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The greater context of the following is derived from an article was published in the Journal of Clinical Orthodontics, 31:9, 1997. This article has been reproduced here with the permission of its author, John J. Sheridan DDS, MSD.
THE PHYSIOLOGIC RATIONALE OF AIR-ROTOR STRIPPING (ARS)
About fifteen years ago bonding replaced banding as a method of attaching orthodontic appliances to teeth. This development created a window of opportunity because the proximal surfaces of posterior teeth were no longer covered with metal bands. They were visible, approachable, and therefore strippable. Air-rotor stripping (the sequential removal of buccal section interproximal enamel) is possible because of this development. It allows the access necessary to slightly reduce the formidable enamel bulks that constitute the interdental buccal section contact points 40.
ARS was described in 1985 1. Subsequent literature and encouraging clinical observations have contributed to its accelerating acceptance 2-9. However, when there's reticence to adopt ARS, other than picking up a handpiece, it may be based on the assumption that stripping proximal enamel surfaces may provoke pathology. I will argue that dental tissues respond to the physiological trigger of interproximal abrasion by non-pathological adaptation, and an ARS site is feasibly more resistant to carious and periodontal disease than unaltered enamel.
Proximal stripping has been described in the literature for decades 10-13. There has been speculation that pathology could be induced but, that's as far as it ever gets, i.e., no verification, observation or data. However, there is a physiologic rationale for ARS and it's centered in the defining principals of inquiry: the valid observations and corroborative data that are evident in the literature of orthodontics, anthropology, periodontology and cariology.
ANTHROPOLOGY
An acceptable capsulation of the massive anthropological data on interdental abrasion is that it's a natural process correlated with diet and lifestyle and compensated by mechanisms not unlike the damage control efficiency of an immune system, i.e. thicker enamel bulks on surfaces prone to abrasion, secondary dentin, and passive eruption. These processes worked symbiotically for millions of years within thousands of cultures, collectively establishing the immediate, and compelling processes that are on-call to compensate the abrasive dynamics of the chewing system. These phenomena, although atavistic, are as evident in contemporary populations as they were to Paleolithic savages 20-23.
It's tempting to extrapolate the observations of anthropology into justification for ARS, but the flaw is obvious. This convenient simplicity begs the question of whether the positive response of dental tissue to natural abrasion, occurring slowly in primitive societies, gives license to the immediacy of ARS and cold rotating steel. Although ARS is not equitable with abrasive diets and vigorous mastication, the end results are essentially the same: interdental tissue reduction; alteration of tooth size ratios; broadening of contact areas; and enamel surfaces that are more amenable to the hardening process of remineralization 24,25,33,39. The point of contention is whether these ARS effects mimic nature or do they bypass natural protective processes. Corroborative data is necessary to sort this out.
PERIODONTAL IMPLICATIONS
If the closure of a 1.0mm ARS space is periodontally suspect, then closing minor naturally occurring posterior spaces must also be judged suspicious, because the effect is the same: crestal bone and interdental soft tissues are orthodontically compressed. Clinicians routinely close naturally occurring minor posterior spaces without thought of inducing pathology because tissue adapts to the attenuated space. This is natures way; physiological adaptation to environmental change. To exclude interdental medullary bone, the most adaptive in the body is at odds with even the most rudimentary appreciation of bone biology 18-19.
Older periodontal studies presumed, without data, that compressing the interradicular tissue could be a precursor of periodontal distress 26-28. Uncritical acceptance of these remarks is no longer appropriate. Alveolar bone will, of course, be compressed as the interradicular spaces become narrower due to the reduction of enamel. However, there's no compelling evidence linking this with disease 16,17,29,30. Conversely, greater, rather than lesser, interproximal spaces may grease the rails of the pathological express.
Tal 17, measured horizontal bone destruction by laying flaps on anterior and posterior teeth. He reported that intrabony pockets were less common when interproximal distances decreased, and more common when the distance between adjacent teeth increased. He stated "The correlation between the interproximal distance and the presence of intraboney pockets was positive and statistically significant." That is, the smaller the distance the less the predilection for intraboney pockets, and the larger the distance the greater the tendency for intraboney pockets.
Heins, Thomas, and Newton 16 amplified Tal's work. Measuring horizontal, and vertical bony defects on posterior teeth, they came to the same conclusion, stating "No findings supported the contention that bone in narrow interradicular spaces is at great risk" and this was in presence of periodontal disease. Also, "Data indicate that some wider, rather than narrow, interradicular spaces may be more likely to experience bone loss."
Heins and Weider 30, working in the heart of ARS country with second premolar-first molar and first molar-second molar interproximal spaces, found that bone was apparent and healthy when root surfaces were as close as 0.3 mm. When root surfaces were closer, interproximal bone was not observed. Even then, the roots shared a common periodontal ligament in the fenestration, established by the absence of bone, was non-pathological in nature or inference. This study indicates the robust adaptability of supporting structures to even the most minimal interradicular space.
If periodontal distress is induced, by compressing interdental tissues, then there must be a specific interdental distance, or at least a range, that cannot be violated. I am not aware of any controlled study that defines these parameters. If this supposedly critical distance is not defined, how can it possibly be argued that it cannot be modified Especially, when there is countering, amplified data to the contrary. From aforementioned citations it was shown that Tal 17, and Heins, Thomas, and Newton 16 provided data that indicate narrower interdental spaces show less disease potential in the presence of pathology. While Heins and Weider 30 provide data for physiological adaptation to attenuated space in the absence of pathology.
Periodontal disease is age related and primarily correlated with the presence of plaque, not the effects of reduced interdental tissue or altered contact points 14,15,35-37. Nevertheless, any stripping system, including ARS, generates some degree of abrasive grooves on the enamel surface that could feasibility induce plaque accumulation in these declivities. The feasibility is there but we must appraise the literature to determine the actuality
IMPLICATIONS FOR CARIES SUSCEPTIBILITY
Radlanski et al. 31 examined posterior interdental enamel after ARS, and reported that furrows, resulting from the stripping, caused increased plaque accumulation that could not be removed by flossing. Their conclusions, based on scanning electron micrographs, presumed a possible carious effect of ARS. However, their findings indicated that it could occur, not that it did occur.
In a follow-up study, the same prime authors 7 reversed their original conclusions--they recanted. Stating, "Even though plaque accumulation would be expected, the SEM analysis revealed no incidence of caries in the artificially produced furrows. Therefore, interdental stripping can be considered a reasonable therapeutic technique, especially if care is taken to avoid abrasion in more gingivally located enamel."
El-Mangoury et al. 6 a team consisting of four Ph.D's in the biological sciences, working specifically with ARS sites, reported that "Posterior interproximal enamel reduction does not appear to expose the enamel to pathological changes that could lead to caries, but to a period of demineralization, followed by remineralization." And, "The roughness produced by ARS does not predispose to caries." Also, "The results of this study establish a sound biological foundation for Sheridan's air rotor stripping technique."
Brudevold 25 reported that smooth surface enamel abrasion initially causes rapid demineralization. This, in turn, opens nucleation sites for accelerated remineralization. Within minutes salivary buffers are neutralizing the abraded site, and remineralization, the healing and fortifying process, can begin within one hour. When complete, the remineralized enamel face is more resistant to acid (carious) attack. He stated "The rapid rate of the initial phase of intraoral mineralization [due to mechanical abrasion] reveals a powerful mechanism for protecting the dentition against demineralization." These observations were due to:
Hanachi 39 working with iodide ion penetration technology, recorded the differential balance on enamel cycled through demineralizing and then remineralizing media. He compared this data to unstripped controls cycled in similar fashion. His results amplified Brudevold's work; stripped enamel surfaces have more potential for remineralization [hardening] than unaltered controls.
A recent in vitro report reported that ARS initially induces excessive demineralization with an implication that caries will be induced 32. The essential balancing factor of remineralization was inexplicably ignored. This must be defined, because demineralization cannot be evaluated in isolation. It's a physiologic impossibility in the oral cavity. Repeated documentation by contemporary cariologists indicate that it's the balance between demineralization and remineralization on abraded surfaces that must be appraised, because that is the reality 29,33,34. More demineralization, potential for pathology; more remineralization, potential for stronger enamel surfaces.
Nevertheless, the newly developed safe-tipped stripping burs preclude inadvertent scaring of the enamel, and ultra-fine finishing burs can reduce interproximal ridges and grooves, induced by ARS, to 15 microns . Radlanski found that function will reduce them even further 7. Therefore, the stripped interproximal enamel texture approaches that of unaltered surfaces.
CONCLUSION
Correlating Air-rotor stripping with pathology is, at best, arguable. Even so, compared with the only other options for moderate crowding (> 10.0 mm) extraction or expansion, ARS is a sensible treatment option. Electing to expand teeth into the harsh environs of cortical plate is a dubious option to closing minor ARS spaces within the vascular fecundity of medullary bone 18,37,38. If, expansion is contemplated, judicious ARS could, at least, reduce the amount needed to compensate crowding.
ARS does not eliminate the rationale for removing teeth. I believe the extraction of teeth is necessary to compensate severe crowding. However, ARS may be more applicable for the resolution of moderate crowding.
ARS is not a technique that circumvents the need to study, to think, to assimilate, and to develop judgment. It requires adherence to the discipline of published guidelines involving: limiting interdental reduction to 1mm/contact point; measuring and charting the accruing space; paralleling of enamel walls; finishing proximal walls as smoothly as possible; contouring to resemble original morphology; and above all, adherence to the criteria of well-finished cases.
There is a natural reluctance to venture beyond the coziness of familiar expertise and risk making celebrated blunders. This haunting prospect looms especially distressing in orthodontics where mastery of detail is so highly prized. However, ARS is no longer untested. It has been validated in the clinic, examined in the literature, and appears to be a sensible treatment option.
John J. Sheridan DDS, MSD
Professor of Orthodontics
LSU School of Dentistry
REFERENCES
