Published online Feb 7, 2023. doi: 10.3748/wjg.v29.i5.825
Peer-review started: September 27, 2022
First decision: October 20, 2022
Revised: October 29, 2022
Accepted: January 11, 2023
Article in press: January 11, 2023
Published online: February 7, 2023
Processing time: 132 Days and 1 Hours
Given that the liver is involved in many metabolic mechanisms, it is not surprising that chronic liver disease (CLD) could have numerous complications. Secondary osteoporosis and increased bone fragility are frequently overlooked complications in CLD patients. Previous studies implied that up to one-third of these individuals meet diagnostic criteria for osteopenia or osteoporosis. Recent publications indicated that CLD-induced bone fragility depends on the etiology, duration, and stage of liver disease. Therefore, the increased fracture risk in CLD patients puts a severe socioeconomic burden on the health system and urgently requires more effective prevention, diagnosis, and treatment measures. The pathogenesis of CLD-induced bone loss is multifactorial and still insufficiently understood, especially considering the relative impact of increased bone resorption and reduced bone formation in these individuals. It is essential to note that inconsistent findings regarding bone mineral density measurement were previously reported in these individuals. Bone mineral density is widely used as the “golden standard” in the clinical assessment of bone fragility although it is not adequate to predict individual fracture risk. Therefore, microscale bone alterations (bone microstructure, mechanical properties, and cellular indices) were analyzed in CLD individuals. These studies further support the thesis that bone strength could be compromised in CLD individuals, implying that an individualized approach to fracture risk assessment and subsequent therapy is necessary for CLD patients. However, more well-designed studies are required to solve the bone fragility puzzle in CLD patients.
Core Tip: Secondary osteoporosis and increased bone fragility are frequently overlooked complications in patients with chronic liver disease (CLD). Recent publications agree that CLD-induced bone fragility depends on the etiology, duration, and stage of liver disease, but certain ambiguities are still present. Importantly, etiopathogenetic mechanisms leading to CLD-induced bone loss are still insufficiently clarified. Given that available clinical tools for fracture risk assessment are not entirely reliable, evaluating small-length structural bone properties could improve understanding of the multifactorial nature of bone fragility in CLD patients, which could set a base for the development of more effective preventive and therapeutic strategies.