Complications (occurring within the first 6 months postoperatively, e.g., infection) and remaining deficits (after a minimum of 6 months and not changing over time, e.g., bony or sensory deficit) should be clearly separated from each other. Knowledge of permanent deficits and bone healing after different therapeutic approaches is important for decision making. Patients should be informed not only about complications but also about the risk of permanent deficits for each method.

Trabecular BMD and trabecular bone microstructure in particular are severely altered in patients with clinical OI-I and OI-III-IV. Low TBS and DXL and their significant associations to HR-pQCT parameters of trabecular bone support this conclusion.

Summary Liver cirrhosis leads to bone loss. To date, information on bone quality (three-dimensional microarchitecture) and, thus, bone strength is scarce. We observed decreased bone quality at both assessed sites, independent of disease severity. Therefore, all patients should undergo early-stage screening for osteoporosis. Introduction Recent studies found low bone mineral density in cirrhosis, but data on bone microstructure are scarce. This study assessed weight-bearing and non-weight-bearing bones in patients with cirrhosis and healthy controls. The primary objective was to evaluate trabecular and cortical microarchitecture. Methods This was a single-center study in patients with recently diagnosed hepatic cirrhosis. Thirty-two patients and 32 controls participated in this study. After determining the type of cirrhosis, the parameters of bone microarchitecture were assessed by high-resolution peripheral quantitative computed tomography. Results Both cortical and trabecular microarchitectures showed significant alterations. At the radius, trabecular bone volume fraction was 17% lower (corrected p = 0.028), and, at the tibia, differences were slightly more pronounced. Trabecular bone volume fraction was 19% lower ( p = 0.024), cortical bone mineral density 7% ( p = 0.007), and cortical thickness 28% ( p = 0.001), while cortical porosity was 32% higher ( p = 0.023), compared to controls. Areal bone mineral density was lower (lumbar spine − 13%, total hip − 11%, total body − 9%, radius − 17%, and calcaneus − 26%). There was no correlation between disease severity and microarchitecture. Areal bone mineral density (aBMD) measured by dual-energy X-ray absorptiometry (DXA) correlated well with parameters of cortical and trabecular microarchitecture. Conclusions Hepatic cirrhosis deteriorates both trabecular and cortical microarchitecture, regardless of disease severity. Areal bone mineral density is diminished at all sites as a sign of generalized affection. In patients with hepatic cirrhosis, regardless of its origin or disease severity, aBMD measurements are an appropriate tool for osteologic screening.

Home-based TDT could achieve a sustained reduction in PLP and should be considered as a possible alternative to established treatment methods.