Can we predict who’s going to get arthritis?


Two studies have recently been published that may help us better predict who is at risk for developing arthritis.

The first study, published in the August 2009 edition of Arthritis & Rheumatism  involved an analysis of 912 healthy individuals, including 60 who had severe osteoarthritis that led to knee or hip replacement between 1990 and 2005.  Those study volunteers who had high levels of vascular cell adhesion molecule 1 (VCAM-1) at the start of the study were most likely to require a joint replacement.  VCAM-1 is expressed in cartilage and other connective tissue.  Lead author Georg Schett from the University of Erlangen-Nuremburg in Germany stated, “The level of VACAm-1 emerged as a significant predictor of the risk of joint replacement due to severe OA, equaling or even surpassing the effects of age.”

This study was the first to establish a laboratory biomarker for the risk of severe osteoarthritis.

Biomarkers are tissue markers that have predictive value either as an indicator of likelihood of disease or even a predictor of likelihood of response to a given therapy.

Another study, appearing in the February 2010 issue of Arthritis & Rheumatism,  was one where researchers in Sweden analyzed the blood samples of 342 people, 86 of whom went on to develop rheumatoid arthritis up to five years after giving blood. Overall, the people who ultimately developed rheumatoid arthritis had higher levels of cytokines (immune-related protein messengers) and other substances involved in inflammation in their blood compared to those who didn’t develop the disease.

“Our findings present an opportunity for better predicting the risk of developing RA and possibly preventing disease progression,” concluded Dr. Rantapää-Dahlqvist, one of the authors.

The nice thing about both studies is the possible predictive value.  Knowing ahead of time who is at risk can certainly help clinicians keep a closer eye on symptoms.

Blood biomarkers, in general, though, have weak predictive value when it comes to treatment. What is lacking is a good library of tissue biomarkers (biomarkers from joint tissue) which can help predict what therapy a patient will best respond to.

We are currently involved in a number of studies at our center to identify those tissue  biomarkers in patients with  various forms of arthritis.

If you have rheumatoid arthritis or osteoarthritis, please contact us to see if you might be eligible for one of these studies.  You can call us at 301 694 5800 or email us at aocmd@aocm.org.

Or just leave a message here.


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Does SAM-e Work for Osteoarthritis


I’m an osteoarthritis junky.  Whatever I can find that might work, I look at.  Many patients have told me that take SAM-e.

All I’ve been able to find is anecdotal reports.

The Cochrane Report recently came out with their analysis of the existing data.  The Cochrane report is really the final word.  They do an exhaustive analysis of everything and their conclusions are usually excellent.  They looked at SAM-e and this is what they found…

OBJECTIVES: We set out to compare S-Adenosylmethionine (SAMe) with placebo or no specific intervention in terms of effects on pain and function and safety outcomes in patients with knee or hip osteoarthritis.

SEARCH STRATEGY: We searched CENTRAL, MEDLINE, EMBASE, CINAHL and PEDro up to 5 August 2008, checked conference proceedings and reference lists, and contacted authors.

SELECTION CRITERIA: Randomised or quasi-randomised controlled trials that compared SAMe at any dosage and in any formulation with placebo or no intervention in patients with osteoarthritis of the knee or hip.

DATA COLLECTION AND ANALYSIS: Two independent authors extracted data using standardised forms. We contacted investigators to obtain missing outcome information. We calculated standardised mean differences (SMDs) for pain and function, and relative risks for safety outcomes. We combined trials using inverse-variance random-effects meta-analysis.

MAIN RESULTS: Four trials including 656 patients were included in the systematic review, all compared SAMe with placebo. The methodological quality and the quality of reporting were poor. For pain, the analysis indicated a small SMD of -0.17 (95% CI -0.34 to 0.01), corresponding to a difference in pain scores between SAMe and placebo of 0.4 cm on a 10 cm VAS, with no between trial heterogeneity (I(2) = 0). For function, the analysis suggested a SMD of 0.02 (95% CI -0.68 to 0.71) with a moderate degree of between-trial heterogeneity (I2 = 54%). The meta-analyses of the number of patients experiencing any adverse event, and withdrawals or drop-outs due to adverse events, resulted in relative risks of 1.27 (95% CI 0.94 to 1.71) and 0.94 (95% CI 0.48 to 1.86), respectively, but confidence intervals were wide and tests for overall effect were not significant. No trial provided information concerning the occurrence of serious adverse events.

AUTHORS’ CONCLUSIONS: The current systematic review is inconclusive, hampered by the inclusion of mainly small trials of questionable quality. The effects of SAMe on both pain and function may be potentially clinically relevant and, although effects are expected to be small, deserve further clinical evaluation in adequately sized randomised, parallel-group trials in patients with knee or hip osteoarthritis. Meanwhile, routine use of SAMe should not be advised.

To see the whole post, go to the Medscape post…

http://www.medscape.com/medline/abstract/19821403?cid=med&src=nlbest


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Ankle replacements for arthritis coming of age?


My mother-in-law forwarded this article to me.  Up until recently, ankle replacements have not been very good.  Looks like things are changing.
HEALTH | January 18, 2010
Well: Ankles Gain as Candidates for Joint Replacement
By TARA PARKER-POPE
As baby boomers enter their 60s and 70s, demand for surgery to replace ankles with artificial joints is expected to grow. (http://well.blogs.nytimes.com/2010/01/18/ankles-gain-as-candidates-for-joint-replacement/?emc=eta1)

(I’m also wondering whether this might also be a place where stem cell therapies might also be an option.)

My thanks to Marcia Hearst and hope all is well with her.  She’s a great mother-in-law.


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Why I think the Dutch PRP study ain't much…


A recent study

[de Vos RJ, Weir A, van Schie HTM, et al. Platelet-Rich Plasma Injection for Chronic Achilles Tendinopathy: A Randomized Controlled Trial. JAMA. 2010;303(2):144-149]

cast a negative light on the use of platelet-rich plasma (PRP) for chronic Achilles tendonitis.

Dutch researchers randomly assigned 54 patients suffering from Achilles tendinopathy to receive either platelet-rich plasma injections or a placebo shot of saline.

Both groups also did conventional rehabilitation consisting of 180 heel drops (an exercise in which the toes are placed on the edge of a step and the heels are lowered toward the step below) daily for 12 weeks.

Results showed no difference between the two groups at six, 12 or 24 weeks after the procedure. Both groups improved about 20 points on a standardized scale that measures pain and function.

Robert-Jan de Vos, MD, in the Department of Orthopedics at Erasmus Medical Center, the lead author, says researchers don’t know why the injections didn’t work and they’re very disappointed by the results.

“These tendon injuries are very hard to treat,” Dr. De Vos said in an article reported in Arthritis Today.  He continued,  “We know that less than 50 percent of the patients with chronic Achilles tendinopathy are free of symptoms after one year. We still cannot prescribe a very promising conservative treatment, which is frustrating for the patients and treating doctors.”

Author’s note:

Many people will point to this study and say that PRP doesn’t work.  My take on it is this.  I think it was a well designed study. Really.  However, there are many explanations for the outcomes reported.

First, the technique used by the person performing the procedure was described as placing three holes in the tendon.  Those of us who do a significant number of Achilles tendon cases know that using a single entry point only and putting that single entry point on the top of the Achilles at an acute angle going from proximal to distal is critical.  Otherwise, the PRP leaks out and the patient won’t have as good a result.

Second any time a tendon is poked with holes without any other type of treatment given, it will improve.  The injury itself sets up an inflammatory response which leads to more healing.

The platelet concentration used was not mentioned.  Some PRP machines only provide a concentration of 2-3 times normal.  That’s not enough.  A good concentrate contains 7-10 times baseline counts of platelets.

No mention of tendon architecture changes was made.  I bet the tendon structure was improved in the PRP group (if a high enough platelet concentrate was used.)

This is a problem when a single study is touted as “being the gospel”. There’s more to the story


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Actemra Approved for Severe, Unresponsive, Rheumatoid Arthritis


Excerpts from an article written by Yael Waknine appearing in Medscape January 13, 2010: ….The FDA has approved tocilizumab intravenous infusion (Actemra) for the once-monthly treatment of moderately to severely active rheumatoid arthritis (RA) in adults who have had an inadequate response to 1 or more tumor necrosis factor (TNF) antagonist therapies.

…Actemra is the first interleukin 6 receptor–inhibiting monoclonal antibody and may be used alone or in combination with methotrexate or other disease-modifying antirheumatic drugs (DMARDS). It is expected to be available in the United States the week of January 18, 2010.

The recommended starting dose for tocilizumab is 4 mg/kg administered once every 4 weeks as a 60-minute single drip infusion, followed by an increase to 8 mg/kg based on clinical response.

Tocilizumab should not be used during active infection… Patients should be screened and treated for latent tuberculosis before starting treatment and monitored thereafter…

Because of the increased risk for infection, tocilizumab should not be used in combination with other biologic DMARDS, such as TNF inhibitors, IL-1 inhibiting drugs, B-cell depleters, and selective costimulation modulators (Basically, all other biologic groups).

Adverse events most commonly reported …include upper respiratory tract infection, nasopharyngitis, headache, high blood pressure, and liver enzyme elevations that were generally mild and reversible. Other laboratory changes, including increases in low-density lipoprotein cholesterol levels and decreased neutrophil and platelet counts, have also been observed and may require a decrease in dosage to 4 mg/kg. Serious adverse effects may include infection, gastrointestinal perforation, and hypersensitivity reactions, including anaphylaxis. As with other immunosuppressive therapies, tocilizumab may increase the risk for cancer.

Author’s note: This is a major advance for RA patients.  It is inconvenient as far as needing intravenous infusion. And there are many potential side effects to be on the lookout for.   Still it is a different mode of action and many patients who have failed other approaches may respond to this drug


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Progress on Stem Cells for Osteoarthritis


A recent article entitled, “The Latest Front in the War on Arthritis”,  in the Lab Journal Edition of the January 4, Wall Street Journal (Shirley S. Wang) described the work being done on a horse model to try and recreate cartilage using stem cell concentrate.

The article profiled the efforts of Dr. Constance Chu, an associate professor and director of the Cartilage Restoration Center at the University of Pittsburgh, and Lisa Fortier, an associate professor of large-animal surgery at Cornell University’s veterinary school.

The two scientists are doing work comparing stem cells versus a commonly used cartilage repair treatment in the U.S. called “microfracture” on former racehorses and rodeo horses to determine which is more effective.

Cartilage, the gristle that caps the ends of long bones at the hip, knee and other joints, can be “weakened with overuse and age, and can be permanently damaged when someone suffers an injury.  Cartilage that has been torn or injured doesn’t naturally grow back, and treatment options remain limited” Wang writes.

Over the long term, cartilage injury increases the risk of osteoarthritis, a painful chronic condition and the most common form of arthritis. It affects almost 27 million Americans, according to the Arthritis Foundation.

To reduce pain, improve functioning and slow disease progression, osteoarthritis is usually treated with a combination of medication, physical therapy to strengthen muscles and improve joint flexibility flexibility, a weight-loss program, as well as splints and braces.

Additionally, patients may undergo arthroscopic surgery to repair cartilage tears and remove loose tissue.  And they may eventually go on to joint-replacement surgery. Some alternatives to traditional therapy include the use of the supplement glucosamine, which research shows may promote cartilage repair and formation, and vitamins like C and E that may help slow cartilage erosion and reduce pain.

And though cartilage-repair surgery has improved over the years, the repaired scar tissue isn’t as strong as real cartilage.

The main challenge is that the structure of cartilage, which is critical to its supporting weight, is hard to mimic, says Fei Wang, director of the Musculoskeletal Tissue Engineering and Regenerative Medicine Program at the National Institute of Arthritis and Musculoskeletal and Skin Diseases in Bethesda, Md.

“It’s easy to generate a piece of tissue, but it’s not so easy to generate a tissue that works,” says Dr. Wang.

Not only is cartilage repair difficult, but it is hard to diagnose as well. Patients don’t feel pain—cartilage doesn’t contain any nerve endings—and there aren’t good tools for detecting injury to it until cartilage becomes permanently damaged. People often don’t know they have a problem until they develop serious disease that causes pain after the cartilage has further eroded.

With microfracture, surgeons punch tiny holes into the bone beneath the damaged cartilage, causing blood and bone marrow to fill the holes. The theory is that some of the bone marrow contains stem cells—which are cells that can grow into different types of cells—and other growth-promoting cells in the blood, a process that generates cartilage-like scar tissue. But this tissue isn’t as strong and doesn’t work as well as real cartilage, and the long-term benefits of the surgery aren’t well researched, according to Ranjan Gupta, professor and chairman of orthopedic surgery at the University of California, Irvine.

Currently, “all of our best efforts create inferior tissue to what we are born with,” says Dr. Chu. Cartilage transplant appears to be effective in filling the damaged cartilage, but isn’t widely available because it is difficult to find healthy cartilage for use in the transplant. “Just because we can’t get [the tissue] perfect unless it’s through transplant doesn’t mean we shouldn’t keep trying to improve the repair,” says Dr. Chu.

Ms Wang writes, “In the current study, she and her colleagues hypothesize that the more stem cells that are used to repair cartilage at the site of the damage, the better the regeneration of the tissue should be. They first create a dime-sized cartilage injury in the horse’s stifle joints, which resemble the human knee, and then test two different ways of concentrating the stem cells after taking them from the horse’s own bone marrow to see if either is better than microfracture and how they compare with each other.”

“Each horse in the study will be examined at 10 days and three months post-surgery for signs of cartilage repair. So far, 11 out of a total 12 horses have had the surgery. By three months, the injury should be filled with new tissue,” says Dr. Chu.

If the use of blood concentrate in the horses appears to repair cartilage better than microfracture, Dr. Chu plans to undertake a similar clinical study on humans, which she estimates would begin in about two years.

Author’s note: This was a well balanced and well written article describing the current state of affairs.  We have learned a tremendous amount about osteoarthritis and stem cells already from animal models .

At our center, we are using autologous  (a patient’s own stem cells) stem cell concentrates to regionally treat osteoarthritis of the knee and hip.  So far, our data looks promising.  We are also trying to develop stratification profiles of our patients to determine who is and who isn’t a good candidate because this procedure doesn’t work for everyone. Finally, we are developing better approaches and framework structures for the stem cells to grow in to give the patient the best chance for success.


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Does running lead to knee osteoarthritis?


This question is a common one that is aked of many rheumatologists, orthopedists, and family practice docs.  The answer changes every week.  This latest study contradicts a study presented by radiologists at their national meeting earlier this year.

So anyway, here it is…

Running may not increase risk of developing osteoarthritis later in life.

Time (12/25, Narayan) reported, “The common wisdom is that regular running or vigorous sport-playing during youth subjects the joints to so much wear and tear that it increases a person’s risk of developing osteoarthritis later in life.” Now, however, “an emerging body of research” indicates there is “no connection between running and arthritis,” and that “regular, vigorous exercise…may even help protect people from joint problems later on.” For example, a 2008 study following 1,000 active runners and non-runners “for 21 years” found that “the runners’ knees were no more or less healthy than the non-runners’ knees,” no matter “how much the runners ran,” and a 2007 study of 1,279 seniors found that “the most active people had the same risk of arthritis as the least active.”

So, if you’re as confused as I am, so be it!


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Carpal tunnel and Woman's Day


An article in the January 2010 issue of Woman’s Day magazine described carpal tunnel syndrome- the diagnosis and treatment.  Near the end was a sentence that said that surgery should be considered a treatment of last resort.  I agree 100% with that assertion, but the author  neglected to mention many options.

My colleagues and I presented a paper at the American College of Rheumatology meeting in November 2009 describing a minimally invasive procedure using a small needle and ultrasound guidance.

This technique has prevented the need for surgery in many patients.  While not 100% effective for everybody, it sure beats the knife. Here it is…

Ultrasound-Guided Percutaneous Injection, Hydrodissection, and Fenestration for Carpal Tunnel Syndrome

Tuesday, October 20, 2009

Hall D (Pennsylvania Convention Center)

Daniel G. Malone, University of Wisconsin, Madison, WI, Thomas B. Clark, MSKUS, Vista, CA and Nathan Wei, Arthritis & Osteo Ctr of MD, Frederick, MD

Purpose: Carpal tunnel syndrome, caused by compression of the median nerve deep to the flexor retinaculum, is the most common entrapment neuropathy.  Most patients are initially treated with conservative measures such as splinting.   When conservative measures fail, interventional techniques are considered the next step.  Many studies have appeared comparing open surgical flexor retinaculum release to blind injections of corticosteroids into the carpal tunnel, but neither technique has proven superior to the other.  Advantages of injection are: lower level of invasiveness, faster recovery, and ease of the technique.  Occasional failures and complications occur with all techniques.
Method: We have been using an ultrasound-guided procedure of percutaneous hydrodissection of the median nerve away from the deep surface of the flexor retinaculum, followed by fenestration of the flexor retinaculum along a path parallel to the long axis of the arm, starting from the level of the distal palmar crease and progressing proximally to the level of the radio-lunate joint, the intent being to lower the pressure exerted by the flexor retinaculum on the nerve (panel 1).  We have treated a series of 39 wrists in 29 patients with electrically-proven carpal tunnel syndrome, using this technique of hydrodissection and fenestration, performed using standard injection equipment and a GE LogiQ e ultrasound system with a 12 MHz linear array probe.  All patients had typical carpal tunnel syndrome symptoms and presented to us for interventional treatment, conservative measures having failed.  No patient had had previous surgery, and 2 had had blind carpal tunnel steroid injections, without hydrodissection or fenestration.  Outcomes were defined as:
Excellent-all symptoms resolved,
Fair-some residual symptoms, or return of symptoms, but improved compared to prior to procedure,
Failure-required open surgical release.
Follow-up periods after procedure ranged from 5-64 weeks, averaging 38 weeks (as of late June 09).  Patients were contacted by telephone, or seen in follow-up in clinic, to determine outcomes.
Results:
Excellent—31 wrists
Fair—5 wrists
Failure—3 wrists

No complications were encountered.
Conclusion:
Ultrasound-guided hydrodissection and fenestration is a viable, easy, relatively non-invasive therapy for carpal tunnel syndrome that can result in prolonged symptom relief, and may be a way to postpone, or even obviate the need for, open release.

Keywords: carpal tunnel syndrome and ultrasound

Disclosure: D. G. Malone, General Electric, 5 ; T. B. Clark, General Electric, 5 ; N. Wei, None.


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My heel kills… could it be plantar fasciitis?


Plantar fasciitis is an extremely common problem, particularly in the summer when people walk around in flip flps all the time.  But I still see alot of it now in people where it is a chronic condition.

And chronic conditions call for the heavy artillery.

I can’t stand it when I hear about a patient getting a cortisone shot for this condition.  It just shouldn’t be done.

Let me tell you what should and can be done…

A tibial nerve block using ultrasound guidance anesthetizes the bottom of the heel.  Then using ultrasound guidance I can poke small holes in the plantar fascia and get rid of any spurs that are there at the same time.  Then I inject PRP (platelet-rich plasma), a derivative of a patient’s own blood.  The PRP is loaded with growth and healing factors which help the plantar fascia to regenerate new tissue. And- gets rid of the pain!

Just did this procedure last week in a patient.  He’s doing great!


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Cluck… cluck… cluck… how to get your rheumatoid arthritis unstuck!


Every once in awhile, there’s a study that warms your heart.  Here’s one that stimulates the appetite.

An oral supplement of collagen from chicken breast cartilage may ease the symptoms of rheumatoid arthritis, but not quite as effectively as conventional treatment, according to results of a randomized trial.

Chicken type II collagen supplementation for patients with rheumatoid arthritis (RA) reduced pain, stiffness, and tender and swollen joint counts significantly compared with baseline in a recent report in the journal, Arthritis Research & Therapy.  According to lead author, Wei Wei, MD, PhD, (no relation to me… as far as I know) of Anhui Medical University in Hefei, China, and his colleagues.

The supplement was not as effective as methotrexate, using  American College of Rheumatology (ACR) measurement criteria.

However, since it has few, if any, side effects, chicken collagen could represent “a promising alternative therapeutic strategy that may be used as a nutritional supplement against RA,” they concluded in their report.

At present, conventional RA  treatments aim at suppressing the immune response since RA is an autoimmune process.

But “the supplements may work by inducing oral tolerance, modulating the immune response to type II collagen, which is a major protein in joint cartilage and a potential antigen in the autoimmune process,” the researchers explained.

After 24 weeks of treatment, the chicken collagen supplement had significantly improved the following outcomes compared with baseline:

  • Pain on the visual analog scale (3.58 versus 6.02, P<0.01)
  • Morning stiffness (36.12 versus 99.26 minutes, P<0.01)
  • Tender joint count (6.34 versus 13.34, P<0.01)
  • Swollen joint count (4.26 versus 10.38, P<0.01)
  • Health Assessment Questionnaire score (0.43 versus 0.82, P<0.01)
  • Physician assessment on the visual analog scale (3.81 versus 5.83, P<0.01)
  • Patient assessment on the visual analog scale (3.92 versus 6.01, P<0.01)

Methotrexate improved all these indicators to a significantly greater degree than the chicken collagen supplement for pain, Health Assessment Questionnaire score, and patient assessment.

And, chicken collagen was significantly less effective than methotrexate at reducing RA disease activity measured on the 28-joint disease activity score (DAS28, P=0.019).

Adverse event rates, as predicted were significantly lower with the collagen supplements compared with methotrexate.

I like chicken… fried chicken, roasted chicken, broiled chicken, grilled chicken, chicken soup, chicken gravy, chicken croquettes, chicken stew, chicken pot pie…

Mark Victor Hansen and Jack Canfield were right… chicken soup is good for the soul… and also for your joints, I guess.


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