I would add to what you said that the time it takes to develop a problem depends where the MB2 joins with MB1. If it joins very close to the apex the time needed to develop a problem is shorter. Also the severity of the problem depends really on how big of a bacteria reservoir is the MB2. The bigger the reservoir the bigger the problem. Someone mentioned about finding the MB2. As a general practitioner I can honestly say it’s not easy. I use 3.5x loupes and sometimes it’s easy and sometimes it’s impossible without larger magnification. The fact of the matter is that you need very good eye of sight in order to find MB2, besides proper technique and files.
Buy some 6.5 loupes and that should help. I definitely feel more confident treating the mandibular molars rather than max molar. If you don’t find mb2 you definitely always wonder if you might have missed it. Even a middle mesial and second distal is way easier to find than mb2.
Also about mb2 what is difficult is that insurances pay low rates and expect fast results. I assume you would run your practice differently if your price lists were 50% , 25% ,10% of your current price (you get the point ). I had a 26 a few weeks ago and I tried my best to find the mb2 but I could not. Most Rct - dentists that I know of who work with these insurances complain they do not find mb2 often.
There's no question practitioners are not compensated enough for the complexity of a root canal procedure; but I'm sure it's ethical in anyway to think that leaving 1/4 of the infection tissue behind is legitimate because of insurance. This is something that our organizing bodies should do a better job explaining to insurance companies. Furthermore, if people don't have the tooth tools, time, and expertise to find all the canals, then it makes sense to me to refer or provide more predictable care by acquiring the skills through deliberate practice on extracted teeth, etc.
I agree... but unfortunately cost and access to this technology is not that easy... therefore, it can not yet be considered Standard of Care. But it's definitely excellence of care.
Why some of those cases with missed MB2s stay asymptomatic until a restorative dentist like myself decides to put a crown on the uncrowned molar or replace an existing crown due to open contacts for example. The MB2 flares up after being asymptomatic for years and the patient might end up blaming the restorative dentist for that.
I'm not sure one can blame the restorative dentist for it. If the tooth was out of occlusion putting it in occlusion will certainly bring to attention a chronic apical infection that was previously not poked. Now, if the restorative dentist replaces the core and gets into the chamber or places a post before the crown, then yes, contaminating likely occurred during reaccessing the core. Posts placed without a rubber dam result into five times more failure than posts placed under complete aseptic technique and under a rubber dam based on one study.
@@kavityphiller4891 yes, there’s no question high occlusion can cause symptoms; but so can an untreated MB2. You only have to look at CBCT of 100 cases with these symptoms after treatment to see how many of them actually have periapical radiolucencies and untreated canals that one can not see in the straight up PA radiograph. Again, it’s not an either or.. both can be true in their own situation. Cheers!
Albeit rare, you also see cases where either hyper plastic pulpits, or even furcal/lateral canal exists keep the rest of the pulp vital. But arrested caries are different concept.
Thanks for sharing mentor ...I have few questions please ! In vital cases where Mb2 has a separate Exit will it fail by time if untreated ? What is the fate of the vital pulp left in Mb2 ? Can bacteria in untreated Mb2 leak through a well treated Mb1 obturated with bc sealer & gutta-percha ? Thanks
Yes, if the vital tissue in MB2 that joins MB1 is cut off from circulation it will clearly go necrotic. If necrosis is sterile and no microbes are around, then it will simply a pulpless tooth; but if the pulp dies and there's any microbes around (the more likely scenario) the necrotic tissue will get infected and it the microbes will have enough substrate to work their way up slowly and contaminate the space once again. If you are in that 25% where you have a separate exit then it will work like a pulpotomy. It may or may not survive, once again, based on how much contamination is present. Of course, this problem doesn't happen regularly or else we would have a lot of problems with MB roots and molars; but it happens enough in the long run where many of these teeth end up having an issue downstream. CBCT imaging is very helpful in knowing what's going on and which ones are accessible and which ones are not. A microscope is really necessary for the best outcome. Best wishes.
@@AANasseh thank you for your reply It's a near 8 minutes video but made lots of questions pop ups in my mind ... again I understood that even with bc sealer it will leak by time if a Necrotic or even vital Mb2 was untreated & joining Mb1 ? Correct ? In the video you said it's Asymptomatic most of the time why ? Thanks
@@minamoheb9793 That’s a long answer that has to do with the genetic profile of each of us as it relates to our immune system and it’s unique response to microbes. There’s a whole world of understanding between the systemic response to microbes that runs parallel to the mechanical aspects of clinical work. This would require its own video. Maybe one of these days I would do something on that. 👍
Great video. As a general dentist doing 380 rct per year it’s very hard to find MB2 without a microscope. Does a microscope help finding it? Could you show some cases where it took you time to find it so I use that as a road map? I use ESX system what file system is more flexible for calcified and curved canals. Thank you Dr
It's very difficult to capture the actual time it takes to find the MB2 and it's also super boring to watch! LOL! That's why most videos are edited so the procedure is shorter... but this my not be able idea to make a video to show real time how long does it take. About your file system, ESX is a great system... I would continue using it but add two specific files to your armamentarium for those tougher type of cases. I would add the EndoSequence Scout size 17/06 and EndoSequence Scout 17/04 (or alternatively 15/04). You can use those files to create a path for yourself that then the ESX will complete the shaping for. That's pretty much the basis of the EndoSequence Blend protocol that Dr. Koch and I developed. Cheers! :)
i enjoy your channel! and now my dilemma: i don't do a lot of endo's but usually every 2 weeks an upper molar. i use the DOM for one year and still it takes a lot of time and patience for me personally to locate,acces the first 3mm, and then get to lenght+shape. it usually takes for me at least 30 minutes but mostly 50min only for mb2. is it ok for a beginner like me in using DOM to have such long treatment time for an mb2? thank you a lot Doctor!
Hi! No. My treatments take about 30minutes of clinical work in molars. I schedule one hour but that's mostly anesthesia and connecting and explaining to the patient. I think the best way to improve your MB2 finding skills is to make it a practice of having a bunch of extracted first/second molars available and then starting to section or access them anytime you find a down time or if a patient cancels. This will only help improve your skills under the scope and what you should look for. Furthermore, you want to make your mistakes on extracted teeth where you can learn the most rather than real teeth.
@@AANasseh thank you alot for your response! I will do as you said and trying to improve my instrumentation technique! I though I was doing something wrong!
@@cosminhuplea5694 You're not doing anything wrong. You just don' know ugh now when is the time to stop and how fast can you get to the point where you stop. In order to do that you need more understanding of the root anatomy and location of the MB2 which you will really no gain unless you do a good 30 exacted upper molars! I know it's boring as hell but it will make you better for sure! Good luck! :)
Sorry, I must say that there is very strong evidence over multiple studies that caries under a well sealed restoration is fully arrested- nothing happens “over time”- This is a very pervasive myth among dentists- now, there are still tons of great reasons to fully remove all the caries- we know that it can be tough to verify for 100% certainty that a restoration is fully sealed when there are any less than ideal conditions - ie a huge percentage of cases
Unfortunately this is merely a theory. It is not proven by any level of certainty that you are proposing. There are scientists on both sides of this issue with valid points. As an Endodontist who has done a lot of endos, I can’t tell you how often I go into these symptomatic cases after a restoration only to find remaining Caries. If Carie’s would stop under a good restoration then there’s would be no need for endo. I. Fact, there would be no endo or endo failure if you simply sealed the top. This is obviously an incorrect assumption since plenty of endo cases fail despite excellent restorations that are well sealed on top (such as excellent cast p/cores and crowns with endo lesions. There’s plenty of collagenases produced by certain microbes that can provide slow growth and spread of the microbes. It’s not as fast but the idea that merely covering the decay will necessarily kill the microbes stands in face of clinical reality. It would be good to interview a good microbiologist in this area. Thanks for bringing up the subject matter! :) 👍
I respect your opinion and experience- thanks for the reply- I do find the studies pretty convincing but am totally open to the fact that, well, I could be wrong (as I have been before!)_. If you have any interest, I can send you a couple links to the studies- but your point is very well taken: biological systems, bacterial populations etc are complex and difficult to predict- the best thing, usually, is to remove all the - short of that, yes, use sdf etc
@@kavityphiller4891 It's entirely possible that some caries composition can be decimated by coverage; but it's also possible that different caries compositions behave differently. We currently have a poor understanding of the variety of biome in caries and how it actually manifests in terms of clinical symptoms and outcomes. We're actually currently doing a clinical research project at our school (Harvard PG Endo) where we are collecting caries samples in symptomatic and asymptomatic irreversible pulpitis caused by caries and will be doing DNA Checkerboard hybridization to find the composition of the microbes between these two groups. We're trying to see if there's a difference, which will potentially indicate the presence or absence of symptoms associated with different lesions. It's a promising idea that can hopefully start an area of investigation where very little is known. You would think this is already done but there's very little research in this area. Cheers! :)
I would add to what you said that the time it takes to develop a problem depends where the MB2 joins with MB1. If it joins very close to the apex the time needed to develop a problem is shorter.
Also the severity of the problem depends really on how big of a bacteria reservoir is the MB2. The bigger the reservoir the bigger the problem.
Someone mentioned about finding the MB2. As a general practitioner I can honestly say it’s not easy. I use 3.5x loupes and sometimes it’s easy and sometimes it’s impossible without larger magnification. The fact of the matter is that you need very good eye of sight in order to find MB2, besides proper technique and files.
I agree with that. There are way too many factors involved in decision making here. Cheers!
Buy some 6.5 loupes and that should help. I definitely feel more confident treating the mandibular molars rather than max molar. If you don’t find mb2 you definitely always wonder if you might have missed it. Even a middle mesial and second distal is way easier to find than mb2.
@@celts03 I didn't know 6.5x loupes are available. Will check into that.
Valuable doubt answered 👍
My first 1st view on this channel
Legend
Also about mb2 what is difficult is that insurances pay low rates and expect fast results. I assume you would run your practice differently if your price lists were 50% , 25% ,10% of your current price (you get the point ). I had a 26 a few weeks ago and I tried my best to find the mb2 but I could not. Most Rct - dentists that I know of who work with these insurances complain they do not find mb2 often.
There's no question practitioners are not compensated enough for the complexity of a root canal procedure; but I'm sure it's ethical in anyway to think that leaving 1/4 of the infection tissue behind is legitimate because of insurance. This is something that our organizing bodies should do a better job explaining to insurance companies. Furthermore, if people don't have the tooth tools, time, and expertise to find all the canals, then it makes sense to me to refer or provide more predictable care by acquiring the skills through deliberate practice on extracted teeth, etc.
It really should just be standard of care for every tooth to get CBCT image prior to tx. No more guess work
I agree... but unfortunately cost and access to this technology is not that easy... therefore, it can not yet be considered Standard of Care. But it's definitely excellence of care.
thanks for sharing!
I m finding mb2 canals in almost every molars... But without magnification my eyes are really stressed out now...
thaxxx
Why some of those cases with missed MB2s stay asymptomatic until a restorative dentist like myself decides to put a crown on the uncrowned molar or replace an existing crown due to open contacts for example. The MB2 flares up after being asymptomatic for years and the patient might end up blaming the restorative dentist for that.
I'm not sure one can blame the restorative dentist for it. If the tooth was out of occlusion putting it in occlusion will certainly bring to attention a chronic apical infection that was previously not poked. Now, if the restorative dentist replaces the core and gets into the chamber or places a post before the crown, then yes, contaminating likely occurred during reaccessing the core. Posts placed without a rubber dam result into five times more failure than posts placed under complete aseptic technique and under a rubber dam based on one study.
Or the occlusion on the crown is a smidge high, results in trauma to the pdl, restorative dentist thinks “oh, this must be a flare up of mb2”-
@@kavityphiller4891 yes, there’s no question high occlusion can cause symptoms; but so can an untreated MB2. You only have to look at CBCT of 100 cases with these symptoms after treatment to see how many of them actually have periapical radiolucencies and untreated canals that one can not see in the straight up PA radiograph.
Again, it’s not an either or.. both can be true in their own situation. Cheers!
Weird to compare it to Caries bc there is arrested Caries
Albeit rare, you also see cases where either hyper plastic pulpits, or even furcal/lateral canal exists keep the rest of the pulp vital. But arrested caries are different concept.
Thanks for sharing mentor ...I have few questions please !
In vital cases where Mb2 has a separate Exit will it fail by time if untreated ? What is the fate of the vital pulp left in Mb2 ?
Can bacteria in untreated Mb2 leak through a well treated Mb1 obturated with bc sealer & gutta-percha ?
Thanks
Yes, if the vital tissue in MB2 that joins MB1 is cut off from circulation it will clearly go necrotic. If necrosis is sterile and no microbes are around, then it will simply a pulpless tooth; but if the pulp dies and there's any microbes around (the more likely scenario) the necrotic tissue will get infected and it the microbes will have enough substrate to work their way up slowly and contaminate the space once again. If you are in that 25% where you have a separate exit then it will work like a pulpotomy. It may or may not survive, once again, based on how much contamination is present. Of course, this problem doesn't happen regularly or else we would have a lot of problems with MB roots and molars; but it happens enough in the long run where many of these teeth end up having an issue downstream. CBCT imaging is very helpful in knowing what's going on and which ones are accessible and which ones are not. A microscope is really necessary for the best outcome. Best wishes.
@@AANasseh thank you for your reply
It's a near 8 minutes video but made lots of questions pop ups in my mind ... again I understood that even with bc sealer it will leak by time if a Necrotic or even vital Mb2 was untreated & joining Mb1 ? Correct ?
In the video you said it's Asymptomatic most of the time why ?
Thanks
@@minamoheb9793 That’s a long answer that has to do with the genetic profile of each of us as it relates to our immune system and it’s unique response to microbes. There’s a whole world of understanding between the systemic response to microbes that runs parallel to the mechanical aspects of clinical work. This would require its own video. Maybe one of these days I would do something on that. 👍
Great video. As a general dentist doing 380 rct per year it’s very hard to find MB2 without a microscope. Does a microscope help finding it? Could you show some cases where it took you time to find it so I use that as a road map? I use ESX system what file system is more flexible for calcified and curved canals. Thank you Dr
It's very difficult to capture the actual time it takes to find the MB2 and it's also super boring to watch! LOL! That's why most videos are edited so the procedure is shorter... but this my not be able idea to make a video to show real time how long does it take. About your file system, ESX is a great system... I would continue using it but add two specific files to your armamentarium for those tougher type of cases. I would add the EndoSequence Scout size 17/06 and EndoSequence Scout 17/04 (or alternatively 15/04). You can use those files to create a path for yourself that then the ESX will complete the shaping for. That's pretty much the basis of the EndoSequence Blend protocol that Dr. Koch and I developed. Cheers! :)
i enjoy your channel! and now my dilemma: i don't do a lot of endo's but usually every 2 weeks an upper molar. i use the DOM for one year and still it takes a lot of time and patience for me personally to locate,acces the first 3mm, and then get to lenght+shape. it usually takes for me at least 30 minutes but mostly 50min only for mb2. is it ok for a beginner like me in using DOM to have such long treatment time for an mb2? thank you a lot Doctor!
Hi! No. My treatments take about 30minutes of clinical work in molars. I schedule one hour but that's mostly anesthesia and connecting and explaining to the patient. I think the best way to improve your MB2 finding skills is to make it a practice of having a bunch of extracted first/second molars available and then starting to section or access them anytime you find a down time or if a patient cancels. This will only help improve your skills under the scope and what you should look for. Furthermore, you want to make your mistakes on extracted teeth where you can learn the most rather than real teeth.
@@AANasseh thank you alot for your response! I will do as you said and trying to improve my instrumentation technique! I though I was doing something wrong!
@@cosminhuplea5694 You're not doing anything wrong. You just don' know ugh now when is the time to stop and how fast can you get to the point where you stop. In order to do that you need more understanding of the root anatomy and location of the MB2 which you will really no gain unless you do a good 30 exacted upper molars! I know it's boring as hell but it will make you better for sure! Good luck! :)
Sorry, I must say that there is very strong evidence over multiple studies that caries under a well sealed restoration is fully arrested- nothing happens “over time”- This is a very pervasive myth among dentists- now, there are still tons of great reasons to fully remove all the caries- we know that it can be tough to verify for 100% certainty that a restoration is fully sealed when there are any less than ideal conditions - ie a huge percentage of cases
Unfortunately this is merely a theory. It is not proven by any level of certainty that you are proposing. There are scientists on both sides of this issue with valid points. As an Endodontist who has done a lot of endos, I can’t tell you how often I go into these symptomatic cases after a restoration only to find remaining Caries. If Carie’s would stop under a good restoration then there’s would be no need for endo. I. Fact, there would be no endo or endo failure if you simply sealed the top. This is obviously an incorrect assumption since plenty of endo cases fail despite excellent restorations that are well sealed on top (such as excellent cast p/cores and crowns with endo lesions. There’s plenty of collagenases produced by certain microbes that can provide slow growth and spread of the microbes. It’s not as fast but the idea that merely covering the decay will necessarily kill the microbes stands in face of clinical reality.
It would be good to interview a good microbiologist in this area. Thanks for bringing up the subject matter! :) 👍
I respect your opinion and experience- thanks for the reply- I do find the studies pretty convincing but am totally open to the fact that, well, I could be wrong (as I have been before!)_. If you have any interest, I can send you a couple links to the studies- but your point is very well taken: biological systems, bacterial populations etc are complex and difficult to predict- the best thing, usually, is to remove all the - short of that, yes, use sdf etc
@@kavityphiller4891 It's entirely possible that some caries composition can be decimated by coverage; but it's also possible that different caries compositions behave differently. We currently have a poor understanding of the variety of biome in caries and how it actually manifests in terms of clinical symptoms and outcomes. We're actually currently doing a clinical research project at our school (Harvard PG Endo) where we are collecting caries samples in symptomatic and asymptomatic irreversible pulpitis caused by caries and will be doing DNA Checkerboard hybridization to find the composition of the microbes between these two groups. We're trying to see if there's a difference, which will potentially indicate the presence or absence of symptoms associated with different lesions. It's a promising idea that can hopefully start an area of investigation where very little is known. You would think this is already done but there's very little research in this area. Cheers! :)