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TEXTBOOK : CLINICAL AND MOLECULAR ADVANCES IN ANKYLOSING SPONDYLITIS

ANKYLOSING SPONDYLITIS
Edited by Jacome Bruges-Armas .
Open Access .
178 pages .

Ankylosing Spondylitis (AS) was first described possibly at the end of the XVII century by Buckley (1931) and Connor, but it was only recognized after the radiologic descriptions of Bechterew, Strumpell and Marie, during the XIX century. In 1964 the American Rheumatism Association classified AS as a distinct disease. About forty years ago (1973), Schlosstein and Brewerton published simultaneously but independently the association of AS with the Class I allele B*27.
Since then, AS has been the target of intense research and an enormous amount of information has been gathered about this disease. Now it is known that AS is one of a group of several diseases known as Spondyloarthritis (SpA): AS, reactive arthritis, unspecified spondyloarthritis, psoriatic arthritis, and entheropathic arthritis.
Also, during the last ten years research has been focused on the understanding of the molecular and cellular processes involved in AS pathogenesis. Genome Wide Association Studies (GWAS) were followed by other studies using candidate genes which allowed the identification of non-HLA genes associated with AS susceptibility.
The more detailed knowledge of the molecular and cellular mechanisms, and the identification of biomarkers and their signaling pathways, contributed to the development of anti-TNFα and anti-IL6 molecules which are highly effective in the treatment of AS. These drugs radically changed the treatment of SpA and improved significantly the quality of life of the patients. With the deeper knowledge of the cellular mechanisms of AS, further therapeutic improvements will follow.
In this book, we have tried through original research and revised chapters, to update the clinical and molecular knowledge of AS and SpA.
The chapters in the first section, “Clinical Manifestations, Bone Density Measurements and Axial Fractures Treatment”, cover general and more specific clinical aspects of SpA. Spinal and axial joints are affected in AS, but the hallmark of this disease is the axial aggression, sometimes restricted to the sacroiliac joint, better characterized in the early stages by MRI. Peripheral joints may be involved in 30% of cases, and the earlier involvement of these joints may be an indicator of a more aggressive disease. Extraarticular manifestations are quite common in AS, namely enthesitis, acute anterior uveitis (AUU), cardiac involvement, pulmonary fibrosis, and secondary renal amyloidosis. Psoriatic arthritis has several subgroups and the sub-classification of this disease may be difficult even for the rheumatologist. Up to 50% of AS patients may have gut inflammation when examined by colonoscopy, and SpA may be found in 1- 12% of patients with Crohn`s Disease and Ulcerative Colitis, with higher incidence of peripheral arthritis; sacroiliitis may occur asymptomatic or with typical symptoms.
Reactive arthritis tends to be more aggressive and as a longer duration in HLA-B*27 positive cases (50%). Asymmetrical acute peripheral arthritis, enthesitis, acute sacroiliitis, urogenital inflammation, and ocular manifestations are common and may last several months to two years. The importance of clinical measurements to evaluate pain, morning stiffness, and functional ability is well evaluated with the BASDAI and BASFI questionnaires. Several measurements may be used by the clinician, to check and control spinal function and flexibility.
The chapter on the incidence, clinical features, pathophysiology, signs, symptoms, and current management of the Temporomandibular Joint (TMJ), reviews how AS affects this joint. TMJ is involved in 4% to 32% of cases, and ranges from mild disease to ankylosis which is exceptional. The non-surgical treatment of TMJ in AS is the most effective way of managing over 80% of patients. Non-pharmacological treatment includes fabrication of intra oral splints, physiotherapy, and patient education. The pharmacological treatment includes NSAIDS, Coxibs, corticosteroids, and anti-TNF agents. The surgical treatment – injection of steroids, joint lavage and total joint replacement -, is indicated in patients with marked trismus, or in cases of the failure of other non-surgical therapies.
The third chapter in this section is dedicated to bone mineral density (BMD) changes in patients with SpA. BMD has been investigated mainly in patients with AS. The authors investigated BMD changes in AS and in other diseases belonging to the SpA group – ReA (Reactive Arthritis), PsA (Psoriatic Arthritis), EnA (Entheropathic Arthritis) - to assess the relationship between changes in BMD and specific diseaserelated variables like duration, physical disability and immobility, activity of the disease, and medications. The results were also compared with a group of patients with Rheumatoid Arthritis (RA) and healthy people. Several conclusions were obtained but possibly the most relevant are: 1) BMD was identical between patients with SpA and RA; 2) Similar changes were found in patients from the various SpA groups....

Dr Jacome Bruges-Armas
Hospital of the Holy Spirit, The Azores,
Portugal
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CONTENTS :

Part 1 of the Textbook : Clinical Manifestations, Bone Density Measurements and Axial Fractures Treatment .


 1 Clinical Features of Ankylosing Spondylitis 3 Jeanette Wolf

 2 Ankylosing Apondylitis of Temporomandibular Joint (TMJ) 15 Raveendra Manemi, Rooprashmi Kenchangoudar and Peter Revington

 3 Bone Mineral Density Changes in Patients with Spondyloarthropathies 27 Lina Vencevičienė, Rimantas Vencevičius and Irena Butrimienė

 4 Surgical Treatment After Spinal Trauma in Patients with Ankylosing Spondylitis 55 Stamatios A. Papadakis, Konstantinos Kateros, Spyridon Galanakos, George Machairas, Pavlos Katonis and George Sapkas

Part 2 of the Textbook : HLA and Non-MHC Genes, Immune Response, and Gene Expression Studies .


 5 HLA-B27 and Ankylosing Spondylitis 73 Wen-Chan Tsai

 6 Humoral Immune Response to Salmonella Antigens and Polymorphisms in Receptors for the Fc of IgG in Patients with Ankylosing Spondylitis 85 Ma. de Jesús Durán-Avelar, Norberto Vibanco-Pérez, Angélica N. Rodríguez-Ocampo, Juan Manuel Agraz-Cibrian, Salvador Peña-Virgen and José Francisco Zambrano-Zaragoza

 7 Genetics in Ankylosing Spondylitis – Beyond HLA-B*27 Bruno Filipe Bettencourt, Iris Foroni, Ana Rita Couto, Manuela Lima and Jácome Bruges-Armas

 8 Lessons from Genomic Profiling in AS 135 Fernando M. Pimentel-Santos, Jaime C. Branco and Gethin Thomas




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Published by: younes younes - Saturday, June 8, 2013

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