Osteonecrosis of the jaw (ONJ) can be associated with nitrogen-containing bisphosphonates (NBPs) therapy. Various mechanisms of NBP-associated ONJ have been proposed and there is currently no consensus of the underlying pathogenesis. The detailed medical and dental histories of 30 ONJ patients treated with NBPs for malignant diseases (24) or osteoporosis (6) were analyzed. The necrotic bone was resected and analyzed histologically after demineralization. In 10 patients the perinecrotic bone was also resected and processed without demineralization. Alveolar bone samples from 5 healthy patients were used as controls. In 14 ONJ patients, serial technetium-99m-methylene diphosphonate scintigraphic scans were also available and confronted to the other data. Strong radionuclide uptake was detected in some patients several months before clinical diagnosis of ONJ. The medullary spaces of the necrotic bone were filled with bacterial aggregates. In the perinecrotic bone, the bacteria-free bone marrow characteristically showed an inflammatory reaction. The number of medullary inflammatory cells taken as an index of inflammation allowed us to discriminate two inflammation grades in the ONJ samples. Low-grade inflammation, characterized by marrow fibrosis and low inflammatory cells infiltration, increased numbers of TRAP + monoand multineacleated cells was seen in patients with bone exposure b 2 cm 2 . High-grade inflammation, associated with larger lesions, showed amounts of tartrate-resistant acid phosphatase + /calcitonin receptor − mono-and multinucleated cells, osteocyte apoptosis, hypervascularization and high inflammatory cell infiltration. The clinical extent of ONJ was statistically linked to the numbers of inflammatory cell. Taken together these data suggest that bone necrosis precedes clinical onset and is an inflammation-associated process. We hypothesize that from an initial focus, bone damage spreads centrifugally, both deeper into the jaw and towards the mucosa before the oral bone exposure and the clinical diagnosis of ONJ.
Our preliminary data obtained in a limited number of patients shows that contrast-enhanced FDG PET/CT offers good sensitivity in the detection and assessment of pancreatic cancer, but at the price of a relatively low specificity. Enhanced PET/CT seems to be superior to unenhanced PET/CT. Further larger prospective studies are needed to establish its value for pre-surgical diagnosis and staging in pancreatic cancer.
Treatment with rosiglitazone increased the production of thyroglobulin in some patients with thyroid cancers, but only rarely restored scintigraphically significant iodine trapping. It remains to be shown whether longer treatment periods might result in a more efficient redifferentiating effect.
Even 6 months after acute pyelonephritis 72% of dimercapto-succinic acid defects improved, demonstrating that some of the lesions may be not definitive. The number of scars was significantly associated with loss of renal growth at 3 years.
A lthough the degree of lumen obstruction is a relevant marker of the risk of stroke, the recognition of the role of the vulnerable plaque has opened new insights in the field of atherothrombotic stroke. [1][2][3][4] Vulnerability is dictated in part by plaque morphology, which, in turn, is influenced by pathophysiologic mechanisms at the cellular and molecular level. Thus, a certain number of features of plaque morphology may play an important role in the occurrence of cerebrovascular events. [5][6][7] An unstable plaque, on the one hand, has a thin fibrous cap that contains large numbers of macrophages and T lymphocytes and a small number of smooth muscle cells. A stable plaque, on the other hand, has a thicker cap with larger numbers of smooth muscle cells and less inflammation. [8][9][10] Intensive research has been performed aimed at optimizing different imaging modalities to precisely analyze the arterial wall morphology, plaque composition, and degree of local inflammation. Among them, positron emission tomography (PET) using 18 fluoro-2-deoxy-d-glucose (18FdG) as a radiotracer has shown promise for detection of local inflammation in atherosclerotic plaques.11 Indeed, high levels of glucose metabolism are typically seen in tissue with inflammatory activity. 12 Moreover, significant positive correlations between histopathologic findings and degree of plaque inflammation depicted by 18FdG uptake have been documented. [13][14][15][16][17][18] Accordingly, a few clinical studies suggested a potential role of 18FdG-PET-computed tomography (CT) for the diagnosis of high-risk carotid plaques. Rudd et al 13 showed that PET-CT might be used to image inflammatory cell activity within the carotid plaque. The study involved only 8 patients but was capable to demonstrate that 18FdG uptake was significantly higher within the symptomatic as compared with the contralateral plaque. Another study showed in a retrospective analysis Background and Purpose-We investigated whether uptake of 18 fluoro-2-deoxy-d-glucose (18FdG) positron emission tomography-computed tomography (PET-CT) correlated to clinical symptoms and presence of microembolic signals (MES) detected by transcranial doppler in patients with carotid stenosis. Methods-18FdG-PET-CT and MES detection was performed in consecutive patients with 50% to 99% symptomatic or asymptomatic carotid stenoses. Uptake index was defined by a target to background ratio (TBR) between maximum standardized uptake value of the carotid plaque and the mean standardized uptake value of the jugular veins. End points for analysis were presence of symptoms and presence of MES. 22,23 A recent study showed a correlation between 18FdG-PET-MRI and presence of MES in 16 patients presenting with recent transient ischemic attack or minor stroke and 50% to 99% stenosis of the ipsilateral carotid bifurcation. There was a significant difference in the target to background ratio (TBR) values between MES positive (+) and MES negative (−) patients, reinforcing the notion that embolization occurring dist...
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