Objectives: The purpose of this study was to present the CT and MRI findings of patients with fibrous dysplasia (FD) of the spine. Methods: Among the patients with pathologically proven skeletal FD, 12 (8 males and 4 females; mean age, 43 years) who were evaluated with either spine CT or MRI were included. The number and location of the involved vertebral segments, the presence of lytic lesions, ground-glass opacity (GGO), an expansile nature, cortical disruption, a sclerotic rim, a decrease in body height and contour deformity were examined on CT scans (n512), while signal intensity, enhancement patterns and the presence of a dark signal rim on the lesion were examined using MRI (n59). Results: Nine patients had polyostotic FD, including one with an isolated spinal localisation, while three had monostotic FD. An expansile nature (n53) and osteolytic lesions with GGO (n53) were seen. On CT images, GGO was noted in all patients. An expansile nature (n511) and presence of lytic lesions (n511) were noted. A decrease in body height (n59) and sclerotic rim formation (n59) were indicated. Contour deformities were visible in six patients. The MRI findings were non-specific. Dark signal rims were visible on MRI in seven patients. Conclusion: Typical imaging findings of extraspinal FD were noted on spine CT scans. These characteristic CT imaging findings of spinal FD may be helpful in differentiating FD from other common spine diseases. Fibrous dysplasia (FD) is a developmental defect of osteoblastic differentiation and bone maturation of unknown origin [1]. FD may affect the skeleton either in isolation (monostotic FD, rate, 70-80%; and polyostotic FD, rate, 20-30%) or in variable combination with endocrine and cutaneous abnormalities (McCune-Albright syndrome) [2][3][4][5]. Although patients afflicted with FD may present at any age, they are typically young and in the first and second decades of life [6]. After puberty, dysplastic areas rarely expand [7]. In general, the progression of the skeletal lesions tends to be exhausted once patients have reached adult age [7]. The diagnosis of FD is difficult in adult patients because cases in older patients, especially those involving the spine, are rare.FD represents approximately 7% of all benign tumourlike bone lesions [8]. However, the spine is affected in only 2.5% of cases, and FD of the spine is very rarely observed without there being disease elsewhere in the body [9]. Spinal involvement occurs mostly in the polyostotic form of FD; it is unusual for it to occur in the monostotic form [9,10]. When present in the elderly with multiple vertebral lesions, a biopsy may be indicated because metastatic disease or multiple myeloma may simulate a benign non-aggressive process. Therefore, active diagnosis and radiological familiarity of spinal FD are thought to be essential for preventing unnecessary examinations or procedures.The purpose of this study was to present the CT and MRI findings of spinal FD, which is rare, and to assess the efficacy of CT in the diagnosis of FD. Me...
SummaryRecently, parasite infections or parasite-derived products have been suggested as a therapeutic strategy with suppression of immunopathology, which involves the induction of regulatory T cells or/and T helper type 2 (Th2) responses. In a recent study, researchers reported that constructed recombinant galectin (rTl-gal) isolated from an adult worm of the gastrointestinal nematode parasite Toxascaris leonina attenuated clinical symptoms of inflammatory bowel disease in mice treated with dextran sulphate sodium. Noting the role of rTl-gal in inflammatory disease, we attempted to investigate the effect of the parasite via its rTl-gal on neuronal autoimmune disease using experimental autoimmune encephalomyelitis (EAE), a mouse inflammatory and demyelinating autoimmune disease model of human multiple sclerosis. In this model, rTl-gal-treated experimental autoimmune encephalomyelitis (EAE) mice failed to recover after the peak of the disease, leading to persistent central nervous system (CNS) damage, such as demyelination, gliosis and axonal damage. Further, rTl-gal-treated EAE mice markedly increased the number of CD45R/B220 1 B cells in both infiltrated inflammation and the periphery, along with the increased production of autoantibody [antimyelin oligodendrocyte glycoprotein (MOG) ] in serum at chronic stage. Upon antigen restimulation, rTl-gal treatment affected the release of overall cytokines, especially interferon (IFN)-g and tumour necrosis factor (TNF)-a. Our results suggest that galectin isolated from a gastrointestinal parasite can deliver a harmful effect to EAE contrary to its beneficial effect on inflammatory bowel disease.
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