Review Article
Current Concepts in the Management of Dupuytren
Disease of the Hand
Downloaded from http://journals.lww.com/jaaos by UR3kvIZBWwEWcmHlottFWtVUUrADVUrexsB+GuFNwzzvg+Cx8+OSsmzZNYWC/uNprZpDBm42zR/pYht+Nd7hcNXyDV/4/bHMlJr+WQLsq0k0He+SfQReejMaEVl97oYmLbknDi8SMMJbOJnpIS4B3LYhcn2GXS6lO1475z+ikah8HJ6FLOKTWQ== on 04/26/2022
Joseph A. Gil, MD
Matthew R. Akelman, MD
Andrew M. Hresko, MD
Edward Akelman, MD
From the Department of Orthopaedic Surgery
(Gil, Hresko, and E. Akelman), Alpert Medical
School of Brown University, Providence, RI,
and the Department of Orthopaedic Surgery
(M. R. Akelman), Wake Forest School of
Medicine, Winston-Salem, NC.
None of the following authors or any immediate
family member has received anything of value
from or has stock or stock options held in a
commercial company or institution related
directly or indirectly to the subject of this article:
Gil, M. R. Akelman, Hresko, and E. Akelman.
J Am Acad Orthop Surg 2021;29:462-469
DOI: 10.5435/JAAOS-D-20-00190
Copyright 2021 by the American Academy of
Orthopaedic Surgeons.
462
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ABSTRACT
Dupuytren disease is a fibroproliferative disorder of the palmar fascia of
the hand. Little agreement and remarkable variability exists in treatment
algorithms between surgeons. Because the cellular and molecular
etiology of Dupuytren has been elucidated, ongoing efforts have been
made to identify potential chemotherapeutic targets that could
modulate the phenotypic expression of the disease. Although these
efforts may dramatically alter the approach to treating this disease in the
future, these approaches are largely experimental at this point. Over the
past decade, the mainstay nonsurgical options have continued to be
percutaneous needle aponeurotomy and collagenase Clostridium
hystoliticum, and the most common surgical option is limited
fasciectomy.
D
upuytren disease (DD) is a fibroproliferative disorder of the palmar
fascia of the hand. Excessive deposition of collagen initially results in
formation of isolated nodules palpable beneath the skin and later
causes the formation of thick cords along the paths of normal fascial ligaments
and bands in the palm and digits. Contraction of cords over time can cause
fixed flexion contracture at the metacarpal phalangeal (MCP) and proximal
interphalangeal (PIP) joints that limits function of the affected digit.1 Related
fibroproliferative disorders in the dorsal knuckles (Garrod knuckle pads),
plantar fascia (Ledderhose disease), and/or penis (Peyronie disease) may also
occur as ectopic disease in a subset of DD patients with DD diathesis.
The prevalence of DD in Western countries is between 0.6% and 31.6%.2
This wide range is due in part to substantial regional variation. Prevalence is
generally highest in Scandinavian and Northern European populations, with
lower rates in Southern Europe and only sporadic cases reported in Asia and
Africa.3 DD most commonly presents in men older than 40 years and
typically involves the ulnar digits. The ratio of male-to-female patients in US
populations has been reported as 1.4:1 and 1.7:1, although estimates in
Europe show a stronger male dominance.4,5 Additional risk factors include
older age, Caucasian race, smoking, and alcohol abuse.3,5 Systemic con-
ditions including diabetes, liver disease, and epilepsy have been associated
with an increased risk of developing DD, whereas obesity has been associated
with decreased disease risk.5,6 Although there has long been debate about the
role of hand activity in the pathogenesis of DD, meta-analysis supports a
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relationship between DD and work exposure. Both
manual work and vibrational exposure were found to be
independently associated with an increased risk of DD.7
Pathophysiology
DD tissue is characterized by increased collagen and
extracellular matrix production. Unlike normal palmar
fascia, diseased areas have a predominance of type III
collagen, leading to an abnormally high ratio of type III to
type I collagen.8 The predominance of type III collagen
varies over the disease course. The type III/type I ratio is
highest during initial proliferation of abnormal tissue,
then becomes lower as cords mature and contract.8
The prototypical histologic findings of DD are pro-
liferation of fibroblasts and their differentiation into
myofibroblasts (Figure 1). The differentiated myofi-
broblast is considered the primary pathologic cell of
DD. Its fibroblast lineage allows it to produce collagen,
although similarities to smooth muscle, including pres-
ence of a-smooth muscle actin (a-SMA), contribute to
skin dimpling and contracture formation. The profi-
brotic cytokine transforming growth factor b (TGF-b) is
integral in the development of DD because it plays a role
in differentiation of fibroblasts to myofibroblasts,
stimulation of collagen production by myofibroblasts,
and contraction of myofibroblasts.9
Wang et al10 recently studied the effects of blocking TGF-
b expression in stem cells derived from DD tissue. They
found that both dexamethasone and knockdown of TGF-b
expression using RNA interference suppressed differentia-
tion of stem cells into myofibroblasts with similar effec-
tiveness. Furthermore, blocking TGF-b expression with
dexamethasone reduced expression of a-SMA and type III
collagen in a dose-dependent manner. Endogenous TGF-b
expression was higher in DD-derived stem cells than in bone
marrow stem cells, indicating overexpression of TGF-b as a
key pathologic factor in early Dupuytren.10 These findings
indicate a potential role for corticosteroids in DD treatment.
Nanchahal et al11 found that immunomodulation
may disrupt pathologic protein expression in DD tissue.
In a proof-of-concept phase 2a clinical trial, they found
that injection of adalimumab into palmar nodules re-
sulted in down regulation of the myofibroblast pheno-
type compared with placebo as evidenced by reduction
of a-SMA and type I procollagen proteins. These find-
ings may be an early step in identifying a chemothera-
peutic agent that can be safely used in early stages of DD
to thwart progression of disease tissue into cords and
associated flexion contractures.
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Joseph A. Gil, MD, et al
Review Article
Growing evidence exists that the renin-angiotensin-
aldosterone system may also play a role in the patho-
genesis of DD. A histologic study of DD surgical samples
by Stephen et al12 showed extensive expression of the
angiotensin II receptor type 2. Chisholm et al13 exposed
dermal fibroblasts to a selective inhibitor of the angio-
tensin II receptor type 2 receptor in vitro and found
reduced expression of many profibrotic genes including
TGF-b. In vivo exposure of human DD tissue in a
xenograft animal model to this same inhibitor resulted
in decreased myofibroblast differentiation. The role of
the renin-angiotensin-aldosterone system in DD war-
rants further study because it is a potential future target
for pharmacologic treatment with ACE inhibitors that
are currently widely used in cardiac and renal disease.
As the cellular and molecular etiology of DD becomes
better elucidated, further efforts will be made to identify
novel targets that could modulate the phenotypic
expression of the disease. Although these efforts—
including ACE inhibitors, immunomodulation, and
others—will likely dramatically alter the approach to
treating this disease in the future, these approaches are
largely experimental at this time.
Genetics
As is indicated by DD predilection for specific populations, a
strong genetic predisposition exists to the disease. Recent
genome-wide association studies (GWAS) have greatly
increased understanding of the genetics of DD and have
emphasized the important role of overactivation of the Wnt
pathways of extracellular signaling. A GWAS by Ng et al14
confirmed over 20 previously identified gene loci as being
associated with DD, most of which encode proteins that
participate in Wnt pathways. Their analysis highlighted a
mutation associated with the gene encoding SFRP4 as the
genetic variation most highly associated with the disease.
SFRP4 binds to WNT3A and acts as an antagonist of Wnt
signaling. Because WNT3A increases a-SMA expression in
myofibroblasts, decreased activity of SFRP4 may lead to
increased a-SMA activation that ultimately contributes to
contracture formation. Immunohistochemical analysis
showed reduced SFRP4 secretion from cells in fibrotic DD
tissue compared with those in nearby normal palmar fascia
in patients with the high-risk homozygous genotype.14
Riesmeijer et al used the mutations identified in pre-
vious GWAS to formulate a weighted genetic risk score to
predict for DD recurrence after fasciectomy. The score
was based on genotype at identified single-nucleotide
polymorphisms. They found the weighted genetic risk
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Management of Dupuytren Disease

Figure 1

A, Figure demonstrating the typical histological appearance of mature fibroblasts in collagenous tissue; collagen fibers are stained pink.
The fibroblast nuclei (F) are condensed and elongated in the direction of collagen fibers. The cytoplasm is relatively scanty and barely
visible. The cell is long and thin with fine cytoplasmic processes extending into the matrix. B, Figure demonstrating active fibroblasts
called myofibroblasts (M) in repair of damaged tissue with early fibrosis/scarring. The nuclei are large with prominent nucleoli and the
cytoplasm is extensive and basophilic. A few eosinophils (Eo) and lymphocytes (L) are present. (Reproduced with permission from
Supporting/Connective Tissues. In: Young B, O’Dowd G, Woodford P, eds: Wheater’s Functional Histology: A Textbook and Colour
Atlas—6th Ed. Philadelphia, PA, Elsevier, 2014, pp 65-81.)

score to be more accurate at predicting recurrence than sibling or parent with the disease, male sex, and Northern
were disease pattern and patient history factors.15 European decent.15

Diagnosis
Initially, DD of the hand presents with painless localized
palm skin thickening, pitting, or palmar nodules (Figure
2). The differential diagnoses include stenosing teno-
synovitis, skin callus, or soft-tissue tumor. The ring
finger is most often affected, followed by the small
finger, middle finger, index finger, and thumb. Gener-
ally, the disease begins in the palm and progresses to the
MCP and PIP joints, although in some cases, disease
may be isolated to the digits.4,5 As the disease pro-
gresses, cumulative deposition of collagen and the
contractility of the myofibroblasts result in cords and
progressive contractures at the MCP, PIP, and distal
interphalangeal (DIP) joints that lead to loss of function.
Fifty percent of patients with palmar nodules progress to
develop cords. Once the MCP contracture 30° or
greater, or any degree exists of PIP contracture, surgical
intervention is considered. A positive table top test is one
diagnostic tool that is often used to indicate patients for
an intervention to resolve the contracture.1
Patients with DD diathesis have a predisposition to
developing more severe contractures that progress more
rapidly and are at higher risk for recurrence (71% versus
23%). These patients are more likely to present with
ectopic sites of disease including the dorsal PIP skin
(Garrod nodes), penile fibromatoses (Peyronie disease),
and plantar fibromatosis (Ledderhose disease). Addi-
tional features of DD diathesis include age of onset
younger than 50, bilateral hands affected, male sex, a
Classification
The three sequential histologic stages described by
Luck16 in 1953 remain the preferred microscopic clas-
sification of DD. In the proliferative stage, fibroblasts
are abundant and histologic nodules with dense cellu-
larity of no purposeful arrangement develop. Nodules in
this stage seem highly vascular. The involutional stage is
characterized by alignment of fibroblasts along lines of
stress that pass through nodules and maturation of fi-
broblasts into myofibroblasts. In addition, the propor-
tion of collagen in affected tissues increases and
contraction begins. In the final residual stage, nodules
regress, cords become hypocellular and scar-like, and
contracture development becomes more pronounced.
Lam et al recognized that changes in the ratio of type
III to type I collagen in DD tissue correspond to Luck
stages. They advocated for augmenting the definitions of
Luck stages based on the percentage of collagen that is
type III: stage I (proliferative) . 35%, stage II (involu-
tional) 20% to 35%, and stage III (residual) , 20%.8
In clinical settings, the most valuable and widely used
classification is Tubiana staging (Table 1). This system
assesses each ray individually based on the total flexion
contracture at the MCP and PIP joints, with a modified
staging system for the thumb that incorporates the
degree of first web space contracture. Additional
notation localizes lesions to the palm or digit, highlights
extensive contracture at the PIP joint and hyperexten-
sion at the DIP joint, and accounts for postoperative

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Figure 2
Figure demonstrating diffuse nodular skin involvement of the
palm without digital contractures in Dupuytren disease.
Prominence of the dermal papillae exists over the nodules
over the metacarpal phalangeal joints (Courtesy of Edward
Akelman, MD, Providence, RI).
conditions that may influence the observed degree of
contracture.17
Nonsurgical Management
Given the challenging postoperative recovery and high
recurrence rates associated with DD fasciectomy, a per-
sistent motivation exists to optimize nonsurgical strate-
gies. Several pharmacologic and radiation therapy
interventions have been trialed in response to new in-
sights into the pathophysiology of the disease. However,
the most commonly used nonsurgical options have con-
tinued to be percutaneous needle aponeurotomy (PNA)
and collagenase Clostridium hystoliticum (CCH).
Percutaneous Needle Aponeurotomy
Given the appeal of less invasive treatment options for DD,
PNA has gained popularity.18 Needle aponeurotomy is
associated with quick healing time, rapid recovery, and
less time out of work compared with open fasciectomy.
The technique involves a systematic percutaneous release
of the cord from proximal to distal until the contracture is
resolved (Figure 3). This can be done in the office or
procedure suite under local anesthesia. The patient is
awake and provides immediate feedback regarding
inadvertent contact with nerves. The patient begins
therapy immediately after the procedure.18
Immediate success rates are comparable with surgical
release. Molenkamp et al19 reviewed their series of 451
patients after PNA and reported that PNA is a safe and
effective treatment strategy in DD with a 85% correction of
preop passive extension deficit. Of the 56 patients with a
complication (12%), 43 were skin tears, five superficial
infection, six transient parasthesias, one nerve laceration,
and one tendon rupture. Mansha et al20 reviewed their
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Joseph A. Gil, MD, et al
Review Article
experience with PNA in 68 patients with 73 fingers treated.
They reported that at the 15-month follow-up, only 5.8%
had recurrence. They reported no complications. Longer-
term recurrence rates after PNA have been reported to be
between 12% and 58% at 2 to 3 years.21,22
Collagenase Clostridium Histoliticum
CCH is a relatively novel, office-based option for man-
aging DD contractures.23 This agent lyses cord tissue
allowing for disruption of the cord with gentle manip-
ulation. In 2009, Hurst and colleagues conducted a
phase 3 clinical trial demonstrating the efficacy of CCH
in managing DD contractures. Of 308 patients with
contractures of 20° of more at the MCP or PIP joint,
64% of the patients had reduction of contracture to 0°
to 5° at 30 days after the last injection. In addition,
range motion improved from 44° to 80°. This trial
paved the way for mainstream approval of using CCH
for the Dupuytren in the United States.24
Over a 3-year span after the US Food and Drug
Administration approved the treatment of DD with CCH
injection in 2010, CCH use increased annually, PNA use
remained stable, whereas surgery for DD contracture
decreased. Ultimately, it was estimated that CCH and
PNA accounted for 40% of all treatment for DD in
2013.25 In the Veterans Affairs Hospital System, a
fivefold increase in CCH use occurred between 2010
and 2014 with a corresponding decrease in open fas-
ciectomy.26 In addition, with the introduction of CCH,
there was a nearly threefold increase in patients pre-
senting with DD suggesting the appeal of a nonsurgical
alternative.26
Simón-Pérez et al27 prospectively followed a cohort of
patients after CCH in an attempt to identify factors
influencing recurrence and progression of Dupuytren.
They reported a 23% recurrence or progression rate at the
4-year follow-up. They found that the rate of recurrence
and progression was higher in patients with Tubiana
grades III and IV, PIP joint contractures, and age younger
than 60 years. Patients with the lowest recurrence rate
had a single cord affecting the MCP, Tubiana grade II, and
were older than 60 years. Cook et al28 compared single
versus concurrent injections over 8 years and found that
there were no differences in clinical success rate or change
in contracture per joint and no difference in skin tear rates.
They did report that there was a higher incidence of
lymphadenopathy with concurrent injections compared
with those receiving single injections.
Given the high recurrence rate after CCH, Bear et al29
evaluated the safety and efficacy of using a second series
of CCH injections to treat recurrence of contracture after
465
Management of Dupuytren Disease
Table 1. Tubiana Stages of Dupuytren Contracture
Index, middle, ring, and small fingersa
0 No deformity
N Palmar or digital nodule without contracture
1 Total flexion deformityb 0°-45°
2 Total flexion deformity 45°-90°
3 Total flexion deformity 90°-135°
4 Total flexion deformity .135°
Thumb
0 First web space contracturec .45°, total
flexion deformity 0°-45°
1 First web space contracture 30°-45°, total
flexion deformity 45°-90°
2 First web space contracture 15°-30°, total
flexion deformity 90°-135°
3 First web space contracture 0°-15°, total
flexion deformity .135°
Additional notations
P Lesion in palm
D Lesion in digit
b
PIP contracture .70°
H Fixed DIP hyperextension
DIP = distal interphalangeal, PIP = proximal interphalangeal
a
Each ray assessed independently.
b
Sum of flexion contracture at the metacarpal phalangeal and PIP
joints.
c
Maximal angle between first and second metacarpals.
initial CCH treatment. In a series of 50 patients, they
found that 86% had resolution of contracture after up to
three CCH injections separated a month apart (69%
single injection, 24% two injections, and 8% three in-
jections). Although CCH remains an attractive option for
patients who prefer to avoid PNA or open fasciectomy,
cost consideration may continue to limit its applicability
in DD. Leafblad et al30 reported that the cumulative cost
per digit after PNA, CCH, and open fasciectomy at 5
years was $1,540, $5,952, and $5,507, respectively.
Several trials have directly compared outcomes after
CCH and PNA. Stromberg and colleagues conducted a
randomized trial comparing clinical and patient-
reported outcomes between patients who had PNA ver-
sus CCH.22 At the 2-year follow-up, no notable differ-
ence existed in recurrence of contracture at the MP, with
13% rate of recurrence with CCH versus 12% with
PNA. No notable differences exist in the reduction of
PIP contracture, range of motion, or patient-reported
outcomes. Other authors have found PNA to be a safer
and more effective comparted with CCH. Skov and
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colleagues23 prospectively compared the outcomes of
CCH and PNA in a randomized trial. They found that
clinical improvement was maintained in only 7% of
patients after CCH and 29% of patients after PNA at 2
years post-treatment. They compared the transient
complication profile within 30 days after procedure,
which included wound complication, skin rupture, pain,
nerve irritation, hyperesthesia, edema, itch, rash,
lymphadenopathy, nausea, and arthralgias, and
reported that 93% of patients had a complication after
CCH compared with only 24% after PNA. Sanjuan-
Cerveró et al31 conducted a meta-analysis to assess the
safety and efficacy of CCH compared with PNA and
fasciectomy. They found that CCH had a 3.24 increased
odds of adverse effects compared with those treated
with fasciectomy or PNA. They found no difference
between the three options in joint motion in the short
and medium term. Although long-term complications
associated with CCH remain rare despite its widespread
use, some of these reported complications include ten-
don rupture, complex regional pain syndrome, extensive
skin loss, and ischemic finger.32
Cost analysis investigations comparing the cost
effectiveness PNA, fasciectomy, and CCH are inconclu-
sive.33 Baltzer and Binhammer34 did an analysis com-
paring the cost effectiveness of fasciectomy, PNA, and
CCH. They stated that PNA was the most cost-effective
option for managing contracture in a single finger. The
cost effectiveness improved when PNA was used to treat
recurrence. They reported that fasciotomy is not a cost
effective option. Yoon et al35 compared the cost effec-
tiveness of these treatment options in patients with
recurrent DD. They found that limited fasciectomy is a
cost-effective option for managing high severity (.45°)
MCP joint contractures. By contrast, they found that
PNA is the most cost-effective option for managing
recurrent low severity (,45°) MCP and PIP con-
tractures. In addition, they reported that CCH is not a
cost-effective option in any recurrent case. Although
these cost effectiveness analyses provide some insight
that could help cost-effective strategies for managing
Dupuytren contractures, the generalizability is limited
because the results depend on the healthcare system
examined and the cost modeling methodology.
Experimental Options
Clinical trials have demonstrated a potential role for
corticosteroids in the treatment of DD. Yin and colleagues
injected 37 patients (49 affected hands) with DD nodules
with triamcinolone. They reported that at 5 years, only
two patients had reactivation of the treated nodules, which
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 Joseph A. Gil, MD, et al

Review Article
Figure 3

Percutaneous needle aponeurotomy technique maneuvers. The targeted area is anethesthesized (A). The bevel of a needle is used to
clear (B) a path over the cord. The needle is then advanced to perforate (C) the cord and a side-to-side sweeping maneuver and (D) is
done until the cord is released from superficial to deep.

is notably lower than the reported rate of progression from
nodules to more advanced disease.36 Likewise, McMillan
and Binhammer37 found that adding a corticosteroid
injection improved the efficacy of PNA. Their random-
ized trial comparing PNA plus triamcinolone injection
versus PNA alone found that PNA plus triamcinolone
injection had a notably greater degree of correction of
flexion deformity at 6 months.
Radiation therapy has been advocated as treatment
strategy that can inhibit fibroblast proliferation and
promote an anti-inflammatory effect by suppressing the
immune response and activating the nitric oxide syn-
thetase pathway. A systematic review of radiation ther-
apy treatment for DD reported disease regression from
0% to 56% with progression ranging from 2% to 86%.
The literature was found to be of low quality and too
scarce to recommend this as an effective modality for
treating Dupuytren.38
Surgical Management
Open Fasciectomy
Fasciectomy options include limited fasciectomy, radi-
cal fasciectomy, and dermatofasciectomy.39 Radical
fasciectomy entails concomitant excision of adjacent
pathologic and normal palmar aponeurosis. The pur-
pose of removing adjacent healthy palmar aponeurosis
is to reduce the chance for recurrence by preemptively
removing tissue that could potentially progress into
diseased tissue.39 Dermatofasciectomy involves the
additional removal of the overlying skin and covering
the wound with a full thickness skin graft.39 Given that
these more invasive surgeries do not notably improve
recurrence rate compared with limited fasciectomy and
have higher complication rates, currently, the most
commonly used surgical intervention for DD is limited
fasciectomy.39 Limited fasciectomy involves removal of
the entire diseased portion of the aponeurosis from
proximal to distal while paying close attention to the
neurovascular bundles because they are displaced out
of their normal position.1 Complications of limited
fasciectomy include neurovascular injury, transient
neurapraxia or ischemia, finger stiffness, flexor tendon
injury, delayed wound healing and necrosis, hema-
toma, and infection.40
Several studies have found reduced recurrence after
limited fasciectomy compared with nonsurgical treat-
ments. Leafblad et al30 recently reported that at 2 years,

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Management of Dupuytren Disease
reintervention rates were tenfold higher for CCH and
sixfold higher for PNA compared with open fas-
ciectomy. At 5 years, approximately 50% of CCH and
PNA required a reintervention, whereas only 4%
required a reintervention after open fascectomy. Soreide
et al conducted an extensive systematic review of the
treatment of DD reporting that although PNA
provides a higher patient satisfaction and is associated
with fewer complications than both CCH and limited
fasciectomy, the recurrence is lowest after limited fas-
ciectomy.41 Overall, they concluded that limited evi-
dence exists to guide the choice of management of
patients with DD.
Role of Postoperative Therapy and Orthosis
Although supervised therapy remains an essential
component of the treatment algorithm for DD, the role
of extension orthoses postoperatively has become less
clear. Collis et al42 conducted a randomized trial
comparing supervised hand therapy plus night exten-
sion orthosis or hand therapy alone. They found no
differences for total active extension 3 months after
surgical release suggesting that application of exten-
sion orthoses should be reserved for cases in which
rapid onset exists of extension loss after surgery.
Similarly, Jerosch-Herold et al43 randomized 154 pa-
tients to supervised hand therapy plus night extension
orthosis or hand therapy alone. At the 12-month
follow-up, they found no difference in total extension
deficit, DASH, or patient satisfaction. They concluded
that routine prescription of nighttime extension splints
is not indicated, unless the patients present with a
recurrence of contracture.
Summary
DD is a fibroproliferative disorder of the palmar fascia of
the hand. Little agreement and remarkable variability
exist in treatment algorithms among hand surgeons. In
addition, currently limited evidence exists to guide the
management of patients with DD. Future research
examining the source of these discrepancies in the man-
agement of DD may help in devising an evidence-based
algorithm for this problem. As the cellular and molecular
etiology of DD has been elucidated, ongoing efforts have
been made to identify potential chemotherapeutic targets
that could modulate the phenotypic expression of the
disease. Over the past decade, the mainstay nonsurgical
options continue to be PNA and CCH and the most
common surgical option is limited fasciectomy.
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References
References printed in bold type are those published
within the past 5 years.
1. Black EM, Blazar PE: Dupuytren disease: An evolving understanding of
an age-old disease. J Am Acad Orthop Surg 2011;19:746-757.
2. Lanting R, Broekstra DC, Werker PMN, van den Heuvel ER: A systematic
review and meta-analysis on the prevalence of Dupuytren disease in the
general population of Western countries. Plast Reconstr Surg 2014;133:
593-603.
3. Hindocha S, McGrouther DA, Bayat A: Epidemiological evaluation of
Dupuytren’s disease incidence and prevalence rates in relation to etiology.
HAND 2009;4:256-269.
4. Anthony SG, Lozano-Calderon SA, Simmons BP, Jupiter JB: Gender
ratio of Dupuytren’s disease in the modern U.S. Population. HAND. 2008;
3:87-90.
5. Hacquebord JH, Chiu VY, Harness NG: The risk of Dupuytren
surgery in obese individuals. J Hand Surg Am 2017;42:149-155.
6. Broekstra DC, Groen H, Molenkamp S, Werker PMN, van den
Heuvel ER: A systematic review and meta-analysis on the strength
and consistency of the associations between Dupuytren disease and
diabetes mellitus, liver disease, and epilepsy. Plast Reconstr Surg
2018;141:367e-379e.
7. Descatha A, Jauffret P, Chastang J-F, Roquelaure Y, Leclerc A: Should
we consider Dupuytren’s contracture as work-related? A review and meta-
analysis of an old debate. BMC Musculoskelet Disord 2011;12:96.
8. Lam WL, Rawlins JM, Karoo ROS, Naylor I, Sharpe DT: Re-visiting
Luck’s classification: A histological analysis of Dupuytren’s disease. J
Hand Surg Eur Vol 2010;35:312-317.
9. Zhang AY, Kargel JS: The basic science of Dupuytren disease.
Hand Clin 2018;34:301-305.
10. Wang JP, Yu HHM, Chiang ER, Wang JY, Chou PH, Hung SC:
Corticosteroid inhibits differentiation of palmar fibromatosis-derived
stem cells (FSCs) through downregulation of transforming growth
factor-b1 (TGF-b1). PLoS One 2018;13:e0198326.
11. Nanchahal J, Ball C, Davidson D, et al: Anti-tumour necrosis factor
therapy for Dupuytren’s disease: A randomised dose response proof
of concept phase 2a clinical trial. EBioMedicine 2018;33:282-288.
12. Stephen C, Touil L, Vaiude P, Singh J, McKirdy S: Angiotensin
receptors in Dupuytren’s disease: A target for pharmacological
treatment? J Plast Surg Hand Surg 2018;52:37-39.
13. Chisholm J, Gareau AJ, Byun S, et al: Effect of compound 21, a
selective angiotensin II type 2 receptor agonist, in a murine xenograft
model of Dupuytren disease. Plast Reconstr Surg 2017;140:
686e-696e.
14. Ng M, Thakkar D, Southam L, et al: A genome-wide association
study of Dupuytren disease reveals 17 additional variants implicated
in fibrosis. Am J Hum Genet 2017;101:417-427.
15. Riesmeijer SA, Manley OWG, Ng M, et al: A weighted genetic risk
score predicts surgical recurrence independent of high-risk clinical
features in Dupuytren’s disease. Plast Reconstr Surg 2019;143:
512-518.
16. Luck JV: Dupuytren’s contracture; a new concept of the pathogenesis
correlated with surgical management. J Bone Joint Surg Am 1959;41:
635-664.
17. Tubiana R: Dupuytren’s disease of the radial side of the hand. Hand
Clin 1999;15:149-159.
18. Eaton C: Percutaneous fasciotomy for Dupuytren’s contracture. J
Hand Surg Am 2011;36:910-915.
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© American Academy of Orthopaedic Surgeons

19. Molenkamp S, Schouten TAM, Broekstra DC, Werker PMN,
Moolenburgh JD: Early postoperative results of percutaneous needle
fasciotomy in 451 patients with Dupuytren disease. Plast Reconstr
Surg 2017;139:1415-1421.
20. Mansha M, Flynn D, Stothard J: Safety and effectiveness of
percutaneous needle fasciotomy for Dupuytren’s disease in the palm.
J Hand Microsurg 2017;09:115-119.
21. Foucher G, Medina J, Navarro R: Percutaneous needle aponeurotomy:
Complications and results. J Hand Surg Am 2003;28 B:427-431.
22. Strömberg J, Ibsen Sörensen A, Fridén J: Percutaneous needle
fasciotomy versus collagenase treatment for Dupuytren contracture.
J Bone Joint Surg Am 2018;100:1079-1086.
23. Skov ST, Bisgaard T, Søndergaard P, Lange J: Injectable
collagenase versus percutaneous needle fasciotomy for Dupuytren
contracture in proximal interphalangeal joints: A randomized
controlled trial. J Hand Surg Am 2017;42:321-328.
24. Hurst LC, Badalamente MA, Hentz VR, et al: Injectable collagenase
clostridium histolyticum for Dupuytren’s contracture. N Engl J Med 2009;
361:968-979.
25. Zhao JZ, Hadley S, Floyd E, Earp BE, Blazar PE: The impact of
collagenase clostridium histolyticum introduction on Dupuytren treatment
patterns in the United States. J Hand Surg Am 2016;41:963-968.
26. Duquette S, Kuster R, Evans T, et al: Treatment of Dupuytren
contracture with injectable collagenase within the veterans affairs
system. JAMA Surg 2017;152:204.
27. Simón-Pérez C, Alı́a-Ortega J, Garcı́a-Medrano B, et al: Factors
influencing recurrence and progression of Dupuytren’s disease
treated by collagenase clostridium histolitycum. Int Orthop 2018;42:
859-866.
28. Cook J, Waughtel J, Andreoni AR, Sakharpe A, Friedman DW:
Collagenase clostridium histolyticum for Dupuytren’s contracture:
Comparing single and concurrent injections. Plast Reconstr Surg
2019;143:782e-787e.
29. Bear BJ, Peimer CA, Kaplan FTD, Kaufman GJ, Tursi JP, Smith T:
Treatment of recurrent Dupuytren contracture in joints previously
effectively treated with collagenase clostridium histolyticum. J Hand
Surg Am 2017;42:391.
30. Leafblad ND, Wagner E, Wanderman NR, et al: Outcomes and
direct costs of needle aponeurotomy, collagenase injection, and
fasciectomy in the treatment of Dupuytren contracture. J Hand Surg
Am 2019;44:919-927.
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Joseph A. Gil, MD, et al
Review Article
31. Sanjuan-Cerveró R, Carrera-Hueso FJ, Vazquez-Ferreiro P,
Ramon-Barrios MA: Efficacy and adverse effects of collagenase use
in the treatment of Dupuytren’s disease. Bone Joint J 2018;100:
73-80.
32. Wozniczka J, Canepa C, Mirarchi A, Solomon JS: Complications
following collagenase treatment for Dupuytren contracture. Hand (N
Y) 2017;12:148-151.
33. Dritsaki M, Rivero-Arias O, Gray A, Ball C, Nanchahal J: What do
we know about managing Dupuytren’s disease cost-effectively? BMC
Musculoskelet Disord 2018;19:34.
34. Baltzer H, Binhammer PA: Cost-effectiveness in the management of
Dupuytren’s contracture: A Canadian cost-utility analysis of current and
future management strategies. Bone Joint J 2013;95:1094-1100.
35. Yoon AP, Kane RL, Hutton DW, Chung KC: Cost-effectiveness of
recurrent Dupuytren contracture treatment. JAMA Netw Open 2020;3:
e2019861.
36. Reilly RM, Stern PJ, Goldfarb CA: A retrospective review of the
management of Dupuytren’s nodules. J Hand Surg Am 2005;30:
1014-1018.
37. McMillan C, Binhammer P: Steroid injection and needle aponeurotomy
for Dupuytren contracture: A randomized, controlled study. J Hand Surg
Am 2012;37:1307-1312.
38. Kadhum M, Smock E, Khan A, Fleming A: Radiotherapy in
Dupuytren’s disease: A systematic review of the evidence. J Hand
Surg Eur Vol 2017;42:689-692.
39. Hovius SER, Zhou C: Advances in minimally invasive treatment of
Dupuytren disease. Hand Clin 2018;34:417-426.
40. Eberlin KR, Mudgal CS: Complications of treatment for Dupuytren
disease. Hand Clin 2018;34:387-394.
41. Soreide E, Murad MH, Denbeigh JM, et al: Treatment of
Dupuytren’s contracture. Bone Joint J 2018;100:1138-1145.
42. Collis J, Collocott S, Hing W, Kelly E: The effect of night extension
orthoses following surgical release of Dupuytren contracture: A
single-center, randomized, controlled trial. J Hand Surg Am 2013;
38.
43. Jerosch-Herold C, Shepstone L, Chojnowski AJ, Larson D,
Barrett E, Vaughan SP: Night-time splinting after fasciectomy or
dermo-fasciectomy for Dupuytren’s contracture: A pragmatic, multi-
centre, randomised controlled trial. BMC Musculoskelet Disord 2011;
12:136.
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