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Escitalopram exposure compromises osteogenic potential of human osteoblastic cells
Augusto Del Pintor Pasotti1, Rodrigo Mendes Ferreiro Girondo1, Bruno Haddad1
1Faculdade São Leopoldo Mandic, Campinas, Brazil.
Objective:
This study aimed to assess the impact of escitalopram on bone metabolism by evaluating its effects on cell viability and proliferation, wound-healing capacity, osteogenic activity, bone formation markers, and collagen deposition.
Design:
The effects of escitalopram were studied on human osteoblastic SAOS-2 cells. Escitalopram (1-1000 µM) was tested in a dose-response curve. Cell viability was measured by MTT assay, and proliferation by hemocytometer counting. Cell migration was examined with the Scratch assay over 72 h. Osteogenic differentiation was assessed by gene expression of RUNX2, Osterix (Osx), bone sialoprotein (BSP), type I collagen (COL1), and osteocalcin (OCN) using RT-qPCR. Alkaline phosphatase (ALP) activity was analyzed at 4 and 8 days. Mineralization was determined by Alizarin Red staining (days 10, 14, 21). For last, Immunofluorescence was carried out for collagen 1 staining (days 3, 7 and 10).
Results:
Escitalopram induced cytotoxicity in doses greater than 100 µM, reducing cell viability within 24 h. At non-toxic concentrations (≤30 µM), proliferation was enhanced in 30 µM after 7 days. Conversely, escilalopram reduced the migration capacity in a concentration-dependent manner. Moreover, the gene expression of RUNX2, OSX, BSP, COL1, and OCN were diminished when exposed to escitalopram. In the functional tests, escitalopram significantly decreases ALP activity at day 4, but not at day 8. Mineralization was dose-dependently impaired at 14 and 21 days. Collagen type I immunofluorescence exhibit weaker staining when escitalopram exposure.
Conclusion:
Escitalopram compromises osteoblast differentiation, extracellular matrix formation, and migratory potential. These results provide mechanistic insight into the adverse skeletal effects of SSRIs and suggest the need for monitoring bone health in long-term users.
Insights
Escitalopram negatively impacts bone health by harming osteoblasts, reducing their ability to form bone and migrate. Long-term users of this SSRI may require bone health monitoring.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Selective serotonin reuptake inhibitors (SSRIs) like escitalopram are widely prescribed.
- Potential adverse effects of SSRIs on bone metabolism are not fully understood.
- Osteoblasts are crucial for bone formation and maintenance.
Purpose of the Study:
- To investigate the effects of escitalopram on human osteoblastic cells.
- To evaluate escitalopram's impact on cell viability, proliferation, migration, and osteogenic differentiation.
- To assess markers of bone formation and collagen deposition.
Main Methods:
- Human osteoblastic SAOS-2 cells were treated with varying concentrations of escitalopram.
- Cell viability (MTT assay), proliferation (hemocytometer), and migration (Scratch assay) were measured.
- Osteogenic gene expression (RUNX2, Osx, BSP, COL1, OCN), alkaline phosphatase (ALP) activity, mineralization (Alizarin Red), and collagen I deposition (immunofluorescence) were analyzed.
Main Results:
- Escitalopram exhibited cytotoxicity at concentrations >100 µM.
- Non-toxic doses (≤30 µM) enhanced proliferation but reduced cell migration.
- Gene expression of key osteogenic markers and collagen deposition were significantly decreased.
- Mineralization and ALP activity were dose-dependently impaired.
Conclusions:
- Escitalopram impairs osteoblast differentiation, extracellular matrix formation, and cell migration.
- These findings suggest potential adverse skeletal effects associated with escitalopram use.
- Monitoring bone health in patients on long-term escitalopram therapy is recommended.
