Smoking and periodontal disease, smoking as a risk factor, incidence of smoking, effects of smoking on periodontium, smoking and gingivitis and smoking and periodontitis, effect of surgical and non surgical therapy on smokers
Smoking and its influence on Periodontium and Periodontal Health
Enlists mechanism of nicotine addiction, its ill effects on individual aspects of the oral cavity and ways to quit smoking to improve health
This document discusses the effects of smoking on periodontal disease. It notes that cigarette smoke contains over 400 toxic substances and that nicotine is the main alkaloid that is responsible for the addictive potential of tobacco. It then summarizes various studies that found higher rates of periodontal disease in smokers compared to non-smokers. The document also outlines how smoking can impact clinical signs of inflammation, the gingival epithelium, gingival bleeding, the gingival crevicular fluid, and the subgingival microflora. It discusses the negative effects of smoking on periodontal treatment and healing. The importance of smoking cessation is emphasized, with models and methods for quitting smoking presented.
Smoking is a major risk factor for periodontal disease. The document discusses how smoking increases the prevalence and severity of periodontal disease by altering the host-bacterial balance in the mouth. Smokers have higher levels of periodontal pathogens, a suppressed immune response, and reduced blood flow in the gingiva. As a result, smokers respond less well to nonsurgical and surgical periodontal treatments, have higher failure rates of dental implants, and are more likely to continue losing teeth and bone even with maintenance therapy. However, smoking cessation improves treatment outcomes and periodontal health by reversing many of these harmful effects. The document emphasizes that smoking cessation should be an integral part of treating periodontal disease in smokers.
This document summarizes the effects of aging and smoking on the periodontium. Key points include:
- Aging leads to thinning gingival epithelium and changes in connective tissue, ligament, cementum and bone. It does not inevitably cause recession.
- Smoking significantly increases the risk and severity of periodontitis by impairing the immune response and altering the subgingival microbiota. Current smokers have more periodontal pathogens and greater periodontal breakdown than former smokers or nonsmokers.
- Both aging and smoking negatively impact treatment outcomes. Smokers generally respond less well to nonsurgical and surgical periodontal therapies and have higher rates of refractory periodontitis.
This document discusses the effects of smoking on periodontium. It begins with an introduction and overview of how smoking affects the oral environment and periodontal tissues. It then covers the classification of smokers, constituents of tobacco smoke and their mechanisms of action in damaging tissues. The effects of smoking include increased periodontal pathogens, impaired healing, decreased inflammation and blood flow. Smoking also negatively impacts the response to periodontal treatments and increases risk of recurrence. However, smoking cessation can help recovery of tissues and positive treatment outcomes through improved circulation, microbial shifts and immune response. The document concludes with steps for smoking cessation programs and pharmacotherapy options.
This document discusses risk assessment in periodontal disease. It defines risk assessment as identifying populations at increased risk of developing periodontal disease and assessing their risk of current or future disease. Key risk factors discussed include tobacco smoking, diabetes, genetic factors, age, gender and socioeconomic status. Tobacco smoking is identified as a major risk factor, increasing the likelihood and severity of periodontal disease through effects on the immune system, blood vessels, bacterial microbiome and other physiological systems. The use of risk assessment tools to evaluate multiple risk factors can help with clinical decision making and reducing oral healthcare costs.
Smoking and periodontal disease, smoking as a risk factor, incidence of smoking, effects of smoking on periodontium, smoking and gingivitis and smoking and periodontitis, effect of surgical and non surgical therapy on smokers
Smoking and its influence on Periodontium and Periodontal Health
Enlists mechanism of nicotine addiction, its ill effects on individual aspects of the oral cavity and ways to quit smoking to improve health
This document discusses the effects of smoking on periodontal disease. It notes that cigarette smoke contains over 400 toxic substances and that nicotine is the main alkaloid that is responsible for the addictive potential of tobacco. It then summarizes various studies that found higher rates of periodontal disease in smokers compared to non-smokers. The document also outlines how smoking can impact clinical signs of inflammation, the gingival epithelium, gingival bleeding, the gingival crevicular fluid, and the subgingival microflora. It discusses the negative effects of smoking on periodontal treatment and healing. The importance of smoking cessation is emphasized, with models and methods for quitting smoking presented.
Smoking is a major risk factor for periodontal disease. The document discusses how smoking increases the prevalence and severity of periodontal disease by altering the host-bacterial balance in the mouth. Smokers have higher levels of periodontal pathogens, a suppressed immune response, and reduced blood flow in the gingiva. As a result, smokers respond less well to nonsurgical and surgical periodontal treatments, have higher failure rates of dental implants, and are more likely to continue losing teeth and bone even with maintenance therapy. However, smoking cessation improves treatment outcomes and periodontal health by reversing many of these harmful effects. The document emphasizes that smoking cessation should be an integral part of treating periodontal disease in smokers.
This document summarizes the effects of aging and smoking on the periodontium. Key points include:
- Aging leads to thinning gingival epithelium and changes in connective tissue, ligament, cementum and bone. It does not inevitably cause recession.
- Smoking significantly increases the risk and severity of periodontitis by impairing the immune response and altering the subgingival microbiota. Current smokers have more periodontal pathogens and greater periodontal breakdown than former smokers or nonsmokers.
- Both aging and smoking negatively impact treatment outcomes. Smokers generally respond less well to nonsurgical and surgical periodontal therapies and have higher rates of refractory periodontitis.
This document discusses the effects of smoking on periodontium. It begins with an introduction and overview of how smoking affects the oral environment and periodontal tissues. It then covers the classification of smokers, constituents of tobacco smoke and their mechanisms of action in damaging tissues. The effects of smoking include increased periodontal pathogens, impaired healing, decreased inflammation and blood flow. Smoking also negatively impacts the response to periodontal treatments and increases risk of recurrence. However, smoking cessation can help recovery of tissues and positive treatment outcomes through improved circulation, microbial shifts and immune response. The document concludes with steps for smoking cessation programs and pharmacotherapy options.
This document discusses risk assessment in periodontal disease. It defines risk assessment as identifying populations at increased risk of developing periodontal disease and assessing their risk of current or future disease. Key risk factors discussed include tobacco smoking, diabetes, genetic factors, age, gender and socioeconomic status. Tobacco smoking is identified as a major risk factor, increasing the likelihood and severity of periodontal disease through effects on the immune system, blood vessels, bacterial microbiome and other physiological systems. The use of risk assessment tools to evaluate multiple risk factors can help with clinical decision making and reducing oral healthcare costs.
This document discusses the effects of smoking on periodontal disease. It states that smoking promotes a more anaerobic environment in the gingival pockets which can lead to increased growth of pathogens. Smoking also causes disease masking, where the tissues appear healthier than they are due to vasoconstriction reducing blood flow and inflammation. Specific oral conditions linked to smoking include acute necrotizing ulcerating gingivitis, nicotinic stomatitis, and accelerated alveolar bone loss. Nicotine is highlighted as the most pharmacologically active compound in cigarettes and can have detrimental effects on periodontal cells and promote collagen breakdown and delayed apoptosis of cells. The conclusion reiterates that smoking increases the severity of periodontal disease and
Smoking has significant negative effects on the periodontium and increases the risk and severity of periodontal disease in several ways:
1) Smoking alters the subgingival microbiota in favor of pathogenic species and impairs the host immune response, making the tissues more susceptible to bacterial infection.
2) Components of smoke such as nicotine, carbon monoxide, and tar are toxic to periodontal tissues and cells, impairing wound healing and reducing blood flow and oxygen levels in the gingiva.
3) Smokers have higher rates of periodontitis, greater attachment and bone loss, and their periodontal disease is less responsive to treatment compared to non-smokers. Quitting smoking can reduce disease
Tobacco . Its definition, available forms , fatal dose , contents , pathophysiology , pharmacokinetics and toxicology. Diagnosis and treatment of toxicity.
Smoking has significant negative effects on periodontal health and outcomes of periodontal treatment. It increases the prevalence and severity of periodontal disease, affects the pathogenesis by altering the microbiome and inflammatory response, and decreases the response to nonsurgical and surgical periodontal therapies. Dentists play an important role in educating patients on the harms of smoking and counseling those who use tobacco on methods for cessation using pharmacotherapy and behavioral support. Smoking cessation improves periodontal treatment outcomes by allowing the periodontium to recover.
Smoking has various long-term and short-term health effects. Long-term effects include decreased fertility, lower birth weights, increased risk of miscarriage and birth complications, increased risk of cervical cancer, and increased risk of developing emphysema, chronic bronchitis, COPD, cataracts, macular degeneration, heart disease, and stroke. Short-term effects include increased heart rate and blood pressure, exacerbation of allergies and irritation of the eyes and nose, increased stomach acid, and bad breath. Smoking is not an effective means of weight loss and can imbalance oxygen demand and supply while providing only a short-term boost to memory.
Dr. Priyanka Kumawat presented on smoking cessation treatments. Key points:
1) Quitting smoking reduces health risks but is difficult due to nicotine addiction. Over 1 billion people smoke worldwide and smoking causes many cancers and pulmonary/cardiovascular diseases.
2) FDA-approved smoking cessation treatments include nicotine replacement therapies, bupropion, and varenicline. Emerging treatments include e-cigarettes, vaccines, and drugs targeting nicotine receptors or withdrawal symptoms.
3) All smokers trying to quit should be offered medication. Higher doses of nicotine replacements may help highly dependent smokers. Second-line drugs like clonidine may help those unable to use first-line
This document discusses the history and health effects of smoking. It begins with the origins of tobacco use among Native Americans and its spread to Europe. It then discusses the addictive properties of nicotine and how cigarettes effectively deliver nicotine to the brain. The document outlines the various health risks of smoking such as increased risk of lung cancer, COPD, and heart disease. It also discusses challenges with smoking cessation and methods that can be used to help people quit smoking such as nicotine replacement therapies, bupropion, and varenicline. The document concludes by discussing approaches to harm reduction for smokers unable or unwilling to quit.
This document discusses the history and health effects of smoking. It begins by outlining the origins of tobacco use among Native Americans and its spread to Europe. It then details the addictive properties of nicotine and how cigarettes effectively deliver nicotine to the brain. The document covers the social and cultural role of smoking as well as initiatives to reduce it. Finally, it outlines strategies for smoking cessation and the health benefits of quitting, including reduced risk of lung cancer, heart disease and improved lung function.
Smoking represents the most readily preventable risk factor for morbidity and mortality.
Smoking related disease will kill one in 10 adults globally.
There are more than 6 million smoker in KSA that represent about 30% from population in 2004.
Smoking and Cardiovascular Disease:
coronary artery disease
cardiac arrhythmias.
Atherosclerosis
Cigarette smoking increases blood cholesterol levels, causing a buildup of arterial plaque that narrows the blood vessels over time.
Blood Clots
Low Blood Oxygen
stroke
A 61-year-old female patient presented with increased shortness of breath, productive cough, and fatigue. She had a smoking history of 35 pack-years. Spirometry showed an FEV1 of 55%, consistent with moderate COPD. The patient was referred to pulmonary rehabilitation and smoking cessation programs. She successfully quit smoking after 12 weeks. Medications of tiotropium and salbutamol were prescribed according to guidelines. The patient benefited from non-pharmacological approaches and medication management of her COPD.
This document discusses the effects of smoking on periodontal health. It covers epidemiological evidence that smoking increases the risk of periodontitis 2-5 times and is a major risk factor. The toxic chemicals in tobacco such as nicotine, carbon monoxide, and tar are discussed. These chemicals can impair the immune response and increase periodontal pathogens, leading to inflammation and tissue destruction. Clinical signs of periodontitis are made worse in smokers, such as increased attachment and bone loss. Smoking is also a major risk factor for oral cancer. The document examines the effects of smoking on gingival blood flow, wound healing, and the complications it can cause for periodontal therapy.
Smoking has significant negative effects on periodontal health and outcomes of periodontal therapy. According to the document, smoking is a major risk factor for periodontitis, with smokers being 2-4 times more likely to develop periodontitis than non-smokers. Smoking reduces blood flow and oxygen to the gingiva, inhibits immune response, increases periodontal pathogens, and reduces fibroblast function, all of which promote periodontal disease and make treatment more challenging. The document examines in detail the epidemiological evidence linking smoking to periodontal disease as well as the mechanisms by which smoking damages periodontal tissues.
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document notes that nicotine is highly addictive and explains the physical, mental, and social factors that contribute to tobacco addiction. It discusses reasons to quit smoking and the health benefits of doing so. Finally, it provides tips and strategies for quitting, as well as addressing common concerns people have about the quitting process.
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document covers nicotine addiction and reasons for tobacco use, as well as the significant health and economic costs of smoking. Finally, it discusses strategies and health benefits for quitting smoking.
This study examined the acute effects of cigarette smoking on coronary blood vessels. Twenty-four long-term smokers underwent cardiac catheterization. Smoking one cigarette caused immediate constriction of both proximal and distal epicardial arteries of 5-8%, returning to baseline within 30 minutes. Coronary blood flow velocity decreased by 7% and resistance increased by 21% despite increased heart rate and blood pressure. The control group showed no vascular changes. Smoking acutely constricts epicardial arteries and increases coronary resistance, potentially contributing to cardiovascular harm.
This document discusses the harmful effects of smoking on periodontal health. It states that smoking is a major risk factor for periodontal disease and increases the prevalence and severity of periodontitis. Smoking can retard fibroblast growth, reduce collagen and fibronectin, and increase collagen breakdown in the gums. It impairs the immune response to bacterial pathogens in the mouth. Smokers are 4 times more likely to develop periodontitis than non-smokers. Smoking cessation is recommended using the 5 A's approach and pharmacotherapy like nicotine replacement or bupropion can help with withdrawal symptoms.
This document provides an overview of smoking cessation. It begins with an introduction discussing the negative health impacts of smoking and statistics on smoking rates. It then covers the chemical components in cigarettes and negative effects of smoking on various parts of the body. Benefits of smoking cessation are outlined. The document also summarizes several research studies on smoking cessation methods and their effectiveness, including enhanced motivational interviewing versus brief advice, nicotine replacement therapy, and a randomized trial of nicotine replacement therapy patches in pregnancy. Barriers to smoking cessation and electronic cigarettes are also discussed.
Anesthetic consideration in smokers,alcoholics and addictsAftab Hussain
Anaesthetic consideration in smokers alcoholic and drug addicts. As an anaesthesiologist we must be aware with the problems associated with their management and interaction with anaesthetics.
Oral lesions that associated with Tobacco useAhmed Saleem
This document discusses tobacco-induced oral mucosal lesions. It begins by explaining what tobacco is and how it is consumed. Tobacco use causes many types of cancer and diseases due to harmful chemicals. Tobacco smoke and smokeless tobacco products contain carcinogens like nitrosamines, polycyclic aromatic hydrocarbons, and radioactive elements. Long-term contact of tobacco with the oral mucosa can induce non-neoplastic lesions like betel chewer's mucosa, leukoedema, nicotine stomatitis, and lichenoid lesions. It can also cause potentially malignant lesions like leukoplakia and erythroplakia. Leukoplakia is the most common potentially malignant oral lesion associated
This document summarizes a forensic odontology case from India involving the 2012 gang rape and murder of "Nirbhaya" in Delhi. Police requested assistance from the forensic odontology department to analyze bite marks found on the victim's body. Dr. Ashit Acharya led the investigation and compared the dental molds of five accused individuals to the bite marks. The analysis found matches between the molds and marks, helping identify the perpetrators of the brutal crime.
The document discusses ketone bodies, which are formed in the liver from fatty acid breakdown and include acetoacetate, beta-hydroxybutyrate, and acetone. These water-soluble molecules provide an energy source for other tissues and are produced more during starvation or uncontrolled diabetes. Ketosis refers to high levels of ketone bodies in the blood and urine, while ketoacidosis is a dangerous condition where ketone levels become severely high, causing a metabolic acidosis. Treatment involves insulin administration and fluid/electrolyte management to prevent complications like dehydration.
Weitere ähnliche Inhalte
Ähnlich wie Smoking and Periodontal Disease presentation
This document discusses the effects of smoking on periodontal disease. It states that smoking promotes a more anaerobic environment in the gingival pockets which can lead to increased growth of pathogens. Smoking also causes disease masking, where the tissues appear healthier than they are due to vasoconstriction reducing blood flow and inflammation. Specific oral conditions linked to smoking include acute necrotizing ulcerating gingivitis, nicotinic stomatitis, and accelerated alveolar bone loss. Nicotine is highlighted as the most pharmacologically active compound in cigarettes and can have detrimental effects on periodontal cells and promote collagen breakdown and delayed apoptosis of cells. The conclusion reiterates that smoking increases the severity of periodontal disease and
Smoking has significant negative effects on the periodontium and increases the risk and severity of periodontal disease in several ways:
1) Smoking alters the subgingival microbiota in favor of pathogenic species and impairs the host immune response, making the tissues more susceptible to bacterial infection.
2) Components of smoke such as nicotine, carbon monoxide, and tar are toxic to periodontal tissues and cells, impairing wound healing and reducing blood flow and oxygen levels in the gingiva.
3) Smokers have higher rates of periodontitis, greater attachment and bone loss, and their periodontal disease is less responsive to treatment compared to non-smokers. Quitting smoking can reduce disease
Tobacco . Its definition, available forms , fatal dose , contents , pathophysiology , pharmacokinetics and toxicology. Diagnosis and treatment of toxicity.
Smoking has significant negative effects on periodontal health and outcomes of periodontal treatment. It increases the prevalence and severity of periodontal disease, affects the pathogenesis by altering the microbiome and inflammatory response, and decreases the response to nonsurgical and surgical periodontal therapies. Dentists play an important role in educating patients on the harms of smoking and counseling those who use tobacco on methods for cessation using pharmacotherapy and behavioral support. Smoking cessation improves periodontal treatment outcomes by allowing the periodontium to recover.
Smoking has various long-term and short-term health effects. Long-term effects include decreased fertility, lower birth weights, increased risk of miscarriage and birth complications, increased risk of cervical cancer, and increased risk of developing emphysema, chronic bronchitis, COPD, cataracts, macular degeneration, heart disease, and stroke. Short-term effects include increased heart rate and blood pressure, exacerbation of allergies and irritation of the eyes and nose, increased stomach acid, and bad breath. Smoking is not an effective means of weight loss and can imbalance oxygen demand and supply while providing only a short-term boost to memory.
Dr. Priyanka Kumawat presented on smoking cessation treatments. Key points:
1) Quitting smoking reduces health risks but is difficult due to nicotine addiction. Over 1 billion people smoke worldwide and smoking causes many cancers and pulmonary/cardiovascular diseases.
2) FDA-approved smoking cessation treatments include nicotine replacement therapies, bupropion, and varenicline. Emerging treatments include e-cigarettes, vaccines, and drugs targeting nicotine receptors or withdrawal symptoms.
3) All smokers trying to quit should be offered medication. Higher doses of nicotine replacements may help highly dependent smokers. Second-line drugs like clonidine may help those unable to use first-line
This document discusses the history and health effects of smoking. It begins with the origins of tobacco use among Native Americans and its spread to Europe. It then discusses the addictive properties of nicotine and how cigarettes effectively deliver nicotine to the brain. The document outlines the various health risks of smoking such as increased risk of lung cancer, COPD, and heart disease. It also discusses challenges with smoking cessation and methods that can be used to help people quit smoking such as nicotine replacement therapies, bupropion, and varenicline. The document concludes by discussing approaches to harm reduction for smokers unable or unwilling to quit.
This document discusses the history and health effects of smoking. It begins by outlining the origins of tobacco use among Native Americans and its spread to Europe. It then details the addictive properties of nicotine and how cigarettes effectively deliver nicotine to the brain. The document covers the social and cultural role of smoking as well as initiatives to reduce it. Finally, it outlines strategies for smoking cessation and the health benefits of quitting, including reduced risk of lung cancer, heart disease and improved lung function.
Smoking represents the most readily preventable risk factor for morbidity and mortality.
Smoking related disease will kill one in 10 adults globally.
There are more than 6 million smoker in KSA that represent about 30% from population in 2004.
Smoking and Cardiovascular Disease:
coronary artery disease
cardiac arrhythmias.
Atherosclerosis
Cigarette smoking increases blood cholesterol levels, causing a buildup of arterial plaque that narrows the blood vessels over time.
Blood Clots
Low Blood Oxygen
stroke
A 61-year-old female patient presented with increased shortness of breath, productive cough, and fatigue. She had a smoking history of 35 pack-years. Spirometry showed an FEV1 of 55%, consistent with moderate COPD. The patient was referred to pulmonary rehabilitation and smoking cessation programs. She successfully quit smoking after 12 weeks. Medications of tiotropium and salbutamol were prescribed according to guidelines. The patient benefited from non-pharmacological approaches and medication management of her COPD.
This document discusses the effects of smoking on periodontal health. It covers epidemiological evidence that smoking increases the risk of periodontitis 2-5 times and is a major risk factor. The toxic chemicals in tobacco such as nicotine, carbon monoxide, and tar are discussed. These chemicals can impair the immune response and increase periodontal pathogens, leading to inflammation and tissue destruction. Clinical signs of periodontitis are made worse in smokers, such as increased attachment and bone loss. Smoking is also a major risk factor for oral cancer. The document examines the effects of smoking on gingival blood flow, wound healing, and the complications it can cause for periodontal therapy.
Smoking has significant negative effects on periodontal health and outcomes of periodontal therapy. According to the document, smoking is a major risk factor for periodontitis, with smokers being 2-4 times more likely to develop periodontitis than non-smokers. Smoking reduces blood flow and oxygen to the gingiva, inhibits immune response, increases periodontal pathogens, and reduces fibroblast function, all of which promote periodontal disease and make treatment more challenging. The document examines in detail the epidemiological evidence linking smoking to periodontal disease as well as the mechanisms by which smoking damages periodontal tissues.
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document notes that nicotine is highly addictive and explains the physical, mental, and social factors that contribute to tobacco addiction. It discusses reasons to quit smoking and the health benefits of doing so. Finally, it provides tips and strategies for quitting, as well as addressing common concerns people have about the quitting process.
This document provides information about tobacco cessation and the harms of smoking. It discusses how smoking harms smokers' health, causing various cancers and respiratory diseases. It also outlines the negative health effects of secondhand smoke exposure. The document covers nicotine addiction and reasons for tobacco use, as well as the significant health and economic costs of smoking. Finally, it discusses strategies and health benefits for quitting smoking.
This study examined the acute effects of cigarette smoking on coronary blood vessels. Twenty-four long-term smokers underwent cardiac catheterization. Smoking one cigarette caused immediate constriction of both proximal and distal epicardial arteries of 5-8%, returning to baseline within 30 minutes. Coronary blood flow velocity decreased by 7% and resistance increased by 21% despite increased heart rate and blood pressure. The control group showed no vascular changes. Smoking acutely constricts epicardial arteries and increases coronary resistance, potentially contributing to cardiovascular harm.
This document discusses the harmful effects of smoking on periodontal health. It states that smoking is a major risk factor for periodontal disease and increases the prevalence and severity of periodontitis. Smoking can retard fibroblast growth, reduce collagen and fibronectin, and increase collagen breakdown in the gums. It impairs the immune response to bacterial pathogens in the mouth. Smokers are 4 times more likely to develop periodontitis than non-smokers. Smoking cessation is recommended using the 5 A's approach and pharmacotherapy like nicotine replacement or bupropion can help with withdrawal symptoms.
This document provides an overview of smoking cessation. It begins with an introduction discussing the negative health impacts of smoking and statistics on smoking rates. It then covers the chemical components in cigarettes and negative effects of smoking on various parts of the body. Benefits of smoking cessation are outlined. The document also summarizes several research studies on smoking cessation methods and their effectiveness, including enhanced motivational interviewing versus brief advice, nicotine replacement therapy, and a randomized trial of nicotine replacement therapy patches in pregnancy. Barriers to smoking cessation and electronic cigarettes are also discussed.
Anesthetic consideration in smokers,alcoholics and addictsAftab Hussain
Anaesthetic consideration in smokers alcoholic and drug addicts. As an anaesthesiologist we must be aware with the problems associated with their management and interaction with anaesthetics.
Oral lesions that associated with Tobacco useAhmed Saleem
This document discusses tobacco-induced oral mucosal lesions. It begins by explaining what tobacco is and how it is consumed. Tobacco use causes many types of cancer and diseases due to harmful chemicals. Tobacco smoke and smokeless tobacco products contain carcinogens like nitrosamines, polycyclic aromatic hydrocarbons, and radioactive elements. Long-term contact of tobacco with the oral mucosa can induce non-neoplastic lesions like betel chewer's mucosa, leukoedema, nicotine stomatitis, and lichenoid lesions. It can also cause potentially malignant lesions like leukoplakia and erythroplakia. Leukoplakia is the most common potentially malignant oral lesion associated
Ähnlich wie Smoking and Periodontal Disease presentation (20)
This document summarizes a forensic odontology case from India involving the 2012 gang rape and murder of "Nirbhaya" in Delhi. Police requested assistance from the forensic odontology department to analyze bite marks found on the victim's body. Dr. Ashit Acharya led the investigation and compared the dental molds of five accused individuals to the bite marks. The analysis found matches between the molds and marks, helping identify the perpetrators of the brutal crime.
The document discusses ketone bodies, which are formed in the liver from fatty acid breakdown and include acetoacetate, beta-hydroxybutyrate, and acetone. These water-soluble molecules provide an energy source for other tissues and are produced more during starvation or uncontrolled diabetes. Ketosis refers to high levels of ketone bodies in the blood and urine, while ketoacidosis is a dangerous condition where ketone levels become severely high, causing a metabolic acidosis. Treatment involves insulin administration and fluid/electrolyte management to prevent complications like dehydration.
Mycobacterium tuberculosis causes tuberculosis. It is an acid-fast, rod-shaped bacterium that is ingested by alveolar macrophages in the lungs. Inside macrophages, the bacteria inhibit lysosome fusion to avoid being killed, allowing proliferation. This forms lesions called tubercles or Ghon complexes that spread to lymph nodes. In some people, the immune system controls the infection, while in others the bacteria become dormant but can reactivate when immunity is compromised, causing active tuberculosis.
Rod-shaped acid-fast bacteria called Mycobacterium tuberculosis causes tuberculosis. It enters the lungs through inhaled droplets from an infected person. Macrophages engulf the bacteria but they prevent the phagosome from fusing with lysosomes, allowing the bacteria to proliferate inside macrophages. This forms lesions called tubercles or granulomas and can spread to other organs. Symptoms include fever, night sweats, weight loss and coughing blood. Diagnosis involves tests like tuberculin skin tests, chest x-rays, and sputum smears and cultures. Treatment depends on whether the infection is latent or active, using drugs like isoniazid and rifampin.
This document discusses various physical properties of dental materials including brittleness, ductility, malleability, and hardness. Brittleness refers to a material's inability to plastically deform before fracturing. Ductility is the ability to sustain deformation under tension without fracturing, while malleability refers to the ability under compression. Hardness is measured by a material's resistance to indentation or scratching. Common tests for properties include Vickers, Knoop, and Rockwell tests.
This document discusses various antiseptics and disinfectants. It defines antiseptics as chemical substances used to destroy or inhibit bacteria on living surfaces, while disinfectants destroy bacteria on inanimate surfaces. It then categorizes and describes common antiseptics and disinfectants such as phenol derivatives, iodine, alcohols, chlorhexidine and provides their mechanisms of action and uses. Ideal antiseptics are described as having broad-spectrum activity, rapid onset, durability and low toxicity. Factors affecting the action of antiseptics and disinfectants and their general uses are also summarized.
This document discusses alcohols including their history, forms, pharmacokinetics, pharmacodynamics, treatment of alcoholism, and methyl alcohol poisoning. It covers how alcohols are absorbed and metabolized in the liver, their central nervous system depressant effects, and reinforcing mechanisms related to dopamine and opioid systems. Tolerance and withdrawal symptoms are also summarized. Treatment of alcoholism includes disulfiram to induce nausea when drinking, naltrexone to reduce reward, and acamprosate for anti-craving effects. Methyl alcohol poisoning is discussed along with supportive treatments and use of ethanol or fomepizole to preferentially block methyl alcohol metabolism.
This document discusses antidiabetic drugs used to treat diabetes mellitus. It defines diabetes as a chronic disease characterized by high blood glucose levels that can damage major organs over time. The document outlines the classification, mechanisms of action, indications, and adverse effects of various hypoglycemic agents (that release insulin) and antihyperglycemic agents (that do not release insulin) used to treat type 1 and type 2 diabetes. These include insulins, sulfonylureas, meglitinide analogs, GLP-1 analogs, DPP-4 inhibitors, biguanides, thiazolidinediones, and alpha-glucosidase inhibitors. Metformin is typically the first-line
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
2. Introduction
• Tobacco smoking is an addictive habit first introduced
in Europe. Smoking is now recognized as the most
important cause of preventable death and disease.
• Currently, the most of adult population smoke cigarettes.
However, nowadays, the smokers are changing to
lower-tar brands.
• Consumption is rising in developing countries,
particularly where tobacco production brings great
economic benefits.
3. • Smoking is associated with a wide spectrum of
diseases including:-
Stroke, coronary artery disease, peripheral
artery disease, gastric ulcer and cancers of
the mouth, larynx, esophagus, pancreas,
bladder and uterine cervix.
It is also a major cause of chronic obstructive
pulmonary disease and a risk factor for low
birth weight babies.
Approximately 50% of regular smokers are
killed by their habit and smoking causes 30%
of cancer deaths.
4. • Cigarette smoke is a very complex mixture of
substances with over 4000 known constituents.
These include:-
carbon monoxide, hydrogen cyanide, reactive
oxidizing radicals, a high number of carcinogens,
and the main psychoactive and addictive molecule
– nicotine
• Many of these components could modify the host
response in periodontitis.
5. • Inter-subject smoking variation includes
frequency of inhalation, depth of inhalation,
length of the cigarette stub left, presence or
absence of a filter, and the brand of cigarette.
• The patient's exposure to tobacco smoke can be
measured in several ways including interviewing
the subject using simple questions or more
sophisticated questionnaires and biochemical
analyses.
6. • The tests include exhaled carbon monoxide in
the breath, which is commonly measured in
smoking cessation clinics, and cotinine (a
metabolite of nicotine) in saliva, plasma/serum,
or urine.
• Cotinine measurements are more reliable in
determining a subject's exposure to tobacco smoke
because the half-life is 14-20 hours compared with
the shorter half-life of nicotine which is 2-3
hours.
7. • The mean plasma and salivary cotinine
concentrations of regular smokers are
approximately 300ng/ml and urine
concentrations are about 1500 ng/ml.
• Nonsmokers typically have plasma/saliva
concentrations under 2ng/ml, but this
may be raised slightly due to environmental
exposure (passive smoking).
8. Nicotine Effect……….
• Inhalation of tobacco smoke allows very rapid
absorption of nicotine into the blood and transport to
the brain, which is faster than an intravenous infusion.
• Nicotine in tobacco smoke from most cigarettes is
not well absorbed through the oral mucosa because the
nicotine is in an ionized form as a result of the pH
(5.5).
• In contrast cigar and pipe smoke is more alkaline
(pH 8.5), which allows good absorption of un-ionized
nicotine through the buccal mucosa.
9. • Nicotine is absorbed rapidly in the lung where
the smoke is well buffered.
• The administration of nicotine causes :-
A rise in the blood pressure, an increase in
heart rate, an increase in respiratory rate and
decreased skin temperature due to peripheral
vasoconstriction.
• However, at other body sites, such as skeletal
muscle, nicotine produces vasodilatation.
10. Periodontal Disease In Smokers
• Pindborg (1947) was one of the first investigators to
study the relationship between smoking and
periodontal disease.
• He discovered a higher prevalence of acute
necrotizing ulcerative gingivitis
The typical appearance of
necrotizing ulcerative
gingivitis in a heavy
smoker with poor oral
hygiene.
11. Smokers with periodontitis, have:
1. Deeper probing depths and a larger number of deep
pockets
2. More attachment loss including more gingival
recession
3. More alveolar bone loss
4. More tooth loss
5. Less gingivitis and less bleeding on probing
6. More teeth with furcation involvement
12. Smoking and gingival inflammation
• A reduction in clinical signs of gingivitis has been
reported in smokers and this effect is independent of
plaque levels.
• Heavy smokers may have grayish discoloration and
hyperkeratosis of the gingiva:
An increased number of keratinized cells has been
found in the gingiva of smokers. Changes in the
epithelium were described as keratotic,
hyperkeratotic, and hyperplastic.
13. Smoking and gingival bleeding
• Smoking is known to produce peripheral
vasoconstriction, in some subjects, this is preceded
by vasodilatation.
• Degree of inhalation of tobacco smoke and the rate
of nicotine absorption.
Nicotine from cigarettes stimulates the sympathetic
ganglia to produce neurotransmitters including
catecholamines.
14. These affect the alpha-receptors in blood vessels
which in turn causes vasoconstriction.
The vasoconstriction of peripheral blood vessels
caused by smoking can also affect the periodontal
tissue as smokers have less overt signs of
gingivitis than nonsmokers and clinical signs of
gingival inflammation such as redness, bleeding,
and exudation are not evident in smokers.
The vasoconstrictive actions of nicotine may be
responsible for the decreased gingival blood flow.
15. Effects of Smoking on the Etiology and
Pathogenesis of Periodontal Disease
16. Smoking and oral
microorganisms
• Smoking has important effects on oral bacteria.
• Cigarette smoking could cause a lowering of the
oxidation-reduction potential, and this could cause
an increase in anaerobic plaque bacteria.
• There was a statistically significant shift in the
proportion of Gram-positive to Gram-negative
bacteria in 3-day-old plaque from smokers when
compared with non-smokers.
17. • Tobacco smoke contains phenols and cyanides,
which can account for antibacterial and toxic
properties.
• Smokers harbored significantly higher levels and
were at significantly greater risk of infection with
Tanarella forsythia than non-smokers.
• Adjusting for disease severity, Porphyromonas
gingivalis was also more likely to subgingivally
infect smokers than non-smokers
18. Effects on the host response
• Nicotine metabolites can concentrate in the
periodontium and their effects include the
promotion of vasoconstriction; and the
impairment of the functional activity of
polymorphs and macrophages.
• The numbers of neutrophils in peripheral blood
are also increased by tobacco use and their
migration through capillary walls.
19. Physiology
• Clinical signs of inflammation are less pronounced
in smokers than in nonsmokers.
• This may result from alterations in the
inflammatory response in smokers, as outlined
previously, or from alterations in the vascular
response of the gingival tissues.
• Although no significant differences in the
vascular density of healthy gingiva have been
observed between smokers and nonsmokers, the
response of the microcirculation to plaque
accumulation appears to be altered in smokers
compared with nonsmokers.
20. • With developing inflammation, a rise in GCF
flow, bleeding on probing, and gingival blood
vessels are less in smokers than nonsmokers. In
addition, the oxygen concentration in healthy
gingival tissues appears to be less in smokers than
nonsmokers, although this condition is reversed in
the presence of moderate inflammation.
• Subgingival temperatures are lower in smokers
than nonsmokers, and recovery from the
vasoconstriction caused by local anesthetic
administration takes longer in smokers.
21. • These cumulative data suggest that
significant alterations are present in the
gingival microvasculature of smokers
compared with nonsmokers and that these
changes lead to decreased blood flow and
decreased clinical signs of inflammation.
• This explains the long observed
phenomenon of a transient increase in
gingival bleeding when a smoker quits.
23. • Following non-surgical therapy, healing in terms
of gingival bleeding reduction and pocket-depth
reduction was less favorable in smokers.
• The clinical results showed a statistically
significant reduction of pocket depth and number
of diseased sites in both smokers and non-smoker
patients.
• These findings are in agreement with recent long-
term results which suggest that tobacco smoking
interferes with the healing process following non-
surgical periodontal therapy.
24. • James and colleagues investigated the in vitro
effect of nicotine on fibroblast activity. They
found that it inhibited attachment and growth of
periodontal ligament fibroblasts.
• The results of these studies all indicate that
smoking has a deleterious effect on wound
healing and may help to explain why smokers
respond less favourably to periodontal therapy.
25. Maintenance Therapy
• The detrimental effect of smoking on treatment
outcomes appears to be long-lasting and
independent of the frequency of maintenance
therapy.
• After four different modalities of therapy,
including scaling and root planing, modified
Widman flap surgery, and osseous surgery,
maintenance therapy was performed by a hygienist
every 3 months for 7 years.
• Smokers consistently had deeper pockets than
nonsmokers and less gain in attachment when
evaluated each year for the 7-year period.
26. • Even with more intensive maintenance
therapy, Smokers possess deeper and more
residual pockets than nonsmokers, even
though no significant differences in plaque or
bleeding on probing scores were found.
• Smokers also tend to experience more
periodontal breakdown than nonsmokers after
therapy.
27. • In studies of patients who failed to respond to
conventional therapy, including different combinations
of oral hygiene instruction, scaling and root planing,
surgery, and antibiotics, approximately 90% of these
poorly responding patients were smokers.
• It is clear from these studies that smokers (1) may
present with periodontal disease at an early age, (2)
may be difficult to treat effectively with conventional
therapeutic strategies, and (3) may continue to have
progressive or recurrent periodontitis. For this
reason, smoking cessation counseling must be a
cornerstone of periodontal therapy in smokers.
28. Smoking Cessation
• Various methods for helping patients to quit
smoking in the dental environment have been
described.
• ASK: Ask the patient about their smoking
status.
• This should be part of the medical history.
29. • ADVISE: Advise smokers of the associations
between oral disease and smoking.
Be informative, honest, and helpful but not judgmental.
• ASSESS: Assess the patient's interest and readiness
to attempt smoking cessation.
Patients may not yet be in an action phase to quit
smoking, which is why it is always important to make
these assessments every time you see the patient.
• ASSIST: Assist the patient in their quit attempt.
If you are trained, many techniques can be used.
Alternatively, assist the patient in seeking the help they
need.
30. • ARRANGE: Arrange follow-up or referral to
professional smoking cessation services.
The most important aspect of this is to keep in
regular contact particularly around the quit date and
in the immediate period after.
31. Effects of Smoking Cessation on
Periodontal Treatment Outcomes
• Studies have demonstrated that smokers have
significantly worse periodontal status (deeper
probing depths, more attachment loss, and bone
loss) than either former smokers or nonsmokers
and usually have poorer treatment outcomes.
32. • There are very few intervention studies on the
effect of smoking cessation on periodontal
treatment outcomes (i.e., studies in which
smokers were helped to quit and the effect on
periodontal status was then assessed).
• Two short-term studies have indicated that
smoking has a negative impact on the gingival
vasculature and that these changes are reversible
upon quitting smoking.
33. • One intervention study has assessed the impact of
smoking cessation on outcomes after nonsurgical
periodontal treatment.
• This study employed dental hygienists who were
trained as smoking cessation advisors and
achieved a 20% quit rate at 12 months in a
population of smokers who also had periodontitis
using a variety of strategies, including
Counseling, Nicotine Replacement Therapy,
and Bupropion.
34. Nicotine Replacement Therapy
• Nicotine replacement therapy (NRT) gives
you nicotine – in the form of gum, patches,
sprays, inhalers, or lozenges – but not the
other harmful chemicals in tobacco.
• NRT can help relieve some of the physical
withdrawal symptoms so that you can focus
on the psychological (emotional) aspects of
quitting.
35. • To conclude, smoking is the major risk
factor for periodontitis, and smoking
cessation should be an integral part of
periodontal therapy in patients who smoke
and needs to be considered a priority for the
management of periodontitis in smokers.
36. References
• Carranza’s clinical Periodontology 11th Ed
• Jan Lindhe
• Ana Pejčić, Radmila Obradović, Ljiljana Kesić, Draginja
Kojović : SMOKING AND PERIODONTAL DISEASE A
REVIEW, Medicine and Biology Vol.14, No 2, 2007, pp. 53
– 59
• Bergstrom J, Eliasson S, Dock J. Exposure to tobacco
smoking and periodontal health. J Clin Perio 2000; 27: 61-
68.