## 3 Discussion  
According to the literature, oral peri-implant diseases may present as mucositis and peri-implantitis, where both the soft and hard tissue destruction is \"caused by bacteria\" [26; 27]. Real life experience casts doubt on the truthfulness of the statement regarding the bacteria causing bone destruction, as many antimicrobial approaches (antibiotics, bactericidal substances, etc.) are not effective, and because we can observe that even after decades in graves around, the world the soft tissues have been dissolved and disappeared, whereas bones remain intact. It seems that bacteria are not so much interested in consuming bones nor have enough tools to degrade them. It should be highlighted that the large amount of minerals in bone guarantees a bacteria-unfriendly pH, and hence mineralized bone can be considered to be auto-sterile. Bacteria even refuse to consume bones in the case of osteomyelitisitis, while they are located in the true center of the bone, i.e., inside the Haversian canals [28]. The true reason why bacteria bother the peri-implant bone is rather the answer of the body itself: the presence of bacteria (adhering to the exposed rough surfaces of the implant) triggers and increases blood supply in order to increase the number of defense cells. Associated to this the blood supply and the oxygen levels are increased (e.g., in the phase of peri-implant mucositis), and this by itself will lead to a de-mineralization of the bone to make space for vessel-rich granuloma-like tissue (just as in the case of periodontitis). This event should not be mixed up with an immunological reaction, e.g., as an answer to foreign bodies or immune-activating substances. [PERSON] et al. [29] stated that PI starts 2-3 years after the implant placement and that a precursor to PI is peri-implant mucositis (PIM). In the explanation section of this article, we explain why this process lasts so long and why it occurs only after sucessful osseointegration. [PERSON] et al. reported [30], on the contrary, that PI is oberved already after 12 months and occurs more often if more than five implants per jaw are placed. In their study, they grouped patients into two groups: G1 with up to five implants placed per jaw and G2 with more than five implants placed per jaw. G1 showed PI in 50% of the implants, whereas G2 showed PI in 81.8% of the implants. Assuming that all parameters were equal in both  
Figure 8: (**a**) Full formation of the basal cortical bone and development of large pockets along the vertical part of the implant after the crestal part of the alveolar bone has been resorbed. (**b**) As soon as the pockets resorb, a large part of the implant’s thread becomes visible, but the development output is reduced or has stopped. groups, the only difference between them were more jaw bone under stronger remodelling because more implants had been placed. The volume ratio between bone and implants is in such a situation strongly changing in favor of the implants, and for the jaw bone, it becomes functionally impossible to maintain its bone mass and the pre-operative macro-trajectories (i.e., the bone volume, dimensions, and structural architecture). As a result of the increased remodelling, the bone is more \"optimized\" [16], and hence the crestal bone level receses away from the \"bone level\" of the implants. As a result, the rough (formerly endosseous) surface of the implant is exposed very early and there is not even time for this part of the surface to undergo osseointegration. Infection starts right away. It may be concluded that in the regular case (with up to five implants per jaw placed), it takes 2-3 years until PI begins to occur. If, however, simultaneously more than five rough-surfaced endosseous implants are placed into the same jaw, the overall remodelling can reach an extent (compared to the amount of non-remodelled bone) where vertical bone loss is extensively observable already after 12 months.