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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
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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