ETIOLOGIES FOR FAILURE
Fifty-seven out of 63 research studies2 on this topic concluded that overfills are an etiology for endodontic treatment failure. But again, this does not square with decades of clinical experience and literally millions of root canal procedures done in that time by clinicians who prefer a reasonable amount of surplus to any under-filled canal space. If we think about it a bit, it does seem odd that despite research findings that gutta-percha and most sealers are relatively biocompatible,3-5 we blame these materials for inciting persistent inflammation and infection.6 Did we miss the turn, with our eyes riveted on the obvious and embarrassing evidence of our less-than-perfect control of the case—the overfill—because we have no way to clinically assess the cause of the crash? Did we mistake coincidence for etiology?
One of dentistry’s premier leaders on microbiology in endodontics, Dr. Sjögren7 brought the controversy closer to a realistic clinical answer to the question of etiology with his classic study that clearly correlated the presence of infection with the outcome of the therapy. He showed that fewer en-dodontic treatments were successful when periapical pathosis was seen preoperatively (86%), than when there were no periapical lesions seen preoperatively (96%). Further-more, he showed that the apical level of root filling had no significant influence on the outcome of treatment when previously root-filled teeth with periapical lesions were retreated.
So it’s not the surplus filling material that causes failure, it’s the bacteria. This should not be a surprise, since we know that dental decay and pulp death only occurs in the presence of bacteria.So far, so good. But now consider Sjögren’s other important finding: the apparent disconnect between the apical extent of obturation and success. The conclusion drawn from that finding was that it doesn’t improve clinical outcomes to fill the entire root canal system.
There lies the real watershed—the continental divide—in our specialty. Because of Sjögren’s paper and his observation that the apical extent of obturation is not a predictor of success in the retreatment of infected root canals (as evidenced by the periapical lesion), the majority of clinicians at that time were convinced that it didn’t matter if you treated root canal systems to their full apical and lateral extents. And, as a result, single-cone and cold lateral condensation obturation were viewed to be as effective as any of the methods were more 3-dimensional, specifically those involving condensing heat-softened gutta-percha.
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