Del Valle-Jasso L., Nieto-Aguilar R., Serrato-Ochoa D. 2012. El stripping dental.

Dent. 24; 34-9.

Del Valle-Jasso L., Nieto-Aguilar R., Serrato-Ochoa D. 2012. El stripping dental

en ortodoncia. 1ª. Edición. Editorial Panamericana. México.

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:

 Loss of inert, fully reacted surface enamel.

 Exposure of more reactive enamel surfaces to remineralization.

 The creation of surface porosities that result in an increased surface area for
interaction with preventive and remineralizing agents.

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

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