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?