Increased Fracture Risk in Patients with Rheumatic Disorders and Other Inflammatory Diseases - A Case-Control Study with 53,108 Patients with Fracture

Department of Molecular Medicine and Surgery, Section of Orthopedics and Sports Medicine, Karolinska University Hospital/Karolinska Institutet, S-171 76, Stockholm, Sweden.
The Journal of Rheumatology (Impact Factor: 3.19). 10/2010; 37(11):2247-50. DOI: 10.3899/jrheum.100363
Source: PubMed


To identify the risk of hip and vertebral fractures in patients with rheumatic disorders (RD) and inflammatory bowel diseases (IBD).
This population-based case-control study assessed the fracture risk of patients with rheumatoid arthritis, juvenile idiopathic arthritis (JIA), ankylosing spondylitis (AS), systemic lupus erythematosus, polymyositis/dermatomyositis (PM/DM), systemic sclerosis (SSc), Crohn's disease, and ulcerative colitis (UC). The study cohort comprised 53,108 patients with fracture (66% women) and 370,602 age-matched and sex-matched controls. Conditional logistic regression analysis was performed and results were expressed as OR with corresponding 95% CI.
There was a statistically significant increased fracture risk for all RD and for IBD compared with controls. The magnitude of fracture risk was higher for patients with RD (OR 3, 95% CI 2.9-3.2) than for those with IBD (OR 1.6, 1.4-1.8). The OR in RD ranged from 2.6 (1.3-4.9) for SSc to 4 (3.4-4.6) for AS. The largest increased fracture risk for vertebral fractures was seen in AS (OR 7.1, 6-8.4) and for hip fractures in JIA (OR 4.1, 2.4-6.9).
Our results highlight the existence of an increased fracture risk from a variety of underlying causes in patients with RD and IBD. In many inflammatory diseases, implementation of fracture prevention strategies may be beneficial.

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    • "The protocol was specifically developed for future clinical application to measure foot bone health in people with chronic inflammatory arthritis conditions such as rheumatoid arthritis who are at risk of metatarsal fractures [26]. However this protocol may have a broader application to other clinical populations with suboptimal bone mass, as well as military recruits, and athletic populations such as gymnasts and runners that are susceptible to fatigue-type stress fractures in the foot [27]. "
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    • "Decreasing lumbar vBMD measured with QCT was, in addition, associated with deteriorated peripheral bone microarchitecture, such as thinner trabeculae, higher trabecular separation, and reduced cortical thickness. This may explain the increased frequency of hip and peripheral fractures observed in an earlier study on Swedish AS patients [5]. "
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    ABSTRACT: Osteoporosis of the axial skeleton is a known complication of ankylosing spondylitis (AS), but bone loss affecting the peripheral skeleton is less studied. This study on volumetric bone mineral density (vBMD) and bone microarchitecture in AS was conducted to compare peripheral vBMD in AS patients with that in healthy controls, to study vBMD in axial compared with peripheral bone, and to explore the relation between vertebral fractures, spinal osteoproliferation, and peripheral bone microarchitecture and density. High-resolution peripheral quantitative computed tomography (HRpQCT) of ultradistal radius and tibia and QCT and dual-energy x-ray absorptiometry (DXA) of lumbar spine were performed in 69 male AS patients (NY criteria). Spinal radiographs were assessed for vertebral fractures and syndesmophyte formation (mSASSS). The HRpQCT measurements were compared with the measurements of healthy controls. The AS patients had lower cortical vBMD in radius (P = 0.004) and lower trabecular vBMD in tibia (P = 0.033), than did the controls. Strong correlations were found between trabecular vBMD in lumbar spine, radius (rS = 0.762; P < 0.001), and tibia (rS = 0.712; P < 0.001).When compared with age-matched AS controls, patients with vertebral fractures had lower lumbar cortical vBMD (-22%; P = 0.019), lower cortical cross-sectional area in radius (-28.3%; P = 0.001) and tibia (-24.0%; P = 0.013), and thinner cortical bone in radius (-28.3%; P = 0.001) and tibia (-26.9%; P = 0.016).mSASSS correlated negatively with trabecular vBMD in lumbar spine (rS = -0.620; P < 0.001), radius (rS = -0.400; p = 0.001) and tibia (rS = -0.475; p < 0.001) and also with trabecular thickness in radius (rS = -0.528; P < 0.001) and tibia (rS = -0.488; P < 0.001).Adjusted for age, syndesmophytes were significantly associated with decreasing trabecular vBMD, but increasing cortical vBMD in lumbar spine, but not with increasing cortical thickness or density in peripheral bone. Estimated lumbar vBMD by DXA correlated with trabecular vBMD measured by QCT (rS = 0.636; P < 0.001). Lumbar osteoporosis, syndesmophytes, and vertebral fractures were associated with both lower vBMD and deteriorated microarchitecture in peripheral bone. The results indicate that trabecular bone loss is general, whereas osteoproliferation is local in AS.
    Full-text · Article · Nov 2013 · Arthritis research & therapy
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    • "Thin-ground sections were prepared along the implant axis and Levai–Laczko stained. 2005; Weiss et al. 2010). In line with the clinical findings, rodents with chemically induced colitis exhibited a lower trabecular bone volume early after disease induction (Lin et al. 1996; Hamdani et al. 2008). "
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    ABSTRACT: Crohn's disease is a chronic inflammatory process that has recently been associated with a higher risk of early implant failure. Herein we provide information on the impact of colitis on peri-implant bone formation using preclinical models of chemically induced colitis. Colitis was induced by intrarectal instillation of 2,4,6-trinitro-benzene-sulfonic-acid (TNBS). Colitis was also induced by feeding rats dextran-sodium-sulfate (DSS) in drinking water. One week after disease induction, titanium miniscrews were inserted into the tibia. Four weeks after implantation, peri-implant bone volume per tissue volume (BV/TV) and bone-to-implant contacts (BIC) were determined by histomorphometric analysis. Cortical histomorphometric parameters were similar in the control (n = 10), DSS (n = 10) and TNBS (n = 8) groups. Cortical BV/TV was 92.2 ± 3.7%, 92.0 ± 3.0% and 92.6 ± 2.7%. Cortical BIC was 81.3 ± 8.8%, 83.2 ± 8.4% and 84.0 ± 7.0%, respectively. No significant differences were observed when comparing the medullary BV/TV and BIC (19.5 ± 6.4%, 16.2 ± 5.6% and 15.4 ± 9.0%) and (48.8 ± 12.9%, 49.2 ± 6.2 and 41.9 ± 11.7%), respectively. Successful induction of colitis was confirmed by loss of body weight and colon morphology. The results suggest bone regeneration around implants is not impaired in chemically induced colitis models. Considering that Crohn's disease can affect any part of the gastrointestinal tract including the mouth, our model only partially reflects the clinical situation.
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