1. Macrophages are bone resorbing cells- i'm thinking true because macrophages
produce pro-inflamm cytokines that resorb bone but unsure if they resorb bone
themselves?
2. LPS is a cytokine- i'm thinking false, they are part of the cell wall of
gram -ve bacteria that stimulate macrophages to produce cytokines but once
again a little unsure.
3. localised periodontitis is treated with azithromycin- unsure about this one
cause if it is chronic then the answer would be false but if it is an agressive
form it could be true with additional perio therapy of course??
4. Is the JE the same as the epithelial attachment? - False, it is apart of it
(the part that attaches to the tooth) but it is not the same??
Lastly the wording of this question really confuses me- is there a linear
association between localised bone loss and tooth mobility? True?
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Here are my answers not entirely sure if theyre correct or not :S
1. macrophages are related to osteoclastic activity however are not immediately involved in bone resorption. Macrophages stimulate the release of pro-inflammatory cytokines which in turn activate T-cells (lymphocytes). T-cells then release RANKL (another cytokine) which attaches onto the pre-osteoclast and helps the formation of the complete osteoclast.
2. LSP isn't a cytokine. LSP or lipopolysaccharide is part of the cell wall of gram negative bacteria which activate both PMNs (the 1st line of defence) and Macrophages (2nd line of defence)
3. All I know that Dr Hirsch has said in regards to the usage of Azithromycin is that it is used in place of tetracyclines. Tetracyclines are used in the position of Amoxil if the patient is allergic to Penicillin
4. I don't think JE is the same as epithelial attachment. They are part of the same group of connective tissues that attaches to the tooth etc. However JE has a different responsibility as the JE is basically in my thinking the gateway for bacterial components to infiltrate into the tissues as well as the exit through which PMNs exit to pallisade over the biofilm bacteria.
5. I think the question is asking; is the relationship between local bone loss and tooth mobility in direct relation to one another. I would though the answer would be false as a patient could have 12mm of recession yet still maintain a non-mobile tooth. I'm quite sure Dr Hirsch has said that a few times in our 2nd and 3rd year notes.
I agree more or less with rob. 1) a macrophage is a pre-osteoclast.. osteoclasts are bone resprobing cells, which are dervived from macrophages, but for marcophaes to resorb bone they need RANKL and all that jazz.. and so marcophages are NOT bone resboring cells.. the are precursors to bone resorbing cells; oesteoclasts.
2. LPS is NOT a cytokine. cytokines are chemicals released by cells which allow them to communicate. LPS on the other hand is an endotoxin found on the cell walls of gram negative bacteria. it is not 'released'.
3. localised periodontitis is generally a chronic disease as it is caused by such things as cracks in the tooth, periapical abcesses... so i would say no. AB's are only used for agressive forms. I would treat first by subging scaling etc around the localised pocket and use ChX gel..
4. The epithelial attachment is NOT the same as the JE. the epithelial attachment is only one small part of the JE. It kind of like saying my finger is the same as my whole body.. it is not... it is part of my whole body... if this makes sense...
5. a linear association referres to 'as the amount of bone loss increases so does the mobility of the tooth'. This is false. e.g. localised attachment down one side of the tooth, if a tooth is ankylosed in one part but there is bone loss in others..if someone knocks their front tooth and it becomes mobile it is mobile without htere being any bone loss.. etc etc.
Hope this helps
I agree with the previous posts. But please note this is only my opinion. I could be wrong.
Questions 2, 4 and 5 are definately false in my opinion.
1. Whilst I believe the proinflammatory affects of macrophages can cause resorbtion of tissue, including bone, I don't think you can class it specifically as a bone resorbing cell (I think that title belongs to osteoclasts alone).
3. Azithromycin is an antibiotic. Antibiotics are only indicated in severe agressive periodontal disease. If the localised perio is the result of an anatomical defect or fracture, antibiotics would not help much. If it is due to Retrograde periodontitis or abscess, antibiotics may be indicated (in conjunction with possible endo therapy or extraction). ANUP may also require antibiotics.
Hope this helps. Again, just my opinion.
All very good answers and well thought out.
With regard to macrophages - both osteoclasts and macrophages are derived from monocytes. Macrophages are not bone resorbing cells, but the enzymes they release in response to inflammation do cause bone resorption.
We have a detailed earlier post on the Epithelial attachment vs the Junctional Epithelium so could you all please refresh your memory to get that one clear in your heads.
Just thought I would add that...
In chronic gingivitis the inflammatory cells are essentially protecive, however due to enzyme activity (collagenase), destruction of collagen cells does occur adjacent to JE. Check out MODULE 2, session 1, page 7, there is an excellent explanation. cheers
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