Biomedical subjects

R J Genco

Publications and source records attributed to R J Genco.

At least 37 records · Page 2Linked to original sources

PubMed1999

Longitudinal study of predictive factors for periodontal disease and tooth loss.

Longitudinal assessment of risk factors for periodontal disease is necessary to provide evidence that a putative risk factor or risk indicator is a true risk factor. The purpose of the present study was to explore longitudinally a variety of markers as possible periodontal risk factors in subjects with little or no periodontal disease at baseline. 415 subjects with mild or little periodontal disease were examined: medical and dental history; socioeconomic profile, clinical measurements, microbial samples and radiographic assessment of bone height were performed at baseline, and at a follow-up examination 2 to 5 years later. Mean probing pocket depth (PPD) at baseline was 1.99+/-0.37 mm while mean overall change was 0.1 mm which amounts to an annual rate of 0.04 mm. Overall mean clinical attachment level (1.75+/-0.6 mm) at baseline resulted in mean attachment change of 0.28 mm (0.12 mm annually). Alveolar crestal height (ACH) at baseline (mean 2.05+/-0.85 mm) resulting in a mean net loss of 0.1 mm. Approximately 10% of all sites presented for the second visit with attachment loss exceeding the threshold (4.4% annually), while only 2.2% of all sites exhibited attachment gain (0.88% annually). Older individuals exhibited greater mean bone loss but the least amount of attachment loss. Current smokers exhibited greater disease progression compared to non-smokers. Tooth morbidity (0.17 teeth/patient/year) was associated with greater baseline CAL and ACH loss, and an assortment of systemic conditions. Subjects who harbored Bacteroides forsythus (Bf) at baseline had greater loss in ACH; likewise, these subjects experienced greater proportions of losing sites and twice as much tooth mortality compared to Bf-negative patients. Baseline clinical parameters correlated strongly with the outcome, i.e., subjects with deeper mean pocket depth at baseline exhibited greater increase in pocket depth overtime; while subjects with greater attachment loss at baseline exhibited greater attachment loss between the 1st and 2nd visits.

Adult↗

PubMed1999

Association of periodontal infections with atherosclerotic and pulmonary diseases.

Chronic infections may influence the severity and/or course of a number of systemic diseases. Periodontal diseases are localized chronic inflammatory conditions of the gingiva and underlying bone and connective tissues induced by bacteria and bacterial products of dental plaque. This paper will discuss the evidence for the role of periodontal disease in the pathogenesis of 2 important systemic diseases, atherosclerosis and pulmonary infections. Both epidemiological and laboratory studies are reviewed to assess the biological basis for the association of periodontal infections and these important diseases. Several potential mechanisms by which periodontal diseases may influence these conditions are also discussed.

Alveolar Process↗

PubMed1999

Role of the amino-terminal region of Porphyromonas gingivalis fimbriae in adherence to epithelial cells.

Porphyromonas gingivalis fimbriae elicit many responses in eukaryotic cells, including mitogenicity, cytokine production, epithelial cell invasion, and cellular immune response. Specific domains of the major fimbrial protein (FimA) have been shown to be important in triggering some of these functions. The goal of the present study was to identify the domain(s) of P. gingivalis FimA responsible for specific interaction with human mucosal epithelial cells. Fimbriated P. gingivalis strains have been shown to bind to buccal epithelial cells, whereas nonfimbriated strains bind at low levels or not at all. This and other studies provide evidence that FimA mediates the adherence of P. gingivalis to oral epithelial cells. To determine the specific region(s) of P. gingivalis FimA involved in epithelial cell binding, specific antipeptide antibodies were used to inhibit the binding of iodinated purified fimbriae as well as the binding of P. gingivalis cells to epithelial cells. Antibodies directed against peptides 49 to 68 (VVMANTAGAMELVGKTLAEVK) and 69 to 90 (ALTTELTAENQEAAGLIMTAEP) were found to highly inhibit both the binding of fimbriae and the binding of P. gingivalis cells to epithelial cells. The antibody against FimA peptides 69 to 90 also reacted with P. gingivalis fimbriae in immunogold labeling and immunoblot analysis, thereby indicating that this peptide domain is exposed on the surface of fimbriae. Our results suggest that the amino-terminal domain corresponding to amino acid residues 49 to 90 of the fimbrillin protein is a major epithelial cell binding domain of P. gingivalis fimbriae.

Amino Acid Sequence↗

PubMed1999

Relationship of stress, distress and inadequate coping behaviors to periodontal disease.

BACKGROUND: The association of stress, distress, and coping behaviors with periodontal disease was assessed. METHODS: A cross-sectional study of 1,426 subjects between the ages of 25 and 74 years in Erie County, New York, was carried out to assess these relationships. Subjects were asked to complete a set of 5 psychosocial questionnaires which measure psychological traits and attitudes including discrete life events and their impact; chronic stress or daily strains; distress; coping styles and strategies; and hassles and uplifts. Clinical assessment of supragingival plaque, gingival bleeding, subgingival calculus, probing depth, clinical attachment level (CAL) and radiographic alveolar crestal height (ACH) was performed, and 8 putative bacterial pathogens from the subgingival flora measured. RESULTS: Reliability of subjects' responses and internal consistencies of all the subscales on the instruments used were high, with Cronbach's alpha ranging from 0.88 for financial strain to 0.99 for job strain, uplifts, and hassles. Logistic regression analysis indicated that, of all the daily strains investigated, only financial strain was significantly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09 to 2.65 and OR = 1.68, 95% CI = 1.20 to 2.37, respectively) after adjusting for age, gender, and cigarette smoking. When coping behaviors were evaluated, it was found that those with more financial strain who were high emotion-focused copers (a form of inadequate coping) had a higher risk of having more severe attachment loss (OR = 2.24, 95% CI = 1.15 to 4.38) and alveolar bone loss (OR = 1.91, 95% CI = 1.15 to 3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. Similar results were found among the low problem-focused copers for AL (OR = 2.21, 95% CI = 1.11 to 4.38) and ACH (OR = 2.12, 95% CI = 1.28 to 3.51). However, subjects with high levels of financial strain who reported high levels of problem-based coping (considered adequate or good coping) had no more periodontal disease than those with low levels of financial strain, suggesting that the effects of stress on periodontal disease can be moderated by adequate coping behaviors. CONCLUSIONS: We find that psychosocial measures of stress associated with financial strain and distress manifest as depression, are significant risk indicators for more severe periodontal disease in adults in an age-adjusted model in which gender (male), smoking, diabetes mellitus, B. forsythus, and P. gingivalis are also significant risk indicators. Of considerable interest is the fact that adequate coping behaviors as evidenced by high levels of problem-based coping, may reduce the stress-associated risk. Further studies also are needed to help establish the time course of stress, distress, and inadequate coping with respect to the onset and progression of periodontal disease, and the mechanisms that explain this association.

Adaptation, Psychological↗

PubMed1998

Structures involved in the interaction of Porphyromonas gingivalis fimbriae and human lactoferrin.

The ability of laboratory and clinical strains of Porphyromonas gingivalis to bind lactoferrin has been assessed (FEMS Immunology and Medical Microbiology, 1996, 14, 135-143). Relative binding for P. gingivalis to lactoferrin varies among strains from 3.78 to 26.62%. We also observed that fimbriated strains of P. gingivalis bind more strongly to lactoferrin as compared to nonfimbriated strains of P. gingivalis. This observation led us to study fimbrial interaction with human lactoferrin and the fine structure of these interactions. Binding of iodinated purified fimbriae was studied using an overlay assay. Iodinated fimbriae bind specifically and strongly to human lactoferrin. When various sugars were used to inhibit binding, only N-acetylgalactosamine and fucose were inhibitory. To confirm further that oligosaccharide of lactoferrin is involved in the interaction, lactoferrin was chemically deglycosylated, and fimbriae failed to bind deglycosylated lactoferrin. Antifimbriae, as well as four antipeptide antibodies against different regions of the P. gingivalis fimbrillin, were used to inhibit the interaction. Antipeptide E, directed against amino acids 81-98 (AAGLIMTAEPKTIVLKAG-C), was found to be the most effective inhibitor for the lactoferrin-fimbriae interaction. These results suggest that the binding of P. gingivalis cells to lactoferrin is lectin like, directed to a oligosaccharide of lactoferrin. Furthermore, these studies suggest that the region of fimbriae that binds to lactoferrin is the N-terminus of the molecule. It is likely that binding of lactoferrin to P. gingivalis cells results in antimicrobial activity directed against these cells by virtue of its ability to deprive the bacterial cell of needed iron.

Amino Acid Sequence↗

PubMed1998

Cloning, expression, and sequencing of a cell surface antigen containing a leucine-rich repeat motif from Bacteroides forsythus ATCC 43037.

Bacteroides forsythus is a recently recognized human periodontopathogen associated with advanced, as well as recurrent, periodontitis. However, very little is known about the mechanism of pathogenesis of this organism. The present study was undertaken to identify the surface molecules of this bacterium that may play roles in its adherence to oral tissues or triggering of a host immune response(s). The gene (bspA) encoding a cell surface-associated protein of B. forsythus with an apparent molecular mass of 98 kDa was isolated by immunoscreening of a B. forsythus gene library constructed in a lambda ZAP II vector. The encoded 98-kDa protein (BspA) contains 14 complete repeats of 23 amino acid residues that show partial homology to leucine-rich repeat motifs. A recombinant protein containing the repeat region was expressed in Escherichia coli, purified, and utilized for antibody production, as well as in vitro binding studies. The purified recombinant protein bound strongly to fibronectin and fibrinogen in a dose-dependent manner and further inhibited the binding of B. forsythus cells to these extracellular matrix (ECM) components. In addition, adult patients with B. forsythus-associated periodontitis expressed specific antibodies against the BspA protein. We report here the cloning and expression of an immunogenic cell surface-associated protein (BspA) of B. forsythus and speculate that it mediates the binding of bacteria to ECM components and clotting factors (fibronectin and fibrinogen, respectively), which may be important in the colonization of the oral cavity by this bacterium and is also a target for the host immune response.

Amino Acid Sequence↗

PubMed1998

Models to evaluate the role of stress in periodontal disease.

We evaluated the association of stress,distress, and coping behaviors with periodontal disease in 1,426 subjects, aged 25 to 74, in Erie County, NY, Demographic characteristics, medical and dental history, and tobacco and alcohol consumption, as well as clinical assessments of supragingival plaque, subgingival flora, gingival bleeding, calculus, probing depth, clinical attachment level (CAL), and radiographic alveolar bone loss (ABL) were obtained for each subject. Subjects also completed a set of 5 psychosocial instruments that measured life events, daily strains, hassles and uplifts, distress, and coping behaviors. Internal consistencies of all subscales on the instruments were high, with Cronbach's alpha ranging from 0.88 to 0.99. Logistic regression indicated that financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.70; 95% CI, 1.09-2.65; and 1.68; 95% CI, 1.20-2.37, respectively) after adjusting for age, gender, and smoking. When those with financial strain were stratified with respect to coping behaviors, it was found that those who exhibited high emotion-focused coping (inadequate coping) had and even higher risk of having more severe attachment loss (OR 2.24; 95% CI, 1.15-4.38) and alveolar bone loss (OR 1.91; 95% CI, 1.15-3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. After further adjusting for number of visits to the dentist, those with financial strain who were high emotion-focused copers still had higher levels of periodontal disease based on CAL (OR 2.12; 95% CI, 1.07-4.18). In contrast, subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain. Salivary cortisol levels were higher in a test group exhibiting severe periodontitis, a high level of financial strain, and high emotion-focused coping, as compared to a control group consisting of those with little or no periodontal disease, low financial strain, and low levels of emotion-focused coping (11.04 +/-4.4 vs/ 8.6 +/- 4.1 nmol/L salivary cortisol, respectively). These findings suggest that psychosocial measures of stress associated with financial strain are significant risk indicators for periodontal disease in adults. Further prospective studies are needed to help establish the time course of stress, distress, and inadequate coping on the onset and progression of periodontal disease, as well as to evaluate the mechanisms by which stress exerts its effects on periodontal infections.

Adaptation, Psychological↗

PubMed1998

Glycemic control and alveolar bone loss progression in type 2 diabetes.

This study tested the hypothesis that the risk for alveolar bone loss is greater, and bone loss progression more severe, for subjects with poorly controlled (PC) type 2 diabetes mellitus (type 2 DM) compared to those without type 2 DM or with better controlled (BC) type 2 DM. The PC group had glycosylated hemoglobin (HbA1) > or = 9%; the BC group had HbA1 < 9%. Data from the longitudinal study of the oral health of residents of the Gila River Indian Community were analyzed. Of the 359 subjects, aged 15 to 57 with less than 25% radiographic bone loss at baseline, 338 did not have type 2 DM, 14 were BC, and 7 were PC. Panoramic radiographs were used to assess interproximal bone level. Bone scores (scale 0-4) corresponding to bone loss of 0%, 1% to 24%, 25% to 49%, 50% to 74%, or > or = 75% were used to identify the worst bone score (WBS) in the dentition. Change in worst bone score at follow-up, the outcome, was specified on a 4-category ordinal scale as no change, or a 1-, 2-, 3-, or 4-category increase over baseline WBS (WBS1). Poorly controlled diabetes, age, calculus, time to follow-up examination, and WBS1 were statistically significant explanatory variables in ordinal logistic regression models. Poorly controlled type 2 DM was positively associated with greater risk for a change in bone score (compared to subjects without type 2 DM) when the covariates were included in the model. The cumulative odds ratio (COR) at each threshold of the ordered response was 11.4 (95% CI = 2.5, 53.3). When contrasted with subjects with BC type 2 DM, the COR for those in the PC group was 5.3 (95% CI = 0.8, 53.3). The COR for subjects with BC type 2 DM was 2.2 (95% CI = 0.7, 6.5), when contrasted to those without type 2 DM. These results suggest that poorer glycemic control leads to both an increased risk for alveolar bone loss and more severe progression over those without type 2 DM, and that there may be a gradient, with the risk for bone loss progression for those with better controlled type 2 DM intermediate to the other 2 groups.

Adolescent↗

PubMed1998

Periodontal disease and diabetes mellitus: a two-way relationship.

Severe periodontal disease often coexists with severe diabetes mellitus. Diabetes is a risk factor for severe periodontal disease. A model is presented whereby severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. We propose that an infection-mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from lipopolysaccharide (LPS) and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response operative in diabetes mellitus. In this model, the combination of these 2 pathways, infection and AGE-mediated cytokine upregulation, helps explain the increase in tissue destruction seen in diabetic periodontitis, and how periodontal infection may complicate the severity of diabetes and the degree of metabolic control, resulting in a 2-way relationship between diabetes mellitus and periodontal disease/infection. This proposed dual pathway of tissue destruction suggests that control of chronic periodontal infection is essential for achieving long-term control of diabetes mellitus. Evidence is presented to support the hypothesis that elimination of periodontal infection by using systemic antibiotics improves metabolic control of diabetes, defined by reduction in glycated hemoglobin or reduction in insulin requirements.

Anti-Bacterial Agents↗

PubMed1998

Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years.

This study tested the hypothesis that persons with non-insulin dependent diabetes mellitus (NIDDM) have greater risk of more severe alveolar bone loss progression over a 2-year period than those without NIDDM. Data from the longitudinal study of the oral health of residents of the Gila River Indian Community were analyzed for 362 subjects, aged 15 to 57, 338 of whom had less than 25% radiographic bone loss at baseline, and who did not develop NIDDM nor lose any teeth during the 2-year study period. The other 24 subjects had NIDDM at baseline, but met the other selection criteria. Bone scores (scale 0-4) from panoramic radiographs corresponded to bone loss of 0%, 1%-24%, 25%-49%, 50%-74%, or 75% and greater. Change in bone score category was computed as the change in worst bone score (WBS) reading after 2 years. Age, calculus, NIDDM status, time to follow-up examination, and baseline WBS were explanatory variables in regression models for ordinal categorical response variables. NIDDM was positively associated with the probability of a change in bone score when the covariates were controlled. The cumulative odds ratio for NIDDM at each threshold of the ordered response was 4.23 (95% C.I. = 1.80, 9.92). In addition to being associated with the incidence of alveolar bone loss (as demonstrated in previous studies), these results suggest an NIDDM-associated increased rate of alveolar bone loss progression.

Adolescent↗

PubMed1998

Radiographic and clinical responses to periodontal therapy.

Mechanical periodontal therapy is widely used for a variety of periodontal conditions. While the clinical efficacy of this treatment has been validated, the radiographic response has not been studied in depth. The purpose of the present study was to examine the clinical and radiographic response to mechanical periodontal therapy, and assess the factors associated with these changes. One hundred and eight patients, with established periodontitis, received oral hygiene instruction and mechanical periodontal therapy for a period of 4 to 5 weeks. Scheduled maintenance visits were performed at 3, 6, 9, and 15 months. Probing depth (PD) and attachment level (AL) measurements were performed at baseline, and at 3 and 15 months. Intraoral radiographs were taken at baseline and 12 to 15 months postsurgery using a Rinn alignment system. Alveolar crestal height (ACH) measurements were performed on a pair of digitized images of the previously taken radiographs. An overall mean of patients' changes for PD, AL, and ACH was initially computed. Active sites (gainers and losers) were determined using a threshold method, and expressed as patient's percentage of active sites (number of active sites of the total sites measured in each patient). Mean overall probing reduction and AL gain was 0.5 mm and 0.44 mm, respectively. Of all sites measured, 16.6% exhibited AL gain, while only 6.2% of all sites exhibited AL loss. Mean overall change in ACH was -0.07 mm, of which 11.8% of all sites exhibited ACH gain, while 15.1% exhibited loss beyond the threshold. Non-smokers presented no change in bone loss, while smokers continued to lose bone at an annual rate of 0.17 mm, despite treatment (P <0.005). Likewise, the average percent of sites per patients showing attachment gain beyond the threshold were much greater in non-smokers (13.9%) compared to 9.0% in smokers (P <0.01). Mean probing reduction was 50% greater among non-smokers (0.6 mm) when compared to smokers (0.4 mm), which was also statistically significant (P <0.05). A positive and significant correlation was established between the percentage of sites with AL gain and sites with ACH gain (Rho =0.40; P=0.0001). It is suggested that monitoring sites for AL and ACH gain expressed as changes beyond a selective threshold is an important outcome variable in treatment studies.

Adult↗

PubMed1998

Is estrogen deficiency a risk factor for periodontal disease?

In recent years, interest in the relationship between osteopenia, osteoporosis, estrogen status, and periodontal disease has grown considerably. A substantial number of studies have attempted to address this important question. Despite the large body of evidence, controversy persists concerning a possible association between these conditions. Whether loss of oral bone is related to loss of systemic bone and whether estrogen deficiency modulates loss of oral bone are subjects of more specific debate. This article reviews the direct and indirect scientific evidence supporting the role of estrogen deficiency as a risk factor for periodontal disease. A model is proposed for the biological basis of such increased risk. The article also suggests essential criteria for the design of studies examining the relationship between osteopenia, osteoporosis, estrogen deficiency, and periodontal disease.

Alveolar Bone Loss↗

PubMed1997

Secretion of Porphyromonas gingivalis fimbrillin polypeptides by recombinant Streptococcus gordonii.

The fimbriae of Porphyromonas gingivalis plays an important role in the pathogenesis of periodontal disease. A structural subunit of the P. gingivalis fimbriae, fimbrillin, has been shown to promote adherence of the bacteria to host surfaces and also induce an immune response. Biologically active domains of fimbrillin responsible for adherence or eliciting immune responses have been determined. In a previous study, we engineered the human oral commensal organism Streptococcus gordonii to express such biologically active domains on the surface of the bacteria as a vaccine delivery system. In this study we report an alternative approach of secreting fimbrillin polypeptide domains into the medium by modification of the surface-expression system described earlier. Such recombinant S. gordonii, in addition to being a source for antigen presentation to trigger a protective immune response, may have the added advantage of directly blocking the fimbriae-mediated adherence of P. gingivalis to the oral cavity following implantation. This approach can also be utilized for secreting other biologically important therapeutic molecules on mucosal surfaces for modulating local microenvironments.

Bacterial Proteins↗

PubMed1997

High-performance liquid chromatographic separation of Porphyromonas gingivalis fimbriae.

Fimbriae are responsible for the adherence of many bacterial species to the surfaces they eventually colonize. Porphyromonas gingivalis is an important pathogenic agent involved in periodontal disease. Fimbriae of P. gingivalis have been thought to mediate binding of the bacterium to oral surfaces. In order to study the role of fimbriae in microbial adhesion, it is important to purify fimbriae to homogeneity. A simple and rapid reverse-phase high-performance liquid chromatography (HPLC) method is developed to purify P. gingivalis fimbriae. The crude fimbriae were precipitated from sonic extract of P. gingivalis cells with the 40% ammonium sulfate precipitation. The dialyzed crude fimbriae preparation was subjected to reverse-phase HPLC separation. The purity and size of purified fimbrial proteins were confirmed by SDS-polyacrylamide gel electrophoresis(SDS-PAGE) followed by Western immunoblot using polyclonal antibodies against fimbriae. The purified major fimbrial protein from strain 33277 of P. gingivalis had apparent molecular mass of 41 kDa. The method is useful for analytical as well as preparative purification with 25% yields from the ammonium sulfate-precipitated crude fimbriae preparation, and represents increased speed and efficiency over earlier published methods.

Bacterial Proteins↗

PubMed1997

Interleukin-1 gene expression in macrophages induced by surface protein components of Porphyromonas gingivalis: role of tyrosine kinases in signal transduction.

We examined interleukin-beta (IL-1 beta) mRNA expression and protein tyrosine kinase activities induced by surface protein components of Porphyromonas gingivalis to gain insights into signaling pathways leading to macrophage responses. Reverse transcriptase-polymerase chain reaction analyses showed that native fimbriae, full-length recombinant fimbrillin, and a lectin-like 12-kDa antigen of P. gingivalis induced rapid expression of mRNA encoding IL-1 beta in BALB/c and lympopolysaccharide-hyporesponsive C3H/HeJ peritoneal macrophages. The antigens also specifically activated tyrosine kinase(s) in macrophages. The ability of the surface protein components to induce the cytokine mRNA accumulation was markedly abrogated by tyrosine kinase inhibitors. The findings reported here suggest that IL-1 beta expression in macrophages is a functional consequence of tyrosine kinase activation by the P. gingivalis surface protein components.

Adhesins, Bacterial↗

PubMed1997

Longitudinal study of prognostic factors in established periodontitis patients.

Numerous indicators for disease progression have been described in the last decade. The purpose of this study was to examine, longitudinally, a large battery of clinical, microbiological, and immunological indicators, to try to determine whether the presence of one or a combination of these parameters at baseline, would correlate positively with increased attachment and or bone loss (true prognostic factors). Following initial screening, 79 patients with established periodontitis were monitored longitudinally for one year. Whole mouth clinical measurements, plaque gingival and calculus indices, together with pocket depth and attachment level measurements, were repeated every three months. Full mouth radiographic survey, performed at baseline and 12 months, served to determine changes in crestal bone height using an image enhancement technique. Subgingival plaque samples were taken at baseline and every 3 months. Immunofluorescence assays were performed for the a battery of target microorganisms. Serum and GCF samples for IgG subclasses analysis were obtained at each visit and assayed using ELISA techniques. Likewise blood, samples were also drawn at each visit for a quantitative analysis of serum cotinine level. The overall mean attachment loss (AL) and bone loss (BL) were almost identical (0.159 mm and 0.164 mm, respectively). Individual patients variation was large (-0.733 to +1.004 mm). An overall 6.89% of sites were active; individual patients' means ranged from 0-28.9%. Mean pocket depth (PD) showed minimal change over the study period (-0.033 mm) thus suggesting that most if not all the AL was accompained by concomitant gingival recession. Smokers exhibited greater AL and radiographic BL compared to non-smokers. Likewise, patients' cotinine level showed direct correlation with outcomes of progressive periodontal breakdown. Past severity of periodontal involvement, as reflected in the patients baseline PD, AL and crestal bone height, showed good correlation with longitudinal changes in the periodontium. This correlation was higher for crestal BL as the outcome variable, while somewhat smaller for change in AL as the outcome variable. Bacteroides forsythus (Bf.), Prevotella intermedia (Pi.) and Porphyromonas gingivalis (Pg.) were frequently found in these patients. The presence of these microorganisms at baseline was associated with further disease progression. Subjects with mean baseline pocket depth equal or greater than 3.2 mm were at greater risk for future bone loss 1 year later (O.R. 2.97; C.I. 1.02-8.70). Smokers were at significantly greater risk for further attachment loss when compared to non-smokers (O.R. 5.41; C.I. 1.50-19.5). Subjects that harbored B. forsythus at baseline, were at seven times greater risk for increased pocket depth (O.R. 7.84; C.I.1.74-35.3). In conclusion, past periodontal destruction, smoking habits, Bf., Pg., & Pi. are prognostic factors for further periodontal breakdown. When designing clinical trials, or when evaluating epidemiological data, it is most important to balance for these factors. Also, treatment strategies should attempt to eliminate or modify these factors.

Adult↗

PubMed1997

Reliability of a self-reported health questionnaire in a periodontal disease study.

This study assesses the reliability of a self-reported health questionnaire completed by 413 subjects aged 25-74 yr in the Erie County Periodontal Disease (ECPD) Study. Specific questions on general and oral health conditions were completed by each subject during a first visit and at a follow-up examination 2 yr later, and the two compared. Results showed that the overall measure of agreement between the two visits is substantial (average kappa, kappa = 0.80). Variation by gender and age were minimal. Questions regarding allergy to medications, oral treatment, reason for tooth extraction, health symptoms and history of systemic diseases exhibited high levels of agreement (kappa ranged from 0.71-0.90). Information on vitamin and mineral intake yielded kappa = 0.63. Oral conditions scored the lowest but were still acceptable (kappa = 0.57). These findings indicate that there were no significant discrepancies in self-reported responses to the health questionnaire used in the ECPD Study. Although the information provided by the subject may not be as accurate as compared to laboratory testing, it is nevertheless a reliable source of information which can be utilized cost-effectively in research studies.

Adult↗

PubMed1997

The relationship between radiographic and clinical changes in the periodontium.

Change in clinical attachment level (CAL) and radiographic change in crestal bone height are often used to assess periodontal breakdown and disease progression. These two variables are also used to monitor the effect of treatment. The purpose of the present longitudinal study was to evaluate the correlation between changes in CAL and alveolar bone loss. Following initial screening, 79 subjects with established periodontitis were monitored quarterly for 1 yr, using a pressure-sensitive automated probe. CAL and relative attachment level (RAL) were recorded at 6 sites for each tooth. Radiographs were obtained at baseline and 1 yr. Crestal bone changes were determined using an image enhancement technique. Mean change in attachment level was 0.16 mm. Similarly, mean proximal bone loss measured radiographically was 0.16 mm. In 6.9% of all the sites, and 13.7% of all pooled interproximal sites, AL loss was in excess of the threshold defined as 2 s.d. of repeated measurements (mean 1.54 mm). Similar percentages of sites (12.9%) had radiographic evidence of proximal bone loss exceeding the threshold (0.55-1.08 mm). A site-based analysis of active sites revealed an overall poor correlation between the 2 variables (kappa value = 0.03) which was the result of a very poor sensitivity (0.16) despite a relatively good specificity (0.81). A patient-based comparison of clinical and radiographical changes revealed an overall kappa value of 0.08, with sensitivity and specificity of 0.51 and 0.56, respectively. However, baseline CAL and crestal bone height showed good correlation (r = 0.73; p = 0.0001). It is suggested that changes in CAL and radiographic bone level progress somewhat independently. Over a short-term period of time they might not follow the same course; however, in the long term, these differences seem to level off. For longitudinal monitoring of disease progression and response to therapy both methods may be needed; while for cross-sectional evaluation and long-term prospective studies, either variable may be used alone.

Adult↗