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Oral pathogens directly aspirated into the lungs. There is evidence in the literature indicating that periodontal organisms such as Porphyromonas gingivalis and Aggregatibacter actinomycetemomitans are involved in aspiration pneumonia (13–15). Furthermore, it is important to understand that the dental biofilm can be colonized by pulmonary pathogens, thus strengthening the idea that the oral cavity may constitute a reservoir for pathogens that are responsible for aspiration pneumonia in high-risk patients (16–19).

Salivary enzymes associated with periodontal disease modify respiratory tract mucosal surfaces. In this hypothesis salivary enzymes associated with periodontal disease modify respiratory tract mucosal surfaces and promote adhesion and colonization by respiratory pathogens, with consequent aspiration into the lungs thereby causing infection. The possible mechanisms of mucosal surface modification leading to enhanced adhesion include: (a) modification of the mucosal epithelium due to high levels of proteolytic periodontal bacteria and their specific enzymes such as mannosidase, fucosidase, hexosaminidase, and sialidase; (b) loss of surface fibronectin, the protein that covers the mucosa resulting in de-masking of surface receptors; (c) removal of surface fibronectin by hydrolytic enzymes; and (d) release of cytokines. However, it is known that even though saliva contains a great variety of hydrolytic enzymes, salivary enzymatic activity is related to an individual's oral hygiene and periodontal condition (20, 21). Moreover, the source of these salivary enzymes has been attributed to both the oral microbiota (20, 22–26) and to polymorphonuclear leukocytes entering the saliva from the gingival sulcus/pocket. Thus, the worse the oral hygiene and the poorer the oral condition, the higher the enzymatic activity will be and the greater the possibility of mucosal changes, thereby increasing the adhesion and colonization by respiratory pathogens (27).

Hydrolytic enzymes from periodontopathic bacteria may destroy the salivary film that protects against pathogenic bacteria. This may reduce the ability of mucins to adhere to pathogens such as Haemophilus influenzae, thus leaving them free to adhere to mucosal receptors in the respiratory tract. In turn, this results in fewer non-specific host defense mechanisms in high-risk individuals. P. gingivalis, for example, produces enzymes that degrade these salivary molecules as well as producing other enzymes that degrade the salivary film on the mucosal surface, thereby exposing adhesion receptors to respiratory pathogens. In the same way as cited previously, individuals with poor oral hygiene may have high levels of hydrolytic enzymes in their saliva.

The presence of a large variety of cytokines and other biologically active molecules continually released from periodontal tissues and peripheral mononuclear cells. In cases of untreated periodontal disease in high-risk individuals, the presence of a large variety of cytokines and other biologically active molecules continually released from periodontal tissues and peripheral mononuclear cells may alter the respiratory epithelium and promote colonization by respiratory pathogens via the upregulation of adhesion receptor expression on the mucosal surfaces, thereby resulting in infection.