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Published on: March 14, 2017
Impact of iron overload on bone remodeling in thalassemia
Pokpong Piriyakhuntorn1, Adisak Tantiworawit1, Mattabhorn Phimphilai2
1Division of Hematology, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Insights
Iron overload in thalassemia patients impairs bone remodeling by increasing oxidative stress, affecting osteoblasts and osteoclasts. This review summarizes mechanisms and treatments for iron overload-induced bone disease.
Area of Science:
- Hematology
- Bone Biology
- Pathophysiology
Background:
- Iron overload is a common complication in thalassemia, leading to organ damage, particularly bone disease.
- Osteoporosis is a frequent and severe complication in thalassemia patients, persisting despite iron chelation therapy.
Purpose of the Study:
- To summarize cellular mechanisms of iron overload-associated bone remodeling in thalassemia.
- To review current treatments and potential interventions for this condition.
Main Methods:
- A review of publications in the PubMed database before December 2019.
- Keywords included iron overload, thalassemia, osteoporosis, osteoblast, and osteoclast.
- Included pre-clinical studies and clinical trials.
Main Results:
- Iron overload increases reactive oxygen species (ROS) production, impairing bone remodeling.
- Oxidative stress inhibits osteoblast activity and promotes osteoclast activation.
- Thalassemia patients exhibit increased bone resorption and reduced bone formation.
Conclusions:
- Understanding cellular mechanisms is crucial for managing iron overload-induced bone disease.
- Further research into novel agents is needed to alleviate bone remodeling issues in iron overload conditions.
Introduction:
Iron overload, a state with excessive iron storage in the body, is a common complication in thalassemia patients which leads to multiple organ dysfunctions including the bone. Iron overload-induced bone disease is one of the most common and severe complications of thalassemia including osteoporosis. Currently, osteoporosis is still frequently found in thalassemia even with widely available iron chelation therapy.
Study Selection:
Relevant publications published before December 2019 in PubMed database were reviewed. Both pre-clinical studies and clinical trials were obtained using iron overload, thalassemia, osteoporosis, osteoblast, and osteoclast as keywords.
Results:
Increased ROS production is a hallmark of iron overload-induced impaired bone remodeling. At the cellular level, oxidative stress affects bone remodeling by both osteoblast inhibition and osteoclast activation via many signaling pathways. In thalassemia patients, it has been shown that bone resorption was increased while bone formation was concurrently reduced.
Conclusion:
In this review, reports on the cellular mechanisms of iron overload-associated bone remodeling are comprehensively summarized and presented to provide current understanding this pathological condition. Moreover, current treatments and potential interventions for attenuating bone remodeling in iron overload are also summarized to pave ways for the future discoveries of novel agents that alleviate this condition.
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