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
6 comments:
sorry.. just realised module 4 session 2 isn't epidemiology stuff. Its about disease activity(that he didn't cover in lect).. still tho.. how much detail dowe need to know from that seeing as he didn't even go over it ?? :D
1) CAL is measured from the CEJ to the end of the pocket. So basically recession + pocket depth.
2) Looking at session 2B it seems to be on diagnostic tests in perio. I think basically he wants us to know that you can't really test for perio cos no ideal test exists. Eg radiographs are good, but they are 2D images of a 3D structure and microbiological tests are pretty useless (cause-and-effect between specific bacteria hasn't been determined).
3) I think we just need to know that they act as programmers of the cell-mediated immune response (as they are T-cell lymphocytes)...but I'm not 100% sure...
4) Was this in one of the lectures, lol, cos i don't remember it. I agree though, it would be very cool
Hope this helps!
Hey tim.. i though PAL(periodontal atachment loss) was from CEJ to base of Pocket.. But i am reading about CAL( whichis clinical attachment loss) is that the same thing.. coz thats why i though it was recession coz it was clinical and i figured you can see that clinically?????
I think they're the same thing. Have a look at pg 171 of the textbook, it talks about the interpretation of pocket probing depths, it's really good. It says that Clinical Attachment Level (CAL) is from the CEJ to the PDL fibres (the point at which the probe tip stops).
Hey Nicole,
In regards to chronic inflammation asprins inhibition of the cyclooxygenase pathway and the subsequent reduction of prostaglandin synthesis would imply that hormones, such as interferon, are down-regulated and hence cell lysis (cell dying e.g. collateral damage) is reduced. Then strictly yes. However, ibuprofen would be considered more effective, especially if the person is on other anticoagulants. If there is no inflammatory processes then this wouldn't help.
hope this helps
Wow ... well done guys.. you have nailed it and worked out the answers to your questions!
http://www.perio.org/resources-products/posppr3-2.html#11
Have a look at these papers by American Association of periodontology.. easy to read summaries that put everything into context. Explore this site its excellent.
Arsenical paste is not something that hygienists use guys...
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
Happy discovery
Sophie
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