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Updated: Feb 25, 2026
Adult Zebrafish Injury Models to Study the Effects of Prednisolone in Regenerating Bone Tissue
Published on: October 18, 2018
Immune Suppressive and Bone Inhibitory Effects of Prednisolone in Growing and Regenerating Zebrafish Tissues
Karina Geurtzen1, Aude Vernet2, Andrew Freidin3
1Center for Regenerative Therapies Dresden (CRTD) and Biotechnology Center, Technische Universität Dresden, Dresden, Germany.
Abstract:
Glucocorticoids are widely used as therapeutic agents to treat immune-mediated diseases in humans because of their anti-inflammatory and immunosuppressive effects. However, glucocorticoids have various adverse effects, in particular rapid and pronounced bone loss associated with fractures in glucocorticoid-induced osteoporosis, a common form of secondary osteoporosis. In zebrafish, which are increasingly used to study processes of bone regeneration and disease, glucocorticoids show detrimental effects on bone tissue; however, the underlying cellular mechanisms are incompletely understood. Here, we show that treatment with the glucocorticoid prednisolone impacts on the number, activity and differentiation of osteoblasts, osteoclasts, and immune cells during ontogenetic growth, homeostasis, and regeneration of zebrafish bone. Macrophage numbers are reduced in both larval and adult tissues, correlating with decreased generation of myelomonocytes and enhanced apoptosis of these cells. In contrast, osteoblasts fail to proliferate, show decreased activity, and undergo incomplete differentiation. In addition, prednisolone treatment mitigates the number and recruitment of osteoclasts to sites of bone regeneration in adult fish. In combination, these effects delay bone growth and impair bone regeneration. Our study demonstrates the many-faceted effects of glucocorticoids in non-mammalian vertebrates and helps to further establish the zebrafish as a model to study glucocorticoid-induced osteoporosis. © 2017 American Society for Bone and Mineral Research.
Insights
Glucocorticoids like prednisolone harm zebrafish bone health by disrupting immune cells, osteoblasts, and osteoclasts. This impairs bone growth and regeneration, highlighting zebrafish as a model for glucocorticoid-induced osteoporosis.
Area of Science:
- Endocrinology
- Osteoporosis Research
- Zebrafish Model Organisms
Background:
- Glucocorticoids are vital for treating immune diseases but cause significant bone loss (glucocorticoid-induced osteoporosis).
- Cellular mechanisms behind glucocorticoid's detrimental bone effects, especially in non-mammalian models, remain unclear.
Purpose of the Study:
- To investigate the cellular mechanisms of glucocorticoid action on zebrafish bone during growth, homeostasis, and regeneration.
- To establish the zebrafish as a model for studying glucocorticoid-induced osteoporosis.
Main Methods:
- Treatment of zebrafish with the glucocorticoid prednisolone.
- Analysis of osteoblast, osteoclast, and immune cell populations, activity, and differentiation.
- Assessment of bone growth and regeneration processes.
Main Results:
- Prednisolone reduced macrophage numbers and increased apoptosis in myelomonocytes.
- Osteoblasts exhibited reduced proliferation, activity, and differentiation.
- Osteoclast numbers and recruitment were diminished, delaying bone regeneration.
Conclusions:
- Glucocorticoids exert multifaceted detrimental effects on zebrafish bone cells and regeneration.
- Zebrafish serve as a valuable model for understanding glucocorticoid-induced osteoporosis mechanisms.
