Arthrofibrosis, student in need of information

[amnsmit]

Hello everyone,
I am a PT student and am doing research about arthofibrosis. I am doing my studies in the Netherlands and have found out that the PTs here are not aware of arthrofibrosis, some don't even know what it is. During my research I have found many american and German sites. Is there anyone here who knows of if there is a standard treatment protocol? Is PT alone enough to help those with arthrofibrosis?
I hope someone can help! :)

Thank You,
Annemarie

[bernard]

Hello Annemarie and welcome on SomaSimple,

I must admit that the last patient with such a condition was seen at the office in 1980. :oops:
I found some interesting papers =>

http://www.physsportsmed.com/issues/2001/03_01/eakin.htm

http://www.ajronline.org/cgi/content/abstract/182/2/337

http://www.physioroom.com/experts/expertupdate/interview_dshelbourne_20030701_2.php

http://www.ajsm.org/cgi/content/full/29/6/822

I'm digging a bit more with pubmed and gives the results in a few.

Nari and Diane may have some replies to add there?

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15378321

Arch Orthop Trauma Surg. 2004 Nov;124(9):585-91. Epub 2004 Sep 18. Related Articles, Links


alpha-Smooth muscle actin containing contractile fibroblastic cells in human knee arthrofibrosis tissueWinner of the AGA-DonJoy Award 2003.

Unterhauser FN, Bosch U, Zeichen J, Weiler A.

Sektion Sporttraumatologie & Arthroskopie, Unfall- & Wiederherstellungschirurgie, Charite, Campus Virchow-Klinikum, Humboldt Universitat, Augustenburger Platz 1, 13353, Berlin, Germany, frank.unterhauser@charite.de.

INTRODUCTION. Primary arthrofibrosis is of major concern after joint trauma or knee ligament surgery. The underlying mechanism in detail remains unclear. Highly differentiated fibroblastic cells, so-called myofibroblasts, express the actin isoform alpha-smooth muscle actin (ASMA) and have been found to play a major role in tissue contraction during wound healing and organ fibrosis. We therefore studied the expression of myofibroblasts in human primary knee arthrofibrosis tissue. MATERIALS AND METHODS. Tissue samples were taken from the infrapatellar fat pad and intercondylar region of nine patients who underwent revision surgery due to arthrofibrosis after anterior cruciate ligament (ACL) reconstruction (study group). Control tissue was taken from five patients who underwent primary ACL reconstruction (control group I) and from eight patients, who underwent second-look arthroscopy after primary ACL reconstruction (control group II). ASMA containing fibroblasts were immunostained with a monoclonal antibody. Histomorphometry was performed for total cell amount, ASMA containing fibroblasts, and vessel cross-sections. RESULTS. The arthrofibrosis group showed a tenfold higher amount of ASMA containing myofibroblasts (23.4% vs. 2.3%) than in control group I. There was a significantly higher total cell count and lower vessel density than in control group I. Control group II showed an upregulation of myofibroblasts almost five times that in control group I; nevertheless there was no evidence of scar formation or tissue fibrosis. CONCLUSIONS. Myofibroblasts are responsible for scar tissue contraction during wound healing. In arthrofibrosis tissue fibroblast contraction may be involved in tissue fibrosis and contraction with consecutive loss of motion. We found that myofibroblasts are upregulated in arthrofibrosis tissue. ACL reconstruction itself caused an up regulation of myofibroblast content. Nevertheless these patients did not show any clinical or histological signs of arthrofibrosis. Thus it is reasonable to assume that the ratio of myofibroblasts and total cell amount in connective tissue are responsible for the onset of arthrofibrosis. Address the expression of this highly differentiated cell type may therefore present a target for future therapeutic interventions.

PMID: 15378321 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15122136

Arthroscopy. 2004 May;20(5):469-73. Related Articles, Links


Screening for arthrofibrosis after anterior cruciate ligament reconstruction: analysis of association with human leukocyte antigen.

Skutek M, Elsner HA, Slateva K, Mayr HO, Weig TG, van Griensven M, Krettek C, Bosch U.

Laboratory of Histology and Cell Biology, Department of Traumasurgery, Hannover Medical School, Hannover, Germany. skutek@aol.com

PURPOSE: Arthrofibrosis represents a severe complication of trauma and reconstructive joint surgery because of generalized connective tissue proliferation resulting in painful joint stiffness. It often appears stereotypical in terms of its clinical and pathologic features, comprising excess deposition of extracellular matrix proteins such as collagen type I, III, and VI and proliferation of fibroblasts. However, trauma and surgery around joints does not always lead to fibrosis, suggesting a genetic predisposition. For a number of autoimmune diseases, strong associations have been described. The objective of the study was to investigate whether an association of HLA (human leukocyte antigen) with primary arthrofibrosis exists. TYPE OF STUDY: Retrospective cohort study. METHODS: Seventeen patients with primary arthrofibrosis after autologous anterior cruciate ligament (ACL) reconstruction were identified and clinically reviewed. Blood samples were taken, and DNA was isolated by column extraction method. DNA samples were typed for the loci HLA-A, -B, -C, -DRB1, and -DQB1. Results were compared with the frequencies of allelic groups as determined for the caucasoid population. RESULTS: HLA-Cw*07 was significantly less often found in the patient group than in the general population (P =.022). The opposite effect was seen for Cw*08, which was found in 17.6% of the patient group but only in 3.8% of the reference group (P =.045). A significant difference was also seen for DQB1*06, because 23.5% of the patients but 48.6% of the reference group possessed an allelic variant of this group (P =.048). However, according to the relatively small number of patients, a statistical bias cannot be excluded. CONCLUSIONS: A possible link may exist between arthrofibrosis and HLA-Cw*07- and DQB1*06-negative as well as Cw*08-positive individuals. Further investigation is necesessary to confirm or vitiate the possible association. LEVEL OF EVIDENCE: Level IV.

PMID: 15122136 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12690864

Instr Course Lect. 2003;52:369-81. Related Articles, Links


Arthrofibrosis of the knee following ligament surgery.

DeHaven KE, Cosgarea AJ, Sebastianelli WJ.

Department of Orthopaedics, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.

Arthrofibrosis of the knee is one of the most serious complications that can result from ligament surgery. Reported incidence of arthrofibrosis following anterior cruciate ligament reconstruction ranges from 4% to 35%. The loss of motion caused by arthrofibrosis can be even more disabling than the instability for which the reconstruction was performed, often requiring extensive physical therapy and/or surgical lysis of adhesions. With aggressive rehabilitation and modifications in the bracing of knees undergoing ligament reconstruction, the incidence of this complication has decreased significantly. Additionally, delaying anterior cruciate ligament reconstruction until the acute inflammatory period has resolved has also been shown to be a significant factor in the reduction of postoperative knee stiffness.

Publication Types:
Review
Review, Tutorial

PMID: 12690864 [PubMed - indexed for MEDLINE]

[nari]

I can't really add anything more, Bernard, as these articles seem to cover the condition well.

It has a rather high percentage of occurence with ACLRs - around 10-12% from memory.

It is iatrogenic, it would seem, resulting from too early intervention of surgery and not waiting until the knee has become non-irritable. Surgeons used to wait until months and months down the track before repair - now it is a rush to get the owner of the knee 'back to fitness'...?


Nari

[bernard]

Nari,

It is a fate! Our world is going to fast and people are in a hurry!
Now, because I have some knowledge about neurodynamics, I'm very soft with ACL patients and we gain more quickly ROM with no pain at all!

The surgeons do not undertand the stuff, here (I'm not following the hurting protocol).

[nari]

I have seen a patient (18yo female) with arthrofibrosis very recently (last week and then again this week). This prompted some digging in the literature, and although so far I have only read one article, Nari's summary is very good. The study was a German study (2004), looking at about 250 ACL reconstruction patients and risk factors for complications. The biggets risk factors were:

early surgery (they stated within 4 weeks of injury)
irritation in the joint (I assume the presence of ongoing inflammation)
loss of range of motion at time of surgery
early muscle retraining

The patient I saw developed stiffness in the knee after the ACLR. She was having physiotherapy and doing hydrotherapy, but without great gains. She then had an arthroscopy, and the operation report quotes extensive scarring within the knee joint, with the intercondylar notch full of adhesions. The ACL graft was intact. The surgeon cleared the adhesions and performed a manipulation under anaesthesia (before the arthroscopy) quoting "audible tearing of adhesions". Unfortunately, the patient is really not much better. Her ROM is 10-25 degrees, with a soft extension end-fee but a solid flexion end-feel. After some training, she was able to relax her quadriceps (verified with sEMG and palpation) but despite this flexion remained unchanged with active, passive, or post-isometric relaxation attemps

Aside from seeing me for an opinion (she was refered because there was a suspicion of CRPS), she has been going to another physiotherapist three times a week. It doesn't seem to be helping. I don't know what the prognosis is. She has no resting pain, no spontaneous pain, no features of sympathetic dystrophy. It only hurts when knee flexion is attempted. I did not think I could offer any assitance.

Pablo

[fapt]

Hi amnsmit

It is a interesting topic here. I have never heard this before.
I try to look some papers told this disease...
PT needs to open mind to search some new fields and develop the professional...
This is a good way to talk about another unusually topic :)

By the way, where is the Netherlands ...
Can you shoe me your country map?
:oops:
Thanks

[bernard]

Lin,

The Netherlands is situated in Europe close to Belgium and France.

[bernard]

Hi Again,

It is a quite a rare condition in France, I saw 3 cases in 25 years but because rehabilitation needs to be more productive, it is possible the trend changes in the bad direction?

[fapt]

hi all
this is a rare case in the word, and in Taiwan, there are not many this kind of patients. I have never seen before... Maybe fewer patients in Taiwan.

[oljoha]

Hello everyone,
I am a PT student and am doing research about arthofibrosis. I am doing my studies in the Netherlands and have found out that the PTs here are not aware of arthrofibrosis, some don't even know what it is. During my research I have found many american and German sites. Is there anyone here who knows of if there is a standard treatment protocol? Is PT alone enough to help those with arthrofibrosis?
I hope someone can help! :)

Thank You,
Annemarie

Welcome. What shool and where are you from? I studied in Eindhoven... long time ago...

Ole