Aim. To investigate whether endothelial toxicity is specific for calcium phosphate bions (CPB) by evaluating cytokine secretion profile of endothelial cells exposed to either CPB or magnesium phosphate bions (MPB) similar to CPB in size and shape. Materials and Methods. For the experiments, we used an immortalized human vein endothelial cell line EA.hy 926. Cells were seeded into 6-well plates (3*105 cells, 1900 µL DMEM/F12 culture medium) with the further: 1) addition of 100 µL CPB, MPB, or 1x phosphate buffered saline (PBS) upon 1 h following culture for 24 h (non-confluent cell culture); 2) culture for 44 h and subsequent addition of 100 µL either CPB, MPB, or PBS following culture for 4 h (confluent cell culture). Upon the collection of cell culture supernatant (n=11 wells per group), the levels of pro-atherosclerotic cytokines (interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12, IL-23, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and soluble vascular cell adhesion molecule (sVCAM)-1) were measured utilizing an enzyme-linked immunosorbent assay. Statistical analysis was performed using one-way analysis of variance, Tukey’s multiple comparisons test, discriminant analysis, and principal component analysis. Results. Exposure to MPB did not cause any changes in cytokine secretion profile in a non-confluent cell culture. In contrast, exposure to CPB increased the level of secreted IL-8 compared to either MPB-treated or control cells and promoted release of IL-6 in comparison with the control cells. Furthermore, in a confluent cell culture, exposure to CPB also enhanced secretion of IL-6 compared to either MPB-treated or control cells and raised the level of secreted IL-8 in comparison with MPB-treated cells. Both discriminant and principal component analysis demonstrated that, regardless of the cell confluence, the cytokine secretion profile of CPB-treated cells significantly differed from those of either MPB-treated or, a fortiori, control cells. Conclusion. Endothelial toxicity of CPB is caused by specific chemical profile but not physical features, and is largely defined by the induction of IL-6 and IL-8 release in endothelial cells.