## 4 Discussion
When the oral cavity imitating models were used (Figure 1), all antiseptics were able to eradicate multi-layer biofilms (Figure 6) preformed on HA surfaces over 24 h of contact time. These results were comprehensive, with data presented by in Table 1, where we showed that the MBECs reached by all antiseptics within this particular time frame were of very low values. Because antiseptics are usually not applied for such long contact times, we performed analysis of their activity for 1 h and 30 min (Figures 7 and 8, respectively). Results presented show that _P. aeruginosa_ and _C. albicans_ displayed a higher resistance to all antiseptics released from BC than _S. aureus_, _E. faecalis_, and _A. actinomycetemcomitans_. _P. aeruginosa_ was also the most resistant to antiseptics for applications using the microdilution and disc-diffusion methodology (Tables 1 and 2, respectively). The high tolerance of this Gram-negative bacteria against various antimicrobials is well-recognized [43]. In contrast to results presented in Tables 1 and 2, _C. albicans_was moderately sensitive to B-antiseptic in the oral cavity model for 30 min and 1 h of contact time (Figures 7 and 8, respectively). We assumed that povidence-iodine released from BC (please refer to Figure 1 for description of this setting) could be partially inhibited by components of the artificial saliva and could display a lower activity against biofilms preformed on HA surfaces. This hypothesis could explain discrepancies in the results obtained by means of disc-diffusion versus oral-cavity-simulating methodologies. It should be noted that the high reactivity of povidence-iodine with various inhibitors (including blood, pus, fat, protein-containing solutions, or even glove powder) was already presented by [PERSON] et al. [44]. Altogether, results presented in Figures 7 and 8 show that for short contact times of 30 min and 1 h, the applicability of antiseptic BC dressings was higher when the biofilms to be eradicated are formed by _S. aureus, E. faecalis_, and _A. actinomycetemomians_ than by _P. aeruginosa_ and _C. albicans_. Nevertheless, all antiseptics released from the BC carriers displayed a high activity against oral biofilms formed in vitro in our experimental model. We are aware that the application of other models of biofilm testing, such as the Amsterdam Active Adhesion Model [45], could provide valuable data and additionally elucidate phenomena concerning the interaction between the BC dressing, drug release, and biofilm eradication. However, the methodology and results presented in our manuscript also may be translated to specific conditions of a pathologically altered oral cavity, where the flow of saliva to the infection site is disturbed. Therefore, to some extent, these results can be used to estimate the efficacy of antiseptics released from a BC carrier in the eradication of pathogenic oral biofilms. It should be noted that our in vitro study is of a preliminary character. However, only in vivo results may be considered conclusive for the matter discussed above, and the data we provide here is a necessary investigative step, which justifies and rationalizes the undertaking of further animal model and clinical studies. Finally, we performed a proof-of-concept analysis and applied antiseptic BC dressings on oral cavity typodont models and bovine tissue to investigate the dressing behavior on topologically-challenging surfaces of the oral cavity. The dressings stuck firmly to particular surfaces resembling teeth (Figure 9) and gingival tissue (Figure 10). One can hypothesize that BC dressings may display sufficient mechanical properties to be applied in an oral cavity. However, the elasticity modulus value of BC was lower than the analogous parameter presented by other teams for collagen fibrils (100-360 MPa) [46; 47], and it was higher than the elasticity of chitosan (7.06 MPa [48]), which is one of the biopolymers frequently used as a carrier in oral mucosal delivery systems.