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An examination of 5616 endodontically treated and retreated maxillary first and second molars was made in an attempt to determine the percentage of MB2 canals that could be located routinely, and evaluate if there were any significant differences between initial treatments and retreatments. The teeth examined were 3578 first molars and 2038 second molars treated consecutively over a 5-yr period by six endodontists. Overall the MB2 canal was found in 2133 (60%) first molars, and 712 (35%) second molars. The incidence of a MB2 canal in first molar retreatments was 66% compared to a 58% incidence in initial treatments. Whereas in second molars the retreatment incidence was 40% compared to 34% in initial treatments. The significant difference in the incidence of a MB2 canal between initial treatments and retreatments suggests that failure to find and treat existing MB2 canals will decrease the long-term prognosis.

An examination of 1873 conventionally treated and retreated maxillary first and second molars was made in an attempt to determine the percentage of second mesiobuccal (MB2) canals that could be located routinely and evaluate if there were any significant differences between initial treatments and retreatments. The teeth examined were 1193 first molars and 680 second molars treated consecutively over a 2-yr period by five endodontists. Overall the MB2 canal was found in 724 (61%) first molars and 245 (36%) second molars. The incidence of a MB2 canal in first molar retreatments was 67% compared to a 59% incidence in initial treatments. Whereas in second molars, the retreatment incidence was 44% compared with 35% in initial treatments. The significant difference in the incidence of a MB2 canal between initial treatments and retreatments suggests that failure to find and treat existing MB2 canals will decrease the long-term prognosis.

The tomosyn/Sro7 family is thought to play an important role in cell surface trafficking both as an effector of Rab family GTPases and as a regulator of plasma-membrane SNARE function. Recent work has determined the binding site of GTP-bound Sec4 on Sro7. Here we examine the effect of mutations in Sro7 that block Sec4 binding in determining the role of this interaction in Sro7 function. Using an in vitro vesicle:vesicle tethering assay, we find that most of Sro7’s ability to tether vesicles is blocked by mutations that disrupt binding to Sec4-GTP. Similarly, genetic analysis demonstrates that the interaction with Sec4 is important for most of Sro7’s functions in vivo. The interaction of Sro7 with Sec4 appears to be particularly important when exocyst function is compromised. This provides strong evidence that Sro7 and the exocyst act as dual effector pathways downstream of Sec4. We also demonstrate that Sro7 tethering requires the presence of Sec4 on both opposing membranes and that homo-oligomerization of Sro7 occurs during vesicle tethering. This suggests a simple model for Sro7 function as a Rab effector in tethering post-Golgi vesicles to the plasma membrane in a pathway parallel to that of the exocyst complex.