Generalized Aggressive Periodontitis and Correlated Factors: An Histomorphometric Study (original) (raw)
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Periodontitis Stage III–IV, Grade C and Correlated Factors: A Histomorphometric Study
Biomedicines
Background: Periodontitis is a disease that leads to serious functional and esthetic dysfunctions. Periodontitis exists in different forms, and its etiology is related to multiple component causes. Two key processes involved in the evolution of this pathology are angiogenesis and inflammatory infiltrate. The aim of this study was to understand if important factors such as smoking, gender, age, plaque, pus, and probing pocket depth could influence the histomorphological pattern of generalized stage III–IV, grade C periodontitis (GPIII–IVC), which is a particular form of periodontitis. Methods: Eighteen subjects with GPIII–IVC were enrolled in this study. The percentage of inflammatory cells and the vascular area were measured and evaluated in relation to each periodontal disease-associated factor. Results: Females showed a significant increase in the percentage of inflammatory cells compared to males (6.29% vs. 2.28%, p-value = 0.020) and it was higher in non-smokers than in smokers ...
Salivary and serum markers of angiogenesis in periodontitis in relation to smoking
Clinical Oral Investigations, 2020
Objective Angiogenesis is essential in maintenance of periodontal homeostasis, and it is regulated by growth factors and cytokines, including basic fibroblast growth factor (b-FGF), endoglin, platelet and endothelial cell adhesion molecule (PECAM-1), vascular endothelial growth factor (VEGF), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1). In this study, the salivary and serum concentrations of these angiogenesisrelated proteins in relation to smoking and periodontitis were examined. Material and methods Full-mouth periodontal status together with unstimulated whole saliva and serum samples was collected from 78 individuals, including 40 periodontitis patients (20 smokers and 20 nonsmokers) and 38 periodontally healthy controls (20 smokers and 18 nonsmokers). The Luminex®-xMAP™ technique was used for protein analyses. Results Concentrations of all tested proteins in saliva as well as VEGF in serum were significantly higher in periodontitis patients than in healthy controls. In smokers, serum concentrations of endoglin (p = 0.017) and sICAM-1 (p = 0.001) were elevated in comparison to nonsmokers. After adjusting for smoking and gender, periodontitis associated significantly with salivary concentrations of b-FGF, PECAM-1, VEGF, sICAM-1, and sVCAM-1 (p < 0.01). Conclusion Taken together, salivary concentrations of b-FGF, PECAM-1, and VEGF associate with periodontitis. The suppressive effect of smoking on salivary marker levels is limited to periodontitis patients only. Clinical relevance Smoking-related suppression of salivary marker levels is observed only in periodontitis patients.
Journal of Dentomaxillofacial Radiology, Pathology and Surgery, 2016
Cigarette smoking is a risk factor for progression of periodontitis, which effects on the incidence, extent and severity of the periodontal disease and no other known factors can be harmful as much as smoking to the periodontal tissues. The purpose of this study was to determine clinical and histopathological effects of smoking on free gingiva in smokers and non-smokers with chronic periodontitis. Materials and Methods: Biopsies were obtained from palatal gingiva of first and second molar of 72 patients with chronic periodontitis (36 smokers and 36 non-smokers). These samples were sent to the pathologic laboratory for microscopic examinations, and then the data were analyzed by SPSS version 21. Results: Histopathological examination showed that smoking increase the thickness of the outer and inner epithelium of free gingiva, Collagenized connective tissue, and CAL; and decrease the vascular density. Conclusion: It seems that the reduction of the clinical signs of inflammation in the gingival tissue of smokers are because of changes in gingival epithelium and connective tissue due to smoking.
Journal of International Society of Preventive and Community Dentistry , 2020
Aim: Cigarette smoking has been recognized as an important risk factor in periodontal diseases. One of the suggested mechanisms behind this association is that nicotine alters the microcirculation and causes vasoconstriction and reduced blood flow through the periodontal tissues. Scarce information is currently available relative to the microvascular alterations associated with smoking and the distribution of capillaries through the various areas of the gingival tissues. The aims of this study were to assess, in human interproximal gingival biopsies, the number and diameter of gingival capillaries in periodontally affected smokers and nonsmokers using the CD34 immunohistochemical staining method. The pattern of distribution of vessels in the different areas of the gingival tissues was also assessed. Materials and Methods: Systemically healthy patients with moderate chronic periodontitis and ranging in age between 30 and 60 years were recruited for the study from the patient population attending the Periodontology Department of the Faculty of Dental Medicine at the Lebanese University of Beirut. The patients were selected to have a group of 10 patients (Group SP) of smokers (>10 cigarettes/day for the last 10 years) and a second group (Group NP) consisting of nonsmoking periodontally affected patients. Three to four weeks following initial preparation, one interproximal gingival biopsy was obtained from each patient. Immunohistochemical staining with CD34 mouse monoclonal antibody was used to identify the endothelial cells of the blood vessels within each sample. Twelve biopsy samples (five in Group NP and seven in Group SP) were chosen for the measurement of the number and diameter of vessels in three regions of the connective tissue of the biopsy under a blinded protocol. Results: In the two groups, the quantitative distribution of small, medium, and large vessels followed a similar trend with the number of small vessels being significantly greater than both medium and large vessels. Small vessels prevailed in the peripheral regions, whereas large vessels were more abundant in the deeper connective tissue areas. The total number of vessels seemed unaffected by chronic cigarette smoking in both groups in the entire biopsy area and in the separate connective tissue regions. Quantitative alteration in the total number of gingival capillaries was not observed in chronic smokers. A redistribution of small and large vessels in the superficial and deeper connective tissue areas of the gingival papilla was noted as a result of smoking in periodontal patients. Conclusion: The quantitative distribution of small, medium, and large vessels follows a similar trend with the content in small vessels being significantly more important than both medium and large vessels. Smoking and periodontitis result in a redistribution of small and large vessels in the superficial and deeper connective tissue areas of the gingival papilla compared to nonsmoking periodontal patients. The significance and clinical implications of such rearrangement of vasculature within the gingival tissue need to be further investigated.
Influence of smoking on clinical parameters and gingival crevicular fluid volume in patients with chronic periodontitis." Oral Health Dent Manag 13(2): 469-473. BACKGROUND: Tobacco smoking is regarded as one of the most significant risk factors for the development and progression of periodontal disease. In particular, studies have shown an alteration in Gingival Crevicular Fluid (GCF) volume and its components in smokers. OBJECTIVE: The purpose of this study was to compare the GCF volume in smoking and non-smoking Saudi subjects with chronic periodontitis. METHODS: In this study, 30 smoking patients and 30 non-smoking patients with chronic periodontitis were enrolled. Periodontal Probing Depth (PPD), Clinical Attachment Level (CAL), Plaque Index (PI), and Bleeding on Probing (BOP) were measured to assess the pattern of periodontal destruction for each patient at six sites in selected teeth. Gingival inflammation was registered at six sites, where Gingival Crevicular Fluid (GCF) was also collected. The GCF volume was measured with a Periotron 8000(R). Comparisons were made between smoking and non-smoking groups with periodontitis. RESULTS: Smokers demonstrated significantly deeper periodontal pockets (4.64+/-0.30 mm) than non-smokers (4.24+/-0.38 mm). Smoking subjects also presented significantly greater attachment loss (3.08+/-0.28 mm) than non-smoking subjects (2.74+/-0.42 mm), whereas the GCF volume was found to be significantly lower in smokers (0.25+/-0.04 mul) than in non-smokers (0.31+/-0.05 mul) (P<0.01). Among smoking subjects, lingual sites showed reduced GCF levels compared to facial sites (0.22+/-0.03 mul vs. 0.25+/-0.03 mul). CONCLUSION: Smoking appears to have considerable adverse effects on the inflammatory process, thereby promoting the progression of periodontal disease in smokers. CLINICAL SIGNIFICANCE: The adverse effect of smoking on the initiation and progression of periodontal disease is highlighted in this study. In particular, estimation of the GCF volume may serve as an indicator to assess the severity as well as the prognosis of periodontitis in smokers.
Oral health and dental management, 2014
Tobacco smoking is regarded as one of the most significant risk factors for the development and progression of periodontal disease. In particular, studies have shown an alteration in Gingival Crevicular Fluid (GCF) volume and its components in smokers. The purpose of this study was to compare the GCF volume in smoking and non-smoking Saudi subjects with chronic periodontitis. In this study, 30 smoking patients and 30 non-smoking patients with chronic periodontitis were enrolled. Periodontal Probing Depth (PPD), Clinical Attachment Level (CAL), Plaque Index (PI), and Bleeding on Probing (BOP) were measured to assess the pattern of periodontal destruction for each patient at six sites in selected teeth. Gingival inflammation was registered at six sites, where Gingival Crevicular Fluid (GCF) was also collected. The GCF volume was measured with a Periotron 8000®. Comparisons were made between smoking and non-smoking groups with periodontitis. Smokers demonstrated significantly deeper pe...
Introduction and objectives: Periodontal disease (periodontitis) and atheromatous disease share not only risk factors such as smoking and diabetes, but also a complex multifactorial process of chronic inflammation stimulating mediators that accelerate endothelial dysfunction and/or mechanisms of cross-reacting antibodies against the periodontal flora and endothelial cell proteins; this may explain the association between both pathologies. The aim of our study was to add evidence about the relationship between periodontal disease (periodontitis) and vascular disease, using acute vascular events as the primary endpoint. Methods: A case-control study was conducted. A total of 30 cases and 32 controls were included in a non-randomized selection. Results: The presence of periodontal disease was significantly higher in cases than it was in controls (70 % vs. 40 %; OR [95 % CI]: 3.41 [1.19-9.76]; p=0.02). Also, plaque and gingival indexes were significantly higher in cases (PI: 1.74 ± 0.64 vs. 0.99 ± 0.69, respectively, p <0.01; GI: 1.61 ± 0.66 vs. 0.98 ± 0.55, respectively, p <0.01). Conclusion: This study demonstrates a strong association between periodontal disease and acute vascular events, the former having an even greater impact than traditional risk factors.
Journal of Dental Health, Oral Disorders & Therapy
Introduction and objectives: Periodontal disease (periodontitis) and atheromatous disease share not only risk factors such as smoking and diabetes, but also a complex multifactorial process of chronic inflammation stimulating mediators that accelerate endothelial dysfunction and/or mechanisms of cross-reacting antibodies against the periodontal flora and endothelial cell proteins; this may explain the association between both pathologies. The aim of our study was to add evidence about the relationship between periodontal disease (periodontitis) and vascular disease, using acute vascular events as the primary endpoint. Methods: A case-control study was conducted. A total of 30 cases and 32 controls were included in a non-randomized selection. Results: The presence of periodontal disease was significantly higher in cases than it was in controls (70 % vs. 40 %; OR [95 % CI]: 3.41 [1.19-9.76]; p=0.02). Also, plaque and gingival indexes were significantly higher in cases (PI: 1.74 ± 0.64 vs. 0.99 ± 0.69, respectively, p <0.01; GI: 1.61 ± 0.66 vs. 0.98 ± 0.55, respectively, p <0.01). Conclusion: This study demonstrates a strong association between periodontal disease and acute vascular events, the former having an even greater impact than traditional risk factors.