more questions

only a few more questions now:
1:this is a silly question but so measuring periodontalpockets-we measure from the gingival margin to the base of the pocket.(is this base of the pocket also regarded as the alveolar crest?) coz i dont think it is??

2: the spread of inflammation-i know we alreadydiscussed but in summary can we say
collagen sackis damaged-Alveolar bone(as PDL has good resistance to inflammation) -then the PDL then apical migration of JE? coz this was in the modules but then on the next page it said the apical migration of JE occured after the collagen break down, which makes more sense??

ok thats all for now. THANKS!!

Furcation Involvement

Hi guys,

In mod 6 Session 1, i've got longer root trunk requires more attachment loss before the furcation becomes involved, so what does this mean in terms of perio? So are molars with longer roots at less risk of furcation involvement? So 6's would be at less risk compared to 7's because of their longer roots?

I recall a tricky question about this in the revision session and Sophie provided us with an explanation but can't remember the explanation itself..

Thanks guys.

Last few thoughts

1. What is Prostaglandin E2 and what role does it play in perio disease?
2. How do Macrophages control the activity of fibroblasts and lymphocytes?
3. Does the incidence of advanced periodontitis differs in developed and developing countries?
4. Discuss the design of gracey curets and their working angle.
Go for it!!!

HELP..

Whyam i the only one asking all these questions?? not very comforting.. lol
anyways i have a few questions that i nede some clarification with
1: IS stress a risk factor for ANUG.. I think yes but some notes i found in my last sem revision stuff has made me second guess myself?

2. with medication induced gingival overgrowth-does this only occur due to hypoplasia of the tisues or is it also associated with inflammation?

3. Does ANUG cause bone loss. coz i didn't think it did but once again i found a question in last sem notes that has that it does cause bone loss.. I thought ANUG doesnt but ANUP does.

Hopefully others are having more luck studying..I am seriously loosing concentration knowing we are so close to finishing for the year and my brain is just not working..
THANKS for the help team.. someone post some questions so im not the only one. :P

More perio FUN!

1) is ACTH and CRH the same thing(main stress hormones)

2)This one may be for Sophie, or if anyone else wants to answer go for it
but say we have a patient that is new to our clinic but they have previously had periodontal treatment at another clinic and we have the notes of their pocket depths etc and they had moderate generalised perio as thier diagnosis, and we are seeing them say 2 years after their initial perio exam(coz they had to go away and travel for work but they maintained good oral health habits etc) adn we do thier charts and theyhave no new pockets and no gingival inflammation and they bone loss has not increased any more... But they still have their original moderate bone loss.. Do we say their diagnosis is still moderate generalised perio(even though its not progressing atthat time??)
I know we cant measure activity of perio via diagnostic tests etc and so im guessing we would just say moderate generalised perio but i justwanted some clarification
(hope my little scanario makes sense):D

3) can we use Azithromycin to treat ANUG

4) is localised periodontitis always agressive??

How does inflammation of the gingival tissues spread to the underlying periodontal structures?

What are LPSs and what role do they play in periodontal pathogenesis?

perio questions

hey guys a few questions thathave popped up during my revision that i hope u can help me out with.
1) in the margins of my page i had written GTR(guided tissue regeneration) and that it is best in class 2 defect(furcations) however im not really sure what it is,what this refers to and if it is relevent.. others opinoin or notes on this would be great

2)accessory canals in furcations. do accessory canals increase the chance of endo-perio lesions occuring. As Hirsch said i think last semester-endoperio can occur anywhere along the root surface so is this due to accesory canals??

3)I had in my notes also this. Cytokines in smoking are those associated with bone destruction(PGE-2) and not the ones associated with.......... ( i didn't get this last bit and i was hoping someone may have also copied down this sentence with the last part)

4) in perio modules Hirsch refers to 4a's for smoking, but we kow there are 5a's.I was just wondering for like this exam do we justassume there is only 4 as' thathe mentions and then in practice follow 5a principles?? i dunno just thought a question might pop up like( there are 4a's to help with smoking cessation) and i would be like ummmmm well... lol..
THANKS guys.
im sure i will have more eventually

Smoking

Does smoking change the nature of the biofilm?

Lets start blogging

1. Differential Diagnosis

Ok guys, we have not really spent much time on differential diagnosis.
Can someone have a go at discussing the process of differential diagnosis if a patient presented with a condition that seemed a little out of the ordinary. What steps would you follow and why?

2. Pathogenesis

What is collagenase and where does it come from and what role does it play?

What is LPS, where does it originated from and what are its effects?

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.