**Bisphosphonate Induced Osteonecrosis of the Jaw**

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zoralsurgeon

noegruslaroz
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Hello,

I am a Sr. undergrad student entering DS in the fall. I'm in a biology seminar capstone course in which I have to write a 30 page paper and give an hour lecture. I am currently writing my 30 page paper (yes, reading lots of info. from Marx!) on Osteonecrosis of the Jaw and making revisions as we speak.

I was wondering if someone could please help me out!!

1.) During treatment of ONJ are patients normally taken off of the BPs when prescribed the chlorhexidine rinse, antibiotics, and/or surgery?? (I am assuming so?)

2.) For treatment of metabolic bone diseases like Osteoporosis and Paget's disease, why do we use BPs (drugs that inhibit osteoclasts) rather than a drug that would do the opposite - activate more osteoblasts...?

3.) Other than the high bone turnover rates in the maxilla and mandible as Marx shows vs. a tibia, why are the maxilla and mandible prime locations for the onset of ONJ? Much of the research I've found shows that dental extractions, implants, trauma, etc. lead to ONJ in maxillofacial region...any take on this?

4.) Can ONJ develop if no bone is exposed in mouth?

5.) Obviously, mandible and maxilla are composed of very strong, spongy, trabecular bone...which is an area of high bone turnover...why do osteoclasts break down so much bone in the maxilla and mandible?? Is it because the stress put on it all the time from chewing?? Plz. explain!

Any assistance would be GREATLY appreciated 🙂

-Z
 
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During treatment of ONJ are patients normally taken off of the BPs when prescribed the chlorhexidine rinse, antibiotics, and/or surgery?? (I am assuming so?)

-Z

Look at the half life of the oral and/or IV bisphosphs and you'll have your answer. It's not like taking aspirin.
 
Look at the half life of the oral and/or IV bisphosphs and you'll have your answer. It's not like taking aspirin.

Okay great, so it depends on the specific BP, gotcha. Nitrogen containing have longer half-lives...okay. makes sense.

Any idea on the second question I have? Why do we use BPs as drugs that inhibit osteoclast bone resorption rather than use drugs that activate the proliferation and formation of osteoblasts?! Do these drugs even exist?! Any ideas!?!
 
dentists don't typically prescribe bisphosphonates. for this question you would need to check the medical forums.
 
Okay great, so it depends on the specific BP, gotcha. Nitrogen containing have longer half-lives...okay. makes sense.

Any idea on the second question I have? Why do we use BPs as drugs that inhibit osteoclast bone resorption rather than use drugs that activate the proliferation and formation of osteoblasts?! Do these drugs even exist?! Any ideas!?!

That's an awesome question! I'd love to know the answer. Does it have to do with preventing uncontrolled osteoblast differentiation and bone generation? I would suspect it would be more difficult to control creation of new bone than it would be to reduce destruction of existing bone... could be that simple.
 
Remember that osteoclast formation is a secondary product of osteoblast formation via the RANK/RANKL system, so a downstream effect of generating more osteoblasts would be a large increase in osteoclast formation.

Stimulating osteoblast proliferation would only work if you also inhibited osteoclast differentiation, but if that's the case, why not just inhibit osteoclast differentiation only?
 
haha, very true. makes a lot of sense actually!

Any idea on the other questions!?

Remember that osteoclast formation is a secondary product of osteoblast formation via the RANK/RANKL system, so a downstream effect of generating more osteoblasts would be a large increase in osteoclast formation.

Stimulating osteoblast proliferation would only work if you also inhibited osteoclast differentiation, but if that's the case, why not just inhibit osteoclast differentiation only?
 
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