Abstract:SummaryRadiographs and spinal bone mineral density (BMD) were evaluated from 342 elderly men regarding possible effects of diffuse idiopathic skeletal hyperostosis (DISH) on vertebral fractures and densitometry measurements. Prevalent vertebral fractures were more frequent among men with DISH compared to men with no DISH even after fracture prevalence was adjusted for BMD. Paravertebral calcifications should be considered in patients with DISH when interpreting BMD measurements because both dual X-ray absorpti… Show more
“…A recent study comparing DXA and QCT in older men with diffuse idiopathic skeletal hyperostosis demonstrated that QCT was better suited to differentiate men with and without vertebral fractures [47].…”
The radiologist has a number of roles not only in diagnosing but also in treating osteoporosis. Radiologists diagnose fragility fractures with all imaging modalities, which includes magnetic resonance imaging (MRI) demonstrating radiologically occult insufficiency fractures, but also lateral chest radiographs showing asymptomatic vertebral fractures. In particular MRI fragility fractures may have a nonspecific appearance and the radiologists needs to be familiar with the typical locations and findings, to differentiate these fractures from neoplastic lesions. It should be noted that radiologists do not simply need to diagnose fractures related to osteoporosis but also to diagnose those fractures which are complications of osteoporosis related pharmacotherapy. In addition to using standard radiological techniques radiologists also use dual-energy x-ray absorptiometry (DXA) and quantitative computed tomography (QCT) to quantitatively assess bone mineral density for diagnosing osteoporosis or osteopenia as well as to monitor therapy. DXA measurements of the femoral neck are also used to calculate osteoporotic fracture risk based on the Fracture Risk Assessment Tool (FRAX) score, which is universally available. Some of the new technologies such as high-resolution peripheral computed tomography (HR-pQCT) and MR spectroscopy allow assessment of bone architecture and bone marrow composition to characterize fracture risk. Finally radiologists are also involved in the therapy of osteoporotic fractures by using vertebroplasty, kyphoplasty, and sacroplasty. This review article will focus on standard techniques and new concepts in diagnosing and managing osteoporosis.
“…A recent study comparing DXA and QCT in older men with diffuse idiopathic skeletal hyperostosis demonstrated that QCT was better suited to differentiate men with and without vertebral fractures [47].…”
The radiologist has a number of roles not only in diagnosing but also in treating osteoporosis. Radiologists diagnose fragility fractures with all imaging modalities, which includes magnetic resonance imaging (MRI) demonstrating radiologically occult insufficiency fractures, but also lateral chest radiographs showing asymptomatic vertebral fractures. In particular MRI fragility fractures may have a nonspecific appearance and the radiologists needs to be familiar with the typical locations and findings, to differentiate these fractures from neoplastic lesions. It should be noted that radiologists do not simply need to diagnose fractures related to osteoporosis but also to diagnose those fractures which are complications of osteoporosis related pharmacotherapy. In addition to using standard radiological techniques radiologists also use dual-energy x-ray absorptiometry (DXA) and quantitative computed tomography (QCT) to quantitatively assess bone mineral density for diagnosing osteoporosis or osteopenia as well as to monitor therapy. DXA measurements of the femoral neck are also used to calculate osteoporotic fracture risk based on the Fracture Risk Assessment Tool (FRAX) score, which is universally available. Some of the new technologies such as high-resolution peripheral computed tomography (HR-pQCT) and MR spectroscopy allow assessment of bone architecture and bone marrow composition to characterize fracture risk. Finally radiologists are also involved in the therapy of osteoporotic fractures by using vertebroplasty, kyphoplasty, and sacroplasty. This review article will focus on standard techniques and new concepts in diagnosing and managing osteoporosis.
“…(7) DISH often manifests as back pain associated with limited range of spinal motion, but can progress to the extent that lesions interfere with neighboring structures, including compression of the spinal cord and nerve roots. (8,9) Lesions in DISH can also cause dysphagia, (10) and DISH is associated with increased susceptibility to spinal fractures (11) and postsurgical heterotopic ossifications. (12) Correlative studies have associated obesity, hypertension, diabetes mellitus, hyperinsulinemia, dyslipidemia, elevated growth hormone levels, elevated insulin-like growth factor-1, and hyperuricemia with DISH.…”
Diffuse idiopathic skeletal hyperostosis (DISH) is a noninflammatory spondyloarthropathy, characterized by ectopic calcification of spinal tissues. Symptoms include spine pain and stiffness, and in severe cases dysphagia and spinal cord compression. The etiology of DISH is unknown and there are no specific treatments. Recent studies have suggested a role for purine metabolism in the regulation of biomineralization. Equilibrative nucleoside transporter 1 (ENT1) transfers hydrophilic nucleosides, such as adenosine, across the plasma membrane. In mice lacking ENT1, we observed the development of calcified lesions resembling DISH. By 12 months of age, ENT1 -/-mice exhibited signs of spine stiffness, hind limb dysfunction, and paralysis. Micro-computed tomography (mCT) revealed ectopic mineralization of paraspinal tissues in the cervical-thoracic region at 2 months of age, which extended to the lumbar and caudal regions with advancing age. Energy-dispersive X-ray microanalysis of lesions revealed a high content of calcium and phosphorus with a ratio similar to that of cortical bone. At 12 months of age, histological examination of ENT1 -/-mice revealed large, irregular accumulations of eosinophilic material in paraspinal ligaments and entheses, intervertebral discs, and sternocostal articulations. There was no evidence of mineralization in appendicular joints or blood vessels, indicating specificity for the axial skeleton. Plasma adenosine levels were significantly greater in ENT1 -/-mice than in wild-type, consistent with loss of ENT1-a primary adenosine uptake pathway. There was a significant reduction in the expression of Enpp1, Ank, and Alpl in intervertebral discs from ENT1 -/-mice compared to wild-type mice. Elevated plasma levels of inorganic pyrophosphate in ENT1 -/-mice indicated generalized disruption of pyrophosphate homeostasis. This is the first report of a role for ENT1 in regulating the calcification of soft tissues. Moreover, ENT1 -/-mice may be a useful model for investigating pathogenesis and evaluating therapeutics for the prevention of mineralization in DISH and related disorders. ß
“…The risk of spinal injury is compounded by alteration in bone metabolism that accompanies both of these conditions, although with some differences. Increased prevalence of vertebral fractures is seen in patients with AS with diminished relative bone mineral density (11) with similar reports of increased prevalence of vertebral fractures in patients with DISH, although paradoxically with increased bone mineral density on conventional testing (5).…”
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