AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Dupuytren contracture is a palmar fibromatosis of uncertain etiology. Reports were first seen in 17th century European medical literature, well before the eponymous Baron Dupuytren, a prominent French surgeon, performed his first palmar fasciotomy in 1831. Dupuytren presented his findings at a lecture, the exact words of which were subsequently disseminated widely by his students, leading to the adoption of his name for the condition.

The syndrome is characterized by fibrosis of the palmar fascia leading to flexural contraction of the digits, which is often progressive. Both the proximal interphalangeal (PIP) joint and the metacarpophalangeal (MCP) joint may be affected. Although many cases appear to be idiopathic and without coexistent conditions, a variety of associated diseases have been reported.

Therapies include conservative medical and surgical modalities. Although the condition is not fatal, significant morbidity can occur if patients remain untreated.

For additional information, see the following articles from eMedicine and Medscape:

• Dupuytren Contracture (orthopedic surgery focus)
• Dupuytren Contracture (rheumatology focus)
• Dupuytren Contracture (physical medicine and rehabilitation focus)
• New Approach for Dupuytren's Contracture: A Newsmaker Interview With Charles Eaton, MD
• Viewpoint: When Is Surgery Warranted in Dupuytren's Contracture?

Pathophysiology

The etiology and the mechanisms of formation have not been fully determined. The disease affects the palmar fascia, not the tendons, although the cordlike fascial thickening can be mistaken for a thickened tendon.

In the fascia, 3 stages have been described, as follows:

• Proliferative phase: Local fascial fibroplasia and development of a nodule, in which myofibroblasts proliferate, occur.
• Involutional phase: Myofibroblasts align themselves along the 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.

These cellular changes are similar to those that occur in localized microvascular ischemia and scar formation, leading some authors to believe that these factors may be the causes of the initial fibroblast and myofibroblast proliferation. Microvascular ischemia occurs as a result of the conversion of adenosine triphosphate to hypoxanthine, which is then oxidized by xanthine oxidase. This conversion releases free radicals, which induce fibroblast proliferation and the production of interleukin (IL)–1.

Various mediators released by platelets and macrophages have been implicated in the pathogenesis of Dupuytren contracture. These mediators include IL-1 and transforming growth factors (TGFs)–beta1 and –beta2. TGF-beta1 and –beta2 have 4 main effects, as follows:

• Differentiation of fibroblasts to myofibroblasts
• Increased production of components of the extracellular matrix, including collagen type III
• Splicing of fibronectin
• Activation of platelets to produce lysophosphatidic acid (LPA)

The linkage of alpha5-beta1 integrin to extracellular fibronectin, as well as the interaction of TGF-alpha and epidermal growth factor-receptor during the proliferative and involutional phases,¹ appear to have a role in enhancing tissue contractility in palmar fibromatosis. LPA and prostaglandin factor 2 are agonists that induce myofibroblast contraction. 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.

Inflammation and skin tension may also cause fibromatosis. Histologically, the lesion shows characteristic bundles of fibroblasts separated by collagen fibers. Multinucleated giant cells may also be present. Lymphocytes, macrophages, and increased numbers of S100-positive Langerhans cells and CD45⁺ cells have been found in nodules and at dermoepidermal junctions. One report suggested a role of factor XIIIa⁺ cells in the affected tissue.

The interaction of matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinases (TIMP), and A disintegration and metalloproteinase domain with thrombospondin motif (ADAMTS) is also responsible for Dupuytren changes. In particular, levels of MMP-1, MMP-3, MMP-7, MMP-14, TIMP-1, and ADAMTS-14 are all increased in affected tissues, resulting in increased collagen biosynthesis, decreased collagenolysis, and contraction.²

Continuing research into the pathogenesis of Dupuytren contracture has yielded information that may be valuable in understanding and developing new therapies for this disease, as follows:

• TGF-beta1 at 1-10 ng/mL induces myofibroblast proliferation, leading to contraction. However, according to one report, at 20-30 ng/mL, negative feedback inhibition of TGF-beta1 occurs, resulting in decreased myofibroblast activity.
• N-acetyl-L-cysteine (NAC), a substance that has antifibrotic properties in hepatic stellate cells and rat fibroblasts, has also been shown to down-regulate the Smad signaling pathway (downstream of TGF-beta1), leading to decreased expression of fibrogenesis-related proteins.³

Frequency

United States

No prospective studies have been performed to determine the incidence of Dupuytren contracture, but a cross-sectional study looking at the prevalence 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

Studies have been performed worldwide, yet a range of frequencies has been reported. The highest frequency was reported in Scotland, where 200 patients were examined and 39% of men and 21% of women older than 60 years were affected with Dupuytren contracture. In Japan, 19.7% of men and 9% of women older than 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.

Mortality/Morbidity

No mortality occurs from this disease. Morbidity occurs from progressive contraction of the affected digits, resulting in both cosmetic and functional disability. With severe flexion deformity, the nail of the affected digit may penetrate the palmar skin. Infection secondary to this trauma has been reported.

Race

Most patients appear to be of Northern European descent, especially Scotland and the Scandinavian countries. The disease is less likely to occur in African and Asian populations. Case reports and series have shown that persons of any race can be affected.⁴

Sex

All studies show a male preponderance earlier in life, with men presenting for treatment in the fifth decade and women presenting a decade later. Typical male-to-female ratios of 3-9:1 have been reported. By the ninth decade of life, no sexual difference in incidence is found. Men are more likely than women to undergo surgery for the disease.

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 infants⁵ but is considered rare.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

Patients describe feeling a knot or thickening on the palmar surface or, less frequently, on the digits, typically the proximal palmar aspect. Often, the thickening has been present for many years and may be slowly progressive.

The fourth digit (ring finger) is most frequently affected, followed by the fifth digit. The disease can be bilateral, but it is generally not symmetric in severity. Hand dominance is not a factor. Nodules typically are painless. Tenosynovitis can develop and lead to pain when the nodules are large. With progressive disease, flexion deformity can develop. Patients report an inability to straighten the fingers.

Dupuytren diathesis, first described in 1963 by Hueston, is seen in patients with an early age of onset (<40 y in men, <50 y in women), bilateral hand involvement, a strong family history, and ectopic lesions. These are considered risk factors for disease recurrence and extension. More recently, a proposal to modify these factors includes male sex as another risk factor.⁶

Related fibromatoses, including Peyronie disease (affecting the penis), Ledderhose disease (affecting the plantar surface), and Garrod knuckle pads (affecting the dorsal PIP joints), may occur. Wrist involvement has been described,⁷ but whether this is a variant of Dupuytren contracture or another similar process involving myofibroblast proliferation is uncertain.

Physical

Physical findings depend on the stage at which the disease is observed. Although the fourth and fifth digits are most commonly involved, any digit can be affected.

• In the earliest stage, localized thickening of the palmar skin and underlying subcutaneous tissue with loss of skin mobility occurs. A depression, puckering, or pitting of the skin may be present in the affected area.
• With the nodular stage, nodules initially are palpable; later, nodules are visible. Nodules are firm, fixed, and usually well localized. When the disease affects the palm, the nodules are usually located adjacent to the palmar crease, typically in line with the ring (fourth) and/or little (fifth) fingers. Digital nodules are located near the PIP joint or at the MCP joint. Of those involving the little finger, a quarter have abductor digiti minimi involvement.⁸
• In the cord stage, the cord is a linear thickening and can resemble the tendon. Progressive contraction of the cord leads to a flexion deformity of the digit. Flexion deformity usually occurs at the MCP joint. Disease located in the digits produces flexion at the PIP joint. MCP joint contracture should be measured while passive extension is applied to the PIP joint. PIP joint contracture is measured while the MCP joint is held in flexion. These maneuvers eliminate artificial contractures. When 30° of flexion deformity is present at the MCP joint, the patient is unable to place the palm flat against a hard surface.

Knuckle pads may be present on the dorsal aspect of the PIP joints, and this indicates more aggressive disease. Additionally, swan-neck deformities and boutonnière deformities have been reported with this disease.

Causes

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.⁹ Still, one study derived a sibling recurrence-risk ratio of 2.9 (range, 2.6-3.3; 95% confidence interval for population prevalence), with a lower age of onset and more severe disease in patients with a positive family history.¹⁰ Furthermore, DNA microarray analysis has demonstrated that the gene MafB, involved in tissue development and cellular differentiation, is up-regulated in Dupuytren cord tissue.¹¹

A separate 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.¹² Another study of 20 patients with apparent maternal inheritance identified a polymorphism in the mitochondrial 16s rRNA region present in 90% of their DNA.¹³ Others believe that Dupuytren contracture has a multifactorial inheritance, similar to diabetes or hypertension.

Many conditions or factors have been associated with Dupuytren contracture. The following have shown the strongest associations:

• 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.
• Alcoholic liver disease: Individuals with alcoholism and 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 studies¹⁴ have disputed the association.
• Diabetes: Of patients with Dupuytren contracture, 5% have diabetes. At greatest risk are persons with type 1 diabetes mellitus, followed by those who take metformin and sulfonylureas. One theory suggests that as many as two thirds of patients with long-standing type 1 diabetes (>20 y) have some degree of Dupuytren contracture. Persons with type 2 diabetes with Dupuytren disease have a 4-fold increased risk of developing microalbuminuria compared with type 2 diabetes patients without Dupuytren disease.
• Smoking: 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.
• Autoantibodies to connective tissue: Significant associations have been found with HLA-DR3 and autoantibodies to collagen types I-IV.
• Androgen receptors: Two studies have shown increased sensitivity to androgens in the palmar fascia.^{15, 16} This may account for the male predominance of the disease.
• Manual work: In general, only persons who work in occupations exposed to vibration appear to be at increased risk.
• 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Callus
Epithelioid sarcoma (rare condition; tends to be progressive and becomes more diffuse than a localized Dupuytren nodule or cord)
Ganglion cyst
Stenosing tenosynovitis
Giant cell tumor of the tendon sheath
Prolapsed flexor tendon
Ulnar nerve palsy
Camptodactyly
Fibromas and fibromatoses

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

Diabetes mellitus has been associated with Dupuytren contracture. A fasting blood glucose level should be obtained if diabetes mellitus is suggested by the patient's clinical history and physical examination findings.

Imaging Studies

Ultrasonography of a thickened cord may be useful prior to intralesional injections so that the underlying tendon can be identified and avoided during the injection.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

In the early stages (<15° of contracture at the MCP joint and no PIP joint contractures), Dupuytren contracture can be treated medically.

Multiple therapies have been tried in small, uncontrolled reports. Many have been unsuccessful, including splinting, dimethylsulfoxide injection, vitamin E cream application, allopurinol and colchicine administration, physical therapy, and ultrasonic therapy. One case report also proposed the use of hyperbaric oxygen therapy for treatment during the early phase of Dupuytren contracture.¹⁷

Some promise has been shown using slow skeletal traction followed by surgery; in addition, calcium channel blockers, interferon-gamma injections, tamoxifen, and topical corticosteroids combined with topical retinoids have all been shown to have some efficacy. The following additional (and mostly experimental) treatments have also been proposed:

• Triamcinolone acetonide: Intralesional triamcinolone acetonide (Kenalog-40) injections of 40 mg/mL have yielded subjective improvement of Dupuytren nodules in some patients.¹⁸
• Collagenase enzymatic fasciotomy: This new treatment is still investigational.^{19, 20} The phase 3 trial was a randomized, double-blind, placebo-controlled trial followed by an open-level extension. Patients were given a maximum of 3 injections at the primary joint at 4- to 6-week intervals. During the double-blind phase, 91% of patients treated with collagenase achieved clinical success (to normal 0° ±5°). In the open-label phase, 77% of joints achieved clinical success. Overall, 54 (87%) of 62 joints achieved success (90% MCP, 84% PIP). Five recurrences were recorded, occurring between 6 and 24 months and ranging from 20-40° regression. Adverse events included local injection reactions (most common) and skin lacerations at cord rupture.²¹
• 5-Fluorouracil: This agent has been shown to cause a dose-dependent selective and specific decrease in collagen production by fibroblasts and inhibit fibroblast proliferation and myofibroblast differentiation.^{22, 23} However, TGF-beta1 gene expression and procollagen types I and III mRNA are not affected. After undergoing clinical trials, this treatment may be useful as an adjuvant therapy to surgery in reducing extracellular matrix production and recurrence of Dupuytren contracture.
• Radiation therapy: An uncontrolled study looked at radiation therapy in patients with established Dupuytren contracture. After the 1-year follow-up period, 53% of sites regressed, 38% were stable, and 9% progressed. The authors are awaiting a 5-year follow-up evaluation to determine long-term results. Local adverse effects developed in 38% of patients.
• Imiquimod: Because it is an immune modulator that down-regulates TGF-beta and fibroblast growth factor-2, this medication has been proposed as a therapy.²⁴ However, currently no reports describe experimental use of imiquimod for Dupuytren contracture.
• Botulinum toxin: This has also been proposed as an intralesional therapy for Dupuytren contracture, based on its inhibition of Rho GTPase, which is necessary for activation of the IL-1 inflammation pathway.²⁵ As with imiquimod, no reports currently describe clinical use of botulinum toxin for this condition.

Surgical Care

Surgery is indicated when contraction is 20° or more at the MCP joint and 30° or more at the PIP joint. As with all elective surgeries, the patient's age, comorbid conditions, and ability to comply with postoperative care and rehabilitation determine whether surgery is appropriate.

Skin overlying the contracture is closed either primarily (using skin grafts) or by secondary intent. The synthesis technique is a method of wound closure that incorporates the advantages of tissue rearrangement, the open-palm technique, and full-thickness skin grafting. One study showed a decreased healing time and recurrence rate using the synthesis technique versus the traditional open-palm technique.²⁶

Finally, one study found that improvement in the PIP joint contracture has a greater correlation with hand function at 6 and 12 months after surgery than improvement in the MCP joint contracture. The results of another study revealed the severity of contracture preoperatively had a significant negative effect on hand power, and older patients experienced less functional benefit from selective fasciectomy.²⁷

Surgical methods are as follows:

• Fasciectomy
• • Radical fasciectomy involves excision of the entire palmar fascia. The procedure involves excision of healthy tissue in an effort to prevent recurrence. Dupuytren contracture has recurred following surgery, and this procedure is not commonly used.
  • In selective fasciectomy, clinically apparent disease is excised. Areas not treated still may develop disease. This method is commonly used to treat both primary and recurrent disease. Skin incisions may be transverse, longitudinal, or diagonal/zigzag (eg, Z-plasty, Y-V-plasty, Bruner-type zigzag incision). Local advancement flaps, including an ulnar-based skin flap²⁸ and palmar intermetacarpal flap,²⁹ have been described.
  • Segmental fasciectomy involves removal of one or more segments of diseased fascia through multiple small incisions.
  • Open-palm technique (McCash) involves a transverse skin incision and division of the aponeurosis; healing is by secondary intention.
  • In the surgical synthesis technique (dermofasciectomy), 2 incisions are made, one from the distal interphalangeal joint of the affected joint to the distal palmar flexion crease, and a transverse palmar incision, to form an L shape. A selective fasciectomy is performed, with partial closure of the incision site. A full-thickness skin graft is harvested from the hypothenar eminence during this surgery. A portion of the palm is left open, and an extension splint is applied. After 4 days, the splint is removed, the wound is cleaned, and the skin graft is applied to the palm. The palm is splinted again for 1 week.
• Fasciotomy
• • Limited open fasciotomy and percutaneous needle fasciotomy may be performed. Diseased tissue is not removed, but is incised.
  • In several studies, percutaneous needle fasciotomy resulted in short-term improvement (77% in one study), but the recurrence rate was high (65% at 32 mo in the same study).³⁰ In addition, in a 6-week follow-up comparison of outcomes between limited open fasciotomy and percutaneous needle fasciotomy, the authors concluded that percutaneous needle fasciotomy was a good alternative to limited open fasciotomy in the short term in patients with early disease.³¹ Thus, these techniques are best reserved for patients unable to comply with postfasciectomy care, for elderly patients who are debilitated, or for patients who are willing to accept primarily short-term improvement.
  • Soft tissue reconstruction using various flaps may be performed after the fasciotomy to correct skin defects introduced as a result of the surgery.
• Amputation: This may be an alternative for primary or recurrent severe disease when flexion contracture is greater than 90° or if the digit has vascular compromise. Some patients may prefer amputation to the postoperative care required for fascial surgery.

Consultations

Consult a hand surgeon for evaluation and possible treatment of patients who are symptomatic and have more than 15° of contracture.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Outpatient Care

A volar forearm–based splint is applied 2-5 days after surgery, with the wrist in a neutral position and the fingers extended. The splint is worn during the daytime for approximately 2 weeks, while nighttime splinting continues for 3-6 months.

The patient should perform flexion and extension active range-of-motion exercises. Particular attention is paid to restoring grip. Passive stretching is performed. According to one study, therapy that avoids applied mechanical tension in the early postoperative phase results in fewer complications, with no digital motion lost to extension.³²

Complications

Postsurgical recurrence rates reportedly vary from 17-50%. Higher rates are seen in patients with earlier onset, radial side and bilateral hand involvement, positive family history, evidence of fibrosing disorders elsewhere, and disease of the PIP joint, especially if the PIP joint contracture was 60° or more. Incomplete correction of PIP joint flexion contracture during surgery and poor postoperative compliance with therapy also worsened recurrent contractures.³³

Risks of surgery in the palm include infection and damage to vessels, tendons, and nerves. Hematomas, skin slough, scar contraction, and carpal tunnel syndrome have also been reported. A false aneurysm and division of the flexor digitorum profundus were reported in an anticoagulated patient following percutaneous needle fasciotomy.³⁴

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.³⁵

Prognosis

Without treatment, spontaneous resolution does not occur. 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.

Recurrence rates have been related to the initial severity of disease, the presence of multiple lesions, and the coexistence of diabetes mellitus. Long-term postoperative recurrence rates have been as high as 63%.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Intralesional injection of corticosteroids can result in tendon rupture.
• Failure to check blood glucose levels and/or refer a symptomatic patient to a primary care physician may result in missing a diagnosis of diabetes.
• Failure to consult a hand surgeon for a patient with a contracture of greater than 15° may result in progressive or irreparable contractures.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Editor-in-Chief, William James, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

1. 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].
2. 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].
3. Kopp J, Seyhan H, Müller B, Lanczak J, Pausch E, Gressner AM. 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].
4. 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].
5. Bebbington A, Savage R. Dupuytren's disease in an infant. J Bone Joint Surg Br. Jan 2005;87(1):111-3. [Medline].
6. Wilbrand S, Ekbom A, Gerdin B. The sex ratio and rate of reoperation for Dupuytren's contracture in men and women. J Hand Surg [Br]. Aug 1999;24(4):456-9. [Medline].
7. Habash A, Rinker B. Dupuytren's disease involving the wrist. J Hand Surg [Am]. Mar 2007;32(3):352-4. [Medline].
8. 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].
9. Burge P. Genetics of Dupuytren's disease. Hand Clin. Feb 1999;15(1):63-71. [Medline].
10. 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].
11. 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].
12. Hu FZ, Nystrom A, Ahmed A, Palmquist M, Dopico R, Mossberg I, 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].
13. Bayat A, Walter J, Lambe H, Watson JS, Stanley JK, Marino M, 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].
14. Gudmundsson KG, Arngrímsson R, Jónsson T. Dupuytren's disease, alcohol consumption and alcoholism. Scand J Prim Health Care. Sep 2001;19(3):186-90. [Medline].
15. 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].
16. 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].
17. Yildiz S, Karacaoglu E, Pehlivan O. Hyperbaric oxygen for the treatment of early-phase Dupuytren's contracture. Microsurgery. 2004;24(1):26-9. [Medline].
18. 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].
19. 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].
20. Hurst LC, Badalamente MA. Nonoperative treatment of Dupuytren's disease. Hand Clin. Feb 1999;15(1):97-107, vii. [Medline].
21. 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].
22. 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].
23. 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].
24. Namazi H. Imiquimod: a potential weapon against Dupuytren contracture. Med Hypotheses. 2006;66(5):991-2. [Medline].
25. Namazi H, Abdinejad F. Botulinum Toxin as a novel addition to the antidupuytren armamentarium. Med Hypotheses. 2007;68(1):240-1. [Medline].
26. Skoff HD. The surgical treatment of Dupuytren's contracture: a synthesis of techniques. Plast Reconstr Surg. Feb 2004;113(2):540-4. [Medline].
27. 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].
28. 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].
29. 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].
30. van Rijssen AL, Werker PM. Percutaneous needle fasciotomy in dupuytren's disease. J Hand Surg [Br]. Oct 2006;31(5):498-501. [Medline].
31. 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].
32. 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].
33. 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].
34. 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].
35. 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].
36. Abe Y, Rokkaku T, Ofuchi S, Tokunaga S, Takahashi K, Moriya H. An objective method to evaluate the risk of recurrence and extension of Dupuytren's disease. J Hand Surg [Br]. Oct 2004;29(5):427-30. [Medline].
37. Al-Qattan MM. Factors in the pathogenesis of Dupuytren's contracture. J Hand Surg [Am]. Nov 2006;31(9):1527-34. [Medline].
38. Benson LS, Williams CS, Kahle M. Dupuytren's contracture. J Am Acad Orthop Surg. Jan-Feb 1998;6(1):24-35. [Medline].
39. Bulstrode NW, Jemec B, Smith PJ. The complications of Dupuytren's contracture surgery. J Hand Surg [Am]. Sep 2005;30(5):1021-5. [Medline].
40. Draviaraj KP, Chakrabarti I. Functional outcome after surgery for Dupuytren's contracture: a prospective study. J Hand Surg [Am]. Sep 2004;29(5):804-8. [Medline].
41. Fitzgerald AM, Kirkpatrick JJ, Naylor IL. Dupuytren's disease. The way forward?. J Hand Surg [Br]. Aug 1999;24(4):395-9. [Medline].
42. 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].
43. Lubahn JD, Pollard M, Cooney T. Immunohistochemical evidence of nerve growth factor in Dupuytren's diseased palmar fascia. J Hand Surg [Am]. Mar 2007;32(3):337-42. [Medline].
44. Rayan GM. Clinical presentation and types of Dupuytren's disease. Hand Clin. Feb 1999;15(1):87-96, vii. [Medline].
45. Ross DC. Epidemiology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):53-62, vi. [Medline].
46. Roush TF, Stern PJ. Results following surgery for recurrent Dupuytren's disease. J Hand Surg [Am]. Mar 2000;25(2):291-6. [Medline].
47. Saar JD, Grothaus PC. Dupuytren's disease: an overview. Plast Reconstr Surg. Jul 2000;106(1):125-34; quiz 135-6. [Medline].
48. Shaw RB Jr, Chong AK, Zhang A, Hentz VR, Chang J. Dupuytren's disease: history, diagnosis, and treatment. Plast Reconstr Surg. Sep 2007;120(3):44e-54e. [Medline].
49. Thurston AJ. Dupuytren's disease. J Bone Joint Surg Br. May 2003;85(4):469-77. [Medline].
50. Yi IS, Johnson G, Moneim MS. Etiology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):43-51, vi. [Medline].

Article Last Updated: Jan 18, 2008