Spondylitis Association of America
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Integrated Biomechanical Influences On Ankylosing Spondylitis
The characteristic spinal deformities and lesions of AS occur at anatomical sites where ligaments, tendons, or joint capsules anchor or attach to bone (1-5). The epidemiological patterns of AS can offer essential clues to possible initiating pathways of the disease. The sex- and age-specific onset patterns of AS in the population are unique (6,7). The clinical condition develops about two or three times more frequently in males than females, and that M:F sex ratio increases with greater severity of skeletal lesions and deformities.
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(Article originally published in the Summer 2009 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

New Genes Provide Additional Targets For Spondylitis Treatment
The genetics of ankylosing spondylitis (AS) came into clearer focus nearly a year ago, with the discovery of two genes that increase the risk of developing the disease. Scientists now have found what they believe may be the last pieces of the genetic puzzle to this potentially crippling disease.
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(Article originally published in the Winter 2008 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

The TASC Genetic Study Uncovers Two New Genes Implicated in Ankylosing Spondylitis
The good news is in. We are delighted to tell you that due, in large part, to your continued commitment to AS genetic research since 1996, a critical milestone has been achieved with the discovery of two new genes implicated in AS. The new genes have been identified as ARTS1* and IL-23R*. This new finding means that researchers now have uncovered roughly 70% of the genetic contribution toward susceptibility toward AS.
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(Article originally published in the Winter 2007 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Genetics and Ankylosing Spondylitis Susceptibility: The Next Step-the TASC Study
One of the indisputable facts about ankylosing spondylitis (AS) is that hereditary factors play a critical role in its cause. We have known for many years that AS and the related conditions associated with spondyloarthritis (such as psoriasis, iritis or uveitis, and inflammatory bowel disease) occur more frequently in family members of AS patients than in the general population. For nearly 35 years we have known that one hereditary factor, HLA-B27, is extremely important in susceptibility. The significance of HLA-B27 became even clearer with the development of the HLA-B27 transgenic rat in 1990, a model that continues to teach us about the immunology of this disease.
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(Article originally published in the Fall 2007 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Genetics, Environment and Lifestyles of People with Spondyloarthritis-Unlocking the Secrets
As many of you know from scanning these pages and by attending the SAA Patient Educational Seminars during the past several years, a great deal has been happening in spondyloarthritis research.

In brief, up until June 1998, there was very little activity in AS research in the U.S. except for a very small dedicated group of researchers. Then in 1998, under the guidance of Dr. John D. Reveille, the SAA initiated, with member support, the AS Family Genetic Project. Following suit, during the next en years, the situation in AS research in the United States vastly improved as interest grew and activity increased as more researchers became involved in this group of diseases:
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(Article originally published in the Summer 2007 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Expanding The Research Horizon In Ankylosing Spondylitis - Understanding the Role of HLA-B27
Most patients with ankylosing spondylitis (AS) recognize HLA-B27 as a genetic marker that they carry. Indeed, it is found in the vast majority (90-95%) of patients with this disease, compared to less than one of ten healthy people. It is inherited from one parent, and in rare cases both, and is often accompanied by the knowledge that someone else in the extended family has AS or another HLA-B27-associated disease. We also know that HLA-B27 does not work alone. Several additional genes contribute to AS, and major efforts in North America and around the world are dedicated to finding the location of these genes in the human genome. What is often less well appreciated is that HLA-B27 is already a major focus of research, and understanding its role in disease will provide a key piece to this puzzle.
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(Article originally published in the Winter 2006 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Ankylosing Spondylitis Research: Celebrating A Major Research Milestone
Thanks to 400 very special families who have participated in the AS Family Genetic Project, we have reached a major milestone. Since the project began six years ago, we have obtained an impressive collection of data and DNA, identified regions on seven chromosomes that lead to susceptibility to AS, and have contributed to a study that identified a chromosome for uveitis (eye inflammation).
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(Article originally published in the September/October 2005 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Psoriatic arthritis and psoriasis: role of patient advocacy organizations in the twenty first century
The SAA was invited to co-author a paper in a supplement of the leading academic journal, Annals of Rheumatic Diseases. GRAPPA, the international group of rheumatologists and dermatologists advancing knowledge in psoriasis and psoriatic arthritis was responsible for the development of the supplement which included 31 papers, ranging from pathophysiology through the clinical management of psoriatic arthritis.
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(Article originally published in the May / June 2005 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Researchers uncover genetic region involved with a cause of potential loss of vision in people with AS
Ankylosing spondylitis (AS) is a rheumatic disease of largely genetic origin, which means that it runs in families. It affects not only the joints and bones; other parts of the body can also be impacted. These include the heart, the lungs and the eyes.
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(Article originally published in the March / April 2005 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

Important breakthroughs as a result of the AS Family Genetic Study
“A new and exciting day is dawning in AS.” These words were spoken recently by Dr. John Reveille presenting at the SAA Educational Forum in San Antonio, TX. Dr. Reveille, certainly, is fully cognizant of the progress since he has been working closely with the SAA for 7 years to advance research in AS. As many of our readers already know, having participated directly in the AS Family Genetic Study, much already has been accomplished through the collaboration between the University of Texas, Houston, the Spondylitis Association and the National Institutes of Health. The study set out to identify families with sibling pairs who have AS in order to locate areas on chromosomes where genes causing the disease might be found. Another goal of the study has been to examine at least five candidate genes from these chromosomal areas. A “candidate” gene is one that is located in a chromosome region suspected of being involved in a specific disease. This has been accomplished.
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(Article originally published in the November / December 2004 issue of our magazine, Spondylitis Plus. SAA Members can click here to download this issue in the Spondylitis Plus archive.)

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