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

Question 1

What are the approaches to smoking cessation?

Answer 1

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

Question 2

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

Answer 2

• 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

Question 3

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

Answer 3

• 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

Question 4

Smoking staining, plaque and calculus

Answer 4

• 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

Question 5

Smoking and gingiva

Answer 5

• 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

Question 6

What are the biological effects of smoking?

Answer 6

• 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)

Question 7

Smoking and vascularity

Answer 7

• 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)

Question 8

smoking and inflammatory and immune response

Answer 8

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

Question 9

smoking and GCF

Answer 9

• 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

Question 10

smoking and subgingival plaque biofilm

Answer 10

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

Question 11

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

Answer 11

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

Question 12

Healing in smokers

Answer 12

• 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

Question 13

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

Answer 13

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

Question 14

What are genetic risk factors in periodontitis ?

Answer 14

• 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

Question 15

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

Answer 15

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