Faculty Bibliography

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).

The incidence of end-stage renal disease (ESRD) is increasing and patients receiving renal replacement therapy including hemodialysis, peritoneal dialysis or renal transplantation will comprise an enlarging segment of the dental patient population. Renal replacement therapy can affect periodontal tissues including gingival hyperplasia in immune suppressed renal transplantation patients and increased levels of plaque, calculus and gingival inflammation and possible increased prevalence and severity of destructive periodontal diseases in ESRD patients on dialysis maintenance therapy. Also, the presence of undiagnosed periodontitis may have significant effects on the medical management of the ESRD patient. Periodontitis has been found to contribute to systemic inflammatory burden including the elevation of C-reactive protein (CRP) in the general population. Atherosclerotic complications including myocardial infarction and stroke are the primary causes of mortality in the ESRD population and, in contrast to that of the general population, the best predictor of all cause and cardiac death in this population is CRP. Consequently, periodontitis may be a covert but treatable source of systemic inflammation in the ESRD population. The objective of this review was to explore the interaction between chronic renal disease, renal replacement therapy and periodontal diseases based upon the results of studies published within the last decade

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

We have developed an experimental model to help identify and characterize factors necessary for periodontal connective tissue attachment formation on dental implants. In this pilot study, we report the effect of autogenous periodontal cell grafts, with and without the a pplication of enamel matrix derivative (EMD), on the implant-connective tissue interface. Periodontal ligament (PDL) and gingival connective tissue (GCT) cultures were established from an adult minipig. Implants were placed in osteotomies prepared with exaggerated countersinks that served as recipient sites for autogenous cell grafts in bilateral edentulated posterior mandibular sextants. In addition, 1 side received an application of EMD before placement of the autogenous cell grafts. A bioabsorbable membrane covering the coronal portion of the implants was placed before closure. After 8 weeks, quantitative histomorphometric and qualitative light microscopic analyses revealed that the implants that received gelatin vehicle alone were surrounded by bone, whereas the implants that received GCT cell grafts were mostly surrounded by fibrous connective tissue. In contrast, implants that received PDL cells without the application of EMD demonstrated good bone contact, but strands of epithelium were observed in the implant-connective tissue interface. Implants that received PDL cells and EMD also had good bone contact but without evidence of epithelium. A cementum-like interface was not observed in any of the groups. Results of this pilot study suggest that EMD and the type of cell populations present in the implant wound-healing environment may alter the implant-connective tissue interface

Destructive periodontal diseases have been associated with increased risk of atherosclerotic complications, including myocardial infarction (MI) and stroke. This finding comes at a time when our understanding of atherosclerotic complications are changing from a focus on the occlusion of arteries, due to the buildup of plaque deposits, to an increased awareness of the role of inflammation in plaque rupture and thrombus formation. The role of inflammation can have great significance to the dental profession if inflammatory cells and factors derived from chronic infections, such as destructive periodontal diseases, are shown to contribute to plaque rupture. This 'Perspectives' feature will review the role of inflammation in atherosclerotic complications, and the association between destructive periodontal diseases, systemic inflammation and atherosclerotic complications. It will also highlight ongoing research designed to determine whether destructive periodontal diseases contribute to atherosclerotic complications

The periodontal ligament has the potential to regenerate a complete periodontal connective tissue attachment, starting with the deposition of cementum, on pathologically exposed root surfaces as well as several materials including titanium oxide. However, most commonly used dental materials result in a fibrous encapsulation or a chronic inflammatory response after periodontal wound healing rather than the formation of a periodontal connective tissue attachment. Recently, an extract of porcine enamel matrix (Emdogain(R), EMD) has been reported inductive of cementum formation in both in vivo and in vitro studies. The aim of this study was to determine the effect of EMD, when applied to materials previously reported not supportive of periodontal connective tissue formation, on the periodontal connective tissue-material interface obtained with these materials in vivo. Bilateral osteotomies were performed on the mandible of a Yucatan minipig exposing the buccal root surface of four premolars. A series of four preparations were placed in each root surface that were subsequently filled with calcium hydroxide, gutta percha, mineral trioxide aggregate (MTA), or left unfilled. One side, in addition, received an application of EMD prior to surgical closure. A bioabsorbable surgical barrier membrane was placed over the osteotomy sites to exclude gingival connective tissue from the wound-healing environment. The mucoperiosteal flaps were then readapted and sutured in position. The animal was euthanized 10 weeks after the procedure, block sections obtained and prepared for light microscopy. Results demonstrated complete regeneration of alveolar bone and periodontal ligament in all four teeth from the EMD-treated side. Fibers from the periodontal ligament were observed to insert into a mineralized matrix consistent with cementum on all four root preparations. In contrast, massive root resorption without regeneration of alveolar bone was found on all teeth from the side not treated with EMD. The results of this pilot study suggest that the application of EMD to material surfaces that normally do not support periodontal connective tissue attachment formation can alter the type of periodontal connective tissue interface obtained with these materials.

Cells within the periodontal ligament have the potential to regenerate a periodontal connective tissue attachment on pathologically exposed root surfaces as well as on several material surfaces including titanium. However, rather than a periodontal connective tissue attachment, a fibrous encapsulation or chronic inflammatory response has been reported at the material connective tissue interface for most dental materials. Cementum is the first tissue of the periodontal connective tissue attachment to develop and the secretion of enamel matrix related proteins on the newly mineralized dentin surface precedes and is thought to induce cementum formation. Enamel matrix-related proteins may also function in the adult because the application of an acid extract of porcine enamel protein matrix (Emdogain(R), EMD) on pathologically exposed root surfaces has been shown to result in cementum regeneration. Therefore, the objective of the present study was to determine whether the application of EMD to materials that do not normally support cementogenesis in vivo would alter the in vitro phenotype of periodontal ligament (PDL) cells including the synthesis of cementum-associated extracellular matrix proteins. Primary PDL cells were established from 21-day-old Sprague-Dawley rats, and were cultured on four materials commonly encountered in dental practice (gutta percha, calcium hydroxide, amalgam, and super EBA cement) with and without the application of EMD. After 7 or 14 days of culture, total-DNA content, collagen synthesis, alkaline phosphatase activity, and the synthesis of a 42-kDa cementum-associated extracellular matrix protein were determined. PDL cells cultured on all materials had decreased total DNA content. The application of EMD further decreased total DNA content. PDL cells cultured on gutta percha and calcium hydroxide with the application of EMD had similar levels of collagen synthesis and alkaline phosphatase activity but also expressed a 42-kDa cementum extracellular matrix-associated protein when compared to the other groups. These results suggest that EMD can alter the phenotype of PDL cells when cultured on these dental materials.

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.