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Smoking-related disease?

Cancer: lung, mouth, pharynx, larynx, bladder, pancreas, kidney, oesophagus, stomach, kidney, leukaemia
Potentially fatal: ischaemic/respiratory heart disease, obstructive lung disease eg bronchitis, stroke, pneumonia, aortic aneurysm, foetal/neonate death
Non-fatal: periodontal diseases, low birth weight baby


Tobacco smoking is related to:

• Periodontitis
• Periodontitis that is refractory to treatment
Necrotising Periodontal Diseases (NUG/NUP)


Smokeless tobacco is related to:

• Localised recession manifesting as attachment loss and also increased oral cancer risk
Severe active periodontal disease


Earlier studies showed tobacco smokers had :

• higher levels periodontal disease
• poorer oral hygiene (OH)
• hypothesised that poorer OH may be responsible for higher disease levels ie smoking indirectly affected periodontium
Current data support direct effects of smoking on periodontium


• Cross-sectional and longitudinal studies have shown :

• Smokers have :

tobacco smoking is a risk factor for periodontal disease

• greater bone loss and attachment loss
• increased numbers deep(er) pockets
than non-smokers with similar plaque levels


Clinical Appearance of periodontium in smokers

• 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 specific features

• 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


microbiology of smoking-related disease

• Review of 14 studies found that:
• In 6 studies no microbiological differences found in smokers & non-smokers
In 8 studies, trend for smokers to harbour more potential periodontal pathogens


pathogenesis of smoking-related disease
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
- Adverse effect on micro-circulation, gingival circulation, blood flow.
-Possible vasoconstriction of gingival capillaries but evidence inconsistent
-Chronic hypoxia of periodontal tissues
• High proportion of small blood vessels in smokers compared with large vessels, but no difference in vascular density
Fewer gingival vessels in smokers


Smoker evidence suggests

• Evidence suggests
• Inflammatory response in smokers with periodontitis may not be accompanied by equivalent 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


Smokers overall

• Less gingival redness
• Less bleeding on probing
• Fewer vessels clinically and histologically
Healing response may be affected by impairment of revascularisation


smoker microbiology

• Microbial profile of smoking associated periodontitis is distinct from non-smokers
• Significant differences in prevalence and abundance of disease-associated as well as health-compatible organisms


effect of smoking on periodontal treatment - clinical characteristic

• Relatively -earlier onset, rapid disease progression
Poorer response to nonsurgical therapy


effect of smoking on periodontal treatment - 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 glycol and/or vegetable glycerine, and flavourings.


effect of smoking on periodontal treatment - 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 i inflammation & GCF, iIgG titres to A.a and poorer periodontal outcome in smokers, although no microbial differences found


effect of smoking on periodontal treatment - cessation

• Brief advice from a health professional can result in up to 5% of patients quitting smoking
• After smoking cessation, time dependent changes:
• recovery of inflammatory response leads to transient increased bleeding (approx 6m)
return to normal architecture (approx 12m)


effect of smoking on periodontal treatment - cessation extended

• 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


effect of smoking on periodontal treatment- clinical implications

• You should advise your patients of the adverse effects of smoking on their oral and periodontal health (+general health)
• Record giving advice in patient’s notes (NB medico-legal reasons)
• You should explain poorer response to periodontal therapy
Give smoking cessation counselling


Toxic substrate smoking

• >4,000 reported toxic substances in cigarette smoke:
• 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 which measures exposure to tobacco smoke


nectrotising gingivitis

• 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


Stress as a risk factor

• Stress known to affect host immune response
Individual more susceptible to periodontal disease


effects of stress

• Behavioural changes
• Activation of biological system activation of Hypothalamic-Pituitary-Adrenal Axis increased circulating glucocorticoids and epinephrine levels in the body immune suppression – e.g. reduction in lymphocyte population, lymphocyte proliferation, natural killer cell activity and antibody production and re-activation of latent viral infections
• OR
Chronic state of inflammation through activation of macrophages, dendritic cells and endothelium Release of pro-inflammatory cytokines


correlation between stress and periodontal disease

• Correlation between periodontal disease and stress
• The effects of stress modified by the ability to cope
• Traumatic events, such as death of a spouse, increased the risk of periodontal disease but individuals with increased ability to cope with a stressful stimulus had reduced impact on the progression of periodontal disease (Hugoson et al, 2002)
Passive coping strategies associated with more pronounced perio disease with less disease and better treatment outcomes with active coping strategies (Wimmer et al, 2005)


define psychological stress

• Psychological stress can be defined as the physiological and psychological changes that occur in the body when an external demand or stressor taxes an individuals' adaptive capacity (Cohen S, 1995)
Psychological stress refers to the emotional and physiological reactions experienced when a person confronts a life event, such as marital conflict, financial debt or death of loved one, that exceeds his or her ability to cope effectively with the situation (Warren KR et al 2014)


What does stress induce

Stress induced response transmitted to the hypothalamus-pituitary-adrenal axis
Corticotrophin-releasing hormone (CRH) from pituitary
Glucocorticoids from adrenal cortex which decrease production of proinflammatory cytokines


Types of stress

• Disasters or Crises: e.g. major floods, earthquakes or wars
• Major life events: e.g. marital separation, imprisonment, death of a close family member
• Micro-stressors: e.g. daily hassles can have the same negative impact as any major stressful event – different for each individual
Also categorised as – acute stressor: short term and time limited events /chronic stressors: conditions that are long-lasting