Frank A. Scannapieco

Colonization of dental plaque by respiratory pathogens in medical intensive care patients

Objective:To assess the prevalence of oral colonization by respiratory pathogens in a group of ICU patients, with specific attention to dental plaque and the oral mucosa. Design:Prospective, nonrandomized study with age-matched controls. Settings:Medical ICU in a tertiary-care Veterans Affairs Medical Center and a dental school outpatient preventive dentistry clinic. Patients:Nonconsecutive, unselected patients admitted to the medical ICU during a 2-month period; controls were age-matched patients seen for the first time in the preventive dentistry clinic. Interventions:None. Measurements:Oral hygienic status was assessed in both groups using a semiquantitative system. Quantitative cultures of dental plaque and buccal mucosa were done within 12 hrs of medical ICU admission and every third day thereafter until discharge/death from the medical ICU. In controls, cultures of plaque and buccal mucosa were done on the initial visit only. Severity of illness of medical ICU patients was quantitated using the Acute Physiology and Chronic Health Evaluation (APACHE II) system and McCabe-Jackson criteria. Main Results:Oral hygiene of medical ICU patients was poor. These patients had a mean plaque score (1.9 ± 0.2) that was significantly greater than that same score seen in outpatients of the preventive dentistry clinic (1.4 ± 0.1; p < .005). Plaque and/or oral mucosa of 22 (65%) of 34 medical ICU patients were colonized by respiratory pathogens, in contrast to only four (16%) of 25 preventive dentistry clinic patients (p < .005). The potential respiratory pathogens cultured from medical ICU patients included methicillinresistant Staphylococcus aureus, Pseudomonas aeruginosa, and ten genera of Gram-negative bacilli. Colonization by respiratory pathogens was statistically associated with concomitant antibiotic therapy within the medical ICU group of patients, but not with severity of illness. Although medical ICU patients tended to have more dental plaque than preventive dentistry clinic patients, there was no statistically significant association noted between the presence of dental plaque and respiratory pathogen colonization. Conclusions:These findings suggest that bacteria commonly causing nosocomial pneumonia colonize the dental plaque and oral mucosa of intensive care patients. In many cases, this colonization occurs by large numbers of bacteria. Dental plaque may be an important reservoir of these pathogens in medical ICU patients. Efforts to improve oral hygiene in medical ICU patients could reduce plaque load and possibly reduce oropharyngeal colonization.

Attributable mortality of ventilator-associated pneumonia: a meta-analysis of individual patient data from randomised prevention studies

BACKGROUND Estimating attributable mortality of ventilator-associated pneumonia has been hampered by confounding factors, small sample sizes, and the difficulty of doing relevant subgroup analyses. We estimated the attributable mortality using the individual original patient data of published randomised trials of ventilator-associated pneumonia prevention. METHODS We identified relevant studies through systematic review. We analysed individual patient data in a one-stage meta-analytical approach (in which we defined attributable mortality as the ratio between the relative risk reductions [RRR] of mortality and ventilator-associated pneumonia) and in competing risk analyses. Predefined subgroups included surgical, trauma, and medical patients, and patients with different categories of severity of illness scores. FINDINGS Individual patient data were available for 6284 patients from 24 trials. The overall attributable mortality was 13%, with higher mortality rates in surgical patients and patients with mid-range severity scores at admission (ie, acute physiology and chronic health evaluation score [APACHE] 20-29 and simplified acute physiology score [SAPS 2] 35-58). Attributable mortality was close to zero in trauma, medical patients, and patients with low or high severity of illness scores. Competing risk analyses could be done for 5162 patients from 19 studies, and the overall daily hazard for intensive care unit (ICU) mortality after ventilator-associated pneumonia was 1·13 (95% CI 0·98-1·31). The overall daily risk of discharge after ventilator-associated pneumonia was 0·74 (0·68-0·80), leading to an overall cumulative risk for dying in the ICU of 2·20 (1·91-2·54). Highest cumulative risks for dying from ventilator-associated pneumonia were noted for surgical patients (2·97, 95% CI 2·24-3·94) and patients with mid-range severity scores at admission (ie, cumulative risks of 2·49 [1·81-3·44] for patients with APACHE scores of 20-29 and 2·72 [1·95-3·78] for those with SAPS 2 scores of 35-58). INTERPRETATION The overall attributable mortality of ventilator-associated pneumonia is 13%, with higher rates for surgical patients and patients with a mid-range severity score at admission. Attributable mortality is mainly caused by prolonged exposure to the risk of dying due to increased length of ICU stay. FUNDING None.

Saliva-Bacterium Interactions in Oral Microbial Ecology

Saliva is thought to have a significant impact on the colonization of microorganisms in the oral cavity. Salivary components may participate in this process by one of four general mechanisms: binding to microorganisms to facilitate their clearance from the oral cavity, serving as receptors in oral pellicles for microbial adhesion to host surfaces, inhibiting microbial growth or mediating microbial killing, and serving as microbial nutritional substrates. This article reviews information pertinent to the molecular interaction of salivary components with bacteria (primarily the oral streptococci and Actinomyces) and explores the implications of these interactions for oral bacterial colonization and dental plaque formation. Knowledge of the molecular mechanisms controlling bacterial colonization of the oral cavity may suggest methods to prevent not only dental plaque formation but also serious medical infections that may follow microbial colonization of the oral cavity.

Relationships between periodontal disease and bacterial pneumonia.

Bacterial pneumonia is a prevalent and costly infection that is a significant cause of morbidity and mortality in patients of all ages. The continuing emergence of antibiotic-resistant bacteria (e.g., penicillin-resistant pneumococci) suggests that bacterial pneumonia will assume increasing importance in the coming years. Thus, knowledge of the pathogenesis of, and risk factors for, bacterial pneumonia is critical to the development of strategies for prevention and treatment of these infections. Bacterial pneumonia in adults is the result of aspiration of oropharyngeal flora into the lower respiratory tract and failure of host defense mechanisms to eliminate the contaminating bacteria, which multiply in the lung and cause infection. It is recognized that community-acquired pneumonia and lung abscesses can be the result of infection by anaerobic bacteria; dental plaque would seem to be a logical source of these bacteria, especially in patients with periodontal disease. It is also possible that patients with high risk for pneumonia, such as hospitalized patients and nursing home residents, are likely to pay less attention to personal hygiene than healthy patients. One important dimension of this personal neglect may be diminished attention to oral hygiene. Poor oral hygiene and periodontal disease may promote oropharyngeal colonization by potential respiratory pathogens (PRPs) including Enterobacteriaceae (Klebsiella pneumoniae, Escherichia coli, Enterobacter species, etc.), Pseudomonas aeruginosa, and Staphylococcus aureus. This paper provides the rationale for the development of this hypothesis especially as it pertains to mechanically ventilated intensive care unit patients and nursing home residents, two patient groups with a high risk for bacterial pneumonia. J Periodontol 1996;67:1114-1122.

Salivary α-Amylase: Role in Dental Plaque and Caries Formation

Salivary α-amylase, one of the most plentiful components in human saliva, has at least three distinct biological functions. The enzymatic activity of a-amylase undoubtedly plays a role in carbohydrate digestion. Amylase in solution binds with high affinity to a selected group of oral streptococci, a function that may contribute to bacterial clearance and nutrition. The fact that a-amylase is also found in acquired enamel pellicle suggests a role in the adhesion of a-amylase-binding bacteria. All of these biological activities seem to depend on an intact enzyme conformation. Binding of a-amylase to bacteria and teeth may have important implications for dental plaque and caries formation. a-Amylase bound to bacteria in plaque may facilitate dietary starch hydrolysis to provide additional glucose for metabolism by plaque microorganisms in close proximity to the tooth surface. The resulting lactic acid produced may be added to the pool of acid in plaque to contribute to tooth demineralization.

Chronic Periodontitis and the Incidence of Head and Neck Squamous Cell Carcinoma

Substantial evidence supports an association between chronic infections/inflammation, and cancer. The aim of this study was to assess the effect of chronic periodontitis on head and neck squamous cell carcinoma (HNSCC). The study population consisted of new patients at the Department of Dentistry and Maxillofacial Prosthetics, Roswell Park Cancer Institute between 1999 and 2005. Cases were patients diagnosed with primary HNSCC. Controls were all patients seen during the same time period but negative for malignancy. Patients age <21 years, edentulous, immunocompromised, and those with history of cancer were excluded. Periodontitis was measured by alveolar bone loss (ABL) from panoramic radiographs by one examiner blind to cancer status. A total of 473 patients (266 cases and 207 controls) were included in the study. Each millimeter of ABL was associated with >4-fold increased risk of HNSCC (odds ratio, 4.36; 95% confidence interval, 3.16-6.01) after adjustment for age, gender, race/ethnicity, marital status, smoking status, alcohol use, and missing teeth. The strength of the association was greatest in the oral cavity, followed by oropharynx and larynx. The association persisted in subjects who never used tobacco and alcohol. There was a significant interaction between smoking and ABL (P = 0.03). Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than those without periodontitis (32.8% versus 11.5%; P = 0.038). This study suggests that chronic periodontitis is an independent risk factor for HNSCC and smoking modifies this association. These results have implications for practical and safe strategies for prevention, diagnosis, and treatment of HNSCC. (Cancer Epidemiol Biomarkers Prev 2009;18(9):2406–12)

A randomized trial of chlorhexidine gluconate on oral bacterial pathogens in mechanically ventilated patients.

IntroductionDental plaque biofilms are colonized by respiratory pathogens in mechanically-ventilated intensive care unit patients. Thus, improvements in oral hygiene in these patients may prevent ventilator-associated pneumonia. The goal of this study was to determine the minimum frequency (once or twice a day) for 0.12% chlorhexidine gluconate application necessary to reduce oral colonization by pathogens in 175 intubated patients in a trauma intensive care unit.MethodsA randomized, double-blind, placebo-controlled clinical trial tested oral topical 0.12% chlorhexidine gluconate or placebo (vehicle alone), applied once or twice a day by staff nurses. Quantitation of colonization of the oral cavity by respiratory pathogens (teeth/denture/buccal mucosa) was measured.ResultsSubjects were recruited from 1 March, 2004 until 30 November, 2007. While 175 subjects were randomized, microbiologic baseline data was available for 146 subjects, with 115 subjects having full outcome assessment after at least 48 hours. Chlorhexidine reduced the number of Staphylococcus aureus, but not the total number of enterics, Pseudomonas or Acinetobacter in the dental plaque of test subjects. A non-significant reduction in pneumonia rate was noted in groups treated with chlorhexidine compared with the placebo group (OR = 0.54, 95% CI: 0.23 to 1.25, P = 0.15). No evidence for resistance to chlorhexidine was noted, and no adverse events were observed. No differences were noted in microbiologic or clinical outcomes between treatment arms.ConclusionsWhile decontamination of the oral cavity with chlorhexidine did not reduce the total number of potential respiratory pathogens, it did reduce the number of S. aureus in dental plaque of trauma intensive care patients.Trial Registrationclinicaltrials.gov NCT00123123.

Genetic Relationships between Respiratory Pathogens Isolated from Dental Plaque and Bronchoalveolar Lavage Fluid from Patients in the Intensive Care Unit Undergoing Mechanical Ventilation

BACKGROUND Ventilator-associated pneumonia (VAP) is a leading cause of morbidity and mortality in patients hospitalized in intensive care units. Recent studies suggest that dental plaque biofilms serve as a reservoir for respiratory pathogens. The goal of this study was to determine the genetic relationship between strains of respiratory pathogens first isolated from the oral cavity and later isolated from bronchoalveolar lavage fluid from the same patient undergoing mechanical ventilation with suspected VAP. METHODS Plaque and tracheal secretion samples were obtained on the day of hospital admission and every other day thereafter until discharge from the intensive care unit from 100 patients who underwent mechanical ventilation. Bronchoalveolar lavage was performed for 30 patients with suspected VAP. Pulse-field gel electrophoresis and multilocus sequence typing were used to determine the genetic relatedness of strains obtained from oral, tracheal, and bronchoalveolar lavage samples. RESULTS Isolates of Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter species, and enteric species recovered from plaque from most patients were indistinguishable from isolates recovered from bronchoalveolar lavage fluid (i.e., had >95% similarity of pulse-field gel electrophoresis patterns). Nearly one-half of the Pseudomonas strains showed identical genetic profiles between patients, which suggested a common environmental source of infection. CONCLUSIONS Respiratory pathogens isolated from the lung are often genetically indistinguishable from strains of the same species isolated from the oral cavity in patients who receive mechanical ventilation who are admitted to the hospital from the community. Thus, dental plaque serves as an important reservoir for respiratory pathogens in patients who undergo mechanical ventilation.

Salivary Amylase Promotes Adhesion of Oral Streptococci to Hydroxyapatite

Recent studies have demonstrated that several species of oral streptococci, such as Streptococcus gordonii, bind soluble salivary a-amylase. The goal of the present study was to determine if amylase immobilized onto a surface such as hydroxyapatite can serve as an adhesion receptor for S. gordonii. Initially, human parotid saliva was fractionated on Bio-Gel P60, and fractions were screened for their ability to promote adhesion of S. gordonii to hydroxyapatite. Fractions containing a-amylase and proline-rich proteins promoted the adhesion of [3H]-labeled S. gordonii to hydroxyapatite. Similar findings were obtained with purified amylase and acidic proline-rich protein 1 (PRP1). Incubation of S. gordonii G9B in the presence of starch and maltotriose increased the binding of this strain to amylase-coated hydroxyapatite, while the adhesion of S. sanguis 10556 to amylase-coated hydroxyapatite was not affected by these saccharides. These results suggest that amylase may serve as a hydroxyapatite pellicle receptor for amylase-binding streptococci. Furthermore, starch and starch metabolites may enhance the adhesion of amylase-binding streptococci to amylase in dental pellicles to augment the formation of dental plaque.

Does Periodontal Therapy Reduce the Risk for Systemic Diseases

Periodontal disease is treated by various approaches, including simple oral hygiene practices, professional mechanical debridement, antimicrobial therapy and periodontal surgery. There is evidence to associate periodontal disease with several systemic diseases and conditions, including myocardial infarction, adverse pregnancy outcomes, diabetes mellitus, and respiratory disease. This article reviews the published literature that describes the effects of periodontal treatment on cardiovascular diseases, adverse pregnancy outcomes, diabetes mellitus, and respiratory disease. While some progress has been made, further research is required to understand the value of periodontal interventions in the prevention of systemic diseases.