445257780-Smoking-and-Periodontium-pptx.pptx

SMOKING AND PERIODONAL DISEASE MECHANISM

1. SMOKING AND PERIODONTIUM

2. INTRODUCTION Tobacco smoking has a devastating effect on the health and well being of the public and remains the nations leading avoidable cause of premature mortality and disability. It is also well established that cigarette smoking is a major risk factor in the incidence and severity of several forms of periodontal diseases.

3. Using the criteria by CENTER FOR DISEASE CONTROL [CDC] smokers were defined as; CURRENT SMOKERS are defined as those who have smoked >or = 100 cigarettes over their life time and smoked at the time of interview.   FORMER SMOKERS are who had smoked > or = 100 cigarettes but were not smoking at the time of interview. NON SMOKERS who had not smoked > or = cigarettes in their life time

4. HISTORY TOBACCO is a plant whose history traces back to about 6000 B.C. when it was believed that it began growing in the North and South America. When Columbus came to America, he met some natives who inhaled smoke from leaves through a long wooden tube which they called ‘ Tobago or tobaca’. From this came the name applied to the plant. Natives also rolled the dried leaves of the tobacco plant in corn husks and inhaled through their mouths. Those were the first cigars and cigarettes. Soon after this sailors brought tobacco to Europe. The main reason why it flourished in Europe is because of its healing properties.

5. HISTORY The generic name NICOTINA TOBACCUM was named after the French ambassador to Portugal , “ JEAN NICOT ” who introduced tobacco into the French court in 1560. The Portuguese brought the tobacco to the durbar of Akbar in the 17th century. Akbar was asked to smoke it after the smoke was passed through water, thus discovering the ‘ Tukka ’.

6. HOW IT IS CONSUMED IN INDIA? 72 % tobacco users in India are bidi smokers 12.5 % were cigarette smokers 16 % were using smokeless forms. Thus tobacco habits are practiced in various forms and many of them are specific to certain areas of India

7. BROADLY TOBACCO CAN CAN BE CLASSIFIED AS Smoked tobacco - cigarette, bidis chelum, dhumti, chutta, cheroot. Chewed tobacco- pan masala, pan with tobacco Tobacco applications - mishri ,tobacco with tooth powders and pastes Inhaled tobacco - snuff

8. COMPOSITON Thousands of different compounds have been identified in tobacco smoke and some occur in concentration judged to be harmful to health [US DEPT OF HEALTH EDUCATION AND WELFARE 1976]. Some of these substances are indisputably carcinogenic and has been implicated in the etiology of oral neoplasias [ Pindborg 1980 ].

9. Nicotine –C 10 H 14 N 2 . an alkaloid exists in all parts of the tobacco plant but notably in the leaves. Hence, the leaves are mostly used. poisonous at high concentrations 3 to 4 drops of pure nicotine taken into the stomach would probably prove fatal for an adult, i.e., about 60mg. Nicotine content is higher in smokeless forms than cigarettes [4.5mg v/s 1mg].

10. Benzathracene, Hydrogen cyanide are undoubtedly noxious substances, but also have antibacterial properties. [Wynder and Hoffman 1967]. Polycyclic aromatic hydrocarbons and n-Nitroso compounds which are the main carcinogens.   Tar -cause lung cancer and bronchial disorders. An average cigarette contains 15mg of tar. person who smokes a pack of cigarette per day inhales about 8 ounces of tar each year. Carbon monoxide Phenol Napthylamines -causes irritation of throat and respiratory passage. A nuclear reactive substance is also product of tobacco, after some years of time the lungs of the smoker could be compared to a nuclear reactor. [ ISP-issue 3;Vol-4;page –42 ]

11. PARTS OF TOBACCO SMOKE It is an aerosol consisting of particles forming a mainstream smoke and a side stream smoke On inhaling, at least 50 % of this smoke is retained in the lungs and some of the droplets are deposited directly in the bronchial tubes.

12. Nicotine is the most pharmacologically active compound in tobacco smoke, mostly absorbed through the alveoli but nicotine can also be absorbed slowly through the oral mucosa. When tobacco is chewed or smoked the nicotine is released from tobacco as the free base and absorbed into the blood stream from where it is distributed to the brain. Nicotine has actions on almost all organs of the body but has a particular predilection for brain and other nervous tissues. PHARMACOLOGY OF NICOTINE

13. Nicotine from tobacco smoke can reach the brain faster than it would if it were injected into the vein through a syringe. Nicotine mimics the actions of acetylcholine by a competitive blockade of acetylcholine at autonomic ganglia initially stimulating subsequently depressing synaptic transmission. ACTS AS AN STIMULANT OF CNS, CVS AND ENDOCRINE SYSTEMS . PHARMACOLOGY OF NICOTINE

14. Nicotine has pronounced effect on CVS thereby increasing the heart rate, cardiac output and blood pressure by autonomic stimulation and stimulates adrenalin thereby also causing peripheral vasoconstriction [Stimmel et al 1979] Direct action on the blood vessels and capillaries to produce vasoconstriction has also been reported [Larson et al 1961] PHARMACOLOGY OF NICOTINE

15. Eliminated chiefly in urine Completely eliminated in about 16 hours partly by the lung, saliva and sweat. Also seen in breast milk of lactating mothers who smoke excessively. SERIOUS CONSEQUENCE IS MAINLY DRUG DEPENDENCE. PHARMACOLOGY OF NICOTINE

16. Prevalence Prevalence of smoking world wide is higher in individuals older than 34 years of age. Higher in males than females (highest prevalence in non Hispanic black men 38.6%.) Current smoking is more common in adults of low income group compared with medium or high income group and increases with the decreasing years of education. In Erie County study population, there was a strong positive relationship between bone loss and mean pack years of smoking

17. Prevalence Increased prevalence and severity of Periodontitis is seen in smoking adults. (smokers 4 times MORE periodontitis ) Former smokers were 1.68 times more likely to have periodontitis than who have never smoked. In subjects smoking less than or equal to 9 cigarettes per day the odds for having periodontitis was 2.79 times whereas subject smoking greater than or equal to 31 cigarettes per day were nearly 6 times more likely to have Periodontitis. CIGARETTE SMOKING HAS BEEN EVIDENCED WITH INCREASED SEVERITY OF GENERALIZED AGGRESSIVE PERIODONTITIS.  

18. Bone loss is twice than non smokers and proceeds more rapidly even in the presence of excellent plaque control Cigar / pipe smokers showed severity intermediate between current smokers and non smokers . Prevalence

19. EFFECTS OF SMOKING

20. EFFECT OF SMOKING ON THE PREVALENCE AND SEVERITY OF PERIODONTAL DISEASE

21. EFFECTS ON GINGIVAL & PERIODONTAL TISSUES Smoking adversely affects periodontal health. Smokers are high risk group for periodontal disease and smoking history is a useful clinical prediction for future disease activity

22. In a study of 142 patients with chronic periodontitis plaque samples from the deep pockets showed no differences in the counts of A.Actinomycetamcomitans, Porphyromonas gingivalis and Prevotella intermedia. In a similar study of 615 patients the prevalence of A.Actinomycetamcomitans, Porphyromonas gingivalis and Prevotella intermedia and Ekinella corrodens was not found to be significantly different from non smokers and smokers. In contrast , other studies have shown differences in the microbial composition of subgingival plaque in smokers. In a study of 798 patients it was found that smokers had significantly higher levels of Bacteroides forsythus.   EFFECTS ON MICROBIOLOGY

23. Of particular interest was the observation that smokers do not respond to mechanical therapy as well as non smokers and that this is associated with increasing levels of B.forsythus, A.Actinomycetamcomitans, Porphyromonas gingivalis remaining in the pockets after therapy.   A recent study using checkerboard DNA-DNA hybridization technology in 272 adults examining all the teeth except third molars found Ekinella nodatum, Fusobacterium nucleatum, P.intermedia, Peptostreptococcus, Prevotella nigrescens, B.forsythus,P.gingivalis, and Treponema denticola were significantly more prevalent in current smokers than non and former smokers EFFECTS ON MICROBIOLOGY

24. Down regulation of the immune response to bacterial challenge. Critical functions of neutrophils such as chemotaxis, phagocytosis and killing are impaired. Reduced levels of IgG2 has been reported in smokers. (smokershave less protection against periodontal infection.) Elevated levels of TNF-α and PGE2 neutrophil elastase , matrix metalloproteinase – 8 are seen. Thus data suggests; Smoking may impair the response of neutrophils to periodontal infections but also elevates the tissue destructive enzymes. EFFECTS ON IMMUNOLOGY

25. EFFECTS OF SMOKING ON ETIO-PATHOGENESIS OF PERIODONTAL DISEASE

26. No effect on the rate of plaque accumulation. Colonization of shallow periodontal pockets by periodontal pathogens. Levels of periodontal pathogens in deep periodontal pockets Altered neutrophil chemotaxis, phagocytosis and oxidative burst. TNF-α and PGE2 in GCF production of PGE2 by monocytes in response to LPS MICROBIOLOGY IMMUNOLOGY

27. Gingival blood vessels with increased inflammation. GCF flow and bleeding on probing with increased inflammation. Sub-gingival temperature. Time needed to recover from local anesthesia.   PHYSIOLOGY

28. EFFECTS ON GINGIVA No striking gingival changes though it has direct toxic effect on gingiva has been reported. Heavy smokers have GRAYISH DISCOLORATION and hyperkeratosis of gingiva. There is decreased INFLAMMATION and EDEMA .   Nicotine causes decreased fibronectin production by gingival fibroblast. This leads to decreased cellular adhesion, spreading and migration which is an important cellular process during wound repair. Smoking causes decrease in number of circulating cells and less oxygen reaching gingiva, thus WEAKENING ITS DEFENCE AND REPARATIVE PROCESS

29. EFFECTS ON GINGIVA Gingivitis toxica : Charaterised by destruction of gingiva and underlined bone. Pindborg in 1951 stated that 98 % of ANUG patients were smokers. Smoking and ANUG are both reflections of stress. Increased susceptibility of smokers to ANUG include - Vasoconstriction of gingival blood vessels. - Reduced activity of oral leucocytes - Proliferation of anaerobic fusospirochaetal microbes  

30. EFFECTS ON GINGIVA Metallothionein (MT) It is a free radical scavenger in gingiva. Samples of gingiva from smokers showed high level of MT in prickle cell layer of epithelium. This increased level of MT will prevent gingival against free radical injury. Hence inflammation is much greater in periodontal tissues of smokers than gingiva.    

31. EFFECTS ON PERIODONTAL LIGAMENT Altering periodontal host response. (impairing normal function of host response & destruction of surrounding periodontal tissues.) It is shown that nicotine can be stored in and released from periodontal fibroblasts and significantly affects growth of PDL FIBROBLASTS . Fibroblasts exposed to nicotine show reduced proliferation, migration, and attachment to root surfaces . Fibroblasts nonspecifically bind and internalize nicotine which could in turn result in an alteration of cell metabolism including collagen synthesis and protein secretion

32. EFFECTS ON ALVEOLAR BONE; S moking has been significantly associated with severity of bone loss This could be due to Decreased immunity, Decreased bone metabolism and turnover, Decreased intestinal absorption of calcium, Toxic effect on osteoblasts, Increased proliferation of anaerobic bacteria , Suppresses proliferation of osteoblasts , Stimulates alkaline phosphatase activity.

33. EFFECTS ON ALVEOLAR BONE A new disease category, SMOKING ASSOCIATED PERIODONTITIS [SAP] , has been proposed, which gives unique characteristics of smokers with periodontitis Clinical features of SAP Relatively early on set of disease at age of 20-30 years. Rapid disease progression Gingiva appears to be fibrotic in thick rolled margins. Minimal gingival inflammation or edema Decreased reduction in pocket depths after scaling. Repocketing within one year of surgical treatment Resistance to conventional therapy Increased pocket depth in anterior & mostly maxillary lingual sites

34. CNS CVS PERIPHERAL VASCULATURE RESPIRATORY TRACT GI TRACT IMMUNE SYSTEM OPTIC NERVE NUTRITION Smoking and systemic involvement

35. Effects on CNS After entering blood stream it rapidly reaches the brain where it mimics the action of ACETYL CHOLINE of autonomic ganglia, initially stimulating and subsequently depressing synaptic transmission. Responsible for dependence Elevates the mood Person feels a sense of pleasure and excitement They are in an emotional state.

36. Effect on CVS Increases heart rate cardiac output blood pressure These are all due to autonomic stimulation. Malignant hyper tension and coronary artery disease are the most common diseases with smoking

37. EFFECT OF PERIPHERAL VASCULATURE Due to stimulation of adrenalin there is vasoconstriction of peripheral blood vessels, which also elevates blood pressure.   EFFECTS ON RESPIRATORY SYSTEM Most of the nicotine enter the lungs and absorbed through the alveoli causing chronic bronchitis, emphysema and all types of lung cancer, except pleural malignancy.  

38. EFFECTS ON GI TRACT There is increased predilection for Esophageal carcinoma and Peptic ulceration EFFECT ON IMMUNE SYSTEM Has an immuno suppressive effects on the host Impaired PMNL motility, chemotaxis,phagocytosis Decreased antibody production especially IgG2 ( IgG2 important for opsonization) Negative immuno regulatory effect

39. EFFECT ON OPTIC NERVE Excess of tobacco smoking along with alcohol consumption and poor nutrition often causes toxic optic neuropathy . Pipe smokers are at high risk for this condition Heavy smoking alters the tumor suppressor gene P53. P53 mutations have been reported to be absent in non smokers and non alcoholics.

40. Effects on NUTRITION SIGNIFICANT TOLL ON THE NUTRIENT STATUS OF THE INDIVIDUAL Smokers have a lower intake of numerous essential nutrients involving vitamin A, C, beta keratin, folic acid and dietary fibers. Smokers require twice as much as vitamin C as non smokers (metabolize the vitamin more rapidly) Smoking influences both hunger and body weight tending to postpone feelings of hunger and to reduce body weight. HENCE SMOKING IN FEMALES HAS AN INCREASING STRIDE

41. EFFECT OF SMOKING ON ORAL CAVITY

42. The mouth receives the brunt of hot, irritating and toxic substances contained in smoke from burning tobacco.   Each puff of a cigarette contains about 18 mg is solid particulate matter and rest consists of carbon dioxide and carbon mono-oxide mixed with oxygen and nitrogen from air. Risk of oral cancer is six times with cigarette or cigar smoking & 16 times with the usage of pipe smoking

43. EFFECT OF SMOKING ON ORAL CAVITY Halitosis Stains Caries Hairy tongue Cancer Palate Leukoplakia OSMF Oral hygeine Smokers Melanosis Attrition Ulceration Saliva

44. HALITOSIS Foul offensive odor, characteristically seen in smokers. Not only causes bad breath by itself but also encourages development of hairy tongue which traps food debris. Smoking also decreases salivary flow and increases the severity of the condition. (Krupp et al )  

45. STAINING OF TEETH Pigmented deposits that appear on teeth are called stains. Tobacco stains are tenacious brown or black deposits seen on the teeth. Staining results from coal tar combustion products from penetration of pits and fissure on the enamel and dentin by tobacco juices

46. DENTAL CARIES Smokers frequently use candy or breath mints in a futile attempt to avoid offensive breath. This candy/mints causes tooth erosion as it contains citric acid. Prolonged usage for more than 8-10 years to mask halitosis leads to destruction of tooth enamel by causing erosion and dental caries.

47. As the bacteria and food debris become trapped between this piled up keratin a burning sensation on tongue and halitosis develop leading to hairy tongue HAIRY TONGUE Mostly seen in heavy pipe smokers. Characterized by development of elongated, thick densely matted and stained hair like filament which represent a profuse over growth of the filiform papilla. The elongated papilla develops when the particulate matter and gases in tobacco smoke prevent the surface cells from sloughing normally.

48. ORAL CANCER Squamous cell carcinoma- most common of malignancy to occur in the oral cavity (90-95%). The various sites include Vermilion border of the lip Lower labial mucosa Labial commisure Buccal mucosa, Tongue where 80% occur in anterior 2/3 mostly on the lateral margin and ventral surface of the tongue

49. Palate : Smoker’s palate [nicotinic stomatitis]. Discoloration of palate occurs and is characterized by prominent mucous glands Inflammation of the orifices of glands Diffuse erythema Wrinkled ‘COBBLESTONE’ surface on the palate will occur.

50. ORAL SUB MUCOUS FIBROSIS : Pre cancerous condition, predominantly occur in Indians. Burning sensation followed by hyper-salivation or dryness of mouth is seen. LEUKOPLAKIA Smoking is an important etiologic factor Common in buccal mucosa

51. Poor oral hygiene is seen Reluctant for maintenance   ORAL HYGIENE

52. Smokers melanosis Benign pigmentation of oral mucosa . Predominantly observed on anterior mandibular attached and inter dental gingiva. Often seen in the third decade of life. This occurs secondary to tobacco smoking.

53. Attrition and other effects on teeth Pipe smoking can cause attrition of teeth Teeth involved can be intruded and those remain without occlusal support can show evidence of hyper-function. This could lead to increased tooth mobility and tooth loss.

54. HYPERKERATOTIC / ULCERATIVE LESIONS Thermal changes in tissues it contact. Habitually pipe and mouth piece used with cigar and cigarette directs a steady flow of stream of heat to an isolated area where an ulcerative and hyper-keratotic lesion develops.   SALIVA Increased flow rate of saliva. This is a ( reflex phenomenon produced by irritant particulate matter) Toxic material can cause inhibition of function of oral salivary leucocytes Level of nicotine in saliva- 96 ng –1.6ng /ml Cotinine a primary metabolite remain constant over a period of time and range from 106ng-1ugm /ml.

55. ORAL EFFECTS OF SMOKELESS TOBACCO

56. TWO MAIN TYPES OF SMOKELESS TOBACCO Chewing Tobacco Snuff

57. CHEWING TOBACCO Loose leaf Processed cigar type tobacco loosely packed in small strips Plug Small oblng blocks of semi-soft tobacco Place tobacco next to the gingival/buccal mucosa

58. Snuff (finely ground tobacco) Moist Used by dipping Placing it between the gum and the cheek or under the upper or lower lip Dry Placed in oral cavity or sniffed through the nose

59. Physiologic Dependence Withdrawal Tolerance

60. Nicotine Withdrawal Symptoms Anxiety Irritability Poor concentration Restlessness Craving GI problems Headaches drowsy

61. Adverse Medical Consequences Many problems affecting different systems in the body Central Nervous System Heart Disease Hypertension Lipids Diabetes

62. PREVENTION

63. Benefits of Smoking Cessation 10-12 weeks after smoking cessation- an increased gingival inflammation and bleeding on probing occurs for several months [recovery of inflammatory response]. After one year smoking cessation, the gingival loses the fibrotic, thickened appearance and assumes as more normal anatomy. Periodontal status stabilizes and attachment loss ceases or slows. IT MAY TAKE A NUMBER OF YEARS AFTER CESSATION BEFORE THE RATE OF TOOTH LOSS IS SIMILAR TO THAT OF NON SMOKERS.

64. Recommended agents to manage nicotine withdrawal NICOTINE REPLACEMENT AGENTS Often preferred route for clinical use ( better compliance) A patch is applied to a different skin area each day to minimize irritation. Used for 16-24 hours and are available in three strengths. The largest patch is used for initial 4 weeks and the next smaller sizes for two week stepped withdrawal periods . HABITROL [Novartis] Nicotine 21mg,14mg,7mg Nicoderm [Smithkline Beecham] - 21mg/hr;14mg/hr;7mg/hr.

65. GUM 4mg of nicotine gum is preferred when allergy is encountered with patches. One piece should be used for every 1-2 hours for 6 weeks, then every 2-4 hrs for 3 weeks and 4-8 hrs for 3 weeks. Patient s must be instructed to chew each piece until a peppery taste is noticeable , and then to park the gum as nicotine absorption occurs. The ‘chew and park’ routine is followed for 30 minutes per piece. Patient advised to stop using acidic liquids like coffee, fruit juices at least 15 minutes since nicotine is not absorbed in an acidic environment. Nicorette[ smithklime beecham] 2 mg/4mgm.  

66. Nicotine spray It is an option that stimulates the rapid delivery effect of cigarette smoking. One spray into each nostril -8-16 times /day . Nasal spray -Nicotrol NS [McNeil consumer] (nicotine 0.5mg).

67. NON NICOTINE AGENTS Bupropion Hcl [Zyban (Glaxo)] It is an nicotine replacement alternative equivalent to patch.

68. EFFECTS OF SMOKING ON RESPONSE TO PERIODONTAL THERAPY

69. NON-SURGICAL Current smokers do not respond to treatment as non smokers on former smokers. The majority of clinical reports support the observation that pocket depth reduction is more effective in non smokers than in smokers . Average pocket reductions of 2.5mm for non smokers and 1.9mm for smokers were observed in pockets that averaged 7mm before treatment, even though plaque scores were less than favorable.

70. NON-SURGICAL Decreased clinical response to scaling and root planning, Reduction in pocket depth, Gain in clinical attachment levels, Negative impact of smoking with increased level of plaque control.  TO CONCLUDE SMOKERS RESPOND LESS WELL TO NON SURGICAL THERAPY THAN NON SMOKERS.

71. SURGICAL Smokers [heavy-20 cigarettes/day: light-19 cigarettes] consistently showed less pocket reduction and less gain in clinical attachment levels than the non smokers. These patients were followed up for 7 years [continued with supportive periodontal therapy]. During these years, deterioration of furcation areas was greater in heavy and light smokers when compared with non smokers.

72. SURGICAL SMOKING HAS SHOWN TO HAVE A NEGATIVE IMPACT ON THE OUTCOMES OF GTR AND THE TREATMENT OF INTRA-BONY DEFECTS BY BONE ALLO-GRAFTS.   By 12 months after GTR therapy, smokers gained less than half as much clinical attachment as non smokers. In another study, 78 smokers showed less gain in clinical attachment, more gingival recession, less gain in bone fill of the defect. In addition, GTR membranes were exposed in all smokers and approximately half of non smokers

73. SURGICAL use of decalcified freeze dried bone allograft[DFDBA]for the treatment of intrabony defects-smokers showed less percentage reduction in presurgical pocket depth. By 6 months, smokers [3mm] showed significantly less reduction of deep pockets [>7mm] than non smokers [4mm] and significantly less gain in clinical attachment [18 v/s 2.8]. Patients also received supportive periodontal therapy for 6 months of significance was the observation that only 16 % of deep pockets returned to- 3mm where as 47 % of deep pockets in non smokers returned to 3mm after completion of therapy.  Root coverage following thick free gingival graft procedures is reportedly diminished by heavy cigarette smoking, and there is a conflicting reports on smoking’s effect on the success of sub epithelial connective tissue grafts.  

74. ON IMPLANTS Effect on implant is unclear. Studies showed that implant success rates are reduced in smokers. In one of the study overall implant success rates up to 6 years among current smokers were approximately 89%as compared to 95% in non smokers. A longitudinal study has shown that marginal bone loss was greater over a 15 year period around implants supporting mandibular fixed prosthesis in current smokers as compared to former or never smokers

75. Recurrent [refractory]Periodontitis Because of difficulty in controlling the disease in smokers, they become refractory to traditional periodontal treatment and also tend to show more periodontal breakdown than non smokers after therapy. Increased need for re-treatment in smokers. Increased need for antibiotics in smokers to control the negative effects of periodontal infection on surgical outcomes. Increased tooth loss in smokers after surgical therapy

76. PUTTING TOBACCO IN GOOD USE Plant transformation scientists at the International Center for Genetic Engineering and Biotechnology, Delhi have now created a factory for gamma interferon in the chloroplasts of tobacco leaf cells. This is a human protein and a life saving drug that can boost the immune system, thus help to treat cancers, asthma genetic disorders and arthritis.   With 50 gm of tobacco leaves yielding 20gm of the special protein , it does not seem like a bad market proposition.

77. CONCLUSION Cigarette smoking is a major risk factor and smokers are a high risk group for periodontitis. It is very difficult to treat them with conventional therapy and may have progressive or recurrent periodontitis leading to tooth loss.   As mentioned, smoking cessation is clearly beneficial and counseling for smoking prevention should be included in the protocol for managing patients with periodontal disease.   Thus motivation towards a positive change should be achieved by each individual – After all whose life is it any way?!