chronic periodontitis/니코틴

Accumulating evidence suggests that tobacco smoking affects the susceptibility to and severity of chronic periodontitis. Epigenetics may explain the role of smoking in the development and progress of periodontal disease. In this study, we performed transcriptomic and methylomic analyses of

Introduction: Smokeless tobacco (SLT) jeopardizes periodontal health and also produces an imbalance between reactive oxygen species (ROS) and antioxidants (AO) such as glutathione. Glutathione is an important redox regulator in saliva and

OBJECTIVE To evaluate the awareness of cigarette smoking as a risk factor for chronic periodontitis in patients either undergoing active periodontal treatment (APT) or enrolled in supportive periodontal therapy (SPT). METHODS Comprehensive tobacco use history was collected with a questionnaire in 50

BACKGROUND Periodontitis is a common inflammatory disease with complex and multi-factorial origin. Tobacco usage has shown its adverse effect on periodontal health. Various components within saliva not only protect the integrity of oral tissues, but also provide clues to local and systemic diseases

BACKGROUND Oxidative Stress (OS) is implicated in the pathogenesis of many systemic and oral diseases such as periodontal disease. Smokeless tobacco extract produces apoptosis and causes an imbalance between reactive oxygen species and antioxidants, such as Gamma Glutamyl Transpeptidase (GGT).

Detrimental effect of bad oral habits, such as smoking and chewing tobacco, on chronic periodontitis (CP) manifest chronic inflammation of gingival tissues which majorly results gum bleeding, teeth loss. Genetic association study of Interleukin 1 beta (IL1ß) has been conducted in CP patients having

Tobacco smoking is a serious health and social problem. The aim of the study was investigation of the influence of tobacco smoking on the state of dentition and effects of conservative treatment of the chronic, moderately advanced periodontitis by comparison of API, SBI, PPD and CAL indices before

OBJECTIVE Smoking is an important environmental risk factor involved in the causation and progression of periodontal disease. Smoking can impair various components of the host immune response and immune system. The virulence factors of periodontal pathogens stimulate inflammatory cytokine expression

BACKGROUND The purpose of this study is to examine the relationship between salivary LL-37 levels and clinical severity in patients with chronic periodontitis (CP). The presence/absence of four periodontopathic bacteria and salivary cotinine levels were also examined to assess the impact of these

Apoptosis provides a mechanism for clearance of unwanted cells in a variety of situations in which programmed or physiological cell death occurs; but the premature death of defensive cells could promote infection, inflammation and concomitant disease. We detected high values of apoptosis in

BACKGROUND The destructive periodontal disease is the result of a complex interaction between the subgingival microflora and nonbacterial factors, specifically host and environmental factors. Principal susceptibility factors are genetic conditions of the immunoinflammatory response but tobacco

The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) secretion by peripheral blood mononuclear cells

The aim of the study was to estimate the influence of tobacco smoking and the clinical type of periodontitis on the chosen parameters of oxidative stress (superoxide anion generation on the ground of cytochrome c reduction in the whole blood, the concentration of autoantibodies for oxidized