Although it has been established that aspiration of pharyngeal bacteria is the major route of infection in the development of nosocomial pneumonia, colonization of the pharyngeal mucosa by respiratory pathogens has been shown to be a transient phenomenon. It has been suggested that the dental plaque may constitute an additional, possibly more stable, reservoir of respiratory pathogens. The purpose of this study was to assess the prevalence of oral colonization by potential respiratory pathogens in a group of elderly (mean age = 75.9 yrs) chronic-care-facility residents (n = 28) and a group of age-, gender-, and race-matched outpatient control subjects (n = 30), with specific attention to plaque present on tooth, denture, and oral mucosal surfaces. Plaque scores on teeth and dentures were significantly higher in the chronic-care-facility (CCF) subjects than in the dental outpatient control (DOC) subjects (PII 2.3 vs. 1.2 and denture plaque 1.4 vs. 0.3). While no subjects in the DOC group were found to be colonized with respiratory pathogens (> 1.0% of the cultivable aerobic flora), 14.3% (4/28) of the CCF subjects were found to be colonized. Oral colonization with respiratory pathogens in CCF subjects was associated with the presence of chronic obstructive pulmonary disease (COPD) and higher plaque scores. These results suggest that deficient dental plaque control and the presence of COPD may be related to respiratory pathogen colonization of dental plaque in chronic-care-facility residents.

Two hundred and thirty-eight Caucasians were studied for ABO blood typing and for HL-A antigens. The subjects were divided into normal, necrotizing ulcerative gingivitis, chronic gingivitis, periodontosis and periodontitis groups. Results showed the chronic gingivitis group was significantly different in ABO grouping than the control group with the gingivitis subjects having a larger percentage of AB types and a smaller percentage of O types. The periodontosis group showed a trend toward more A and B blood groups and a smaller percentage of O groups than the controls. Compared to the normal group there was a significant reduction in HL-A2 antigen frequency in the periodontitis groups and a trend in reduced frequency in the periodontosis group.

The frequency of HL-A2 was significantly low (21%) in patients with periodontitis when compared to controls who were free of periodontal disease (61%). The effect was most pronounced in females in whom HL-A2 was present in 12.5% (2 out of 16). This finding suggests that genes controlling susceptibility to microbial agents may be linked to the HL-A LOCUS.

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