Comparisons of radiographs taken by different methods - panoramic compared with periapical views and even periapical views compared with other periapical views - is notoriously misleading, since the angle of the x-ray cone is not standardized and movement of the teeth may well be more virtual than actual. From the series of views that you have illustrated, I see little or no movement in either tooth.
As far as my July 2013 bulletin is concerned, I do believe that both canines have undergone 'pre-eruptive intracoronal resorption', and it is entirely possible that this was due to the 2006 trauma. As I wrote in the bulletin, it is generally believed (but not certain) that the resorptive initiation is through an enamel defect in the crown formation which, when it occurs (which is rarely), it is likely to affect the tips of the crowns of permanent canines - as we see here and as I illustrated in the bulletin. Having noted that, does it stop eruption? Apparently not, at least not in my limited experience. Furthermore, having surgically exposed the tooth, the lifeline of the lesion will have been interrupted but closing off the surgical wound completely, without at least filling the resorbed area, will then likely re-ignite the resorption process. This means that the resorption process may still be eating away at the inside of the crown of the tooth. However, it is unlikely to affect the dental pulp - as explained in the bulletin.
From the orthodontic point of view, space has been provided adequately for both teeth and traction has clearly been applied with little complexity. Furthermore, the direction of traction appears to have been correct.
 
So, in the absence of any other explanation why the teeth have not moved, I have to go with the idea that 'pre-eruptive intracoronal resorption' may indeed prevent movement. That being the case, we now have to look at September's renewed exposure adventure a little differently. I use the word adventure, because the entire raison d'etre or modus vivendi of the advice here is based on this questionable assumption.
My advice to the surgeon, therefore, is as follows:-
1. expose the two canines, check the adequacy of the bond and remove any adhesions of tissue (possibly scar tissue) from the crowns of the teeth, but not to extend the exposure into the CEJ area, at the join between crown and root.
2. identify and superficially clean the mush from the resorbed area of the crown - but not to extend the cavity excavation deeper. Most important: absolutely to leave the deeper area of mush untouched, for fear of exposing the vital pulp. Restore the crown with composite material, to seal off the cavity from the surrounding tissues. While I have no problem with the surgeon checking for mobility of the tooth at this stage, I would argue strongly against his/her pushing elevators down the PDL along the root surface, since this will almost certainly cause an ankylosis, if not already present (there are no signs at present).
3. re-suture the full flap back into place. As the orthodontist, I would want to be present at the surgery, to apply immediate traction to both teeth simultaneously, as before, using vertical intermaxillary elastics to support the anchorage and, thereby, avoid intrusion of adjacent teeth.
4. Depending on the method of traction and its power range will depend how frequently Sam should be seen and you should be guided by the orthodontist in this.
5. I would expect to see positive results within 3-4 months. If nothing happens, then the teeth should be extracted.....in which case, I would like you to have them photographed and sent to me (please!) - or, better still, place them in formalin and send them to me for further examination. If they do move, please tell me. It may help someone else, since I will have learned something new!

Whether or not the resorption has stopped in the interim between 2012 and 2013 is irrelevant. The teeth are not erupting and need to be treated one way or another (i.e. extracted or erupted). I am not aware of a lesion like this ceasing its progressive destruction without outside intervention - which means cutting off its nutrient supply line. If the resorption has indeed stopped, the reason could be that the surgical exposure achieved this. As I noted earlier, by re-covering the tissues over the exposed crown, the likelihood is that the nutrient supply line will have been re-established and the progress merely temporarily interrupted and then renewed with healing. Alternatively, the lesion may have been permanently arrested, in which case its resorptive tissue will have become replaced by the surrounding connective tissue. In the absence of a follicle and with connective tissue in direct contact with the dentine, I do not know whether the tooth will respond to orthodontic traction, but probably not. Accordingly, as I see it, logic would suggest surgical re-exposure of the tooth and covering the affected part of the crown with an inert dental restoration (e.g. glass ionomer) in order to separate it from the surrounding connective tissue. This could probably be done in a closed eruption procedure, but preferably, in an open one and then to reapply orthodontic  traction.

The crown resorption that has occurred is due to clastic cells whose origin is the PDL and not the pulp. I see it as analogous in virtually every detail to invasive cervical root resorption (ICRR) that we published in the Angle Orthodontist earlier this year (Becker A, Abramovitz I, Chaushu S. Failure of treatment of impacted canines associated with invasive cervical root resorption. Angle Orthodontist, 2013,83:870-876) and was the subject of our presentation at the AAO meeting in Hawaii last year (it's on the disk from the meeting). Additionally, pre-eruptive crown resorption was the subject of the July 2013 Bulletin on my website at
http://www.dr-adrianbecker.com/page.php?pageId=273
This is not caries, but resorption. According to the research (see list of refs in that article), it attacks the body of the dentine but stops short at the predentine, which has a much higher organic content and probably does not actually get through to expose the pulp. The diagnosis that there is an open connection was presumably made radiographically, which must be viewed with some suspicion. If the resorption mush is cleared away meticulously, as if it were caries, instrumentation will certainly push through the predentine layer. Cutting off the lesion by minimal mush removal and sealing it off (with the deeper mush still inside) with glass ionomer or other filling material, will effectively stop the resorption by starvation - since its nourishment comes from the PDL and not from the pulp. According to the same research (and again relying on the high degree of similarity between this form of crown resorption and ICRR), in advanced stages, bone is deposited in the lesion (see list of references in the article) and I would hazard an informed guess that this is the factor that stops the tooth from responding to extrusive forces - as in a pure ankylosis.
For these reasons, I have recommended surgery to expose the teeth and to seal off the lesions and then to try again. If I am right, the teeth should respond to well directed traction. Once the teeth erupt, then endo can be done under ideal conditions - if it is required for reasons of retention of a crown. Leaving the mush in place and properly sealed, it should not cause a pulpal reaction during this entire period, because it is sterile, uninfected, and now non-progressive. It is not caries and it should not be treated as such, because it contains no bacteria and therefore it does not generate pulp inflammation. 
It is entirely possible that my conclusions are not as well founded as I like to believe, but these points represent my line of thinking and are the basis for the recommendations that I made in my correspondence