Ignite Creation Date:
2024-05-06 @ 2:44 AM
Last Modification Date:
2024-10-26 @ 11:22 AM
Study NCT ID:
NCT02111005
Status:
COMPLETED
Last Update Posted:
2016-03-16
First Post:
2014-03-14
Brief Title:
Smoking Influence on Apoptosis in Periodontitis
Sponsor:
Damascus University
Organization:
Damascus University
Study Overview
Official Title:
Influence of Smoking on Fibroblast Apoptosis in Patients With Chronic and Aggressive Periodontitis
Status:
COMPLETED
Status Verified Date:
2016-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Apoptosis is an evolutionary form of physiological cell death Studies suggest that apoptosis is involved in the pathogenesis of periodontal diseases Human gingival fibroblasts HGF have an important role in the periodontal immune response It is believed that HGF can be diminished andor eliminated by means of apoptosis
Smoking is one of the most common risk factor of periodontal disease Studies indicated that smoking can increase the risk of periodontitis by enhancing the apoptosis of gingival fibroblast
The purpose of this study is to determine and to investigate apoptosis of HGF in gingival biopsies collected from smokers and non smokers who are diagnosed with chronic periodontitis or aggressive periodontitis
Eighty subjects will be invited to participate in this study Patients will be allocated into four groups 20 patients each Gingival biopsies will be obtained from the base of papillae during surgical treatment open flap curettage and will be examined by Immuno-histochemical analysis Immune-staining will be done using p53 monoclonal mouse anti-human antibody
Smoking is one of the most common risk factor of periodontal disease Studies indicated that smoking can increase the risk of periodontitis by enhancing the apoptosis of gingival fibroblast
The purpose of this study is to determine and to investigate apoptosis of HGF in gingival biopsies collected from smokers and non smokers who are diagnosed with chronic periodontitis or aggressive periodontitis
Eighty subjects will be invited to participate in this study Patients will be allocated into four groups 20 patients each Gingival biopsies will be obtained from the base of papillae during surgical treatment open flap curettage and will be examined by Immuno-histochemical analysis Immune-staining will be done using p53 monoclonal mouse anti-human antibody
Detailed Description:
Background
The mechanisms responsible for gingival tissue damage are poorly understood and both immune-mediated reactions and direct cytopathic effects of bacteria maybe involved Based on direct effect of bacteria in cell cultures it has been suggested that apoptosis might play an important role in periodontitis Chen 1994
Programmed cell death apoptosis is normal physiologic process that contributes to maintaining tissue homeostasis The process of apoptosis can be modulated by various stimuli hormones cytokines growth factors infections and immune-responses Renehan et al 2001
Among other factors the products of two genes that encode protein p53 and Bcl-2 have been shown to play fundamental regulatory role in apoptosis P53 is the protein product of tumor-suppressor gene and expression of P53 can induce apoptosis This protein is also implicated in the regulation of tissue dynamics and is specifically thought to induce apoptosis in terminally differentiated cells including inflammatory cells Bulut et al2006
Fibroblast is a type of cell that synthesizes the extracellular and collagen in connective tissue It plays a critical role in wound healing Fibroblasts are the most common cells in connective tissue The main function of fibroblasts is to maintain the structural integrity of connective tissue by continuously secreting precursors of extracellular matrix it was reported that apoptosis levels increased in gingivitis and periodontitis Jarenberg et al 2002
Cigarette smoking is a risk factor for many diseases and recent evidence indicates that smoking adversely influences periodontal health A number of epidemiologic studies have shown strong association between smoking and prevalence and severity of periodontitis Bostrom et al 1998 Whereas the pathogenesis of periodontitis in smokers is poorly understood there are data suggesting that smoking effects on the periodontal tissues include defects in neutrophil function impaired serum antibody responses to periodontal pathogens and potentially diminished gingival fibroblast function Shivanaikar et al 2001 Smokers are considered a high-risk group for periodontitis and smoking history is a useful clinical predictor of future disease activity Hanokia et al 2000
Aims of the study
Investigation of the effects of smoking on fibroblasts apoptosis in smokers with periodontitis compared to non-smokers with periodontitis using immuno-histochemical methods
Comparison of apoptosis levels of gingival fibroblasts between chronic and aggressive periodontitis
Materials and methods
A total of 80 subjects will be invited to participate in this study from the patients referred to the Department of Periodontology Faculty of Dentistry University of Damascus The study will be approved by a specific Review Board Subjects will be recruited according to specific inclusion criteria after completion of medical and dental history questionnaires Patients will sign a consent form after being advised about the nature of the study
The selection of patients will be made according of the criteria approved by the 1999 international world workshop for a classification system of periodontal diseases and conditions Armitage 1999 using five clinical parameters and full mouth or panoramic radiographs for diagnosis
Subjects will be allocated into four groups
Smoking Chronic Periodontitis group ChP-S comprise 20 patients who are smokers and aged 45 years and have presence of 2 non-adjacent sites per quadrant that were not first molars or incisors with probing depth PD 5 mm which bleed on gentle probing The demonstrated radiographic bone loss 30 of the root length patient with poor oral hygiene the amount of accumulated plaque commensurate with the amount of clinical attachment level CAL
Non-smoking Chronic periodontitis group ChP-NS comprise 20 age-sex matched patients who are non-smokers and have chronic periodontitis
Smoking Aggressive Periodontitis group AgP-S comprise 20 patients who are smokers and aged 35 years and diagnosed with rapid attachment loss with periodontal pocket depth PD 4 mm around at least three teeth other than the first molars and incisors Rapid bone destruction 50bone loss at diseased sites Weak relationship between dental plaque and the severity of gingival inflammation
Non-smoking Aggressive periodontitis group AgP-NS comprise 20 age- and sex matched patients who are non-smokers and have aggressive periodontitis
Clinical measurements
A standard periodontal probe will be used for recording periodontal indices at six sites per tooth The examined clinical parameters include bleeding on probing BOP plaque index PI clinical attachment loss CAL and periodontal pocket depth PPD and gingival index GI
Biopsy collection and analysis
The biopsy samples will be obtained from patients during surgical treatment open flap curettage where biopsy is taken from the base area of papilla
Samples will be placed in 10 formalin
The samples will be then installed in paraffin wax
Samples will be analyzed in the by means of p53 monoclonal mouse anti-human antibody
The mechanisms responsible for gingival tissue damage are poorly understood and both immune-mediated reactions and direct cytopathic effects of bacteria maybe involved Based on direct effect of bacteria in cell cultures it has been suggested that apoptosis might play an important role in periodontitis Chen 1994
Programmed cell death apoptosis is normal physiologic process that contributes to maintaining tissue homeostasis The process of apoptosis can be modulated by various stimuli hormones cytokines growth factors infections and immune-responses Renehan et al 2001
Among other factors the products of two genes that encode protein p53 and Bcl-2 have been shown to play fundamental regulatory role in apoptosis P53 is the protein product of tumor-suppressor gene and expression of P53 can induce apoptosis This protein is also implicated in the regulation of tissue dynamics and is specifically thought to induce apoptosis in terminally differentiated cells including inflammatory cells Bulut et al2006
Fibroblast is a type of cell that synthesizes the extracellular and collagen in connective tissue It plays a critical role in wound healing Fibroblasts are the most common cells in connective tissue The main function of fibroblasts is to maintain the structural integrity of connective tissue by continuously secreting precursors of extracellular matrix it was reported that apoptosis levels increased in gingivitis and periodontitis Jarenberg et al 2002
Cigarette smoking is a risk factor for many diseases and recent evidence indicates that smoking adversely influences periodontal health A number of epidemiologic studies have shown strong association between smoking and prevalence and severity of periodontitis Bostrom et al 1998 Whereas the pathogenesis of periodontitis in smokers is poorly understood there are data suggesting that smoking effects on the periodontal tissues include defects in neutrophil function impaired serum antibody responses to periodontal pathogens and potentially diminished gingival fibroblast function Shivanaikar et al 2001 Smokers are considered a high-risk group for periodontitis and smoking history is a useful clinical predictor of future disease activity Hanokia et al 2000
Aims of the study
Investigation of the effects of smoking on fibroblasts apoptosis in smokers with periodontitis compared to non-smokers with periodontitis using immuno-histochemical methods
Comparison of apoptosis levels of gingival fibroblasts between chronic and aggressive periodontitis
Materials and methods
A total of 80 subjects will be invited to participate in this study from the patients referred to the Department of Periodontology Faculty of Dentistry University of Damascus The study will be approved by a specific Review Board Subjects will be recruited according to specific inclusion criteria after completion of medical and dental history questionnaires Patients will sign a consent form after being advised about the nature of the study
The selection of patients will be made according of the criteria approved by the 1999 international world workshop for a classification system of periodontal diseases and conditions Armitage 1999 using five clinical parameters and full mouth or panoramic radiographs for diagnosis
Subjects will be allocated into four groups
Smoking Chronic Periodontitis group ChP-S comprise 20 patients who are smokers and aged 45 years and have presence of 2 non-adjacent sites per quadrant that were not first molars or incisors with probing depth PD 5 mm which bleed on gentle probing The demonstrated radiographic bone loss 30 of the root length patient with poor oral hygiene the amount of accumulated plaque commensurate with the amount of clinical attachment level CAL
Non-smoking Chronic periodontitis group ChP-NS comprise 20 age-sex matched patients who are non-smokers and have chronic periodontitis
Smoking Aggressive Periodontitis group AgP-S comprise 20 patients who are smokers and aged 35 years and diagnosed with rapid attachment loss with periodontal pocket depth PD 4 mm around at least three teeth other than the first molars and incisors Rapid bone destruction 50bone loss at diseased sites Weak relationship between dental plaque and the severity of gingival inflammation
Non-smoking Aggressive periodontitis group AgP-NS comprise 20 age- and sex matched patients who are non-smokers and have aggressive periodontitis
Clinical measurements
A standard periodontal probe will be used for recording periodontal indices at six sites per tooth The examined clinical parameters include bleeding on probing BOP plaque index PI clinical attachment loss CAL and periodontal pocket depth PPD and gingival index GI
Biopsy collection and analysis
The biopsy samples will be obtained from patients during surgical treatment open flap curettage where biopsy is taken from the base area of papilla
Samples will be placed in 10 formalin
The samples will be then installed in paraffin wax
Samples will be analyzed in the by means of p53 monoclonal mouse anti-human antibody
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None