Faculty Bibliography

The purpose of this study was to evaluate the effect of cortical bone perforation on angiogenesis and osteogenesis of the augmented ridge in guided bone regeneration. Eighteen patients who had osseous defects in the mandible were selected. In the test group (n=9), alveolar cortical bone in the area of regeneration was perforated. No decortication was performed in the control group (n=9). Subsequently, defects were augmented by guided bone regeneration using resorbable membrane and bovine bone. After a healing period of 7 months, trephine cores were harvested for histological and histomorphometric analysis of the grafted areas. Histomorphometry demonstrated that the amount of newly formed bone in the test group (27.8%) was greater than that in the control group (25.3%), but the difference was not statistically significant (P=0.13). However, the mean number of microvessels in the test group was significantly higher than that in the control group (P=0.01). This study found that cortical bone perforation favourably affects the amount of new bone formation in the grafted sites after 7 months of healing. Cortical bone perforation significantly increase number of new vessels (angiogenesis) of the regenerated bone. Further randomized clinical trials are required to confirm these results.

This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects of all CAD/CAM designed restorations (including inlays, onlays and crowns) for indirect restoration of teeth in need of a final permanent dental restoration in adults and adolescents with erupted second molars. To compare the effects of CAD/CAM designed restorations (inlays, onlays, crowns) with restorations (inlays, onlays, crowns) designed and produced by other available indirect systems.

AIM: To investigate the association between the use of oral bisphosphonate therapy and dental implant failure. MATERIALS AND METHODS: The case-control study involved 337 female patients, aged 40 years and older, who had 1181 implants placed at the Department of Periodontology and Implant Dentistry at New York University College of Dentistry between January 1997 and December 2004. Cases, defined as women with one or more implant failures, were identified from the departmental database. Controls were then randomly selected for each case. Adjusted odds ratios were estimated using logistic regression models fitted through generalized estimating equations. RESULTS: After adjusting for selected covariates, the odds of oral bisphosphonate use was 2.69 (95% confidence interval [CI], 1.49-4.86) times higher in women for whom implants failed compared with those for whom implants did not fail. Although no significant interaction was observed (p = 0.41), the stratified analyses suggest that the association between oral bisphosphonate use and dental implant failure was stronger in the maxilla (Odds Ratio [OR] = 2.60; 95% CI, 1.36-4.96) than in the mandible (OR = 1.38; 95% CI, 0.51-3.73). CONCLUSION: Findings from this study suggest that dental practitioners should be aware of the increased risk of implant failure associated with oral bisphosphonate use in the population.

Periodontal disease is associated with cardiovascular disease and is thought to accelerate systemic atherosclerosis. Here we examined the relationship between periodontitis and cardiovascular disease mortality in outpatients on hemodialysis using a retrospective analysis of 168 adult patients in New York City and North Carolina. During 18 months of follow-up, cardiovascular disease and all-cause mortality were determined from a centralized dialysis registry. One hundred patients had mild or no periodontal disease but the remaining 68 had moderate-to-severe disease defined as 2 or more teeth with at least 6 mm of inter-proximal attachment loss. At baseline, the proportion of males was significantly lower in the moderate-to-severe group. Compared with mild or no periodontal disease, moderate-to-severe disease was significantly associated with death from cardiovascular causes. Adjustment for age, gender, center and dialysis vintage, smoking status, and history of diabetes mellitus or hypertension did not diminish the strength of this association. Our findings suggest a need for larger studies to confirm this connection, along with intervention trials to determine if treating periodontitis reduces cardiovascular disease mortality in dialysis patients

The relationship between periodontitis and two measures of systemic inflammation, serum albumin and C-reactive protein (CRP), were examined among patients who were receiving chronic outpatient hemodialysis. Adult patients at two locations, North Carolina and New York City, were evaluated by dentist examiners. Six sites per tooth (up to 32 teeth per patient) were examined. A periodontitis case was defined as > or = 60% of sites with attachment level > or = 4 mm. Multivariable logistic regression was used to determine the association of periodontitis with low serum albumin, defined as < 3.5 mg/dl, and with high CRP, defined as > 3.0 mg/dl. A total of 154 patients completed the study. The mean age was 54.6 yr (SD 13.3), and average duration of dialysis was 4.0 yr (3 mo to 16 yr). Eighty-six (54.6%) were men, and 89 (58.2%) were black. Common causes of end-stage kidney disease were hypertension (12.3%), diabetes (22.1%), glomerulonephritis (7.1%), and other (58.4%). The average number of teeth was 20.3 (SD 8.4). Thirty-five (23%) patients were periodontitis cases. Severe periodontitis was associated with low serum albumin (odds ratio 8.20; 95% confidence interval 1.61 to 41.82; P = 0.01) compared with individuals without severe periodontitis disease after adjustment for age, gender, race, diabetes, hypertension, body mass index, smoking, study site, total cholesterol, serum calcium, serum phosphorus, and normalized protein catabolic rate. There was no observed association of severe periodontitis with CRP. Investigation of the potential contribution of periodontitis to serum albumin and possibly to morbidity and mortality among patients with end-stage kidney disease seems warranted

BACKGROUND, AIMS: Differences in prevalence, severity and risk factors for destructive periodontal diseases have been reported for ethnic/racial groups. However, it is not certain whether this disparity is due to ethnicity/race or factors associated with ethnicity/race. Therefore, the present study addressed whether the rates of disease progression and clinical and demographic factors associated with disease progression varied among three ethnic/racial groups. METHODS: The study population consisted of 53 Asian-, 69 African- and 62 Hispanic-Americans. Clinical measurements included probing depth, attachment level, gingival erythema, bleeding upon probing, suppuration and plaque. Disease progression was defined as a > 2 mm loss of attachment 2 months post baseline. The demographic variables examined included occupational status, report of a private dentist, years resident in the United States and smoking history. RESULTS: The rate of attachment loss for the entire population was 0.04 mm or 0.24 mm/year. No significant differences were found among the three ethnic/racial groups. Variables associated with subsequent attachment loss for the entire population were age, male gender, mean whole-mouth plaque, erythema, bleeding upon probing, suppuration, attachment loss and probing depth, and belonging to the "unskilled" occupational group. No differences in risk profiles were found among the 3 ethnic/racial groups. Using stepwise logistic regression analysis, a model was developed to relate the clinical and demographic variables examined with subsequent attachment loss. The model indicated that prior attachment loss, gingival erythema, suppuration, being a current smoker and belonging to the "unskilled" occupational group conferred high risk of > 1 site of attachment loss of > 2 mm. CONCLUSIONS: The results of this study suggest that variables associated with ethnicity/race, such as occupational status, are largely responsible for the observed disparity in destructive periodontal disease progression in these populations.

BACKGROUND: Destructive periodontal diseases have been associated with an increased risk of atherosclerotic complications; however, the potential mechanisms are yet to be defined. Inflammation plays a central role in atherosclerosis since C-reactive protein (CRP), an acute-phase protein monitored as a marker of inflammatory status, has been identified as a major risk factor for atherosclerotic complications. Recent reports that destructive periodontal diseases can increase CRP values present the possibility that the acute-phase response may link these 2 disease processes. The objective of the present investigation was to determine the effect of destructive periodontal disease status, severity, and progression on components of the acute-phase response in an urban minority population. METHODS: Clinical measurements recorded included probing depth, attachment level, gingival erythema, bleeding upon probing, suppuration, and plaque. Disease progression was defined as a >2 mm loss of attachment 2 months post-baseline. Serum antibody was measured by enzyme-linked immunosorbent assay. CRP was measured using a high-sensitivity CRP (hsCRP) assay. A commercial laboratory measured serum glucose (non-fasting), albumin, cholesterol, high-density lipoprotein (HDL), triglycerides, low-density lipoprotein (LDL), and iron. RESULTS: Increased serum IgG antibody to Porphyromonas gingivalis, but not to 5 other species, was associated with periodontal disease status, increased severity, and progression as were age, male gender, and smoking. Cholesterol and LDL were increased in disease, and HDL and iron were increased in health. hsCRP, glucose, and cholesterol increased with disease progression. By regression analysis, IgG antibody to P. gingivalis correlated with age, probing depth, and hsCRP, and negatively correlated with albumin and iron. By logistic regression, subjects who experienced multiple sites of disease progression and elevated antibody to P. gingivalis increased the odds ratio of hsCRP>2.08 mg/l by 14.1 and 5.6, respectively. CONCLUSION: These results suggest that destructive periodontal disease and disease progression are associated with changes in serum components consistent with an acute-phase response

Disparities in the prevalence and severity of destructive periodontal diseases have been reported for American minority populations and have raised the following questions. Are differences in destructive periodontal disease prevalence and severity due to genetic or other confounding variables associated with ethnicity race? Do risk factors for destructive periodontal diseases differ among American minority populations or differ from the population at large? Answers to these questions will have profound impact on the direction of future research and the allocation of resources to address disparities in destructive periodontal diseases in American minority populations. Risk assessment studies that examined a set of clinical, demographic, immunologic, and microbiologic parameters of Asian Americans, African Americans, and Hispanic Americans resident in the greater New York City region suggest that occupational status, monitored as a surrogate variable for socioeconomic status, may be a more robust risk factor than ethnicity/race for destructive periodontal diseases in these populations

Differences in periodontal disease prevalence, severity, subgingival microflora and host immune response have been reported for various ethnic/racial groups, which implies that risk factors for destructive periodontal disease progression may also vary in these populations. As it is possible that these differences may be due to confounding variables other than ethnicity/race, we have measured serum IgG antibody response to six periodontal pathogens, and compared these data with microbiological, clinical and demographic parameters in three urban minority populations. The study population consisted of 23 Asiatic, 48 African-American and 37 Hispanic subjects, who were resident in the greater New York region. Clinical indices that were recorded included pocket depth, attachment level, gingival erythema, bleeding upon probing, suppuration and supragingival plaque. Attachment level measurements were taken twice at each visit, and the difference between the means of pairs of measurements taken at baseline and two months later was used to determine disease progression. Subgingival microbiological species were identified and enumerated using DNA-DNA checkerboard hybridization. Serum IgG antibody levels to Actinobacillus actinomycetemcomitans serotyopes a and b, Bacteroides forsythus, Campylobacter rectus, Porphyromonas gingivalis and Prevotella intermedia were measured by enzyme-linked immunosorbant assay (ELISA). Mean serum IgG antibody to P. gingivalis was found to be higher in the African-American group, while IgG antibody to B. forsythus was lower in the Hispanic group. However, the African-American group also had greater mean probing depth, attachment loss, number of missing teeth and numbers of individuals within the unskilled occupational group. When the data were analyzed by occupational status, mean serum IgG antibody to P. gingivalis increased from professional to skilled to unskilled groups. For the entire study population, prior disease and subsequent attachment loss were associated with elevated serum IgG antibody to P. gingivalis. Increasing pocket depth, attachment level, gingival erythema and age were also positively correlated with serum IgG antibody to P. gingivalis, but not with serum IgG antibody to the other five subgingival species. No correlation was found between whole-mouth bacterial levels and homologous serum IgG antibody levels. These results suggest that elevated serum IgG antibody to P. gingivalis reflects destructive periodontal disease status, and may be considered a risk factor for disease progression in these ethnic/racial populations. In addition, although differences in serum IgG antibody profiles to subgingival species were found among the three ethnic/racial groups, environmental and socioeconomic variables may have a greater influence on serum IgG antibody levels in these populations