Comparison of the Effect of Intra-Tendon Applications of Recombinant
Human Platelet-Derived Growth Factor-BB, Platelet-Rich Plasma,
Steroids in a Rat Achilles Tendon Collagenase Model
Luis A. Solchaga,1Alison Bendele,2Vivek Shah,3Leo B. Snel,1Hans K. Kestler,3Joshua S. Dines,4Christopher K. Hee3
1Research and Development, BioMimetic Therapeutics, LLC, Franklin, Tennessee,
BioMimetic Therapeutics, LLC, Franklin, Tennessee,4Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York
2Bolder BioPATH, Boulder, Colorado,
Received 28 May 2013; accepted 14 August 2013
Published online 9 September 2013 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/jor.22483
(rhPDGF-BB), platelet-rich plasma (PRP) and corticosteroids in a rat tendinopathy model. Seven days after collagenase induction of
tendinopathy, a 30-ml IT injection was administered. Treatments included: saline; 3mg rhPDGF-BB; 10mg rhPDGF-BB; PRP; and
300mg triamcinolone acetonide (TCA). Outcomes were assessed 7 and 21 days after treatment. All groups exhibited good to excellent
repair. Relative to saline, cell proliferation increased 65% in the 10mg rhPDGF-BB group and decreased 74% in the TCA group;
inflammation decreased 65% in the TCA group. At 7 days, maximum load-to-failure was increased in the 3mg rhPDGF-BB group
relative to saline, PRP, and TCA (p<0.025). On day 21, maximum load-to-rupture was increased in the 10mg rhPDGF-BB group
relative to saline, PRP, and TCA (p<0.035) and in the 3mg rhPDGF-BB group compared to saline and TCA (p<0.027). Stiffness in the
10mg rhPDGF-BB group was increased compared to saline, PRP, and TCA (p<0.038). Histology demonstrated similar repair in all
groups. PRP and TCA did not improve mechanical properties compared to saline. Injections of rhPDGF-BB increased maximum load-
to-failure (3 and 10mg) and stiffness (10mg) relative to controls and commonly used treatments. ? 2013 Orthopaedic Research Society.
Published by Wiley Periodicals, Inc. J Orthop Res 32:145–150, 2014.
This study compared the effect of intra-tendon (IT) delivery of recombinant human platelet-derived growth factor-BB
tendinopathy; platelet-derived growth factor-BB; platelet-rich plasma; corticosteroid; biomechanics
Tendinopathy is a painful condition that develops as
result of tendon degeneration1,2and can affect tendons
throughout the body (e.g., rotator cuff, Achilles).
Tendinopathy leads to collagen degeneration, disorga-
nization, increased mucoid ground substance, prolifer-
ation of capillaries and arterioles, loss of mechanical
properties, and concomitant pain. These degenerative
changes occur without macroscopic tearing of the
tendon and may result from a failed healing response
to sub-failure injuries.1–3
Current treatment options for tendinopathy includ-
ing, but not limited to, exercise-based physical thera-
inflammatory drugs, extracorporeal shock wave thera-
py and surgical interventions4–11have met varying
degrees of success. These therapies often treat the
symptoms associated with the condition, but do not
address the underlying cause resulting in persistence
of the degeneration. While not considered a gold-
standard treatment, corticosteroid injections are often
administered for chronic tendinopathies. However,
there are concerns about the long-term safety and
efficacy of this therapy8–10due to adverse changes
within the tendon.12
Growth factors have also been assessed to promote
tendon healing. Autologous growth factors in the form
of platelet-rich plasma (PRP) have been studied;
however variability in the preparation and composi-
tion of PRP makes it difficult to compare results across
studies.13Additionally, variable clinical outcomes fol-
lowing PRP treatment for tendinopathy have been
reported.14,15As an alternative to PRP, recombinant
human platelet-derived growth factor-BB (rhPDGF-
BB) is a readily available, off-the-shelf option that
provides a consistent, therapeutic dose. Utilizing a
variety of delivery methods, animal models of tendon
injury have shown that rhPDGF-BB accelerates ten-
don healing by improving matrix remodeling, in-
proliferation.16–22We have previously reported that
rhPDGF-BB is efficacious in a non-ruptured, degener-
ated, tendinopathy model.23In contrast to corticoste-
roids, rhPDGF-BB addresses chronic tendinopathies
by inducing proliferation and migration of progenitor
cells and tenocytes,17,24–26which stimulate structural
repair of the degenerated tendon.
As a consequence of the deficiencies in clinical
outcome offered by contemporary therapies, the objec-
tive of this study was to compare the effect of intra-
tendon (IT) delivery of rhPDGF-BB, PRP and cortico-
steroids in a rat Achilles tendinopathy model. We
hypothesized that IT delivery of rhPDGF-BB would
result in increased biomechanical strength and im-
proved histological appearance compared to PRP and
Conflict of interest: BioMimetic Therapeutics, Inc.: L.A. Solchaga
(employee, stock/options), A. Bendele (institutional funds to
perform aspects of the study), V. Shah (employee, stock/options),
L.B. Snel (employee, stock/options), H.K. Kestler (employee,
stock/options), J.S. Dines (Scientific Advisory Board, consultant),
and C.K. Hee (employee, stock/options).
Grant sponsor: BioMimetic Therapeutics.
Correspondence to: Luis A. Solchaga (T: þ1-615-236-4511; F: þ1-
615-236-4470; E-mail: firstname.lastname@example.org)
# 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
JOURNAL OF ORTHOPAEDIC RESEARCH JANUARY 2014
MATERIALS AND METHODS
This study was approved by the Institutional Animal Care
and Use Committee at Bolder BioPATH, Inc. Male Sprague-
Dawley rats weighing approximately 315g (Charles River
Labs, St. Constant, Quebec) were used. Rats were housed
four per cage under a 12:12-h light-dark cycle and food and
water were provided ad libitum.
Preparation of Platelet-Rich Plasma
PRP donor animals (n¼18) were sacrificed and each was
used to treat two study animals (one sacrificed at 7 days and
one sacrificed at 21 days post-treatment). PRP was prepared
using a double-spin method.27,28Briefly, 6.5ml of blood was
collected with 1.5ml of acid citrate dextrose-A from the
descending aorta and centrifuged at 220g for 20min. The
plasma was collected and centrifuged again at 480g for
20min. The platelet-poor plasma was removed and the
platelets were resuspended in 900ml of platelet-poor plasma
to form the PRP. Aliquots of whole blood, plasma, and PRP
were collected for quantification of complete blood counts and
of growth factors.
Analysis of Platelet-Rich Plasma
Immediately following preparation, complete blood counts
were performed on samples of whole blood, plasma, and PRP
using a Hemavet 950 FS system to determine red blood cell
(RBC), white blood cell (WBC) and platelet (PLT) counts.
Aliquots of plasma and PRP were frozen at ?80˚C for later
quantification of growth factors. Enzyme-linked immunosor-
bent assays (ELISA) specific for rat PDGF-AB, PDGF-BB,
vascular endothelial growth factor (VEGF), and transforming
growth factor-b1 (TGF-b1) were used according to manufac-
turer’s instructions (Quantikine Immunoassays, R&D Sys-
tems, Minneapolis, MN).
On day-7, rats received an injection of collagenase (50ml of
10mg/ml Type IA in PBS, pH 7.4, 469units/mg; Sigma, St.
Louis, MO) into the right Achilles tendon near the osseo-
tendinous junction using insulin syringes with 28.5G needle
as described previously.23Seven days following the collage-
nase injection (day 0), rats were randomized to one of five
treatment groups (n¼18/time point/group): (i) saline (placebo
control); (ii) 3mg rhPDGF-BB (BioMimetic therapeutics, Inc.,
1.5?1012platelets/L (PRP); or (v) 300mg triamcinolone ace-
tonide (TCA; Bristol-Myers Squibb Company, Princeton, NJ).
These concentrations, adjusted for animal size, are consistent
with other investigations of tendon rupture healing.22,29
Animals received an injection volume of 30ml of the assigned
treatment solution into the damaged Achilles tendon. Rats
were anesthetized with isofluorane during the collagenase
and subsequent treatment injections. Rats were euthanized 7
or 21 days following treatment. Additional animals (n¼18)
were euthanized on the day of treatment (day 0) to establish
the baseline damage from the collagenase treatment.
The calcaneous-Achilles tendon-muscle specimen (n¼5/time
point/group), with skin removed, was fixed in 10% neutral
buffered formalin and decalcified in 10% formic acid. Speci-
mens were embedded in paraffin and serial sections (5mm)
were collected and stained with Hematoxylin and Eosin
(H&E), Masson’s trichrome or immunohistochemical staining
for proliferating cell nuclear antigen (PCNA).
Histopathological assessment of inflammation, extent of
damage, extent of repair and character of the repair were
performed by a board-certified veterinary pathologist masked
to treatment, according to criteria outlined in Table S1.
Proliferating cells within the tendon, identified by PCNA
immunoreactivity, were quantified using three consistent
fields of an ocular micrometer (39.4mm?197mm; 7,762mm2).
PCNA positive cell counts were normalized by the area of the
field of view. Microscopic tendon thickness was measured
with an ocular micrometer at the calcaneal attachment point
and at the midsubstance of the tendon.
At necropsy, the calcaneous-Achilles-gastrocnemius specimen
was dissected from the surrounding tissues, wrapped in
saline soaked gauze, and frozen at ?20˚C until testing. All
treated ankles (n¼13/group/timepoint) were tested. Contra-
lateral ankles (n¼13/timepoint) from the saline-treated
group were used as uninjured controls. Samples were thawed
in phosphate-buffered saline containing proteinase inhibitors
(Roche Diagnostics, Indianapolis, IN) at 4˚C for up to 4h
prior to mechanical testing. The muscle was dissected from
the tendon and the soft tissue removed from the calcaneous
to facilitate gripping. Specimen dimensions were measured
using a custom contact-sensing micrometer. Mechanical
testing was performed on a Bose EnduraTEC test system
(Model 3200, Bose, Eden Prairie, MN) under displacement
control. The resulting load was measured using a 100N load
cell. A 1N tare load was applied to the specimens followed by
10 cycles of cyclic loading between 0.1 and 1N at 0.138Hz. A
uniaxial tensile ramp-to-failure was then applied at a strain
rate of 0.1%/s and the resultant load recorded. The samples
were tested to failure (until fracture the measured load was
<1N).23,29,30All specimens were tested masked to treatment
with no indication of identifiable group classification. The
load–displacement curve was analyzed to determine linear
stiffness and maximum load. The stress–strain curve was
analyzed to determine modulus and ultimate stress.
Statistical analyses were performed using SigmaPlot 12.0. A
one-way ANOVA on ranks with a Tukey’s post-hoc test was
used for analysis of the complete blood counts. A one-tailed t-
test was used for comparison of the growth factor concentra-
tion. Two-way ANOVA with interaction and a Fisher’s LSD
post-hoc test was used for analysis of the biomechanical
data. Non-parametric data (histopathology scores) were ana-
lyzed using a Kruskal–Wallis test. All results are presented
as mean?SEM. The level of significance was set at p<0.05.
RBCs were present in whole blood only (Table 1).
WBCs were present in whole blood and their numbers
were significantly diminished in plasma and PRP.
PLTs were concentrated 3.3-fold in PRP samples
compared to whole blood (p<0.05). Platelet concentra-
tion in plasma was not different from whole blood.
VEGF was not detected in any sample. The concen-
trations of PDGF-AB, PDGF-BB, and TGF-b1 (Table 2)
SOLCHAGA ET AL.
JOURNAL OF ORTHOPAEDIC RESEARCH JANUARY 2014
were significantly increased in the PRP relative to
plasma (p<0.001). A positive correlation (p<0.001)
was observed between growth factor concentration and
Histopathology scores are presented as the median
and range of five specimens (Table 3) evaluated by a
single masked histopathologist. On day 7, the TCA-
treated specimens presented decreased tendon thick-
ness at insertion and midsubstance; decreased cell
proliferation and decreased inflammation relative to
saline treatment; the 10mg rhPDGF-BB dose group
presented increased cell proliferation compared to
saline; no differences were observed in the extent and
character of the repair among the treatment groups.
On day 21 no differences were observed in any of the
elements of assessment among the treatment groups.
Structural mechanical properties (maximum load, ten-
sile extension, and stiffness) are presented in Table 4.
The maximum load for the 3mg rhPDGF-BB dose
group was significantly increased (p?0.025) compared
to the saline, PRP, and TCA groups at day 7 and
significantly increased (p?0.027) compared to the
saline and TCA groups at day 21. The maximum load
(p?0.035) and stiffness (p?0.038) were significantly
increased in the 10mg rhPDGF-BB group compared to
the saline, PRP, and TCA groups at day 21. Material
mechanical properties (ultimate stress, tensile strain,
and modulus) are presented in Table 5. The ultimate
stress was significantly increased in the 3mg rhPDGF-
BB dose group compared to the saline, PRP, and TCA
groups at day 7 (p?0.025) and compared to the PRP
group at day 21 (p?0.025). The ultimate stress
(p?0.025) and modulus (p?0.046) were significantly
increased in the 10mg rhPDGF-BB dose group com-
pared to the saline, PRP, and TCA groups at day 21.
In this study, we compared rhPDGF-BB with cortico-
steroids and PRP in a rat model of tendinopathy. This
that are similar to human tendinopathy such as
hypercellularity, loss of matrix organization, and lack
of inflammatory cell infiltration, however, its main
drawback is that it causes a healing response which is
often absent in tendinopathy patients.35,36This heal-
ing response can mask the effects of the treatments
applied if the time points for assessment are not
carefully defined. Guided by our previous experience,23
we chose relatively short follow-up that would allow us
to assess the effect and, potentially, the mechanism of
action of the treatments applied.
Although there are concerns about their long-term
safety and efficacy,8–10corticosteroid injections are
often administered for chronic tendinopathies. Growth
factors have also been used to promote tendon healing
in the form of PRP; however variability in the prepara-
tion and composition of PRP makes it difficult to
compare results across studies13
responsible for the variability in the clinical outcomes
reported with this therapy.14,15Several preclinical
studies demonstrate that regenerative healing of ten-
dons and ligaments can be accomplished by exploiting
the biological properties of the platelet-derived growth
factor (PDGF) family of growth factors.37–44The safety
profile of rhPDGF-BB has been well-established45,46
and the Food and Drug Administration has approved
rhPDGF-BB-containing formulations (Regranex1Gel
and GEM 21S1) for wound healing and periodontal
The results of this study confirm our previous
findings that a 10mg IT injection of rhPDGF-BB,
promoted cellular proliferation and improved mechani-
cal properties of collagenase-treated tendons.23Consis-
tent with our previous study, this treatment resulted
in early cellular proliferation at day 7 and improved
strength at day 21 compared to the placebo controls.
The mechanism of action of corticosteroid treatment
is very different from that of the PRP and rhPDGF-
BB. Corticosteroids target the pain caused by local
inflammation of the damaged tendon tissue6,8while
PDGF-BB and the growth factors contained in PRP
are chemotactic and mitogenic triggering recruitment
and proliferation of tenocytes to the injured tendon
that may improve the conditions for repair.47As a
result, corticosteroids predictably and significantly
Corticosteroid treatment, consistent with the pro-
posed mechanism of action, significantly reduced in-
flammation, tendon thickness and cell proliferation at
day 7. However, these early effects did not result in
biomechanical improvement over the control group
and it is likely
Plasma, and PRP
Mean Blood Cell Counts for Whole Blood,
Mean?SD.?Different from whole blood; p<0.05.#Different from
and PRP Samples
Average Growth Factor Content in Plasma
Mean?SD. BLQ, below the limit of quantitation.?Different from
COMPARISON OF TREATMENTS IN A TENDINOPATHY MODEL
JOURNAL OF ORTHOPAEDIC RESEARCH JANUARY 2014
indicating that this therapy addresses the pain associ-
ated with tendinopathy albeit not its root cause and
lacks long-term efficacy.48PRP and low dose (3mg)
rhPDGF-BB had little impact on cell proliferation and
tendon thickness and they also lacked sustained
improvement in biomechanical properties suggesting
that low doses of growth factors are insufficient to
trigger a successful repair.
The platelet content and RBC depletion achieved in
the preparation of the PRP for this study are similar
to those achieved by commercially available systems.13
The growth factor content in PRP compared with
whole blood correlated strongly with the platelet
enrichment attained in the PRP preparation. The
concentration of PDGFs in PRP are, however, orders
of magnitude below the dose that was found to be
efficacious in this and in our previous study.23As
such, the lack of improvement of biomechanical prop-
erties in these groups suggests that the level of
concentration of platelets/growth factors necessary for
impacting tendon function is not achievable with the
PRP concentration method studied.
In conclusion, the improved biomechanical strength
of the tendons treated with 10mg of rhPDGF-BB
support the hypothesis that rhPDGF-BB stimulates
tendon repair in this model, resulting in improvements
in the mechanical function. The other treatments (3mg
of rhPDGF-BB, PRP, and TCA) did not yield bio-
mechanical improvements compared to the placebo
(saline) group. Although this model has some intrinsic
Histopathology Scores at Baseline, 7, and 21 Days Post-Treatment
Inflammation Extent of DamageExtent of Repair Character of Repair
Day 0 Day 7Day 21 Day 0Day 7 Day 21 Day 0Day 7Day 21 Day 0Day 7 Day 21
Summary of Structural Biomechanical Properties at Baseline, 7, and 21 Days Post-Treatment
Maximum LoadTensile Extension at Maximum LoadRamping Stiffness
Day 0Day 7Day 21Day 0Day 7Day 21Day 0Day 7Day 21
Summary of Material Biomechanical Properties at Baseline, 7, and 21 Days Post-Treatment
Ultimate Tensile StressTensile Strain at Maximum Stress Ramping Modulus
Day 0Day 7 Day 21Day 0Day 7Day 21Day 0Day 7Day 21
SOLCHAGA ET AL.
JOURNAL OF ORTHOPAEDIC RESEARCH JANUARY 2014
shortcomings and does not lend itself to long-term
follow-up and assessment of the longevity of the
repair, taken together, the results of this study
indicate that rhPDGF-BB, at the correct concentra-
tion, may have benefit as a therapy for tendinopathy.
Future investigations will examine the clinical impact
of rhPDGF-BB on pain abrogation and restoration of
activity following treatment.
We thank Dr. Jeffery O. Hollinger (assistance with study
design), Jack Ratliff (histologic processing), and Patricia
Ward (growth factor analysis).
1. Sharma P, Maffulli N. 2005. Tendon injury and tendinop-
athy: healing and repair. J Bone Joint Surg 87:187–202.
2. Maffulli N, Wong J, Almekinders L. 2003. Types and
epidemiology of tendinopathy. Clin Sports Med 22:675–692.
3. Battery L, Maffulli N. 2011. Inflammation in overuse tendon
injuries. Sports Med Arthrosc 19:213–217.
4. Buchbinder R, Green S, Bell SN, et al. 2009. Surgery for
lateral elbow pain. Cochrane Database Syst Rev 1:1–14.
5. Buchbinder R, Green S, Youd JM, et al. 2005. Shock wave
therapy for lateral elbow pain. Cochrane Database Syst Rev
6. Green S, Buchbinder R, Barnsley L, et al. 2002. Non-
steroidal anti-inflammatory drugs (NSAIDs) for treating
lateral elbow pain in adults. Cochrane Database Syst Rev
7. Smidt N, Assendelft WJJ, Arola H, et al. 2003. Effectiveness
of physiotherapy for lateral epicondylitis: a systematic
review. Ann Med 35:51–62.
8. Smidt N, Assendelft WJ, Van der Windt DA, et al. 2002.
Corticosteroid injections for lateral epicondylitis: a systemat-
ic review. Pain 96:23–40.
9. Smidt N, van der Windt D, Assendelft W, et al. 2002.
Corticosteroid injections, physiotherapy, or a wait-and-see
policy for lateral epicondylitis: a randomised controlled trial.
10. Gosens T, Peerbooms J, van Laar W, et al. 2011. Ongoing
positive effect of platelet-rich plasma versus corticosteroid
injection in lateral epicondylitis. A double-blind randomized
controlled trial with 2-year follow-up. Am J Sports Med
11. Andres B, Murrell G. 2008. Treatment of tendinopathy. Clin
Orthop Relat Res 466:1539–1554.
12. Jobe F, Ciccotti M. 1994. Lateral and medial epicondylitis of
the elbow. J Am Acad Orthop Surg 2:1–8.
13. Castillo T, Pouliot M, Kim H, et al. 2011. Comparison of
growth factor and platelet concentration from commercial
platelet-rich plasma separation systems. Am J Sports Med
14. de Vos RJ, van Veldhoven PLJ, Moen MH, et al. 2010.
Autologous growth factor injections in chronic tendinopathy:
a systematic review. Br Med Bull 95:63–77.
15. Del Buono A, Papalia R, Denaro V, et al. 2011. Platelet rich
plasma and tendinopathy: state of the art. Int J Immunopa-
thol Pharmacol 24:79–83.
16. Chan BP, Fu SC, Qin L, et al. 2006. Supplementation-time
dependence of growth factors in promoting tendon healing.
Clin Orthop Relat Res 448:240–247.
17. Thomopoulos S, Zaegel M, Das R, et al. 2007. PDGF-BB
released in tendon repair using a novel delivery system
promotes cell proliferation and collagen remodeling. J
Orthop Res 25:1358–1368.
18. Thomopoulos S, Das R, Silva MJ, et al. 2009. Enhanced
flexor tendon healing through controlled delivery of PDGF-
BB. J Orthop Res 27:1209–1215.
19. Gelberman R, Thomopoulos S, Sakiyama-Elbert S, et al.
2007. The early effects of sustained platelet-derived growth
factor administration on the functional and structural
properties of repaired intrasynovial flexor tendons: an in
vivo biomechanic study at 3 weeks in canines. J Hand Surg
20. Uggen JC, Dines J, Uggen CW, et al. 2005. Tendon gene
therapy modulates the local repair environment in the
shoulder. J Am Osteopath Assoc 105:20–21.
21. Uggen C, Dines J, McGarry M, et al. 2010. The effect of
recombinant human platelet-derived growth factor BB-coat-
ed sutures on rotator cuff healing in a sheep model.
22. Hee CK, Dines JS, Dines DM, et al. 2011. Augmentation of a
rotator cuff suture repair using rhPDGF-BB and a type I
bovine collagen matrix in an ovine model. Am J Sports Med
23. Shah V, Bendele A, Dines JS, et al. 2013. Dose–response
effect of an intra-tendon application of recombinant human
platelet-derived growth factor-BB (rhPDGF-BB) in a rat
Achilles tendinopathy model. J Orthopaedic Res 31:413–420.
24. Costa MA, Wu C, Pham BV, et al. 2006. Tissue engineering
of flexor tendons: optimization of tenocyte proliferation using
growth factor supplementation. Tissue Eng 12:1937–1943.
25. Thomopoulos S, Harwood F, Silva M, et al. 2005. Effect of
several growth factors on canine flexor tendon fibroblast
proliferation and collagen synthesis in vitro. J Hand Surg
26. Sakiyama-Elbert SE, Das R, Gelberman RH, et al. 2008.
Controlled-release kinetics and biologic activity of platelet-
derived growth factor-BB for use in flexor tendon repair. J
Hand Surg 33:1548–1557.
27. Aspenberg P, Virchenko O. 2004. Platelet concentrate injec-
tion improves Achilles tendon repair in rats. Acta Orthop
28. Virchenko O, Aspenberg P. 2006. How can one platelet
injection after tendon injury lead to a stronger tendon after
4 weeks? Interplay between early regeneration and mechan-
ical stimulation. Acta Orthop 77:806–812.
29. Cummings SH, Grande DA, Hee CK, et al. 2012. Effect of
rhPDGF-BB-coated sutures on achilles tendon healing in a
rat model: a histological and biomechanical study. J Tissue
30. Dines JS, Weber L, Razzano P, et al. 2007. The effect of
growth differentiation factor-5-coated sutures on tendon
repair in a rat model. J Shoulder Elbow Surg 16:S215–S221.
31. Foland JW, Trotter GW, Powers BE, et al. 1992. Effect of
sodium hyaluronate in collagenase-induced superficial digi-
tal flexor tendinitis in horses. Am J Vet Res 53:2371–2376.
32. Soslowsky LJ, Carpenter JE, DeBano CM, et al. 1996.
Development and use of an animal model for investigations
on rotator cuff disease. J Shoulder Elbow Surg 5:383–392.
33. Lui PP, Fu SC, Chan LS, et al. 2009. Chondrocyte phenotype
and ectopic ossification in collagenase-induced tendon degen-
eration. J Histochem Cytochem 57:91–100.
34. Fu SC, Chan KM, Chan LS, et al. 2009. The use of motion
analysis to measure pain-related behaviour in a rat model of
degenerative tendon injuries. J Neurosci Methods 179:309–
35. Dirks RC, Warden SJ. 2011. Models for the study of
tendinopathy. J Musculoskelet Neuronal Interact 11:141–
36. Almekinders LC, Temple JD. 1998. Etiology, diagnosis, and
treatment of tendonitis: an analysis of the literature. Med
Sci Sports Exerc 30:1183–1190.
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JOURNAL OF ORTHOPAEDIC RESEARCH JANUARY 2014