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Patellar Tendinopathy
Recent Developments toward Treatment
Robert A. Christian, B.A., William H. Rossy, M.D., and Orrin H. Sherman, M.D.

Abstract
Patellar tendinopathy (PT) is a clinical and chronic overuse
condition of unknown pathogenesis and etiology marked
by anterior knee pain typically manifested at the inferior
pole of the patella. PT has been referred to as jumpers
knee since it is particularly common among populations
of jumping athletes, such as basketball and volleyball players. Due to its common refractory response to conservative
treatment, a variety of new treatments have emerged recently
that include dry-needling, sclerosing injections, platelet-rich
plasma therapy, arthroscopic surgical procedures, surgical
resection of the inferior patellar pole, extracorporeal shock
wave treatment, and hyperthermia thermotherapy. Since PT
has an unknown pathogenesis and etiology, PT treatment is
more a result of physician experience than evidence-based
science. This review will summarize the current literature
on this topic, identify current research efforts aimed to
understand the pathological changes in abnormal tendons,
provide exposure to the emerging treatment techniques, and
provide suggested direction for future research.

atellar tendinopathy (PT) describes a clinical condition characterized by activity-related anterior knee
pain associated with focal patellar tendon tenderness
localized to the inferior pole of the patella.1,2 PT pain can
also manifest at the distal insertion of the patellar tendon
over the anterior tibial tuberosity. A challenge to patients
and physicians alike, PT is a chronic and degenerative
overuse condition triggered by repetitive microtrauma.3

Robert A. Christian, B.A., Georgetown University School of

Medicine, Washington, DC. William H. Rossy, M.D., and Orrin
H. Sherman, M.D., Department of Orthopaedic Surgery, New York
University, New York, New York.
Correspondence: Robert A. Christian, B.A., Hospital for Joint
Diseases, 301 East 17th Street, Room 1402, New York, New York
10003; rac64@georgetown.edu.

Mechanical overload of the tendon is commonly cited as a

key component with many other contributing extrinsic and
intrinsic factors.4 Due to the uncertainty surrounding PT,
the use of correct terminology is important when describing
the condition.
As an overuse injury, PT should not be confused with
patellar tendonitis, which is an inflammatory discomfort
of the patellar tendon. The term tendonitis implies an
inflammatory nature to the injury, which is not present in
PT. Patellar tendinosis is the histopathological term to
describe the degenerative presentation characteristic of an
overuse injury. A tissue biopsy is needed in order to describe
patellar tendon pain as either tendonitis or tendinosis.1
For these reasons, patellar tendinopathy has been adopted
as the correct clinical term for overuse conditions of the
patella tendon.1,4
Patellar tendinopathy is a common clinical presentation
especially in athletic populations. It is particularly prevalent
among elite jumping athletes, such as basketball and volleyball players with rates of 31.9% and 44.6%, respectively.5
Due to this high prevalence among jumping athletes, PT
has historically been labeled as jumpers knee.6 Since
PT-related pain typically persists for 3 years and has been
reported to persist for greater than 15 years, athletes developing PT symptoms are often forced to deal with chronic
pain, which can reduce training, or even prematurely end
their careers.5,2 Due to its debilitating effects, understanding
and characterizing the symptoms of PT are key for patients.
PT does not have an evidence-based, preferred choice for
treatment. Conservative treatment of symptomatic PT focuses on rest, physical therapy, non-steroidal anti-inflammatory
drugs (NSAIDs), and eccentric muscle training.7-9 In cases
that are non-responsive to these modalities, both patients and
physicians are left searching for alternatives. Treatment of
recurrent PT varies widely and can be broadly grouped into
the following categories: exercise training, injection-based

Christian RA, Rossy WH, Sherman OH. Patellar tendinopathy: recent developments toward treatment. Bull Hosp Jt Dis. 2014;72(3):217-24.

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Bulletin of the Hospital for Joint Diseases 2014;72(3):217-24

treatments, surgical procedures, and other therapies. Due to

its unknown pathogenesis and etiology, treatment is often
based on physician experience, exposure, and comfort with
a specific treatment modalities. These factors have made the
treatment and management of PT resemble more of an art
than a science.8 The goal of this review is to identify recent
research effors aimed at addressing PT in order to best inform
physicians of the currently available treatment modalities.
We will also discuss potential future areas of research with
regard to PT.

History and Physical Examination

Athletes with PT typically present with complaints of anterior knee pain that is exacerbated with knee flexion and
prolonged activity. Often there is no history of direct trauma
to the knee; however, at times, the patient can report a recent
increase in activity level. The pain is typically insidious in
onset and can be localized to the proximal insertion of the
patellar tendon to the patella. In early stages of the disease,
athletes complain of pain only after sporting activities;
however, as the disease progresses, pain can be present
throughout specific activities and in severe cases can be
present during daily activities. Athletes will complain of a
decrease in athletic performance and an inability to complete
training regimens.
The most consistent physical exam finding in these
patients is localized tenderness at the inferior pole of the
patella. The most specific physical exam test to evaluate for
PT is the decline squatting test. In patients with PT, a limited
number of pain-free decline squats can be performed.10

an abnormal tendon with localized widening at the point of

tenderness with hypoechoic areas and can show neovascularization with increased vascular flow (Fig. 1).11 Neovascularization refers to the growth of new vessels into the
tendon with the potential for accompanying nerves, which
have been hypothesized as a source of symptomatic pain.
One cohort study reported that 60% of participants clinically
diagnosed with PT exhibited tendon changes complete with
neovascularization under US.11 These types of patients could
be indicated to receive sclerosing injection therapy, which
will be discussed later.
MRI can also be used to diagnose PT by differentiating between normal and abnormal tendons. An MRI of
an abnormal patellar tendon with PT usually reveals both
increased signal and tendon size at the site of pathologic
tendon changes (Fig. 2).1 In the case of both US and MRI,
it is important to note that abnormal patellar tendon changes
visible on a sonogram or MRI can occur asymptomatically. It has been found that asymptomatic patients with
sonographic tendon changes do have an increased risk of
developing symptoms of PT versus controls moving forward.12 Conversely, both imaging modalities may fail to
show abnormal tendon changes in patients with symptoms
consistent with PT. Due to the weak relationship between
imaging and symptomatology of PT, neither US nor MRI
can replace clinical presentation as the preferred method of
diagnosis of PT.1
A 2007 study by Warden and coworkers compared the
accuracy of MRI and both gray-scale and color-Doppler US.

Imaging
Both ultrasonography (US) and magnetic resonance imaging (MRI) are used to visualize patellar tendons in patients
clinically presenting with symptoms of PT. Ultrasound
examination reveals a variety of symptomatic changes in
patellar tendons with PT. Under ultrasound, normal tendons
appear regular with smooth fiber structure. When patellar
tendons with PT are imaged, the sonogram typically reveals

Figure 1 Gray-scale and color-Doppler ultrasound showing the

sonographic findings characteristic of PT. The sonogram reveals the
hypoechoic, darken area of the patellar tendon, tendon thickening,
and neovascularization.34

Figure 2 MRI scan typical of a symptomatic PT. This MRI reveals a change in signal intensity in the proximal patellar tendon
and increased tendon thickness. Both of these MRI findings are
characteristic of PT.13

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Results indicated that US was more accurate at diagnosing

PT than MRI. While the data revealed both gray-scale and
color-Doppler US to be 83% accurate, gray-scale US had a
higher sensitivity (87% to 70%), and color-Doppler US had
a higher positive predictive value (91% to 81%). Thus, Warden and coworkers argued that the most accurate diagnosis
would come from complementarily using both gray-scale
and color-Doppler ultrasonography.13

Recent Research
Research efforts have taken shape to explore the etiology
and pathogenesis of PT. To this end, several studies have
focused on extracellular matrix (ECM) changes and receptor
expression in PT. Cook and colleagues showed that tendinopathy is associated with changes in the ECM, and recent
research has worked to further characterize these changes.14
Specifically, histopathological analysis of abnormal tendons
with tendinopathy reveals hypercellularity, hypervascularity, lack of inflammatory infiltrates, and disorganization
and loosening of collagen fibrils.15 In 2009, Samiric and
associates set out to biochemically compare proteoglycan
and collagen composition in normal and abnormal patellar
tendons to confirm previous histological tendon studies.6,16-19
This study biochemically verified the previous histological
findings including increased sulfated glycosaminoglycans
(sGAGs) due to increased deposition of large proteoglycans and collagen changes in pathological tendons. While
the study did not find a change in total collagen between
normal and abnormal tendons, there was evidence of a
down-regulation of Type I collagen and fibromodulin and
an up-regulation of Type III collagen and versican. Samiric
and associates concluded that the increased ratio of Type
III to Type I collagen signifies a changes in the metabolic
turnover of pathologic tendons.6
Research examining transporter and receptor expression
in pathologic patellar tendons has also provided insight into
possible contributors to pathogenesis. In 2001, Rolf and coworkers investigated tendon hypercellularity, a characteristic
of PT, by tracking the expression of proliferation cell nuclear
antigen (PCNA) and platelet-derived growth factor receptor
(PDGFR).15 This study found significant hypercellularity
resulting from cell proliferation related to the expression of
PDGFR. With regard to transporter expression, in 2008,
Scott and associates discovered that vesicular glutamate
transporters (VGluT2) are more widespread and numerous
in tenocytes in human tendons inflicted with PT compared to
normal tendons.20 As a result of this transporter overexpression, tendons with PT have higher intratendinous levels of
glutamate than normal tendons. In part due to glutamates
role in controlling apoptosis, proliferation, and necrosis,
Scott and associates proposed that locally-derived glutamate,
possibly from the tenocytes, could play a role in the pathology of tendinosis.
Further research needs to be done to identify and characterize the biochemical changes and their mechanisms present

219

in PT. Research should continue to explore intratendinous

and extracellular changes in PT, mechanisms for hypercellularity, and the source and role of glutamate in tendinopathy
pathogenesis.

Exercise Training and Bracing

Eccentric muscle training became a mainstay in conservative treatment for various types of tendinopathies, mainly
due to studies evaluating Achilles tendinopathy. In these
studies, eccentric strength training proved to be effective
in reducing pain associated with neovascularization present
in Achilles tendinopathy.21,22 The mechanism is not well
understood but supports the theory that eccentric strengthening reduces blood flow through neovessels and eventually causes them to collapse. This collapse of neovessels
may then eliminate the role accompanying nerves can play
in causing symptomatic pain through ischemia. Eccentric
strength training has since been expanded to treat other
tendinopathies with beneficial results.23,24 Furthermore, the
technique of eccentric training has been refined to more
effectively treat PT. In 2004, Purdam and colleagues published a pilot study of eccentric decline squat training to
address PT.25 Results indicated that eccentric squats on the
decline board resulted in a statistically significant reduction
in pain that was not seen in the standard eccentric training
squat group. The benefits of eccentric decline squats were
later confirmed in a subsequent study.26 Eccentric strength
training is now considered a key aspect of conservative
treatment for PT.9,8
Kongsgaard and associates compared the effects of eccentric decline squat training, corticosteroid injections, and
heavy slow resistance training in treating PT.8 Results indicated that all three treatments result in short-term improvement at 12 weeks. Corticosteroid injections, however, were
not able to maintain the same improvement at the 6-month
follow-up as the eccentric training and heavy slow resistance
treatments modalities. Interestingly, heavy slow resistance
training also resulted in the reduction of abnormal tendon
changes characteristic of PT. This study signals the need
for more investigation into heavy slow resistance training
to promote the reduction of PT tendon changes.
Success of eccentric training led Fredberg and coworkers
to study the benefits of prophylactic eccentric training to
reduce the risk of developing PT.12 Since eccentric strength
training has been shown to reduce abnormal ultrasound characteristics in tendons with PT, it was logical to hypothesize
that this training could prophylactically reduce ultrasound
characteristics in asymptomatic abnormal tendons of soccer players and reduce the risk for these tendons to become
symptomatic in the subsequent year. Unfortunately, Fredberg
and coworkers did not find that eccentric training could be
used as prophylaxis. In fact, the results showed that eccentric
training actually increased the risk of developing symptoms
or injury in asymptomatic players with ultrasonographically abnormal patellar tendons. In this way, Fredberg and

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coworkers showed that eccentric training should only be

used on symptomatic PT.
Bracing and patella taping is sometimes used in conjunction with eccentric training and activity modification for the
treatment of PT. Chopat straps and knee taping techniques,
such as Kinesio taping and McConnell taping, have all been
utilized to reduce anterior knee pain in these patients.27 The
goal of bracing and taping is to reduce pain by increasing the
patellofemoral contact area, thereby decreasing joint stress.
These modalities are likely better served for treatment of
patellofemoral pain syndrome rather than chronic patellar
tendinopathy as they do little to unload the insertion of the
patella tendon to the patella.28

Injection Therapies
A variety of injection and needle-based therapies have
emerged in the literature as alternatives to treat PT. These
range from dry needling and autologous blood injections
to platelet-rich plasma (PRP) therapy, sclerosing, and high
volume injections.
Multiple studies have examined the benefits of ultrasound-guided dry needling to fenestrate tendons with
PT.29,30 Housner and associates looked at the variety of
injection therapies and found needling and physical disruption of the tendon to be the common attribute of the treatments.29 In this retrospective study, they found that 72%
of tendons treated with dry needling were able to return to
desired activity level by the 45-month follow-up. Housner
and associates proposed that the dry needing physically
breaks up possible degenerative changes characteristic
of PT, causes bleeding at the bone-tendon boundary, and
may allow for healing components to act on the abnormal
tendon. More research must be done to determine whether
tendon recovery occurs as a result of the treatment or simply due to the passage of time due to long-term follow-up
period utilized in this study. A second study combined
ultrasound-guided dry needling with autologous blood
injections for treating patellar tendinosis.30 In this study,
James and colleagues emphasized the need for injections
to be under ultrasound guidance and reiterated the call for
randomized controlled trials to confirm the positive results
of autologous blood injections.
A recent pilot study by Kon and coworkers investigated
the benefits of applying PRP therapy to treat PT.31 PRP
treatment involves reinjecting a concentration of autologous growth factors derived from blood into an injury site.
Kon and coworkers reported 80% satisfaction resulting
from PRP treatment of PT in this study with statistically
significant improvement both at the end of PRP therapy
and the 6-month follow-up. The investigators cautioned
that stretching and strengthening therapies play an essential
role in rehab following PRP treatment. Since the Kon and
coworkers study was a pilot study, randomized controlled
trials are needed to confirm the use of PRP to treat PT. As
research continues to explore the use of PRP in PT, it is

important to use a standard classification system like the

PRP PAW classification system, proposed by DeLong
and colleagues to facilitate comparing published results.32
This classification system emphasized the importance of
detailing the platelet concentration, activation method,
and the presence of white blood cells in PRP treatments
to allow comparison of PRP treatments and studies.
Sclerosing injections attempt to disrupt the neovascularization that is present in many cases of PT. These
injections are ultrasound-guided to insure localization
around the site of neovascularization. Previous studies
had shown that the presence of neovascularization in
abnormal tendons was related to increased tendon pain
compared to abnormal tendons without neovascularization.14 In this way, the sclerosing agent should eliminate
neovascularization and decrease the pain associated with
PT. It has been hypothesized that new nerves may also
follow the neovascularization, and this may play a role in
causing the associated pain. The nerves may be affected
directly by the sclerosing injection or indirectly through
ischemia with the elimination of neovessels.21 In two key
studies, Hoksrud and associates injected polidocanol to
sclerose neovascularization in tendons diagnosed with
PT.33,34 Their 2006 randomized controlled trial followed
up on a previously successful pilot study21 and found that
polidocanol injections had an 84% success rate after 12
months.34 This study seems to clearly establish polidocanol injections as a treatment alternative that must be
considered in chronic PT. In a second study, Hoksrud and
associates followed patients after sclerosing treatment to
determine the prevalence of neovascularization and posttreatment ultrasound tendon condition.11 Interestingly, they
found that while symptoms and pain had improved as a
result of the treatment, there was no relationship between
post-treatment ultrasound characteristics and reduction in
symptoms. In spite of the published success of sclerosing
injections, the investigators argued that this confirms the
unclear association between structural changes, neovascularization, and symptoms.
High volume ultrasound-guided injections also target the
neovascularization in abnormal tendons similar to sclerosing
injections. In high volume injections, the goal is to mechanically hinder the neovascularization process by injecting a
large volume of fluid between the deep aspect of the patellar tendon and Hoffas body. In a small pilot study (N =
9), Crisp and coworkers found that high volume injections
significantly out-performed the standard eccentric training
therapy.9 The investigators did caution, however, that four
of the patients did not realize a long-term reduction in PT
symptoms. They proposed that neovascularization may not
be the only reason for PT symptoms, which could explain
sclerosing injections not being effective in all cases of PT
as found in other studies. Crisp and coworkers remarked
that it would be interesting to repeat a diagnostic ultrasound
on cases in which high volume injections were ineffective

Bulletin of the Hospital for Joint Diseases 2014;72(3):217-24

in treating PT. Future research should investigate whether

neovascularization has occurred in patients receiving either
sclerosing injections or high volume injections to determine
if neovascularization is responsible for the recurrence of PT
symptoms.

Alternative Treatment Modalities

Recently, attention has been given to alternative treatment
options for those patients who have failed a course of conservative management and who do not yet wish to undergo
surgery. These modalities include treatments such as hyperthermia thermotherapy, extracorporeal shock wave therapy
(ESWT), and TOPAZ radiofrequency coblation.
Hyperthermia thermotherapy utilizes a deep tissueheating source along with a superficial cooling device to
warm deeper tissues while leaving the superficial tissues
cool. A 2002 randomized controlled trial by Giombini and
colleagues compared the efficacy of hyperthermia at 434
MHz to conventional ultrasound therapies in the treatment of
tendinopathies.35 This treatment was adapted from effective
utilization of hyperthermia in the early treatment of muscle
injuries. While the investigators acknowledge the debate
regarding the indication for hyperthermia thermotherapy,
they tout the ability to increase circulation and cellular
metabolism and assert that deep heating has long been
considered part of the treatment of tendinopathies. Thus,
hyperthermia thermotherapy could possibly be indicated
by the findings from the previously mentioned Samiric and
associates study, which proposed a decrease in metabolic
turnover as the explanation for increased sGAG deposition
in abnormal tendons.6 Giombini and coworkers found that
while both hyperthermia at 434 MHz and ultrasound produced statistically significant reductions in pain on palpation
and on isometric contraction, hyperthermia significantly
outperformed ultrasound in the remission of symptoms
during isometric contraction and overall satisfaction.35
Although its mechanism is not well understood, ESWT
has been utilized in clinical treatments for soft tissues and
orthopaedics for a decade. In 2007, Vulpiani and colleagues
published a pilot study to explore the efficacy of using ESWT
to treat PT.7 In this pilot study, ESWT produced a significant reduction of initial pain symptomatology at 1 month,
which continued to improve until 2 years after treatment.
Satisfactory results were found in 43.4%, 63.9%, and 68.8%
of tendons receiving ESWT at the 1-month, short-term, and
2-year follow-up exams.7 As a result, the pilot study seems
to support ESWT as a valid therapy for PT. A key benefit of
ESWT, which Vulpiani and colleagues made sure to note,
is that it does not contraindicate subsequent surgical treatment if found ineffective. The investigators of this review
believe that the effects of shock wave treatment on human
tendons should likely be investigated in the future since
the mechanism of ESWT is not well understood. As a pilot
study, these results need to be confirmed through randomized
controlled trials in order to gain evidence-based support.

221

TOPAZ radiofrequency coblation has been reported in

the literature for use for treatment of recalcitrant plantar
fasciitis, lateral epicondylitis, and rotator cuff tendonitis.36-38
Through the use of the minimally invasive radiofrequency
probe, microtenotomy is performed, which is thought to
promote an angiogenic healing response.36 Although there is
currently no data to support its use on patients with PT, the
fact that there is evidence supporting its use for other chronic
tendon conditions with similar pathogenesis has led some
surgeons to anecdotally turn to this treatment modality as a
last resort. Further studies are needed in order to evaluate
its effectiveness and safety in this patient population.

Surgical Management
Surgical treatment for PT tends to be viewed as a last resort
due to the variety of conservative and less invasive treatments available. With this in mind, PT is often chronic and
refractory to more conservative treatments leaving surgical
intervention as the sole remaining alternative. It has been
estimated that 10% of PT in athletes requires surgical intervention.39 Despite this fact, there remains a lack of consensus
on the ideal surgical approach.
Traditionally, the gold standard for surgical treatment of
PT involved open debridement of the inferior pole of the
patella, as well as debridement of the patella tendon. With
recent advancements in knee arthroscopy, arthroscopic
treatment of PT has become more common. This typically
involves arthroscopic debridement of the adipose tissue of
the anterior fat pad of the knee, debridement of any abnormal
patellar tendon, and longitudinal tenotomies with or without
excision or drilling of the inferior pole of the patella. As
per Santander and coworkers, this arthroscopic approach
attempts to treat the symptomatic pain of PT, while allowing a quicker return to normal activity. In this study, it was
found that 82% of study participants were able to return
to their previous activity level, which was comparable to
results of previous reported open surgery.40 Despite these
findings, this study had limitations, including a small study
population and lack of a control group. In addition, a small
number of elite athletes were in the study population, which
did not allow the merits of the arthroscopic procedure to be
evaluated on patients with high activity and load on their
tendons. Regardless of these limitations, the main goal of
arthroscopic treatment of PT is underscoredto surgically
address symptomatic pain, while allowing a quicker return to
normal activity. This potential for a quicker return to activities with arthroscopic debridement has led to the increasing
number of arthroscopic procedures performed in this patient
population.
When surgically approaching patients with PT, the inferior pole of the patella is the subject of debatedebridement
versus excision. Lorbach and associates attempted to definitively answer this question in 2008, when they designed two
separate studies focusing on the role the inferior pole of the
patella plays in the pathology of PT.39 Their data showed that

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the PT group had a significantly longer non-articular inferior

patellar pole compared to that of the control group. These
findings support a theory that a mechanical impingement
may be involved in the development of PT; this theory was
previously proposed by Johnson and colleagues.41 Despite
the contrast with previous studies regarding the inferior
patellar pole, their second study also showed a significant
reduction of symptoms from arthroscopic resection of the
inferior aspect of the patella.42 Additional research must be
done to conclusively show whether a difference in the length
of the inferior patellar pole exists in patients developing PT
and whether it plays a role in its pathogenesis and symptomatology.

Postoperative Rehabilitation
Postoperative rehabilitation following surgical treatment
of PT is varied. Some protocols suggest prolonged postoperative casting, whereas others recommend early range of
motion. As suggested by the reported variation in the literature, it can be deduced that no one regimen is universally
successful. Despite this, Shelbourne and coworkers applied
the universal orthopaedic concept that increasing stress
across biologic tissue can promote and optimize healing
and evaluated the application of aggressive postoperative
rehabilitation techniques on recovery following patellar tendonectomy for PT. Their study utilized a rehabilitation regimen currently used for ACL patellar autograft donor sites,
which included immediate range of motion, full flexion,
and immediate high-repetition, low-resistance quadriceps
muscle exercise. This analysis showed the application of
patellar tendon donor site rehabilitation for ACL reconstruction to the site of patellar tendonectomy to be effective with
87.5% (14/16 patients) of patients returning to their previous
activity level. The time required to return to a high activity
level was between 3 months and 1 year.43 It has long been
confirmed that stressing patellar tendons can aid in healing
and recovery from injury. This research by Shelbourne and
coworkers could represent a shift in rehabilitation for surgical treatment of PT that would allow for a quicker and more
effective return to activity.

Limitations
While this review summarizes PT research and treatment
today, it has several limitations that restrict our ability to
effectively draw conclusions and make treatment recommendations. Much of the current research investigating
treatment alternatives for PT consists of pilot studies with
small sample sizes with or without a control population. The
lack of randomized controlled trials and large treatment comparison studies makes it difficult to compare results across
studies and provide treatment recommendations. Differing
protocols in literature investigating the same PT treatment
also complicate comparison. In this review, effort was made
to include randomized controlled trials and draw conclusions
wherever possible to direct further research. In addition, the

retrospective nature of a few studies introduced recall bias.

It is also important to note that while PT can be a chronic
condition, Vulpiani and colleagues asserts that non-surgical
treatments can be effective in up to 90% of PT cases.7 It is
possible that rest, as a component of conservative treatment,
can be at least partly responsible for a given treatment result.
This should only further highlight the need for randomized
controlled trials to minimize this concern. In light of these
challenges, this review attempts to provide exposure for
treatment alternatives and raise physician awareness.

Conclusions
As a common chronic overuse condition, PT can be debilitating for many patients and in particular, athletes. Because of
its unknown pathogenesis and etiology, PT can be equally
as difficult for physicians without a clear, evidence-based
treatment of choice. For this reason, treatment selection often
relies on physician comfort with and exposure to a particular
method. This review attempts to address this uncertainty by
summarizing recent research, providing exposure for a variety of published treatments, and giving recommendations
for future research. Recent research efforts have investigated
biochemical changes in abnormal tendons, confirmed the
benefits of eccentric decline training, and explored the
benefits of new treatments, including heavy slow resistance
training, dry-needling, sclerosing injections, platelet-rich
plasma therapy, arthroscopic surgical procedures, resection of the inferior patella pole, extracorporeal shock wave
treatment, and hyperthermia thermotherapy. At this point,
the literature supports the use of eccentric decline training
for the treatment of PT, but does not support prophylactic
eccentric training to lower the risk of developing PT. Heavy
slow resistance training, sclerosing injections, arthroscopic
surgery, and surgical resection of the inferior patellar pole
appear to be promising based on existing research but
still need further confirmation. The remaining treatments
explored in this review require further research to become
evidence-supported therapies for PT. Additional studies,
especially large sample, randomized controlled trials, are
needed to verify the efficacy of many of these treatments
and allow for comparison between therapies. As research
identifies beneficial therapies for PT, studies will be needed
to provide indications for treatment providers and provide
evidence-based guidance for physicians treating PT.
Disclosure Statement
None of the authors have a financial or proprietary interest
in the subject matter or materials discussed, including, but
not limited to, employment, consultancies, stock ownership,
honoraria, and paid expert testimony.

References
1.
2.

Warden SJ, Brukner P. Patellar tendinopathy. Clin Sports Med.

2003 Oct;22(4):743-59.
Kettunen JA, Kvist M, Alanen E, Kujala UM. Long-term prognosis for jumpers knee in male athletes. A prospective follow-

Bulletin of the Hospital for Joint Diseases 2014;72(3):217-24

3.
4.
5.
6.
7.

8.

9.

10.
11.
12.

13.

14.
15.

16.
17.
18.

19.

up study. Am J Sports Med. 2002 Sep-Oct;30(5):689-92.

Alfredson H. The chronic painful Achilles and patellar tendon:
Research on basic biology and treatment. Scand J Med Sci
Sports. 2005 Aug;15(4):252-9.
Crossley KM, Thancanamootoo K, Metcalf BR, et al. Clinical
features of patellar tendinopathy and their implications for
rehabilitation. J Orthop Res. 2007 Sep;25(9):1164-75.
Lian OB, Engebretsen L, Bahr R. Prevalence of jumpers knee
among elite athletes from different sports: A cross-sectional
study. Am J Sports Med. 2005 Apr;33(4):561-7.
Samiric T, Parkinson J, Ilic MZ, et al. Changes in the composition of the extracellular matrix in patellar tendinopathy.
Matrix Biol. 2009 May;28(4):230-6.
Vulpiani MC, Vetrano M, Savoia V, et al. Jumpers knee treatment with extracorporeal shock wave therapy: A long-term
follow-up observational study. J Sports Med Phys Fitness.
2007 Sep;47(3):323-8.
Kongsgaard M, Kovanen V, Aagaard P, et al. Corticosteroid
injections, eccentric decline squat training and heavy slow
resistance training in patellar tendinopathy. Scand J Med Sci
Sports. 2009 Dec;19(6):790-802.
Crisp T, Khan F, Padhiar N, et al. High volume ultrasound
guided injections at the interface between the patellar tendon
and hoffas body are effective in chronic patellar tendinopathy:
A pilot study. Disabil Rehabil. 2008;30(20-22):1625-34.
Cook J, Khan KM, Maffulli N, et al. Overuse tendinosis,
not tendinitis, part2: applying the new approach to patellar
tendinopathy. Phys Sportsmed. 2000 Jun;28(6):31-46.
Hoksrud A, Ohberg L, Alfredson H, Bahr R. Color Doppler
ultrasound findings in patellar tendinopathy (jumpers knee).
Am J Sports Med. 2008 Sep;36(9):1813-20.
Fredberg U, Bolvig L, Andersen NT. Prophylactic training in
asymptomatic soccer players with ultrasonographic abnormalities in Achilles and patellar tendons: The Danish super
league study. Am J Sports Med. 2008 Mar;36(3):451-60.
Warden SJ, Kiss ZS, Malara FA, et al. Comparative accuracy of magnetic resonance imaging and ultrasonography in
confirming clinically diagnosed patellar tendinopathy. Am J
Sports Med. 2007 Mar;35(3):427-36.
Cook JL, Malliaras P, De Luca J, et al. Neovascularization and
pain in abnormal patellar tendons of active jumping athletes.
Clin J Sport Med. 2004 Sep;14(5):296-9.
Rolf CG, Fu BS, Pau A, et al. Increased cell proliferation and
associated expression of PDGFRbeta causing hypercellularity in patellar tendinosis. Rheumatology (Oxford). 2001
Mar;40(3):256-61.
Chard MD, Cawston TE, Riley GP, et al. Rotator cuff degeneration and lateral epicondylitis: A comparative histological
study. Ann Rheum Dis. 1994 Jan;53(1):30-4.
Fu SC, Chan KM, Rolf CG. Increased deposition of sulfated
glycosaminoglycans in human patellar tendinopathy. Clin J
Sport Med. 2007 Mar;17(2):129-34.
Riley GP, Harrall RL, Constant CR, et al. Tendon degeneration
and chronic shoulder pain: Changes in the collagen composition of the human rotator cuff tendons in rotator cuff tendinitis.
Ann Rheum Dis. 1994 Jun;53(6):359-66.
Bank RA, TeKoppele JM, Oostingh G, et al. Lysylhydroxylation and non-reducible crosslinking of human supraspinatus
tendon collagen: Changes with age and in chronic rotator cuff
tendinitis. Ann Rheum Dis. 1999 Jan;58(1):35-41.

223

29. Scott A, Alfredson H, Forsgren S. VGluT2 expression in

painful Achilles and patellar tendinosis: Evidence of local glutamate release by tenocytes. J Orthop Res. 2008
May;26(5):685-92.
21. Ohberg L, Alfredson H. Effects on neovascularisation behind
the good results with eccentric training in chronic mid-portion
Achilles tendinosis?. Knee Surg Sports Traumatol Arthrosc.
2004 Sep;12(5):465-70.
22. Ohberg L, Lorentzon R, Alfredson H. Eccentric training in
patients with chronic Achilles tendinosis: Normalised tendon
structure and decreased thickness at follow up. Br J Sports
Med. 2004 Feb;38(1):8-11; discussion 11.
23. Frohm A, Saartok T, Halvorsen K, Renstrom P. Eccentric
treatment for patellar tendinopathy: A prospective randomised
short-term pilot study of two rehabilitation protocols. Br J
Sports Med. 2007 Jul;41(7):e7. Epub 2007 Feb 8.
24. Visnes H, Bahr R. The evolution of eccentric training as
treatment for patellar tendinopathy (jumpers knee): A critical review of exercise programmes. Br J Sports Med. 2007
Apr;41(4):217-23.
25. Purdam CR, Jonsson P, Alfredson H, et al. A pilot study of the
eccentric decline squat in the management of painful chronic
patellar tendinopathy. Br J Sports Med. 2004 Aug;38(4):395-7.
26. Young MA, Cook JL, Purdam CR, et al. Eccentric decline
squat protocol offers superior results at 12 months compared
with traditional eccentric protocol for patellar tendinopathy
in volleyball players. Br J Sports Med. 2005 Feb;39(2):102-5.
27. Crossley K, Cowan SM, Bennell KL, et al. Patellar taping:
is clinical success supported by scientific evidence? Manual
Therapy. 2000 Aug;5(3):142-50.
28. Khan KM, Maffulli N, Coleman BD, et al. Patellar tendinopathy: some aspects of basic science and clinical management.
Br J Sports Med. 1998 Dec;32(4):346-55.
29. Housner JA, Jacobson JA, Morag Y, et al. Should ultrasoundguided needle fenestration be considered as a treatment option
for recalcitrant patellar tendinopathy? A retrospective study
of 47 cases. Clin J Sport Med. 2010 Nov;20(6):488-90.
30. James SL, Ali K, Pocock C, et al. Ultrasound guided dry needling and autologous blood injection for patellar tendinosis.
Br J Sports Med. 2007 Aug;41(8):518-21; discussion 522.
31. Kon E, Filardo G, Delcogliano M, et al. Platelet-rich plasma:
New clinical application: A pilot study for treatment of
jumpers knee. Injury. 2009 Jun;40(6):598-603.
32. DeLong JM, Russell RP, Mazzocca AD. Platelet-rich
plasma: The PAW classification system. Arthroscopy. 2012
Jul;28(7):998-1009.
33. Alfredson H, Ohberg L. Neovascularisation in chronic painful
patellar tendinosis--promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee
Surg Sports Traumatol Arthrosc. 2005 Mar;13(2):74-80.
34. Hoksrud A, Ohberg L, Alfredson H, Bahr R. Ultrasoundguided sclerosis of neovessels in painful chronic patellar
tendinopathy: A randomized controlled trial. Am J Sports
Med. 2006 Nov;34(11):1738-46.
35. Giombini A, Di Cesare A, Casciello G, et al. Hyperthermia at
434 MHz in the treatment of overuse sport tendinopathies: A
randomised controlled clinical trial. Int J Sports Med. 2002
Apr;23(3):207-11.
36. Tay KS, Ng YC, Singh IR, et al. Open technique is more
effective than percutaneous technique for TOPAZ readiofre-

224

Bulletin of the Hospital for Joint Diseases 2014;72(3):217-24

quency coblastion for plantar fasciitis. Foot Ankle Surg. 2012

Dec;18(4): 287-92.
37. Tasto JP, Cummings J, Medlock V, et al. Microtenotomy
using a radiofrequency probe to treat lateral epicondylitis.
Arthroscopy. 2005 Jul;21(7):851-60.
38. Taverna E, Battistella F, Sansone V, et al. Radiofrequencybased plasma microtenotomy compared with arthroscopic
subacromial decompression yields equivalent outcomes for
rotator cuff tendinosis. Arthroscopy. 2007 Oct;23(10):104251.
39. Lorbach O, Diamantopoulos A, Kammerer KP, Paessler HH.
The influence of the lower patellar pole in the pathogenesis
of chronic patellar tendinopathy. Knee Surg Sports Traumatol
Arthrosc. 2008 Apr;16(4):348-52.

40. Santander J, Zarba E, Iraporda H, Puleo S. Can arthroscopically assisted treatment of chronic patellar tendinopathy
reduce pain and restore function?. Clin Orthop Relat Res.
2012 Apr;470(4):993-7.
41. Johnson DP, Wakeley CJ, Watt I. Magnetic resonance
imaging of patellar tendonitis. J Bone Joint Surg Br. 1996
Mar;78(3):452-7.
42. Lorbach O, Diamantopoulos A, Paessler HH. Arthroscopic
resection of the lower patellar pole in patients with chronic
patellar tendinosis. Arthroscopy. 2008 Feb;24(2):167-73.
43. Shelbourne KD, Henne TD, Gray T. Recalcitrant patellar
tendinosis in elite athletes: Surgical treatment in conjunction
with aggressive postoperative rehabilitation. Am J Sports
Med. 2006 Jul;34(7):1141-6.