ReviewInternational journal of molecular sciences2019
Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 64 citations in OpenAlex.
- Bioactive glasses-mediated ion therapy ameliorates hepatic osteodystrophy by reprogramming the liver-bone axis.Bioactive materials · 2027Article
- The Liver-Bone Axis in Steatotic Liver Disease.Calcified tissue international · 2026Review
- Free Fatty acid-induced disruption of hepatic vitamin D metabolism impairs bone homeostasis in an in vitro 3D human liver-bone model.Archives of toxicology · 2026Article
- Multifunctional scaffold inspired by hepatocyte exosomes promotes bone regeneration by regulating osteogenic differentiation via PI3K/AKT pathway.Materials today. Bio · 2026Article
- Micronutrient deficiencies in hepatic cirrhosis: Navigating challenges to assessment and implications for clinical management: A narrative review.Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition · 2026Review
- Inhibiting hepatocytes MAGL alleviates osteoporosis caused by high-fat diet-induced liver fibrosis in male mice.Journal of the Endocrine Society · 2026Article
- Trabecular bone score enhances fracture risk stratification in patients with metabolic dysfunction-associated steatotic liver disease and type 2 diabetes mellitus.Journal of endocrinological investigation · 2026Article
- The liver-bone axis: an emerging player in disease pathogenesis and therapeutic intervention.Science China. Life sciences · 2026Review
- Identification of the critical immune-related drivers shared by non-alcoholic fatty liver disease and osteoporosis.Cellular and molecular life sciences : CMLS · 2026Article
- Dynamic modelling of liver-bone axis: A microphysiological approach to hepatic osteodystrophy.Bioactive materials · 2026Article
- Elucidating the mechanisms by which acetyl tributyl citrate affects fracture healing: a comprehensive network toxicology study.BMC pharmacology & toxicology · 2026Article
- Article
- Long-term Western diet feeding impairs hepatic vitamin D metabolism and promotes bone loss in mice.EXCLI journal · 2026Article
- Hepatic osteodystrophy: An underrecognized metabolic bone disease.World journal of hepatology · 2025Review
- Vitamin D Deficiency and Chronic Liver Disease: Investigating Predictive Factors and Their Implications for Patient Care in Pakistan.Iranian journal of public health · 2025Article
- Increased BMD in SLD Patients Without Advanced Hepatic Fibrosis: Evidence From the NHANES 2017-2020 Database.Canadian journal of gastroenterology & hepatology · 2025Article
- Mechanisms and targeted prevention of hepatic osteodystrophy caused by a low concentration of di-(2-ethylhexyl)-phthalate.Frontiers in immunology · 2025Article
- Establishment of a human 3D in vitro liver-bone model as a potential system for drug toxicity screening.Archives of toxicology · 2025Article
- Treatment of osteoporosis in the solid organ transplant recipient: an organ-based approach.Therapeutic advances in endocrinology and metabolism · 2025Review
- Osteokines in Nonalcoholic Fatty Liver Disease.Current obesity reports · 2024Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Almost all patients with chronic liver diseases (CLD) show altered bone metabolism. Depending on the etiology, this manifests in a severe osteoporosis in up to 75% of the affected patients. Due to high prevalence, the generic term hepatic osteodystrophy (HOD) evolved, describing altered bone metabolism, decreased bone mineral density, and deterioration of bone structure in patients with CLD. Once developed, HOD is difficult to treat and increases the risk of fragility fractures. Existing fractures affect the quality of life and, more importantly, long-term prognosis of these patients, which presents with increased mortality. Thus, special care is required to support the healing process. However, for early diagnosis (reduce fracture risk) and development of adequate treatment strategies (support healing of existing fractures), it is essential to understand the underlying mechanisms that link disturbed liver function with this bone phenotype. In the present review, we summarize proposed molecular mechanisms favoring the development of HOD and compromising the healing of associated fractures, including alterations in vitamin D metabolism and action, disbalances in transforming growth factor beta (TGF-β) and bone morphogenetic protein (BMP) signaling with histone deacetylases (HDACs) as secondary regulators, as well as alterations in the receptor activator of nuclear factor kappa B ligand (RANKL)-osteoprotegerin (OPG) system mediated by sclerostin. Based on these mechanisms, we give an overview on the limitations of early diagnosis of HOD with established serum markers.
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