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Arthrofibrosis Associated With Total Knee Arthroplasty

The Journal of Arthroplasty 32 (2017) 2604e2611
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The Journal of Arthroplasty
journal homepage: www.arthroplastyjournal.org
Arthrofibrosis Associated With Total Knee Arthroplasty
Victor A. Cheuy, PhD a, *, Jared R.H. Foran, MD b, Roger J. Paxton, PhD a,
Michael J. Bade, PT, PhD a, Joseph A. Zeni, PT, PhD c, Jennifer E. Stevens-Lapsley, PT, PhD a, d
Physical Therapy Program, Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora, Colorado
Panorama Orthopaedics and Spine Center, Golden, Colorado
Department of Physical Therapy, University of Delaware, Newark, Delaware
Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Denver, Colorado
a r t i c l e i n f o
a b s t r a c t
Article history:
Received 17 August 2016
Received in revised form
3 January 2017
Accepted 5 February 2017
Available online 14 February 2017
Background: Arthrofibrosis is a debilitating postoperative complication of total knee arthroplasty (TKA).
It is one of the leading causes of hospital readmission and a predominant reason for TKA failure. The
prevalence of arthrofibrosis will increase as the annual incidence of TKA in the United States rises into
the millions.
Methods: In a narrative review of the literature, the etiology, economic burden, treatment strategies, and
future research directions of arthrofibrosis after TKA are examined.
Results: Characterized by excessive proliferation of scar tissue during an impaired wound healing
response, arthrofibrotic stiffness causes functional deficits in activities of daily living. Postoperative,
supervised physiotherapy remains the first line of defense against the development of arthrofibrosis.
Also, adjuncts to traditional physiotherapy such as splinting and augmented soft tissue mobilization can
be beneficial. The effectiveness of rehabilitation on functional outcomes depends on the appropriate
timing, intensity, and progression of the program, accounting for the patient's ability and level of pain.
Invasive treatments such as manipulation under anesthesia, debridement, and revision arthroplasty
improve range of motion, but can be traumatic and costly. Future studies investigating novel treatments,
early diagnosis, and potential preoperative screening for risk of arthrofibrosis will help target those
patients who will need additional attention and tailored rehabilitation to improve TKA outcomes.
Conclusion: Arthrofibrosis is a multi-faceted complication of TKA, and is difficult to treat without an
early, tailored, comprehensive rehabilitation program. Understanding the risk factors for its development
and the benefits and shortcomings of various interventions are essential to best restore mobility and
© 2017 Elsevier Inc. All rights reserved.
total knee
range of motion
Characterizing Arthrofibrosis
Arthrofibrosis is a well-known complication of injury or trauma,
characterized by the production of excessive fibrous scar tissue in a
joint [1e4]. The major consequence of arthrofibrosis is the loss of
range of motion because of the painful stiffness of proliferated scar
tissue, which interferes with the patient's ability to adequately
perform functional tasks of daily living [5,6]. Arthrofibrosis is a
debilitating complication after knee surgery that may also result in
One or more of the authors of this paper have disclosed potential or pertinent
conflicts of interest, which may include receipt of payment, either direct or indirect,
institutional support, or association with an entity in the biomedical field which
may be perceived to have potential conflict of interest with this work. For full
disclosure statements refer to http://dx.doi.org/10.1016/j.arth.2017.02.005.
* Reprint requests: Victor A. Cheuy, PhD, Mail Stop C244, 13121 East 17th Ave.,
Aurora, CO 80045.
0883-5403/© 2017 Elsevier Inc. All rights reserved.
pain that does not subside at predictable time points, pain with
palpation, lack of patellar movement with quadriceps muscle
contraction, or a knee joint that is warm or swollen unrelated to
effusion [7,8].
There is a lack of consensus on the diagnostic criteria for
arthrofibrosis of the knee, which obscures its true prevalence after
surgical procedures [9,10]. The spectrum of classification ranges
from broadly assessing patient difficulty with activities of daily
living attributable to limited range of motion (including decreased
range of motion preoperatively), to quantitative thresholds of
flexion and/or extension loss [5,11]. These quantitative thresholds
vary and include a flexion contracture of >15 degrees and/or <75
degrees of flexion; >10 degrees of extension deficit and/or <95
degrees of flexion; or a total knee arc range of motion <70 degrees
[12e14]. Imaging techniques have been used to supplement patient
history and clinical examinations, and can be valuable in assisting
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
Fig. 1. Risk factors for arthrofibrosis and typical postoperative care strategies. NSAIDs, nonsteroidal anti-inflammatory drugs; PT, physical therapy; RICE, rest-ice-compressionelevation; ROM, range of motion; TKA, total knee arthroplasty.
with diagnosis and treatment planning [15]. Magnetic resonance
imaging (MRI) and ultrasound have both demonstrated the ability
to detect focal fibrous proliferation based on heterogeneous signal
intensity in the knee, ankle, and foot [15e17]. However, MRI is not
part of the standard of care, even with the development of metal
suppression sequences to reduce artifacts and improve image
quality [18,19]. Advanced imaging is used (if at all) only after patient
history, physical examination, and radiographs all fail to identify
the cause of pain and/or stiffness after total knee arthroplasty (TKA)
[20]. MRI also suffers from the drawbacks of cost, the timeconsuming nature of scans, and concerns over patient claustrophobia and keeping still for extended periods.
The etiology of arthrofibrosis is multifactorial, and numerous
preoperative, intraoperative, and postoperative risk factors have
been identified (Fig. 1). Decreased preoperative knee range of
motion, higher complexity surgery (ie, amount of trauma, length of
surgery), and history of surgery increase the risk of excessive scar
tissue after TKA [21]. Previous studies have shown the rate of
arthrofibrosis doubles or even triples when patients have undergone previous surgeries for multiple ligamentous injuries or surgeries that require immobilization [9,22,23]. Postoperative factors
contributing to arthrofibrosis include poor patient motivation and
immobility, delay in starting a rehabilitation program, lack of
compliance with prescribed rehabilitation, poor pain tolerance, and
infection [5,9,23]. In addition, a genetic predisposition to forming
excessive intraarticular scar tissue after injury and/or surgery has
been implicated in several studies [24e26].
The exact pathophysiology of how these factors cause arthrofibrosis is not completely clear, but what is known is the coordination of cell growth, differentiation, and death controlled by
various cytokines and growth factor signaling is disrupted, directly
affecting tissue homeostasis and organization, and allowing for
uninhibited proliferation of fibroconnective tissue [9,22,27].
Fibrosis can occur in many different organs (eg, skin, liver, lungs),
and can ultimately lead to organ failure [25,28,29]. In the normal
wound healing response, the cascade of biological responses is
tightly regulated. The migration of inflammatory cells and the
proliferation of fibroblasts trigger the release of cytokines, growth
factors, and reactive oxygen species that are responsible for tissue
remodeling and restoring tissue integrity [30]. Once the healing
process is complete, the inflammatory cells undergo apoptosis
(ie, programmed cell death), the release of signaling molecules
stops, and the inflammatory response critical to restoring tissue to
its functional state subsides [30,31]. However, the arthrofibrotic
condition is characterized by a lack of apoptosis in the proinflammatory phase, resulting in an imbalance between synthesis
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
and degradation [29,31]. Persistent transforming growth factor-b
(TGF-b) and bone morphogenetic protein 2 (BMP2) secretion and
downstream responses are thought to contribute to a sustained
inflammatory response [25,28,31,32]. Without apoptosis to balance
proliferation during this time, pathologic scar formation is inevitable, where functional cell types are eventually replaced by connective tissue [33,34]. Proteoglycans, collagens, and extracellular
matrix components aggressively accumulate in the intercellular
space and stiffen, creating a fibrotic state [25,30,31,33]. Interventions directed at some of these potential biological targets
have not been successful, and there has been no specific pharmacological therapy able to prevent or cure arthrofibrosis [29].
Association With TKA
TKA is the standard of care to manage the pain and disability
associated with end-stage knee osteoarthritis, with more than
700,000 TKA surgeries performed annually in the United States
[35]. Arthrofibrosis is a debilitating complication of TKA, with a
reported incidence of between 1% and 13% postoperatively
[4,6,10,13,36]. The range of values can be attributed to the varying
quantitative thresholds of flexion and/or extension loss used to
define arthrofibrosis, as described previously. As a predominant
failure mechanism, arthrofibrosis accounts for 28% of hospital
readmissions due to surgical complications within 90 days of
discharge, and 10% of all revisions within 5 years of initial surgery
within the United States [37,38]. Patients with arthrofibrosis are at
elevated risk for prolonged, high treatment costs, especially for
those whose limited range of motion persists despite varied
treatment techniques [38,39]. One quarter of patients treated with
a motion-restoring surgical procedure still required multiple surgeries, with only 37% reporting satisfactory results [22]. With the
incidence of TKA projected to reach 3.5 million by 2030, the
growing cohort of TKA patients with postoperative arthrofibrosis
provides an important target for research [40].
The excessive scar tissue formation in the knee joint with
arthrofibrosis results in decreased knee extension and flexion range
of motion, leading to tissue contracture, increased pain, and functional deficits in many activities of daily living (eg, standing up,
walking, stair climbing) [11,41e44]. Previous studies have shown
that the functional deficits vary depending on the severity of
flexion loss; approximately 70 degrees of flexion are necessary for
typical gait, 80 -90 for stair ascent and descent, and at least 125
for squatting to pick an object up from the floor [9,43,45]. Loss of
extension can be even more incapacitating and difficult to manage,
as just small limitations in extension range of motion increase
energy consumption and place undue strain on the quadriceps
muscles [9,27,45]. As little as a 5 loss in extension results in altered
gait mechanics (eg, limping) and walking on a 15 flexed knee requires 22% more extensor demand [9,46].
over a primary); those receiving a revision are also twice as likely to
require readmission (higher rates of complications such as infection); and those receiving a revision may have worse outcomes, as
patients may remain stiff even after their procedure [38,49e52]. If
the use of invasive techniques for management of arthrofibrosis
could be minimized while still achieving adequate range of motion,
the costs and incidence of complications associated with arthrofibrosis could be reduced. Rehabilitation is comparatively low cost,
at approximately $1500 per knee arthroplasty [53].
Importance of Initial Management
Physiotherapy rehabilitation is a fundamental component of the
postoperative care after primary TKA. The arthrofibrotic knee represents a difficult challenge for the therapist that requires careful
attention and skill to improve functional outcomes and potentially
save the health care system tens of thousands of dollars per patient
in future medical costs. An effective rehabilitation program emphasizes (1) the management of inflammation, swelling, and pain,
(2) frequent monitoring, and (3) maintaining or restoring range of
motion as soon as arthrofibrosis is recognized [27,54e56]. This is in
contrast to the typical intervention after TKA, in which the
emphasis is on increasing muscle strength of the quadriceps as well
as managing inflammation and swelling. However, because range
of motion is the limiting factor in patients with arthrofibrosis, the
intervention needs to prioritize range of motion deficits early
before the fibrotic tissue has a chance to mature and become
resistant to physiotherapy later on [10]. The arthrofibrotic knee
requires intensive, structured, and well-monitored rehabilitation to
aggressively treat range of motion deficits, and its effectiveness is
also highly dependent on patient motivation and compliance
[5,11,22,57e59]. Concurrently, adequate pain management must be
maintained and progress should be monitored closely [55]. The
intensity of rehabilitation should be aggressive, as intense physical
therapy was found to be the most influential factor for postoperative flexion, while a decrease in days of aggressive inpatient
physical therapy correlated with an increased rate of MUAs [60,61].
Preoperative educational meetings can also engage patients as
active participants in their own healthcare to address motivation
and compliance; attendance of educational meetings was associated with a significantly decreased risk of postoperative stiffness
requiring MUA [59]. Several supplements to a prescribed rehabilitation program exist that target range of motion, with a long-term
goal of avoiding additional operations if possible. These adjuncts to
rehabilitation may help maintain or even promote range of motion
gains achieved with physical therapy, with implementation and
timing of these treatment modalities typically customized to each
patient (see below) [22,41].
Nonsteroidal Anti-Inflammatory Drugs and the Rest-IceCompression-Elevation Method
Economic Burden of Arthrofibrosis Post-TKA
TKA is generally a successful and cost-effective procedure, but
adverse outcomes like arthrofibrosis can lead to costly follow-up
procedures [47]. Although manipulation under anesthesia (MUA)
is typically the initial treatment option for post-TKA arthrofibrosis,
it is no guarantee of improved function, decreased pain, and
increased satisfaction [14,48]. More aggressive procedures may
improve knee range of motion, but are more traumatic and are
associated with an increased risk of continued postoperative
treatment. Furthermore, compared with a primary TKA, a revision
TKA is more costly (1.6 times less cost-effective for the same increase in Western Ontario and McMaster Universities Arthritis Index score, and an increased hospitalization cost of almost $7000
Nonsteroidal anti-inflammatory drugs and the rest-icecompression-elevation method assist with decreasing the inflammatory response, pain, and swelling. Shortening the inflammatory
phase decreases the pathogenesis of scar tissue, whereas proper
pain and swelling management allow rehabilitation to begin or to
continue without excessive patient discomfort [62]. Such symptom
management is important for patient motivation and adherence to
therapy, which are both crucial to successful outcomes, as gains in
range of motion may be lost because of lack of activity or immobility [63]. Therapist supervision is vital in determining if acute
inflammation persists through treatment. Although immediate and
aggressive range of motion exercises improve outcomes for patients with early motion problems, if inflammation is not well
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
Fig. 2. Management algorithm for arthrofibrosis of the knee after total knee arthroplasty.
controlled, such aggressive intervention may have the opposite
effect and actually promote scar tissue formation [64]. In these
cases, a milder, but consistently implemented range of motion
exercise intervention might achieve the best results.
Continuous Passive Motion Devices
Although active motion training is preferred, continuous passive
motion (CPM) devices are occasionally used to promote flexion.
However, several studies have found no advantage in improving
range of motion or any greater benefit when paired with physiotherapy [65e67]. Boese et al [68] randomized a total of 160 subjects
into 3 groups: CPM device on and moving from the immediate
postoperative period, CPM device on and stationary at 90 flexion for
the first night and then moving throughout the rest of their stay, and
no CPM. They found no significant differences in all outcome variables (range of motion, swelling, blood loss, and pain scores) and
that CPM provided no benefit to patients recovering from TKA [68].
systematic review of 12 randomized controlled trials investigating
bracing after ACL reconstruction rehabilitation found no evidence
that range of motion was affected by brace use, findings which may
extend to bracing after TKA as well [69]. Both static progressive
splints, which use stress relaxation to stretch tissues, and dynamic
progressive splints, which apply a low-grade force to the joint to
gradually flex or extend the joint, have been shown to improve
knee flexion deficits by 19 and knee flexion contractures by 7 -19
[39,71]. However, research in this area is limited to only 2 small
cohort studies.
Neuromuscular Electrical Stimulation
Neuromuscular electrical stimulation applies an electrical current that overrides voluntary activation deficits to help re-educate
the quadriceps muscle to contract normally [72]. Improving muscle
function increases the speed of recovery and long-term functional
performance, and may help reduce or prevent extension lag
Soft Tissue Mobilization
Static bracing is often used to maintain full extension range of
motion [8,69]. Unfortunately, an extension brace may worsen
arthrofibrosis due to limited flexion and, if bracing is used, the
recommendation is alternating periods of bracing with periods of
motion so as to limit development of stiffness [8,70]. Bracing is
common practice after anterior cruciate ligament (ACL) reconstruction, and although it is a different pathology of the knee, a
Mechanical soft-tissue stimulation with hand-held instruments
(Astym, Performance Dynamics Inc, Muncie, Indiana) has also been
shown to improve knee flexion deficits by 35 and knee flexion
contractures by 12 in a small cohort of individuals who had failed
to respond to traditional rehabilitation and MUA [74]. The rationale
is the topical application of appropriate shear force and pressure
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
Table 1
Indications and Contraindications for Surgical Treatment Modalities.
MUA [75,76]
90 degrees of flexion at 6-wk follow-up
Within 3 mo of primary TKA
Arthroscopic and open debridement [6,77]
Revision total knee arthroplasty [4]
Recurrent stiffness after physical therapy and MUA
First attempt arthroscopic, then open
More than 3 mo after primary TKA
Clear diagnosis for cause of stiffness, which can be
corrected operatively
Preferably within 2 y of primary TKA
Infection, wound problems
>10 degrees of extension loss (fracture concern)
Component malalignment
Infection, wound problems
Component malalignment
Extrinsic source of stiffness
Insufficient pain and functional limitation to outweigh
risk of additional surgery
MUA, manipulation under anesthesia.
stimulates regeneration of damaged tissues and breakdown of scar
Treatment Modalities Post-TKA After Physical Therapy
Arthrofibrosis is a challenging complication after primary TKA
because deficits in range of motion can persist, mitigating the
therapeutic effects of rehabilitation [41]. Treatment options available after physical therapy are MUA, debridement, and revision TKA
(Fig. 2), whose indications and contraindications are summarized
in Table 1.
Management of arthrofibrosis with MUA is typically the first
option when range of motion has not improved with physiotherapy
in the early postoperative period, as it is the least invasive operative
procedure and the scar tissue has not yet matured [10,48,78,79].
The reported incidence of patients undergoing a MUA after TKA to
address limited range of motion is between 2% and 6%
[48,58,75,76]. The most common technique for MUA is general
anesthesia, muscle relaxants, and a combination of administered
hip and knee flexion [80]. While the patient is under anesthesia, the
physician flexes the hip to 90 , and progressively flexes and extends
the knee while receiving auditory and tactile feedback of the adhesions breaking away, culminating with several 20-30 second
holds at the new maximal knee positions [81].
Historically, there has been disagreement on the optimal interval of time between TKA and MUA [75]. Initially, no major differences were found in knee flexion improvement between MUA
performed early (12 weeks postop) and late (>12 weeks postop)
[82,83]. However, recent research has found an inverse relationship between time to MUA postoperatively and final range of
motion, where earlier MUA increased flexion range of motion 30 42 and overall knee range of motion 31 -47 [13,75,78,80,84,85].
Namba and Inacio [48] compared patients who received MUA
within or beyond 3 months of surgery (1.8 [SD 0.7] vs 5.5 [SD 3.0]
months, respectively), and found that those patients who received
MUA beyond 3 months gained approximately half the flexion
range of motion of the cohort who had MUA within 3 months (17
vs 33 ). Issa et al [86] found that patients who underwent
manipulation within 12 weeks achieved double the mean gain in
flexion (36.5 vs 17 ), over 20 more in total arc range of motion
(119 vs 95 ), and had higher Knee Society objective and function
scores than those who had late MUA. No significant differences in
these outcomes were found between patients who received an
MUA within 6 weeks and between 7 and 12 weeks. A recent survey
of 82 surgeons found confirmatory attitudes toward MUA timing,
where 71% performed MUA within 3 months, while only 19% performed manipulations between 3 and 6 months postoperatively
[5]. With patients typically returning to clinic 4-6 weeks postoperatively, manipulation of those with severely limited motion
should not be delayed much longer, as potential range of motion
gains begin to decrease and incidence of subsequent revision TKA
increase (from 3.8%-5.3%) after 8 weeks post-TKA [58,75,76]. MUA
may not be effective for the severely stiff knee, in which flexion
range of motion is less than 70 , or for those who require multiple
sessions of MUA, as both these clinical presentations tend to have
poorer outcomes and require more aggressive treatment
[14,84,87]. When assessing the clinical benefits of MUA, the patient and surgeon must also weigh the potential complications,
which include fracture, wound dehiscence, patellar tendon avulsions, quadriceps strain or rupture, hemarthrosis, heterotopic bone
formation, and pulmonary embolism [79,85].
When previous interventions like an MUA have failed to restore
adequate range of motion, or if the patient is more than 3 months
post-TKA, arthroscopic or open debridementdalso known as lysis
of adhesionsdis typically considered [10,11]. The reported incidence of patients undergoing a debridement after TKA to address
limited range of motion is 0.8% [88]. Arthroscopic debridement is a
minimally invasive surgical procedure that introduces various
cutting or shaving instruments through multiple arthroscopic
portals to break up focal and diffuse arthrofibrosis [77]. The focus of
the procedure is on the release of adhesions within the suprapatellar pouch, the lateral and medial gutters, and the intercondylar
notch [89]. Previous studies have found arthroscopic debridement
improved flexion range of motion 24 -34 , extension range of
motion 12 -23 , and overall knee range of motion 24 -31
[83,88,90,91]. When arthrofibrosis is severe enough that nonoperative and arthroscopic techniques fail, open debridement is the
more invasive alternative [6,10,45,62]. During the open surgery,
blunt and sharp tools are used to break up adhesions with
enhanced visualization and easier access to all the articular structures that require debridement [62]. Improvement in overall knee
range of motion range averaged 39 with the open method
[13,83,92e94]. Because the gains in range of motion for both
arthroscopic and open debridement are comparable with those
from an MUA, the utility of debridement (specifically open) may
only exist for those patients with severe arthrofibrosis and who
have not responded to any previous treatments [6]. A recent survey
of 82 surgeons found that a majority (55%) do not perform open or
arthroscopic debridement, and only 4% routinely performed
debridement [5]. Although debridement is generally a safe treatment modality, the risks associated with it include damage to the
metal prosthesis, hemarthrosis, extensor mechanism injury, fracture, infection, and neurovascular injury [77].
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
Revision TKA
Revision TKA is the final treatment option available for persistent limited motion if all previous treatments have failed. Previous
research has found that 10% of all revisions within 5 years of initial
surgery are due to arthrofibrosis [37]. A revision involves a partial
or complete replacement of the original prosthesis. Previous literature is scant on the outcomes of revision surgery for arthrofibrosis,
but Ries et al did find an improvement in range of motion in 6
patients, averaging a 50 increase in total knee range of motion
[14,95]. Unfortunately, pain and function scores after revision TKA
for arthrofibrosis have been shown to still lag behind scores for
revision TKA for other reasons (eg, infection, instability, wear, and
loosening) [96]. Arthrofibrosis may still occur after a revision due to
the surgical trauma, postsurgical rehabilitation process, or patient
predisposition, as those patients who require a revision due to
arthrofibrosis are also those with the highest risk for the persistent
development of severe fibrosis. Kim et al [57] found that over 25% of
revision TKAs due to stiffness required a second revision. Greidanus
et al [97] asserted that “most revision patients will never experience an outcome as favorable as their primary procedure.” The
additional risks associated with a revision are similar for primary
TKA surgery and as mentioned previously, including infection,
hemarthrosis, and neurovascular injury [98].
Future Directions
Novel Treatments
Novel operative and nonoperative treatment options for
arthrofibrosis after TKA are being developed, although most still
require larger, prospective, randomized studies. Saltzman et al [99]
has described supplementing arthroscopic debridement with the
use of indwelling epidural catheters begun preoperatively that
continue postoperatively for 6 weeks. The rational for extended
pain analgesia is that inadequate postoperative pain control prevents knee flexion, resulting in adhesion formation and knee
stiffness [5]. Although the retrospective analysis was completed on
a small cohort (n ¼ 20), those receiving epidural catheters showed
improved knee extension, knee flexion, and self-reported pain
levels, with 70% maintaining range of motion success long-term
(6-month follow-up) and minimal complications [99]. Formby
et al [100] used hydraulic distension, a technique typically used to
treat adhesive capsulitis, as a substitute for an MUA. Hydraulic
distension of the knee involves (1) aspirating the suprapatellar
pouch, (2) distending the capsule with irrigation fluid and anesthesia until rupture, (3) aspirating the distension fluid, and (4)
injecting corticosteroid coupled with manipulation of the knee. The
3 patients receiving hydraulic distension showed a 23 increase in
knee flexion postoperatively, which was maintained at follow-up
(average 12 months) with no complications [100].
Smith et al [101] performed a prospective, randomized, doubleblinded, placebo-controlled trial comparing the use of botulinum
toxin A vs placebo for the treatment of knee flexion contracture
after TKA in patients without a specific preexisting neuromuscular
disorder. The authors postulated that botulinum toxin A can been
used to relieve hamstring tightness that developed secondary to a
flexion contracture. The results for 15 knees were that a single injection into the hamstring musculature resulted in a significant
improvement in extension at 1 month and a greater amount of
improvement at 1 year compared with placebo, although both
groups recovered near full extension at the 1-year time point [101].
Treatment options are targeting inhibition of the fibrotic process as
well: Farid et al evaluated low-dose irradiation immediately before
constrained revision TKA to suppress fibroblastic proliferation;
Dixon et al hypothesize an interleukin-1 receptor antagonist, anakinra, can have an inhibitory effect on fibroblasts; and animal
models reveal novel anti-inflammatory agents may reduce knee
stiffness [102e104]. These studies serve as impetus for further
work into interventions during all perioperative phases of TKA.
Certain individuals may develop arthrofibrosis as part of their
healing process, indicative of a genetic component to arthrofibrosis
[26,105]. The development of an assessment of patient susceptibility to arthrofibrosis would aid healthcare professionals in optimizing perioperative care, targeting those at high risk of
complication. For example, a physical therapist could tailor the
rehabilitation program more effectively through improving timing,
level of aggressiveness, and speed of progression based on the
patient's risk level, resulting in faster recovery and better functional
outcomes. Differences in genetic disposition and gene expression
between patients with and without arthrofibrosis is a promising
area of future study.
The genetic targets of interest would be those genes and
signaling pathway regulators that relate most to the fibrogenic
process, capsular remodeling, and long-term inflammatory reactions, all associated with changes in extracellular matrix and
collagen production [25,27]. Although allelic association studies
have implicated a genetic predisposition toward forming excessive
joint scar tissue after injury and/or surgery, a genome-wide association study (GWAS) would offer a far more robust approach for
establishing a genetic risk profile [24,25,106]. A GWAS takes into
account the entire genome, unbiased with respect to selecting
certain single nucleotide polymorphisms. A meta-analysis of multiple GWAS could identify target single nucleotide polymorphisms
associated with arthrofibrosis and better inform future candidate
gene studies. Determining the genetic variation and what is
differentially expressed in those with postoperative arthrofibrosis
could then be applied preoperatively through a screening tool to
determine patient risk. This knowledge would guide the health care
professionals in modifying the timing and aggressiveness of
noninvasive postoperative care before the rapid formation of scar
tissue, and ideally prevent the need for invasive procedures such as
arthroscopic/open arthrolysis or revision TKA in the future. Identification of those individuals at high risk for severe arthrofibrosis
could even become a contraindication to receiving a primary TKA.
Arthrofibrosis is a multi-faceted complication of TKA, and is
difficult to treat without an early, tailored, comprehensive rehabilitation program. Understanding the risk factors for its development, as well as the benefits and shortcomings of various
interventions are essential to best restore mobility and function
(Fig. 1). Future studies investigating early diagnosis and potential
preoperative screening for risk of arthrofibrosis will help target
those patients who will need additional attention to prevent prolonged, expensive healthcare costs.
[1] Sanders T, Kremers H, Bryan A, Kremers W, Stuart M, Krych A. Procedural
intervention for arthrofibrosis after ACL reconstruction: trends over two
decades. Knee Surg Sports Traumatol Arthrosc 2015:1e6. http://dx.doi.org/
[2] Parvataneni HK, Shah VP, Howard H, Cole N, Ranawat AS, Ranawat CS.
Controlling pain after total hip and knee arthroplasty using a multimodal
protocol with local periarticular injections: a prospective randomized study.
J Arthroplasty 2007;22:33e8. http://dx.doi.org/10.1016/j.arth.2007.03.034.
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
[3] Vezeridis PS, Goel DP, Shah AA, Sung S-Y, Warner JJP. Postarthroscopic
arthrofibrosis of the shoulder. Sports Med Arthrosc 2010;18:198e206.
[4] Donaldson JR, Tudor F, Gollish J. Revision surgery for the stiff total knee
arthroplasty. Bone Joint J 2016;98-B:622e7.
[5] Vun SH, Shields DW, Sen A, Shareef S, Sinha S, Campbell AC. A national
questionnaire survey on knee manipulation following total knee arthroplasty. J Orthop 2015;12:193e6. http://dx.doi.org/10.1016/j.jor.2015.05.016.
[6] Manrique J, Gomez MM, Parvizi J. Stiffness after total knee arthroplasty.
J Knee Surg 2015;28:119e26. http://dx.doi.org/10.1055/s-0034-1396079.
[7] Solanki RB, Bhise AR. Arthrofibrosis following total knee arthroplasty. Int J
Physiother Res 2014;2:762e5. http://dx.doi.org/10.16965/ijpr.2014.686.
[8] Millett PJ, Johnson B, Carlson J, Krishnan S, Steadman JR. Rehabilitation of the
arthrofibrotic knee. Am J Orthop (Belle Mead NJ) 2003;32:531e8.
[9] Magit D, Wolff A, Sutton K, Medvecky MJ. Arthrofibrosis of the knee. J Am
Acad Orthop Surg 2007;15:682e94.
[10] Kalson NS, Borthwick LA, Mann DA, Deehan DJ, Lewis P, Mann C, et al. International consensus on the definition and classification of fibrosis of the
knee joint. Bone Joint J 2016;98-B:1479e88.
[11] Bong MR, Di Cesare PE. Stiffness after total knee arthroplasty. J Am Acad
Orthop Surg 2004;12:164e71.
[12] Christensen CP, Crawford JJ, Olin MD, Vail TP. Revision of the stiff total knee
arthroplasty. J Arthroplasty 2002;17:409e15. http://dx.doi.org/10.1054/
[13] Yercan HS, Sugun TS, Bussiere C, Ait Si Selmi T, Davies A, Neyret P. Stiffness
after total knee arthroplasty: prevalence, management and outcomes. Knee
2006;13:111e7. http://dx.doi.org/10.1016/j.knee.2005.10.001.
[14] Kim J, Nelson CL, Lotke PA. Stiffness after total knee arthroplasty. Prevalence
of the complication and outcomes of revision. J Bone Joint Surg Am 2004;86A:1479e84. http://dx.doi.org/10.1016/j.arth.2004.02.008.
[15] Linklater J, Fessa C. Imaging findings in arthrofibrosis of the ankle and foot.
Semin Musculoskelet Radiol 2012;1:185e91. http://dx.doi.org/10.1055/s0032-1320059.
C, Velleman M, Suleman FE. MRI findings of cyclops lesions of the
[16] Minne
knee. SA Orthop J 2012;11:56e60.
[17] Devu S, M UM, Rajani S, Marda SS, Mvr S, Devu S. Cyclops - the giant in
postoperative knee. Innov J Med Heal Sci 2014;4:298e300.
[18] Talbot BS, Weinberg EP. MR imaging with metal-suppression sequences for
evaluation of total joint arthroplasty. Radiographics 2015;36:209e25. http://
[19] Sneag DB, Bogner EA. Magnetic resonance imaging evaluation of the painful
total knee arthroplasty. Semin Musculoskelet Radiol 2015;19:40e8.
[20] Scuderi GR. Techniques in revision hip and knee arthroplasty: expert consult.
Philadelphia, PA: Elsevier Saunders; 2014.
[21] Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee
arthroplasties failing today-has anything changed after 10 years?
J Arthroplasty 2014;29:1774e8. http://dx.doi.org/10.1016/j.arth.2013.07.024.
[22] Stephenson JJ, Quimbo RA, Gu T. Knee-attributable medical costs and risk of
re-surgery among patients utilizing non-surgical treatment options for knee
arthrofibrosis in a managed care population. Curr Med Res Opin 2010;26:
1109e18. http://dx.doi.org/10.1185/03007991003676479.
[23] Haller JM, Holt DC, Mcfadden ML, Higgins TF, Kubiak EN, Mcfadden ML.
Arthrofibrosis of the knee following a fracture of the tibial plateau. Bone Joint
J 2015;9797:109e14. http://dx.doi.org/10.1302/0301-620X.97B1.
[24] Campbell TM, Trudel G, Wong KK, Laneuville O. Genome wide gene
expression analysis of the posterior capsule in patients with osteoarthritis
and knee flexion contracture. J Rheumatol 2014;41:2232e9. http://
[25] Hold GL, Untiveros P, Saunders KA, El-Omar EM. Role of host genetics in
fibrosis. Fibrogenesis Tissue Repair 2009;2:6. http://dx.doi.org/10.1186/
[26] Su EP, Su SL. The stiff total knee replacement: evaluation and treatment. Semin
Arthroplasty 2013;24:142e8. http://dx.doi.org/10.1053/j.sart.2013.08.007.
[27] Gillespie MJ, Friedland J, Dehaven KE. Arthrofibrosis: etiology, classification,
histopathology, and treatment. Oper Tech Sports Med 1998;6:102e10.
[28] Remst DFG, Blaney Davidson EN, Vitters EL, Blom AB, Stoop R, Snabel JM,
et al. Osteoarthritis-related fibrosis is associated with both elevated
pyridinoline cross-link formation and lysyl hydroxylase 2b expression.
[29] Watson RS, Gouze E, Levings PP, Bush ML, Kay JD, Jorgensen MS, et al. Gene
delivery of TGF-beta1 induces arthrofibrosis and chondrometaplasia of
synovium in vivo. Lab Invest 2010;90:1615e27. http://dx.doi.org/10.1038/
[30] Freeman TA, Parvizi J, Della Valle CJ, Steinbeck MJ. Reactive oxygen and nitrogen species induce protein and DNA modifications driving arthrofibrosis
following total knee arthroplasty. Fibrogenesis Tissue Repair 2009;2:5.
[31] Faust I, Traut P, Nolting F, Petschallies J, Neumann E, Kunisch E, et al. Human
xylosyltransferasesemediators of arthrofibrosis? New pathomechanistic insights into arthrofibrotic remodeling after knee replacement therapy. Sci Rep
2015;5:12537. http://dx.doi.org/10.1038/srep12537.
[32] Pfitzner T, Geissler S, Duda G, Perka C, Matziolis G. Increased BMP expression
in arthrofibrosis after TKA. Knee Surg Sports Traumatol Arthrosc 2012;20:
1803e8. http://dx.doi.org/10.1007/s00167-011-1774-8.
€ tting C, Kuhn J, Kleesiek K. Human xylosyltransferases in health and dis[33] Go
ease. Cell Mol Life Sci 2007;64:1498e517. http://dx.doi.org/10.1007/s00018007-7069-z.
[34] Black DW. Treatment of knee arthrofibrosis and quadriceps insufficiency
after patellar tendon repair: a case report including use of the graston
technique. Int J Ther Massage Bodywork 2010;3:14e21. http://dx.doi.org/
[35] Rissman CM, Keeney BJ, Ercolano EM, Koenig KM. Predictors of facility
discharge, range of motion, and patient-reported physical function improvement after primary total knee arthroplasty: a prospective cohort analysis.
J Arthroplasty 2016;31:36e41. http://dx.doi.org/10.1016/j.arth.2015.09.002.
[36] Desai AS, Karmegam A, Dramis A, Board TN, Raut V. Manipulation for stiffness following total knee arthroplasty: when and how often to do it? Eur J
Orthop Surg Traumatol 2014;24:1291e5. http://dx.doi.org/10.1007/s00590013-1387-7.
[37] Schroer WC, Berend KR, Lombardi AV, Barnes CL, Bolognesi MP, Berend ME,
et al. Why are total knees failing today? Etiology of total knee revision in
2010 and 2011. J Arthroplasty 2013;28:116e9. http://dx.doi.org/10.1016/
[38] Schairer WW, Vail TP, Bozic KJ. What are the rates and causes of hospital
readmission after total knee arthroplasty? Clin Orthop Relat Res 2014;472:
181e7. http://dx.doi.org/10.1007/s11999-013-3030-7.
[39] Bonutti PM, Marulanda GA, McGrath MS, Mont MA, Zywiel MG. Static progressive stretch improves range of motion in arthrofibrosis following total
knee arthroplasty. Knee Surg Sports Traumatol Arthrosc 2010;18:194e9.
[40] Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and
revision hip and knee arthroplasty in the United States from 2005 to 2030.
J Bone Joint Surg Am 2007;89:780e5. http://dx.doi.org/10.2106/JBJS.F.00222.
[41] Seyler TM, Marker DR, Bhave A, Plate JF, Marulanda GA, Bonutti PM, et al.
Functional problems and arthrofibrosis following total knee arthroplasty.
J Bone Joint Surg Am 2007;89(Suppl 3):59e69. http://dx.doi.org/10.2106/
[42] Bhave A, Mont M, Tennis S, Nickey M, Starr R, Etienne G. Functional problems
and treatment solutions after total hip and knee joint arthroplasty. J Bone Joint
Surg Am 2005;87(Suppl 2):9e21. http://dx.doi.org/10.2106/JBJS.E.00628.
[43] Laubenthal KN, Smidt GL, Kettelkamp DB. A quantitative analysis of knee
motion during activities of daily living. Phys Ther 1972;52:34e43.
[44] Unterhauser FN, Bosch U, Zeichen J, Weiler A. Alpha-smooth muscle actin
containing contractile fibroblastic cells in human knee arthrofibrosis tissue.
Arch Orthop Trauma Surg 2004;124:5855e91. http://dx.doi.org/10.1007/
[45] Creighton RA, Bach BR. Arthrofibrosis: evaluation, prevention, and treatment. Tech Knee Surg 2005;4:163e72. http://dx.doi.org/10.1097/
[46] Perry J, Antonelli D, Ford W. Analysis of knee-joint forces during flexed-knee
stance. J Bone Joint Surg Am 1975;57:961e7.
[47] Pfefferle KJ, Shemory ST, Dilisio MF, Fening SD, Gradisar IM. Risk factors for
manipulation after total knee arthroplasty: a pooled electronic health record
database study. J Arthroplasty 2014;29:2036e8. http://dx.doi.org/10.1016/
[48] Namba RS, Inacio M. Early and late manipulation improve flexion after total
knee arthroplasty. J Arthroplasty 2007;22:58e61. http://dx.doi.org/10.1016/
[49] Bozic KJ, Kamath AF, Ong K, Lau E, Kurtz S, Chan V, et al. Comparative
epidemiology of revision arthroplasty: failed THA poses greater clinical and
economic burdens than failed TKA. Clin Orthop Relat Res 2015;473:2131e8.
[50] Burns AWR, Bourne RB, Chesworth BM, MacDonald SJ, Rorabeck CH. Cost
effectiveness of revision total knee arthroplasty. Clin Orthop Relat Res
2006;446:29e33. http://dx.doi.org/10.1097/01.blo.0000214420.14088.76.
[51] Vincent KR, Vincent HK, Lee LW, Alfano AP. Inpatient rehabilitation outcomes
in primary and revision total knee arthroplasty patients. Clin Orthop Relat Res
2006;446:201e7. http://dx.doi.org/10.1097/01.blo.0000214435.72398.0e.
[52] Maradit Kremers H, Visscher SL, Moriarty JP, Reinalda MS, Kremers WK,
Naessens JM, et al. Determinants of direct medical costs in primary and
revision total knee arthroplasty knee. Clin Orthop Relat Res 2013;471:
206e14. http://dx.doi.org/10.1007/s11999-012-2508-z.
[53] Graver R, Da Deppo L, Harris E, Feingass S. The total economic cost of primary
total joint replacement surgery in the United States. 2010 Annual Meeting of
the American Academy of Orthopaedic Surgeons, New Orleans. 2010.
[54] Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M. Arthrofibrosis in
acute anterior cruciate ligament reconstruction. The effect of timing of
reconstruction and rehabilitation. Am J Sports Med 1991;19:332e6. http://
[55] Ranawat CS, Ranawat AS, Mehta A. Total knee arthroplasty rehabilitation
protocol: what makes the difference? J Arthroplasty 2003;18:27e30. http://
[56] Westby MD, Brittain A, Backman CL. Expert consensus on best practices for
post-acute rehabilitation after total hip and knee arthroplasty: a Canada and
V.A. Cheuy et al. / The Journal of Arthroplasty 32 (2017) 2604e2611
United States Delphi study. Arthritis Care Res (Hoboken) 2014;66:411e23.
Kim GK, Mortazavi SMJ, Parvizi J, Purtill JJ. Revision for stiffness following
TKA: a predictable procedure? Knee 2012;19:332e4. http://dx.doi.org/
Werner BC, Carr JB, Wiggins JC, Gwathmey FW, Browne JA. Manipulation
under anesthesia after total knee arthroplasty is associated with an increased
incidence of subsequent revision surgery. J Arthroplasty 2015;30:72e5.
Livbjerg AE, Froekjaer S, Simonsen O, Rathleff MS. Pre-operative patient
education is associated with decreased risk of arthrofibrosis after total knee
arthroplasty: a case control study. J Arthroplasty 2013;28:1282e5. http://
Shoji H, Solomonow M, Yoshino S, D'Ambrosia R, Dabezies E. Factors
affecting postoperative flexion in total knee arthroplasty. Orthopedics
Mauerhan DR, Mokris JG, Ly A, Kiebzak GM. Relationship between length of
stay and manipulation rate after total knee arthroplasty. J Arthroplasty
1998;13:896e900. http://dx.doi.org/10.1016/S0883-5403(98)90196-6.
Millett PJ, Williams RJ, Wickiewicz TL. Open debridement and soft tissue
release as a salvage procedure for the severely arthrofibrotic knee. Am J
Sports Med 1999;27:552e61.
Kim Y-M, Joo YB. Prognostic factors of arthroscopic adhesiolysis for arthrofibrosis of the knee. Knee Surg Relat Res 2013;25:202. http://dx.doi.org/
Schiavone Panni A, Cerciello S, Vasso M, Tartarone M. Stiffness in total knee
arthroplasty. J Orthop Traumatol 2009;10:111e8. http://dx.doi.org/10.1007/
Pope RO, Corcoran S, McCaul K, Howie DW. Continuous passive motion after
primary total knee arthroplasty. Does it offer any benefits? J Bone Joint Surg
Br 1997;79:914e7.
LA, Davies DM, Jones CA, Cinats JG. Exercise combined with
continuous passive motion or slider board therapy compared with exercise
only: a randomized controlled trial of patients following total knee arthroplasty. Phys Ther 2001;81:1029e37.
Joshi RN, White PB, Murray-Weir M, Alexiades MM, Sculco TP, Ranawat AS.
Prospective randomized trial of the efficacy of continuous passive motion post
total knee arthroplasty: experience of the hospital for special surgery.
J Arthroplasty 2015;30:2364e9. http://dx.doi.org/10.1016/j.arth.2015.06.006.
Boese CK, Weis M, Phillips T, Lawton-Peters S, Gallo T, Centeno L. The efficacy
of continuous passive motion after total knee arthroplasty: a comparison of
three protocols. J Arthroplasty 2014;29:1158e62. http://dx.doi.org/10.1016/
Wright RW, Fetzer GB. Bracing after ACL reconstruction: a systematic review.
Clin Orthop Relat Res 2007;455:162e8. http://dx.doi.org/10.1097/
Azim K, Parsley B, Brinker M. Chronic patellar tendon rupture and arthrofibrosis after total knee arthroplasty. Curr Orthop Pract 2015;26:204e7.
McGrath MS, Mont MA, Siddiqui JA, Baker E, Bhave A. Evaluation of a custom
device for the treatment of flexion contractures after total knee arthroplasty.
Clin Orthop Relat Res 2009;467:1485e92. http://dx.doi.org/10.1007/s11999009-0804-z.
Stevens-Lapsley JE, Balter JE, Wolfe P, Eckhoff DG, Kohrt WM. Early neuromuscular electrical stimulation to improve quadriceps muscle strength after
total knee arthroplasty: a randomized controlled trial. Phys Ther 2012;92:
210e26. http://dx.doi.org/10.2522/ptj.20110124.
Bade MJ, Stevens-Lapsley JE. Restoration of physical function in patients
following total knee arthroplasty: an update on rehabilitation practices. Curr
Opin Rheumatol 2012;24:208e14. http://dx.doi.org/10.1097/BOR.0b0
Chughtai M, Mont MA, Cherian C, Cherian JJ, Elmallah RDK, Naziri Q, et al.
A novel, nonoperative treatment demonstrates success for stiff total knee
arthroplasty after failure of conventional therapy. J Knee Surg 2016;29:
188e93. http://dx.doi.org/10.1055/s-0035-1569482.
Bawa HS, Wera GD, Kraay MJ, Marcus RE, Goldberg VM. Predictors of range
of motion in patients undergoing manipulation after TKA knee. Clin Orthop
Relat Res 2013;471:258e63. http://dx.doi.org/10.1007/s11999-012-2591-1.
Cates HE, Schmidt JM. Closed manipulation after total knee arthroplasty:
outcome and affecting variables. Orthopedics 2009;32:398. http://dx.doi.org/
Enad JG. Arthroscopic lysis of adhesions for the stiff total knee arthroplasty.
Arthrosc Tech 2014;3:e611e4. http://dx.doi.org/10.1016/j.eats.2014.07.001.
Issa K, Kapadia BH, Kester M, Khanuja HS, Delanois RE, Mont MA. Clinical,
objective, and functional outcomes of manipulation under anesthesia to treat
knee stiffness following total knee arthroplasty. J Arthroplasty 2014;29:
548e52. http://dx.doi.org/10.1016/j.arth.2013.07.046.
Mohammed R, Syed S, Ahmed N. Manipulation under anaesthesia for stiffness following knee arthroplasty. Ann R Coll Surg Engl 2009;91:220e3.
Fitzsimmons SE, Vazquez EA, Bronson MJ. How to treat the stiff total knee
arthroplasty?: A systematic review. Clin Orthop Relat Res 2010;468:
1096e106. http://dx.doi.org/10.1007/s11999-010-1230-y.
€fer R, Lahrmann J, Kluba T. Stiffness after knee arthrotomy:
Ipach I, Scha
evaluation of prevalence and results after manipulation under anaesthesia.
Orthop Traumatol Surg Res 2011;97:292e6. http://dx.doi.org/10.1016/
Keating EM, Ritter MA, Harty LD, Haas G, Meding JB, Faris PM, et al.
Manipulation after total knee arthroplasty. J Bone Joint Surg Am 2007;89:
282e6. http://dx.doi.org/10.2106/JBJS.E.00205.
Scranton PE. Management of knee pain and stiffness after total knee
arthroplasty. J Arthroplasty 2001;16:428e35. http://dx.doi.org/10.1054/
Ipach I, Mittag F, Lahrmann J, Kunze B, Kluba T. Arthrofibrosis after TKA influence factors on the absolute flexion and gain in flexion after manipulation under anaesthesia. BMC Musculoskelet Disord 2011;12:184. http://
Pariente GM, Lombardi AV, Berend KR, Mallory TH, Adams JB. Manipulation
with prolonged epidural analgesia for treatment of TKA complicated by
arthrofibrosis. Surg Technol Int 2006;15:221e4.
Issa K, Banerjee S, Kester MA, Khanuja HS, Delanois RE, Mont MA. The effect
of timing of manipulation under anesthesia to improve range of motion and
functional outcomes following total knee arthroplasty. J Bone Joint Surg Am
2014;96:1349e57. http://dx.doi.org/10.2106/JBJS.M.00899.
Choi HR, Siliski JM, Malchau H, Kwon YM. Effect of repeated manipulation on
range of motion in patients with stiff total knee arthroplasty. Orthopedics
Tjoumakaris FP, Tucker BS, Post Z, Pepe MD, Orozco F, Ong AC. Arthroscopic
lysis of adhesions for the stiff total knee: results after failed manipulation.
Orthopedics 2014;37:e482e7.
Hegazy AM, Elsoufy MA. Arthroscopic arthrolysis for arthrofibrosis of the
knee after total knee replacement. HSS J 2011;7:130e3. http://dx.doi.org/
Jerosch J, Aldawoudy AM. Arthroscopic treatment of patients with moderate
arthrofibrosis after total knee replacement. Knee Surg Sports Traumatol
Arthrosc 2007;15:71e7. http://dx.doi.org/10.1007/s00167-006-0099-5.
Schwarzkopf R, William A, Deering RM, Fitz W. Arthroscopic lysis of adhesions for stiff total knee arthroplasty. Orthopedics 2013;36:e1544e8.
Hutchinson JRM, Parish EN, Cross MJ. Results of open arthrolysis for the
treatment of stiffness after total knee replacement. Bone Joint J 2005;87:
Mont MA, Seyler TM, Marulanda GA, Delanois RE, Bhave A. Surgical treatment and customized rehabilitation for stiff knee arthroplasties. Clin Orthop
Relat Res 2006;446:193e200.
Babis GC, Trousdale RT, Pagnano MW, Morrey BF. Poor outcomes of isolated
tibial insert exchange and arthrolysis for the management of stiffness
following total knee arthroplasty. J Bone Joint Surg Am 2001;83:1534e6.
Ries MD, Badalamente M. Arthrofibrosis after total knee arthroplasty. Clin
Orthop Relat Res 2000:177e83.
Pun SY, Ries MD. Effect of gender and preoperative diagnosis on results of
revision total knee arthroplasty. Clin Orthop Relat Res 2008;466:2701e5.
Greidanus NV, Peterson RC, Masri BA, Garbuz DS. Quality of life outcomes in
revision versus primary total knee arthroplasty. J Arthroplasty 2011;26:
615e20. http://dx.doi.org/10.1016/j.arth.2010.04.026.
Mortazavi SMJ, Schwartzenberger J, Austin MS, Purtill JJ, Parvizi J. Revision
total knee arthroplasty infection: incidence and predictors. Clin Orthop Relat
Res 2010;468:2052e9. http://dx.doi.org/10.1007/s11999-010-1308-6.
Saltzman BM, Dave A, Young A, Ahuja M, Amin SD, Bush-Joseph CA. Prolonged epidural infusion improves functional outcomes following knee
arthroscopy in patients with arthrofibrosis after total knee arthroplasty: a
retrospective evaluation. J Knee Surg 2016;29:40e6. http://dx.doi.org/
Formby PM, Donohue MA, Cannova CJ, Caulfield JP. Hydraulic distension of
the knee: a novel treatment for arthrofibrosis after total knee replacement
(case series). ANZ J Surg 2016;86:480e2. http://dx.doi.org/10.1111/
Smith EB, Shafi KA, Greis AC, Maltenfort MG, Chen AF. Decreased flexion
contracture after total knee arthroplasty using Botulinum toxin A: a randomized controlled trial. Knee Surg Sports Traumatol Arthrosc 2016;24:
3229e34. http://dx.doi.org/10.1007/s00167-016-4277-9.
Farid YR, Thakral R, Finn HA. Low-dose irradiation and constrained revision for
severe, idiopathic, arthrofibrosis following total knee arthroplasty. J Arthroplasty
2013;28:1314e20. http://dx.doi.org/10.1016/j.arth.2012.11.009.
Dixon D, Coates J, del Carpio Pons A, Horabin J, Walker A, Abdul N, et al.
A potential mode of action for Anakinra in patients with arthrofibrosis
following total knee arthroplasty. Sci Rep 2015;5:16466. http://dx.doi.org/
Efird W, Kellam P, Yeazell S, Weinhold P, Dahners LE. An evaluation of
prophylactic treatments to prevent post traumatic joint stiffness. J Orthop
Res 2014;32:1520e4. http://dx.doi.org/10.1002/jor.22700.
Parvizi J, Tarity T, Steinbeck MJ, Politi R, Joshi A, Purtill J, et al. Management
of stiffness following total knee arthroplasty. J Bone Joint Surg Am 2006;88A:175e81.
Skutek M, Elsner H-A, Slateva K, Mayr H-O, Weig T-G, van Griensven M,
et al. Screening for arthrofibrosis after anterior cruciate ligament reconstruction: analysis of association with human leukocyte antigen. Arthrosc J