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

Round 2.....

Ok.
have started reading over notes again.. and here are the strats of my questions:
1: Fenestrations are anatomical defects in bone..(windows) but they shouldn't technically cause any clinical problems(perio pocket readings) unless they are close to the alveolar crest.. Is this correct??
2:Is a dental abscess the same as a periodontal abscess.??? as it says that inflammatory causes of perio can be caused by retrograde perio;dental abscess and then below that it says periodontal abscess is another cause..???

3: and lastely.. one of the few questions that i am sure i got from in todays exam... Module 4 says that obesity is something we should look for when diagnosing perio...bu can someone explain to me... How is being obese associated with perio??? coz all ican think of is that it mayyyyyy possibly lead to increase in diabetes risk???

OKthats all for now Dont worry..guaranteed there will be more.

exam time

Hi Sophie..Just clarifying exam time.. On access adelaide/in your email it says 1:50, but on the blog you said 1:20?

Azithromycin

just a clarification:

Azithromycin is used totreat ANUG (along with metranidazole, and Amoxil) and is used in generalised perio...Is it also used in localized perio???coz in the notes in orange book it says it is used in severe perio-but doesn't actually specify localised/generalised

a few simple questions

Hey hey.. and as we get closer :S
I have a couple of quick questions
in perio and gingivitis..the gingival fibre netwrok is NOT comletely destroyed right?? And so, it isn't destroyed but does affect the contour and consistency.. Ohh and if it was completely destroyed then you wouldn't be able to get healing??? Is this right--sorry just my thought processes all coming out now..

2)what is epithelial attachment( i know i should know this..sorry Sophie im sure your shaking your head). I just need it clarified coz once again have confused myself. :D
Thanks guys..

Modules 4&5

1)is CAL the same thing as recession?
2) when discussing generalised/localised.. Does this refer to ><30% of the whole mouth, or just the arch, as gingivitis and perio can both differ in patterns between and within arches?
3)Module 4, Session 2 epidemiology stuff... How much detail do we need to know(i havetaken the basic principles from it, but do we need to learn % and history etc??
4)Th1 & Th2 cells. functionof each as iam getting contrdictions form notes and textbook about which one does which, or do we just need to know that theyare involved in the anti-inflammatory response??
5) when talking about aspirin and NSAID supressing prostyglandins.. does this mean that essentially aspirin could be used to assist in reducing the bone loss is perio??(Coz that would be cool :D)
6)sophie-question for you.. Dr Hirsch talked about use of an Arsenical paste to reduce pain for patients if they have had an endo-perio lesion-is this something that as hygienists we could do if a patient came in with pain? or was this something that was meant for the dental students?

and just for a hint pg 66 of textbook had a nice little summary of perio/gingivitis that i think just made it come together a bit for me.So maybe have a read if you all like.:D
THANKS

Perio Modules 2 &3

Hey guys..
i justhave a few Questions that i got a bit confued with today...hopefully you guys can shine some light on these for me!!
1)so with chronic gingivitis-it says that there is no loss of CT attachment but only migration of JE-so, does this mean that pocket readings that can be obtained are due to pseudopockets??like from the inflammation..Or are they actually classed as perio pockets...?? if this question confuses anyone.. ignore it, coz i think i am just confusing myself..

2)What is inflammatory infiltrate? i just thought it was lots of inflammatory cells?is this right?

3)ANUG-text book says it is very rarely generalised, however the notes(in module)say that it can occur either localised or generlaised-with very severe cases often being associated with some bone loss?? Is this what others found as well..
Maybe sophie you could clarify the localised/generalized bit??

4)notes says chronic gingivitis has a cause effect relation ship with plaque- thats fine.. But then further in-the notes say that chronic diseases are not associated with cause-effect and that they are multifactorial??? Confused??
Is this just because gingivitis is really a 'disease'as such but more an inflammatory reaction???

and last one-Module 2, sesion 3 pg 25- my box for ANUG/ANUP and ANUG/HIV is blank-- did i miss something here or did he skip this stuff??

THANKS GUYS!!

More revision questions...

1. 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?
See how you go....

Sophie

Here's the first question for perio revision.

Is biofilm a risk factor for chronic periodontitis? Justify your answer.