What is MTAD?
It is an irrigant consisting of tetracycline (to kill bacteria, so to speak), citric acid (to get rid of smear layer increasing the likelihood of killing bacteria), detergent (to reduce surface tension again increasing the likelihood of getting to bacteria in fin, ramification and all hard to reach region of the root canal system)
Why has MTAD been developed?
I guess it could have something to do with an ineffectiveness of current root canal disinfection protocol (instrumentation+0.5%NaOCL irrigation+EDTA+1wk of calcium hydroxide dressing) especially in retreatment of fail cases. A study has shown that with the above protocol, around 17% of their retreatment cases remained culture positive (Sundqvist et al. 1998). Another clinical study looked into the effects of instrumentation and 0.5% NaOCL on E. faecalis (Peciuliene et al. 2001) in retreatment cases. Despite the facts that 0.5%NaOCL is very effective in killing E. faecalis in vitro, this clinical study showed that 30% of the cases remained E. faecalis positive. It clearly demonstrated that 0.5%NaOCL cannot predictably eliminate E. faecalis clinically. This article also suggested that alternative irrigant in retreatment of a fail cases might be needed.
Also it could be a process gearing towards single-visit endodontics.
How should MTAD be used?
First as a replacement of current irrigating protocol (NaOCl+EDTA). Personally, I don’t think it should be used in this way for the simple reason that MTAD doesn’t have tissue dissolving property as NaOCl does.
Second MTAD can be used as an adjunct (as a final flush) additional to either NaOCl+EDTA or NaOCl alone. To me, this way is more logical. And I will explore further based on this premises, OK?
I’m trying not to muck around and just cut to the chase here.
Can MTAD improve treatment outcome?
Short answer would be “don’t know” long answer can be long……really long.
Logic
Now let’s look at it logically. Tetracycline is bacteriostatic meaning it only stops bacteria from growing but does not kill bacteria per se. It works as systemic antibiotic because body defense mechanism can get to bacteria and destroy it. Basically tetracycline helps tip the balance in favor of body immune response. However, in root canal, where immune system is in complete absence (necrotic->no blood supply->no defense mechanism), how can it kill bacteria????
Evidence
Now before any innovations (MTAD included) should be adopted, wouldn’t it be prudent (as a health care provider) to demand to see evidence showing their benefits?
High level evidence
Is there any clinical evidence showing improvement in treatment outcome because of MTAD? So far there’s none and I can tell you now that there will never be. In well executed endodontic treatment, the success (healing) rate is in the area of 90% (Friedman 2002). Suppose MTAD can improve healing rate to 95% (this considered to be very very small difference from epidemiological perspective). To show that it is significant statistically (at 80% power, p = 0.05), a sample size of 870 is required (Sokal & Rohlf 1995). I can tell you (again) that the trial of this size will extremely unlikely to be conducted in our field.
So where evidence does not exist and will never exist, should we be using that thing on our patients??
Low level evidence
There are plenty of laboratory studies around supporting the benefit of MTAD. Many studies showed a high smear layer removal property of MTAD (Torabinejad et al. 2003). I couldn’t care less if it removes smear layer. EDTA has done a great job with half the price (in fact it’s much less ;). Many showed other points (Machnick et al. 2003a, Machnick et al. 2003b, Park et al. 2004). Again I couldn’t care less if MTAD does any of those.
What I want to see (but haven’t seen so far) is that (NaOCl+MTAD) or (NaOCl+EDTA+MTAD) can reduce bacterial load to a greater extent than NaOCl+EDTA. Basically, even the low level evidence, it is still far from conclusive.
Conclusion
There’s nothing replacing high level of professionalism, accepting to nothing but the highest treatment standard and to persevere in cultivating the utmost clinical dexterity.
As I mention earlier, well-executed endodontic treatment has a very high healing rate. Technical quality of the treatment has, probably, much higher impact on treatment outcome than one single irrigant.
Unfortunately there’s no magic bullet or magic wand here.
References:
Friedman S (2002) Prognosis of initial endodontic therapy Endodontic Topics 2, 59-88.
Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003a) Effect of MTAD on flexural strength and modulus of elasticity of dentin J Endod 29, 747-50.
Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003b) Effect of MTAD on the bond strength to enamel and dentin J Endod 29, 818-21.
Park DS, Torabinejad M, Shabahang S (2004) The effect of MTAD on the coronal leakage of obturated root canals J Endod 30, 890-2.
Peciuliene V, Reynaud AH, Balciuniene I, Haapasalo M (2001) Isolation of yeasts and enteric bacteria in root-filled teeth with chronic apical periodontitis. International Endodontic Journal 34, 429-34.
Sokal RR, Rohlf FJ (1995) Biometry: the principles and practice of statistics in biological research, 3rd edn. New York: W.H. Freeman.
Sundqvist G, Figdor D, Persson S, Sjogren U (1998) Microbiologic analysis of teeth with failed endodontic treatment and the outcome of conservative re-treatment Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Endodontics 85, 86-93.
Torabinejad M, Cho Y, Khademi AA, Bakland LK, Shabahang S (2003) The effect of various concentrations of sodium hypochlorite on the ability of MTAD to remove the smear layer J Endod 29, 233-9.
It is an irrigant consisting of tetracycline (to kill bacteria, so to speak), citric acid (to get rid of smear layer increasing the likelihood of killing bacteria), detergent (to reduce surface tension again increasing the likelihood of getting to bacteria in fin, ramification and all hard to reach region of the root canal system)
Why has MTAD been developed?
I guess it could have something to do with an ineffectiveness of current root canal disinfection protocol (instrumentation+0.5%NaOCL irrigation+EDTA+1wk of calcium hydroxide dressing) especially in retreatment of fail cases. A study has shown that with the above protocol, around 17% of their retreatment cases remained culture positive (Sundqvist et al. 1998). Another clinical study looked into the effects of instrumentation and 0.5% NaOCL on E. faecalis (Peciuliene et al. 2001) in retreatment cases. Despite the facts that 0.5%NaOCL is very effective in killing E. faecalis in vitro, this clinical study showed that 30% of the cases remained E. faecalis positive. It clearly demonstrated that 0.5%NaOCL cannot predictably eliminate E. faecalis clinically. This article also suggested that alternative irrigant in retreatment of a fail cases might be needed.
Also it could be a process gearing towards single-visit endodontics.
How should MTAD be used?
First as a replacement of current irrigating protocol (NaOCl+EDTA). Personally, I don’t think it should be used in this way for the simple reason that MTAD doesn’t have tissue dissolving property as NaOCl does.
Second MTAD can be used as an adjunct (as a final flush) additional to either NaOCl+EDTA or NaOCl alone. To me, this way is more logical. And I will explore further based on this premises, OK?
I’m trying not to muck around and just cut to the chase here.
Can MTAD improve treatment outcome?
Short answer would be “don’t know” long answer can be long……really long.
Logic
Now let’s look at it logically. Tetracycline is bacteriostatic meaning it only stops bacteria from growing but does not kill bacteria per se. It works as systemic antibiotic because body defense mechanism can get to bacteria and destroy it. Basically tetracycline helps tip the balance in favor of body immune response. However, in root canal, where immune system is in complete absence (necrotic->no blood supply->no defense mechanism), how can it kill bacteria????
Evidence
Now before any innovations (MTAD included) should be adopted, wouldn’t it be prudent (as a health care provider) to demand to see evidence showing their benefits?
High level evidence
Is there any clinical evidence showing improvement in treatment outcome because of MTAD? So far there’s none and I can tell you now that there will never be. In well executed endodontic treatment, the success (healing) rate is in the area of 90% (Friedman 2002). Suppose MTAD can improve healing rate to 95% (this considered to be very very small difference from epidemiological perspective). To show that it is significant statistically (at 80% power, p = 0.05), a sample size of 870 is required (Sokal & Rohlf 1995). I can tell you (again) that the trial of this size will extremely unlikely to be conducted in our field.
So where evidence does not exist and will never exist, should we be using that thing on our patients??
Low level evidence
There are plenty of laboratory studies around supporting the benefit of MTAD. Many studies showed a high smear layer removal property of MTAD (Torabinejad et al. 2003). I couldn’t care less if it removes smear layer. EDTA has done a great job with half the price (in fact it’s much less ;). Many showed other points (Machnick et al. 2003a, Machnick et al. 2003b, Park et al. 2004). Again I couldn’t care less if MTAD does any of those.
What I want to see (but haven’t seen so far) is that (NaOCl+MTAD) or (NaOCl+EDTA+MTAD) can reduce bacterial load to a greater extent than NaOCl+EDTA. Basically, even the low level evidence, it is still far from conclusive.
Conclusion
There’s nothing replacing high level of professionalism, accepting to nothing but the highest treatment standard and to persevere in cultivating the utmost clinical dexterity.
As I mention earlier, well-executed endodontic treatment has a very high healing rate. Technical quality of the treatment has, probably, much higher impact on treatment outcome than one single irrigant.
Unfortunately there’s no magic bullet or magic wand here.
References:
Friedman S (2002) Prognosis of initial endodontic therapy Endodontic Topics 2, 59-88.
Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003a) Effect of MTAD on flexural strength and modulus of elasticity of dentin J Endod 29, 747-50.
Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003b) Effect of MTAD on the bond strength to enamel and dentin J Endod 29, 818-21.
Park DS, Torabinejad M, Shabahang S (2004) The effect of MTAD on the coronal leakage of obturated root canals J Endod 30, 890-2.
Peciuliene V, Reynaud AH, Balciuniene I, Haapasalo M (2001) Isolation of yeasts and enteric bacteria in root-filled teeth with chronic apical periodontitis. International Endodontic Journal 34, 429-34.
Sokal RR, Rohlf FJ (1995) Biometry: the principles and practice of statistics in biological research, 3rd edn. New York: W.H. Freeman.
Sundqvist G, Figdor D, Persson S, Sjogren U (1998) Microbiologic analysis of teeth with failed endodontic treatment and the outcome of conservative re-treatment Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Endodontics 85, 86-93.
Torabinejad M, Cho Y, Khademi AA, Bakland LK, Shabahang S (2003) The effect of various concentrations of sodium hypochlorite on the ability of MTAD to remove the smear layer J Endod 29, 233-9.
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