CLINICAL CONTROVERSIES IN ORAL AND MAXILLOFACIAL SURGERY: PART TWO

J Oral Maxillofac Surg

62:489-496, 2004

Platelet-Rich Plasma: Evidence to Support

Its Use
Robert E. Marx, DDS*
Platelet-rich plasma (PRP) is an autologous concentration of human platelets in a small volume of plasma.
Therefore, the term PRP is preferred to autologous
platelet gel, plasma-rich growth factors (PRGFs), or a
mere autologous platelet concentrate. Because it is a
concentration of platelets, it is also a concentration of
the 7 fundamental protein growth factors proved to
be actively secreted by platelets to initiate all wound
healing. These growth factors include the 3 isomeres
of platelet-derived growth factor (PDGF, PDGF,
and PDGF), 2 of the numerous transforming
growth factors- (TGF1 and TGF2), vascular endothelial growth factor, and epithelial growth factor. All
of these growth factors have been documented to
exist in platelets.1,2 Because these concentrated platelets are suspended in a small volume of plasma, PRP is
more that just a platelet concentrate; it also contains
the 3 proteins in blood known to act as cell adhesion
molecules for osteoconduction and as a matrix for
bone, connective tissue, and epithelial migration.
These cell adhesion molecules are fibrin itself, fibronectin, and vitronectin.
PRP development via centrifugation has been
greatly simplified so that it can be used in the office
setting as well as the operating room. However, the
centrifugation process must be sterile and precisely
suited to platelet separation from red blood cells and
their sequestration in high concentrations without
lysing the platelets or damaging them so that they no
longer can actively secrete their growth factors.
Therefore, not all currently marketed PRP devices are
equal; some do not concentrate viably active platelets
in sufficient numbers to produce a healing enhance-

ment. This has led to and explains most of the criticisms regarding the efficacy of PRP. In addition, there
have been some research efforts to study PRP in
animal models that have a blood volume that is too
small to produce PRP; therefore, these studies have
used donor blood. This of course is homologous, not
autologous, and therefore is not true PRP. The use of
donor animal blood platelets imparts an overt immune reaction and leads to false-negative results that
may falsely be ascribed to PRP.
True PRP is always autologous and is not homologous. An example of this confusion is the use of
lyophilized donor platelets. Homologous platelets are
not viable and could not possibly secrete bioactive
growth factors. Homologous platelets are also antigenic due to their abundance of cell membranes.
Certainly, antiplatelet antibodies could develop from
this product and second set reactions would follow.
Such substances offer no useful comparison to PRP.
Regarding autologous PRP, clinicians must read the
literature and assess the results of studies relating to
PRP as to whether a Food and Drug Administration
(FDA)-cleared device produced the PRP and whether
platelet concentrations and growth factors were documented. At the time of this writing, only 2 office
devices used to develop PRP have been cleared by the
FDA (Smart PReP; Harvest Technologies Inc, Plymouth, MA; and the Platelet Concentration Collection
System [PCCS]; 3i Implant Innovations, Inc, West
Palm Beach, FL).2 A study conducted in our laboratories and repeated by the Center for Blood Research in
Boston, MA, indicated that of all of the devices tested,
these 2 FDA-cleared PRP devices produced the greatest platelet concentrations and, most important, release of a therapeutic level of bioactive growth factors
(Tables 1 and 2). Studies suggesting that there is no
benefit from PRP can often be traced to poor-quality
PRP produced by inadequate devices. Studies by
Weibrich and Klies,3 for instance, documented the
inadequacy of such devices. They found this one
particular device to be deficient in developing therapeutic levels of platelets compared with other devices
and was not cleared by the Certification Europe organization, which is the European counterpart to the US

*Professor of Surgery and Chief, Department of Oral and Maxillofacial Surgery, University of Miami School of Medicine and Jackson Memorial Hospital, Miami, FL.
Address correspondence and reprint requests to Dr Marx: Department of Oral and Maxillofacial Surgery, University of Miami
Jackson Memorial Hospital, 9380 SW 150th St, Suite 190, Miami, FL
33157; e-mail: [email protected]
2004 American Association of Oral and Maxillofacial Surgeons

0278-2391/04/6204-0018$30.00/0
doi:10.1016/j.joms.2003.12.003

489

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IN SUPPORT OF PLATELET-RICH PLASMA

Table 1. GROWTH FACTOR YIELDS PER DEVICE

Device

Mean PRP
Volume
(mL)

PDGF-
(ng/mL)

TGF-
(ng/mL)

Laboratory Centrifuge (Anitua Protocol)26

Laboratory Centrifuge (Landesberg Protocol)27
Clinaseal Sealed Technology Centrifuge*
ACE Surgical
AG Curasan
3i PCCS
Harvest Technologies SmartPReP

9.5 4.1
10.6 2.4
7.6 1.5
7.8 0.6
7.6 1.5
7.0 1.5
7.4 0.5

35 11.3
26 13.7
46 15.3
35 17.2
39 11.4
103 27
133 29.2

52 7.6
50 10.8
55 18.7
43 17.9
39 16.4
144 31.1
170 42.3

*Clinaseal Sealed Technology Centrifuge; Salvin Dental Specialties Inc, Charlotte, NC.
ACE Surgical, Brockton, MA.
AG Curasan, Kleinostheim, Germany.

FDA. Our own testing concurs with their findings.

Therefore, the clinician must look at such PRP-negative literature to assess whether PRP with therapeutic
platelet levels was really used.
The prudent clinician who uses PRP or the clinician
judging whether the healing enhancement of PRP
would offer a benefit to his or her patients should
assess the literature with scientific scrutiny and ask
the following critical questions.

How Does PRP Work?

PRP works via the degranulation of the granules
in platelets, which contain the synthesized and prepackaged growth factors. The active secretion of
these growth factors is initiated by the clotting process of blood and begins within 10 minutes after
clotting. More than 95% of the presynthesized growth
factors are secreted within 1 hour.2 Therefore, PRP
must be developed in an anticoagulated state and
should be used on the graft, flap, or wound, within 10
minutes of clot initiation. Studies that have not used
anticoagulated whole blood, which is then clotted to

activate the PRP, are not really studies of PRP and

therefore are misleading. Related to this, PRP has
been shown to remain sterile and the concentrated
platelets viable for up to 8 hours once developed in
the anticoagulated state and placed on a sterile surgical table. Like most growth factors such as bone
morphogeneic protein (BMP) and similar to collagen,
the growth factors within the granules of platelets
are incomplete because they must be soluble. As the
clotting process activates the platelets, the growth
factors are secreted from the cell through the cell
membrane. In this process, the granules fuse to the
platelet cell membrane where the protein growth
factor is completed to a bioactive state by the addition
of histones and carbohydrate side chains to these
proteins. Therefore, platelets damaged or rendered
nonviable by PRP processing will not secrete bioactive growth factors and may result in disappointing
outcomes.
The secreted growth factors immediately bind to
the external surface of cell membranes of cells in the
graft, flap, or wound via transmembrane receptors.
Studies have shown that adult mesenchymal stem

Table 2. PLATELET YIELDS PER DEVICE

Device

Mean PRP
Volume
(mL)

Mean Platelet
Concentration
103

Platelet
Yield (%)

Increase Above
Baseline (%)

Laboratory Centrifuge (Anitua Protocol)26

Laboratory Centrifuge (Landesberg Protocol)27
Clinaseal Sealed Technology Centrifuge*
ACE Surgical
AG Curasan
3i PCCS
Harvest Technologies SmartPReP

9.5 4.1
10.6 2.4
7.6 1.5
7.8 0.6
7.6 1.5
7.0 1.5
7.4 0.5

433 129
336 141
401 267
493 245
344 192
939 284
1,086 227

35 168
30 10.3
39 16.3
33 10.2
29 14.1
61 8.9
62 4.4

190
150
164
180
139
324
404

*Clinaseal Sealed Technology Centrifuge; Salvin Dental Specialties Inc, Charlotte, NC.
ACE Surgical, Brockton, MA.
AG Curasan, Kleinostheim, Germany.

491

ROBERT E. MARX

FIGURE 1. Proliferation of human mesenchymal stem cells (hMSCs)

is proportional to platelet concentrations in PRP. (SF, fetal calf serum;
GM, growth medium; PB, phosphate buffer; PPP, platelet poor
plasma.)

cells, osteoblasts, fibroblasts, endothelial cells, and

epidermal cells express the cell membrane receptors
to growth factors in PRP.1 These transmembrane receptors in turn induce an activation of an endogenous
internal signal protein, which causes the expression
of (unlocks) a normal gene sequence of the cell such
as cellular proliferation, matrix formation, osteoid
production, collagen synthesis, etc. The importance
of this knowledge is that the PRP growth factors
never enter the cell or its nucleus, they are not mutagenic, and they act through the stimulation of normal healing, just much faster. Therefore, PRP has no
ability to induce tumor formation and has never done
so.4,5
After the initial burst of PRP-related growth factors,
the platelets synthesize and secrete additional growth
factors for the remaining 7 days of their life span.
Once the platelet is exhausted and dies off, the macrophage, which has arrived in the region via the
vascular in-growth stimulated by the platelets, assumes the function of wound healing regulation by
secreting some of the same growth factors as well as
others. Therefore, the number of platelets in the
blood clot within the graft, wound, or adherent to a
flap sets the rate of wound healing. PRP merely increases this number.

How Many Platelets are Enough?

This question has been elegantly answered by the
work of Haynesworth et al,6 who showed that the
proliferation of adult mesenchymal stem cells and
their differentiation were directly related to the platelet concentration. They showed a dose-response
curve, which indicated that a sufficient cellular re-

sponse to platelet concentrations first began when a

4- to 5-fold increase over baseline platelet numbers
was achieved (Fig 1). A similar study by Lui et al7
showed that fibroblast proliferation and type I collagen production were also enhanced by increasing
platelet concentrations and that much of the response
was pH dependent with the best responses occurring
at more acidic pH levels. Together these studies not
only documented the necessity of devices to concentrate sufficient platelets but also explained both the
enhanced bone regeneration results associated with
PRP and the enhanced soft tissue results. Because
most individuals have a baseline blood platelet count
of 200,000 75,000/L, a PRP platelet count of 1
million/L as measured in the standard 6-mL aliquot
has become the benchmark for therapeutic PRP.
The importance of this knowledge is that our studies
have indicated that only the aforementioned FDAcleared devices consistently achieve this therapeutic
level of platelet concentration and hence growth factor release (Tables 1 and 2).

Does PRP Really Work?

The vast majority of publications report a significant enhancement of healing when PRP is used. Some
of these publications that report positive results in
either or both bone and soft tissue healing are Marx et
al,1 with autogenous mandibular bone grafts; Garg,8
with composites of autogenous bone grafts and bone
substitutes in sinus lifts and other surgeries; Man et
al,9 with cosmetic surgeries; Adler and Kent,10 specifically with face lift surgeries; Camargo et al,11 with
intrabony periodontal defects; Kim et al,12 with periimplant defects; Kassolis et al,13 with freeze-dried
bone allografts in sinus lift surgeries; Abuzeni and
Alexander,14 with cosmetic dermal fat grafts; and
Monteleone et al,15 with skin graft healing enhancement. These studies document the observed enhancement of bone regeneration as well as the enhancement of soft tissue healing. However, there have also
been publications that concluded that there was little
or no benefit from PRP: Froum et al,16 with sinus lift
grafts; Aghaloo et al,17 with cranial defects in rabbits;
and Shanaman et al,18 in ridge augmentations together
with demineralized freeze-dried bone allografts. How
does the reader then reconcile these apparently conflicting publications? The best way is to review the
level of science each publication represents, assessing
the quality of PRP used in each study and the controls
used.
If the reader analyzes some of the aforementioned
articles, they see that articles purporting little benefit
from PRP often do not use real PRP, use damaged
platelets, may have not activated the platelets, or have

492

FIGURE 2. Human bone graft histology at 4 months without plateletrich plasma. There is a 59% trabecular bone density, active resorption
remodeling, and a preponderance of immature bone (hematoxylin
and eosin stain, original magnification 4).

statistically insufficient data to draw a valid conclusion. An example is the article by Froum et al.16 This
study included only 3 patients and introduced multiple independent variables to confound their results.
One patient received only anorganic bovine bone and
a BioGide membrane (Luitpold/Osteohealth, Shirley,
NY) with PRP; another patient received anorganic
bovine bone with 5% autogenous bone, a BioGide
membrane, and PRP; and the third received only anorganic bovine bone and a Gore-Tex membrane (W.L.
Gore and Associates, Flagstaff, AZ) with PRP. In 1
case, immediate test implants were also placed that
were not placed in the other 2. In addition, this study
reported using a large draw Metronic unit (Tempe,
AZ) and did not test the platelet concentrations as in
other studies. Although studies such as this are often
referenced and quoted as showing little PRP benefit,
their conclusions cannot be accepted as valid, particularly if judged against the studies by Marx et al,1 in
which 88 patients were used with strict controls; by
Adler and Kent,10 in which 20 patients were used
with split side controls and platelet counts were documented; in Camargo et al,11 in which 18 patients
were used with identical techniques and materials in
a split mouth design; and in Monteleone et al,15 in
which 20 patients were used in a side-by-side, same
patient control design of skin graft donor sites. All of
these studies concluded a profound enhancement by
PRP.
Another study often quoted or referenced as showing little benefit from PRP is the study by Aghaloo et
al.17 Their study used non critical-sized defects in the
New Zealand White rabbit model. Their results
showed no benefit of PRP alone in the defect but
actually showed significant enhancement when PRP
was combined with autogenous bone compared with

IN SUPPORT OF PLATELET-RICH PLASMA

autogenous bone alone. This finding is consistent

with those of Marx et al,1 Garg,8 and others and is
actually a study supporting the use of PRP if read in its
entirety. Similarly, the study by Shanaman et al18 is
frequently quoted as showing no positive results with
PRP related to their study of only 3 patients for ridge
augmentation, yet the authors specifically state in
their discussion, The histologic observations suggest
that PRP in combination with DFDBA [demineralized
freeze-dried bone allografts] and covered with a barrier membrane supports new bone formation. In
addition, the core biopsy photomicrographs of PRPenhanced grafts from this study show significant
new bone formation, and the clinical photographs of
the ridges as described by the authors showed extensive defect fill with a hard bone-like material
within the defect area observed. The confusion
about the interpretation of this study as being positive
or negative toward PRP once again relates to the
science or nonscience of this study. This was not a
study per se but rather a case report of only 3 cases
without any controls. The documentation presented
by the authors was stated to be and was shown to be
a bone regeneration enhancement with PRP. Yet the
authors perhaps inadvertently implied a negative PRP
interpretation when they stated, The results of this
case series appear comparable to other GBR [guidedbone regeneration] studies without the use of PRP.
The reader should now see the value of statistically
significant numbers as opposed to a case series of
just 3 cases. The reader should also appreciate the use
of study controls versus no controls and that the use
of the word appear is a poor substitute for controlled data.
Perhaps the best proof of the absolute clinical efficacy and value of PRP can be seen directly in the
published photographs of bone grafts at 4 months

FIGURE 3. Human bone graft histology at 4 months with platelet-rich

plasma enhancement. There is an 80% trabecular bone density, the
bone is mature, and there is no evidence of active resorption remodeling (hematoxylin and eosin stain, original magnification 4).

ROBERT E. MARX

FIGURE 4. Split-thickness skin graft donor sites at 0.016 inch in

depth comparing a control site with a platelet-rich plasmatreated site
at the time of initial placement. Note the old skin graft donor site above
the platelet-rich plasmatreated site is scarred, contracted, and
hyperpigmented.

without PRP versus those with PRP (Figs 2, 3) and the

photographs of skin healing at various stages without
PRP in contrast to skin healing with PRP (Figs 4, 5).
Figure 2 represents an autogenous bone graft healing
at 4 months without PRP. It has a 59% trabecular bone
density, and 70% of that bone is in an immature stage
as evidenced by a random pattern of large osteocytic
lacunae without lamellar architecture. Only 30% has
lamellar architecture, indicating that the graft itself
primarily remains within a resorption-remodeling cycle as also evidenced by osteoclastic resorption. By
contrast, Figure 3 represents a size- and age-matched
autogenous bone graft healing at 4 months with PRP.
This histology has 80% trabecular bone density, and
85% of that bone is in a mature state as evidenced by
lamellar architecture and smaller osteocytic lacunae

FIGURE 5. The same split-thickness skin graft donor sites as seen in

Figure 4 now at 6 days. The control site has a peripheral erythema and
is covered by granulation tissue. There is minimal epithelialization. The
platelet-rich plasmatreated site has no peripheral erythema. The granulation tissue has already been replaced by a thin epithelial cover at
this early stage.

493

FIGURE 6. Histology specimen of the split-thickness skin graft donor

site control at 6 days. There is no epithelial budding, and the connective tissue shows macrophages and young plump fibroblasts without
significant collagen production (hematoxylin and eosin stain, original
magnification 10).

as well as mature haversian systems. There also is no

evidence of active resorption and remodeling, indicating a level of stable maturity.
Figures 4 and 5 represent side-by-side controlled
split-thickness skin graft donor sites of 0.016 inch in
depth at the time of their placement and after 6 days
of healing. This dramatic side-by-side comparison represents seeing is believing evidence. The graft site
without PRP in Figure 5 has peripheral erythema and
abundant granulation tissue with only 5% or less epithelialization seen at the edges. The graft site of the
same size and depth and on the same individual at 6
days with PRP use has no peripheral erythema and
already has a 95% thin epithelial covering. This is
further proved by histology specimens from each of
these 2 sites taken at 6 days (Figs 6, 7). The non-PRP
histology shows no epithelial budding and granula-

FIGURE 7. Histology specimen of split-thickness skin graft donor site

treated with platelet-rich plasma at 6 days. Prominent epithelial budding is noted and the underlying connective tissue shows a mature
dermis development with collagen deposition (hematoxylin and eosin
stain, original magnification 10).

494

FIGURE 8. Split-thickness skin graft donor site control of 0.016 inch

in depth at 45 days. Note the abundant subsurface vascularity indicative of a thin epithelial cover and the persistence of the hypervascular
phase of healing, which represents an immaturity of the healing
process.

tion tissue consisting only of macrophages and plump

young fibroblasts. The PRP-treated site instead shows
obvious epithelial budding and a mature dermis beneath. Figures 8 and 9 show another individuals splitthickness skin graft donor sites at 45 days without
PRP and with PRP, respectively. Note the dense subsurface vascularity of the non-PRP site, which is indicative of a thin epithelial cover and incomplete
healing. Note the absence of such subsurface vascularity at the PRP site, indicative of the involution of
this vascular phase of healing, the greater thickness of
the epithelial cover, and a more advanced healing.
Finally, Figure 10 shows the individual side-by-side
donor sites of Figure 4, now at 6 months. It is evident
that the site without PRP has more scarring and a
greater loss of pigmented cells than the PRP site,
indicating that the PRP effect of faster and more

IN SUPPORT OF PLATELET-RICH PLASMA

FIGURE 10. The split-thickness skin graft side-by-side donor sites from
Figures 4 and 5 seen now at 6 months. Note that the control side has
more scarring, is contracted, and has a greater variation in
pigmentation.

complete healing reduces scar and promotes a greater

melanocyte survival.

What Clinical Situations Benefit from

PRP?
Because PRP enhances osteoprogenitor cells in the
host bone and in bone grafts,1,19 it has found clinical
applications in fully autogenous bone grafts and composites of autogenous bone grafts with a variety of
bone substitutes with as little as 20% autogenous
bone.8 Therefore, PRP has shown improved results in
continuity defects,1,20 sinus lift augmentation grafting,13,21 horizontal and vertical ridge augmentations,8
ridge preservation grafting,22 and periodontal/peri-implant defects.12 We have also observed PRP to allow
earlier implant loading and improved osseointegration when used in compromised bone such as osteoporotic bone and bone after radiotherapy. Because
PRP also enhances soft tissue mucosal and skin healing, it is used in connective tissue grafts, palatal grafts,
gingival grafts, mucosal flaps together with Alloderm
(BioHorizons, Birmingham, AL) for root coverage,
skin graft donor and recipient sites, dermal fat grafts,
face lifts, blepharoplasty, and laser resurfacing surgery.

What is the Safety of PRP?

FIGURE 9. Split-thickness skin graft donor site of 0.016 inch in depth

in the same patient treated with platelet-rich plasma at 45 days. Note
the absence of subsurface vascularity indicative of a more mature
healing process and a greater thickness of the overlying epithelium.

Because it is an autogenous preparation, PRP is

inherently safe and therefore free from concerns over
transmissible diseases such as HIV, hepatitis, West
Nile fever, and Cruetzfeld-Jacob disease (CJD) (mad
cow disease). It therefore is also well accepted by
patients. Related to the issue of CJD, concerns have
been advanced about the use of bovine thrombin as
the clotting initiator. However, bovine thrombin has a

495

ROBERT E. MARX

completely negative history of CJD in more than 10

million uses in a wide variety of surgeries worldwide.
Because the transmission vector of CJD is a prion that
to date has been found only in neural tissues of the
central nervous system in cattle, sheep, cats, humans,
etc and because bovine thrombin is derived solely
from blood and is also heat processed for purification,
it remains in standard use today in many surgeries and
is the safe initiator of clotting related to PRP.
Of more reasonable clinical concern are the rare
cases where bovine thrombin was used as a hemostatic agent in open orthopedic, neurosurgical, and
cardiovascular surgeries and later bleeding episodes
were encountered.23,24 Although less than 20 such
cases have been reported, these adverse events have
been thoroughly investigated. The second set bleeding episodes in these patients were not due to antibodies against bovine thrombin or human thrombin
but instead due to antibodies that developed to bovine factor Va that was a contaminant in certain bovine thrombin commercial preparations.23-25 These
antibodies, which developed to bovine factor Va,
cross-reacted with human factor Va and thereby produced coagulopathies and these rare bleeding episodes. Since 1997, the processing of bovine thrombin
by Gentrac (Jones Medical Industries, St Louis, MO)
has eliminated contamination of bovine thrombin
with bovine factor Va from pre-1997 levels of 50
mg/mL to less than 0.2 mg/mL and thus no further
cases related to this specific preparation have been
reported.25 In addition, the bovine thrombin preparations used in the reported cases were high dose
(10,000 units) and were applied directly onto open
wounds where absorption into the systemic circulation is certain. The use of bovine thrombin in PRP is
low dose (200 units), is topical with no entry into
the systemic circulation, and is already clotted when
it comes into contact with human tissues. It is therefore not absorbed systemically but is engulfed and
digested by the macrophages that also digest the clot
itself.

Does PRP Promote Infections?

Some have empirically suggested that PRP may promote infections due to the flawed logic that it is a
blood clot and that blood agar is used in microbiology
laboratories to culture bacteria. However, PRP is no
different in substrate than the blood clot that forms in
every wound and therefore could not support bacterial growth any more than any other blood clot. In
fact, PRP has a pH of 6.5 to 6.7 compared with a
mature blood clot of 7.0 to 7.2. It has thus been
countersuggested that PRP actually inhibits bacterial
growth. To this end, no clear studies or data are

available. Our experience comparing similar bone

grafts and skin wounds with and without PRP shows
no promotion or inhibition of infection complications. Each has an incidence of 2.0% to 3.5%. However, the clinician should know that preparation of
PRP must use an aseptic technique.

Is the Value of PRP Limited to Soft

Tissue?
Some have also implied that the value of PRP is
mostly related to soft tissue healing enhancement
because platelets do not contain BMP. Indeed, PRP
does not contain any BMP and it is not osteoinductive.
However, all bone graft healing and osteoconduction
into bony defects and around the numerous bone
substitutes used today arise from adult mesenchymal
stem cells and their lineage, leading to osteoblasts, all
of which have already been proved to respond to PRP
with accelerated bone formation.1,6,26 In fact, the first
randomized trial of PRP versus non-PRP grafts focused
specifically on and documented PRPs enhancement
of bone formation1 (Figs 3, 4).
Today, PRP remains the sole growth factor preparation available to oral and maxillofacial surgeons and
other specialties of dentistry for outpatient use. The
recent withdrawal of the application for FDA approval of recombinant human BMP-2 (rhBMP-2) for
craniofacial, oral surgical, and dental applications
is a disappointment to the entire profession but underscores the value of PRP. The value of PRP is its
proven effectiveness, its safety, its cost effectiveness, and its availability in an easy-to-develop manner
and its FDA approval if developed by an FDA-cleared
device.

References
1. Marx RE, Carlson ER, Eichstaedt R, et al: Platelet rich plasma:
Growth factor enhancement for bone grafts. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 85:638, 1998
2. Kevy S, Jacobson M: Preparation of growth factors enriched
autologous platelet gel. Proceedings of the 27th Annual Meeting of Service Biomaterials, April 2001
3. Weibrich G, Kleis WKG: Curasan PRP kit vs PCCS PRP system:
Collection efficiency and platelet counts of two different methods for the preparation of platelet rich plasma. Clin Oral Implant Res 13:437, 2002
4. Schmitz JP, Hollinger JO: The biology of platelet-rich plasma
(letter to the editor). J Oral Maxillofac Surg 59:1119, 2001
5. Marx RE: The biology of platelet-rich plasma (reply to letter to
the editor). J Oral Maxillofac Surg 59:1120, 2001
6. Haynesworth SE, Kadiyala S, Liang LN, et al: Mitogenic stimulation of human mesenchymal stem cells by platelet release
suggest a mechanism for enhancement of bone repair by platelet concentrates. Presented at the 48th Meeting of the Orthopedic Research Society, Boston, MA, 2002
7. Lui Y, Kalen A, Risto O, et al: Fibroblast proliferation due to
exposure to a platelet concentrate in vitro is pH dependent.
Wound Repair Regen 10:336, 2002

496
8. Garg AK: The use of platelet rich plasma to enhance the
success of bone grafts around dental implants. Dent Implantol
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poor plasma (fibrin glue) in cosmetic surgery. Plast Reconstr
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humans. J Periodont Res 37:300, 2002
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in the treatment of bone defects around implants. Int J Oral
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13. Kassolis JD, Rosen PS, Reynolds MA: Alveolar ridge and sinus
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with freeze-dried bone allograft. Case series. J Periodont 71:
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Francisco, CA, September 22, 2000
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IN SUPPORT OF PLATELET-RICH PLASMA

18. Shanaman R, Filstein MR, Danesh-Meyer MJ: Localized ridge
augmentation using GBR and platelet rich plasma: Three case
reports. Int J Periodont Restor Dent 21:343, 2001
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human osteoblast-like cells by thrombocyte concentrates in
vitro. Mund Kiefer Geschtschir 6:168, 2002
20. Fennis JPM, Stoelinga PJW, Jansen JA: Mandibular reconstruction: A clinical and radiographic animal study on the use of
autogenous scaffolds and platelet rich plasma. Int J Oral Maxillofac Surg 31:281, 2002
21. Lozada JL, Caplanis N, Proussaefs P, et al: Platelet rich plasma
application in sinus graft surgery: Part I, background and processing techniques. J Oral Implantol 27:38, 2001
22. Carlson NE, Roach RB Jr: Platelet rich plasma: Clinical applications in dentistry. J Am Dent Assoc 133:1383, 2002
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