1. Is biofilm a risk factor for chronic periodontitis? Justify your answer.
How is ANUG treated?
2. What is considered to be the primary stress hormone?
3. Make a list of how smoking effects the periodontal tissues.
4. How long does it take for chronic gingivitis to heal after treatment?
5. Is CAL the same thing as recession?
6. Obesity is something we should look for when diagnosing perio. How is being obese associated with perio?
7. What are the causes of localised periodontitis?
8. What type of bone loss is associated with localised periodontitis?
9. What type of microbial flora is found in localised periodontitis?
These questions should stimulate some awesome discussion. Lets get going!!!
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ReplyDeleteTaken from Wilkins 2009. pg 506
Gingivitis
- inflammatory response to dental biofilm accumulation is reduced compared to non-smokers. [As smoking causes vasoconstriction]
Periodontitis
- smoking increases the rate and severity of perio destruction
- increases bone loss, attachment loss and pocket depths
- subgingival temp lowered
- lowers immune response (compromised number of PMNs) and delayed healing (vasocontriction)
- decresed chemotaxis and phagotocytosis
- altered anitoby production (IgG)
smoking also causes increased macrophage activity, and thus higher chance of endotoxin LPS causing macrophages to produce pro-inflammatory cytokines which contribute to periodontal breakdown.
ReplyDeleteCan anyone tell me what happens to the keratin layer in smokers? What implications does this have on oral health?
ReplyDeleteCorticotropin releasing hormone (CRH) is the primary stress hormone.
ReplyDeleteACTH - Stress hormones significantly interfere with wound healing.
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ReplyDeleteSmoking and Perio
ReplyDelete(systemic-effects)
*blood flow (acute vs chronic)
*impaired PMN chemotaxis & phagocytosis, (ascorbic acid depletion)
*alteration of immune function
*nicotine induces macrophages to produce large amounts of pro-inflammatory chemicals
*reduction in mineral content of skeletal bone
(Local effects)
*rapid mucosal absorption of nicotine contributes to its addictive nature
*binding of nicotine to tooth surface
*binding of nicotine by fibroblasts resulting in impaired function
*no consistent differences in periodontopathogens between smokers & non-smokers
Smoking can cause hyperkeratosis. This is the abnormal thickening of the keratin layer (stratum corneum) of the epithelium.
ReplyDeleteAlso! During an intra oral exam, the soft tissues would feel 'leathery', because of this.
ReplyDeleteGood work there guys. Renae, excellent response to keratin question. This is important to remember as reduced blood flow plus extra keratin contributes to the pale looking colour of the gingival tissues, masking signs of inflammation.
ReplyDeleteWhat happens with the keratin on the buccal mucosa as an example?
1) anug is treated through antibiotics, debridement, plaque control and if required CHX rinse.
ReplyDeleteAlso need to address influential factors. so look at OHI, smoking cessation, altering lifestyle factors (stress etc)
Some patient who have ANUG may have HIV, how would you address that factor?
ReplyDeleteGood question Renae
ReplyDeleteLets see what you guys come up with. Also, dont forget to look at what happens to the oral/buccal mucosa in smokers and what does this predispose them to?