Spinal fractures in ankylosing spondylitis: prevalence, prevention and management
نویسندگان
چکیده
Patients with chronic inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosis, inflammatory bowel disease (IBD) and chronic obstructive pulmonary diseases, have an increased risk for bone fragility resulting in an increased risk of vertebral and non vertebral fractures. These diseases are characterized by inflammation-induced bone loss and erosive bone destruction. Therefore, guidelines advocate fracture prevention in such high-risk patients. By contrast, in patients with ankylosing spondylitis (AS), inflammation also induces bone loss and bone erosions, but typically new bone formation is found, both intra-osseous (such as in the sacroiliac joints) and extra-osseous (such as in syndesmophytes). In the early 1970s, Cawley et al. showed, on a postmortem transversally sliced spine specimen of a patient with long-standing AS, the multiple bone changes in vertebrae and their annexes, including intravertebral bone loss, intraand extra-osseous bone sclerosis, syndesmo phytes, disc destruction, disc calcifications and vertebral wedging resulting in hyper kyphosis (Figure 1) [1]. In patients with AS, the risk of vertebral fractures (VFs) is increased, but case finding and prevention of VFs in patients with AS is a clinical challenge (Table 1). First, back pain and hyperkyphosis are mostly attributed to disease-related inflammation and structural damage, and an eventual VF could be overlooked if no imaging of the spine is performed. Second, besides classical VFs in the ankylosed spine, fractures can also occur in the vertebral annexes. Third, the complex combination of bone changes in the vertebrae interferes with the interpretation of the spine bone density. AS belongs to the group of spondyloarthritides, which comprises a wide spectrum of clinical entities with shared features, including AS, as inflammatory back pain and arthritis associated with IBD, Crohn’s disease and ulcerative colitis and psoriatic arthritis [2]. In the concept of spondylo arthritides, AS is the most known type with chronic inflammation mainly of the axial skeleton. Prevalence of AS within the entire group of spondylarthropathies varies between 15 and 50%, according to several authors [3,4]. AS is characterized by enthesitis, sacroiliitis and spinal inflammation. These features may lead to ossification of the spinal ligaments, joints and discs, and to progressive rigidity of the spine. Besides articular and spinal manifestations, patients with AS may suffer from extra-articulair manifestations, such as IBD (5–10% of patients), psoriasis (10–25% of patients) and uveitis (1–53% of patients), where prevalence rates vary depending on clinical and methodological c haracteristics of the studies [5–7]. Ankylosis of the spine (ultimately resulting in a bamboo spine) and thoracic hyperkyphosis are typical clinical features of long-standing AS, but In patients with ankylosing spondylitis (AS), the risk of vertebral fractures (VFs) is increased. Case finding and fractures in patients with AS is a clinical challenge for several reasons. First, back pain and hyperkyphosis are mostly attributed to disease-related inflammation and structural damage in terms of erosions and syndesmophytes, and not to an eventual VF. Second, the most frequent VFs are classical wedging, biconcave or crush VFs as seen in postmenopausal women and the elderly, but once multilevel ankylosis of the spine is manifested, fractures can also occur in other parts and directions of the vertebrae (transvertebral, in the dorsal arch structures and through the ankylosed extravertebral calcifications of ligaments and intervertebral discs) and in the cervical spine. Diagnosis of these atypical fractures is much more difficult. Besides the pathology of fractures in general in patients with AS, VFs are associated with hyperkyphosis of the spine and can result in irreversible neurological complications. In this review, the authors propose a five-step approach for fracture prevention, starting with case finding and the subsequent difficulties in imaging, followed by risk evaluation, differential diagnosis and therapeutic strategies and follow-up, in order to translate current knowledge on fracture risk and fracture prevention, in general, towards patients with AS.
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