Periodontal disease and systemic risk factors session 2 - part 1 patient case Flashcards

1
Q

What are the approaches to smoking cessation?

A
  • pre-contemplators (not interested)
  • Contemplators (interested unready)
  • Active quitters (making an attempt)
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2
Q

What are the 5 A’s Approach (brief intervention)

A
  • Ask: about the smoking use status
  • Advise: about the advantages and value of stopping
  • Assess: how motivated a patient is to stop
  • Assist: those who wish to stop
  • Arrange: monitoring, follow-up and referral
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3
Q

If your patients do not want to stop smoking use the following:

A
  • Relevance: of smoking to the individual
  • Risks: associated with smoking
  • Rewards: of cessation to be stressed
  • Road Blocks: must be identified
  • Repetition: repeat at each consultation
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4
Q

Smoking staining, plaque and calculus

A
  • smoking causes increased salivary flow rate as a response to the irritant particulate matter in smoke
  • Increased parotid flow has raised pH, raised calcium concentration and raised precipitation of calcium phosphate thus calculus deposition occurs
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5
Q

Smoking and gingiva

A
  • results in a reduced inflammatory response and vascularity which can make the gingiva appear healthy, even though there is significant active periodontal disease present
  • smoking is a risk factor for necrotising gingivitis
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6
Q

What are the biological effects of smoking?

A
  • Smoking causes widespread negative effects on the periodontium tissues including:
  • reduced vascularity
  • reduced inflammatory and immune responses
  • more pathogenic plaque biofilm
  • direct toxic effects on various cell types e.g. fibroblasts
  • thermal damage (especially if reverse smoking)
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7
Q

Smoking and vascularity

A
  • From studies nicotine causes little vasoconstriction of periodontal blood vessels
  • smoking actually impairs the vaculature of periodontal tissues
  • the reduced vaculature results in less gingival redness, less bleeding on probing and fewer vessels visible both clinically and histologically in smokers
  • these vascular changes may also have to be part of the reason why smokers have poorer gingival healing. Think of the potential impairment of revacularisation
  • After stopping smoking there is a rapid recovery of both the inflammatory response and vascularity of the periodontal tissues (rebound effect)
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8
Q

smoking and inflammatory and immune response

A

there are higher levels of matrix metalloproteinases (MMPs- collagenases) and prostaglandin E2 (PGE2) which cause tissue breakdown, if smokers compared to non-smokers

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9
Q

smoking and GCF

A
  • smokers have lower resting gingival crevicular fluid
  • reduced GCF flow in smokers results in several negative effects:
  • reduces the ability of immunoglobulins and other defense molecules to reach the periodontal pocket
  • reduces the flushing out of the gingival crevice/periodontal pocket which helps to remove bacteria and their waste
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10
Q

smoking and subgingival plaque biofilm

A

recent studies have shown that periodontal healthy smokers (pocket depths less than 4mm) have subgingival plaque biofilms which are significantly different from healthy non-smokers. In smokers the biofilm is more with higher levels of pathogenic species and is more anaerobic in nature

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11
Q

In non smokers pocket depth reduction following PMPR is due to 3 factors:

A
  • reduction in inflammatory swelling
  • improved tissue resistance
  • small possible gain in attachment
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12
Q

Healing in smokers

A
  • inflammatory swelling makes up less of the pocket depth. the reduction of inflammatory swelling following treatment contribute as much to pocket depth reduction in smokers
  • healing is further impaired in smokers due to lower numbers of fibroblast reduced epithelial cell function, in addition to the reduced host response reduced vacularity
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13
Q

How do u assess the patient’s genetic susceptibility to periodontitis

A
  • Extent of previous periodontal disease (bone loss/loss of attachment possibly level of bop)
  • age
  • level of oral hygiene
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14
Q

What are genetic risk factors in periodontitis ?

A
  • Genetics is an important determinant in individual susceptibility for periodontitis
  • No single genetic change is fully responsible for determining genetic response of periodontitis
  • Natural variations within the structure of genes (polymorphisms) results in altered protein production
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15
Q

What are examples of periodontitis as a manifestation of systemic disease?

A
  • Down’s syndrome
  • Papillon-Lefevre syndrome
  • Chediak-Higashi syndrome
  • Ehlers-Danlos syndrome
  • Hypophosphatasia
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