The Alveolus Bone Is Not a Process

Recent revelations in the literature about OTE suggest that knowledge of the alveolus bone has suffered greatly from two major misconceptions. First, it is not a process. A bony process, like the zygomatic or mastoid, is a projection of a larger body for muscle attachment or mechanical advantage. So, physiology of an anatomical “process” should be identical to that of its basal bone. But the alveolus bone is somewhat independent of the maxillary or mandibular corpus in origin, function, and fate. In congenital anodontia, it is absent, and its behavior reflects that of the tooth roots, not the subjacent corpi.

In dentistry, since the term “process” has been used for centuries, it is naturally assumed to be a structural and behavioral extension of the basal bone, i.e., maxillary or mandibular body. But observing the absence of alveolus in congenital anodontia one must logically question the legitimacy of that term. Thus, we propose it be referred to as simply “the alveolus.” The alveolus bone is developmentally, structurally, and functionally unique, similar to and contiguous with the underlying body of bone. But it is neither anatomically continuous nor physiologically identical.

The alveolus bone lives, thrives, and dies by virtue of root positions.

If we posit that arch length deficiency (crowding) reflects ectopic eruption and the alveolus bone emerges only upon tooth eruption, then logically the teeth are not erupting ectopically because of a “small bone.” The opposite is true: the bone is small because the teeth are crowded. Since the bone development will “follow” the root to some degree, we posit that one should evaluate potential space (available space) by measuring the circumference of the labial alveolus rather than relying on mere visual inspection or adding the sums of mesiodistal widths of teeth.

The second major misconception about the alveolus is that its form, its phenotype, is immutable and thus, risks dehiscence when arches are expanded. Our experience with the alveolus bone suggests that it its not immutable; it is in fact, under the right conditions, very malleable and invites expansion to accommodate an entire natural dentition.

Epigenetics and the Waddington Landscape

In 1957, Conrad Waddington, a biologist and polymath, described mammalian development as unidirectional,³ which means that embryonic stem cells develop into a more mature differentiated state. Explaining interruptions in the developmental expression of the genotype, he drew a “developmental landscape” (Figure 1.2).

Waddington’s Epigenetic Landscape (Figure 1.2) is a visual metaphor showing how stem cell differentiation is analogous to a ball rolling down an incline. Here, we use it to demonstrate epigenetic alteration of a developmental trajectory with OTE. At the top of the incline, the ball symbolizes tissue in development during healing, where it mimics its original ontogeny. The pull of gravity down the incline symbolizes the force of nature in natural development or, in our case, the force of therapeutic manipulation.

During the process, the cells become specialized by deleting or inactivating unnecessary genetic information. Since normal cells do not lose differentiation potential, i.e., transformative information during their differentiation, they can differentiate into virtually any tissue element. And tissue mimics that cellular differentiation. In cell development genes are just silenced but can be reactivated by exposure to defining stimuli called “epigenetic perturbation.” We submit that SAD, PAOO, and other OTE protocols constitute the same. This is the key to alveolus bone malleability and the orthodontic stability it renders. Loading a healing bone overcomes any determinative barrier, termed “canalization” (ridges in the landscape).

The term “epigenetics” was coined by Waddington to introduce the idea that some threshold environmental phenomena can modify the expression of chromosomes. He contended that a focus on natural selection as a determinate of structural phenotype must also consider the nonheritable role of epigenetic dynamics. The limit is dictated by a physiologic negotiation between the genomic options and the environmental perturbation which the genome “recognizes” and uses to select from a variety of expressions depending on the developmental environment. That is, DNA is not destiny nor a blueprint for a fixed and immutable phenotype. The DNA is rather like a survival manual, telling the tissue how to react depending on whatever environmental challenge presents. This “challenge” is termed an “epigenetic perturbation.” This recognition and allowance for alveolar phenotypic expansion in turn depends on the threshold of epigenetic perturbation, (infection, surgery, metabolic disorders, methylation, etc.). These possible perturbing factors include the influence of orthodontic forces loading a healing bone. Siegal and Bergman (2002) argued that phenotype is “robust to changes,” and we interpret that as a reference to the potential stability of orthodontic clinical outcomes. The robustness they refer to in epigenetic terminology is visualized as “canalization,” analogous to “energy wells,” which is the result of “long‐term natural selection for optimal phenotypes.” We contend that in wound healing, which is a regional redux of embryological development, this process is mimicked and, thus, can be applied to the wound healing of decorticated bone and stem cells, endogenous or grafted.

Without an influential perturbation, a healing bone normally reverts to its original phenotype. In the case of infection, fibroplasia replaces parenchymal regeneration thus forming scar tissue, itself a qualitative change in phenotype. If a broken bone is immobilized and heals well, it will endorse normal environmental stresses, e.g., running, walking, load bearing, and return to its original form. However, if fixation is inadequate and movement occurs under a cast, the movement is an exogenous influence sufficient to overcome normal robustness (canalization). Then a hypertrophic nonunion may occur. If there is an inadequate blood supply to the fracture, an atrophic nonunion will develop. Each of these forms of clinical outcome represents an altered trajectory down a developmental canal. Sufficient to maintain an osteopenic state, the orthodontic load will also prevent recalcification, providing less resistance to OTM. The fundamental biological principle at work in this phenomenon is the fact that a healing wound mimics the original development of phenotype. That is, a healing wound recapitulates regional ontogeny.

In Figure 1.2, Waddington’s epigenetic landscape model, (a) represents malocclusion development as an unperturbed genetic expression hits an ectopic eruption problematic enough to qualify as an “epigenetic perturbation.” (b) Illustrates a perturbation during healing and reprogramming of development to an alternative morphotype along a novel developmental trajectory. Ridges represent barriers to differential development and valleys (canals) represent stable morphotypes. Overcoming the ridges requires a kind of “energy of activation” and a threshold of “epigenetic perturbation.” This may take the form of infection as in scar formation, surgery skill in the hands of a plastic surgeon, or PAOO in the hands of a skilled orthodontist–periodontist team. The therapeutic intervention is designated by the red arrows, changing trajectory “a” to trajectory “b.” The result is a reengineered alveolus, morphotype (a) to morphotype (b) a larger alveolus bone, which is secure in orthodontic stability by deep canalization.

Thus, rather than the DNA acting as exact “blueprint” for a fixed and immutable phenotypic form, the type of genetic expression and the final configuration of the alveolus bone depends upon (i) the genomic options available, (ii) the physical resources available, e.g., grafted scaffolding, (iii) the limits to which soft tissue periosteum can be extended (stretched or “relieved of tension”) during surgery, and (iv) general regenerative capacity of the individual set by age, physical health, metabolic robustness of local tissue, atrophic, and degree of vascularity or fibrosis, i.e., the cell/fiber element ratio.

One of the great advantages of SFOT is that alveolar bone can be enlarged sufficiently to accommodate an idealized dental arch rather than modifying a normal healthy dentition, with odontoplasty or healthy teeth extractions, to match inferior bone. In a way, the ability to “build a better bone” renders, the extraction–expansion debate somewhat moot as a simplistic and false dichotomy, just as epigenetics has rendered the nature–nurture debate into an anachronistic dichotomy.

From Osteotomy to Corticotomy to Tissue Engineering

When reviewing the history of the corticotomy, one discovers that it originated in attempts to minimize the harsh side effects of major segmental osteotomy. The history is complicated by the fact that early writers used the terms osteotomy and corticotomy synonymously. So, much of the early literature is vague and prone to misinterpretation. An osteotomy starts with a linear decortication of bone and ends with a physical “movement” or “mobilization” (read: fracture) of a section of bone the way one might break a twig from the branch of a tree. Thus, “mobilization” is a euphemism for a kind of purposeful fracturing of bone sometimes literally done with a mallet and chisel. Whereas a corticotomy is limited to gentle incisions without any luxation or fracture. When studying OTE one must keep in mind the fundamental effects and esoteric mechanisms which facilitate the phenomena.

These effects, “observed” in the mind of the doctor during OTE occur sub‐clinically at the tissue and cell level. They are less clearly defined than clinic‐level gross anatomy, a level to which most orthodontists are accustomed. Therefore, new thinking must occur which could not have been appreciated by the specialty’s earlier advocates. Ironically, the mechanism that made OTE successful may have been singularly intuited as early as the 19th century by John Nutting Farrar (1839–1913) around 1888. He was referring to orthodontic effects from a “whole bone” perspective when he wrote,

… The softening of the socket breaks the fixedness or rigidity of the tooth leaving it comparatively easy to move, either by resorption of the tissues or by bending of the alveolar process or both (Emphasis added)

Farrar Revisited: Bending Bone and CPO

Farrar’s writing invites natural queries about the optimal threshold for bone fractures but is more germane to OTE, the thresholds for therapeutic bone modeling. The answers lie just beyond the scope of classical orthodontic literature residing instead within the fields of recent orthopedic and osteology (Mavcic and Antolic, 2012).

This bending of the whole alveolus bone stimulates regenerative osseous metabolism, compensatory bone resorption, and deposition, which occurs in areas of shear loading. The net result is a reconfiguration of cortical and trabecular architecture consistent with Wolff’s Law (Wolff, 1892). For example, in Figure 1.3 if a premolar is loaded with a buccal vector, the alveolus is bent buccally causing it to assume a relatively convex surface on the palatal aspect and a concavity on the buccal aspect. This buccal bending produces shear tension on the palatal convex surface signified by (−) and shear compression signified by (+) on the labial surface (Figure 1.3).

Close analysis of a loaded alveolus depicted in Figures 1.3a, b, an exaggerated diagram of OTM, shows a much more complicated vector system. One key to reconciliation of the medical–dental paradox is to imagine the cribriform plate and periodontal ligament as analogous to endosteal elements. Figure 1.3b is a closer look at the complicated vector system in Figure 1.3a.

In Figure 1.3, orthodontic force (F) is applied to the palatal side of a bicuspid. The alveolus palatal cortical plate and the buccal cortical plate are distorted, (“bent”) buccally in the direction of the sum vector (V). Note the asterisk representing the area of hyalinization, an ischemic necrosis (infarct) of the crestal periodontal ligament.

Observe in Figure 1.3b, how force (F) induces shear tension on the palatal subperiosteal cortical surface and shear compression on the palatal cribriform plate. On the buccal alveolus cortex, the palatal surface of the buccal alveolus cortex also “senses” shear tension. As the same force bends the alveolus in the direction of vector (V), it produces shear tension on the palatal aspect of the buccal cortex and shear compression on the buccal aspect of the buccal cortex. In periodontal terminology, this shear loading‐osteogenesis creates “buttressing bone” and is often attributed to trauma from occlusion.

These buttressing bone phenomena are limited by genotypic codes, but the expression of those codes depends upon the environmental perturbations they encounter. In summary, we propose that the bone apposition and resorption patterns seen in the periodontal ligament during OTM are due to differential shear forces during alveolus “bone bending,” simultaneous with periodontal ligament infarction, i.e., (hyalinization “H” in Figure 1.3). We contend that the surrounding osteopenia caused by the bone bending is amplified by the OTE‐induced Regional Acceleratory Phenomenon (RAP). Further the mobility phenomenon is referred to, in periodontal terms, as primary mobility. When mobility is caused by progressive loss of the attachment apparatus the appropriate term is secondary mobility. The concern about the exaggerated OTE and ODO‐induced mobility is not to be confused with secondary mobility caused by attachment loss. Patients should be explicitly reassured that OTE/ODO mobility is a therapeutic asset and is completely reversible in the retention period as the bone quickly recalcifies to its original density.

The two seemingly contradictory clichés of orthopedics and orthodontics about how load affects bone physiology, (load causes osteoclasia in dentistry; load causes osteogenesis in medical orthopedics) are thus reconciled if one considers the cribriform plate and periodontal ligament as a kind of “modified endosteum,” and a distinction is made between the orthodontic model of compression loading and the medical orthopedic model of shear loading. As force (F) is applied to the tooth, in Figure 1.3, it does indeed move in the socket, but pressures and tensions are applied with a myriad of component vectors. Therefore, we propose that the “pressure–tension” metaphor is so simplistic that it acts as a kind of facile intellectual red herring.” This intellectual “detour” inhibits a full conceptualization of bone dynamics during PAOO and alveolus enlargement. This leads the reader away from a more sophisticated and accurate bone physiology that allows alveolus phenotype change and, therefore, increased orthodontic stability.

In other words, the reaction of orthodontic load we posit is better explained by the shear tension or shear compression analysis of the bone cortices and periosteum. Hyalinization of the periodontal ligament provides little knowledge about “whole bone” periosteal strain. This mechanism to explain OTM within the alveolus bone and cribriform plate is superior to the pressure–tension hypothesis because it is consistent with basic science and general orthopedic principles. Looking beyond the ligament with a “whole bone” perspective gives a more realistic and comprehensive assessment of bone‐under‐load. It also explains the universal clinical successes of both SFOT in general and ODO (or PAOO) in particular.

This principle of compensatory periosteal osteogenesis (CPO) can be seen when a palatal alveolus bone – not dental – expander (Figure 1.4a) is activated. The purpose, to expand the palatal alveolus bone with acrylic panels, and stimulate bone deposition on the concave buccal surface of bone. This appositional behavior of woven bone on the buccal alveolar aspect can only be explained by what we call CPO. Figure 1.4 demonstrates a real‐life application of the schema in Figure 1.3. The behavior of the convex buccal subperiosteal bony surface is osteogenic when the alveolus expander panels are subjected to 150 g of lateral load. This nonsurgical phenotype alteration is how a larger alveolus bone is developed in a natural way that accommodates a fully aligned dentition (Figure 1.4a–d).

Histophysiology of Orthodontically Driven Osteogenesis

The “whole bone perspective,” discussed above, is a new way of looking at alveolar bone reactions to orthodontic loads and vector sums. The focus on periodontal ligament change is legion in our literature. But to fully understand OTE one must go beyond the ligament of the periodontium. The “hyalinization phenomenon” occupies an inordinate place in orthodontic literature. In 2008, Williams and Murphy documented the effects of “bone bending” with unequivocal biopsy images after using a Series 2000^® appliance (Max‐2000^®). It developed a low‐force magnitude for slow alveolus expansion in a case where healthy tooth extraction would compromise facial esthetics. The effect of the appliance captures the optimal loading threshold necessary for subperiosteal, coupled osteoclasia/osteoblastic activity in the alveolar cortices, as the bone is slightly distorted (“bent”) buccally. It is thus demonstrated here that the concept of “moving the root out of a (supposedly) static and immutable state” is misleading. The idea that the entire “alveolar housing” is immutable must be corrected in the orthodontic literature.

So, when patients refuse surgery to correct a posterior crossbite a safer, more stable, and periodontally healthier alternative lies with biomechanics of alveolus expansion. When speed is desired, PAOO can do the job. At cell level, it appears that the Max‐2000^® appliance and PAOO accomplish the same objective. Surgery simply elicits the phenomenon more dramatically and faster. Long‐term stability also appears to be the same. This theoretical concept of osteogenesis by shear loading has been alluded to previously in medical orthopedic literature and expanded in Melsen’s excellent textbook (Melsen, 2022), where she refers to a “… change in surface curvature of the alveolar walls.” All contemporary orthodontists should read this most elegant summary of basic alveolar osteology to fully understand bone shear strain in all patients.

This “whole‐bone” perspective posits the alveolus bone, cf. alveolar “process,” as a separate operative organ independent of its contiguous corpus. As the whole bone is orthodontically bent, buccally each osteon and indeed, each cell is deformed. We propose a kind of “peri‐orthodontic hypothesis”,⁴ which contends that this bends protein molecules and DNA, opening obscure binding sites on important developmental molecules. This, in turn, elicits an epigenetic perturbation and redesigns the morphogenesis to a novel homeostatic phenotype unique in alveolus shape, mass, and volume at the molecular level. The value of this new perspective is that it conforms well with contemporary basic biological sciences, particularly molecular biology, and epigenetics (Allis and Caparros, 2015).

In this regard, alveolar subperiosteal tissue and periodontal ligament act no differently than the periosteum and endosteum, respectively, in any long bone. Indeed, the father of limb‐lengthening surgery, Dr. Gavriil Ilizarov, mimicked the SFOT for the lengthening of legs and restructuring limbs deformed by accident, congenital factors, or poor management of prior fractures. Therefore, a lot of recent medical and basic orthopedic science can be transferred to and from alveolus bone science. This phenomenon, facilitated by corticotomy protocols, may be employed to reduce the degree of clinical relapse that still plagues orthodontics after 100 years of clinical trial and error. Standard orthodontic protocols, merely moving teeth without surgery, cannot overcome the natural tissue phenotype “canalization” that resists change (Figure 1.2). Traditional orthodontic biomechanical schemes create internal tension which rebound like an orthodontic elastic. The rebound is manifest as relapse, necessitating life‐long retention.

Cell‐Level Orthodontics

Bone cells, as homologs in other tissues as well, sense changes in their mechanical environments, internally throughout the cytoskeleton and externally through focal adhesions to the extracellular matrix (Ingber, 2003, 2008). This area of cell‐level biomechanics was essentially beyond the control of most orthodontists who relied instead on gross anatomical and clinical events to intuit cellular activity. With the introduction of tissue engineering concepts and a revival of corticotomy‐facilitated orthodontics, a new interest in cell‐ and tissue‐level phenomena has emerged. This is how the alveolus bone lives, thrives, and dies by virtue of its functional matrix, tooth roots (Moss, 1997a–d). This is because of the behavioral imperatives identified by Wolff’s law and Frost’s “mechanostat” model (Frost, 2003).

What skeletal muscle can do to bone morphogenesis at the gross anatomical level is analogous to effects of microstrain at the cell level. Engineering bone morphogenesis is a threshold phenomenon; too much or too little is dysfunctional. The influence of mechanical stimuli at the cell and tissue level, mechanobiology, is not the domain of bone alone; indeed, the pathoses of atherosclerotic cardiovascular disease are directly related to mechanobiological changes in vessel walls. With modern analytic methodologies and a body of science, too extensive for the scope of this writing,⁴ responses to all tissue can now be studied and modulated, be they integumental or neuronal, mucosal, or bony. This is the essence of tissue engineering science. Thus, orthodontic scientists have a legitimate claim to equity in mechano‐biology as well as biomechanics.

Timid Surgery and Its Consequences

Where adequate bone volume is present SAD is the treatment of choice. In the SAD protocol perforations and linear decortication 2–8 mm into the bone are performed with impunity. Although the depth of penetration depends upon the surgeon’s discretion, this author recommends deep perforations. Many doctors are happy with a simple flap reflection and a placement of small but effete divots 2–4 mm deep (Figure 1.5). But, this will not give access to medullary stem cells and elicits only a mild osteopenia. Then the doctor erroneously concludes “SFOT does not work”, (Figure 1.5).

In Figure 1.5, note the rather shallow, diffusely located, and bloodless (arrows) “divots” used as cortical decortication. This pattern achieves little more than simple flap reflection would create; it renders effete osteopenic (RAP) effects. So, in one respect, a failure to deliver definitive, deep, and hemorrhagic punctate decortications squanders the opportunity to engineer an efficient OTM course. This may be the reason why critics of SFOT encountered experimental failures. Nothing works well when it is done incorrectly.

Thus, complete decortication is correctly aggressive after elevation of a mucoperiosteal flap. This area has sufficient bone to decorticate without concomitant bone grafting. In most SFOT, the postoperative discomfort is not necessarily related to the degree of decortication. When a bone graft is added to a SAD, the appropriate term is PAOO. A previously employed term is accelerated osteogenic orthodontics (AOO⁵), but the two acronyms can be used interchangeably. The cells may be of autogenous origins (Nowzari et al., 2008) or donor stem cells (viable cell allograft) (Murphy et al., 2012). Experience suggests that in most cases, demineralized human bone or xenogeneic graft suffices (Brugnami et al., 2018, 2021a, b). But this author prefers stem cell alveolus therapy (SCAT) for regeneration because of its superior osteogenic potency.

Finally, it is important here to interject a practical guide to discomfort management. Aggressive and timid decortication being equally benign, discomfort comes mainly form protracted time spent in flap reflection, unnecessarily excessive flap reflection, and dehydration of tissue. So, in properly executed SFOT, most discomfort is handled by appropriate doses of nonsteroidal anti‐inflammatory pharmaceutical agents with little need for opioid analgesics. Prescribing a single dose of nonsteroidal anti‐inflammatory drugs (NSAIDs) prior to surgery is a helpful prophylaxis in pain amelioration. Also, remember that pain has both physical and psychological components. So, combining analgesics with a selective serotonin reuptake inhibitor (SSRI), e.g., benzodiazepines PRN is also helpful.

German Roots

Many historians cite Cunningham’s German article of 1894 as the first published article to address SFOT, after his lecture in Chicago the previous year. While having some rudimentary characteristics in common with modern cortectomies, scrutiny of Cunningham’s SFOT procedure suggests it has no relation to modern SFOT beyond a crude surgical approach. Cunningham’s treatment was really a luxated segmental osteotomy in today’s clinical parlance.

His singular goal of making teeth move faster has since evolved to more global objectives and variations on the corticotomy theme. But his prototype has indeed spawned interesting incarnations throughout the 20th and 21st centuries in many different countries and cultures.

Ironically, despite numerous derivative articles describing surgical facilitations of orthodontic treatment in the German literature, it languished there for more than half a century. For example, in 1921 Cohn‐Stock, citing “Angle’s method,” removed the palatal bone near the maxillary teeth to facilitate retrusion of single or multiple teeth. Five years later, Skogsborg (1926) wrote about “permanent fixation of the teeth after orthodontic treatment” by dividing the interdental bone, with a procedure he called “septotomy.”

Then, just before World War II, Bichlmayr (1931) described a surgical technique to accelerate tooth movement and reduce relapse. This surgery was performed in the palatal aspect of the anterior sextant by seemingly ablating large areas of cortex and medullar bone (spongiosa) (Figure 1.6b). This ablative technique was apparently employed also with canine retraction after bicuspid extraction, by excising the buccal and lingual cortical plates at the extraction site. Although this procedure seemed bold to American orthodontists, it became popular in the German scientific community. Later, Ascher (1947) published a similar procedure, claiming that it reduced treatment duration by 20%–25%. Analyses of these procedures were combined with a critique of the Bichlmayr’s procedure by Neuman in 1955.

The Introduction Into English

The seminal American work, published in English by Köle, built upon the German predecessors and summarized a series of surgical techniques to facilitate orthodontic therapy. One was a decortication of the dentoalveolar process to facilitate OTM. He compared his interdental decortication with the more morbid procedure of Bichlmayr claiming that only the cortex should be removed.

He specifically mentioned the advantage of singular cortex removal leaving the spongiosa intact to serve “… as a nutritive pedicle to the bone denuded of its mucoperiosteum.” With some notable refinements, this is the basic technique that is used today without a subapical osteotomy. The Kole surgery (Figure 1.6a) was limited to the cortex of the dental alveolus, but subapical decortication was embellished by extending buccal and lingual cortical plate incisions until they communicated through the subapical spongiosa. Buccolingual communication is now considered unnecessarily morbid and eschewed by evidence‐based SAD and PAOO protocols.

The rationale for the decortication as Kole explained was, “… the main resistance to movement is encountered in the cortical layer,” thus, ignoring the change in physiology (RAP) that Frost has so vividly discussed. The literature in the early half of the 20th century seems to miss the central point, viz. SFOT is not intended to eliminate a mechanical impediment as Kole implies. It is somewhat illogical that the cortex should be the main impediment to efficient OTM because the teeth move through medullary bone, not cortical bone. SFOT is a physiology modulation. Figure 1.8 demonstrates this point dramatizing the stark difference between normally calcified bone and osteopenic bone.

Early bias and the lack of cell‐level perspective are reasons why the literature of this period is merely anecdotal, dismissive, and often incorrect. Ironically, this body of data is still used to justify specious criticisms of 21st century SFOT. In Figure 1.6, we can see how Kole contrasted his technique (Figure 1.6a), with that of Bichlmayr’s technique (Figure 1.6b). The Bischlmayr technique seems to ablate an entire segment of palatal bone prior to incisor retraction. Kole’s method however, is similar to the modern technique employed by contemporary periodontist–orthodontist teams. Note, however, that Kole carried the linear decortications to the crest of the alveolus bone (arrow). Most modern surgeons categorically disdain this extension.

But it should be noted that integrating SAD with OTM will not grow new bone mass. In fact, in a steady‐state alveolus, it may reduce alveolar bone mass (Figure 1.23 (1b) and (1c). This is what “moving bone out of the alveolar housing” means. So, applying Cunningham’s derivatives indiscriminately can indeed result in a net loss of supporting bone. This dilemma of risking bone loss for the sake of faster OTM was solved by the prodigious efforts of many doctors in the Wilckodontics^® research group, representing the academic aegis of Case Western Reserve University. But the inspiration for all the American innovators belongs to a Japanese doctor.

Suya and the Asian Connection

Suya (1991), a Japanese clinician, stimulated significant academic interest in the United States and rejuvenated the Asian orthodontic community for nearly two decades. For example, his paper reintroduced refinements of Kole’s work into the American mind with a report on “corticotomy‐facilitated orthodontics.” Suya’s contention was well received because it demonstrated that conservative intervention could yield dramatic results. He also substantiated that opinion by reporting his experiences with over 300 patients. Importantly, Suya did not connect the buccal and labial incisions like Kole (1959) but relied purely on linear interproximal decortication. Although Suya, unfortunately, contended that the facilitated tooth movement was the result of “bony block” movement, his contribution to the world literature evoked many questions about the exact pattern of cortical cuts. We now know that the style of decortication, divots, lines, or other patterns is irrelevant. Only the sum of therapeutic perturbations is significant. For some patients, minor divots will suffice. Others might require a nearly complete cortex decortication. But biodiversity rules all. So, experience and surgeon discretion are important drivers of success. In any case, the decortication must elicit bleeding from the spongiosa.

Suya’s refinement of Kole’s methods has essentially set the standard for decortication procedures that followed in the postmodern era. Korean literature included a discussion by Kim (S‐C), as early as 2003, and a thorough discussion of the corticotomy phenomenon in that year, which stimulated further inquiry in the Korean peninsula very soon. Practical application of the protocols was published in 2009 (Kim et al., 2009a, b). The fact that Suya’s method requires a surgical flap reflection was recognized as an intimidating requirement for some clinical and patient cohorts. So, knowing how fast mucosal wounds heal encouraged other investigators to develop more conservative protocols. Kim (SJ) followed with a published transmucosal procedure (TMP) called corticision the same year (Figure 1.7). Corticision is a so‐called “flapless decortication”.

1980s: Anholm and the Loma Linda Investigation

Following communications with prior visionaries of the 1980s, periodontists and orthodontists collaborated in the first major university studies of the phenomenon at California’s Loma Linda University (LLU). A series of excellent research papers were created at that school, but support for the SFOT was tempered. Anholm et al. (1986), sobered by minor attachment loss in a male patient, were cautious in their praise of SFOT. Some limited crestal attachment loss can certainly occur if the periodontal (mucoperiosteal) flap is reflected off the bone for a protracted period; it gets dehydrated, and papillae may temporarily shrink (Figure 1.20). So, effective decortication surgery should be sterile, sure, and swift.

Gantes (1990), also at LLU, was a little more supportive of SFOT’s merits when he reported decortication on buccal and lingual surfaces on five orthodontic patients, with immediate orthodontic activation. His interproximal “vertical grooves” extended apically “beyond the apex levels of the teeth” with horizontal connections at the apical end. It is surprising that at a university follow‐up was possible since patients are often handed off to new orthodontists as classes graduate. Nonetheless, it is to the school’s credit that the Gantes data demonstrate a clinically significant 50% reduction in treatment duration.

After the completion of the orthodontic treatment in five patients, the outcomes according to Gantes, “… showed that the corticotomy procedure caused minimal change in the periodontal apparatus” offsetting Dr. Anholm’s fears. The parameters for periodontal health assessment were standard well‐accepted indices: plaque scores, probing depths, and probing attachment levels. So, it is ironic that Gantes advised that a corticotomy should be avoided on patients having “any form of periodontal pathology or deformity.” Under this rubric of “untouchables,” he included gingival recession, buccal or lingual bony dehiscence, and teeth with reduced periodontium. We disagree with his proscriptions. We have successfully treated every one of these periodontal problems with SAD or PAOO/SCAT. Patients who have reduced (compromised) periodontal support are no exception. As the case presented in this chapter demonstrates, reduced periodontium and active periodontal infection need not be contraindications for SFOT, as long as the proper technique is employed.

Even if no bone is used, and SAD is the only surgery employed, there is no reason to believe that dehiscence would worsen by virtue of the surgery. Indeed, recession is commonly treated with periodontal surgery. Regarding gingival recession, if the surgical flap is replaced coronally over receded gingival margins, and the root surface is properly prepared, a new attachment or a stable long‐epithelial attachment can be achieved as reasonable clinical outcomes. And, the outcomes are stable if maintenance achieves low bleeding indices. Orthodontic non‐extraction may exacerbate a dehiscence, but surgery would not necessarily affect this unfortunate phenotype. It is unclear why Gantes included this proviso because no rationale was given. The categorical and vague nature of this admonition discredits it in the context of 21st‐century periodontal science.

A 20th Century Summary

From Bichlmayr in Germany to Köle in the English literature, to the turn of the new century, it becomes obvious that thinning of the alveolar volume in the direction of the tooth movement is a critically important consideration in the protocols of any orthodontic‐driven corticotomy procedure. When one applies this nuanced philosophy to the surgical preparations, it becomes much easier to keep the entire OTM treatment times under 12 months except in cases of severe Class III or Class II skeletal dysplasia.

Yet, even severe skeletal dysplasia can be treated fast and better if SFOT is coordinated with orthognathic surgery. This is when SFOT accelerates the universal first step in OTM, leveling and aligning. Orthognathic surgery can achieve the second phase, arch coordination (congruency) within hours. The third phase of OTM, “detailing” is perhaps the most difficult part of OTM. But SFOT makes this phase easier also. Moreover, the immediate post‐orthognathic surgical condition is notorious for displaying excellent physiologic tooth mobility. Rather than waiting to attempt detailing until the surgery “heals” (read: recalcifies), it is better to intervene early in the postoperative course to take advantage of the generalized iatrogenic mobility. This author begins OTM during the surgical procedure after the last suture is placed. This has been achieved with clinical impunity for over a decade.

Most treatment times range from 3 to 9 months with Class I and mild Class II malocclusions. Twelve months in severe Class II cases and less than 3 months in Class I moderate crowded cases are reasonable OTM goals. Independent clinicians often claim that severe skeletal posterior cross bites and anterior open bites are universally daunting challenges, but they may also be treated successfully in about 10–12 months despite the fact they represent a basal bone skeletal dysplasia. Where clinicians face maxillary transverse deficiency, it is doubtful that PAOO has any effect on the basal bone. But it can be employed in Class II cases if decortication and grafting are performed on this basal component. Wilcko has demonstrated this principle in his famous case of Patient X (Figure 1.8) whom he treated with serial PAOO at pogonion and gnathion. However, for transverse deficiencies, it should be noted that expansion of the palatal suture and maxilla per se is irrelevant if the alveolus bone itself is sufficiently enlarged. This is what PAOO is designed to achieve.

As the century closed, the specialty of dentoalveolar surgical orthodontics was reaching the end of clinical art and the beginning of a protracted journey through the gauntlet of scientific scrutiny. SFOT specialists remained dutifully skeptical but undaunted because, with the consistently gratifying clinical results and unimpeachable anecdotal consistency around a shrinking world, their collective confidence continued to grow.

The Entry of Academics

By the year 2007, intellectual collaboration among clinical researchers and other universities around the world inspired by scholastic leadership at Case Western Reserve University resulted in significant documentation of the SAD and PAOO efficacy. Clinical researchers resolved for the last time much of the contention among the earlier clinicians by subjecting SAD to detailed analysis and rigorous standards of evidence‐based science. This is important because it positioned corticotomy procedures at the exalted level of university‐based analysis and the kind of controlled experimentation that it demands. At the time, these early 21st‐century studies of SFOT were unparalleled; in retrospect, their findings seem epochal.

“Wilckodontics,” PAOO^TM/AOO^TM, and Tissue Engineering

After studying the publication of Suya (1991), Wilcko group led us intrepidly into the 21st century. Dr. M. Thomas Wilcko, a periodontist, collaborated with his brother William, an orthodontist, in Erie, Pennsylvania, United States, to develop a more stable and benign SFOT. Concerned with the destructive periodontal effects of banded therapy and encouraged by the results of SAD, the brothers surmised that alveolus inadequacy might play a factor in relapse. So, in 1996, they conducted case studies to a very high standard of excellence. Finally, they added an allogeneic bone graft between the decorticated cortices and replaced flaps. The Wilckos also popularized the notion that a corticotomy induces a regional osteopenia (Figure 1.9), the so‐called RAP.

The Wilckos’ computerized tomography of the results also documented a definitive alteration of alveolus morphology, Wilcko et al. published their seminal academic works within the next 7 years, referring to the grafted protocols as AOO^TM.⁷ Later, it was renamed the PAOO^TM technique. The difference between the two is merely semantic, so they are essentially synonyms.

Sadly, many dental schools initially shunned these innovative efforts. Even worse, some prejudiced professional associations even expressed hostility to the Wilcko efforts. This is, however, the personal cost which innovative leaders predictably must pay for novel data which appears to be iconoclastic. New data can threaten some intransigent vested interests simply by being new. But, undaunted by institutional cynicism, they began teaching their innovation in a proprietary school called “Wilckodontics.” They trademarked the name of the school for the protection of the unique protocol lest it be adulterated to the detriment of patients’ welfare. Among cynics, the school’s name and trademark were mistakenly misinterpreted as a legal gambit to monopolize the surgical technique. But nothing could be further from the truth.

The legal trademark was intended to protect patients and the integrity of the school’s name. Ironically, the trend of “patenting science” is now becoming increasingly popular, but this is still not the case with the Wilcko philosophy. The trend toward healthcare corporatization is inevitable and was heralded by Paul Starr’s prescient work, The Transformation of American Medicine, two decades earlier. The 1982 sociological treatise is still worth reading for those interested in the future of healthcare delivery patterns. But the Wilcko mission was scholastic, not commercial. Interestingly, as with Mary Shelly’s gothic novel, Frankenstein, the school’s name was transmogrified by some readers and misappropriated for the creation itself. So, the term “Wilckodontics” in contemporary vernacular is a general reference to any and all SFOT iterations.

Since the 1990s, the Wilcko collaborators have remained true to their noble mission, relying on empirical proof of their brainchild, collegially sharing data through their school, wisely eschewing crass commercialization, and validating the worth of their protocol by independent corroboration internationally. The combination of grafting, decortication, and accelerated adjustment schedules was an ingenious addition to the orthodontic profession because it enriched the studies at the Loma Linda School of Dentistry with a rationale and depth of scholarship others seemed to misunderstand.

The Wilcko group protocols went even further by developing protocols for space closure in extraction cases, as Kole did before them. But the Wilcko wisely added more. They combined buccal and lingual grafted corticotomies with total extraction site ablation. This unnamed procedure leaves only the mesial and distal cribriform plates of adjacent teeth during extraction site closure. As the adjacent teeth move toward one another, a new alveolus naturally forms around them, aided by the graft of demineralized freeze‐dried bone allograft (DFDBA).

At the dawn of the 21st century, further refinements of PAOO and other variations of SFOT were investigated under the aegis of Case Western Reserve University and the profoundly rigorous analyses of Professor DJ Ferguson. This data spread thereafter throughout the world. Ironically, some of the most disciplined studies came out of the so‐called Third World.⁶ The introduction of PAOO to the SFOT collage marked a particular quantum leap into 21st‐century tissue engineering. Remember, the word “engineering” means the art of manipulating natural forces to a predetermined design. The tantalizing dynamics and biological phenomena of this clinical approach evoke the biomathematics of nonlinear complexity and fractal geometry. These progressions and patterns expose the enigmatic patterns of mammalian morphogenesis and geometric destiny of individual cells. These topics are too profoundly esoteric for the scope of this practical discussion but warrant further study.⁷

As with many great innovations in science, the difference between profundity or meaningless novelty, innovation, or apostasy often depends on the consistency of observation, psychosocial acceptance, degree of institutional inertia, political advocacy, and even the serendipity of fickle fortune. All these determinants are presently alive and beneficent for the young visionary orthodontist.

According to the strict Wilcko protocol, 1998–2020, tooth movement was typically initiated sometime during the week preceding the surgery. So, the surgery at that time was performed in strained bone ab initio. Thereafter, the strain was perpetuated by activation of the orthodontic fixed appliance every 2 weeks. Since the time PAOO was introduced, timing of the adjustment periods has been shortened by this author to semiweekly or even daily adjustments. SFOT is so effective that simple space closure can be achieved with finger pressure in less than a minute.⁸ The creation of bone de novo was a revelation to many periodontists. Prior to this observation, it was considered axiomatic that one “… cannot grow bone on a flat surface.” Yet, PAOO did just that. The secret is coincident and nonresonant wound loading.

The first publication by Wilcko et al. was preceded by 8 years of research and clinical investigation that reduced morbidity and, in some cases, even obviated the need for orthognathic surgery. What began as performing corticotomy surgeries without bone grafting on both younger adolescents and adults flowered into a major subspecialty of dentoalveolar phenotype morphogenesis. The Wilcko group made it obvious to everyone that accelerated care reduces bacterial load, enhances stability, reduces the pain of mechanical adjustments, precludes damage to the attached gingiva, and can even increase the zone of attached gingiva. All these historical banes of traditional fixed appliance care are reduced with PAOO and conform to the definition of “best” discussed earlier in this chapter.

Prior to this research, corticotomy‐based surgeries were only recommended for individuals 18 years of age or older following the cessation of growth. This age limit now appears to be antiquated. Indeed, due to the tremendous rate of adolescent development, leveling, and aligning can be achieved in a matter of weeks, not months in adolescents younger than 18. High‐resolution surface scans of computerized tomography clearly showed a demineralization–remineralization process at work and stable, enlarged alveoli. The explanation Dr. Wilcko first suggested was “bone matrix transportation” rather than a bony block movement.

Building on that astute observation, we introduced a modified term combining specific technical terms derived from orthopedic, periodontal, and orthodontic literature. Our term is periodontal matrix translation (PMT). This term is entirely consistent with Frost’s RAP and Wilckos’ thesis. But PMT is more accurate. The terminology refinement proposes that only the decalcified cribriform bone, periodontal ligament, and root are the translating entities. The two terms are essentially synonymous, but the one we proffer is more traditionally consistent. Thus, in summary, the PAOO is purely a natural osseous reaction not an idiosyncratic phenomenon. PAOO requires no modification of fixed appliances. It is also indifferent to any style of biomechanical adjustments (Begg, Tweed, etc.), as long as the internal osseous strain is constant.

The Small Window Myth

Critics who have not taken formal instruction in SFOT or are inexperienced often claim that the SFOT procedures have a limited window of opportunity. They reason that, since an osteopenic state, (purportedly but fallaciously) lasts for such a limited time, it cannot facilitate OTM (Buschang et al., 2012). Even though they acknowledge acceleration is possible, e.g., a doubling of movement rate, they fall victim to the myth of short duration. The truth is: there is no window.

Quoting Buschang, “the amount of time during which corticotomy have an effect on tooth movements is limited to 1–2 months.” This is true only if the OTE protocols are executed erroneously, or therapy is interrupted for a protracted period. However, when instructed well, the orthodontists’ biomechanical protocol can load the bone in a way that elicits a constant strain in the healing alveolus. So, there is really no such thing as a small 1–2 month “window of opportunity.” The small window concept is a myth. The osteopenic state (RAP) can be maintained indefinitely allowing recalcification to occur in the retention phase of treatment. This is perfectly analogous to a fracture nonunion that recalcifies once total immobilization is secured. In case the treated alveolus recalcification occurs too soon, an osteopenic state will return within a couple of weeks if strain is reinstated and/or transmucosal perforations are employed. The clinical truth is this: RAP (transient osteopenia) can be sustained indefinitely.

Even when RAP is evinced, sometimes, bodily translation of a tooth through the long axis of the alveolus may be delayed to a millimeter per month when no significant entry into interproximal bone is made. This is the error of timid surgery. But sometimes even with appropriate intramedullary perforation is achieved a complete treatment failure can occur; such is the nature of biological systems. It is a wise man who acknowledges that every island of knowledge which science discovers is surrounded by a shore of ignorance. These are idiopathic occurrences. They are idiosyncratic and rare.

Despite the knowledge that sometimes things simply do not work in idiosyncratic patients, so‐called “failure” must be minimized by assiduous scholarship and confident intervention. For example, a timid punctate decortication (Figure 1.5), in the opinion of this author, should be abandoned in favor of deep linear decortication 4–8 mm deep and in clusters no more than 4 mm apart. The millimeter depth is only a general guideline that must be individualized for each patient and each location within that patient. The goal is intramedullary penetration through the cortex, to elicit hemorrhage, not merely within a cortex. This will ensure medullary osteopenia which is much more important than its cortical counterpart.

Therefore, if a thin cortex perforation elicits bleeding with a 2 mm decortication, then it is the correct procedure for that individual patient. Whereas other patients may require a 4–5 mm perforation. And, if more mobility is needed, the penetrations should be doubled in each example. Decortication does not always mean partial decortication; it can also refer to a complete decortication in situ. In cases of very dense bone, a total resection of the cortices is necessary. PAOO and non‐grafted SFOT principles, however manifest in the hands of an experienced surgeon, complete many cases as fast as 4 mm per month. This will not be achieved with a reticent surgeon.

The “Need” for Extraction Myth

Bicuspid extraction therapy is often presented as “needed” because the alveolus bone supposedly cannot be moved facially to accommodate arch expansion. It is also claimed that “the teeth should not be moved beyond the limits of the alveolar housing” (presuming the alveolus is immutable). Second, the extraction choice is often justified because the doctor wishes to reduce morbidity. That is, he or she claims a desire to reduce the risk of “periodontal damage, e.g., gingival dehiscence.” Third, the doctor decides unilaterally that the patient’s profile would be better served if the teeth were not protrusive. This is the kind of specious reasoning that leads to perfunctory extractions which on closer inspection are neither indicated by contemporary science nor desired by hapless patients. Too often biomechanical extraction protocols are little more than short‐order recipes for convenient and predictable tooth alignment without consideration of the patients’ subjective opinion of their own facial appearance. Improper extraction faces get even worse through the ravages of time (Figure 1.13).

We propose that none of these excuses are justified. First, the erroneous notion of alveolus immutability of the alveolus has been disproven by years of “black swan” arguments. Professor Ferguson’s intrepid work is particularly impressive in this regard because of his unabashed scholastic excellence. He has the uncanny ability to breach obscured scientific truths and present them in pedagogically facile ways. His research culminated in a new definition of the tooth movement envelope. The Ferguson Limits of Movement (Figure 1.14) clearly defines the new limits to which the alveolus bone can be expanded. Second, even if periodontal dehiscence occurs, (unlikely when infection is managed) a gingival graft to restore the zone of attached gingival is far less morbid than extracting two to four healthy teeth. Third, the definition of facial beauty ultimately is a patient decision, and with changing culture, more protrusive, so‐called “full smiles” are in vogue.

Where the projection of future facial form is in doubt or where the patient is ambivalent, a resort to Pascal’s Wager maximizes future options. If the non‐extraction course is followed only to discover that it produces too much lower facial protrusion, patients still have the option to change their minds and retract anterior sextants. The perfunctory and injudicious extraction of bicuspids to suit the doctor’s singular artistic vision is a misappropriation of patents’ prerogatives. In cases where SFOT can enlarge the alveolus, ignoring patients’ opinions, for the sake of expediency or a doctor’s artistic sentiments is simply too facile and solipsistic to serve seriously deliberative and rational decision theories.

Some may claim that only the doctor is uniquely trained in the definition of good esthetics. Often what they believe are benignly authoritarian decisions on esthetic matters is couched in expressions like “… work well for most patients” or “… art that works well in my hands.” However, when that arbitrary decision involves injudicious tooth extraction to match a deformed bone, the retreat into the orthodontist’s singularly subjective sense of beauty rings hollow as a banal rationalization.

On the contrary, we claim that routine extraction therapy “recipes,” with their unpredictable potential to flatten facial profiles in maturity, evoke serious questions about what constitutes universal definitions of desirable facial esthetics. The generation of PAOO‐augmented profiles with serial augmentation protocols call for guidelines about how far one should go with augmentation therapy. But a fear of excessive protrusion is an idle fear. A critical discussion of traditional orthodontic standards is in order here.

On Beauty

Existing concepts of optimal esthetics are available to all orthodontists and are integral to their training. But as cultural values change, some clinicians appear to be relying on outdated concepts of facial beauty, starting with Angle’s veneration of the Apollo Belvedere profile. It is noteworthy to remember that this Victorian standard also coincided with the eugenics movement and social Darwinism where prognathic lower facial profiles were considered simian and “primitive.” It is the extraction protocols that tend to produce this archetype for better or worse. Now, relative bimaxillary protrusions reflect an emerging social standard of high esthetic value. The Apollo profile is beginning to fade as a desirable standard. We propose that the Victorian profile is too flattened, viz. “dished‐in,” to meet contemporary standards of social esthetics, as judged by a naso‐pogonion “E‐line” (Ricketts, 1968) (Figures 1.10 and 1.11).

Marquardt, a facial reconstruction surgeon, heartily endorses the use of his ideas in orthodontic therapy. His Golden Decagon can serve as a geometric template or intellectual metaphor (Jefferson, 2004; Bashour, 2006) (Figure 1.11). Mathematical imperatives seem to appear more prominently in popular facial profiles. These have been studied for decades by Dr. Steven Marquardt with a profound justification. It seems that universal geometric pattern, expressed as a ratio called Phi, is a ubiquitous phenomenon in nature and even in purely inanimate physical systems. As part of what Plato called the “World of Forms” and Jungian Archetype, it is thought that Phi can predict the social acceptance of some faces over others.

Calling upon an eclectic literature ranging from physics to biology, to metaphysics, Marquardt has developed an esthetic matrix that can be overlaid on photographs to quantitate how much deviation a facial form differs from his geometrical archetype (www.beautyanalysis.com). These kinds of precise quantitations are superior to subjective evaluations, outdated notions, or popular esthetic nostrums. They give both plastic surgeons and orthodontists a very useful instrument to confirm professional assessment (Figure 1.12).

Figures 1.11, 1.12, and 1.13 harshly illustrate just how extraction treatments – often unnecessary in the age of PAOO/SCAT – can unpredictably devolve into unattractive lower faces in adulthood. Even when a midline discrepancy is obvious, a generous display of teeth presents a more esthetic appearance than iatrogenically flattened profiles, as demonstrated in Figure 1.12 (Figure 1.13).

A prominent nose and chin combined with arch length deficiencies has always presented a conundrum for previous generations of orthodontists with no good alternatives: Not extracting teeth would allow a malocclusion to prevail. Even extracting healthy posterior teeth and allowing facial profile to remain static can be very unpredictable and biomechanically challenging. When adult teeth are extracted in an adolescent, postpubertal predictions of facial form can be very unreliable. Finally, deferring treatment to maturity is unacceptable to older adolescents and adults. So, extraction became de rigeuer and injudicious extraction became more common from the earliest days of orthodontics. It was thought that extractions rendered a more stable outcome. But Little et al. (1988) found that the 80%–90% relapse rate was equally evident regardless of extraction or non‐extraction treatment. Both plans are equally unstable because most orthodontists are not yet aware of the fact that traditional OTM does not change alveolar phenotype; it merely strains it. And what is strained relapses.

However, the success of PAOO vitiates the previous imperative to extract healthy teeth simply to align the dentition or render less relapse. Now that PAOO allows expansion of the alveolus bone with impunity, alveolar bone augmentation is emerging as the professional standard of care to build a better bone.

The unesthetic outcome gets worse with age. Figure 1.13 illustrates that injudicious extraction of healthy teeth is tantamount to amputation of a facial growth site. The predominant idea of years past is that a recessive low face was less primitive looking than a prominent dentition seen in primates. This patient in Figure 1.13 approximates that of Apollo Belvedere, the Victorian archetype, and eugenics ideal. As she ages her lower facial profile becomes relatively retruded. Such profiles are even today cited for their “strong chin” a reference to pseudoscience physiognomy, the philosophy that character can be assessed by the shape of bones. Such a notion finds comfort in social prejudice and misplaced art; anathemas to science.

Professor Ricketts set an enviable standard in 1968 that helped define optimal esthetics and is still widely employed standard of facial value. He stated that the lips in the Caucasian are “… contained within a line from the nose to the chin, the lower lip is closer to the line than the upper, the lips are smooth in contour, and the mouth is closed with no strain” (The so‐called “E‐line,” “E” for esthetics, as displayed in Figures 1.10b and 1.11).

In retrospect, the E‐line and the Marquardt mask have worked well in establishing attractive facial profiles for generations of orthodontists and have such an enduring quality that they should not be summarily dismissed. The closer we can come to predictable beauty the stronger the profession becomes. And yet, conformity does not necessarily produce the most beautiful facial esthetics. Average faces are attractive, and yet, exceptional beauty is not average (Alley and Cunningham, 1991). So individualization is still a strong clinical imperative. We must ask patients what they call “attractive.” The correct measure of appropriate case development, the sine qua non, is concordance, a “meeting of minds,” between and doctor and the patient. This can only be forged with fully informed consent, meaningful dialogue, and an adroit use of Pascal’s wage.

From PAOO to SCAT; Dead Cells to Living Tissue

The original component of PAOO that made a significant difference in alveolus augmentation was the addition of Demineralized Freeze‐Dried Bone Allograft (DFDBA), a common component in infrabony defect regeneration. Mixed with clindamycin, the trademarked protocol of Wilckodontics^® proved to be successful in “growing bone on a flat surface” heretofore thought to be impossible. The reason the Wilcko group was so successful was that their graft was placed on decorticated bone and – most importantly – it was loaded. The loading stimulated endogenous mesenchymal stem cells (MSCs) (pericytes) to differentiate into osteoblasts. PAOO employs the potentials of “dead cells” to serve as an osteoinductive scaffolding for endogenous bone growth. But if the host’s stem cells are minimal or effete so is the regeneration.

PAOO, despite its manifest efficacy, lacked a method of ensuring the graft was robust in a way to quantify the number of robust cells in situ. Fortunately, the introduction of living stem cells to the graft solved this problem. Supplemental exogenous multipotent stem cell allografts⁹ with potent growth factors can fortify in a complementary way, the minimal numbers, and effete stem cells of the host (Murphy et al., 2015). One no longer needs rely on merely endogenous elements liberated from the medullary bone and blood when an excellent FDA‐approved stem cell product has been extensively in medical orthopedics for many years.

The exogenous stem cells, euphemistically referred to as “viable cell matrices,” are attached to a DFDBA “vehicle” for easy handling. The stem cells are taken from biopsies in healthy patients under the age of thirty to ensure safety and robustness. The stem cell product boasts millions of multipotent MSCs/cc in a DFDBA vehicle that is easily handled. Originally, the population was not expanded in cell culture. But since its introduction cryogenic technology has changed to allow expansion and “banking” of robust MSCs, in either endogenous or allogeneic grafts.

DFABA is only osteoinductive stimulating the regenerative potential in situ, and in older patients, a robust potential is absent. Nowzari, (2008) was the first to recognize this and published a variation on the Wilcko protocol. By using an autograft harvested from the mandibular ramus. Nowzari added extra robustness to the healing wound by the autograft and presumably engineered faster regeneration of the new alveolus form. The first disadvantage to the Nowzari technique is that it requires a second surgical site for harvest. The second disadvantage is the weakness of autogenous cells in older patients. Refined protocols using a viable stem cell admixture to an autograft makes a productive enhancement. The stem cell approach to alveolus expansion surgery was first published by this author (Murphy et al., 2012) during a prolific period of clinical innovation inspired by the Wilcko group’s “revolution.” And the SCAT is even better in time. Because the allograft contained living cells, the healing is more subdued and even recruit endogenous latent stem cells to differentiate as well. This is a manifest advantage in regenerative surgery. This author’s protocol is demonstrated step‐by‐step in Figure 1.22a–h.

The development of stem cell regeneration to facilitate this standard more predictably in orthodontic therapy is discussed in length elsewhere (Murphy et al., 2012, 2015), but a brief reiteration is appropriate. The progression of human development, from the conceptual to the empirical, from the rudimentary to the sophisticated, and from the unpredictable to the routine is a trajectory of fits and starts. Likewise, from the perfunctory extraction of healthy teeth to the molding of beautiful faces, intellectual leaps, retreats, and rational adjustments are to be expected. Such was the quantum leap of viable MSCs into medical orthopedics, periodontal regeneration, and OTE. MSC regeneration of the dental alveolus is exceptionally compatible with the standard PAOO protocol published by Wilkco.

Because of supportive literature and our own extensive experience, we propose that the clinical standard for long bone regeneration (Chaparro and Linero, 2016) and the emerging choice for a variety of regenerative protocols (Safari et al., 2018) should also be considered the preferred choice for alveolus augmentation in PAOO. SCAT has been the treatment of choice in the author’s office for over a decade with commendable and predictable outcomes. While not yet universally appreciated, when proffered fairly, SCAT is also the first choice of many patients. The Ferguson research group contributions, 2005–2014, have strengthened the PAOO rationale and demonstrate how far we can go with it in their “new envelope of movement.”

SCAT achieves that goal more robustly and more predictably than DFDBA or autografts, and in the future, stem cell grafting will constitute a 21st‐century gold standard (Figure 1.14).

The Ferguson Envelope of Movement tells us that the alternative is here.

There will probably never be a total replacement for bicuspid extraction or its justification in clinical art. For the exigencies of private practice extraction therapy, despite its limitation, is inescapable. The need for “camouflage‐biomechanics” in cases of Class II skeletal dysplasia and correction of disfiguring bimaxillary protrusion certainly define a perpetual need to occasionally sacrifice some dental units. Even SCAT and a singular PAOO protocol to reconstitute more esthetic protrusive lip posture have limits. But SCAT is an emerging first choice in many erstwhile orthopedic surgical theories, so it must be considered in orthodontists who value facial beauty over simple tooth alignment.

Stem cell engineering of bone tissue even has a place in extraction therapy. Stem cell supplements aid ridge retention and extraction site healing. Moreover, surgical manipulations of the vacant alveolus can accelerate anterior teeth retraction en masse safely without anchorage loss. Because of these merits, unproductive, inert synthetic material for bone tissue engineering will probably lose favor in the future among enlightened doctors. Thus, it behooves all progressive clinicians, to learn about SCAT.

Beyond the Ligament with Mechano‐biology

Given a basic understanding of stem cell biology, we turn to its practical application in clinical practice. One aspect of “cell‐level” orthodontics that merits greater consideration in orthodontic curricula is mechanobiology (Van der Meulen and Huiskes, 2002). This is a relatively new science that investigates the effects of exogenous force reflected on and within cells (Ingber, 2008). A good education in stereochemistry and protein chemistry is extremely helpful in understanding clinical outcomes. This is the kind of biology which essentially defines the biology of orthopedically strained stem cells and the reason pre‐doctoral educational requirements demand significant proficiency in organic chemistry and physics. It is these disciplines which form the conceptual basis of molecular and mechano‐biology.

The concept of an engineered alveolus phenotype introduced at the start of the new century, (Murphy, 2005a, b) acknowledges the traditional explanation of tissue behavior in the periodontal ligament but asks for more. This focus on the ligament alone has occupied orthodontists for too long, and using it to singularly describe the full spectrum of mechano‐physiology in the subjacent bone is inadequate.

Newer concepts go beyond the ligament to champion the theories of subperiosteal cell dynamics as a determinate of treatment stability. The original model of hyalinization of the periodontal ligament was always at odds with the medical orthopedic model, and the two divergent views were only recently reconciled. Yet the so‐called “pressure–tension model,” despite the early criticism by Baumrind half a century ago (Baumrind, 1969) persists anachronistically to dominate the clinical worldview and the curricula of many academic institutions. The pressure–tension model was published around the end of the 19th century (Sandstedt, 1904, 1905) and should not be consumed whole as a comprehensive explanation of alveolar bone physiology.

The pressure–tension hypothesis been criticized as effete and parochial as late as 2006 by Meikle who just as easily could have been explaining PAOO. He argues,

Contrary to the impression gained from the literature, tooth movement is not confined to events within the periodontal ligament. Orthodontic tooth movement involves two interrelated processes: (1) deflection or bending of the alveolar bone and (2) remodeling (sic.) of the periodontal tissues. (Emphasis added)

The new model, “appositional osteogenesis,” a compensatory subperiosteal phenomenon, when bone is distorted, did not get much recognition until Ilizarov popularized distraction osteogenesis. Ironically, an indirect reference to the phenomenon antedates Ilizarov’s data by nearly a century. A 19th‐century observation by Farrer (1889) notes that orthodontic biomechanical adjustments can bend the alveolus bone en toto. This “whole bone” concept has been alluded to by Melsen (Burstone, 1988) and others. It appears that bending of the whole alveolus bone results in shear compression which affects the subperiosteal cells’ cytoskeletons, causes canaliculi fluid perturbations, and, at the cell level, transduces strain to biochemical and behavioral changes inside the stem cell cytoplasm.

The OTE based on this “Peri‐orthodontic Hypothesis” seeks to explain the effects of both PAOO and even some nonsurgical appliance therapy where the classic “pressure–tension hypothesis” falls short. The peri‐orthodontic hypothesis beings with Popper’s (2002) falsification principal vis a vis the ligament focus. We propose that it is the physiologically adaptive mechanisms in the entire periosteum, not just the PDL, which effect a reengineering of the alveolus form to a larger or more accommodating phenotype after PAOO and to a more robust form with SCAT. The healing of the bone under load amplifies the natural appositional modeling of bone that effects osteoclasia on the convex side (Figure 1.15) of a bone and osteoblastic osteogenesis on the concave surface of a bent bone (Figure 1.3). This bending, we proffer, accounts for the striking success seen in Wilckos’ tomographs (Figure 1.23).

But neither surgery alone nor orthodontic pressure alone can achieve permanent change in the alveolus or ensure impressive stability; both must be orchestrated simultaneously. Happily, there is no need for any orthodontist to change his or her favorite biomechanical style. All biomechanical protocols will work with PAOO and SCAT if the adjustment appointments are scheduled no farther apart than 1–2 weeks to perpetuate the RAP and activate stem cells.

This hypothesis is biologically valid, and the creation of a more accommodating alveolus phenotype is possible, because – at the cell level – wound healing recapitulates regional ontogeny, viz. the basic function of a stem cell in utero is not much different from its function in a healing SFOT “wound.” In other words, the stem cell in situ simply responds to local epigenetic perturbations and does not “know” if it is residing in a developing fetus or the healing wound of a mature adult. Any alveolus healing wound, supplemented with MSCs and subjected to physiologic orthodontic forces, creates a phenotype reflecting epigenetic perturbations which the orthodontist (cum tissue engineer) decides to induce. Reiterating, at the cell level, a stem cell responds only to local environmental chemical or physical stimuli.

Some criticisms of this new heuristic model have been presented, but most are specious because they lack a sufficiently authoritative biological basis and rely on the intergenerational didactics among clinical artisans for validation. But a challenge to a clinic‐level paradigm is not without merit; a heretical idea that works certainly has precedent in science. But if new theory is to have scientific gravitas, it must be appropriate for cultural needs, and contribute to better results, albeit inconvenient and disruptive. When new ideas are algorithmically sound, supported by biological science, and logically consistent, they should enjoy reasonable appeal to open‐minded fellows and earn a legitimate place in the pantheon of accepted clinical therapeutics.

The Mechanosome

At cell‐level biology, there is a missing link between genetic expression and clinical skeletal change. That link may be the mechanosome. In 2003, Bidwell and Pavalko proposed a theory of mechanotransduction that involved a hypothetical entity called a “mechanosome” (Figure 1.17). The mechanosome hypothesis explains that deformation of bone deforms bone cells, and that in turn ultimately deforms target genes. That is to say, bending bone bends genes. This DNA physical distortion ostensibly is the “instructional mechanism” which alters the gene’s morphogenetic expression, i.e., overcomes Waddington’s canalization. The Bidwell and Pavalko hypothesis suggests that bending bone bends DNA in a way analogous to stereochemical phenomena.

In 2010, they explained that the mechanosome is not a single object or intracellular organelle but rather a mechanosome transduction pathway. This pathway is a cascading series of molecular interactions. The origin of mechanosomes, they explained was

“… the transient formation of complexes comprised of adhesion‐associated molecules and nucleocytoplasmic shuttling ATFs, transferred information from the membrane to the nucleus.” They cited β‐catenin/LEF‐1 and Nmp4/p130C … as mechanosomal archetypes.

In 2010, Bidwell noted that

… the load‐induced nuclear translocation of β‐catenin/LEF‐1 is accepted as a … significant component of bone mechano‐transduction, and Nmp4 has been characterized as a general inhibitor of bone anabolism.

Intracellular and transmembrane cytoskeletal proteins (Figure 1.16) target specific genes sensitive to mechanical stimulation via this transduction cascade (Figure 1.17).

This ultimately “reprograms” DNA with a new “transcription message,” in a way not dissimilar to new software reprogramming a computer hard drive. The Bidwell–Pavalko hypothesis of mechanotransduction is intriguing as a working model until future explications reveal a better explanation.

In summary, orthodontic force application, immediately translated to gross anatomical deformation of alveolus bone, changes the conformation of cytoplasmic proteins, and distorts cytoskeletal tensional integrity (tensegrity) with presumptive strains. This is consistent with the findings of Ingber et al. (2003, 2008) and Mao (2002) widely respected clinical tissue engineers. The physical stimulation of the membrane launches mechanome activation at focal adhesins while concomitantly putting genes into position for direct chemical interaction with the mechanosome messengers. Upon arrival at the target gene, this transcription factor conceptually adds data to the physically altered DNA conformation to influence the desired genetic expression as the new DNA “message” forms a more stable architectural form.

Apparently, these phenomena are determinate engines involved in techniques to engineer novel genetic expression and morphogenesis and are predictable due to the fact that wound healing recapitulates regional ontogeny. It is crucial to recall that a wound or load separately is not capable of eliciting such profound change in permanent alveolus architecture. It is synergistic interaction that delivers the clinical outcome, an emergent event from a multifaceted chaotic, or nonlinear complex dynamical system.

Enter the Exosome

A natural progression from the Wilkos’ PAOO flows to stem cell regeneration and then to MSC products, passing ultimately to exosome injections.¹⁰ Significant exosome developments have occurred in the last decade. An exosome is a small, spherical, membrane‐bound vesicle containing genomic material which is released by short‐lived MSCs. They are produced and released by all stem cells regardless of embryologic characteristics. Exosomes, once released from stem cells, are termed “extracellular vesicles” (EV) (Figure 1.18a–c).

EV’s liaise cell‐to‐cell communication by transferring cellular data, proteins, and RNA, among cells. This intercellular communication is important for regulating immune responses, cellular signaling, and waste removal. Overall, exosomes are commercially available¹¹ and can play a crucial role in the regenerative process. We have found that adding exosomes to bone grafts of any kind can add significant regenerative potential which may potentiate the effects of epigenetic perturbation and orthodontic loading.

TMP and MOP Nonsurgical Alternatives

Where sufficient labial bone is present, one may ask if a nonsurgical alternative can evoke an effective perturbation. Just as the surgical evolution trended toward less morbidity, the same evolution applies to nonsurgical techniques. The question begged is: Can a minimal‐intervention technique be employed successfully and comfortably in an out‐patient setting to achieve the same outcomes as the surgical techniques. This question was answered affirmatively in 2005 when we introduced a reasonable alternative to surgical flap reflection (Murphy, 2005a, b, 2006). A significant cohort of patients absolutely will never submit to elective surgery yet desire a well‐treated smile. The objective of this alternative was to solicit RAP without the stigmata of oral surgery.

After studying PAOO and understanding the RAP phenomenon, the author designed a non‐SFOT. Encouraged by the results of physiologic manipulation of the osteogenic/osteoclastic dynamic, a series of small alveolus bone perforations were made directly through the gingiva without reflecting a surgical flap. The procedure demonstrated excellent accelerated OTM and is called “Trans‐Medullary Perturbation”, (TMP), technically a kind of “medull‐otomy”. It worked very well when sufficient bone can be identified with tomography and the arch length deficiencies were minor. It is also important to note that the perforations went 4–8 mm deep into the alveolus medulla (spongiosa). The effect appeared within a week and created a profound increase in physiologic tooth mobility. It is especially noteworthy when serial perforation is employed a fortnight apart. In such cases, movement of the teeth could be achieved with simple finger pressure within a few minutes. And, in such cases no attachment loss was evident (Murphy, 2014) if the perforations did not impinge within 3–4 mm of the alveolus osseous crest.

This nonsurgical perforation was first introduced to orthodontists in 2005 at the Eighth International Conference of the Harvard Society for the Advancement of Orthodontics in Phuket, Thailand and again at the annual meeting of the American Academy of Periodontology the same year. It is significant and encouraging that the procedure was well received in both venues. So as of this writing, TMP has been working well for nearly 20 years.

A subsequent replication of TMP was introduced in New York City and validated in humans 7 years later (Alikhani et al., 2012). The procedure, less definitive than TMP was called micro‐osteoperforation (MOP). The MOP perforation technique differs significantly from TMP because it cuts less deeply into the cortex. It has been shown to be effective by local advocates but when combined with a flap is identical to the punctate perforations that the Wilcko brothers introduced in 2001.

Nonetheless, it has been shown by Alikhani et al. (2012) that TMP can double the rate of dental translation and may be an effective treatment adjunct. The scientific justification for TMP was essentially a replication of the Wilcko (2000, 2001) technique only “flapless.” It is noteworthy that superficial perforation may fail to recruit significantly more RAP just as timid surgery fails. That is why TMP was designed to penetrate 4–8 into the medullary bone for maximum effectiveness. Others have confirmed the efficacy of the TMP procedure by replicating the protocols in laboratory animals (Teixeira et al., 2010) and humans (Alikhani et al., 2012; Alansari et al., 2017; Feizbakhsh et al., 2018).

TMP is executed under local anesthesia with epinephrine‐fortified lidocaine. This method helps form a blood clot to protect the perforated site; patients report little to no pain. The mild post‐operative discomfort is ironic since a deep penetration elicits a transient but profoundly therapeutic osteopenia. Their discomfort is easily managed with one to two doses of NSAIDs. The images herein, (and in Figure 1.19) were first presented in 2005 as mentioned above, at that presentation it was emphasized that TMP success depends upon a release of medullary stem cells in addition to the osteopenia. It is the deep medullary stimulation that accounts for the efficacy of TMP in contrast to the effete response to MOP penetration of merely the cortical bone.

This author’s theory thus successfully ran the gauntlet of skepticism and is now successfully employed for several clinical challenges. The difference between TMP and its derivative, MOP is that the latter produces divots too shallow for many cases. But for minor tooth movement, MOP should suffice. TMP can be used for any case normally planned for surgery, but not in cases where bony support is questionable. Conceptually, molecular‐level alterations of genetic expression with surgical perturbation and TMP are the same. So, TMP may also enhance stability if phenotype is altered significantly. But such stability studies have not yet been published.

The clinical success of the TMP innovation has been summarized well in a review by Chou and Alikhani (2017). But there is some disagreement on how well shallow perforations may work. The authors note “Three MOPs with a depth of 4 mm can be … effective method to increase the rate of tooth movement. However, … depths of 4–7 mm does not additionally enhance tooth movement.” (Ozkan and Arici, 2021) Our experience is just the opposite. We speculate that no coordinated osseous strain accompanied the authors’ perforations. This is why, we generally sink perforations at least four to eight deep and perturb the medullary bone with sweeping movements within 3–4 mm of each other. This is intended to elicit medullary osteopenia, the medium through which teeth move. Medullary RAP will not follow innocuous shallow divots in thick cortices. In our experience – given wide biological diversity – that greater depth penetration can indeed turn a failing case into success. But often the failure is declared too early in treatment. Some failure to accelerate OTM can also be attributed to the natural OTM latency period seen in traditional OTM. Thus, patience and the willingness to apply multiple doses of TMP will usually salvage a refractory response.

The failure of Chau and Alikhani to achieve RAP with deeper perforations brings out a basic problem with clinical studies; they do not always replicate protocols faithfully. A good example of inadequate penetration and inadequate clinical management was published by Swapp (2015) and Cramer (2019).

To their credit, Swapp et al. (2015) claimed the effect of accelerated tooth movement requires penetration into the medullary bone which confirms our observations. Referring to the corticision study of Kim and Tae (2003), they say:

… tooth movements that were 3.75 times faster than the controls.

… the blade was driven up to 10 mm into the cortical bone; this is significantly deeper than any reported corticotomy procedure and might have been expected to damage both the cortical and trabecular bone surrounding the teeth that were moved. These studies suggest that the awl injuries produced in this study might not have been deep enough to affect the bone mesial to the root being moved. (Emphasis added.)

All cases must be individualized beyond the perfunctory compliance with TMP protocols. This is why, we generally sink perforations four to eight deep with a sweeping motion and cluster them within 3–4 mm of each other. Swapp’s research affirms that the term MOP should be relegated to shallow penetration, as the term TMP refers to more definitive spongiosa management and less on mere cortical management pe se.

It should be noted that some cases (in concordance with biological principles of wide variance) will demonstrate almost complete recalcitrance to therapy, regardless of extreme decortication efforts. From a logical point of view of view, definitive perforations of TMP as an SFOT intermitent supplement can release endogenous medullary stem cells which are necessary for augmentation success and morphotype modification. This produces a more profound immediate effect (Ozkan and Arici, 2021) which can lend greater stability over time.

The Problems with Orthodontics

A failure to achieve sufficient osteopenic state to escape canalization and facilitate clinical OTM will occur for specific reasons, some known and preventable, e.g., inadequate depth of perforation, poor patient compliance, and a myriad of idiopathic factors common to biological systems. The job we have at hand is to elaborate on the phenomenon for the edification of our colleagues and to protect patients from untoward events. Therefore, it is not our responsibility, in this chapter, to prove that TMP can work. That has been demonstrated. As the burden of proof that all swans are white is vitiated by an observation of one black swan, our cases for over a decade document many “black swans.”

All that critics have achieved with their experimental failure was to demonstrate that their experimental design was inappropriate, or they have documented the obvious: biology is not always predictable. The results of individual failures do not demonstrate a universal truth. Logically, they may only claim that a technique is not universally possible for all doctors. True. It is not possible to replicate protocol if one performs it wrong.

PAOO and SCAT Step‐by‐Step

PAOO/SCAT and corrective periodontal surgeries can be conducted simultaneously according to expert consensus. The protocol for using PAOO/SCAT with infected periodontia is illustrated in Figure 1.22a–h. The protocol follows:

1. Place all brackets on the labial surface of teeth as the manufacturer suggests.
2. Reflect a full mucoperiosteal surgical flap to a depth necessary to visualize the alveolus bone. It is not always necessary to reflect the flap completely into the vestibule because that will cause excessive postoperative edema and facial ecchymosis. But do not reflect the maxillary incisive papilla (Figure 1.21, black arrow). Flap reflection may occur on the labial surface only coupled with TMP on the palatal surface as the incisive papilla is untouched.
3. Debride all accretions, root‐plane the root surface, then proceed with periodontal osseous recontouring at the surgeon’s discretion.
4. Decorticate the alveolus cortex until copious medullary bleeding is observed but do not approach within 3–4 mm of the osseous crest.
5. Soak the root surfaces with ethylenediaminetetraacetic acid (EDTA).
6. Suture the surgical flap with a continuous (“sling”) suture at doctor’s discretion forming a pouch to accept the graft. This ensures easy graft containment.
7. Apply graft abundantly to the root surfaces and “overfill” as desired.
8. Coronally position the surgical flap 1–2 mm coronal to cementoenamel junctions (CEJ).
9. Immediately activate the “wound” with a nickel–titanium archwire after the last suture is tied.
10. Cover the sutured wound with 2‐octyl‐cyanoacrylate dressing and prescribe NSAIDs¹² for discomfort. Proceed with orthodontic therapy activating the wires weekly or semiweekly, as the orthodontic success dictates.
11. After a few weeks, advise the patient of the activation objective and tell them to return when that objective, e.g., space closure, can be achieved, in days or even hours after activation.
12. Continue to activate as necessary depending upon the patient’s unique response. Avoid any arbitrary schedule, e.g., fortnight intervals. Adjustment goals may be accomplished within days or hours when the osteopenic state is well managed.

Flap reflection in the esthetic zone risks loss of papillae in the case of a flap marginal slough, a rare but significant event. But if a labial flap is reflected off the maxillary midline the appearance of an open midline, embrasure may unfairly be attributed to the clinical style of the surgeon. Another alternative to PAOO that might ensure embrasure integrity in the esthetic zone is to operate with a split flap (Figure 1.21, white arrow) or place initial incisions solely within the attached gingiva, not the sulcus (Figure 1.21).

Figure 1.21 demonstrates papillary integrity (black Arrow) can also be preserved with a single split labial flap (white arrow) leaving the palatal interproximal tissue intact. These practical gambits may compromise RAP somewhat since buccal and lingual flaps are reflected as dictated in the original PAOO protocol. But we have been very pleased with the outcomes of a singular labial flap combined with lingual TMP.

Figure 1.22a–g demonstrates the management of these so‐called “hot lesion” (severely inflamed periodontal infection). Initial therapy was excluded from the treatment plan to take advantage of the rich supply of growth factors and endogenous undifferentiated MSCs in such lesions. A protracted initial therapy of scaling and subgingival root planning eliminates these robust healing agents. It is well known that there is no difference in clinical outcome quality if scaling and root planning are performed during surgery or before. The advantage of performing initial therapy is to become familiar with the psychological state of the patient. The other advantage of initial therapy is that it reduces surgical time. However, the loss of healing potential in regenerative surgery is too great a price to pay for excessive initial therapy. Note, in Figure 1.22c, d, the copious bleeding that was created by the deep and numerous decortication pattern. This bleeding is a blessing to any regenerative procedure. So are “hot lesions.”

After the periodontal lesions were debrided and the teeth were root‐planed, physiologic topography was created with standard periodontal osseous recontouring. But where deep infrabony pockets precluded aggressive osseous recontouring, e.g., the circumferential defect around tooth #25 regenerative treatment with viable stem cell allograft was selected by the patient. Immediately after the periodontal lesion was debrided, a generalized corticotomy ensued. The sequence of osseous recontouring vis a vis decortication lies within the surgeon’s discretion. The stem cell allograft was placed according to the PAOO protocol. The mucoperiosteal flap was sutured to place and followed by a cyanoacrylate dressing; “wound activation” here was achieved with a 0.018” nickel–titanium arch wire in full bracket engagement.

A subsequent biopsy and microscopic inspection (Figure 1.22h) of the grafted site demonstrated abundant osseous regeneration (white arrow) adjacent to a DFDBA matrix/carrier (green arrow). OTM did not interfere with osteogenesis, as clinical tooth alignment was accelerated. The asterisk in Figure 1.22f indicates the location from which the biopsy was taken after 3 months. It is true as a generality that tooth movement should not be done in areas of active but untreated periodontal infection. But occasionally periodontal infection treatment can indeed be done simultaneously with orthodontic treatment in this coordinated manner. The bone is just as stable because an improved phenotype was created by load placed on the graft differentiation, as the roots were moved into the desire location during bone healing. This phenomenon is entirely consistent with Moss’s functional matrix theory: the roots of the teeth constitute the functional matrix of a new alveolus phenotype (Figures 1.23 and 1.24).

Figure 1.23, a Wilcko document, illustrates how copious bone can be created de novo with the PAOO protocol. The original surgery in this case was performed on January 7, 1997. Surgical reentry to inspect the bone stability was performed 8 years later January 6, 2005. In Figure 1.24a, note the bony dehiscence on teeth #27 and #29. These are common sites of bony dehiscence, gingival recession, and minimal zones of keratinized attached gingiva. In Figure 1.24b, the outlined dehiscence and fenestrations are more discernable. Often these cases present with the clinical topography of an old‐fashioned washboard. In such cases, this “washboard effect” has often been proposed as an indication for bicuspid extraction regardless of how it might affect facial appearance. This extraction indication is no longer valid.

In cases of retrusive and thin lips, an injudicious bicuspid extraction would seriously compromise facial appearance. When we have the fate of a child’s face for a lifetime, prudence and serious consideration of PAOO as an explicit element of informed consent is, in our modest view, a professional imperative. Figures 1.23 (2b) and (2c) demonstrate how much stable bone can be created with PAOO. Since this is a new phenotype both the dental pattern and the integrity of the alveolus bone are extremely stable. An eight‐year stability has been clinically demonstrated in this case. Basic logic tells us that stability of bone at eight years argues for stability indefinitely if the roots are maintained as the functional matrix of the new phenotype.

In summary, stability of the bony phenotype is caused by loading a healing bone graft. A labial loading stimulates endogenous and grafted stem cells to differentiate into a new bony form. That is, the key to success lies in the simultaneous interaction of bone graft differentiation and load. Neither the singular effect of incisor advancement nor grafts alone will suffice. Unloaded grafts on the labial alveolus cortex will normally resorb over time when the graft is not loaded during healing and graft differentiation, and incisor advancement will only bring minimal bone with it. This is not the case with PAOO/SCAT; it is manifestly a bone‐generating machine.

Ortho‐Infection

A discussion of OTM is painfully incomplete without addressing the potential for its predictable and irreversible tissue damage by other oral infections, e.g., hyperplastic gingivitis and focal decalcification. The syndrome¹² is so closely related to traditional fixed appliance therapy that we refer to as, Ortho‐Infection.

Hyperplastic gingivitis, periodontitis, and focal decalcification (so‐called “white spots”) are the most common side effects of fixed‐appliance OTM. Some speculate that SFOT may amplify the damage of the side effects. This is not true; indeed, the opposite is true. Accelerated orthodontic care reduces the chance of side effects most notably, apical root resorption, adjustment pain, caries, and periodontal infection. All these complications are time‐sensitive. Periodontal infections are particularly onerous because they are self‐perpetuating with a net tissue loss. First, let us consider the most serious, periodontitis. For 50 years, we have known that irreversible crestal attachment (bone) loss may occur in orthodontically treated adolescents.

In the classic study by Zachrisson and Alnaes (1974), the article states “The orthodontic patients demonstrated slightly, but significantly more loss of attachment clinically than did the reference subjects.” We object to this interpretation of empirical data. The mean loss was 0.41 mm which seems insignificant. But the devil lies in the statistical details. The report by Zachrisson and Alnaes pooled data. A closer look at the Zachrisson and Alnaes data demonstrate that a cohort of individual patients did indeed suffer clinically significant attachment loss. Data pooling is misleading to conscientious clinicians. It obscures important findings in a sea of numbers. The error of pooling lets the authors to emphasize an arithmetic mean, a descriptive statistic important to discern general trends when standard deviations are also reported. But an arithmetic mean can be an intellectual trap to practical clinicians who treat individual patients (A jocular adage in statistical classes is that a man can drown in a lake that only averages 2 ft deep if he just steps into one small spot that is 20 ft deep). The objective of microbial management is to create a microecological niche in which commensal organisms can thrive. So, a clinically relevant measure of lesion occurrence is not the midpoint on a Gaussian frequency distribution. Rather, a measure of range demonstrates a worst‐case scenario for the individuals we treat. We treat individuals not arithmetic means. More academic efforts should be directed toward the infection that we orthodontists are not taught to see, often ignore, yet always create. The individualized creation of a commensal niche can be achieved with astute patient collaboration.

However, the modern abandonment of orthodontic bands, with inevitable “overhangs,” in favor of bonded brackets is a very good start. Beyond that improvement, all too often only a perfunctory acknowledgment of the infection problem is made with a token admonition to “brush better.” The problems are more serious in adult patients and very problematic when surgery is involved. So, clinicians should be periodontally vigilant and, solicit ancillary supportive care.

As orthodontists, we operate in a bacterial stew of pathogens and commensal microorganisms. Yet, very little bacteriology is taught in orthodontic training programs. This is unfortunate because the bacterial biofilm in which pathogens thrive is ubiquitous. So, its effect on treatment must be acknowledged and constantly modulated. Knowing how a bacterial niche is created around orthodontic appliances gives us insight into many side effects. It must be noted that these infection side effects are predictable in the aggregate but not necessarily foreseeable in the particular. Thus, a kind of universal precaution must always be maintained, and every patient must be informed individually of untoward bacterial events.

Compliance Dialogue

Patient:

 This brushing method causes gums bleeding; isn’t that bad?

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