Current understanding of periodontal disease derives from studies mostly conducted in developed countries. However, the disease process among those studied populations may be confounded by the professional dental care. There have been few attempts to investigate factors related to the disease among populations of developing countries where the natural history of the disease is minimally confounded by care. This imbalance is evident in risk assessment research on the associations between periodontal disease and smoking-one of the most significant risk factors for the disease. Also, most studies on smoking used convenience or purposive samples, which may bias the findings. Therefore, there is a need for research conducted among a representative sample of a developing country. The present study aimed to describe the prevalence, extent and severity of chronic adult periodontitis among representative Vietnamese middle-aged adults. Also, it aimed to investigate smoking, which is highly prevalent in Vietnam, as a risk indicator for periodontal disease in a population with minimal access to dental care. The study was designed as a cross-sectional population-based study with a multistage, stratified random sample with probability of selection proportional to population size. The US National Institute of Dental Research (NIDR) protocol was used to assess loss of periodontal attachment among 575 dentate subjects in two randomly selected provinces. Assessment was made at mesial and buccal sites of every present tooth, excluding third molars. A parallel social survey collected socio-demographic information and smoking history, which were assessed for possible association with the disease status. Periodontal disease was highly prevalent among the sample. The patterns of the disease were similar to those reported from other populations. Virtually all subjects expressed some levels of disease, whereas only a few subjects or sites had severe disease. Bivariate analyses revealed significant associations between smoking and lower socio-economic status with more severe expression of the disease. Smoking was consistently associated with poorer periodontal status irrespective of outcome measure investigated. Multivariate models showed that smoking was the most predictive factor for the disease. The Odds Ratio of having severe periodontitis (that is, having 2+sites with loss of attachment more than or equal to 5 mm and 1+sites with pocket depth more than or equal to 4 mm) was 7.93 for heavy smokers compared to non-smokers. A dose-response effect of the association between smoking and the outcomes of the disease was also evident. The study provided a picture of the periodontal status of the representative sample from Vietnamese middle-aged adult population where the disease was less confounded by dental care. Furthermore, the study contributes consistency, strength and dose-response effect to the association of smoking as a risk indicator for periodontal destruction. The study should be used to assist the public health agencies in planning appropriate policies for Vietnam to address smoking and periodontal disease. / Thesis (M.Sc.)--Dental School, 2001.

Thesis (M.D.S.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 83-102) Also available in print.

Objectives: Periodontal disease is a chronic inflammation resulting in periodontal attachment loss. Keratinocyte Growth Factor-1 (KGF-1) is upregulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial-specific Keratinocyte Growth Factor Receptor (KGFR). First, we examined KGF-1 and KGFR expression and localization in human periodontal tissues. Second, we extended these studies by developing an in vitro mechanical wound model to mimic trauma to the periodontal pocket epithelium and examined ligand independent KGFR activation and cell migration. Methods: In our study of human gingival tissues, we used immunohistochemistry and laser capture microdissection with RT-PCR to analyze KGF-1 and KGFR expression and localization. To study ligand independent KGFR phosphorylation, KGFR internalization along the wound edge was imaged using immunohistochemical staining and KGFR phosphorylation confirmed using immunoprecipitation with western blotting. Wounding induced oxidative stress was detected using DCFH-DA (2',7'-dichlorofluorescin diacetate) and modulated by pretreatment with an antioxidant. Changes in migration were examined in the presence or absence of pathway specific inhibitors. Results: KGF-1 protein localized to areas of junctional and basal oral epithelial cells was significantly increased in periodontal pocket epithelium (p<0.01) and oral epithelium (p<0.05) of disease-associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, and was increased in disease-associated pocket epithelium (p<0.05). Laser capture microdissection with RT-PCR confirmedKGF-1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. In our cell culture model, mechanical wounding induced ligand independent KGFR activation. ROS (Reactive Oxygen Species) generation along the wound edge was associated with KGFR activation and scavenging of ROS reduced KGFR phosphorylation. The c-Src family inhibitor, PP1, significantly inhibited KGFR phosphorylation. Functionally cell migration was reduced by PP1 (82.7%), SU5402(70%) and PD98059 (57%). Conclusions: KGF-1 and KGFR proteins are expressed in health but significantly induced in human diseased periodontal tissues. Microwounding associated generation of ROS mediates KGFR phosphorylation via c-Src kinase signaling and induced wound edge cell migration. Therefore, regulation of epithelial cell behavior associated with the onset and progression of periodontal disease may possibly be mediated by two related but distinct mechanisms. (1) Ligand-dependent activation of KGFR due to upregulation of KGF-1. (2) Ligand-independent activation of KGFR due to chronic microwounding.

El estudio evaluó la concentración de inmunoglobulina G (IgG) en saliva total en la enfermedad periodontal y su papel como marcador biológico en esta patología Se incluyeron 50 individuos sanos y 40 pacientes periodontales como grupos control y estudio respectivamente. El grupo de estudio se dividió en subgrupos de 20 individuos: gingivitis y periodontitis. El examen clínico evaluó placa dentaria, sangrado al sondaje y profundidad de sondaje. Las evaluaciones se efectuaron antes y después del tratamiento periodontal de Fase I. En ambos momentos se tomaron muestras de saliva total para determinar la concentración de IgG mediante el análisis espectrofotométrico de su absorbancia. Se encontró que a mayor progresión de la enfermedad periodontal los niveles de IgG eran más elevados encontrándose una diferencia significativa entre pacientes sanos, con gingivitis y periodontitis. Sin embargo el grado de severidad de la gingivitis no constituía un factor relevante para la variación del nivel de IgG. Entre los casos leves y severos de periodontitis se encontró una diferencia significativa en los niveles de IgG. / This study evaluated the concentration of inmunogluline G (IgG) in whole saliva in peridontal disease and its role as a biological marker in this patology. To realize the study, 50 healthy patients and 40 patients were incluyed as control and study group respectively. The study group was divided in subgroup with 20 patients: gingivitis and periodontitis. The clinical examination was realized evaluating dental plaque, probing bleeding and probing depth. The evaluation were performed before and after the phase I periodontal treatment. At each moment, we took whole saliva samples to determine the IgG concentration through espectrophotometric analysis of its absorbance. We found that the greater progression of the periodontal disease, more elevated was the IgG level IgG establishing a significant difference between the healthy patients and individuals with gingivitis and periodontitis. However, the severity of gingivitis didn’t constitute a outstanding factor for significant differences in IgG concentration between slight and severe cases. On the other hand, between slight and severe cases of patients with periodontitis, we found a significant difference at IgG levels.

abstract / Dentistry / Doctoral / Doctor of Philosophy

Objectives: Periodontal disease is a chronic inflammation resulting in periodontal attachment loss. Keratinocyte Growth Factor-1 (KGF-1) is upregulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial-specific Keratinocyte Growth Factor Receptor (KGFR). First, we examined KGF-1 and KGFR expression and localization in human periodontal tissues. Second, we extended these studies by developing an in vitro mechanical wound model to mimic trauma to the periodontal pocket epithelium and examined ligand independent KGFR activation and cell migration. Methods: In our study of human gingival tissues, we used immunohistochemistry and laser capture microdissection with RT-PCR to analyze KGF-1 and KGFR expression and localization. To study ligand independent KGFR phosphorylation, KGFR internalization along the wound edge was imaged using immunohistochemical staining and KGFR phosphorylation confirmed using immunoprecipitation with western blotting. Wounding induced oxidative stress was detected using DCFH-DA (2',7'-dichlorofluorescin diacetate) and modulated by pretreatment with an antioxidant. Changes in migration were examined in the presence or absence of pathway specific inhibitors. Results: KGF-1 protein localized to areas of junctional and basal oral epithelial cells was significantly increased in periodontal pocket epithelium (p<0.01) and oral epithelium (p<0.05) of disease-associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, and was increased in disease-associated pocket epithelium (p<0.05). Laser capture microdissection with RT-PCR confirmedKGF-1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. In our cell culture model, mechanical wounding induced ligand independent KGFR activation. ROS (Reactive Oxygen Species) generation along the wound edge was associated with KGFR activation and scavenging of ROS reduced KGFR phosphorylation. The c-Src family inhibitor, PP1, significantly inhibited KGFR phosphorylation. Functionally cell migration was reduced by PP1 (82.7%), SU5402(70%) and PD98059 (57%). Conclusions: KGF-1 and KGFR proteins are expressed in health but significantly induced in human diseased periodontal tissues. Microwounding associated generation of ROS mediates KGFR phosphorylation via c-Src kinase signaling and induced wound edge cell migration. Therefore, regulation of epithelial cell behavior associated with the onset and progression of periodontal disease may possibly be mediated by two related but distinct mechanisms. (1) Ligand-dependent activation of KGFR due to upregulation of KGF-1. (2) Ligand-independent activation of KGFR due to chronic microwounding.

Current understanding of periodontal disease derives from studies mostly conducted in developed countries. However, the disease process among those studied populations may be confounded by the professional dental care. There have been few attempts to investigate factors related to the disease among populations of developing countries where the natural history of the disease is minimally confounded by care. This imbalance is evident in risk assessment research on the associations between periodontal disease and smoking-one of the most significant risk factors for the disease. Also, most studies on smoking used convenience or purposive samples, which may bias the findings. Therefore, there is a need for research conducted among a representative sample of a developing country. The present study aimed to describe the prevalence, extent and severity of chronic adult periodontitis among representative Vietnamese middle-aged adults. Also, it aimed to investigate smoking, which is highly prevalent in Vietnam, as a risk indicator for periodontal disease in a population with minimal access to dental care. The study was designed as a cross-sectional population-based study with a multistage, stratified random sample with probability of selection proportional to population size. The US National Institute of Dental Research (NIDR) protocol was used to assess loss of periodontal attachment among 575 dentate subjects in two randomly selected provinces. Assessment was made at mesial and buccal sites of every present tooth, excluding third molars. A parallel social survey collected socio-demographic information and smoking history, which were assessed for possible association with the disease status. Periodontal disease was highly prevalent among the sample. The patterns of the disease were similar to those reported from other populations. Virtually all subjects expressed some levels of disease, whereas only a few subjects or sites had severe disease. Bivariate analyses revealed significant associations between smoking and lower socio-economic status with more severe expression of the disease. Smoking was consistently associated with poorer periodontal status irrespective of outcome measure investigated. Multivariate models showed that smoking was the most predictive factor for the disease. The Odds Ratio of having severe periodontitis (that is, having 2+sites with loss of attachment more than or equal to 5 mm and 1+sites with pocket depth more than or equal to 4 mm) was 7.93 for heavy smokers compared to non-smokers. A dose-response effect of the association between smoking and the outcomes of the disease was also evident. The study provided a picture of the periodontal status of the representative sample from Vietnamese middle-aged adult population where the disease was less confounded by dental care. Furthermore, the study contributes consistency, strength and dose-response effect to the association of smoking as a risk indicator for periodontal destruction. The study should be used to assist the public health agencies in planning appropriate policies for Vietnam to address smoking and periodontal disease. / Thesis (M.Sc.)--Dental School, 2001.

Thesis (M.D.S.)--University of Adelaide, 1983. / Mounted ill. Includes bibliographical references (leaves [221-240]).

Thesis (M.S.)--School of Dentistry. University of Missouri--Kansas City, 2006. / "A thesis in oral biology." Advisor: Simon R. MacNeill. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Nov. 12, 2007. Includes bibliographical references (leaves 56-60). Online version of the print edition.

Thesis (M.D.S.)--University of Adelaide, Dept. of Dentistry, 1989? / "Addenda" [i.e. Errata] on fly-leaf. Includes bibliographical references (leaves 159-176).