## 4 Discussion  
In this study, we investigated the pathogenic bacteria for the postoperative pneumonia after cancer surgery under general anesthesia. By decision analysis, pathogens that can be predict the incidence postoperative pneumonia were presented. Figure 3: tSNE analysis of the oral microbiome; (**a**) Baseline; (**b**) Before cancer operation. Figure 2: Decision tree for the prediction of incidence of pneumonia by specific species; (**a**): Baseline; (**b**): Before cancer operation. “+”: incidence of pneumonia, “-”: without incidence of pneumonia. Figure 1 shows the changes in the proportion of oral microbiome. At the phylum level, _Bacteroides_ and _Proteobacteria_ were major components of Gram-negative bacteria and _Frimicutes_ and _Actinobacteria_ were major components of Gram-positive bacteria. The proportion of Gram-positive bacteria were decreased, and Gram-negative bacteria were increased. However, a clear difference between the two groups was not observed. The changes may be derived from the effect of lung dysbiosis by mechanical ventilation. A previous report had shown that mechanical ventilation was associated with changes in the respiratory microbiome [25]. The component of respiratory microbiome was different between patients with or without ventilation-associated pneumonia [26]. A \"microbial shift\" occurred in dental plaque, with colonization by potential VAP pathogens and reverted back to having a predominantly normal oral microbiota after extubation [27,28]. At the genus level, Streptococci and _Veillonella_ were decreased, and _Neisseria_ was increased after cancer operation in the control group. _Streptococci_ and _Veillonella_ congregate and promote the formation of early biofilm [29, 30, 31]. _Neisseria_ increase at the stage of dental biofilm re-development [32]. The plaque control record was lower in the control group. The amount of biofilm before a cancer operation may reflect on the results. _Neisseria_ and _Granulicatella_ were decreased in pneumonia group after a cancer operation. Most of the species belong to these two genera are commensal bacteria of oral microbiome [32, 33, 34]. MALDI-TOF mass spectrometry made it possible to identify the pathogens in biofilm [35]. At the initial visit, _Perplyromonas gingivalis_ and _Fusobacterium nucleatum_ were a high risk for the incidence of postoperative pneumonia. These species were periodontal pathogens. Effect of the _Perplyromonas gingivalis_ on the pneumonia has been intensively studied. Human respiratory epithelial cell lines induced proinflammatory cytokines [36]. Gingipains, which is known as proteolytic enzymes produced by _Perplyromonas gingivalis_ manipulate innate immune responses and induce TNF, IL-6, IL-17 and C-reactive protein [37]. Outer membrane vesicles produced by induced cell death in lung epithelial cells [38]. However, when comparing infectious pneumonia and noninfectious pulmonary disease, the proportion of periodonotopathic bacterial DNA did not differ between the two groups [39]. Periodontal pathogens may play an indicator for the prediction of postoperative pneumonia. Further study is necessary to detect periodontal pathogens directly from the inflated respiratory tissue. As the O'Leary plaque control records at both initial visit and after preoperative oral care management, remaining dental plaque may contain increased pathogens. For cases included in our study we did not take into consideration the possible associated pathology of respiratory allergies and asthma that can modify the commensal flora at the level of the aerodigestive tract and increase the risk of postoperative pneumonia [40]. In addition, we could set up the medical history completely. Diabetes is a risk for postoperative pneumonia [41]. It is one of the limitations of this study. A previous report had shown that _Fusobacterium nucleatum_, which is periodontal commensal and pathogen, can occasionally cause remote infections [42].