Historical review and rationale for corticotomy-accelerated tooth movement

Europe is the birthplace of corticotomy-related surgeries. In 1931, Bichlmayr introduced a surgical technique for rapid correction of severe maxillary protrusion with orthodontic appliances. Wedges of bone were first removed to reduce the volume of bone through which the roots of the maxillary anterior teeth would need to be retracted. In 1959, Köle expanded on this philosophy by addressing additional movements, including space closure and crossbite correction. Similar to the method of Bichlmayr, a reduction in bone thickness was often used. Major movements were corrected in 6 to 12 weeks without significant apical root resorption. Some of Köle’s surgical preparations resulted in the appearance of outlined blocks of bone; when taken in conjunction with his incorrect assumption that the mineralized bone was moving with the roots of the teeth, others deemed the mechanism “bony block” (tooth-bone unit) movement. Consequently, corticotomy surgery evolved mostly into circumscribing cuts, and bone thinning was deemphasized, thus leading to almost 4 decades of confusion concerning the correct mechanism of facilitated movement.

Interestingly, in 1987, Rynearson demonstrated in nonhuman primates that the cortical plates in corticotomized maxillary second premolars did not move during space closing. The misconception of “bony block” movement prevailed, however, until 2001, when Wilcko et al reported that a surface-computed tomographic evaluation of corticotomized patients clearly showed a transient localized demineralization-remineralization process consistent with the accelerated wound-healing pattern of the regional acceleratory phenomenon. The apparent demineralization of the alveolar bone over the buccal and lingual root prominences left a collagenous soft-tissue matrix of bone, which was carried with the root surfaces (bone matrix transportation) and then remineralized in retention. The remineralization was fairly complete in adolescent patients, but in adults only partial remineralization of the soft-tissue matrix was observed. Therefore, in adults there was a net loss in bone volume with lingering labial and lingual dehiscences that had still not resolved after 11.5 years of retention.

As early as 1965, many effects of regional acceleratory phenomenon were introduced by Kolǎŕ et al. It was not until 1983, however, that Frost introduced the regional acceleratory phenomenon as an operational entity to clinicians. In 1994, Yaffe et al were the first to report a robust regional acceleratory phenomenon response in the jawbones of rats by merely reflecting and replacing mucoperiosteal flaps. In 2007, Sebaoun et al reported that intramarrow penetrations in rats resulted in a transient demineralization-remineralization process and increased bone turnover. In 2011, Baloul et al reported on tooth movement in rats after intramarrow penetrations. In the mesial movement of maxillary first molars, the total displacement in the selective alveolar decortication plus tooth movement group was 6.94 mm compared with 5.3 mm for the traditional orthodontic group. The corticotomized teeth showed only a 24% increase in the distance of tooth movement. We suggest that an even greater differential in the amount of tooth movement would have been realized if a different morphologic situation had been provided (a thin layer of bone in the direction of movement) in addition to the regional acceleratory phenomenon.

When closing extraction spaces, our findings agree with those of Iino et al and Gantes et al. If space closure is performed at first premolar sites with only circumscribing corticotomy cuts or with inadequate bone thinning such as partial ostectomies, the space closure can take 7 or more months to complete. This can result in total treatment times expanding to a year or longer. However, if the bone is thinned adequately in the direction of the intended tooth movement, premolar site closure can be accomplished in 3 to 4 weeks with orthopedic forces or in 6 to 8 weeks with lighter orthodontic forces. With the proper surgical technique, these space-closing cases can be routinely completed in 8 to 10 months or less. If orthopedic appliances are used for space closing or other movements, it is advisable to wait 3 to 4 weeks after surgery before activating them to allow the thinned bone to demineralize. All indications are that a coupled bone remodeling response is taking place, but with a thin layer of activated bone, the rate of demineralization will outweigh the rate of remineralization, and the demineralized bone matrix can be sustained with continued tooth movement.

Excessive root resorption does not appear to have been an issue with corticotomy-facilitated orthodontics. Because of the demineralized state of the bone during treatment and the fact that normal orthodontic forces are used, rapid movement occurs from the lack of osseous resistance and not from excessive orthodontic force. In an evaluation of maxillary central incisors, the findings of Machado et al would actually indicate a slight (1.1 mm) decrease in apical root resorption. This decrease might not be clinically significant, but at least it is reassuring to know that rapid tooth movement after corticotomy surgery will not result in increased root resorption. Iino et al have additionally demonstrated decreased hyalinization of the periodontal ligament in corticotomized dogs, and it is well known that hyalinization can be a precursor to root resorption.

Rothe et al reported that patients with thinner mandibular cortices are at increased risk for dental relapse, and this could certainly be used as one argument for increasing the alveolar volume. Additionally, we suggest that increased alveolar volume could increase the probability of maintaining attachment levels, especially when there is a discrepancy involving a wide root and a narrow alveolus. It will not provide for improved attachment levels. Clinicians must also be aware that if there is preexisting bone loss from periodontal disease, corticotomy surgery becomes pocket reduction surgery, and the teeth will appear longer commensurate with the degree of preexisting bone and attachment loss regardless of whether alveolar augmentation is performed.

There are limitations to what corticotomy-facilitated orthodontics can offer. We do not represent that ankylosed teeth can be reliably moved nor can teeth be moved through devitalized bone, a situation that can occur in conjunction with long-term cortical steroid or bisphosphonate therapy. Corticotomy-facilitated tooth movement is a periodontal ligament-mediated sterile inflammatory process, so the use of nonsteroidal anti-inflammatory drugs will reduce the inflammatory response and therefore tend to counteract the regional acceleratory phenomenon effect. Since its benefits and capabilities are impressive, doctors sometimes think of periodontally accelerated osteogenic orthodontics when nothing else works. This is not a rescue technique but, rather, a tool to be used with knowledgeable thought and design.

Many surgical and nonsurgical methods and devices are being used and represented to accelerate tooth movement. Each might have its merits, but in the absence of correct surgical intervention, these can only provide a degree of the regional acceleratory phenomenon. Accelerated movements require both physiologic and morphologic issues to be addressed. However, inadequate decortication techniques do not create the robust regional acceleratory phenomenon needed for many accelerated movements, and they actually reduce the amount of bone support by the nature of the procedure. An important aspect of the periodontally accelerated osteogenic orthodontics technique, in addition to shortened treatment times, is the ability to address alveolar insufficiencies with bone augmentation to increase the likelihood of creating intact buccal and lingual plates of bone.