Dupuytren Contracture 

  • Author: Stephanie Danielle Mathew, DO; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Dec 8, 2011
 

Background

Dupuytren contracture results from contracture of the palmar fascia within the hand, possibly resulting in a fixed flexion deformity of the metacarpophalangeal (MCP) joints and the proximal interphalangeal (PIP) joints. This condition usually affects the fourth and fifth digits (the ring and small fingers). (See the images below.)

Arrow denotes the cord often present in Dupuytren Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present. This photo shows a patient with an inability to exThis photo shows a patient with an inability to extend the fourth and fifth digits. The differential diagnosis includes Dupuytren contracture, which is a flexion contracture most commonly involving digits 4 and/or 5.

The condition is a fibrosing disorder that results in slowly progressive thickening and shortening of the palmar fascia, leading to the debilitating digital contractures. Dupuytren contracture belongs to the group of fibromatoses that include plantar fibromatosis (Ledderhose disease), penile fibromatosis (Peyronie disease), and fibromatosis of the dorsal proximal interphalangeal (PIP) joints (Garrod nodes or knuckle pads).[1] Although many cases appear to be idiopathic and without coexisting conditions, a variety of associated diseases have been reported. (See Etiology.)

Dupuytren contracture is most commonly observed in persons of Northern European descent and affects 4-6% of whites worldwide.[2] Many individuals have bilateral disease (45%); in unilateral cases, the right side is more often affected.[3] The ring finger is most commonly involved, followed by the fifth digit and then the middle finger. The index finger and the thumb are typically spared. (See Epidemiology and Presentation.)

Although the cause of Dupuytren disease is unknown, a family history is often present. Males are 3 times as likely to develop disease and are more likely to have higher disease severity.[4, 5] Male predominance may be related to expression of androgen receptors in Dupuytren fascia. (See Etiology and Epidemiology.)[6]

Additional risk factors include manual labor with vibration exposure, prior hand trauma, alcoholism, smoking, diabetes mellitus, hyperlipidemia, Peyronie disease, and complex regional pain syndrome.[7] Rheumatoid arthritis seems to protect against the development of Dupuytren disease. (See Etiology.)

Therapies include conservative medical and surgical modalities. Although the condition is not fatal, significant morbidity can occur if patients remain untreated. (See Prognosis, Treatment, and Medication.)

Stages of Dupuytren disease

Dupuytren disease occurs in the following 3 stages:

  • Proliferative phase - Local fascial fibroplasia and development of a nodule, in which myofibroblasts proliferate, occur (see the image below), with palmar skin blanching on finger extension; in early disease, some patients may report tenderness and discomfort associated with the nodules
  • Involutional phase - Contracture develops, with associated nodular thickening of the palmar fascia; myofibroblasts are predominant during this phase and align themselves along tension lines within the nodule
  • Residual phase - The nodular tissue disappears, leaving acellular tissue and thick bands of collagen; the ratio of type III collagen to type I collagen increases, which is the reverse of the normal pattern in the palmar fascia[8]

Grades of severity

The grading system for Dupuytren disease severity is as follows (see the images below)[9] :

  • Grade 1 - Thickened nodule and band in the palmar aponeurosis; may have associated skin abnormalities
  • Grade 2 - Development of pretendinous and digital cords with limitation of finger extension
  • Grade 3 - Presence of flexion contractureArrow denotes the cord often present in Dupuytren Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present. Arrow denotes the typical cords of Dupuytren contrArrow denotes the typical cords of Dupuytren contracture. These cords are usually painless. Note the metacarpophalangeal joint contracture. This photo demonstrates the presence of a nodule aThis photo demonstrates the presence of a nodule as well as skin blanching with extension of the affected digits. Three clinical grades of Dupuytren disease. Three clinical grades of Dupuytren disease.
Next

Patient education

Patients must have realistic expectations that surgery can relieve some disability but that it cannot cure Dupuytren disease. Discuss all potential complications of the procedure, including complex regional pain syndrome. In addition, explain that intense rehabilitation with an occupational therapist is necessary postoperatively for an optimal outcome.

Previous
Next

Anatomy

In the normal hand, the palmar aponeurosis runs longitudinally from the wrist, crosses over the superficial transverse palmar ligament, and splits into pretendinous bands to each digit. (See the image below.)

Normal anatomy of digital ligaments. Normal anatomy of digital ligaments.

In the distal palm and fingers, the following superficial fascial components are typically involved in Dupuytren disease:

  • Pretendinous band
  • Spiral band
  • Lateral digital sheet
  • Grayson ligament
  • Natatory ligament

The extension of a palmar fascial band to the index finger frequently ends in the skin on the radial side of the hand. The band to the thumb is inconsistent. The insertion of the pretendinous bands to the skin distal to the distal palmar crease is by means of a bifurcate insertion into the side of the finger dorsal to the neurovascular bundle. A natatory ligament runs transversely across each web space distal to the MCP joint, giving fibers that blend with each lateral digital sheet and to the superficial aspect of the flexor tendon sheath.

The superficial transverse ligament lies deep to the pretendinous bands, proximal to the MCP joints and the natatory ligament. In the fingers, the Cleland ligament, Landsmeer ligaments (oblique retinacular ligaments), and other deeper fascial layers are usually spared in Dupuytren disease.[10, 11]

According to Luck, normal longitudinal components of the superficial palmar aponeurosis are referred to as bands; diseased tissue is referred to as cords.[12] Cardinal features of Dupuytren disease are the nodule, the cord, and the digital flexion contracture. The bands and cords are characterized as follows (see the images below):

  • The pretendinous cord is formed from pretendinous bands
  • The spiral cord is made up of the pretendinous band, spiral band, lateral digital sheet, and Grayson ligament; this often occurs in the ring and small fingers and winds around the neurovascular bundle
  • The lateral cord is formed from the lateral digital band and is rarely observed, except on the ulnar aspect of the small finger
  • The central cord has no defined fascial precursor; it is the most common cause of proximal PIP contracture
  • The natatory cord contributes to web space contractures and passes superficial to neurovascular bundlesVisible cord characteristic of Dupuytren disease wVisible cord characteristic of Dupuytren disease with planned markings for surgical release. Dissection of a diseased cord. Dissection of a diseased cord. Parts of the palmar and digital fascia that becomeParts of the palmar and digital fascia that become diseased in Dupuytren disease (left). Diseased fascia that is associated with the pretendinous cord (center). Diseased fascia that is not associated with the pretendinous cord (right). Normal parts of the fascia that produce the spiralNormal parts of the fascia that produce the spiral cord (left). The spiral cord demonstrating medial displacement of the neurovascular bundle in Dupuytren disease (right).

Spiral and lateral cords displace the neurovascular bundle toward the digital midline, while a central cord may encase the neurovascular bundle and usually is directed toward one side of the finger. The central, lateral, and spiral cords terminate on the tendon sheath of the adjacent middle phalanx. One or more may be found in any individual patient, but they seldom occur on both sides of the same finger. McFarlane describes displacement of the neurovascular bundle superficially and toward the digital midline by a spiral cord, which makes it more vulnerable to injury during surgery.[13] With increasing degrees of flexion contracture, nerve compression and vascular embarrassment may also occur.

In the thumb, 3 fascial structures may be involved: the natatory ligament, the pretendinous band, and the superficial transverse ligament of the palm. Knuckle pads may develop with fibrosis in the dorsal subcutaneous wrinkle ligaments (of McGrouther) dorsally at the PIP joints. These often indicate progressive disease.

Previous
Next

Etiology

The palmar fascia within the hand may develop nodular, hypertrophic degeneration of uncertain etiology. The dense nodular fascia may become adherent to the overlying skin as the hypertrophic degeneration progresses, sometimes extending distally into the involved digit. This anatomic change may result in contracture of the involved fascia, causing fixed flexion of the MCP joint and sometimes of the PIP joint as well. The most commonly affected area is the ulnar aspect of the hand (digits 4 and 5).

Myofibroblasts are the primary cell type in Dupuytren disease.[14] Vi et al hypothesized that when the protein periostin is secreted by disease cord myofibroblasts into the extracellular matrix, it causes the disease to progress by promoting the transition of palmar fascia fibroblasts into a myofibroblast phenotype.[15]

Investigators have proposed several hypotheses for the pathogenesis of Dupuytren disease. Al-Qattan hypothesizes that an individual with a genetic predisposition to develop Dupuytren disease experiences a second inciting event (ie, smoking, diabetes, trauma, alcoholism), which results in microvascular ischemia.[6]

The localized ischemia causes 2 events to take place in the palmar fascia: (1) the conversion of adenosine triphosphate to hypoxanthine and (2) the conversion of xanthine dehydrogenase to xanthine oxidase.

Xanthine oxidase acts as a catalyst for the oxidation of hypoxanthine to xanthine and uric acid; this conversion results in the production of free radicals. Free radicals result in fibroblast proliferation and the production of numerous cytokines. Interleukin 1 (IL-1) is the most abundant cytokine in Dupuytren disease and, via its receptor, upregulates the production of transforming growth factor beta (TGF-beta), fibroblast growth factor, epidermal derived growth factor, and platelet-derived growth factor.[16, 17]

This milieu of cytokines and growth factors results in (1) the proliferation of fibroblasts and their differentiation into myofibroblasts (levels of nerve growth factor, which induces fibroblast transformation to myofibroblasts, were also found to be increased in persons with Dupuytren tissue, especially during stages II-III.); (2) the splicing of fibronectin, affecting collagen binding; and (3) platelet activation to produce lysophosphatidic acid (LPA).

LPA is a signaling molecule for cell proliferation and myofibroblast contraction. After binding to its receptor on myofibroblasts, LPA leads to a decrease in cyclic adenosine monophosphate and an increase in intracellular calcium levels. These 2 events mediate smooth muscle contraction of the myofibrils within the myofibroblast.

Normal palmar fascia is primarily composed of type I collagen; Dupuytren disease is associated with an increase in type III collagen. Excess type III collagen production occurs from an increased density of fibroblasts secondary to increased stimulation and diminished apoptosis, as well as an imbalance between the collagenases and their endogenous inhibitors. Dupuytren fascia exhibits an increased ratio of tissue inhibitors of metalloproteinases (TIMP) to matrix metalloproteinases (MMP).[18, 19, 20]

The myofibroblasts are indirectly connected to collagen, and the contractile force is transmitted from the intracellular actin microfilaments to the collagen bundles. Ultimately, the end result is contracture from excess deposition of type III collagen and the formation of cross links between myofibroblasts and collagen.

Synthesis theory

Hueston advanced the extrinsic theory, suggesting that Dupuytren’s nodules arise de novo and progress to cords.[21] Vasomotor disturbance and neurovascular mediation by the skin were suggested by Hueston as possible contributors to the development of Dupuytren disease. In contrast, McFarlane postulated the intrinsic theory, that the cords of more advanced Dupuytren disease are derived from normal fascia.[13] A combination of these ideas forms the synthesis theory, which states that the nodules and pretendinous cords represent different forms of the disease.[10]

Genetic factors

The cause of Dupuytren contracture remains unknown. Genetic factors are thought to play a role in Dupuytren disease; however, currently no link has been established.[22, 23] Still, one study derived a sibling recurrence-risk ratio of 2.9 (range, 2.6-3.3). In addition, those patients with a family history of Dupuytren contracture tend to have a younger age of onset and more severe disease.[24] Furthermore, deoxyribonucleic acid (DNA) microarray analysis has demonstrated that the gene MafB, involved in tissue development and cellular differentiation, is upregulated in Dupuytren cord tissue.[25, 26]

Al-Qattan described a maternally transmitted inheritance within the mitochondrial genome in 90% of patients. The defective mitochondria generate high levels of free radicals and defective apoptosis and are therefore directly related to disease pathogenesis.[6]

Other studies suggest an autosomal dominant pattern of inheritance with variable penetrance.[9] An analysis of an autosomal dominant pattern of inheritance, with incomplete penetrance, in 5 generations of a Swedish family, mapped the affected gene (not yet identified) to 16q.[27] Another study of 20 patients with apparent maternal inheritance identified a polymorphism in the mitochondrial 16s rRNA region present in 90% of their DNA.[28] Still, others believe that Dupuytren contracture has a multifactorial inheritance, similar to diabetes or hypertension.

Some authors suggest an error in growth and regulation of the fibroblast resulting from chromosomal abnormalities similar to those cells undergoing neoplastic changes. Trisomy 7 and 8 have been identified in the fibroblasts excised from some patients.[29] Nodules may display features of a benign neoplasm.[30]

Additional risk factors

There is conflicting literature regarding whether certain conditions represent independent risk factors for the development of Dupuytren contracture. A large, retrospective study by Loos and colleagues on 2919 hands on which surgery had been performed revealed no statistically significant evidence that the occurrence of Dupuytren contracture could be correlated with the presence of diabetes, with alcoholism, or with smoking.[31]

Another report, however, found different results, noting an association between Dupuytren contracture and several conditions (eg, alcoholism, diabetes, epilepsy, pulmonary disease), as well as a link with smoking.[32] Nonetheless, even if such associations exist, no clear causal relationship has been established in the literature.

HLA-DRB1*15 and HLA-DR3 have been identified in numerous patients, suggesting an immunologic influence. Each confers about a 2-3 times relative risk for the development of Dupuytren disease.[33, 34]

Most likely, an inciting disease or event in a genetically predisposed individual causes a cascade of events that may include processes that promote the formation of growth factors and free radicals that ultimately leads to abnormal fibroproliferation and the appearance of the characteristic Garrod nodule. Even when homeostasis is ultimately achieved and fibroblastic growth lessens, the pathologic nodule and cord remain.

Local trauma or injury

Many hand surgeons believe that trauma to the hand or the distal part of the forearm, such as falling on an outstretched hand, may precipitate the onset. (A positive family history may play a role in occupational and traumatic cases of Dupuytren disease.)

However, numerous population-based studies have failed to conclusively link Dupuytren disease to trauma. In reviewing available studies on the question of the work-relatedness of Dupuytren disease, Liss stated "No controlled studies of acute trauma and Dupuytren’s contracture were identified."[35]

In their discussion of Dupuytren disease and occupational exposure, Melhom and Ackerman reviewed 46 available studies, including those cited by Liss, and concluded that evidence associated Dupuytren disease with vibration (discussed below) but not with highly repetitive or forceful work.[36]

The debate continues, with reports by Lucas et al finding increased Dupuytren disease in a group of French male civil servants with greater occupational exposure to vibration and manual work.[37] Case reports of Dupuytren disease occurring after surgical injury to the hand also appear, with the authors suggesting that injury can trigger the onset of Dupuytren disease.[38, 39]

Manual labor with vibration exposure

A history of manual labor with vibration exposure or recurrent trauma has been found to result in a 5-fold increase in the incidence of Dupuytren disease.[35]

Although in reviewing available studies on the question of the work-relatedness of Dupuytren disease, Liss found no link between acute trauma and Dupuytren’s contracture, he did find acceptable studies linking occupational exposure to vibration with a higher incidence of Dupuytren disease.[35, 40, 41, 42] Notably, the exposure in one study was severe enough to cause persistent symptomatic circulatory disturbance ("vibration white finger"); in another, the exposure was associated with other soft tissue "wasting" and peripheral nerve damage.

In a review of 46 available studies,[36] Melhom and Ackerman concluded that evidence associated Dupuytren disease with vibration but not with highly repetitive or forceful work generally.

Diabetes

Dupuytren disease among patients with diabetes ranges from 1.6-32%, and the prevalence of diabetes in patients with Dupuytren disease is 5%.[4] The use of insulin and oral hypoglycemic are strongly associated with Dupuytren disease. The disease seems to occur at a younger age and tends to be more severe in those with type 1 diabetes. Patients with diabetes mellitus and Dupuytren disease have a 4-fold increased risk of developing microalbuminuria than do persons with diabetes alone.[43, 44]

One study showed a higher incidence of retinopathy and Dupuytren contracture in diabetic patients and attributed the cause to microangiopathic changes.

Alcoholic liver disease

Individuals with alcoholism-related liver disease have an increased prevalence of Dupuytren contracture (approximately 20%) compared with control populations. Patients with liver disease from other causes do not appear to be at increased risk. The reason for this is unknown, and some studies have disputed the association.[45, 46]

Smokers

A 3-fold increased risk for Dupuytren contracture is seen in individuals who smoke, even when studies control for alcohol use, perhaps due to microvascular impairment.[47]

Autoantibodies to connective tissue

Significant associations have been found with HLA-DRB1*15,[48] HLA-DR3 and autoantibodies to collagen types I-IV.

Androgen receptors

Two studies have shown increased sensitivity to androgens in the palmar fascia.[49, 50] This may account for the male predominance of the disease.

Epilepsy and use of epileptic medications

Although implicated in previous studies, little conclusive evidence has been reported to link epilepsy and antiepileptic medications to the development of Dupuytren contracture. Phenobarbitone, in particular, results in increased LPA levels.

Although the incidence of Dupuytren disease is 2-3 times higher in individuals with epilepsy, opinions about the cause differ. One group of investigators concluded that electroencephalogram (EEG) abnormalities were more common in patients with Dupuytren disease than in persons with other clinical conditions.

Another study showed a correlation between increased barbiturate medication and a higher occurrence of Dupuytren disease, whereas other studies implicated a genetic link between the 2 diseases.[51]

HIV

There are conflicting results about whether the human immunodeficiency virus (HIV) is implicated in some cases of Dupuytren disease.[52] Bower et al demonstrated an increased incidence in patients with both Dupuytren contracture and HIV infection, whereas a study by French researchers showed no statistically significant difference in these patients compared with the general population.[53]

Previous
Next

Epidemiology

Occurrence in the United States

Dupuytren disease is common in the United States, with a prevalence of 4%; this reflects immigration from Northern Europe.[7] A cross-sectional study looking at the prevalence of Dupuytren contracture in 5000 patients admitted to a New York City hospital for unrelated conditions showed a rate of 4.8%, with a male-to-female ratio of 3:1.

International occurrence

In Northern Europe, the prevalence of Dupuytren contracture ranges from 4-39%. In Norwegian populations, 30% of males older than age 60 years are affected. The incidence of Dupuytren disease in the British population was calculated at 34.4 per 100,000 for men aged 40-84 years.[7] In men older than age 60 years, a 28% prevalence was reported in Australia, and a 19% prevalence was reported in Spain.[54]

The highest frequency of Dupuytren contracture has been reported in Scotland, where 200 patients were examined and 39% of men and 21% of women older than age 60 years were affected with the disease. In Japan, 19.7% of men and 9% of women older than age 60 years in nursing homes had the disease. In Spain, the disease was seen in 9.9% of individuals aged 45-54 years, while the rate increased to 25.5% in patients older than 75 years. In Iceland, rates of 7.2% in men aged 45-49 years and 39.5% in men aged 70-74 years have been reported. Sporadic cases of Dupuytren contracture have been reported in Africa and Asia.[7]

Race-related demographics

Case reports and series have shown that persons of any race can be affected by Dupuytren contracture.[55] However, most patients appear to be of Northern European (particularly Scottish and Scandinavian) descent. Ling demonstrated that the prevalence of Dupuytren disease in a Celtic family was 24%, which increased to 74% with the inclusion of close relatives.[56]

The disease is less likely to occur in African and Asian populations.[57] The disease prevalence in Asians is 3% and usually involves the palm rather than the digits. Therefore, it is less likely to be clinically significant and the incidence may be underreported. Dupuytren contracture has been reported in East Africa, Zimbabwe and Tanzania.[7]

Dupuytren is uncommon (< 1%) among Indians, Native Americans, and patients of Hispanic descent.[7]

Sex-related demographics

Approximately 80% of affected individuals are male, and this is consistent throughout all countries and races. The disease onset in males tends to occur in the fifth to sixth decade. Men tend to present a decade earlier than females. (Hueston, however, suggested that the male-to-female incidence rate may actually be less, because the disease is less severe in women; therefore, this condition may go unnoticed in women until later in life.[58] )

The disease course tends to be more rapid and severe in males and increases in incidence with advancing age.[43] Men are more likely than women to undergo surgery for the disease. By the ninth decade of life, however, no sexual difference in incidence is found.

Age-related demographics

The incidence of Dupuytren's increases with age. The average age of onset in men is in the sixth decade, with onset occurring later in women, in the seventh decade. Dupuytren contracture has been reported in children and infants but is considered rare.[59]

Younger individuals with a positive family history for the Dupuytren disease have been reported. In addition, they often have other fibromatoses, such as plantar fibromatosis, knuckle pads, and penile fibromatosis, although this diathesis occurs in less than 1% of the patients with Dupuytren disease. Among patients affected with Dupuytren disease, only 10-20% develops knuckle pads, and about 10% develop plantar fibromatosis. Factors such as family history, age younger than 40 years, presence of related fibromatoses, and disease on the radial side of the hand indicate an increased severity of the disease and an increased likelihood of recurrence.

Previous
Next

Prognosis

Resolution of Dupuytren contracture does not occur without treatment. Progression is unpredictable, and not all cases progress to contraction deformity. Patients with an early onset of disease appear to have a more aggressive course, often requiring surgery.

The long-term overall recurrence of Dupuytren disease is approximately 30% and can be in the same area of the hand or in a new area.[60] MCP joint contractures are readily corrected with surgery (80-96%) but can recur 11% of the time.[61]

PIP joint contractures are corrected in only 25-56% of cases and are actually exacerbated by surgery in 25%.[61]

Severe hand osteoarthritis is a relative contraindication to surgery, as these patients are at high risk for worsening of hand function postoperatively.

Recurrence rates have been related to the initial severity of disease, the presence of multiple lesions, and the coexistence of diabetes mellitus.

Complications

The predominant complication in Dupuytren contracture is progressive flexion contracture of the digits, with associated functional disability.

The overall incidence of surgical complication is 20%. The most common complications include postoperative joint stiffness and loss of preoperative flexion. A postoperative rehabilitation program is necessary to decrease these risks. Other complications include hematoma, skin loss or scarring, infection, nerve injury, vascular injury, prolonged edema, and complex regional pain syndrome.

Complex regional pain syndrome, formerly known as reflex sympathetic dystrophy, occurs in 1-8% of patients who undergo surgery for Dupuytren contracture. The complication occurs twice as often in women. One study also found that the risk of developing complex regional pain syndrome is higher in patients who undergo surgery with intravenous regional anesthesia with lidocaine alone or with general anesthesia.[62]

The effects of morbidity in Dupuytren contracture are generally limited to lifestyle changes. MCP and PIP joint contractures may interfere with activities of daily living and the nodules can be painful. Occasionally, Dupuytren contracture is associated with plantar fascial thickening (Ledderhose disease), involvement of the penis (Peyronie disease), or involvement of the knuckle pads (Garrod nodes). These associations tend to reflect more aggressive disease.[63] No mortality occurs from Dupuytren contracture.

Previous
Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Stephanie Danielle Mathew, DO  Fellow, Department of Rheumatology, San Antonio Uniformed Services Health Education Consortium

Stephanie Danielle Mathew, DO is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and American Osteopathic Association

Disclosure: Nothing to disclose.

Coauthor(s)

Daniel F Battafarano, DO, FACP, FACR  Clinical Professor of Medicine, University of Texas Health Science Center at San Antonio; Associate Professor of Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Chief of Rheumatology Service, San Antonio Military Medical Center

Daniel F Battafarano, DO, FACP, FACR is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Milton B Armstrong, MD, FACS Associate Professor of Clinical Surgery, Associate Professor of Clinical Orthopedics, Department of Surgery, University of Miami Miller School of Medicine

Milton B Armstrong, MD, FACS is a member of the following medical societies: American Association for Hand Surgery, American Association of Plastic Surgeons, American Cleft Palate/Craniofacial Association, American College of Surgeons, American Medical Association, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, and National Medical Association

Disclosure: Nothing to disclose.

D Glynn Bolitho, MD, PhD, FACS, FRCSC, FCS(SA) Associate Clinical Professor, Department of Plastic Surgery, University of California at San Diego; Private Practice, LaJolla, California

D Glynn Bolitho, MD, PhD, FACS, FRCSC, FCS(SA) is a member of the following medical societies: American College of Surgeons, American Medical Assocation, American Society for Aesthetic Plastic Surgery, American Society of Maxillofacial Surgeons, American Society of Plastic Surgeons, California Society of Plastic Surgeons, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Rene Cailliet, MD Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center

Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association

Disclosure: Nothing to disclose.

David W Chang, MD, FACS Associate Professor, Department of Plastic Surgery, MD Anderson Cancer Center, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Theresa Dressler Conologue, DO, FAAD Physician, Department of Dermatology, Geisinger Medical Center

Theresa Dressler Conologue, DO, FAAD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, and American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Evan R Farmer, MD Clinical Professor of Pathology and Dermatology, Department of Pathology, Virginia Commonwealth University School of Medicine

Evan R Farmer, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Medical Association, American Society of Dermatopathology, and International Society of Dermatology

Disclosure: Nothing to disclose.

Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

William D James, MD is a member of the following medical societies: American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Elselvier

Felisa S Lewis, MD Staff Physician, Department of Dermatology, Madigan Army Medical Center

Felisa S Lewis, MD, is a member of the following medical societies: American Academy of Dermatology, International Society of Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Carlos J Lozada, MD Director of Rheumatology Fellowship Program, Professor, Department of Medicine, Division of Rheumatology and Immunology, University of Miami, Leonard M Miller School of Medicine

Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Pfizer Honoraria Speaking and teaching; Amgen Honoraria Speaking and teaching

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joseph A Molnar, MD, PhD, FACS Director, Wound Care Center, Associate Director of Burn Unit, Associate Professor, Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine

Joseph A Molnar, MD, PhD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, American Society of Plastic Surgeons, North Carolina Medical Society, Peripheral Nerve Society, Undersea and Hyperbaric Medical Society, and Wound Healing Society

Disclosure: KCI, Inc. Honoraria Speaking and teaching; Integra Life Sciences Honoraria Speaking and teaching; Clincal Cell Culture Grant/research funds Co-investigator; KCI, Inc Wake Forest University receives royalties Other

Don R Revis Jr, MD Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine

Don R Revis Jr, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons

Disclosure: Nothing to disclose.

Frank R Rogers, MD, MBA Associate Professor, Division of Plastic and Reconstructive Surgery, Director, Undergraduate Education, Department of Surgery, Loma Linda University School of Medicine

Frank R Rogers, MD, MBA is a member of the following medical societies: American Association for Hand Surgery, American College of Physician Executives, American College of Surgeons, American Society of Plastic and Reconstructive Surgery, and Association for Surgical Education

Disclosure: Nothing to disclose.

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Kristina Shaffer, MD, MPH Consulting Staff, Department of Dermatology, Dermatology Consultants

Kristina Shaffer, MD, MPH is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose

Dev Sinha, MD Research Associate/Physiatrist Observership, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Disclosure: Nothing to disclose.

Todd P Stitik, MD Professor, Department of Physical Medicine and Rehabilitation; Director, Outpatient Occupational/Musculoskeletal Medicine, UMDNJ-New Jersey School of Medicine

Todd P Stitik, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, Phi Beta Kappa, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Wendy Wing-Heen-Lo Wong, MD Research Fellow in Plastic and Reconstructive Surgery, Department of Plastic Surgery, Loma Linda University School of Medicine

Wendy Wing-Heen-Lo Wong, MD is a member of the following medical societies: American Medical Association and American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston

Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of Medscape Reference gratefully acknowledge the previous contributions of Debra Ibrahim, New York College of Osteopathic Medicine Class of 2008, Evish Kamrava, St. George's University School of Medicine Class of 2009, Jason Lee, St. George's University School of Medicine Class of 2010, Cyrus Kao, St. George's University School of Medicine Class of 2011, and Robert Mathew, to the development or revision of a source article.

References

  1. Verheyden CN. The history of Dupuytren's contracture. Clin Plast Surg. Oct 1983;10(4):619-25. [Medline].

  2. Hurst LC, Badalamente MA, Hentz VR, et al. Injectable collagenase clostridium histolyticum for Dupuytren's contracture. N Engl J Med. Sep 3 2009;361(10):968-79. [Medline].

  3. Wheeless Clifford. Wheeless' Textbook of Orthopedics: Dupuytren's Contracture. Ortho Preferred. Available at http://wheelessonline.com/ortho/dupuytrens_contracture. Accessed September 22 2010.

  4. Geoghegan JM, Forbes J, Clark DI, Smith C, Hubbard R. Dupuytren's Disease Risk Factors. J Hand Surg. 2004/10;29B:423-426. [Medline].

  5. Anthony SG, Lozano-Calderon SA, Simmons BP, Jupiter JB. Gender ratio of Dupuytren's disease in the modern U.S. population. Hand (N Y). Jun 2008;3(2):87-90. [Medline]. [Full Text].

  6. Al-Qattan MM. Factors in the pathogenesis of Dupuytren's contracture. J Hand Surg Am. Nov 2006;31(9):1527-34. [Medline].

  7. Hindocha S, McGrouther DA, Bayat A. Epidemiological evaluation of Dupuytren's disease incidence and prevalence rates in relation to etiology. Hand (N Y). Sep 2009;4(3):256-69. [Medline]. [Full Text].

  8. Fitzgerald AM, Kirkpatrick JJ, Naylor IL. Dupuytren's disease. The way forward?. J Hand Surg Br. Aug 1999;24(4):395-9. [Medline].

  9. Trojian TH, Chu SM. Dupuytren's disease: diagnosis and treatment. Am Fam Physician. Jul 1 2007;76(1):86-9. [Medline].

  10. Strickland JW, Leibovic SJ. Anatomy and pathogenesis of the digital cords and nodules. Hand Clin. Nov 1991;7(4):645-57; discussion 659-60. [Medline].

  11. McFarlane RM. The anatomy of Dupuytren's disease. Bull Hosp Jt Dis Orthop Inst. Fall 1984;44(2):318-37. [Medline].

  12. LUCK JV. Dupuytren's contracture; a new concept of the pathogenesis correlated with surgical management. J Bone Joint Surg Am. Jun 1959;41-A(4):635-64. [Medline].

  13. McFarlane RM. Patterns of the diseased fascia in the fingers in Dupuytren's contracture. Displacement of the neurovascular bundle. Plast Reconstr Surg. Jul 1974;54(1):31-44. [Medline].

  14. Bansal V, Naidu SH. Dupuytren's disease. Curr Opin Orthop. 2005;16(4):236-9.

  15. Vi L, Feng L, Zhu RD, Wu Y, Satish L, Gan BS, et al. Periostin differentially induces proliferation, contraction and apoptosis of primary Dupuytren's disease and adjacent palmar fascia cells. Exp Cell Res. Dec 10 2009;315(20):3574-86. [Medline].

  16. Augoff K, Tabola R, Kula J, Gosk J, Rutowski R. Epidermal growth factor receptor (EGF-R) in Dupuytren's disease. J Hand Surg Br. Dec 2005;30(6):570-3. [Medline].

  17. Kopp J, Seyhan H, Müller B, et al. N-acetyl-L-cysteine abrogates fibrogenic properties of fibroblasts isolated from Dupuytren's disease by blunting TGF-beta signalling. J Cell Mol Med. Jan-Mar 2006;10(1):157-65. [Medline].

  18. Ulrich D, Ulrich F, Piatkowski A, Pallua N. Expression of matrix metalloproteinases and their inhibitors in cords and nodules of patients with Dupuytren's disease. Arch Orthop Trauma Surg. Nov 2009;129(11):1453-9. [Medline].

  19. Johnston P, Chojnowski AJ, Davidson RK, Riley GP, Donell ST, Clark IM. A complete expression profile of matrix-degrading metalloproteinases in Dupuytren's disease. J Hand Surg Am. Mar 2007;32(3):343-51. [Medline].

  20. Johnston P, Larson D, Clark IM, Chojnowski AJ. Metalloproteinase gene expression correlates with clinical outcome in Dupuytren's disease. J Hand Surg Am. Sep 2008;33(7):1160-7. [Medline].

  21. MACCALLUM P, HUESTON JT. The pathology of Dupuytren's contracture. Aust N Z J Surg. May 1962;31:241-53. [Medline].

  22. Forsman M, Pääkkönen V, Tjäderhane L, et al. The expression of myoglobin and ROR2 protein in Dupuytren's disease. J Surg Res. May 15 2008;146(2):271-5. [Medline].

  23. Burge P. Genetics of Dupuytren's disease. Hand Clin. Feb 1999;15(1):63-71. [Medline].

  24. Hindocha S, John S, Stanley JK, Watson SJ, Bayat A. The heritability of Dupuytren's disease: familial aggregation and its clinical significance. J Hand Surg Am. Feb 2006;31(2):204-10. [Medline].

  25. Lee LC, Zhang AY, Chong AK, Pham H, Longaker MT, Chang J. Expression of a novel gene, MafB, in Dupuytren's disease. J Hand Surg Am. Feb 2006;31(2):211-8. [Medline].

  26. Shih B, Wijeratne D, Armstrong DJ, Lindau T, Day P, Bayat A. Identification of biomarkers in Dupuytren's disease by comparative analysis of fibroblasts versus tissue biopsies in disease-specific phenotypes. J Hand Surg Am. Jan 2009;34(1):124-36. [Medline].

  27. Hu FZ, Nystrom A, Ahmed A, et al. Mapping of an autosomal dominant gene for Dupuytren's contracture to chromosome 16q in a Swedish family. Clin Genet. Nov 2005;68(5):424-9. [Medline].

  28. Bayat A, Walter J, Lambe H, et al. Identification of a novel mitochondrial mutation in Dupuytren's disease using multiplex DHPLC. Plast Reconstr Surg. Jan 2005;115(1):134-41. [Medline].

  29. Dal Cin P, De Smet L, Sciot R, Van Damme B, Van den Berghe H. Trisomy 7 and trisomy 8 in dividing and non-dividing tumor cells in Dupuytren's disease. Cancer Genet Cytogenet. Jan 15 1999;108(2):137-40. [Medline].

  30. WARREN RF. The pathology of Dupuytren's contracture. Br J Plast Surg. Oct 1953;6(3):224-30. [Medline].

  31. Loos B, Puschkin V, Horch RE. 50 years experience with Dupuytren's contracture in the Erlangen University Hospital--a retrospective analysis of 2919 operated hands from 1956 to 2006. BMC Musculoskelet Disord. Jul 4 2007;8:60. [Medline]. [Full Text].

  32. Hnanicek J, Cimburova M, Putova I, et al. Lack of association of iron metabolism and Dupuytren's disease. J Eur Acad Dermatol Venereol. Apr 2008;22(4):476-80. [Medline].

  33. McCarty S, Farhatullah S, Bayat A. Role of the HLA System in the Pathogenesis of Dupuytren's Disease. Hand. 2010/2;5:241-250.

  34. Neumuller J, Menzel J, Millesi H. Prevalence of HLA-DR3 and autoantibodies to connective tissue components in Dupuytren's contracture. Clin Immunol Immunopathol. May 1994;71(2):142-8. [Medline].

  35. Liss GM, Stock SR. Can Dupuytren's contracture be work-related?: review of the evidence. Am J Ind Med. May 1996;29(5):521-32. [Medline].

  36. Melhom JM, Ackerman III WE. Guides to the Evaluation of Disease and Injury Causation. American Medical Association Press; 2007:147-152 and 191-202.

  37. Lucas G, Brichet A, Roquelaure Y, Leclerc A, Descatha A. Dupuytren's disease: personal factors and occupational exposure. Am J Ind Med. Jan 2008;51(1):9-15. [Medline].

  38. Lanzettá M, Morrison WA. Dupuytren's disease occurring after a surgical injury to the hand. J Hand Surg Br. Aug 1996;21(4):481-3. [Medline].

  39. Kelly SA, Burke FD, Elliot D. Injury to the distal radius as a trigger to the onset of Dupuytren's disease. J Hand Surg Br. Apr 1992;17(2):225-9. [Medline].

  40. Thomas PR, Clarke D. Vibration white finger and Dupuytren's contracture: are they related?. Occup Med (Lond). Aug 1992;42(3):155-8. [Medline].

  41. Cocco PL, Frau P, Rapallo M, Casula D. [Occupational exposure to vibration and Dupuytren's disease: a case-controlled study]. Med Lav. Sep-Oct 1987;78(5):386-92. [Medline].

  42. Dasgupta AK, Harrison J. Effects of vibration on the hand-arm system of miners in India. Occup Med (Lond). Feb 1996;46(1):71-8. [Medline].

  43. Thurston A. Dupuytren's disease or Cooper's contracture?: Kenneth Fitzpatrick Russell Memorial Lecture. ANZ J Surg. Jul 2003;73(7):529-35. [Medline].

  44. Noble J, Heathcote JG, Cohen H. Diabetes mellitus in the aetiology of Dupuytren's disease. J Bone Joint Surg Br. May 1984;66(3):322-5. [Medline].

  45. Gudmundsson KG, Arngrimsson R, Jonsson T. Dupuytren's disease, alcohol consumption and alcoholism. Scand J Prim Health Care. Sep 2001;19(3):186-90. [Medline].

  46. Bradlow A, Mowat AG. Dupuytren's contracture and alcohol. Ann Rheum Dis. Apr 1986;45(4):304-7. [Medline]. [Full Text].

  47. Burge P, Hoy G, Regan P, Milne R. Smoking, alcohol and the risk of Dupuytren's contracture. J Bone Joint Surg Br. Mar 1997;79(2):206-10. [Medline]. [Full Text].

  48. Brown JJ, Ollier W, Thomson W, Bayat A. Positive association of HLA-DRB1*15 with Dupuytren's disease in Caucasians. Tissue Antigens. Aug 2008;72(2):166-70. [Medline].

  49. Kuhn MA, Wang X, Payne WG, Ko F, Robson MC. Tamoxifen decreases fibroblast function and downregulates TGF(beta2) in dupuytren's affected palmar fascia. J Surg Res. Apr 2002;103(2):146-52. [Medline].

  50. Pagnotta A, Specchia N, Soccetti A, Manzotti S, Greco F. Responsiveness of Dupuytren's disease fibroblasts to 5 alpha-dihydrotestosterone. J Hand Surg Am. Nov 2003;28(6):1029-34. [Medline].

  51. Critchley EM, Vakil SD, Hayward HW, Owen VM. Dupuytren's disease in epilepsy: result of prolonged administration of anticonvulsants. J Neurol Neurosurg Psychiatry. May 1976;39(5):498-503. [Medline]. [Full Text].

  52. Ross DC. Epidemiology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):53-62, vi. [Medline].

  53. Bower M, Nelson M, Gazzard BG. Dupuytren's contractures in patients infected with HIV. BMJ. Jan 20 1990;300(6718):164-5. [Medline]. [Full Text].

  54. McFarlane RM. On the origin and spread of Dupuytren's disease. J Hand Surg Am. May 2002;27(3):385-90. [Medline].

  55. Saboeiro AP, Porkorny JJ, Shehadi SI, Virgo KS, Johnson FE. Racial distribution of Dupuytren's disease in Department of Veterans Affairs patients. Plast Reconstr Surg. Jul 2000;106(1):71-5. [Medline].

  56. LING RS. THE GENETIC FACTOR IN DUPUYTREN'S DISEASE. J Bone Joint Surg Br. Nov 1963;45:709-18. [Medline].

  57. Gonzalez MH, Sobeski J, Grindel S, Chunprapaph B, Weinzweig N. Dupuytren's disease in African-Americans. J Hand Surg Br. Jun 1998;23(3):306-7. [Medline].

  58. Hueston JT. The incidence of Dupuytren's contracture. Med J Aust. 1960;2:999-1002.

  59. Bebbington A, Savage R. Dupuytren's disease in an infant. J Bone Joint Surg Br. Jan 2005;87(1):111-3. [Medline].

  60. Bulstrode NW, Jemec B, Smith PJ. The complications of Dupuytren's contracture surgery. J Hand Surg Am. Sep 2005;30(5):1021-5. [Medline].

  61. Högemann A, Wolfhard U, Kendoff D, Board TN, Olivier LC. Results of total aponeurectomy for Dupuytren's contracture in 61 patients: a retrospective clinical study. Arch Orthop Trauma Surg. Feb 2009;129(2):195-201. [Medline].

  62. Reuben SS, Pristas R, Dixon D, Faruqi S, Madabhushi L, Wenner S. The incidence of complex regional pain syndrome after fasciectomy for Dupuytren's contracture: a prospective observational study of four anesthetic techniques. Anesth Analg. Feb 2006;102(2):499-503. [Medline].

  63. Hindocha S, Stanley JK, Watson S, Bayat A. Dupuytren's diathesis revisited: Evaluation of prognostic indicators for risk of disease recurrence. J Hand Surg Am. Dec 2006;31(10):1626-34. [Medline].

  64. Bayat A, Cunliffe EJ, McGrouther DA. Assessment of clinical severity in Dupuytren's disease. Br J Hosp Med (Lond). Nov 2007;68(11):604-9. [Medline].

  65. Meathrel KE, Thoma A. Abductor digiti minimi involvement in Dupuytren's contracture of the small finger. J Hand Surg Am. May 2004;29(3):510-3. [Medline].

  66. Balaguer T, David S, Ihrai T, Cardot N, Daideri G, Lebreton E. Histological staging and Dupuytren's disease recurrence or extension after surgical treatment: a retrospective study of 124 patients. J Hand Surg Eur Vol. Aug 2009;34(4):493-6. [Medline].

  67. Lam WL, Rawlins JM, Karoo RO, Naylor I, Sharpe DT. Re-visiting Luck's classification: a histological analysis of Dupuytren's disease. J Hand Surg Eur Vol. May 2010;35(4):312-7. [Medline].

  68. Watt AJ, Curtin CM, Hentz VR. Collagenase injection as nonsurgical treatment of Dupuytren's disease: 8-year follow-up. J Hand Surg Am. Apr 2010;35(4):534-9, 539.e1. [Medline].

  69. Badalamente MA, Hurst LC, Hentz VR. Collagen as a clinical target: nonoperative treatment of Dupuytren's disease. J Hand Surg Am. Sep 2002;27(5):788-98. [Medline].

  70. Hurst LC, Badalamente MA. Nonoperative treatment of Dupuytren's disease. Hand Clin. Feb 1999;15(1):97-107, vii. [Medline].

  71. Starkweather KD, Lattuga S, Hurst LC, et al. Collagenase in the treatment of Dupuytren's disease: an in vitro study. J Hand Surg Am. May 1996;21(3):490-5. [Medline].

  72. Rayan GM. Nonoperative treatment of Dupuytren's disease. J Hand Surg Am. Sep 2008;33(7):1208-10. [Medline].

  73. Betz N, Ott OJ, Adamietz B, Sauer R, Fietkau R, Keilholz L. Radiotherapy in early-stage Dupuytren's contracture. Long-term results after 13 years. Strahlenther Onkol. Feb 2010;186(2):82-90. [Medline].

  74. Ketchum LD, Donahue TK. The injection of nodules of Dupuytren's disease with triamcinolone acetonide. J Hand Surg Am. Nov 2000;25(6):1157-62. [Medline].

  75. Badalamente MA, Hurst LC. Efficacy and safety of injectable mixed collagenase subtypes in the treatment of Dupuytren's contracture. J Hand Surg Am. Jul-Aug 2007;32(6):767-74. [Medline].

  76. Collagenase Clostridium Histolyticum [package insert]. Malver, PA: Auxilium Pharmaceuticals; 2010. [Full Text].

  77. Bulstrode NW, Mudera V, McGrouther DA, Grobbelaar AO, Cambrey AD. 5-fluorouracil selectively inhibits collagen synthesis. Plast Reconstr Surg. Jul 2005;116(1):209-21; discussion 222-3. [Medline].

  78. Jemec B, Linge C, Grobbelaar AO, Smith PJ, Sanders R, McGrouther DA. The effect of 5-fluorouracil on Dupuytren fibroblast proliferation and differentiation. Chir Main. Feb 2000;19(1):15-22. [Medline].

  79. Namazi H. Imiquimod: a potential weapon against Dupuytren contracture. Med Hypotheses. 2006;66(5):991-2. [Medline].

  80. Namazi H, Abdinejad F. Botulinum Toxin as a novel addition to the antidupuytren armamentarium. Med Hypotheses. 2007;68(1):240-1. [Medline].

  81. Townley WA, Cambrey AD, Khaw PT, Grobbelaar AO. Matrix metalloproteinase inhibition reduces contraction by dupuytren fibroblasts. J Hand Surg Am. Nov 2008;33(9):1608-16. [Medline].

  82. Yildiz S, Karacaoglu E, Pehlivan O. Hyperbaric oxygen for the treatment of early-phase Dupuytren's contracture. Microsurgery. 2004;24(1):26-9. [Medline].

  83. Denkler, Keith. Surgical Complications Associated With Fasciectomy for Dupuytren's Disease: A 20-Year Review of the English Literature. Eplasty [serial online]. Jan 27, 2010;10:e15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20204055. Accessed November 3, 2010. [Medline]. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828055/.

  84. Anwar MU, Al Ghazal SK, Boome RS. Results of surgical treatment of Dupuytren's disease in women: a review of 109 consecutive patients. J Hand Surg Am. Nov 2007;32(9):1423-8. [Medline].

  85. Mavrogenis AF, Spyridonos SG, Ignatiadis IA, et al. Partial fasciectomy for Dupuytren's contractures. J Surg Orthop Adv. Summer 2009;18(2):106-10. [Medline].

  86. Misra A, Jain A, Ghazanfar R, Johnston T, Nanchahal J. Predicting the outcome of surgery for the proximal interphalangeal joint in Dupuytren's disease. J Hand Surg Am. Feb 2007;32(2):240-5. [Medline].

  87. Donaldson OW, Pearson D, Reynolds R, Bhatia RK. The association between intraoperative correction of Dupuytren's disease and residual postoperative contracture. J Hand Surg Eur Vol. Mar 2010;35(3):220-3. [Medline].

  88. Zyluk A, Jagielski W. The effect of the severity of the Dupuytren's contracture on the function of the hand before and after surgery. J Hand Surg Eur Vol. Jun 2007;32(3):326-9. [Medline].

  89. Lilly SI, Stern PJ. Simultaneous carpal tunnel release and Dupuytren's fasciectomy. J Hand Surg Am. May 2010;35(5):754-9. [Medline].

  90. van Rijssen AL, Gerbrandy FS, Ter Linden H, Klip H, Werker PM. A comparison of the direct outcomes of percutaneous needle fasciotomy and limited fasciectomy for Dupuytren's disease: a 6-week follow-up study. J Hand Surg Am. May-Jun 2006;31(5):717-25. [Medline].

  91. van Rijssen AL, Werker PM. Percutaneous needle fasciotomy in dupuytren's disease. J Hand Surg Br. Oct 2006;31(5):498-501. [Medline].

  92. Cheng HS, Hung LK, Tse WL, Ho PC. Needle aponeurotomy for Dupuytren's contracture. J Orthop Surg (Hong Kong). Apr 2008;16(1):88-90. [Medline].

  93. Symes T, Stothard J. Two significant complications following percutaneous needle fasciotomy in a patient on anticoagulants. J Hand Surg Br. Dec 2006;31(6):606-7. [Medline].

  94. Foucher G, Medina J, Navarro R. Percutaneous needle aponeurotomy: complications and results. J Hand Surg Br. Oct 2003;28(5):427-31. [Medline].

  95. Moermans JP. Long-term results after segmental aponeurectomy for Dupuytren's disease. J Hand Surg Br. Dec 1996;21(6):797-800. [Medline].

  96. Moermans JP. Segmental aponeurectomy in Dupuytren's disease. J Hand Surg Br. Aug 1991;16(3):243-54. [Medline].

  97. Ali SN, McMurtrie A, Rayatt S, Roberts JO. Ulnar-based skin flap for Dupuytren's fasciectomy. Scand J Plast Reconstr Surg Hand Surg. 2006;40(5):307-10. [Medline].

  98. Pelissier P, Gardet H, Pinsolle V. The palmar intermetacarpal flap in Dupuytren's contracture. J Hand Surg Eur Vol. Feb 2007;32(1):113. [Medline].

  99. HUESTON JT. Limited fasciectomy for Dupuytren's contracture. Plast Reconstr Surg Transplant Bull. Jun 1961;27:569-85. [Medline].

  100. Tripoli M, Merle M. The "Jacobsen Flap" for the treatment of stages III-IV Dupuytren's disease: a review of 98 cases. J Hand Surg Eur Vol. Dec 2008;33(6):779-82. [Medline].

  101. Skoff HD. The surgical treatment of Dupuytren's contracture: a synthesis of techniques. Plast Reconstr Surg. Feb 2004;113(2):540-4. [Medline].

  102. Ullah AS, Dias JJ, Bhowal B. Does a 'firebreak' full-thickness skin graft prevent recurrence after surgery for Dupuytren's contracture?: a prospective, randomised trial. J Bone Joint Surg Br. Mar 2009;91(3):374-8. [Medline].

  103. Villani F, Choughri H, Pelissier P. [Importance of skin graft in preventing recurrence of Dupuytren's contracture]. Chir Main. Dec 2009;28(6):349-51. [Medline].

  104. Mullins PA. Postsurgical rehabilitation of Dupuytren's disease. Hand Clin. Feb 1999;15(1):167-74, viii. [Medline].

  105. Jerosch-Herold C, Shepstone L, Chojnowski AJ, Larson D. Splinting after contracture release for Dupuytren's contracture (SCoRD): protocol of a pragmatic, multi-centre, randomized controlled trial. BMC Musculoskelet Disord. Apr 30 2008;9:62. [Medline]. [Full Text].

  106. Evans RB, Dell PC, Fiolkowski P. A clinical report of the effect of mechanical stress on functional results after fasciectomy for Dupuytren's contracture. J Hand Ther. Oct-Dec 2002;15(4):331-9. [Medline].

 
Previous
Next
 
Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present.
Arrow denotes the typical cords of Dupuytren contracture. These cords are usually painless. Note the metacarpophalangeal joint contracture.
This photo demonstrates the presence of a nodule as well as skin blanching with extension of the affected digits.
Ultrasound of the palm in Dupuytren disease of the fourth digit; the Dupuytren nodule and thickening of the palmar fascia with puckering of the skin is noted. Green arrow: Flexor tendon; Red arrow: Dupuytren nodule; Blue arrow: Thickened palmar fascia; Yellow arrow: Puckering of the skin.
This photo shows a patient with an inability to extend the fourth and fifth digits. The differential diagnosis includes Dupuytren contracture, which is a flexion contracture most commonly involving digits 4 and/or 5.
Visible cord characteristic of Dupuytren disease with planned markings for surgical release.
Dissection of a diseased cord.
Normal anatomy of digital ligaments.
Three clinical grades of Dupuytren disease.
Parts of the palmar and digital fascia that become diseased in Dupuytren disease (left). Diseased fascia that is associated with the pretendinous cord (center). Diseased fascia that is not associated with the pretendinous cord (right).
Normal parts of the fascia that produce the spiral cord (left). The spiral cord demonstrating medial displacement of the neurovascular bundle in Dupuytren disease (right).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.