## 4 Discussion  
The surface topography and roughness of dental implants exert a substantial influence on the behavior of osteogenic cells in vitro [24]. In the present study, we observed that the roughness patterns of the MS and SBAS surfaces were similar and showed moderate hydrophilicity. The laser-modified surface with and without HA, however, had a high roughness, with valleys, peaks and absolute hydrophilicity. These surface properties can affect how cells respond and may influence the rate and extent of bone deposition [4]. For a surface with moderate roughness, it is advantageous for cells to adhere stably, promoting their growth and subsequent proliferation; on the other hand, superhydrophobic and superhydrophobic surfaces are not conducive to cell attachment and growth [9]. In general, laser-modified surfaces can accelerate bone healing around implanted materials [4; 36; 37], through their ability to enhance osteoblast differentiation, increase matrix mineralization, and increase the expression of genes specific to bone formation [24]. Moreover, laser-treated implants with HA coating exhibit higher torque values and increased new bone volume compared to machined and acid-etched implants [4; 5]. Nevertheless, there is concern regarding the HA coating of implant surfaces due to the risk of fragmentation. Fragmentation may lead to HA particles potentially triggering leukocyte activation and consequently provoking an inflammatory response [29]. However, the possible role of HA coating to affect the viability and the inflammatory status of mesenchymal cells is less clear. The present study revealed that the laser-modified surface prompted alterations in the morphology of both MC3T3-E1 and ST2 cells, with an additional impact of HA coating. With HA coating, the cell shape was altered, and less cells with nuclear staining were noticed. Support for our findings comes from others showing that MC3T3-E1 cells were less spread and elongated on an HA surface compared to a tissue culture surface [32]. Consistently, HA coating reduced cell viability in MC3T3-E1 and ST2 cells, similar to the results from previous reports in a tissue culture dish serving as the controls [32]. Previous studies have established that the structure of HA nanoparticles significantly influences immediate inflammation, regardless of their chemical composition and charge [20]. HA nanoparticles have the capacity to enhance the release of pro-inflammatory agents such as IL1, along with chemotactic factors like IL8, macrophage inflammatory proteins, and matrix metalloproteinase 9. HA also activates polymorphonuclear neutrophils, possibly contributing to implant-related inflammation [29]. Furthermore, HA particles can trigger the production of IL18 in human monocytes due to their specific characteristics [38]. In light of these results, and to understand if the lower viability translates into an inflam  
Figure 5: Effect of HA-mediated in IL6 secretion in ST2 cells. (**A**) IL6 expression. The RT-PCR analysis was performed in accordance with the procedure described in the Materials and Methods section, and the data depict the expression levels of IL6 normalized to the control, represented by MS surface. (**B**) Immunoassay showed that HA increased the expression of IL6 in ST2 cells. Each format shape represents the levels of IL6 from individual experiments and are presented with mean and SD values. Statistical analysis was carried out through a one-way ANOVA, and corrected \(p\)-values were indicated. matory response, the expression of IL6 was determined. Consistent with the lower viability, HA coating caused higher GAPDH values, reflecting lower cell numbers. Interestingly, HA coating caused an increased IL6 on the level of gene expression and protein in the supernatant of the MC3T3-E1 and ST2 cells.