Faculty Bibliography

An emerging body of evidence has associated moderate to severe periodontitis with atherosclerotic complications. The contribution of periodontitis to systemic inflammation may account for this association in view of the pivotal role inflammation plays in atherosclerotic complications. Periodontal therapy has been shown to decrease systemic inflammation and to improve early atherosclerotic events; however, to date, periodontal therapy has not been shown to decrease subsequent atherosclerotic complications although aggressive treatment in at-risk populations appears warranted

Atherosclerotic complications, including myocardial infarction and stroke, are highly prevalent and associated with increased systemic inflammation in patients who have end-stage renal disease (ESRD) and are receiving renal hemodialysis maintenance therapy. In the general population, an increasing body of evidence suggests periodontitis can contribute to systemic inflammation and may contribute to atherosclerotic complications. In addition, results of recent interventional trials suggest effective periodontal therapy may decrease systemic inflammation as well as endothelial dysfunction, an early predictor of atherosclerotic complications. Because moderate-to-severe periodontitis appears to be highly prevalent in the renal hemodialysis population, effective periodontal therapy may reduce systemic inflammation and thereby become a treatment consideration for this population. This article will acquaint dental practitioners with ESRD and the association between systemic inflammation and mortality. Also discussed are the possible contributions of destructive periodontal diseases to systemic inflammation and the dental management of patients receiving renal replacement therapies

The complications of chronic kidney disease (CKD) present the anaesthetist with a number of clinical challenges related in part to altered drug handling and to difficulties with vascular access and fluid balance. Safe anaesthetic management requires an understanding of CKD pathophysiology to prevent aggravation of pre-existing disease. This review will consider some recent changes in the management of adult patients with CKD as they affect the anaesthetist. It will consider medical problems associated with CKD together with new developments in perioperative management.

BACKGROUND: Recent studies have reported an association between poor dental health and acute coronary syndrome (ACS). The purpose of this study was to correlate the presence of periodontitis with serum endotoxin/lipopolysaccharides (LPS), lipid profiles, troponin, and immunoglobulin G (IgG) antibody to Porphyromonas gingivalis in control patients or patients with ACS or angina at the time of hospital admission. METHODS: Blood samples from 194 subjects presenting with ACS, angina, or non-cardiac chest pain were analyzed for endotoxin/LPS (Limulus amebocyte lysate assay), lipid profile, troponin, and IgG antibody to P. gingivalis. Data were collected from hospital charts and dental records, and health questionnaire responses. RESULTS: Subjects with ACS or angina were more likely to have poor oral care, fewer remaining teeth, and increased alveolar radiographic bone loss compared to subjects with chest pain. In all subjects, endotoxin/LPS and IgG antibody to P. gingivalis tended to increase in association with increased radiographic bone loss. Endotoxin/LPS increased directly with triglyceride and troponin levels (P = 0.04 and P = 0.006, respectively) and inversely with high-density lipoprotein (HDL) levels (P = 0.002). IgG antibody to P. gingivalis levels was directly correlated with very low-density lipoprotein (P = 0.03) and triglycerides (P = 0.06) and inversely with low-density lipoprotein (P = 0.01). CONCLUSIONS: Results showed more alveolar bone loss in patients with cardiac disease than in patients without cardiac disease, but there was no difference between the groups in the serum levels of endotoxin/LPS or IgG antibody to P. gingivalis. However, there were associations between endotoxin/LPS and levels of serum triglycerides, troponin, and HDL.

In previous cross-sectional or case-control studies, clinical periodontal disease has been associated with gestational diabetes mellitus. To test the hypothesis that, in comparison with women who do not develop gestational diabetes mellitus, those who do develop it will have had a greater exposure to clinical and other periodontal parameters, we measured clinical, bacteriological (in plaque and cervico-vaginal samples), immunological, and inflammatory mediator parameters 7 weeks before the diagnosis of gestational diabetes mellitus in 265 predominantly Hispanic (83%) women in New York. Twenty-two cases of gestational diabetes mellitus emerged from the cohort (8.3%). When the cases were compared with healthy control individuals, higher pre-pregnancy body mass index (p=0.004), vaginal levels of Tannerella forsythia (p=0.01), serum C-reactive protein (p=0.01), and prior gestational diabetes mellitus (p=0.006) emerged as risk factors, even though the clinical periodontal disease failed to reach statistical significance (50% in those with gestational diabetes mellitus vs. 37.3% in the healthy group; p=0.38).

PURPOSE: This two armed, self-controlled, investigator blinded, clinical study tested the efficacy of an ultraviolet (UV) light toothbrush holder (Violight) to decrease toothbrush bacterial contamination. METHODS: 25 subjects were randomly assigned to control or experimental groups and received two toothbrushes for home use on either even or odd days. The control group rinsed both toothbrushes after use in cold tap water with no mechanical manipulation. The experimental group rinsed one toothbrush in cold running water while storing the other toothbrush in the Violight toothbrush holder after use. The toothbrushes were returned after 2 weeks use in sealed plastic bags and were analyzed for the number of colony forming units (CFU) of S. mutans, S. salivarius, lactobacilli, E. coli, and other coliforms, and total bacterial counts by culture. An additional analysis of the total bacterial profile was performed using denaturing gradient gel electrophoresis (DGGE). RESULTS: The Violight toothbrush holder reduced total CFU by an average of 86% (ANCOVA, P = 0.037). In addition, a tendency was noted for a reduction in total bacterial population as detected by DGGE.

Alzheimer's disease (AD) affects approximately 4.5 million people in the U.S. and this number will increase as the population ages and the life-span increases. Therefore, of paramount importance is identifying mechanisms and factors that affect the risk of developing AD. The etiology and pathogenic mechanisms for AD have not been defined, although inflammation within the brain is thought to play a role. Consistent with this hypothesis, studies suggest that peripheral infections contribute to the inflammatory state of the central nervous system. Periodontitis is a prevalent, persistent peripheral infection associated with gram negative, anaerobic bacteria that are capable of exhibiting localized and systemic infections in the host. This review offers a hypothetical link between periodontitis and AD and will present possible mechanistic links between periodontitis related inflammation and AD. It will review the pathogenesis of periodontitis and the mechanisms by which periodontal infections may affect the onset and progression of AD. Since periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.

The molecular and cellular mechanisms responsible for the etiology and pathogenesis of Alzheimer's disease (AD) have not been defined; however, inflammation within the brain is thought to play a pivotal role. Studies suggest that peripheral infection/inflammation might affect the inflammatory state of the central nervous system. Chronic periodontitis is a prevalent peripheral infection that is associated with gram-negative anaerobic bacteria and the elevation of serum inflammatory markers including C-reactive protein. Recently, chronic periodontitis has been associated with several systemic diseases including AD. In this article we review the pathogenesis of chronic periodontitis and the role of inflammation in AD. In addition, we propose several potential mechanisms through which chronic periodontitis can possibly contribute to the clinical onset and progression of AD. Because chronic periodontitis is a treatable infection, it might be a readily modifiable risk factor for AD.