Systemic Risk Factors Flashcards
(35 cards)
Statistics of smoking in uk
As in previous years, in 2019 more men smoked than women in the UK. Within allconstituent countries of the UK, 15.9% of men (around 3.8 million) and 12.5% ofwomen (around 3.1 million) reportedbeing current smokers
Nicotine and tobacco
- Smokers start for a range of reasons but keep smoking primarily because of nicotine dependence
- Nicotine is addictive, but it is the many otherharmful constituents in tobacco that kill
- “Smokers smoke for the nicotine but diefrom the tar” (Prof Michael Russell, 1979, early pioneer of Nicotine Replacement Therapy
Smoking related diseases
- Cancer: lung, mouth, pharynx, larynx, bladder, pancreas, kidney, oesophagus,stomach, kidney, leukaemia
- Potentially fatal: ischaemic/respiratory heartdisease, obstructive lung disease eg, bronchitis, stroke, pneumonia, aorticaneurysm, foetal/neonate death
- Non-fatal: periodontal diseases, low birthweight baby
Smoking and periodontal diseases
Tobacco smoking is related to:
- Periodontitis
- Periodontitis that is refractory to treatment
- Necrotising Periodontal Diseases (NG/NP)
Smokeless tobacco is related to:
Localised recession manifesting as attachment loss and also increased oral cancer risk
Severe active periodontal disease
Earlier studies showed that taboacco smokers had
- higher levels periodontal disease• poorer oral hygiene (OH)
- hypothesised that poorer OH may beresponsible for higher disease levels ie smokingindirectly affected periodontium
- Current data support direct effects of smoking on periodontium
Epidemiology
• Cross-sectional and longitudinal studies have shown tobacco smoking is a risk factor for periodontal disease
Smokers have:
- greater bone loss and attachment loss
- increased numbers deep(er) pocketsthan non-smokers
Risk from smoking (classic studies)
Odds ratios for attachment and bone loss in light and heavy smokers
How many and how long?
Smoking correlation for periodontitis
Periodontitis and smoking
- earlier onset
- rapid disease progression
Clinical appearance
- fibrotic ‘tight’ gingiva, rolled margins
- less gingival redness and bleeding
- more severe, widespread disease than same age non-smoking control
- anterior, maxilla palate worst affected
- anterior recession, open embrasures
- nicotine staining, calculus
Necrotising gingivitis
NECROTISING GINGIVITIS (NG)
• Rapid onset, specific features
• painful, interdental necrosis, bleeding gingivae
• necrotic ulcers affecting interdental papillae
• “punched out” appearance
• ulcers painful, covered by grey slough
• gingival bleeding with little provocation
• possible halitosis, “foetor oris”
• possible lymph nodes involvement
• Most adult patients with NPD are smokers
Toxic substances
• >4,000 reported toxic substances in cigarettesmoke:
• Particles - nicotine, benzene, benzo(a)pyrene
• Gases - hydrogen cyanide, carbon monoxide(carboxyhaemaglobin), ammonia,formaldehyde, dimethylnitrosamine, acrolein
• Free radicals (react with cholesterol, leading to atheroma on artery walls)
NB. Cotinine is metabolite of nicotine whichmeasures exposure to tobacco
Pathogenesis - what affects does smoking have in relation to the oral cavity?
Local and systemic effects not fully understood
• Inhibition of phagocytosis of neutrophils (PMNs)
• Reduction in chemotaxis and migration of oral PMNs exposed to nicotine
• Nicotine affects PMNs respiratory burst (affects ability to kill oral pathogens)
• Nicotine adversely affects fibroblast function and penetrates oral epithelium
• Reduced antibody production, serum IgG2
• Altered peripheral blood immuno-regulatoryT-cell subset ratios in some studies
• Reduced bone mineralisation
• Cytotoxic, vasoactive constituents
• Adverse effect on micro-circulation, gingival circulation, blood flow
• Possible vasoconstriction of gingival capillaries but evidence inconsistent
• Chronic hypoxia of periodontal tissues (impacts how well tissues are able to heal)
• High proportion of small blood vessels in smokers compared with large vessels, but no difference in vascular density
• Fewer gingival vessels in smokers
Pathogenesis - what affects does smoking have overall?
- Less gingival redness
- Less bleeding on probing
- Fewer vessels clinically and histologically
- Healing response may be affected by impairment of revascularisation
Pathogenesis - evidence suggests?
• Inflammatory response in smokers with periodontitis may not be accompanied byequivalent increase in vascularity
• Reduction in ICAM-1 expression may affect neutrophil emigration from vessels
Suppressive effect of smoking on vasculature rather than just simple vasoconstrictive effect
Microbiology
Review of 14 studies found that
- in 6 studies, no microbiological differences found in smokers and non smokers
- in 8 studies, trend for smokers to harbour more potential periodontal pathogens
Therapy for smokers
Non surgical therapy same as with non smokers however different treatment outcomes
• Poorer response to non-surgical therapy
• Smokers respond less well to periodontal therapy, non-surgical and surgical
• presumably relates to the local, systemic and microbiological effects of smoking
• Over 90% of refractory patients have been found to be smokers
• 6 month study showed decreased inflammation & GCF, decreased IgG titres to A.a and poorer periodontal outcome in smokers, although nomicrobial differences found
Clinical implication of having a pt who smokes
• You should advise your patients of the adverse effects of smoking on their oral andperiodontal health (+general health)
• Record giving advice in patient’s notes (NBmedico-legal reasons)
• You should explain poorer response toperiodontal therapy• Give smoking cessation counselling
Smoking cessation - what are the time dependent changes in the periodontal tissue?
• Brief advice from a health professional can result in up to 5% of patients quitting smoking
After smoking cessation, time dependent changes in the periodontal tissues:
• recovery of inflammatory response leads to transient increased bleeding (approx 6 months)
• return to normal architecture of gingival tissues (approx 12 months)
Key pillars of smoking cessation
Suggest
• nhs stop smoking services
• Nicotine replacement therapy:
• Buproprion (Zyban); Varenicline (Champix)
• Be practical, supportive & encourage
• Very Brief Advice: 3 As
• Ask (establish and record smoking status)
• Advise (on personal benefits of quitting)
• Act (offer help)
• Smokers are up to 4 times more likely to quit with support
Smoking cessation study
• 1 year longitudinal study
• N=49: plaque, probing depths (PD), BOP, CAL, subtraction radiography
• Smoking cessation advice & non-surgical therapy
• 11 quitters, 11 oscillators, 11 non-quitters, (CO monitor & self reportdiary);15 withdrew
• Improved clinical outcomes, more Pocket Depth reductions in quitters (p<0.05) !!
E-CIGARETTES
E-cigarettes don’t contain tobacco and don’t produce tar or carbon monoxide, two of the most damaging constituents in cigarette smoke.
E-cigarettes work by heating a solution (e-liquid) that typically contains nicotine, propylene glycoland/or vegetable glycerine, and flavourings.
What is another risk factor that affects periodontal disease?
Stress
