Rheumatoid arthritis

===== Symptoms ===== ===== Management ===== ===== Other treatments ===== ===== Tests ===== ===== Diagnosis ===== ===== Epidemiology ===== ===== Types ===== ===== Evidence of infectious cause===== ===== Role of vitamin D metabolism ===== ===== Politics ===== ===== Patient interviews ===== ===== Presentations and publications=====

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Rheumatic diseases

Our Autoimmunity Reviews paper specifically identifies rheumatoid arthritis, systemic lupus erythematosus, and Parkinson's as Th1 diseases. http://dx.doi.org/10.1016/j.autrev.2003.10.001

Fulltext preprint is at http://yarcrip.com/sarcoidosissuccumbs-preprint.htm

Lupus In 'Overlap' With Other Connective Tissue Diseases

Nothing contained in this site is or should be considered, or used as a substitute for, medical advice, diagnosis or treatment by your physician.

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Death risk linked to steroid use for arthritis (filelink) “Patients with rheumatoid arthritis who are treated with low-dose steroids for more than 10 years are more likely to die than patients who are less exposed to these drugs ”

Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| MP Aug04|

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Personal Experience:

marion villa this is a piece of cake my friends… and I am heading for a completely healthy life.

Michele MBK: RA: boost in confidence in resuming life-activities while on MP

John McDonald: RA: Road Back and MP story. other unexpected gains.

Interview with Ival Meyer - arthritis, dyslexia

davbrkr Dave: Lyme 40+ yrs: RA: 1 month-17 days on Phase I

Christina JRA MP summary

Ival RA: MP is the right treatment for RA

Christina: RA - First Anniversary update

Carol: new RA update Phase three

Ival: RA: update: gone back to work. MP 21 months.

Christina: RA - re should I wait to MP?

Carol: RA - MP personal experience

Ival can you work on MP?

Christina RA: food sensitivities lessening. very active. recovering more quickly. Christina re JRA: personal experience.

Ival: RA: my most active month ever since starting the MP.

Help from RA members

John McDonald: RA: My RA “remission” is more secure now

Ival: RA: Here is my little speech I gave at the Los Angeles conference. see DVDs. Ival: RA: I've got my life back Ival: RA improvements..8 months … 1 year….

Has anyone had evidence of joint improvement? Carol RA: summary Carol RA: off thyroid meds

Christina RA personal experience

AmyEliz: RA: my 'positives'…. RA: summary

See also

PAIN CONTROL

see Standard Treatments information link and scroll down

Last edited on Mon Aug 11th, 2008 00:15 by

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Article about the role of VDR in RA: The Vitamin D Receptor regulates rheumatoid arthritis synovial

If we ever have an article on JIA:

Do infections trigger juvenile idiopathic arthritis?²

Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A, Torun MM, Arısoy N, Kocazeybek B.

Rheumatology International, published online before print December 13, 2009.

http://dx.doi.org/10.1007/s00296-009-1253-4

Abstract

Juvenile idiopathic arthritis (JIA) is a disease that was prominent with increased inflammation response in immune system, appeared mostly with peripheral arthritis and endogenous and exogenous antigens play a role in the pathogenesis of disease.

Two major reasons were thinking to be considerably important. First of them is immunological predisposition and the second one is environmental factors. Infections are considered to be the most important between environmental factors but also stress and trauma are also important in the etiology of the disease. However, the relation between JIA and infections is not clearly defined but the relation between adult chronic arthritis and infections was well-defined.

A total of 70 patients, 26 with primer JIA, 20 with recurrent JIA, 24 healthy control were included in this study. Mycoplasma pneumoniae, Chlamydophila pneumoniae and C. Jejuni were detected in 4, 1 and 1 of 10 (38.46%) patients with primer JIA, respectively. Salmonella enteritidis, EBV, M. pneumoniae, C. jejuni and Borrelia burgdorferi were detected in 1, 2, 2, 2, and 1 of the 8(40%) patients with recurrent JIA, respectively. S. enteritidis were isolated in feces culture and also identified by agglutination method. Infection was detected in total 18 (39.13%) of patient groups. C. pneumoniae and C. jejuni were detected in 1 and 1 of 2(8.33) healthy control groups, respectively. Throat culture positivity was not detected in any of the patient and healthy control groups.

In conclusion, etiopathogenesis of JIA is not clearly understood and suggested that various factors can trigger the disease and it is the most common rheumatoid disease of childhood. However, there are some studies focusing especially on one infectious agent but this is the first study including such a big range of infectious agents in the literature for the microorganisms that can be suggested to have a role in the etiopathogenesis of JIA. We have a conclusion in the light of our results and suggest that some microorganisms can trigger and increase the intensity of clinical situation according to the case. When we evaluate the primer and recurrent JIA groups; M. pneumoniae and C.

jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.

http://dx.doi.org/10.1007/s00296-009-1253-4

Calcif Tissue Int. 2010 Jun 26. [Epub ahead of print]Induced Apoptosis of Chondrocytes by Porphyromonas gingivalis as a Possible Pathway for Cartilage Loss in Rheumatoid Arthritis.

Röhner E, Detert J, Kolar P, Hocke A, N'guessan P, Matziolis G, Kanitz V, Bernimoulin JP, Kielbassa A, Burmester GR, Buttgereit F, Pischon N. Department of Rheumatology and Clinical Immunology, Charité University Hospital, Campus Mitte, Charitéplatz 1, 10117, Berlin, Germany, eric.roehner@charite.de. Abstract The role of bacterial infections in the pathogenesis of rheumatoid arthritis (RA) has gained increasing interest. Patients with RA often exhibit periodontal disease, which is associated with pathogens like Porphyromonas gingivalis. The present study examines the direct effects of P. gingivalis on apoptosis of human chondrocytes (a feature of inflammatory joint diseases) as one can assume an interrelation of pathogenesis of RA and P. gingivalis infections. Primary chondrocytes were infected with P. gingivalis. Early apoptotic and dead cell analysis was performed using Annexin-V, 7AAD, and propidium iodide and examined by flow cytometry and fluorescence microscopy. Caspase activation and DNA fragmentation were determined by western blot analysis and TUNEL reaction. Flow cytometry and fluorescence microscopy demonstrated an increase of Annexin-V-positive early apoptotic chondrocytes after infection. Western blot showed upregulation of activated caspase-3 expression, and TUNEL reaction revealed considerable DNA fragmentation following infection. The data show that P. gingivalis promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA. PMID: 20582408

Certain Bacteria May Trigger Inflammation

New technology creates a clearer picture of how bacteria may be linked to autoimmune forms of arthritis.

By Jennifer Davis

12/2/10 New research is homing in on types of bacteria in the body that may be associated with some autoimmune diseases, including rheumatoid arthritis, or RA.

At the recent American College of Rheumatology Annual Scientific Meeting, researchers said that they think specific bacteria that live in the mouth and intestines activate cells that promote inflammation.

“The most important point is that we are now able to answer some of these questions and may be able to better understand potential triggering factors that lead to joint inflammation in RA and other diseases,” says Jose U. Scher, MD, director of New York University’s new Microbiome Center for Rheumatology and Autoimmunity and one of the lead investigators in the study. “We need to be cautious because this hypothesis generates expectations from doctors and patients, and the reality is that there is a lot of work ahead of us before we can come up with conclusions.”

In the study, researchers from New York University’s Langone Medical Center used cutting-edge DNA sequencing technology to identify 100 percent of the bacteria in the mouth and intestines of eight people recently diagnosed with RA, three with psoriatic arthritis and nine who were healthy and didn’t have an autoimmune disease. “What we are doing is testing an old hypothesis with 21st-century technologies,” Dr. Scher explains.

Researchers say the new technology is allowing them to see some differences in those with autoimmune diseases and those without. The RA patients, for example, had more of a bacterial family called prevotellaceae in their intestinal fecal samples, and more of a type of oral bacteria called porphyromonas genus, than healthy patients had.

“We can say we have preliminary results looking at a particular set of bacteria that may seem present at a higher abundance in patients with RA,” Dr. Scher says. “Now we have the technological tools to look at this question, but we can not say we have an answer yet.”

David S. Pisetsky, MD, PhD, a professor of medicine at Duke University Medical Center in Durham, N.C., says the fact that researchers can find and identify hundreds if not thousands of bacteria types provides a level of detail never before seen. He believes that will go a long way in highlighting differences in people with RA from those without it.

“It’s part of an entirely new direction in analyzing the relationship between infection and disease,” Dr. Pisetsky says. “We are filled with bacteria. It’s probably stimulating or modifying our immune system and the question is, are there particular bacteria that would make you more or less likely to get a disease?”

Because studies looking into the relationship of bacteria and autoimmune disease are small and in early stages, it’s hard to tell what, if anything, the information means to patients now, Dr. Pisetsky adds. “I am going to follow [this emerging area of research] with interest to see how it develops.”

From Medscape Medical News Lifetime Risk for RA Much Higher Than Expected

Janis C. Kelly

January 31, 2011 — The first study to determine lifetime risk for inflammatory autoimmune rheumatic disease reports that 1 in 12 women and 1 in 20 men will develop such disorders, and 1 in 28 women and 1 in 59 men will develop rheumatoid arthritis (RA).

Vitamin D receptor regulates TNF-mediated arthritis.Zwerina K, Baum W, Axmann R, Ruiz Heiland G, Distler JH, Smolen J, Hayer S,Zwerina J, Schett G Ann Rheum Dis Mar 2011; Download citation Affiliation 1Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. Abstract OBJECTIVE: /st> Reduced vitamin D intake has been linked to increased susceptibility to develop rheumatoid arthritis (RA) and vitamin D deficiency is associated with increased disease activity in RA patients. The pathophysiological role of vitamin D in joint inflammation is, however, unclear. METHODS: /st> To determine the influence of absent vitamin D signalling in chronic arthritis, vitamin D receptor (VDR)-deficient mice were crossed with human tumour necrosis factor (TNF) transgenic mice (hTNFtg), which spontaneously develop chronic arthritis. RESULTS: /st> Clinical signs and symptoms of chronic arthritis were aggravated in hTNFtg mice lacking functional VDR signalling. Moreover, synovial inflammation was clearly increased in VDR(-/-)hTNFtg mice as compared to hTNFtg mice and was associated with an increased macrophage influx in inflamed joints. In vitro, VDR-deficient monocytes were proinflammatory and hyper-responsive to TNF stimulation associated with prolonged mitogen-activated protein kinase activation and cytokine secretion. Also, VDR(-/-) monocytes showed enhanced potential to differentiate into bone resorbing osteoclasts in vitro. In line, VDR(-/-)hTNFtg mice had significantly increased cartilage damage and synovial bone erosions. CONCLUSIONS: /st> VDR plays an important role in limiting the inflammatory phenotype in a mouse model of RA. Absent VDR signalling causes a proinflammatory monocyte phenotype associated with increased inflammation, cartilage damage and bone erosion.

J Clin Periodontol. 2010 May;37(5):405-11.Effect of Porphyromonas gingivalis-induced inflammation on the development of rheumatoid arthritis. Bartold PM, Marino V, Cantley M, Haynes DR. School of Dentistry, Faculty of Health Sciences, School of Medical Sciences, University of Adelaide, Adelaide, Australia. mark.bartold@adelaide.edu.au Abstract BACKGROUND: Periodontitis is an extra-synovial chronic inflammatory condition, which has been proposed to be inter-related with rheumatoid arthritis. Objective: We investigated the effect of an established extra-synovial chronic inflammatory lesion on the induction and severity of experimental arthritis. MATERIALS AND METHODS: Chronic inflammatory lesions were induced by the implantation of polyurethane sponges impregnated with heat-killed Porphyromonas gingivalis into the backs of DA rats. Thirty-five days later, adjuvant arthritis (AA) was induced in the rats by injecting a mycobacterium cell wall in complete Freund's adjuvant. The development of arthritis was then monitored for 2 weeks. RESULTS: Histological assessment of the implanted sponges confirmed that a chronic inflammatory lesion had been established after 21 days. Following induction of adjuvant arthritis, the severity of disease was scored and paw swelling was measured. Severe arthritis developed more rapidly in animals with a pre-existing P. gingivalis-induced inflammatory lesion elsewhere. CONCLUSIONS: The results show that a pre-existing extra-synovial chronic inflammatory lesion induced by P. gingivalis promotes the development of arthritis in an animal model. These findings provide further evidence for a relationship between the presence of periodontal pathogen-associated inflammation and the development of rheumatoid arthritis. PMID: 20507365

The microbiome and rheumatoid arthritis

The microbiome and rheumatoid arthritisJose U. Scher & Steven B. Abramson About the authors

topof page Abstract

Humans are not (and have never been) alone. From the moment we are born, millions of micro-organisms populate our bodies and coexist with us rather peacefully for the rest of our lives. This microbiome represents the totality of micro-organisms (and their genomes) that we necessarily acquire from the environment. Micro-organisms living in or on us have evolved to extract the energy they require to survive, and in exchange they support the physiological, metabolic and immune capacities that have contributed to our evolutionary success. Although currently categorized as an autoimmune disorder and regarded as a complex genetic disease, the ultimate cause of rheumatoid arthritis (RA) remains elusive. It seems that interplay between predisposing genetic factors and environmental triggers is required for disease manifestation. New insights from DNA sequence-based analyses of gut microbial communities and a renewed interest in mucosal immunology suggest that the microbiome represents an important environmental factor that can influence autoimmune disease manifestation. This Review summarizes the historical clues that suggest a possible role for the microbiota in the pathogenesis of RA, and will focus on new technologies that might provide scientific evidence to support this hypothesis.