Some last minute questions

I've just been thinking about the types of questions that could be ask and that we've seen in those practice runs and I have a couple of queries (I'm probably just panicking now as the exam draws closer)....

Diabetes is a risk factor for chronic periodontitis. This seems like an obvious true at first, but then I was thinking it is a pretty broad statement, and that it really is uncontrolled diabetes that is the risk. So if this statement happened to be in the exam (probably too late for requests) would this be false??? I don't want to over think, but in those practice runs it was this kind of statement that tripped me up...

I was just wondering, how much do we need to know about the cells involved in gingivitis and perio?? Do we just need to know the properties and their role in the inflammatory response (eg PMN is a key cellular 'player' in chronic gingivitis in that through chemotaxis it is drawn to the area of attack where it kills bacteria via phagocytosis and cytotoxic products which also cause tissue destruction) or is there more we need to know? Also, with cytokines, do we need to know specific ones (eg Il-2, Il-8) and what they do or just generally know there are different cytokines that do different things at different times (that sounded really bad...)

Do we need to know %s of people who suffer from gingivitis or perio?? For epidemiology do we just need to know basic facts, study designs, tests, etc?

On the topic of tricky questions, much like the diabetes one, would a statement along the lines of: 'Gingivitis is a painful disease' be false, as chronic gingivitis is not painful, but acute forms are???

That'll be all for now I think, don't wanna confuse/worry people before the exam (too late for that probably!)

Tommorow's Exam

This is probably a stupid question, but I just wanted to clarify tomorrow's exam. Is it just on Modules 2 and 3, with assumed knowledge of Module 1? So therefore the topics we need to know about are:

-Gingivitis (etiology and pathogenesis)
-Treatment of Chronic Gingivitis
-Acute Gingivitis and Systemically Modified Forms of Gingivitis
-Risk Factors and Human Disease
-Risk Factors for Chronic Periodontitis
-Stress and Periodontal Disease

Good luck with the rest of your study guys =)

Last checkpoint for tomorrow

What effects does chronic gingivitis have on the blood vessels supplying the gingival tissues?
What are the causes of chronic gingivitis? What are some of the systemic conditoning factors? How are each of these causes managed?
What is the role of diabetes and periodontal conditions? How does diabetes affect the gingival tissues histologically?
Off you go team......
Sophie

Pathogenesis

Also, as far as pathogenesis is concerned make sure you know what the following are and what their role is:
Macrophages
cytokines- which ones are present where
osteoprotogerin
LPS
Prostaglandin E2
Sophie

Hi guys,

Do Ca channel blockers always cause gingival enlargement or does this only happen in some individuals, as dilantin only affected some individuals?

Thanks,

beth xxo

Have a go at these....

What are the causes of localised periodontitis?
What type of bone loss is associated with localised periodontitis?
What type of microbial flora is found in localised periodontitis?
Sophie

more questions..

to diagnose chronic perio, a series of radiographs needs to be taken over time(as we cant just diagnose from one).. just curious does anyone how often it would be recommended to take each OPG/radiograph? were we ever given a rough time(obviously it will depend onpatient factors etc) but is there an estimate time like every 1-2 years??

in the module-Dr Hirsch refers us to go read other texts(articles etc)..are these articles examinable..coz ill be honest.. i havn't accessed/read them and now im thinking i maybe should have.?? has anyone else looked into these??

with perio treatment(scaling).. this is a dumb questions btw.. so calculus isn't a causative factor for perio.. So the reason that we actually remove calculus and do cleans etc is due to the calc being good at retaining plaque and bacteria(that ARE neccessary causes for periodontitis), and also to increase the ability for the patient to self clean effectively.. Is this right.. just a random thought process in my head last night..

Localised perio..can this be chronic?? im not sure why but i just always thought that local perio was severe.. and i cant really find anywhere that indicates that it is chronic..(apart from the causes such as cracked teeth, fused roots that may not get picked up right away and therfore progress in a cyclickind of way?? also in the module it is talking about localised perio..then the next session is titled treatment of severe perio..so tome this indicates thatlocalised perio is severe?? clarification...........

Why are nightgurads useful therapy in perio?? he says to organise a nightguard sooner rather than later(if indicated) but what are the indications??

Do we need to know the historicla perio indexes( i have mainly focussed on how research is currently done and just briefly why the others weren't good ie.blocked gingivitis + perio, averaged scores for whole mouth etc)..is this basically the levelof detailwe need to know?

Ok.. once again thats it for now..
happy studies guys.. oh yea.. just quickly i found this on interleukins that may help..

iL-1, iL-6, iL-12 = pro-inflammatory cytokines(have slightly different functions for each, but basically are involved in increasing bone resorption and decreasing the bone formation(very basic detail)

iL-8=chemotactic function-target cell is the PMN..

iL-10, iL-13 = anti-inflammatory-increase the # of B-cells(which decreases inflammation response) and inhibits macrophages

prostoglandin E2=hormone like fattyacid that increases inflammation and bone resorption..
pg 47-48 text book. :D