Dexamethasone: chondroprotective corticosteroid or catabolic killer?
While glucocorticoids have been used for over 50 years to treat rheumatoid and osteoarthritis pain, the prescription of glucocorticoids remains controversial because of potentially harmful side effects at the molecular, cellular and tissue levels. One member of the glucocorticoid family, dexamethaso...
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| Format: | Article |
| Language: | English |
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European Cells and Materials
2020
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| Online Access: | https://hdl.handle.net/1721.1/126296 |
| _version_ | 1826217382261030912 |
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| author | Black, Robert Xavier Grodzinsky, Alan J |
| author2 | Massachusetts Institute of Technology. Department of Biological Engineering |
| author_facet | Massachusetts Institute of Technology. Department of Biological Engineering Black, Robert Xavier Grodzinsky, Alan J |
| author_sort | Black, Robert Xavier |
| collection | MIT |
| description | While glucocorticoids have been used for over 50 years to treat rheumatoid and osteoarthritis pain, the prescription of glucocorticoids remains controversial because of potentially harmful side effects at the molecular, cellular and tissue levels. One member of the glucocorticoid family, dexamethasone (DEX) has recently been demonstrated to rescue cartilage matrix loss and chondrocyte viability in animal studies and cartilage explant models of tissue injury and post-traumatic osteoarthritis, suggesting the possibility of DEX as a disease-modifying drug if used appropriately. However, the literature on the effects of DEX on cartilage reveals conflicting results on the drug’s safety, depending on the dose and duration of DEX exposure as well as the model system used. Overall, DEX has been shown to protect against arthritis-related changes in cartilage structure and function, including matrix loss, inflammation and cartilage viability. These beneficial effects are not always observed in model systems using initially healthy cartilage or isolated chondrocytes, where many studies have reported significant increases in chondrocyte apoptosis. It is crucially important to understand under what conditions DEX may be beneficial or harmful to cartilage and other joint tissues and to determine potential for safe use of this glucocorticoid in the clinic as a disease-modifying drug. |
| first_indexed | 2024-09-23T17:03:07Z |
| format | Article |
| id | mit-1721.1/126296 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T17:03:07Z |
| publishDate | 2020 |
| publisher | European Cells and Materials |
| record_format | dspace |
| spelling | mit-1721.1/1262962022-10-03T10:03:07Z Dexamethasone: chondroprotective corticosteroid or catabolic killer? Black, Robert Xavier Grodzinsky, Alan J Massachusetts Institute of Technology. Department of Biological Engineering Massachusetts Institute of Technology. Department of Mechanical Engineering Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science While glucocorticoids have been used for over 50 years to treat rheumatoid and osteoarthritis pain, the prescription of glucocorticoids remains controversial because of potentially harmful side effects at the molecular, cellular and tissue levels. One member of the glucocorticoid family, dexamethasone (DEX) has recently been demonstrated to rescue cartilage matrix loss and chondrocyte viability in animal studies and cartilage explant models of tissue injury and post-traumatic osteoarthritis, suggesting the possibility of DEX as a disease-modifying drug if used appropriately. However, the literature on the effects of DEX on cartilage reveals conflicting results on the drug’s safety, depending on the dose and duration of DEX exposure as well as the model system used. Overall, DEX has been shown to protect against arthritis-related changes in cartilage structure and function, including matrix loss, inflammation and cartilage viability. These beneficial effects are not always observed in model systems using initially healthy cartilage or isolated chondrocytes, where many studies have reported significant increases in chondrocyte apoptosis. It is crucially important to understand under what conditions DEX may be beneficial or harmful to cartilage and other joint tissues and to determine potential for safe use of this glucocorticoid in the clinic as a disease-modifying drug. NIH/NCATS (Grant UG3/UH3 TR00218) 2020-07-21T20:52:55Z 2020-07-21T20:52:55Z 2019-11 2020-03-06T18:48:40Z Article http://purl.org/eprint/type/JournalArticle 1473-2262 https://hdl.handle.net/1721.1/126296 Black, R. and A. J. Grodzinsky. "Dexamethasone: chondroprotective corticosteroid or catabolic killer?." European Cells and Materials 38 (November 2019): 246-263 © 2019 AO Research Institute Davos en http://dx.doi.org/10.22203/ecm.v038a17 European Cells and Materials Creative Commons Attribution-Noncommercial-Share Alike http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf European Cells and Materials European Cells and Materials |
| spellingShingle | Black, Robert Xavier Grodzinsky, Alan J Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title | Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title_full | Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title_fullStr | Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title_full_unstemmed | Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title_short | Dexamethasone: chondroprotective corticosteroid or catabolic killer? |
| title_sort | dexamethasone chondroprotective corticosteroid or catabolic killer |
| url | https://hdl.handle.net/1721.1/126296 |
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