TBS has repeatedly been proven to be predictive of fragility fractures, current and future, and this is largely independent of BMD, CRF, and the FRAX, and when used in conjunction with any one of these measures, it consistently enhances their accuracy. There also is a growing body of evidence indicating that the TBS has particular advantages over BMD for specific causes of increased fracture risk, like chronic corticosteroid excess, type-2 diabetes, and chronic kidney disease, and patients being treated with anti-aromatase and primary hyperparathyroidism, conditions wherein BMD readings are often misleading. TBS enhances performance of the FRAX tool, where its greatest utility appears to lie in its ability to accurately classify those patients whose BMD level lies close to the intervention threshold, aiding in decisions on whether treatment is warranted or not. Furthermore, TBS has also particular advantages over BMD in secondary osteoporosis. While the role of TBS with monitoring could be important as the different molecules impact logically TBS to various degrees, large clinical trials are still needed.

No abstract

Treatment with bDMARDs decreases plasma ecDNA of both nuclear and mitochondrial origin. Dynamics of ecDNA is slower than dynamics of standard clinical markers. Therefore, it is likely to be not useful for monitoring of the disease progress, at least for RA.

A 62-year-old man presented with diabetes insipidus, pulmonary fibrosis, right atrial tumor and bilateral knee osteoarthritis with cystic lesions of distal femur and proximal tibia. Scintigraphy and histological examination of right femur bone biopsy revealed changes characterized for Paget's disease. Re-evaluation of the computer tomography (CT) scans and histological samples revealed diffuse infiltrates of foamy histiocytes in the bone marrow what was consistent with Erdheim-Chester disease. Positron emission tomography/computed tomography (PET/CT) was performed to access the activity and extent of disease.