Management strategies for Dupuytren's

The management options for people with Dupuytren's can appear as confusing as the biology. This review provides a nice overview of Dupuytren's disease and a practical decision tree approach to manage hands affected by Dupuytren's. It's worth a read: http://www.dupuytrenfoundation.org/DupPDFs/2006_Bayat_1586.pdf

Homeopathy for Dupuytren's

HH Reckeweg (1905-1985) in Germany developed the Disease Evolution Table of homeopathic medicine. In this system, Dupuytren's contracture is classified as a mesenchymal-connective tissue cellular-degeneration phase disease. This should be the starting point for homeopathic physicians to begin developing a homeopathic cure for Dupuytren's. See where Dupuytren's fits on the Disease Evolution Table:  http://www.dupuytrenfoundation.org/DupPDFs/1985_Reckeweg.pdf

Machines to Stretch Dupuytren's Cords

There is not yet a perfect solution for PIP contractures from Dupuytren's Disease, or for PIP contractures in general. One approach has been to use temporary skeletal fixation devices to slowly lengthen Dupuytren's cords and scar tissue. The collagen bundles in Dupuytren's cords don't actually stretch: they remodel, disconnecting crosslinks between adjacent strands, sliding adjacent strands relative to each other and then forming new crosslinks. On a microscopic level, this is architecturally the opposite of the process by which Dupuytren's cords shorten. This brief review summarizes the experience of several groups in developing such devices along the road to designing the Digit Widget. http://www.dupuytrenfoundation.org/DupPDFs/2002_Goss.pdf

Tissue markers for Dupuytren's

Is it possible to predict the course of Dupuytren's in an individual? Who will need surgery? Who will have rapid progression or an early recurrence after surgery and who won't? Family and personal history provide general trends, but that's all. Several studies have correlated the cellularity of nodule tissue and the presence of myofibroblasts with the risk for recurrence or "aggressive" Dupuytren's. This study found in addition, alpha smooth muscle antigen and the MK167 gene related Ki-67 protein correlated with aggressive disease, the markers for tenascin and factor XIIIa less so. Unfortunately, these differences were a matter of degree, not absolute. What are the actual pieces of this puzzle?  http://www.dupuytrenfoundation.org/DupPDFs/2005_Forsman_1055.pdf

Dupuytren's, epilepsy, barbiturates and genes: a chemical love ...triangle.

Dupuytren's has been associated with epilepsy. The type or cause of epilepsy doesn't seem to matter. What does matter is the specific medication phenobarbitone. Dupuytren's was not common in epileptics prior to the common use of this medicine, but is very common in people on long term treatment with it: Dupuytren's will be found in half of men having 20 years of pentobarbitone treatment. This is a huge number, and presents a problem: how can this be reconciled with the concept of an inherited disorder if the incidence of pentobarbitone related Dupuytren's is larger than the expected Dupuytren gene pool? Does pentobarbital activate Dupuytren genetic or cytokine pathways in the absence of a genetic risk for Dupuytren's? Once again, more questions than answers. http://www.dupuytrenfoundation.org/DupPDFs/1976_Critchley_1447.pdf

Treatment effectiveness for Dupuytren's needs documentation

Progress into new territory requires an open mind: beware conformity; examine failure; engage outsiders, and be aware of undocumented claims. This interesting report of an injection treatment for Dupuytren's would be worth considering if published in an independent peer reviewed format rather than on the manufacturer's web site: http://www.dupuytrenfoundation.org/DupPDFs/2001_Beller.pdf

Rock Climbing and Dupuytren's - an interesting analysis

Dupuytren's is an inherited systemic disorder of either the threshold or the feedback inhibition of the biology of scar formation, contracture and maturation. It is not spontaneous, but triggered in specific areas having the common characteristic of being subjected to repeated high shearing or stretching forces: palmar fascia, plantar fascia, shoulder capsule, tunica albuginea of the penis. These areas are able to produce the perfect storm of tissue conditions which activate the process. Dupuytren's is not just a reaction to mechanical forces: they are a small, but definite part of the picture, and may just speed up the timescale of activating the process.
http://www.dupuytrenfoundation.org/DupPDFs/2005_Logan_1606.pdf

How the FDA sees Collagenase for Dupuytren's

Why is it taking so long for collagenase injection treatment to be available to treat Dupuytren's? Trials have been ongoing for over 10 years. The answer: collagenase is an extremely potent substance, and the FDA has required very detailed proof not only that it works, but that it is safe, and that it has something to offer better than existing treatment. This FDA presentation provides the actual data from trials on collagenase, the good, the bad and the strange. The bar is pretty low to choose collagenase over fasciectomy, but the question of choosing collagenase over needle aponeurotomy remains unanswered. http://www.dupuytrenfoundation.org/DupPDFs/2009_FDA.pdf

Abstracts can be misleading

Unlike proximal interphalangeal joint contractures from Dupuytren's, metacarpophalangeal joint contractures usually respond so well to fasciectomy or fasciotomy that joint capsule or ligament release is generally not a consideration. Because of this, I was intrigued by the title of this report: a series of patients treated with dermofasciectomy and MP joint release - it's an unusual combination. What I found instead was that the original report must have been lost in translation: the text describes fasciectomy but calls it dermofasciectomy; the pictures show a mix of proximal interphalangeal joint and metacarpopalangeal joint contractures; the statistical analysis reports 1/25 as 2.5% instead of 4% in reporting complications. Reinterpreted along these lines, the results are similar to previous reports of fasciectomy and proximal interphalangeal joint release, which is apparently what this report actually describes. http://www.dupuytrenfoundation.org/DupPDFs/2003_Saleh.pdf

Myofibroblast Biology

Myofibroblast biology is at the heart not only of Dupuytren's, but of other diseases not related to Dupuytren's. Myofibroblasts are major players in pulmonary fibrosis, cirrhosis, renal fibrosis and arteriosclerosis. Studies of myofibroblast biology in these conditions may shed light on potential new treatment strategies for Dupuytren's. Gains in the management of any one myofibroblast related condition may benefit others. This review paper covers myofibroblast biology outside the realm of Dupuytren's and a number of possible targets for biological intervention - for example: could topical nitroglycerin work for Dupuytren's? http://www.dupuytrenfoundation.org/DupPDFs/2007_Hinz_1450.pdf

Pregnancy, Dupuytren's and Relaxin

Relaxin is a natural hormone which does many things and normally increases during pregnancy. It has been shown to have a range of antifibrotic actions: it inhibits collagen synthesis, increases collagenase activity, inhibits the profibrotic factors TGFß and Interleukin1-ß, and prevents fibroblast differentiation into myofibroblasts. How does it work? Is Dupuytren's related to low relaxin levels? Could it have a possible role in treating Dupuytren's? Could pregnancy help prevent Dupuytren's and is that why Dupuytren's is more common in men than women? There are more questions than answers, which is the necessary first step toward progress. http://www.dupuytrenfoundation.org/DupPDFs/2005_Samuel.pdf

A Surgeon's Perspective of Dupuytren's

A very readable review of Dupuytren's Disease from a surgeon's perspective: http://www.dupuytrenfoundation.org/DupPDFs/1985_Hill.pdf

To understand Dupuytren's, first understand women.

Is Dupuytren's a tumor - an independent growth, or is it a reaction of normal tissues to a stimulus? Is a woman one person or several people sharing the same body? This paper answers both questions. Every female human has two X chromosomes, one from each parent, but in any individual cell, only one X chromosome is active, the other permanently inactivated. One X chromosome rules half of a woman's cells, the other rules the other half, and these cells are evenly mixed throughout her body. Now, true neoplastic tumors are clones: one cell reproduces over and over, and so in females all cells of a tumor will have the same active X chromosome. In contrast, reactive tumors are many adjacent cells responding to a common stimulus, and will have a normal mix of active X chromosomes. This fact was used to show that Dupuytren's nodules are not true tumors, not bad cells, but a reaction of normal cells to some stimulus. What is it? http://www.dupuytrenfoundation.org/DupPDFs/2006_Wang_1040.pdf

Fasciotomy versus fasciectomy for Dupuytren's

Fasciectomy and fasciotomy were compared in this study with some interesting observations. Initially after procedure, fasciotomy was better than fasciectomy in straightening fingers, but this advantage was lost over time as fasciotomy had earlier recurrences than fasciectomy. Fasciectomy had better results at correcting PIP joint contractures, both early and late. Recovery time was longer and permanent complications, particularly stiffness, were more common for fasciectomy than fasciotomy: one out of twenty fasciectomy patients lost finger flexion compared to none of the fasciotomy patients. Fasciotomy has evolved considerably since this publication, and it will be interesting to compare fasciectomy with needle fasciotomy and enzymatic fasciotomy when results are available. http://www.dupuytrenfoundation.org/DupPDFs/1976_Rodrigo.pdf

Partial Fasciectomy for Dupuytren's

Dupuytren's patients need two things: first, a way to prevent disease progression and recurrence; second, the simplest, safest way to straighten fingers bent by Dupuytren's. While working and waiting on the first, there are choices for the second. One of these is limited or partial fasciectomy, which has the advantage of quick recovery and low complication rate compared to more extensive fasciectomy. There are several technical variations of this approach. Here's one: http://www.dupuytrenfoundation.org/DupPDFs/1963_Freehafer.pdf

TGF-ß2 and Dupuytren's

What if Dupuytren's is due to slightly abnormal levels of a normal hormone, protein or other molecule in the system? If so, one of the most likely suspects would be Transforming Growth Factor Beta Two: TGF-ß2. This protein is part of the autocrine system (a chemical instant messaging system which lets individual cells communicate with each other) and it has been shown to activate collagen contraction by fibroblasts. This study looked at the behavior of fibroblasts in a 3D living model of normal fibrous tissue, the Fibroblast Populated Collagen Lattice (FPCL), and found that although Dupuytren fibroblasts react more to the effects of TGF-ß2 than normal fibroblasts, they are abnormally active compared to normal fibroblasts even when all TGF-ß2 is removed from the system. Great! One suspect to cross off the list: http://www.dupuytrenfoundation.org/DupPDFs/2004_Tse_1031.pdf

Deformity, aggressiveness and severity of Dupuytren's

When is the most effective time to treat Dupuytren's and what is the best treatment? These are not easy questions. Dupuytren's responds differently and recurs differently in different people: starting with the same deformity (how bent the fingers are), people who do worse are described as having "aggressive" Dupuytren's. Severity is a combination of the measure of deformity and an estimate of aggressiveness. Genes determine whether or not someone will develop Dupuytren's and to a degree how aggressive it will be. External factors, such as alcoholism, amplify aggressiveness. Optimum treatment would be individualized based on severity, but a standard evaluation of all available factors is needed. This report analyzes a new system for estimating severity of Dupuytren's: http://www.dupuytrenfoundation.org/DupPDFs/2008_Hindocha_1014.pdf

Sex and Dupuytren's in Boston

Dupuytren's is fairly common in Boston, but seems different than the European flavor in terms of sex. The numbers on almost 2000 Boston Dupuytren's patients were sorted out, and here's how things roll in Boston: men develop Dupuytren's almost twice as often as women, but it may seem like more because men tend to get the disease at a younger age, are almost twice as likely to have surgery if they do get Dupuytren's, and are more likely to have recurrences after surgery. Why? http://www.dupuytrenfoundation.org/DupPDFs/2007_Anthony.pdf

Monkey model for Dupuytren's

An experimental monkey model of Dupuytren's Disease was performed to confirm or refute the microtrauma hypothesis of Dupuytren's. The outcome: the reaction to rupture of the palmar fascia produced lesions identical to those of early Dupuytren's, although did not lead to contractures during the period of study. The conclusion was that trauma is not the entire picture: "...it seems possible that certain individuals have some alteration of their connective tissues that causes these tissues to respond in an abnormal manner ...to microruptures". http://www.dupuytrenfoundation.org/DupPDFs/1960_Larsen_1088.pdf

What's old is new in Dupuytren's

Larsen's insightful study and review of the demographics and microscopic anatomy of Dupuytren's disease is over 50 years old, but reads like a recent publication. The author describes and ponders the significance of topics which were well known at the time: perivascular inflammation adjacent to but not within the affected areas; iron pigment in the center of active nodules. Non operative treatment with enzyme injections, nutritional supplements, radiotherapy are all discussed. Fasciotomy, fasciectomy and dermofasciectomy with skin graft are described and compared as are problems of postoperative stiffness and recurrence. Koch, Bruner, Boyes and Meyerding all comment. Fascinating, clear and delightful. http://www.dupuytrenfoundation.org/DupPDFs/1958_Larsen.pdf

Nice Overview of Dupuytren's

Time to pause and look at the big picture. Here is a balanced overview of the history, biology, etiology and epidemiology of Dupuytren's Disease: http://www.dupuytrenfoundation.org/DupPDFs/2003_Thurston.pdf

The potential of cryotherapy and Dupuytren's

Myofibroblasts are part of the normal tissue repair response to almost all injuries: cut, crush, burn, chemical injury, infectious gangrene, and others - with one exception: freeze injury. Freeze burns don't contract, possibly because only in freeze injury, the original collagen matrix scaffold is preserved, which may inhibit myofibroblast formation: http://www.dupuytrenfoundation.org/DupPDFs/1984_Ehrlich.pdf. This makes cryotherapy a potential treatment for Dupuytren's related nodules: it might just turn the process off. The problem is how to precisely control the extent of freeze injury: freeze both finger arteries, no more finger. The anatomy of foot involvement is different than the hand, and there is some experience with treating Dupuytren's half-brother, Ledderhose, with cryotherapy. It looks encouraging: http://www.dupuytrenfoundation.org/DupPDFs/2005_Goldstein.pdf.

Is Dupuytren's work related?

A specific gene has not been definitively associated with Dupuytren's, but the best evidence suggests that the primary cause is genetic. There are factors which alter risk, such as diabetes and local trauma, but these are minor compared with the underlying genetic risk. The question of causation is not simply academic: since the time of Dupuytren, lawsuits have been filed to claim payment for Dupuytren's Disease as a work-related injury. Unlike the laws of Man, the laws of Nature are not altered by argument, but the courts continue to debate the issue, as shown in this recent court document: http://www.dupuytrenfoundation.org/DupPDFs/2008_Bridgett.pdf

Vitamin E treatment of Dupuytren's Contracture

Treating Dupuytren's with vitamin E. Does it work? No, according to this 50 year old study, documenting results with before and after plaster casts of the bent fingers. The results: no improvement in the degree of contracture. This is a pretty straightforward clearly documented study, which answers the question "Does three months of vitamin E therapy help straighten fingers bent by Dupuytren's?" Apparently not. It doesn't answer the much more difficult question "Does vitamin E therapy prevent progression of Dupuytren's contracture?". I'd still like to know: http://www.DupuytrenFoundation.org/DupPDFs/1952_Richards_1269.pdf

Not your typical Viking's Dupuytren's

In the Viking era, boats from what is now Denmark travelled west across the North Sea to invade what is now Great Britain, but boats from what is now Sweden travelled south across the Baltic Sea and took rivers deep into what is now southern Europe, where they may have left a genetic trail. This southern European survey shows that the prevalence of Dupuytren's in Bosnia and Herzegovina is higher than one might expect, with a somewhat different age distribution compared to surveys of northern Europe, and the novel finding of a predominance of right hand involvement: http://www.dupuytrenfoundation.org/DupPDFs/2004_Zerajic_1030.pdf

Cell biology and faulty brakes in Dupuytren's

TGF-beta is a protein which lets some cells boss other cells around. It's manufactured and released by some cells, and other cells change what they are doing when they notice that TGF-beta is around. TGF-beta does different things to different cells, always in a domino effect. For example, fibroblasts respond to TGF-beta by accumulating the protein beta-catenin inside the cells, which then triggers another protein, TCF/LEF, inside the cell nucleus to turn on certain genes which then change what that cell does and looks like. See? Dominos. This study reveals an automatic braking system: Normally, TGF-beta triggers fibroblasts to make collagen, and then that collagen steps on the brakes by blocking TGF-beta. This study suggests how this braking system may be broken in Dupuytren's: Not only are Dupuytren's fibroblasts more sensitive to TGF-beta than regular fibroblasts, but Dupuytren fibroblasts manufacture a different mix of collagen (type 1 and type 3) than normal fibroblasts (only type 1), which may not have the same regulatory effect. More studies are in the works - very exciting! http://www.dupuytrenfoundation.org/DupPDFs/2009_Vi.pdf

Oxygen Free Radicals and Dupuytren's

Oxygen free radicals affect Dupuytren's fibroblasts: high levels are toxic, but not only do slightly elevated levels stimulate fibroblast activity, active fibroblasts actually produce oxygen free radicals. Which is the chicken and and which is the egg? This seminal paper reports studies of the effects of oxygen free radicals on Dupuytren and normal fibroblasts, the effect of blocking free radicals with free radical scavengers, and brings up the relationship between mechanical forces, oxygen free radicals and abnormal fibroblast proliferation in Dupuytren's: http://www.dupuytrenfoundation.org/DupPDFs/1990_Murrell_1203.pdf. Cause and effect? We still need to know - more work to do.

Viking blood, blue eyes and other risk factors for Dupuytren's

What is the actual story of the Vikings and Dupuytren's? The full history will never be known, but some fascinating details on this and other risk factors, including blue eyes, are reviewed here: http://www.dupuytrenfoundation.org/DupPDFs/2001_Flatt_1397.pdf. See page 4 for a decision tree showing how to predict the risk of recurrence after surgery based on family history, bilaterality, age of onset and involvement of other areas.

Sorting out the truth

Don't believe everything you read about Dupuytren's - even in respectable journals. I was aware that reflex sympathetic dystrophy (complex regional pain syndrome) was more common after fasciectomy for Dupuytren's than for other hand operations, but there is little published on this. Then, this report came out documenting surprisingly high incidence of this complication, higher than I would have guessed: http://www.dupuytrenfoundation.org/DupPDFs/2006_Reuben_499.pdf. Sadly, the lead author on this and several other academic papers was found to have falsified data, and the accuracy of this particular report will never be known. Too bad - I'd still like to know what the actual numbers were.

Lessons from Peyronie's for Dupuytren's

Peyronie's disease is more common than Dupuytren's - 3 to 9 percent of the population - and shares a similar biology and genetic predisposition. Progress in the treatment of Peyronie's will benefit that of Dupuytren's and vice versa. Taken in this context, these two articles by Hellstrom from 2000 and 2009 are very thought provoking. Animal model? Oral, topical or intralesional medication? Radiation? Shockwave treatment? Could these be applied to Dupuytren's?
http://www.dupuytrenfoundation.org/DupPDFs/2000_Hellstrom.pdf
http://www.dupuytrenfoundation.org/DupPDFs/2009_Hellstrom_397.pdf

Looking at Dupuytren's with MRI

Where is Dupuytren's? It's been known for some time that Dupuytren's involvement can be identified by MRI, as described in these articles:
http://www.dupuytrenfoundation.org/DupPDFs/1993_Yacoe_813.pdf
http://www.dupuytrenfoundation.org/DupPDFs/1994_Miller.pdf
and it's likely that the activity of the process could be mapped, both for predictive value and for targeted treatment to prevent progression. Now, these papers are 15 years old - it's time to revisit this with more up-to-date imaging technology to look again at the usefulness of MRI and Dupuytren's in a longitudinal study - might make a nice PhD thesis...

The Fish Technique for Dupuytren's: Fasciectomy and Skin Graft

Skin grafts are used in a variety of approaches for Dupuytren's: to add skin where it has been shortened (fasciotomy and skin graft, fasciectomy and skin graft); to replace skin where it has been removed to prevent recurrence (dermofasciectomy and skin graft). This study reviews the results of fasciectomy and skin graft. The recurrence rate was better than simple fasciectomy: 7% recurrence rate at four years. The study also reminds us that for Dupuytren's, even smart surgery by skilled surgeons has significant downsides: three of ten patients lost some feeling in their fingers and four out of ten had cold sensitivity as a direct result of surgery. We need even better treatment options.
http://www.dupuytrenfoundation.org/DupPDFs/2006_Roy.pdf

Accidental fasciotomy for Dupuytren's

Fingers bent by Dupuytren's can complicate a fall on an outstretched hand: because the fingers can't stretch back, the force of impact is redistributed, making it more likely to break hand bones. When the fall is hard enough to break something, occasionally what gives is not bone, but the Dupuytren cord. This usually is accompanied by a tear in the skin. Although the final outcome is often surprisingly good, it's not recommended as a primary treatment. This report describes a patient with an unusual traumatic partial rupture of a Dupuytren's cord: http://www.dupuytrenfoundation.org/DupPDFs/1995_Darcangelo.pdf

No advantage to open Proximal Interphalangeal Joint release for Dupuytren's

Proximal interphalangeal joint contractures from Dupuytren's disease take on a life of their own, persisting after the Dupuytren's has been removed. One of the arguments for open fasciectomy is that PIP contractures can be treated by openly releasing the tight joint capsule and ligaments. Unfortunately, gains made in the operating room are lost during the recovery period, and after the dust settles, open joint releases for PIP contractures associated with Dupuytren's are ineffective in the long run, as reviewed in these three reports from three different institutions:
http://www.ncbi.nlm.nih.gov/pubmed/8596787
http://www.ncbi.nlm.nih.gov/pubmed/15142694
http://www.ncbi.nlm.nih.gov/pubmed/14734062

Dupuytren's and Burns

Dupuytren's overlaps in some ways with the local excessive scarring which occur after a burn injury. This report documents the development of progressive Dupuytren's disease developing in a young man after a hand burn, and reviews the conventional teachings regarding Dupuytren's: http://www.dupuytrenfoundation.org/DupPDFs/2008_Balakrishnan_1422.pdf

Gene Expression in Dupuytren's

If Dupuytren's is inherited, what are the genes involved? Difficult question. Every cell in a person's body has the same genes, but every cell is not the same. The differences between cells are not from different genes, but from differences in gene expression: every cell in the body is like a tiny computer; chromosomes are the hard drive and genes are the programs on that hard drive, and to this extent, every cell in a person's body is identical. However, just as two identical computers can run different programs, different genes being expressed are like different programs running. Cells involved with Dupuytren's are running the wrong programs. Just looking at the genes doesn't tell what is actually going wrong - it's necessary to look at the programs which are running, which genes which are being "expressed". This study documents progress in the effort to identify gene expression associated with Dupuytren's, the master key to the puzzle: http://www.dupuytrenfoundation.org/DupPDFs/2008_Satish_1556.pdf

ß-catenin, Wnt and Dupuytren's

Ultimately, Dupuytren's has to do with cell signalling: normal cells are somehow instructed ("signalled") to become abnormal, and adjacent cells interact with each other in a progression of abnormal changes. One of the many ways that cell signal each other is the Wnt signaling pathway, which involves a series of proteins which trigger cascades of events inside individual cells. One of these proteins is ß-catenin. ß-catenin is associated with some processes in which cells physically attach to each other. It can also affect the cell nucleus and activate specific genes. ß-catenin builds up abnormally in Dupuytren cells and may be part of the cause. What causes this? The Wnt pathway is a likely candidate: some ß-catenin interactions are involved in the Wnt pathway. However, this study appears to show that abnormal ß-catenin levels in Dupuytren cells are not due to effects of the Wnt pathway, which brings a better understanding of the biology: one suspect crossed off of the list: http://www.dupuytrenfoundation.org/DupPDFs/2006_O'Gorman_1565.pdf

Stretching may provoke Dupuytren's

The relationships between mechanical forces and the biochemistry of Dupuytren's are only recently being sorted out. Clinically, Dupuytren's activity responds to changes in mechanical stresses: active nodules soften in response to reducing tension by adjacent fasciotomy; disease activity after fasciectomy may be provoked by overly aggressive stretching and splinting. Biochemically, this may relate to the finding that, in contrast to cells from normal fascia, cells from Dupuytren's tissue produce ß-catenin and fibronectin in response to stretching forces: http://www.dupuytrenfoundation.org/DupPDFs/2003_Howard_1029.pdf

The Open Palm Technique for Dupuytren's

The Open Palm Technique for Dupuytren's contracture has advantages - lack of hematoma, lower incidence of sympathetic dystrophy. The classic McCash version of this procedure combines closure of zigzag finger incisions, leaving transverse palm wounds open. The Burkhalter version, developed by Dr. Mann, employs only transverse incisions in the palm and fingers, all of which are left open. Proponents of the Burkhalter technique believe that it leads to fewer recurrences, but there are no studies yet to back this up. Available evidence suggests that individual patient biology is the main influence on recurrence and that the incidence of some complications varies with procedure. This study of the McCash open palm technique confirms that the rates of complications (21%) and recurrence (33% at 2 1/2 years) remain issues even the hands of experienced surgeons: http://www.dupuytrenfoundation.org/DupPDFs/1994_Cools.pdf

Chondroitin Sulfate, Dermatan Sulfate and Dupuytren's

Dermatan sulfate is similar to the nutritional supplement chondroitin sulfate, and used to be called chondroitin sulfate. Dermatan sulfate is unusually abundant in fascia affected by Dupuytren's. Is it the cause or is it the effect of the abnormal biology of Dupuytren's? Maybe both, as discussed in this review: http://www.dupuytrenfoundation.org/DupPDFs/2007_Kozma.pdf

Open fasciotomy for Dupuytren's

 Patients with Dupuytren's need two things, mechanical and biological. The former, a simple and safe way to straighten bent fingers, and the latter, a way to prevent disease progression and recurrence. This article reviews pros and cons of a simple mechanical treatment, open fasciotomy, for severe contractures in a group of elderly patients: http://www.dupuytrenfoundation.org/DupPDFs/2007_Jablecki.pdf

Genetic determined biochemistry and Dupuyren's

The genetic basis of Dupuytren's is explained by the genetic basis of individual biochemistry and enzymatic variation. Sort of. This fascinating review shows how complicated this can be: http://www.dupuytrenfoundation.org/DupPDFs/2008_Zyluk.pdf

Verapamil, tamoxifen, carnitine - options?

One resource for potential medical treatment of Dupuytren's is the literature on medicines which work for related conditions such as Peyronie's. This review examines the rationale and results of propionyl-L-carnitine, acetyl-L-carnitine, verapamil and tamoxifen in treating Peyronie's disease. Is there a role for these in Dupuytren's? http://www.dupuytrenfoundation.org/DupPDFs/2002_Cavallini.pdf

Dupuytren's and Frozen shoulder

About one in six patients with frozen shoulder will also have Dupuytren's disease and vice versa. Frozen shoulder has been called "Dupuytren's of the shoulder": the abnormal tissues are quite similar. However, they are different in other respects - for example, Dupuytren's commonly recurs after surgical treatment, but frozen shoulder does not. This study demonstrates how biomechanical tissue responses to stimulation differs in these two conditions, which may help explain this: http://www.dupuytrenfoundation.org/DupPDFs/2006_Bains_43.pdf

Vascular cause of Dupuytren's?

Diabetes, hypertension, stiff finger joints and Dupuytren's: This study uses retinopathy as an index of vascular disease and suggests that small vessel disease, rather than the effect of blood sugar on collagen, is the link between diabetes and Dupuytren's: http://www.dupuytrenfoundation.org/DupPDFs/1986_Larkin_1218.pdf

Peyronie's Disease and Dupuytren's

Dupuytren's is one manifestation of a systemic fibrotic disorder that can also show up as Ledderhose, frozen shoulder or Peyronie's disease. Fortunately, the majority of people affected show only one of these conditions, but many have to deal with several or all of these. This summary reviews the condition referred to as Peyronie's disease: http://www.dupuytrenfoundation.org/DupPDFs/2009_NIDDK.pdf

A landmark advance in understanding Dupuytren's

Two methods of investigating Dupuytren's have been used: Demographic - family studies, associations with medications, activities, other diseases; and Biological - tissue analysis. The big biologic breakthrough came in 1972 when Gabbiani and others published two articles back to back findings on the biology of myofibroblasts:
http://www.dupuytrenfoundation.org/DupPDFs/1972_Gabbiani_719.pdf
and the role of myofibroblasts in Dupuytren's Disease:
http://www.dupuytrenfoundation.org/DupPDFs/1972_Gabbiani_1115.pdf
We need more breakthroughs like this to develop biologic treatments for Dupuytren's.

Smooth Muscle Actin in Dupuytren's Contracture

The palmar fascia in Duputren's contracture does not contract like a muscle: it's more like the effect of an army of tiny rachets. Adjacent parallel strands of collagen are grabbed by myofibroblasts, which then shorten ("crimp") lengthwise, pulling the strands to overlap more and more, and then gluing these strands together with crosslinks. Crimp, lock, crimp, lock, shortening the fabric in one direction. Crimping is accomplished by the action of one type of smooth muscle actin (SMA) inside myofibroblast cells. This study looks at the presence of SMA in Dupuytren's tissues, and suggests that one of the five types of platelet derived growth factor, PDGF-BB, might be used to selectively block SMA and prevent contracture:
http://www.dupuytrenfoundation.org/DupPDFs/2003_Hindman_1072.pdf

CMMS therapy for stiffness after fasciectomy for Dupuytren's

Stiffness is a common problem after fasciectomy, particularly loss of flexion, and can be resistant to stretching exercises or splints. This therapy program, incorporating a combination of casting and active exercises, helped patients regain motion when they had failed conventional hand therapy: http://www.dupuytrenfoundation.org/DupPDFs/2007_Rose.pdf

NICE evaluation of needle aponeurotomy for Dupuytren's

The source of medical information is critical; objectivity is essential. That's one of the advantages of the UK's NHS independent review process. Read their assessment of needle aponeurotomy:
http://www.dupuytrenfoundation.org/DupPDFs/2004_NICE.pdf

Drugs that provoke Dupuytren's Disease

Looking for ways to stop Dupuytren's, it should be useful to look in reverse at factors which may start it, such as protease inhibitor drugs, as reported here: http://www.dupuytrenfoundation.org/DupPDFs/2002_Florence_1607.pdf

Dupuytren's, Mast cells, Substance P

Dupuytren's is not always painless. Sometimes, active areas itch and burn. This goes along with the finding of elevated levels of mast cells and nerve fibers containing substance P - something also found in interstitial cystitis. Find out more at http://www.dupuytrenfoundation.org/DupPDFs/2006_Schubert_1071.pdf

Aggressive Dupuytren's Disease

This report of Dupuytren's extending from the palm into the forearm reviews the anatomy of involvement and points out the aggressive nature of Dupuytren's in young people. We need more effective biologic treatments: http://www.dupuytrenfoundation.org/DupPDFs/1997_Sinha_1048.pdf

Dupuytren' s Contracture - Microscopic Analysis

This is a classic article on the biology of Dupuytren's. Structural changes in the palmar fascia are associated with type III collagen, which isn't normally found in this tissue. Myofibroblasts are likely the source of this and are associated with disease recurrence.Most important quote: "Clinical recurrence was not related to the age of
the patient at onset, duration, or severity of disease. Recurrence was related to the electron microscopic
findings of myofibroblasts in the nodules and fibroblasts containing prominent microtubules in the fascia
of these patients." Wouldn't it be great to have a way to have this assessment before treatment?
http://www.dupuytrenfoundation.org/DupPDFs/1980_Gelberman_425.pdf

Dupuytren Symposium Website is Live!

The website for the 2010 International Symposium on Dupuytren's Disease is now live, accepting on line registration and submission of abstracts for presentation. http://www.DupuytrenSymposium.com

Dupuytren Foundation is now a Public Charity

It's taken almost two years to wade through the red tape, but hot off the press, The Dupuytren Foundation is finally officially certified as a 501(c)3 Public Charity! See http://dupuytrenfoundation.org/act.htm for documentation.

First International Dupuytren's Symposium

Plans are underway to organize the first International Symposium on Dupuytren's Disease, to be held in South Florida May or June 2010, coordinated jointly by the Dupuytren Foundation and the Dupuytren Society. The goal of the symposium is to raise awareness regarding Dupuytren's disease and related conditions and to promote cooperative efforts to find a cure.
Dupuytren's is the most common of the fibrosing diseases, and inroads into its treatment have potential impact in the management of more life threatening conditions with similar biology. The symposium will be a gathering of researchers and clinicians with a wide spectrum of interests: cell biology, genomics, surgery, pharmacotherapy, radiotherapy, biomechanics - as they relate to Dupuytren's and related conditions. It will be a way to share insights and discuss potential new approaches to work for a cure.

Dupuytren's Skin Graft Controversy

Skin grafting is a time honored technique in the range of options to reduce the incidence of recurrence after fasciectomy for Dupuytren's contracture. There are two general approaches. One is dermofasciectomy: remove a large area of affected skin and resurface the area with a similarly large skin graft. The other is to put in a smaller skin graft to break up the line of pull of the original cord, a firebreak skin graft. Several studies have documented the superiority of dermofasciectomy over fasciectomy, but what about firebreak grafts? Hot off the press, a controlled study http://www.ncbi.nlm.nih.gov/pubmed/19258615?dopt=Abstract reports that fasciectomy with firebreak skin graft doesn't improve results compared to fasciectomy alone. Hmmmph!

Genetic studies are underway for Dupuytren's

The goal of the collaboration of the Dupuytren Foundation and Scripps Research is to identify the genes responsible for Dupuytrens and then develop a targeted intervention to make them stop doing that. Our DNA is like a computer, and our genes are the programs that are either running (upregulated) or not running (downregulated). The genes that result in Dupuytren's are chromosomal malware - a bad program or bad programs. Progress is being made http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2377253&blobtype=pdf with a small number of samples. The Scripps DNA project anticipates a DNA sample selection 10 to 100 times larger than what has been previously available. The future looks bright. We will find a cure.

Hand therapy and splinting are usually a big part of recovery after open surgery for Dupuytren's contracture. Despite a drive for evidence based medicine, evidence for the effectiveness of splinting after open Dupuytren's surgery is still elusive. Debbie Larson and Christina Jerosch-Herold review the issue in this article (link to full text pdf): Clinical effectiveness of post-operative splinting after surgical release of Dupuytren's contracture: a systematic review

Dupuytren's Foundation and Scripps Research

The Dupuytren's Foundation http://www.dupuytrenfoundation.org has officially partnered with Scripps research to establish a DNA bank of tissues affected by Dupuytren's disease. This will be available to researchers interested in studying Dupuytren DNA. So far, 20 samples have been collected. If the gene is identified, progress toward acure will be greatly streamlined. Very exciting. Interested in donating your DNA to the cause? Contact The Hand Center http://www.handcenter.org 561-746-7686