Respiratory Infections

Chronic Obstructive Pulmonary Disease (COPD) & Pulmonary Function

Epidemiologic and intervention studies have suggested an association between poor oral health and respiratory diseases, such as pneumonia and chronic obstructive pulmonary disease (COPD). Increased presence of dental caries, determined by the number of decayed, missing and filled teeth, has also been found to increase pulmonary impairment. A National Health and Nutrition Examination Survey study found a significant 4.5 times increase in chronic respiratory disease in subjects that had poor oral hygiene when compared to those with good oral hygiene. Periodontal bacteria have also been found in infected lung fluids and lung tissues. Limeback noted a relationship between poor oral hygiene and aspiration pneumonia among elderly residents of chronic care facilities. He subsequently found that the nursing homes with the least number of dental visits had the most deaths due to pneumonia. Loesche and Lopatin have studied oral and dental conditions in elderly individuals that may predispose individuals for aspiration pneumonia, and found that individuals with “definite” aspiration pneumonia were 3.3 times more likely to have a higher periodontal disease score than the individuals without pneumonia.

Microorganisms can infect the lower respiratory tracts by four possible routes: aspiration of oropharyngeal contents, inhalation of infectious aerosols, spread of infection from neighboring sites, and hematogenous spread from extrapulmonary sites of infection.

Lower respiratory infections begin by contamination of the lower airway with microorganisms contained in aerosolized droplets, or by aspiration of oral secretions containing microorganisms into the lower respiratory tract causing pneumonia, especially in periodontally compromised patients. Studies have suggested relationships between poor oral health, especially in critically ill and hospitalized patients, and respiratory infections and compromised lung function. Several biological mechanisms through which periodontal bacteria may modulate respiratory infection have been proposed: 1) aspiration of oral pathogens (such as Porphyromonas gingivalis, Actinobacillus  actinomycetemcomitans, etc.) into the lung to cause infection; 2) periodontal disease-associated salivary enzymes aspirated into the lower airway may modify mucosal surfaces to promote adhesion and colonization by respiratory pathogens; 3) destruction of protective salivary molecules by periodontal disease-associated enzymes; and 4) cytokines originating from periodontal tissues which may alter respiratory epithelium, promoting infection by respiratory pathogens.

These diseases share many common risk factors, and it is becoming more evident that these diseases may have common pathogenic pathways.  Oral streptococci, previously thought to be exclusively benign members of the flora, may participate in pneumonia initiation and/or progression. In fact, these bacteria have been found to cause pneumonia in 4% of COPD patients. P. gingivalis was found to cause lung inflammation in laboratory animals. Prevotella species, previously associated with periodontal disease have been found in ventilator-associated pneumonia in hospitalized patients.

The lung is composed of numerous units formed by the progressive branching of the airways. The lower respiratory tracts are normally sterile, despite the fact that secretions from upper respiratory tracts are heavily contaminated with microorganisms from the oral and nasal surfaces. Sterility in the lower respiratory tract is maintained by intact cough reflexes, by the action of tracheobronchial secretions, mucociliary transport of inhaled microorganisms and particulate material from the lower respiratory tract to the oropharynx, and immune and nonimmune defense factors. The defense factors are present in a secretion which also contains surfactant and other proteins such as fibronectin, complement, and immunoglobulins, which coat the pulmonary epithelium. The lung also contains a rich system of resident phagocytic cells which remove microorganisms and particulate debris.

Oral bacteria are routinely found in tonsillar epithelium, and may contaminate the distal respiratory epithelium and cause stimulation of respiratory epithelial cells. Lower respiratory tract infections, including COPD exacerbation, depend on the initial colonization of bacterial pathogens to oral/pharyngeal surfaces, and subsequently shed into the salivary secretions, together with oral bacteria, hydrolytic enzymes, and proinflammatory cytokines. These secretions may potentially contaminate and induce respiratory epithelial alterations. Oral bacteria may also modulate the adhesion of respiratory pathogens to mucosal surfaces by altering the environment of the upper airway enhancing potential lower respiratory pathogen colonization. It is therefore possible that oral pathogen accumulation associated with periodontal disease, along with caries susceptibility, may increase the risk of pulmonary impairment. Periodontal disease may also alter environmental conditions that permit mucosal colonization, along with caries producing bacteria, and infection by respiratory pathogens.


Pneumonia is an infection of pulmonary parenchyma caused by a wide variety of infectious agents; including bacteria, fungi, parasites, and viruses. Pneumonia can be a life-threatening infection, especially in the old and immunocompromised patient, and is a significant cause of morbidity and mortality in patients of all ages.

Total pneumonia mortality in low-risk individuals over 65 years of age is 9 per 100,000 (0.009%), whereas in high-risk individuals who are likely to aspirate, the mortality can be almost 1,000per 100,000 (1%) or higher (Niederman M,Fein A, 1986). Pneumonias can be broadly divided into two types, community acquired and hospital acquired (nosocomial). These types of pneumonia differ in their causative agents.

Generally, accepted risk factors that predispose an older individual to nosocomial pneumonia, include the presence of underlying diseases such as chronic lung disease, congestive heart failure, or diabetes mellitus, mechanical ventilation or intubation, a history of smoking, previous antibiotic treatment, immunosuppression, a long preoperative stay; and prolonged surgical procedures.

Pneumonia can result from infection by anaerobic bacteria. Dental plaque would seem to be a logical source of these bacteria, especially in patients with periodontal disease. Such patients harbor a large number of subgingival bacteria, particularly anaerobic species. Among the oral bacterial species implicated in pneumonia areA. actinomycetemcomitansActinomyces israelii, Capnocytophaga spp., Eikenella corrodensPrevotella intermedia, and Streptococcus constellatus.

Most commonly, bacterial pneumonia results from aspiration of oropharyngeal flora into the lower respiratory tract, failure of host defense mechanisms to eliminate them, multiplication of the microorganisms, and subsequent tissue destruction. It is likely that most pathogens first colonize the surfaces ofthe oral cavity or pharyngeal mucosa before aspiration. These pathogens can colonize from an exogenous source or emerge following overgrowth of the normal oral flora after antibiotic treatment. Common potential respiratory pathogens (PRPs) such as Streptococcus pneumoniae, Mycoplasma pneumoniae, and Haemophilus influenzae can colonize the oropharynx and be aspirated into the lower airways. Other species thought to comprise the normal oral flora, including A. actinomycetemcomitans and anaerobes such as P. gingivalis and Fusobacterium species, can also be aspirated into the lower airways and cause pneumonia.

There are several proposed mechanisms to explain the propensity for PRPs to colonize the oropharynx of susceptible patients. Compromised individuals such as diabetics and alcoholics may be prone to oropharyngeal colonization by PRPs. These individuals are thought to be more likely to aspirate, and are also known to be at greater risk of periodontal disease. Thus, the extensive dental plaque of these subjects may provide surfaces to which PRPs might adhere to provide a reservoir for infection to distal portions of the respiratory tract.

The oral surface of subjects at high risk for pneumonia, such as hospitalized patients, may somehow become modified to provide receptors for the adhesion of PRPs. Poor oral hygiene increases the plaque load and therefore the level of hydrolytic enzymes in saliva. The source of these enzymes has been attributed to plaque bacteria or polymorphonuclear leukocytes, which enter the saliva through the inflamed gingival sulcus. These proteolytic enzymes may alter the characteristics of the mucosal surfaces, resulting in increased colonization by pathogenic bacteria.