The Biologic Basis of Orthodontic Therapy

Periodontal Ligament Structure and Function

Each tooth is attached to and separated from the adjacent alveolar bone by a heavy collagenous supporting structure, the periodontal ligament (PDL). Under normal circumstances, the PDL occupies a space approximately 0.5 mm in width around all parts of the root. By far the major component of the ligament is a network of parallel collagenous fibers, inserting into cementum of the root surface on one side and into a relatively dense bony plate, the lamina dura, on the other side. These supporting fibers run at an angle, attaching farther apically on the tooth than on the adjacent alveolar bone. This arrangement, of course, resists the displacement of the tooth expected during normal function (Figure 8-1).

Although most of the PDL space is taken up with the collagenous fiber bundles that constitute the ligamentous attachment, two other major components of the ligament must be considered. These are (1) the cellular elements, including mesenchymal cells of various types along with vascular and neural elements, and (2) the tissue fluids. Both play an important role in normal function and in making orthodontic tooth movement possible.

The principal cellular elements in the PDL are undifferentiated mesenchymal cells and their progeny in the form of fibroblasts and osteoblasts. The collagen of the ligament is constantly being remodeled and renewed during normal function. The same cells can serve as both fibroblasts, producing new collagenous matrix materials, and fibroclasts, destroying previously produced collagen.¹ Remodeling and recontouring of the bony socket and the cementum of the root is also constantly being carried out, though on a smaller scale, as a response to normal function.

Fibroblasts in the PDL have properties similar to osteoblasts, and new alveolar bone probably is formed by osteoblasts that differentiated from the local cellular population.² Bone and cementum are removed by specialized osteoclasts and cementoclasts, respectively. These multinucleated giant cells are quite different from the osteoblasts and cementoblasts that produce bone and cementum. Despite years of investigation, their origin remains controversial. Most are of hematogenous origin; some may be derived from stem cells found in the local area.³

Although the PDL is not highly vascular, it does contain blood vessels and cells from the vascular system. Nerve endings are also found within the ligament, both the unmyelinated free endings associated with perception of pain and the more complex receptors associated with pressure and positional information (proprioception).

Finally, it is important to recognize that the PDL space is filled with fluid; this fluid is the same as that found in all other tissues, ultimately derived from the vascular system. A fluid-filled chamber with retentive but porous walls could be a description of a shock absorber, and in normal function, the fluid allows the PDL space to play just this role.

Response to Normal Function

During masticatory function, the teeth and periodontal structures are subjected to intermittent heavy forces. Tooth contacts last for 1 second or less; forces are quite heavy, ranging from 1 or 2 kg while soft substances are being chewed, up to as much as 50 kg against a more resistant object. When a tooth is subjected to heavy loads of this type, quick displacement of the tooth within the PDL space is prevented by the incompressible tissue fluid. Instead, the force is transmitted to the alveolar bone, which bends in response.

The extent of bone bending during normal function of the jaws (and other skeletal elements of the body) is often not appreciated. The body of the mandible bends as the mouth is opened and closed, even without heavy masticatory loads. Upon wide opening, the distance between the mandibular molars decreases by 2 to 3 mm. In heavy function, individual teeth are slightly displaced as the bone of the alveolar process bends to allow this to occur, and bending stresses are transmitted over considerable distances. Bone bending in response to normal function generates piezoelectric currents (Figure 8-2) that appear to be an important stimulus to skeletal regeneration and repair (see further discussion later in this chapter). This is the mechanism by which bony architecture is adapted to functional demands.

Very little of the fluid within the PDL space is squeezed out during the first second of pressure application. If pressure against a tooth is maintained, however, the fluid is rapidly expressed, and the tooth displaces within the PDL space, compressing the ligament itself against adjacent bone. Not surprisingly, this hurts. Pain is normally felt after 3 to 5 seconds of heavy force application, indicating that the fluids are expressed and crushing pressure is applied against the PDL in this amount of time (Table 8-1). The resistance provided by tissue fluids allows normal mastication, with its force applications of 1 second or less, to occur without pain.

Although the PDL is beautifully adapted to resist forces of short duration, it rapidly loses its adaptive capability as the tissue fluids are squeezed out of its confined area. Prolonged force, even of low magnitude, produces a different physiologic response—remodeling of the adjacent bone. Orthodontic tooth movement is made possible by the application of prolonged forces. In addition, light prolonged forces in the natural environment—forces from the lips, cheeks, or tongue resting against the teeth—have the same potential as orthodontic forces to cause the teeth to move to a different location (see the discussion of equilibrium factors in Chapter 5).

Role of the Periodontal Ligament in Eruption and Stabilization of the Teeth

The phenomenon of tooth eruption makes it plain that forces generated within the PDL itself can produce tooth movement. After a tooth emerges into the mouth, further eruption depends on metabolic events within the PDL, including but perhaps not limited to formation, cross-linkage, and maturational shortening of collagen fibers (see Chapter 3). This process continues, although at a reduced rate, into adult life. A tooth whose antagonist has been extracted will often begin to erupt again after many years of apparent quiescence.

The continuing presence of this mechanism indicates that it may produce not only eruption of the teeth under appropriate circumstances but also active stabilization of the teeth against prolonged forces of light magnitude. It is commonly observed that light prolonged pressures against the teeth are not in perfect balance, as would seem to be required if tooth movement were not to occur (Figure 8-3). The ability of the PDL to generate a force and thereby contribute to the set of forces that determine the equilibrium situation, probably explains this.

Active stabilization also implies a threshold for orthodontic force, since forces below the stabilization level would be expected to be ineffective. The threshold, of course, would vary depending on the extent to which existing soft tissue pressures were already being resisted by the stabilization mechanism. In some experiments, the threshold for orthodontic force, if one was found at all, appeared extremely low. In other circumstances, a somewhat higher threshold, but still one of only a few grams, seems to exist. The current concept is that active stabilization can overcome prolonged forces of a few grams at most, perhaps up to the 5 to 10 gm/cm² often observed as the magnitude of unbalanced soft tissue resting pressures.

Biologic Control of Tooth Movement

Before discussing in detail the response to orthodontic force, it is necessary to consider the biologic control mechanisms that lead from the stimulus of sustained force application to the response of orthodontic tooth movement. Two possible control elements, biologic electricity and pressure-tension in the PDL that affects blood flow, are contrasted in the two major theories of orthodontic tooth movement. The bioelectric theory relates tooth movement at least in part to changes in bone metabolism controlled by biologic electricity that are produced by light pressure against the teeth. The pressure–tension theory relates tooth movement to cellular changes produced by chemical messengers, traditionally thought to be generated by alterations in blood flow through the PDL. Pressure and tension within the PDL, by reducing (pressure) or increasing (tension) the diameter of blood vessels in the ligament space, could certainly alter blood flow. The two theories are neither incompatible nor mutually exclusive, and it appears that both mechanisms may play a part in the biologic control of tooth movement.⁴

Effects of Force Magnitude

The heavier the sustained pressure, the greater should be the reduction in blood flow through compressed areas of the PDL, up to the point that the vessels are totally collapsed and no further blood flows (Figure 8-6). That this theoretical sequence actually occurs has been demonstrated in animal experiments, in which increasing the force against a tooth causes decreasing perfusion of the PDL on the compression side (see Figures 8-4 and 8-5).⁹ Let us consider the time course of events after application of orthodontic force, contrasting what happens with heavy versus light force (Table 8-2).

When light but prolonged force is applied to a tooth, blood flow through the partially compressed PDL decreases as soon as fluids are expressed from the PDL space and the tooth moves in its socket (i.e., in a few seconds). Within a few hours at most, the resulting change in the chemical environment produces a different pattern of cellular activity. Animal experiments have shown that increased levels of cyclic adenosine monophosphate (cAMP), the “second messenger” for many important cellular functions, including differentiation, appear after about 4 hours of sustained pressure. This amount of time to produce a response correlates rather well with the human response to removable appliances. If a removable appliance is worn less than 4 to 6 hours per day, it will produce no orthodontic effects. Above this duration threshold, tooth movement does occur.

What happens in the first hours after sustained force is placed against a tooth, between the onset of pressure and tension in the PDL and the appearance of second messengers a few hours later? Experiments have shown that prostaglandin and interleukin-1 beta levels increase within the PDL within a short time after the application of pressure, and it is clear now that prostaglandin E (PgE) is an important mediator of the cellular response. Since prostaglandins are released when cells are mechanically deformed, it appears that prostaglandin release is a primary rather than a secondary response to pressure. At the molecular level, we are beginning to understand how these effects are created. Focal adhesion kinase (FAK) appears to be the mechanoreceptor in PDL cells, and its compression is at least part of the reason that PgE₂ is released.¹⁰ Experiments have shown that concentrations of the receptor activator of nuclear factor-kappa ligand (RANKL) and osteoprotegerin (OPG) in gingival crevicular fluid increase during orthodontic tooth movement, which suggests that PDL cells under stress may induce the formation of osteoclasts through upregulation of RANKL.¹¹ Other chemical messengers, particularly members of the cytokine family but also nitric oxide (NO) and other regulators of cellular activity, also are involved.¹² Since drugs of various types can affect both prostaglandin levels and other potential chemical messengers, it is clear that pharmacologic modification of the response to orthodontic force is more than just a theoretical possibility (see further discussion below).

For a tooth to move, osteoclasts must be formed so that they can remove bone from the area adjacent to the compressed part of the PDL. Osteoblasts also are needed to form new bone on the tension side and remodel resorbed areas on the pressure side. Prostaglandins have the interesting property of stimulating both osteoclastic and osteoblastic activity, making it particularly suitable as a mediator of tooth movement. If parathyroid hormone is injected, osteoclasts can be induced in only a few hours, but the response is much slower when mechanical deformation of the PDL is the stimulus, and it can be up to 48 hours before the first osteoclasts appear within and adjacent to the compressed PDL. Studies of cellular kinetics indicate that they arrive in two waves, implying that some (the first wave) may be derived from a local cell population, while others (the larger second wave) are brought in from distant areas via blood flow. These cells attack the adjacent lamina dura, removing bone in the process of “frontal resorption,” and tooth movement begins soon thereafter. At the same time, but lagging somewhat behind so that the PDL space becomes enlarged, osteoblasts (recruited locally from progenitor cells in the PDL) form bone on the tension side and begin remodeling activity on the pressure side.¹³

The course of events is different if the sustained force against the tooth is great enough to totally occlude blood vessels and cut off the blood supply to an area within the PDL. When this happens, rather than cells within the compressed area of the PDL being stimulated to develop into osteoclasts, a sterile necrosis ensues within the compressed area. In clinical orthodontics it is difficult to avoid pressure that produces at least some avascular areas in the PDL, and it has been suggested that releasing pressure against a tooth at intervals, while maintaining the pressure for enough hours to produce the biologic response, could help in maintaining tissue vitality. This seems to be the mechanism by which chewing on a plastic wafer or chewing gum after orthodontic force is applied reduces pain—chewing force briefly displaces the tooth and allows a spurt of blood into compressed areas, thereby reducing the size of necrotic areas in the PDL.

Because of its histologic appearance as the cells disappear, an avascular area in the PDL traditionally has been referred to as hyalinized (see Figure 8-4). Despite the name, the process has nothing to do with the formation of hyaline connective tissue. It represents the inevitable loss of all cells when the blood supply is totally cut off. When this happens, remodeling of bone bordering the necrotic area of the PDL must be accomplished by cells derived from adjacent undamaged areas.

After a delay of several days, cellular elements begin to invade the necrotic (hyalinized) area. More importantly, osteoclasts appear within the adjacent bone marrow spaces and begin an attack on the underside of the bone immediately adjacent to the necrotic PDL area (Figure 8-7). This process is appropriately described as undermining resorption, since the attack is from the underside of the lamina dura. When hyalinization and undermining resorption occur, an inevitable delay in tooth movement results. This is caused first by a delay in stimulating differentiation of cells within the marrow spaces, and second because a considerable thickness of bone must be removed from the underside before any tooth movement can take place. The different time course of tooth movement when frontal resorption is compared with undermining resorption is shown graphically in Figure 8-8.

Not only is tooth movement more efficient when areas of PDL necrosis are avoided, but pain is also lessened. However, even with light forces, small avascular areas are likely to develop in the PDL, and tooth movement will be delayed until these can be removed by undermining resorption. The smooth progression of tooth movement with light force shown in Figure 8-8 may be an unattainable ideal when continuous force is used. In clinical practice, tooth movement usually proceeds in a more stepwise fashion because of the inevitable areas of undermining resorption.

Effects of Force Distribution and Types of Tooth Movement

From the previous discussion, it is apparent that the optimum force levels for orthodontic tooth movement should be just high enough to stimulate cellular activity without completely occluding blood vessels in the PDL. Both the amount of force delivered to a tooth and the area of the PDL over which that force is distributed are important in determining the biologic effect. The PDL response is determined not by force alone, but by force per unit area, or pressure. Since the distribution of force within the PDL, and therefore the pressure, differs with different types of tooth movement, it is necessary to specify the type of tooth movement, as well as the amount of force in discussing optimum force levels for orthodontic purposes.

The simplest form of orthodontic movement is tipping. Tipping movements are produced when a single force (e.g., a spring extending from a removable appliance) is applied against the crown of a tooth. When this is done, the tooth rotates around its “center of resistance,” a point located about halfway down the root. (A further discussion of the center of resistance and its control follows in Chapter 9.) When the tooth rotates in this fashion, the PDL is compressed near the root apex on the same side as the spring and at the crest of the alveolar bone on the opposite side from the spring (Figure 8-9). Maximum pressure in the PDL is created at the alveolar crest and at the root apex. Progressively less pressure is created as the center of resistance is approached, and there is minimum pressure at that point.

In tipping, only one-half of the PDL area that could be loaded actually is. As shown in Figure 8-9, the “loading diagram” consists of two triangles, covering half of the total PDL area. On the other hand, pressure in the two areas where it is concentrated is high in relation to the force applied to the crown. For this reason, forces used to tip teeth must be kept quite low. Both experiments with animals and clinical experience with humans suggest that tipping forces for a single-rooted tooth should not exceed approximately 50 gm, and lighter forces are better for smaller teeth (which have a smaller PDL).

If two forces are applied simultaneously to the crown of a tooth, the tooth can be moved bodily (translated), that is, the root apex and crown move in the same direction the same amount. In this case, the total PDL area is loaded uniformly (Figure 8-10). It is apparent that to produce the same pressure in the PDL and therefore the same biologic response, twice as much force would be required for bodily movement as for tipping. To move a tooth so that it is partially tipped and partially translated would require forces intermediate between those needed for pure tipping and bodily movement (Table 8-3).

In theory, forces to produce rotation of a tooth around its long axis could be much larger than those to produce other tooth movements, since the force could be distributed over the entire PDL rather than over a narrow vertical strip. In fact, however, it is essentially impossible to apply a rotational force so that the tooth does not also tip in its socket, and when this happens, an area of compression is created just as in any other tipping movement. For this reason, appropriate forces for rotation are similar to those for tipping.

Extrusion and intrusion are also special cases. Extrusive movements ideally would produce no areas of compression within the PDL, only tension. Like rotation, this is more a theoretical than a practical possibility, since if the tooth tipped at all while being extruded, areas of compression would be created. Even if compressed areas could be avoided, heavy forces in pure tension would be undesirable unless the goal was to extract the tooth rather than to bring alveolar bone along with the tooth. Extrusive forces, like rotation, should be about the same magnitude as those for tipping.

For many years, it was considered essentially impossible to produce orthodontic intrusion of teeth. Now it is clear that clinically successful intrusion can be accomplished, but only if very light forces are applied to the teeth. Light force is required for intrusion because the force will be concentrated in a small area at the tooth apex (Figure 8-11). As with extrusion, the tooth probably will tip somewhat as it is intruded, but the force still will be concentrated at the apex. Only if the force is kept very light can intrusion be expected.

Effects of Force Duration and Force Decay

The key to producing orthodontic tooth movement is the application of sustained force, which does not mean that the force must be absolutely continuous. It does mean that the force must be present for a considerable percentage of the time, certainly hours rather than minutes per day. As we have noted previously, animal experiments suggest that only after force is maintained for approximately 4 hours do cyclic nucleotide levels in the PDL increase, indicating that this duration of pressure is required to produce the “second messengers” needed to stimulate cellular differentiation.

Clinical experience suggests that there is a threshold for force duration in humans in the 4 to 8 hour range and that increasingly effective tooth movement is produced if force is maintained for longer durations. Although no firm experimental data are available, a plot of efficiency of tooth movement as a function of force duration would probably look like Figure 8-12. Continuous forces, produced by fixed appliances that are not affected by what the patient does, produce more tooth movement than removable appliances unless the removable appliance is present almost all the time. Removable appliances worn for decreasing fractions of time produce decreasing amounts of tooth movement.

Duration of force has another aspect, related to how force magnitude changes as the tooth responds by moving. Only in theory is it possible to make a perfect spring, one that would deliver the same force day after day, no matter how much or how little the tooth moved in response to that force. In reality, some decline in force magnitude (i.e., force decay) is noted with even the springiest device after the tooth has moved a short distance (though with the superelastic nickel–titanium materials discussed in Chapter 10, the decrease is amazingly small). With many orthodontic devices, the force may drop all the way to zero. From this perspective, orthodontic force duration is classified (Figure 8-13) by the rate of decay as:

Both continuous and interrupted forces can be produced by fixed appliances that are constantly present.

Intermittent forces are produced by all patient-activated appliances such as removable plates, headgear, and elastics. Forces generated during normal function (e.g., chewing, swallowing, speaking) can be viewed as a special case of intermittently applied forces, most of which are not maintained for enough hours per day to have significant effects on the position of the teeth.

There is an important interaction between force magnitude and how rapidly the force declines as the tooth responds. Consider first the effect of a nearly continuous force. If this force is quite light, a relatively smooth progression of tooth movement will result from frontal resorption. If the continuous force is heavy, however, tooth movement will be delayed until undermining resorption can remove the bone necessary to allow the tooth movement. At that time, the tooth will change its position rapidly, and the constant force will again compress the tissues, preventing repair of the PDL and creating the need for further undermining resorption and so on. Such a heavy continuous force can be quite destructive to both the periodontal structures and the tooth itself.

Consider now the effect of forces that decay fairly rapidly, so that the force declines to zero after the tooth moves only a short distance. If the initial force level is relatively light, the tooth will move a small amount by frontal resorption and then will remain in that position until the appliance is activated again. If the force level is heavy enough to produce undermining resorption, the tooth will move when the undermining resorption is complete. Then, since the force has dropped to zero at that point, it will remain in that position until the next activation. Although the original force is heavy, after the tooth moves there is a period for regeneration and repair of the PDL before force is applied again.

Theoretically, there is no doubt that light continuous forces produce the most efficient tooth movement. Despite the clinician’s best efforts to keep forces light enough to produce only frontal resorption, some areas of undermining resorption are probably produced in every clinical patient. The heavier forces that produce this response are physiologically acceptable only if the force level quickly drops to zero so that there is a period of repair and regeneration before the next activation or if the force decreases at least to the point that no second and third rounds of undermining resorption occur.

The bottom line: heavy continuous forces are to be avoided; heavy intermittent forces, though less efficient, can be clinically acceptable. To say it another way: the more perfect the spring in the sense of its ability to provide continuous force, the more careful the clinician must be that only light force is applied. Some of the cruder springs used in orthodontic treatment have the paradoxical virtue of producing forces that rapidly decline to zero and are thus incapable of inflicting the biologic damage that can occur from heavy continuous forces. Several clinical studies have indicated that heavy force applications may produce more tooth movement than lighter ones, which can be understood only from consideration of force decay characteristics.

Experience has shown that orthodontic appliances should not be reactivated more frequently than at 3-week intervals. A 4- to 6-week appointment cycle is more typical in clinical practice. Undermining resorption requires 7 to 14 days (longer on the initial application of force, shorter thereafter). When this is the mode of tooth movement and when force levels decline rapidly, tooth movement is essentially complete in this length of time. The wisdom of the interval between adjustments now becomes clear. If the appliance is springy and light forces produce continuous frontal resorption, there is no need for further activation. If the appliance is stiffer and undermining resorption occurs, but then the force drops to zero, the tooth movement occurs in the first 10 days or so, and there is an equal or longer period for PDL regeneration and repair before force is applied again. This repair phase is highly desirable and needed with many appliances. Activating an appliance too frequently, short circuiting the repair process, can produce damage to the teeth or bone that a longer appointment cycle would have prevented or at least minimized.

Drug Effects on the Response to Orthodontic Force

At present, drugs that stimulate tooth movement are unlikely to be encountered, although efforts to produce them continue. A major problem is how they would be applied to the local area where an effect on tooth movement is desired. Direct injection of prostaglandin into the PDL has been shown to increase the rate of tooth movement, but this is quite painful (a bee sting is essentially an injection of prostaglandin) and not very practical. Relaxin, a “pregnancy hormone” discovered in the 1980s, facilitates birth by causing a softening and lengthening of the cervix and pubic symphysis. It works by simultaneously reducing collagen synthesis and increasing collagen breakdown. The effects on collagen seem to make it more than just a pregnancy hormone, especially since its peak levels in pregnancy occur well before birth. Preliminary data in rats showed faster tooth movement with relaxin treatment, but a well-done, double-blinded clinical trial at the University of Florida, in which relaxin or just physiologic saline was injected adjacent to a tooth to be moved, did not show a consistent positive effect,¹⁴ and further clinical trials have been delayed. It seems likely that at some point in the future, drugs to facilitate tooth movement will become clinically useful—but there is no way to know how long it will take to develop them.

Drugs that inhibit tooth movement as a side effect of their use for other problems, however, already are encountered frequently, though not yet prescribed for their tooth-stabilizing effect. Two types of drugs are known to depress the response to orthodontic force and may influence current treatment: prostaglandin inhibitors for pain control (especially the more potent members of this group that are used in treatment of arthritis, like indomethacin),¹⁵ and the bisphosphonates used in treatment of osteoporosis (e.g., Fosamax, Actonel, Boniva, Reclast, Atelvia).

Effects of Local Injury: Corticotomy and Accelerated Tooth Movement

Because remodeling of alveolar bone is the key component of orthodontic tooth movement and bone remodeling is accelerated during wound healing,¹⁸ the idea that teeth could be moved faster after local injury to the alveolar process first appeared early in the history of orthodontics. The pioneer American oral surgeon Hullihan is said to have experimented with moving teeth after making cuts in alveolar bone in the late nineteenth century, and sporadic experiments with this continued into the early twentieth century. The approach was not widely adopted, however, for several reasons that included concerns about infections and bone loss in this pre-antibiotic era. In mid-century, the German surgeon Köle revived the idea that cuts between teeth could produce faster tooth movement.¹⁹ This method was advocated in the United States at that time by Merrill at the University of Oregon and was again suggested in 1978 by Gunderson et al,²⁰ but it was viewed as unnecessarily invasive and was not widely accepted.

The idea that local injury to alveolar bone, in the form of cuts through the cortex of the bone between the teeth, could speed tooth movement was presented again in the late 1990s and has achieved some acceptance as its mechanism has become better understood. At this point, there still are remarkably few papers in the peer-reviewed literature to document the results. The next section is an effort to put injury to alveolar bone, now usually called corticotomy, in a current perspective.

Anchorage: Resistance to Unwanted Tooth Movement

The term anchorage, in its orthodontic application, is defined in an unusual way: the definition as “resistance to unwanted tooth movement” includes a statement of what the dentist desires. The usage, though unusual, is clearest when presented this way. The dentist or orthodontist always constructs an appliance to produce certain desired tooth movements. For every (desired) action, there is an equal and opposite reaction. Inevitably, reaction forces can move other teeth as well if the appliance contacts them. Anchorage, then, is the resistance to reaction forces that is provided usually by other teeth, occasionally by the palate, sometimes by the head or neck (via extraoral force), and more and more often by anchors screwed to the jaws.

At this point, let us focus first on controlling unwanted tooth movement when some teeth are to serve as anchors. In planning orthodontic therapy, it is simply not possible to consider only the teeth whose movement is desired. Reciprocal effects throughout the dental arches must be carefully analyzed, evaluated, and controlled. An important aspect of treatment is maximizing the tooth movement that is desired, while minimizing undesirable side effects.

Mobility and Pain Related to Orthodontic Treatment

Orthodontic tooth movement requires not only a remodeling of bone adjacent to the teeth but also a reorganization of the PDL itself. Fibers become detached from the bone and cementum, then reattach at a later time. Radiographically, it can be observed that the PDL space widens during orthodontic tooth movement. The combination of a wider ligament space and a somewhat disorganized ligament means that some increase in mobility will be observed in every patient.

A moderate increase in mobility is an expected response to orthodontic treatment. The heavier the force, however, the greater the amount of undermining resorption expected, and the greater the mobility that will develop. Excessive mobility is an indication that excessive forces are being encountered. This may occur because the patient is clenching or grinding against a tooth that has moved into a position of traumatic occlusion. If a tooth becomes extremely mobile during orthodontic treatment, it should be taken out of occlusion and all force should be discontinued until the mobility decreases to moderate levels. Unlike root resorption, excessive mobility will usually correct itself without permanent damage.

If heavy pressure is applied to a tooth, pain develops almost immediately as the PDL is literally crushed. There is no excuse for using force levels for orthodontic tooth movement that produce immediate pain of this type. If appropriate orthodontic force is applied, the patient feels little or nothing immediately. Several hours later, however, pain usually appears. The patient feels a mild aching sensation, and the teeth are quite sensitive to pressure, so that biting a hard object hurts. The pain typically lasts for 2 to 4 days, then disappears until the orthodontic appliance is reactivated. At that point, a similar cycle may recur, but for almost all patients, the pain associated with the initial activation of the appliance is the most severe. It is commonly noted that there is a great deal of individual variation in any pain experience, and this is certainly true of orthodontic pain. Some patients report little or no pain even with relatively heavy forces, whereas others experience considerable discomfort with quite light forces.

The pain associated with orthodontic treatment is related to the development of ischemic (hyalinized) areas in the PDL that will undergo sterile necrosis. The increased tenderness to pressure suggests inflammation at the apex, and the mild pulpitis that usually appears soon after orthodontic force is applied probably also contributes to the pain. There does seem to be a relationship between the amount of force used and the amount of pain: all other factors being equal, the greater the force, the greater the pain. This is consistent with the concept that ischemic areas in the PDL are the major pain source, since greater force would produce larger areas of ischemia.

If the source of pain is the development of ischemic areas, strategies to temporarily relieve pressure and allow blood flow through compressed areas should help. In fact, if light forces are used, the amount of pain experienced by patients can be decreased by having them engage in repetitive chewing (of sugarless gum, a plastic wafer placed between the teeth, or whatever) during the first 8 hours after the orthodontic appliance is activated. Presumably this works by temporarily displacing the teeth enough to allow some blood flow through compressed areas, thereby preventing buildup of metabolic products that stimulate pain receptors. Light forces, however, are the key to minimizing pain as a concomitant of orthodontic treatment.

As we have noted previously, many drugs used to control pain have the potential to affect tooth movement because of their effects on prostaglandins. It has been suggested that acetaminophen (Tylenol) should be a better analgesic for orthodontic patients than aspirin, ibuprofen, naproxen, and similar prostaglandin inhibitors because it acts centrally rather than as a prostaglandin inhibitor. The counterargument against acetaminophen is that inflammation in the PDL contributes to the pain. Acetaminophen does not reduce inflammation, but the peripherally acting agents such as ibuprofen do, so they may offer more effective pain control. Based on a number of clinical studies, it now is widely accepted that acetaminophen and the over-the-counter NSAIDs are equally acceptable for controlling pain over the 3 to 4 days after an orthodontic appliance has been activated. It also is of interest that there is a strong placebo effect: reassuring patients and calling them at home the evening after appliances were placed was as effective in reducing pain as either type of drug in a recent and well-done study.³⁰

It is rare but not impossible for orthodontic patients to develop pain and inflammation of soft tissues, not because of the orthodontic force, but because of an allergic reaction. There are two major culprits when this occurs: a reaction to the latex in gloves or elastics and a reaction to the nickel in stainless steel bands, brackets, and wires. Latex allergies can become so severe as to be life threatening. Extreme care should be taken to avoid using latex products in patients reporting a latex allergy. Nickel is allergenic, and nearly 20% of the U.S. population show some skin reaction to nickel-containing materials (such as cheap jewelry and earrings). Fortunately, most children with a skin allergy to nickel have no mucosal response to stainless steel orthodontic appliances (which are about 8% nickel) and tolerate treatment perfectly well, but some do not.³¹ The typical symptoms of nickel allergy in an orthodontic patient are widespread erythema and swelling of oral tissues, developing 1 to 2 days after a stainless steel appliance is placed. For such patients, titanium brackets and tubes can be substituted for stainless steel (see Chapter 10), and beta-titanium archwires can be used instead of nickel-titanium (NiTi) or steel wires. If there is doubt about how a patient with a known nickel allergy will react to an orthodontic appliance, it is wise to bond one or two steel brackets and wait for a week or two to see if there will be an allergic response before placing a complete appliance.

Effects on the Pulp

Although pulpal reactions to orthodontic treatment are minimal, there is probably a modest and transient inflammatory response within the pulp, at least at the beginning of treatment. As we have noted previously, this may contribute to the discomfort that patients often experience for a few days after appliances are placed, but the mild pulpitis has no long-term significance.

There are occasional reports of loss of tooth vitality during orthodontic treatment. Usually, there is a history of previous trauma to the tooth, but poor control of orthodontic force also can be the culprit. If a tooth is subjected to heavy continuous force, a sequence of abrupt movements occurs, as undermining resorption allows increasingly large increments of change. A large enough abrupt movement of the root apex could sever the blood vessels as they enter. Loss of vitality has also been observed when incisor teeth were tipped distally to such an extent that the root apex, moving in the opposite direction, was actually moved outside the alveolar process (see Figure 8-25). Again, such movements probably would sever the blood vessels entering the pulp canal.

Since the response of the PDL, not the pulp, is the key element in orthodontic tooth movement, moving endodontically treated teeth is perfectly feasible. It may be necessary to treat some teeth endodontically, especially in adults receiving adjunctive orthodontic treatment (see Chapter 18), and then reposition them orthodontically. There is no contraindication to doing this. Severe root resorption should not be expected as a consequence of moving a nonvital tooth that has had proper endodontic therapy. One special circumstance is a tooth that experienced severe intrusive trauma and required pulp therapy for that reason.³² If such a tooth must be repositioned orthodontically, resorption seems less likely if a calcium hydroxide fill is maintained until the tooth movement is completed, and then the definitive root canal filling is placed.³³

Effects on Root Structure

Orthodontic treatment requires remodeling of bone adjacent to the tooth roots. For many years, it was thought that the roots were not remodeled in the same way as bone. More recent research has made it plain that when orthodontic forces are applied, there usually is some remodeling of the cementum on the root surface as well as the adjacent bone.

Rygh and coworkers have shown that cementum adjacent to hyalinized (necrotic) areas of the PDL is “marked” by this contact and that clast cells attack this marked cementum when the PDL area is repaired.³⁴ This observation helps explain why heavy continuous orthodontic force can lead to severe root resorption. Even with the most careful control of orthodontic force, however, it is difficult to avoid creating some hyalinized areas in the PDL. It is not surprising therefore that careful examination of the root surfaces of teeth that have been moved reveals repaired areas of resorption of both cementum and dentin of the root (Figure 8-27). It appears that cementum (and dentin, if resorption penetrates through the cementum) is removed from the root surface, then cementum is restored in the same way that alveolar bone is removed and then replaced. Root remodeling, in other words, is a constant feature of orthodontic tooth movement, but permanent loss of root structure would occur only if repair did not replace the initially resorbed cementum.

Repair of the damaged root restores its original contours, unless the attack on the root surface produces large defects at the apex that eventually become separated from the root surface (Figure 8-28). Once an island of cementum or dentin has been cut totally free from the root surface, it will be resorbed and will not be replaced. On the other hand, even deep defects in the form of craters into the root surface will be filled in again with cementum once orthodontic movement stops. Therefore permanent loss of root structure related to orthodontic treatment occurs primarily at the apex. Sometimes there is a reduction in the lateral aspect of the root in the apical region.

Shortening of tooth roots during orthodontic treatment occurs in three distinct forms that must be distinguished when the etiology of resorption is considered.

Effects of Treatment on the Height of Alveolar Bone

At the root apex, if the balance between apposition and resorption of the root surface moves too far toward resorption, irreversible shortening of the root may occur. It seems logical to suspect that this might also happen at the alveolar bone crest and that another effect of orthodontic treatment might be loss of alveolar bone height. Since the presence of orthodontic appliances increases the amount of gingival inflammation, even with good hygiene, this potential side effect of treatment might seem even more likely.

Fortunately, excessive loss of crestal bone height is almost never seen as a complication of orthodontic treatment. Loss of alveolar crest height in one large series of patients averaged less than 0.5 mm and almost never exceeded 1 mm, with the greatest changes at extraction sites.³⁸ Minimal effects on crestal alveolar bone levels also are observed on long-term follow-up of orthodontic patients. The reason is that the position of the teeth determines the position of the alveolar bone. When teeth erupt or are moved, they bring alveolar bone with them. The only exception is tooth movement in the presence of active periodontal disease, and even adults who have had bone loss from periodontal disease can have orthodontic treatment with good bone responses, if the periodontal disease is well controlled.

The relationship between the position of a tooth and alveolar bone height can be seen clearly when teeth erupt too much or too little. In the absence of pathologic factors, a tooth that erupts too much simply carries alveolar bone with it, often for considerable distances. It does not erupt out of the bone. But unless a tooth erupts into an area of the dental arch, alveolar bone will not form there. If a tooth is congenitally absent or extracted at an early age, a permanent defect in the alveolar bone will occur unless another tooth is moved into the area relatively rapidly. This is an argument against very early extraction, as, for instance, the enucleation of an unerupted premolar. Early removal of teeth poses a risk of creating an alveolar bone defect that cannot be overcome by later orthodontic treatment.

Because an erupting tooth brings alveolar bone with it, orthodontic tooth movement can be used to create the alveolar bone needed to support an implant to replace a congenitally missing tooth. For instance, if a maxillary lateral incisor is missing and a prosthetic replacement is planned, it is advantageous to have the permanent canine erupt mesially, into the area of the missing lateral incisor, and then to move it back into its proper position toward the end of the growth period. This stimulates the formation of alveolar bone in the lateral incisor region that otherwise would have not formed.³⁹

The same effects on alveolar bone height are seen with orthodontic extrusion as with eruption: as long as the orthodontic treatment is carried out with reasonable force levels and reasonable speed of tooth movement, a tooth brought into the dental arch by extrusive orthodontic forces will bring alveolar bone with it. The height of the bone attachment along the root will be about the same at the conclusion of movement as at the beginning. In some circumstances, it is possible to induce bone formation where an implant will be required, by extruding the root of an otherwise hopelessly damaged tooth, so that new hard and soft tissue forms in the area. If a tooth is intruded, bone height tends to be lost at the alveolar crest, so that about the same percentage of the root remains embedded in bone as before, even if the intrusion was over a considerable distance.

In most circumstances, this tendency for alveolar bone height to stay at the same level along the root is a therapeutic plus. Occasionally, it would be desirable to change the amount of tooth embedded in bone. For instance, the bone support around periodontally involved teeth could be improved by intruding the teeth and forcing the roots deeper into the bone, if the alveolar bone did not follow the intruding tooth. There are reports of therapeutic benefit from intruding periodontally involved teeth,⁴⁰ but the reduced pocketing relates to the formation of a long junctional epithelium, not to reattachment of the PDL or more extensive bony support. On occasion, it is desirable to elongate the root of a fractured tooth to enable its use as a prosthetic abutment without crown-lengthening surgery. If heavy forces are used to extrude a tooth quickly, a relative loss of attachment may occur, but this deliberately nonphysiologic extrusion is at best traumatic and at worst can lead to ankylosis and/or resorption. Physiologic extrusion or intrusion that brings the alveolar bone along with the tooth, followed by surgical recontouring of gingiva and bone, is preferable.

Principles in Growth Modification

Orthodontic force applied to the teeth has the potential to radiate outward and affect distant skeletal locations, and it now is possible to apply force to implants or screws in the jaws to affect their growth. Orthodontic tooth movement can correct dental malocclusions; to the extent that the distant effects change the pattern of jaw growth, there also is the possibility of correcting skeletal malocclusions.

Our current knowledge of how and why the jaws grow is covered in some detail in Chapters 2 through 4. In brief summary, the maxilla grows by apposition of new bone at its posterior and superior sutures in response to being pushed forward by the lengthening cranial base and pulled downward and forward by the growth of the adjacent soft tissues. Tension at the sutures as the maxilla is displaced from its supporting structures appears to be the stimulus for new bone formation. Somewhat similarly, the mandible is pulled downward and forward by the soft tissues in which it is embedded. In response, the condylar process grows upward and backward to maintain the temporomandibular articulation. If this is so, it seems entirely reasonable that pressures resisting the downward and forward movement of either jaw should decrease the amount of growth, while adding to the forces that pull them downward and forward should increase their growth.

The possibility of modifying the growth of the jaws and face in this way has been accepted, rejected, and then accepted again during the past century. Although the extent to which treatment can produce skeletal change remains controversial, the clinical effectiveness of procedures aimed at modifying growth has been demonstrated in recent years. The possibilities for growth modification treatment and the characteristics of patients who would be good candidates for it are described in Chapter 12. Here, the focus is on how the effects on growth are produced.

Effects of Orthodontic Force on the Maxilla and Midface

Manipulation and control of tooth eruption is properly considered an aspect of orthodontic tooth movement and therefore has been reviewed in some detail in the previous section. The focus of the discussion below is on changes in the jaws, not on dentoalveolar structures, but it is important to keep in mind that in treatment of patients, the dentoalveolar and skeletal effects cannot be divorced so readily.

Effects of Orthodontic Force on the Mandible

If the mandible, like the maxilla, grows largely in response to growth of the surrounding soft tissues, it should be possible to alter its growth in somewhat the same way maxillary growth can be altered, by pushing back against it or pulling it forward. To some extent, that is true, but the attachment of the mandible to the rest of the facial skeleton via the TM joint is very different from the sutural attachment of the maxilla. Not surprisingly, the response of the mandible to force transmitted to the temporomandibular joint also is quite different.

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