Systemic Risk Factors Flashcards

1
Q

Statistics of smoking in uk

A

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

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2
Q

Nicotine and tobacco

A
  • 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
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3
Q

Smoking related diseases

A
  • 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
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4
Q

Smoking and periodontal diseases

A

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

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5
Q

Earlier studies showed that taboacco smokers had

A
  • 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
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6
Q

Epidemiology

A

• 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

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7
Q

Risk from smoking (classic studies)

A
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8
Q

Odds ratios for attachment and bone loss in light and heavy smokers

A
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9
Q

How many and how long?

Smoking correlation for periodontitis

A
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10
Q

Periodontitis and smoking

A
  • earlier onset
  • rapid disease progression
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11
Q

Clinical appearance

A
  • 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
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12
Q

Necrotising gingivitis

A

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

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13
Q

Toxic substances

A

• >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

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14
Q

Pathogenesis - what affects does smoking have in relation to the oral cavity?

A

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

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15
Q

Pathogenesis - what affects does smoking have overall?

A
  • Less gingival redness
  • Less bleeding on probing
  • Fewer vessels clinically and histologically
  • Healing response may be affected by impairment of revascularisation
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16
Q

Pathogenesis - evidence suggests?

A

• 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

17
Q

Microbiology

A

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

18
Q

Therapy for smokers

A

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

19
Q

Clinical implication of having a pt who smokes

A

• 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

20
Q

Smoking cessation - what are the time dependent changes in the periodontal tissue?

A

• 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)

21
Q

Key pillars of smoking cessation

A

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

22
Q

Smoking cessation study

A

• 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) !!

23
Q

E-CIGARETTES

A

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.

24
Q

What is another risk factor that affects periodontal disease?

A

Stress

25
Q

How does stress affect periodontal disease?

A

• Stress known to affect host immune response

• Individual more susceptible to periodontaldisease

26
Q

What is psychological stress?

A

• Psychological stress can be defined as the physiological and psychological changesthat occur in the body when an external demand or stressor taxes an individuals’adaptive capacity.

• Psychological stress refers to the emotional and physiological reactionsexperienced 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

27
Q

Types of physiological stresses

A

• 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 thesame negative impact as any major stressfulevent – different for each individual

• Also categorised as – acute stressor: short termand time limited events /chronic stressors: conditions that are long lasting

28
Q

How is stress induced response created?

A
  1. Stress induced response transmitted to the hypothalamus-pituitary-adrenal axis
  2. Corticotrophin-releasing hormone (CRH) from hypothalamus
  3. Adrenocorticotropic hormone (ACTH) from pituitary
  4. Glucocorticoids from adrenalcortex which decrease production of pro-inflammatory cytokines
29
Q

Effects of stress

A

• 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

30
Q

Smoking is a … for periodontal disease

A

Risk factor

31
Q

Smoking information and cessation advise are integral to a … for periodontal management but smoking cessation should also be addressed as a … for systemic disease by any healthcare worker

A

treatment plan

preventive strategy

32
Q

Nicotine affects body how

A

Antibody decrease \
Less fibroblast function
Reduces bone mineralisation

33
Q

Smoking effects on gingiva

A

Vasoconstriction of blood vessels

Hypoxia periodtonal tissue

Lack of micro circulation

34
Q

Going about smoking

A

Ask
Advise
Act

35
Q

After quitting smoking how long do gums take to heal

A

6 months