placental growth
factor variant unable to recognize Vascular Endothelial Growth
Factor (VEGF) receptor-1 inhibits VEGF-dependent tumor
angiogenesis via heterodimerization,” Cancer Research, vol. 70,
no. 5, pp. 1804–1813, 2010.
[9] D. J. Tobin, A. Gunin, M. Magerl, B. Handijski, and R.
Paus, “Plasticity and cytokinetic dynamics of the hair follicle
mesenchyme: implications for hair growth control,” Journal of
Investigative Dermatology, vol. 120, no. 6, pp. 895–904, 2003.
[10] W. Li, M. Enomoto, M. Ukegawa et al., “Subcutaneous injectionsof platelet-rich plasma into skin flaps modulate proangiogenic
gene expression and improve survival rates,” Plastic and Reconstructive Surgery, vol. 129, no. 4, pp. 858–866, 2012.

[1] M. Takikawa, S. Nakamura, S. Nakamura et al., “Enhanced effectof platelet-rich plasma containing a new carrier on hair growth,”
Dermatologic Surgery, vol. 37, no. 12, pp. 1721–1729, 2011.

[11] M. Semalty, A. Semalty, G. P. Joshi, and M. S. M. Rawat, “Hairgrowth and rejuvenation: an overview,” Journal of Dermatological Treatment, vol. 22, no. 3, pp. 123–132, 2011.

[2] Z. J. Li, H.-I. Choi, D.-K. Choi et al., “Autologous platelet-richplasma: a potential therapeutic tool for promoting hair growth,”
Dermatologic Surgery, vol. 38, no. 7, part 11, pp. 1040–1046, 2012.

[12] V. Cervelli, M. G. Scioli, P. Gentile et al., “Platelet-richplasma greatly potentiates insulin-induced adipogenic differentiation of human adipose-derived stem cells through aBioMed Research International
serine/threonine kinase Akt-dependent mechanism and promotes clinical fat graft maintenance,” Stem Cells Translational
Medicine, vol. 1, no. 3, pp. 206–220, 2012.
[13] V. Cervelli, P. Gentile, M. G. Scioli et al., “Application of plateletrich plasma in plastic surgery: clinical and in vitro evaluation,”
Tissue Engineering C: Methods, vol. 15, no. 4, pp. 625–634, 2009.
[14] V. Cervelli, P. Gentile, B. de Angelis et al., “Application ofenhanced stromal vascular fraction and fat grafting mixed
with PRP in post-traumatic lower extremity ulcers,” Stem Cell
Research, vol. 6, no. 2, pp. 103–111, 2011.
[15] L. Campagnolo, G. Costanza, A. Francesconi, G. Arcuri, I.
Moscatelli, and A. Orlandi, “Sortilin expression is essential
for pro-nerve growth factor-induced apoptosis of rat vascularsmooth muscle cells,” PLoS ONE, vol. 9, no. 1, Article ID e84969,
2014.
[16] A. Francesconi, G. Arcuri, E. Doldo et al., “Age-related increaseof stem marker expression influences vascular smooth muscle
cell properties,” Atherosclerosis, vol. 224, no. 1, pp. 51–57, 2012.
[17] M. A. Stasi, M. G. Scioli, G. Arcuri et al., “Propionyl-l-carnitine
improves postischemic blood flow recovery and arteriogenetic
revascularization and reduces endothelial NADPH-oxidase 4mediated superoxide production,” Arteriosclerosis, Thrombosis,
and Vascular Biology, vol. 30, no. 3, pp. 426–435, 2010.
[18] J. H. Han, O. S. Kwon, J. H. Chung, K. H. Cho, H. C. Eun,and K. H. Kim, “Effect of minoxidil on proliferation andapoptosis in dermal papilla cells of human hair follicle,” Journalof Dermatological Science, vol. 34, no. 2, pp. 91–98, 2004.
[19] A. Tosti and B. M. Piraccini, “Finasteride and the hair cycle,”
Journal of the American Academy of Dermatology, vol. 42, no. 5,
pp. 848–849, 2000.
[20] M. E. Sawaya, U. Blume-Peytavi, D. L. Mullins et al., “Effects offinasteride on apoptosis and regulation of the human hair cycle,”
Journal of Cutaneous Medicine and Surgery, vol. 6, no. 1, pp. 1–9,
2002.
[21] J. P. D. R. Vaccari, M. E. Sawaya, F. Brand III et al., “Caspase-1
level is higher in the scalp in androgenetic alopecia,” Dermatologic Surgery, vol. 38, no. 7, part 11, pp. 1033–1039, 2012.
[22] C. Ferraris, M. Cooklis, R. R. Polakowska, and A. R. Haake,“Induction of apoptosis through the PKC pathway in cultured
dermal papilla fibroblasts,” Experimental Cell Research, vol. 234,
no. 1, pp. 37–46, 1997.
[23] O. S. Kwon, H. K. Pyo, Y. J. Oh et al., “Promotive effect ofminoxidil combined with all-trans retinoic acid (tretinoin) on
human hair growth in vitro,” Journal of Korean Medical Science,
vol. 22, no. 2, pp. 283–289, 2007.
[24] K.-C. Sohn, G. Shi, S. Jang et al., “Pitx2, a 𝛽-catenin-regulatedtranscription factor, regulates the differentiation of outer root
sheath cells cultured in vitro,” Journal of Dermatological Science,
vol. 54, no. 1, pp. 6–11, 2009.
[25] J.-S. Kang, Z. Zheng, M. J. Choi, S.-H. Lee, D.-Y. Kim, andS. B. Cho, “The effect of CD34+ cell-containing autologous
platelet-rich plasma injection on pattern hair loss: a preliminary
study,” Journal of the European Academy of Dermatology and
Venereology, vol. 28, no. 1, pp. 72–79, 2014.
[26] I. Giusti, A. Rughetti, S. D’Ascenzo et al., “Identification of an
optimal concentration of platelet gel for promoting angiogenesis in human endothelial cells,” Transfusion, vol. 49, no. 4, pp.
771–778, 2009.

9