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Permanent Rheumatology Job in AL statewide Alabama with Medical Doctor Associates, Inc.
Tremendous growth requires recruitment of BC/BE Rheumatologist to meet community needs. Excellent financial package with Sign On Bonus/Loan Repayment. Located in the beautiful Tennessee River Valley,
Permanent Rheumatology Job in Not Disclosed Florida with Locum Medical Group
An expanding multi-specialty/multi-facility practice in the Miami, Florida area is seeking a Board Certified Rheumatologist. Each contemporary facility ranges in size from 6,000 to 8,000 square feet with
Permanent Rheumatology Job in Northeast Missouri - MSG Seeks Rheumatologist Missouri with Enterprise Medical Services
Northeast Missouri multi-specialty clinic needs to replace 100% Rheumatologist. Call is 1:1. Financial package includes base salary of $180 - $200k, production bonuses, malpractice, health, life, disability,

Arthritis Research & Therapy - Latest articles

Prognostic factors of 10-year radiographic outcome in early rheumatoid arthritis: a prospective study
Natacha Courvoisier, Maxime Dougados, Alain Cantagrel, Philippe Goupille, Olivier Meyer, Jean Sibilia, Jean Pierre Daures and Bernard Combe Thu, 04 Sep 2008 00:00:00 -0000
IntroductionThe objectives of this study are to determine the predictive factors of long-term radiographic outcome in rheumatoid arthritis (RA) and to describe the relationship between joint damage and disability over the course of the disease. Methods: A cohort of 191 patients with early RA referred from primary care physicians were prospectively followed up for 10 years. To determine the predictive factors of radiographic outcome, univariate analysis of the relationship between baseline values and outcome measures was undertaken using the chi-square or Fisher's exact test. Stepwise multiple logistic regression was performed to select independent prognostic factors. Results: From data available for 112 patients, univariate analysis revealed total Sharp score at 10 years to be significantly correlated with erythrocyte sedimentation rate (ESR), presence and level of IgA rheumatoid factor, presence of an anti-citrullinated protein antibody (ACPA), serum level of matrix metalloproteinase 3 and radiographic score at baseline. Logistic regression identified the most important baseline parameter as an independent prognostic factor of total radiographic score at 10 years to be baseline erosion score (OR=5.64; 95% CI=1.78-17.86). After excluding radiographic scores from the entry parameters, the presence of ACPA and ESR were also predictive of the final total Sharp score. Health assessment questionnaire (HAQ) score was strongly correlated with disease activity parameters, such as disease activity score and pain, at baseline and at 3, 5 and 10 years. No correlation was found between total radiographic Sharp score and HAQ score throughout the study. Conclusions: In this prospective study, baseline radiographic score, ESR and ACPA were the best predictive factors of 10-year radiographic outcome in early RA. HAQ disability was associated with disease activity throughout the 10-year follow-up but not with joint damage. This discrepancy with previous reports may be due in part to the early start of therapy with disease-modifying anti-rheumatic drugs.
Elevated autoantibody content in rheumatoid arthritis synovia with lymphoid aggregates and the effect of rituximab
Sanna Rosengren, Nathan Wei, Kenneth C Kalunian, Nathan J Zvaifler, Arthur Kavanaugh and David L Boyle Mon, 01 Sep 2008 00:00:00 -0000
IntroductionThe purpose of this study was to quantitatively evaluate the contribution of synovial lymphoid aggregates to autoantibody (rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP)) and total immunoglobulin (IgG and IgM) production in rheumatoid arthritis (RA) patients, and the effect thereon of the B-cell depleting antibody, rituximab, in the ARISE trial. Methods: Autoantibodies, total IgM and IgG were quantified by ELISA in extracts of synovial tissues and matched serum from patients with RA or osteoarthritis (OA). Synovial biopsies and serum were obtained at baseline and 8 weeks following rituximab therapy in 14 RA patients. A synovial/serum index (SSI) was calculated as the ratio of synovial to serum antibody/albumin, with values above 1 representing synovial enrichment. Lymphoid aggregates were evaluated histologically. The ARISE trial is registered at ClinicalTrials.gov, number NCT00147966 Results: Anti-CCP IgG, but not RF-IgM, was significantly enriched in RA synovia compared to serum. Total IgM and IgG was also enriched in RA, but not in osteoarthritis. SSI correlated significantly with mRNA content for both IgM and IgG, demonstrating that it reflected synovial immunoglobulin production. RA synovia with lymphocyte aggregates contained significantly elevated RF-IgM and anti-CCP IgG compared to tissues with diffuse lymphoid infiltration. Rituximab treatment did not affect synovial autoantibody or total Ig SSI overall. However, in aggregate-containing tissues, rituximab significantly reduced total IgM and IgG SSI as well as IgM and IgG1 mRNA. Surprisingly, RF-IgM and anti-CCP IgG synovial/serum indices were unchanged by rituximab in aggregate-containing synovia. Conclusions: Combined with earlier observations that synovial lymphoid aggregates survived rituximab treatment, these data suggest that lymphoid aggregates may provide a protective niche for autoantibody producing cells.
The relationship between inflammation and new bone formation in patients with ankylosing spondylitis
Xenofon Baraliakos, Joachim Listing, Martin Rudwaleit, Joachim Sieper and Juergen Braun Mon, 01 Sep 2008 00:00:00 -0000
IntroductionSpinal Inflammation as detected by magnetic resonance imaging and new bone formation as identified by conventional radiographs are characteristic for ankylosing spondylitis. Whether and how spondylitis and syndesmophyte formation are linked is unclear. Our objective was to investigate whether and how spinal inflammation is associated with new bone formation in ankylosing spondylitis. Methods: Spinal magnetic resonance images and conventional radiographs from 39 ankylosing spondylitis patients treated with anti-TNF agents at baseline and after 2 years were analysed for syndesmophyte formation at vertebral edges with or without inflammatory lesions at baseline. Results: Overall, 922 vertebral edges at the cervical and lumbar spine were analysed. At baseline, the proportion of vertebral edges with and without inflammation (magnetic resonance imaging) that showed structural changes (conventional radiographs) was similar (in total 16.6% of all vertebral edges in 71.4% of patients). From the perspective of syndesmophyte formation (n=26, 2.9%) after 2 years, there were more vertebral edges without (62%) than with inflammation (38%) at baseline, respectively (p=0.03). From the perspective of spinal inflammation at baseline (n=153 vertebral edges) more syndesmophytes developed at vertebral edges with (6.5%) than without inflammation (2.1%), respectively (p=0.002, OR: 3.3 (95%CI:1.5 to 7.4)). Inflammation persisted in 31% of the initially inflamed vertebral edges, (n=132) and new lesions developed in 8% of the vertebral edges without inflammation at baseline (n=410). From the perspective of spinal inflammation after 2 years (n=72 vertebral edges), 5.6% of the vertebral edges showed syndesmophyte development, in contrast to 1.9% of the vertebral edges with new syndesmophytes without inflammation (p=0.06). Conclusions: These findings obtained in patients treated with anti-TNF agents suggest linkage and some dissociation of inflammation and new bone formation in ankylosing spondylitis. Although syndesmophytes were found to also develop at sites where no inflammation had been seen by magnetic resonance imaging at baseline, it was more likely that syndesmophytes developed in inflamed vertebral edges. More effective suppression of spinal inflammation may be required to inhibit structural damage in ankylosing spondylitis.
A polymorphism in the human serotonin 5-HT2A receptor gene may protect against systemic sclerosis by reducing platelet aggregation
Lorenzo Beretta, Marta Cossu, Maurizio Marchini, Francesca Cappiello, Andrea Artoni, Giovanna Motta and Raffaella Scorza Mon, 01 Sep 2008 00:00:00 -0000
IntroductionPlatelet aggregation may contribute to the pathogenesis of systemic sclerosis: following activation platelets release significant amounts of serotonin which promotes vasoconstriction, fibrosis and further enhances aggregation. The C+1354T polymorphism in the exonic region of the Serotonin 2A receptor gene determining the His452Tyr substitution, was associated with blunted intracellular responses after serotonin stimulation and may have a role in susceptibility to scleroderma. Methods: One-hundred-fifteen consecutive systemic sclerosis patients and 140 well-matched healthy controls were genotyped by sequence-specific primer-polymerase chain reaction for the His452Tyr substitution of the serotonin 2A receptor gene and associations were sought with scleroderma and its main clinical features. The functional relevance of the His452Tyr substitution was also assessed by evaluating the aggregation of platelet-rich plasma from His452/His452 and His452/Tyr452 healthy individuals after stimulation with adenosine diphosphate +/- serotonin. Results: The T allele of the C+1354T polymorphism was underrepresented in scleroderma patients compared to controls (5.2% vs 12.4%, p<0.001, chi-square test and 1000-fold permutation test) and its carriage reduced the risk for systemic sclerosis (OR=0.39, CI95=0.19 to 0.85 p<0.01). Platelets from His452/Tyr452 healthy subjects more weakly responded to serotonin stimulation compared to platelets from His452/His452 individuals (3.2+/-2.6 vs 9.6+/-8.6-fold increase in aggregation, p=0.017 Kolmogorov-Smirnov test and p=0.003 after correction for baseline adenosine diphosphate-induced aggregation values). Conclusions: The His452Tyr substitution may influence susceptibility to systemic sclerosis by altering platelet aggregation in response to 5-HT.
Biochemical markers of bone turnover and their association with bone marrow lesions
David J Hunter, Michael LaValley, Jiang Li, Doug C Bauer, Michael Nevitt, Jeroen DeGroot, Robin Poole, David Eyre, Ali Guermazi, Daniel Gale, Saara Totterman and David T Felson Fri, 29 Aug 2008 00:00:00 -0000
IntroductionOur objective was to determine if markers of bone resorption and formation could serve as markers for the presence of bone marrow lesions (BMLs). Methods: We conducted an analysis of data from the Boston Osteoarthritis of the Knee Study. Knee MR images were scored for BMLs using a semi-quantitative grading scheme. In addition, a subset of persons with BMLs had a quantitative volume measure of their BML using a proprietary software method. Within the BOKS population 80 subjects with BMLs and 80 subjects without BMLs were selected for the purposes of this case control study. Bone biomarkers assayed included Type I Collagen N-telopeptide (NTx/ Cr), Bone Specific Alkaline Phosphatase (BSAP), and Osteocalcin (OST). The same methods were used and applied to a nested case control sample from the Framingham study where BMD assessments allowed the assessment of this as a covariate. Logistic regression models were fit using BML as the outcome and biomarkers, age, sex and BMI as predictors. An ROC was generated for each model and the area under the curve assessed. Results: 151 subjects from BOKS with knee OA were assessed. The mean (SD) age was 67 (9) years and 60% were male. 69% had maximum BML score > 0, 48% had maximum BML score > 1. The only model that reached statistical significance used maximum score of BML>0 as the outcome. LnNTx demonstrated a significant association with the odds of a bone marrow lesion being present increased 1.4 (95%CI 1.0, 2.0) fold per SD increase in the Ln NTx, with a small partial R2 of 3.05. 144 subjects from the Framingham Osteoarthritis Study of mean age 68 years, BMI 29, and 40% of them were male. 55% of participants had a maximum BML score >0. The relationship between NTx and maximum score of BML>0 revealed a significant association with OR=1.7 (1.1-2.7) after adjusting for age, sex and BMI. Conclusion: Serum NTx was weakly associated with BML presence in both study samples. This relationship was not strong and we would not advocate their use as markers for the presence of BMLs.
Upregulated miR-146a expression in peripheral blood mononuclear cells from rheumatoid arthritis patients
Kaleb M. Pauley, Minoru Satoh, Annie L. Chan, Michael R. Bubb, Westley H. Reeves and Edward K.L. Chan Fri, 29 Aug 2008 00:00:00 -0000
IntroductionMicroRNA are small non-coding RNA molecules that negatively regulate gene expression via degradation or translational repression of their targeted messenger RNAs. It is known that aberrant microRNA expression can play important roles in cancer, but the role of microRNA in autoimmune diseases is only beginning to emerge. In this study, the expression of selected microRNA is examined in rheumatoid arthritis. Methods: Total RNA was isolated from peripheral blood mononuclear cells obtained from rheumatoid arthritis patients, healthy, and disease controls and the expression of miR-146a, miR-155, miR-132, miR-16, and microRNA let-7a was analyzed using quantitative real time polymerase chain reaction. Results: Rheumatoid arthritis peripheral blood mononuclear cells exhibited between 1.8 to 2.6 fold increase in miR-146a, miR-155, miR-132, and miR-16 expression, while let-7a expression was not significantly different compared to healthy controls. In addition, two targets of miR-146a, tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK-1), were similarly expressed between rheumatoid arthritis patients and controls, despite the increased expression of miR-146a in rheumatoid arthritis patients. Repression of tumor necrosis factor receptor-associated factor 6 and/or interleukin-1 receptor-associated kinase 1 in THP-1 cells resulted in up to an 86% reduction in tumor necrosis factor-alpha production, implicating that normal miR-146a function is critical for the regulation of tumor necrosis factor-alpha production. Conclusions: Recent studies have shown that rheumatoid arthritis patient synovial tissue and synovial fibroblasts exhibit increased expression of certain microRNA. Our data thus demonstrate that microRNA expression in rheumatoid arthritis peripheral blood mononuclear cells mimics that of synovial tissue/fibroblasts. The increased microRNA expression in rheumatoid arthritis patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy but this will require confirmation using a large and well-defined cohort. Our data also suggest a possible mechanism contributing to rheumatoid arthritis pathogenesis where miR-146a expression is increased but unable to properly function, leading to prolonged tumor necrosis factor-alpha production in rheumatoid arthritis patients.

Annals of the Rheumatic Diseases current issue

[Editorials] Arthritis and endogenous glucocorticoids: the emerging role of the 11{beta}-HSD enzymes
Buttgereit, F., Zhou, H., Seibel, M. J Tue, 12 Aug 2008 00:00:00 -0000

[Extended reports] Local and systemic glucocorticoid metabolism in inflammatory arthritis
Hardy, R, Rabbitt, E H, Filer, A, Emery, P, Hewison, M, Stewart, P M, Gittoes, N J, Buckley, C D, Raza, K, Cooper, M S Tue, 12 Aug 2008 00:00:00 -0000
Background: Isolated, primary synovial fibroblasts generate active glucocorticoids through expression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). This enzyme produces cortisol from inactive cortisone (and prednisolone from prednisone). Objective: To determine how intact synovial tissue metabolises glucocorticoids and to identify the local and systemic consequences of this activity by examination of glucocorticoid metabolism in patients with rheumatoid arthritis (RA). Methods: Synovial tissue was taken from patients with RA during joint replacement surgery. Glucocorticoid metabolism in explants was assessed by thin-layer chromatography and specific enzyme inhibitors. RT-PCR and immunohistochemistry were used to determine expression and distribution of 11β-HSD enzymes. Systemic glucocorticoid metabolism was examined in patients with RA using gas chromatography/mass spectrometry. Results: Synovial tissue synthesised cortisol from cortisone, confirming functional 11β-HSD1 expression. In patients with RA, enzyme activity correlated with donor erythrocyte sedimentation rate (ESR). Synovial tissues could also convert cortisol back to cortisone. Inhibitor studies and immunohistochemistry suggested this was owing to 11β-HSD2 expression in synovial macrophages, whereas 11β-HSD1 expression occurred primarily in fibroblasts. Synovial fluids exhibited lower cortisone levels than matched serum samples, indicating net local steroid activation. Urinary analyses indicated high 11β-HSD1 activity in untreated patients with RA compared with controls and a significant correlation between total body 11β-HSD1 activity and ESR. Conclusions: Synovial tissue metabolises glucocorticoids, the predominant effect being glucocorticoid activation, and this increases with inflammation. Endogenous glucocorticoid production in the joint is likely to have an impact on local inflammation and bone integrity.
[Extended reports] Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis
Ferrandiz, M L, Maicas, N, Garcia-Arnandis, I, Terencio, M C, Motterlini, R, Devesa, I, Joosten, L A B, van den Berg, W B, Alcaraz, M J Tue, 12 Aug 2008 00:00:00 -0000
Objective: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). Methods: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E2 (PGE2) by radioimmunoassay. Localisation of cyclooxygenase-2 (COX-2), haem oxygenase-1 (HO-1), intercellular adhesion molecule-1 (ICAM-1) and receptor activator of nuclear factor B ligand (RANKL) was examined by immunohistochemistry. Results: Therapeutic administration of CORM-3 suppressed clinical and histopathological manifestations of disease. The levels of PGE2, interleukin (IL)1β, IL2, IL6, IL10 and tumour necrosis factor (TNF) in joint tissues were inhibited by CORM-3. By contrast, CORM-3 augmented IL4. Anti-type II collagen antibodies and COMP levels in serum were reduced by CORM-3. Treatment with CORM-3 decreased cellular infiltration, joint inflammation and destruction, as well as the expression of COX-2, ICAM-1 and RANKL, whereas HO-1 increased. These beneficial effects were due to CO release, as iCORM-3 was ineffective. Conclusion: This study reveals the antiarthritic properties of CORM-3 in the CIA model and supports the notion that CO-RMs could be developed as a novel strategy for the treatment of inflammatory and arthritic conditions.
[Extended reports] Adalimumab effectively reduces the signs and symptoms of active ankylosing spondylitis in patients with total spinal ankylosis
van der Heijde, D, Pangan, A L, Schiff, M H, Braun, J, Borofsky, M, Torre, J, Davis, J C, Wong, R L, Kupper, H, Collantes, E, for the ATLAS Study Group Tue, 12 Aug 2008 00:00:00 -0000
Objective: To evaluate the long-term safety and efficacy of adalimumab in patients with ankylosing spondylitis (AS) and total spinal ankylosis (TSA). Design: Patients (n = 315) with active AS were randomised in a 2:1 ratio to receive adalimumab 40 mg every other week or placebo for 24 weeks followed by open-label adalimumab for up to 5 years. Two-year efficacy and safety data for 11 patients with investigator-defined TSA were evaluated. The primary end point was the ASsessment in AS International Working Group criteria for 20% improvement (ASAS20) at Week 12. On or after Week 12, ASAS20 non-responders could switch to open-label adalimumab. Other efficacy measurements included ASAS40, ASAS 5/6, ASAS partial remission, and 50% improvement in the Bath AS Disease Activity Index (BASDAI 50). Results: 6 of 11 TSA patients were randomised to adalimumab and 5 to placebo. At Week 12, 50% of the adalimumab-treated patients achieved an ASAS20 response and 33% achieved an ASAS40, ASAS 5/6 and BASDAI 50. No placebo-treated patients achieved any response criteria at Week 12. 4 placebo- and 2 adalimumab-treated patients switched to open-label adalimumab before Week 24. After 1 year of adalimumab treatment, 8 of 11 patients achieved an ASAS20 response. After 2 years, 6 of the remaining 8 patients with TSA reported an ASAS20 response. There were no serious adverse events or adverse event-related study discontinuations. Conclusion: In patients with TSA, adalimumab treatment resulted in rapid and clinically significant improvement in the signs and symptoms of active disease. Adalimumab effectiveness and safety were sustained for at least 2 years. Trial registration number: NCT00085644.
[Extended reports] Long-term effects of bosentan on quality of life, survival, safety and tolerability in pulmonary arterial hypertension related to connective tissue diseases
Denton, C P, Pope, J E, Peter, H-H, Gabrielli, A, Boonstra, A, van den Hoogen, F H J, Riemekasten, G, De Vita, S, Morganti, A, Dolberg, M, Berkani, O, Guillevin, L, (on behalf of the TRacleer Use in PAH associated with Scleroderma and Connective Tissue Diseases (TRUST) Investigators) Tue, 12 Aug 2008 00:00:00 -0000
Objectives: This study investigated the long-term effects of bosentan, an oral endothelin ETA/ETB receptor antagonist, in patients with pulmonary arterial hypertension (PAH) exclusively related to connective tissue diseases (CTD). Methods: A total of 53 patients with PAH related to connective tissue diseases (PAH–CTD) in World Health Organization (WHO) functional class III received bosentan 62.5 mg twice a day for 4 weeks and then 125 mg twice a day for 44 weeks in this open non-comparative study. Assessments at weeks 16 and 48 included WHO class, clinical worsening, quality of life (Short-Form Health Survey (SF-36) and health assessment questionnaire (HAQ) modified for scleroderma), and survival (week 48 only). Safety and tolerability were monitored throughout the study. Results: At week 48, WHO class improved in 27% of patients (95% CI 16–42%) and worsened in 16% (95% CI 7–29%). Kaplan–Meier estimates were 68% (95% CI 55–82%) for absence of clinical worsening and 92% (95% CI 85–100%) for survival. Overall changes in quality of life were minimal. There were no unexpected side effects observed during the study. Conclusions: In most patients, bosentan was associated with improvement or stability of clinical status. The 92% estimate for survival at 48 weeks is a significant achievement in this patient population.
[Extended reports] The effectiveness and medication costs of three anti-tumour necrosis factor {alpha} agents in the treatment of rheumatoid arthritis from prospective clinical practice data
Kievit, W, Adang, E M, Fransen, J, Kuper, H H, van de Laar, M A F J, Jansen, T L, De Gendt, C M A, De Rooij, D-J R A M, Brus, H L M, Van Oijen, P C M, Van Riel, P C L M Tue, 12 Aug 2008 00:00:00 -0000
Aim: to evaluate the effects of adalimumab, etanercept and infliximab on disease activity, functional ability and quality of life and the medication costs in a naturalistic design. Methods: All patients from the Dutch Rheumatoid Arthritis Monitoring (DREAM) register starting on tumour necrosis factor (TNF)-blocking agents for the first time were monitored and assessed by trained research nurses every 3 months. The primary outcome was the Disease Activity Score (DAS28) course over the 12 months follow-up, analysed by linear mixed models. Secondary outcomes were the Health Assessment Questionnaire (HAQ), EuroQol five dimensions (EQ-5D) and the Short-Form 36 items (SF36) scores, and medication-related total costs. Results: The DAS28 and SF-36 physical component scale decreased in all three medication groups over 12 months, but the decrease was larger for adalimumab and etanercept in comparison to infliximab (p<0.001). The analyses of the HAQ and the EQ-5D scores showed the same (non-significant) trend, namely that at 12 months, the functionality and quality of life was better for adalimumab and etanercept patients. With regard to the medication costs, infliximab treatment resulted in significantly higher costs over the follow-up period than treatments with either adalimumab or etanercept. The comparison between adalimumab and etanercept showed a significant difference in the 12-month DAS28 course (p = 0.031). There were no additional indications for differences in effectiveness or costs between adalimumab and etanercept. Conclusion: The evaluation of the effectiveness and costs showed that adalimumab and etanercept are more or less equal and favourable compared to infliximab in the first year of treatment.

Arthritis Care & Research

Pay for performance in rheumatology: Will we get the carrot or the stick?
Allan Gibofsky, J. Timothy Harrington Jr. Fri, 29 Aug 2008 08:14:00 -0000
No abstract.
Lifetime risk of symptomatic knee osteoarthritis
Louise Murphy, Todd A. Schwartz, Charles G. Helmick, Jordan B. Renner, Gail Tudor, Gary Koch, Anca Dragomir, William D. Kalsbeek, Gheorghe Luta, Joanne M. Jordan Fri, 29 Aug 2008 08:14:00 -0000
To estimate the lifetime risk of symptomatic knee osteoarthritis (OA), overall and stratified by sex, race, education, history of knee injury, and body mass index (BMI).The lifetime risk of symptomatic OA in at least 1 knee was estimated from logistic regression models with generalized estimating equations among 3,068 participants of the Johnston County Osteoarthritis Project, a longitudinal study of black and white women and men age [ge]45 years living in rural North Carolina. Radiographic, sociodemographic, and symptomatic knee data measured at baseline (1990-1997) and first followup (1999-2003) were analyzed.The lifetime risk of symptomatic knee OA was 44.7% (95% confidence interval [95% CI] 40.0-49.3%). Cohort members with history of a knee injury had a lifetime risk of 56.8% (95% CI 48.4-65.2%). Lifetime risk rose with increasing BMI, with a risk of 2 in 3 among those who were obese.Nearly half of the adults in Johnston County will develop symptomatic knee OA by age 85 years, with lifetime risk highest among obese persons. These current high risks in Johnston County may suggest similar risks in the general US population, especially given the increase in 2 major risk factors for knee OA, aging, and obesity. This underscores the immediate need for greater use of clinical and public health interventions, especially those that address weight loss and self-management, to reduce the impact of having knee OA.
Effects of specialized footwear on joint loads in osteoarthritis of the knee
Najia Shakoor, Roy H. Lidtke, Mondira Sengupta, Louis F. Fogg, Joel A. Block Fri, 29 Aug 2008 08:14:00 -0000
Elevated dynamic joint loads have been associated with the severity and progression of osteoarthritis (OA) of the knee. This study compared the effects of a specialized shoe (the mobility shoe) designed to lower dynamic loads at the knee with self-chosen conventional walking shoes and with a commercially available walking shoe as a control.Subjects with knee OA were evaluated in 2 groups. Group A (n = 28) underwent gait analyses with both their self-chosen walking shoes and the mobility shoes. Group B (n = 20) underwent gait analyses with a control shoe and the mobility shoe. Frontal plane knee loads were compared between the different footwear conditions.Group A demonstrated an 8% reduction in the peak external knee adduction moment with the mobility shoe compared with self-chosen walking shoes (mean ± SD 49 ± 0.80 versus 2.71 ± 0.84 %BW × H; P < 0.05). Group B demonstrated a 12% reduction in the peak external knee adduction moment with the mobility shoe compared with the control shoe (mean ± SD 2.66 ± 0.69 versus 3.07 ± 0.75 %BW × H; P < 0.05).Specialized footwear can effectively reduce joint loads in subjects with knee OA, compared with self-chosen shoes and control walking shoes. Footwear may represent a therapeutic target for the treatment of knee OA. The types of shoes worn by subjects with knee OA should be evaluated more closely in terms of their effects on the disease.

Arthritis & Rheumatism

In this Issue
Fri, 29 Aug 2008 08:13:00 -0000
NO abstract.
Treatment-failure gout: A moving target
N. Lawrence Edwards Fri, 29 Aug 2008 08:13:00 -0000
No abstract.
Genome-wide single-nucleotide polymorphism studies in rheumatology: Hype or hope?
Annette H. M. van der Helm-van Mil, Leonid Padyukov, René E. M. Toes, Lars Klareskog, Tom W. J. Huizinga Fri, 29 Aug 2008 08:13:00 -0000
No abstract.

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