Faculty Bibliography

Pulpitis results in significant morbidity among the elderly, particularly in underserved communities. We collected panoramic oral radiographs from 244 (mean age 67) participants of the Northern Manhattan Study, a prospective cohort study of stroke risk in a multiethnic urban population. Radiographs were evaluated for missing teeth, caries, restorations, periodontal bone loss, adequacy of endodontic treatment, and periapical radiolucencies. In the study 206 subjects were dentate (mean 17.1 teeth). 5.1% of teeth had periapical radiolucencies, and 4.8% had been endodontically treated; 37.5% of endodontically treated teeth had periapical radiolucencies. Teeth with restorations, periodontal bone loss, pulpotomy, and inadequate root canal filling had a significantly higher occurrence of periapical radiolucency (p < 0.05). Among all root filled teeth, only 26% were deemed satisfactory. We conclude that apical periodontitis is widely prevalent and the technical standard of root fillings is poor in this cohort. There is a substantial need for improved dental care among the northern Manhattan elderly.

OBJECTIVES: Studies suggest that elevated circulating tumour necrosis factor-alpha (TNF-alpha) may contribute to insulin resistance in patients with type 2 diabetes. The source of plasma TNF has been thought to be adipocytes associated with obesity, but inflammation and infection result in TNF-alpha production as well. METHODS: We studied 46 patients with type 2 diabetes and chronic periodontitis to determine the relationship between plasma TNF-alpha levels and clinical measures of periodontitis, gingival crevicular fluid (GCF) interleukin-1beta (IL-1beta), plasma endotoxin, serum glucose, and glycated haemoglobin (HbA1c). TNF-alpha levels were measured using a high sensitivity enzyme-linked immunosorbent assay. RESULTS: TNF-alpha showed a significant positive correlation with attachment loss (r=0.40, p=0.009), plasma endotoxin (r=0.33, p=0.03), and GCF IL-1beta (r=0.33, p=0.035), but not probing depth (r=0.28, p=0.07), bleeding on probing (r=0.30, p=0.053), plaque index (r=0.22, p=0.17), serum glucose, HbA1c (r=0.10, p=0.50), or body mass index (r=0.077, p=0.62). A dose-response relationship was observed between periodontitis severity and TNF-alpha (p=0.012). CONCLUSION: The finding that chronic periodontitis is associated with plasma TNF-alpha levels in subjects with type 2 diabetes supports the hypothesis that periodontal infection and inflammation may contribute to insulin resistance.

OBJECTIVES: Polymorphonuclear neutrophil (PMN) dysfunction is associated with diabetes. We examined the gingival crevicular fluid (GCF) beta-glucuronidase (BG) and interleukin-8 (IL-8) levels of periodontitis patients with and without type 2 diabetes mellitus (DM). MATERIAL AND METHODS: Forty five adults with type 2 DM and 32 adults without DM, both with chronic periodontitis were enrolled. GCF was collected from eight posterior sites in each quadrant, and periodontal parameters were recorded. GCF was assayed for IL-8 by ELISA and BG by a fluorometric assay. RESULTS: GCF IL-8 was positively correlated with probing depth (PD), and GCF BG but not clinical attachment level (CAL), bleeding on probing (BOP), or plaque index (PI). In contrast, GCF BG was strongly correlated with each of the clinical measures of periodontal disease. Subjects with DM significantly lower levels of both BG (73.0+/-44.8 versus 121.9+/-84.6 pg/sample; p=0.002) and IL-8 (32.1+/-33.1 versus 90.8+/-83.2 pg/sample; p<0.0001) even after adjustments for age, gender, PD, CAL, BOP, and PI. Neither BG nor IL-8 was correlated with HbA1c levels in subjects with DM. CONCLUSION: These data suggest that an inadequate local response by PMN, partially explained by an altered chemokine gradient, may contribute to periodontal disease in patients with type 2 DM.

BACKGROUND AND PURPOSE: Chronic periodontitis (CP) is associated with stroke and subclinical atherosclerosis, but clinical measurement of CP can be time consuming and invasive. The purpose of this study was to determine whether radiographically assessed CP is associated with nonstenotic carotid artery plaque as an ultrasound measure of subclinical atherosclerosis. METHODS: Panoramic oral radiographs were obtained from 203 stroke-free subjects ages 54 to 94 during the baseline examination of the Oral Infections and Vascular Disease Epidemiology Study (INVEST). CP exposure among dentate subjects was defined either categorically (periodontal bone loss > or =50% [severe] versus <50% bone loss) or via tertile formation (for dose-response investigation), with edentulous subjects categorized separately. In all subjects, high-resolution B-mode carotid ultrasound was performed. Carotid plaque thickness (CPT) and prevalence (present/absent) were recorded. Covariates included age, sex, smoking, diabetes, hypertension, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein cholesterol. RESULTS: Among dentate subjects with severe periodontal bone loss, mean CPT was significantly greater (1.20+/-1.00 mm versus 0.73+/-0.89 mm; P=0.003). CPT increased with more severe bone loss (upper versus lower tertile bone loss; P=0.049; adjusted for age, sex, and hypertension). This apparent dose-response effect was more evident among never-smokers. In a fully adjusted multivariate logistic regression model, severe periodontal bone loss was associated with a nearly 4-fold increase in risk for the presence of carotid artery plaque (adjusted odds ratio, 3.64; CI, 1.37 to 9.65). CONCLUSIONS: Severe periodontal bone loss is associated independently with carotid atherosclerosis. Panoramic oral radiographs may thus provide an efficient means to assess CP in studies of atherosclerosis risk.

BACKGROUND: Patients with diabetes have increased incidence and severity of periodontal disease not accounted for by differences in the subgingival microbial infection. Poor glycemic control has been consistently associated with periodontal disease severity. Also, recent evidence suggests that hyperglycemia may induce inflammatory cytokine production. Few studies, however, have examined local biochemical measures of periodontal inflammation in patients with type 2 diabetes. The aim of this study was to determine whether glycemic control was related to gingival crevicular fluid (GCF) levels of interleukin-1beta (IL-1beta). METHODs: GCF samples were collected from 45 patients with type 2 diabetes and untreated chronic periodontitis. Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and attachment level (AL) were recorded at six sites per tooth. IL-1beta levels were determined from individual GCF samples by enzyme-linked immunoabsorbent assay (ELISA). Individual site and mean patient values were calculated. Glycated hemoglobin (HbA1c) levels were measured from anticoagulated whole blood using an automated affinity chromatography system. Serum glucose was also determined. RESULTS: Clinical periodontal measures (PD, AL, BOP) and measures of glycemic control (HbA1c, random glucose) were significantly correlated with GCF IL-1beta. Patients with greater than 8% HbA1c had significantly higher mean GCF IL-1beta levels than patients with less than 8% HbA1c. In a multivariate model adjusting for age, gender, PD, AL, BOP, and PI, HbA1c and random glucose were independent predictors of high GCF IL-1beta. CONCLUSIONS: Poor glycemic control is associated with elevated GCF IL-1beta. These data are consistent with the hypothesis that hyperglycemia contributes to an heightened inflammatory response, and suggests a mechanism to account for the association between poor glycemic control and periodontal destruction.

BACKGROUND: The objective of this prospective cross-sectional study was to determine if cyclo-oxygenase-2, or COX-2, is overexpressed in the inflamed gingival tissue of patients diagnosed as having moderate-to-severe chronic periodontitis, or CP. METHODS: The authors evaluated clinical measures, crevicular fluid and gingival biopsy specimens from patients with moderate or severe CP (n = 16) and from healthy volunteers (n = 8). Patients were diagnosed as having CP based on clinical attachment loss, or CAL, of at least 5 millimeters at two sites in each quadrant and on evidence of alveolar bone loss as assessed from standard periapical or bite-wing radiographs. Healthy patients exhibited no sites with CAL of more than 2 mm and no evidence of alveolar bone loss. The authors used standard techniques to perform biochemical measures. RESULTS: Levels of interleukin-1 beta, or IL-1beta, in crevicular fluid were more than doubled in the CP group (P < .05). The amounts of COX-2 mRNA and protein also were elevated in gingival tissues from subjects with CP compared with those from healthy subjects. To gain further mechanistic insights, the authors conducted in vitro studies. The results showed that lipopolysaccharide and tumor necrosis factor alpha, or TNF-alpha, induced COX-2 in macrophages, while IL-1beta and TNF-alpha induced COX-2 in oral epithelial cells. CONCLUSIONS: Taken together, these results suggest that levels of COX-2 in gingivae reflect clinical measures of periodontitis and gingival inflammation. CLINICAL IMPLICATIONS: The discovery of increased levels of COX-2 in inflamed gingival tissue suggests that COX-2 represents a pharmacological target for the prevention or treatment of CP.

OBJECTIVES: Studies suggest a genetic influence on levels of interleukin-1beta (IL-1beta) in gingival crevicular fluid (GCF). Levels of IL-1beta in GCF, however, are also dependent upon the clinical parameters at the site of collection, including probing depth (PD) and level of attachment (AL). To examine this issue, IL-1beta in GCF was evaluated from patients with varying degrees of periodontal disease. The influence of both the status of the patient and the probing depth at the sampled sites were considered in the analysis. MATERIAL AND METHODS: GCF IL-1beta was determined by ELISA at 6-8 molar sites from 29 non-smoking adults with mild, moderate, or severe periodontal disease at baseline, 2 weeks, and 24 weeks following scaling and root planing. For later analysis, patients were dichotomized on the basis of disease severity (mild/moderate vs severe). Sampled sites were classified at baseline by PD as, shallow (<4 mm), intermediate (4-6 mm), or deep (>6 mm). RESULTS: PD and AL were each strongly correlated with IL-1beta levels at baseline. However, patients with severe disease had higher levels of IL-1beta in each PD category than those with mild/moderate disease. As compared to patients with mild/moderate disease, IL-1beta levels in shallow sites from patients with severe disease was elevated nearly 2 fold (p<0.001). IL-1beta levels were reduced in all groups at 2 weeks and were still significantly reduced in patients with mild/moderate disease at 24 weeks. At 24 weeks IL-1beta returned to near baseline levels in patients with severe disease. CONCLUSION: While PD and AL are each associated with increased GCF IL-1beta, patients with severe disease show higher IL-1beta GCF levels in shallow sites, suggesting that high GCF IL-1beta expression is in part a host trait, and not strictly a function of clinical parameters.

The aim of this report is to provide early data from an ongoing study examining (i) the relationship between periodontal infections and pre-term low birth weight (PLBW) in a cohort of young, minority, pregnant and post-partum women; and (ii) the effect of periodontal interventions on pregnancy outcome. During the first 2 yr of the study, 213 women were enrolled and examined clinically for dental plaque, calculus, bleeding on probing, and probing depth. Birth outcome data were available for 164 women, including one group (n = 74) subjected to oral prophylaxis during pregnancy, and a second group (n=90) who received no prenatal periodontal treatment. Subgingival plaque samples were available from 145 subjects (4 samples/subject) and were analyzed by checkerboard DNA hybridization with respect to 12 bacterial species. The prevalence of PLBW was 16.5% (27 cases) in this cohort. No differences in clinical periodontal status were observed between PLBW cases and women with normal birth outcome. However, PLBW mothers had significantly higher levels of Bacteroides forsythus and Campylobacter rectus, and consistently elevated counts for the other species examined. PLBW occurred in 18.9% of the women who did not receive periodontal intervention (17 cases), and in 13.5% (10 cases) of those who received such therapy.