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Rezension / Literaturbericht, 2004
THE BIOLOGIC BASIS OF ORTHODONTIC THERAPY
Periodontal and bone response to normal function
Periodontal ligament and bone response to sustained orthodontic force
Biologic control of tooth movement
Pressure tension theory
Effect of force magnitude
Physiologic response to sustained pressure against a tooth
GINGIVAL RESPONSE TO ORTHODONTIC FORCE
Effect of force
Changes in the phenotype of gingival fibroblast and tooth relapse
Effect on root structure
RELATIONSHIP BETWEEN ALTERED TOOTH POISTION AND PERIODONTAL HEALTH AND DISEASE
EFFECT OF ORTHODONTIC TREATMENT ON THE HEIGHT OF ALVEOLAR BONE
ORTHODONICS AND PERIODONTAL PROPHYLAXIS
PERIODONTAL ASPECTS OFADULT ORTHODONTIC TREATMENT
Minimal periodontal involvement
Moderate periodontal involvement
Severe periodontal involvement
Types of orthodontic appliances
Tissue response to certain types of tooth movement
INTERRELATIONSHIP OF ORTHODONTIC TOOTH
MOVEMENT WITH PERIODONTAL HEALTH
Loss Of Periodontal Attachment And Bone Relative To Orthodontic Therapy
Gingival recession relative to orthodontic therapy
Gingival hyperplasia relative to orthodontic therapy
ORTHODONTIC TREATMENT AS A PART OF PERIODONTAL THERAPY
PERIODONTAL CONSIDERATIONS IN AN ORTHODONTIC PAIENT
REVIEW OF LITERATURE
Team work is the essence for the success of any venture. A multidisciplinary approach is often necessary to treat and prevent dental problems in a patient. Orthodontics and periodontics are interrelated in a variety of ways. Orthodontic treatment is based on the principle that if prolonged pressure is applied to a tooth, tooth movement will occur as the bone around the tooth remodels. Bone is selectively removed in same areas and added in others. In essence, the tooth moves through the bone carrying its attachment apparatus with it, as the socket of the tooth migrates. Since the bony response is mediated by the periodontal ligament, tooth movement is primarily a periodontal ligament phenomenon.1
Orthodontic tooth movement, which is the basis of the orthodontic treatment, is possible because of the inherent nature of the periodontium. Many advances have been made in understanding the mechanisms involved in the process of tooth movement. However, there are many pathologic conditions affecting the periodontium which may affect these mechanisms of tooth movement and alter the end result of the orthodontic treatment. Similarly awareness of the pathologic changes or other undesirable changes which can occur in the periodontium as a result of ideal or less than ideal orthodontic procedures would help in better treatment procedure and management of the patients. Altered tooth position may affect periodontal health. Placement of orthodontic appliances causes microbiological changes as well as changes in the periodontium. With the success, in the recent decades of the fixed multi banded appliance, orthodontic treatment in adults has continuously grown in the United States and Europe. It is in connection with adult orthodontics that periodontal factors are becoming more important to the orthodontist.
Orthodontics in the adult patient, specially the periodontally compromised patient requires adequate periodontal considerations to maintain the periodontium in a healthy condition during and after treatment. Minor periodontal surgery may be required to prevent relapse after orthodontic treatment. In addition, since periodontal diseases can secondarily cause malocclusion, very often orthodontic treatment would be an essential adjunct if the periodontal therapy is to succeed.
Orthodontic treatment in adults is now being performed by a team of periodontist and orthodontist. Inter disciplinary co-operation with clinical excellence in both disciplines may transform patients with unattractive dentitions, who show spaced, extruded, or otherwise migrated teeth in inflamed and compromised periodontium, in to persons with attractive, esthetic dentitions and radiant smiles.
Since, there is a close relationship between orthodontic treatment and periodontal health and vice versa, an understanding of the orthodontic periodontal interrelationship will help approach these situations to bring about optimum results.
The empiricism inherent with much clinical experience suggests that a “good” uncrowded dentition may be more conducive to periodontal health than a “bad” crowded dentition. Proper occlusal and masticatory functions are stimulatory to the gingival tissue and the attachment apparatus. On the other hand, a lack of function predisposes to disease in that, it increases plaque retention and calculus formation with its attendant gingival inflammation and cervical caries, leads to increased loss of bony support as compact with functional teeth, and causes a narrowing of the periodontal membrane. Alexander (1970)2 found an increase in gingival inflammation around nonfunctional teeth with a corresponding increase in plaque and subgingival calculus accumulation.
Orthodontic treatment is based on the principle that if prolonged pressure is applied to a tooth, tooth movement will occur as the bone around the tooth remodels. Bone is selectively removed in same areas and added in others. In essence, the tooth moves through the bone carrying its attachment apparatus with it, as the socket of the tooth migrates. Since the bony response is mediated by the periodontal ligament, tooth movement is primarily a periodontal ligament phenomenon.
Forces applied to the teeth can also affect the pattern of bone apposition and resorption at sites distant from the teeth, particularly the sutures of the maxilla and bony surfaces on both sides of the temporomandibular joint. Thus, the biologic response to orthodontic therapy includes not only the response of the periodontal ligament but also the response of growing areas distant from the dentition.
- 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. Major component of this PDL is collagen fibers, inserting in to cementum of the root on one side and the in to the bony plate of lamina dura, on the other side. These fibers run at an angle, attaching further apically on the tooth than on the adjacent alveolar bone. This arrangement resists the displacement of the tooth expected during normal function.
There are two major components of PDL other than collagen fibers which must be considered.
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 movement possible.
The principle cellular elements in 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 fibroblasts, producing new collagenous matrix materials, and fibroclasts, destroying previously produced collagen3. 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. 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. Most are of hematogenous origin4, 5; some are derived from stem cells found in the local area, but not from local osteoprogenitor cells6.
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 PDL space is filled with fluid; this fluid is the same as that found in all other tissues, ultimately derived from vascular system. A fluid filled chamber with retentive but porous walls could be description of a shock absorber, and in normal function, the fluid allows the PDL space to play just the role.
- Response to normal function
During masticatory function, the teeth and periodontal structures are subjected to intermittent heavy forces. Tooth contacts lasts for 1 second or less; forces are quiet heavy, ranging from 1 or 2 kg while soft substances are 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 PDL space is prevented by incompressible tissue fluid. Instead the force is transmitted to the alveolar bone, which bends in response.
illustration not visible in this excerpt
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.
PERIODONTAL LIGAMENT AND BONE RESPONSE TO SUSTAINED ORTHODONTIC FORCE
The response to sustained force against the teeth is a function of force magnitude: heavy forces lead to rapidly developing pain, necrosis of cellular elements within the PDL, and the phenomenon of “undermining resorption” of alveolar bone near the affected tooth. Lighter forces are compatible with survival of cells within the PDL and a remodeling of the tooth socket by a painless “frontal resorption” of the tooth socket. In orthodontic practice, the objective is to produce tooth movement as much as possible by frontal resorption, recognizing that some areas of PDL necrosis and undermining resorption will probably occur despite efforts to prevent this.
It is necessary to consider the biologic control mechanism that leads from the stimulus of sustained force application to the response of orthodontic tooth movement.
è Two control mechanisms have been proposed :
1. Biologic electricity.
2. Pressure- tension theory
This theory relates tooth movement, at least in part to changes in bone metabolism controlled by the electric signals that are produced when alveolar bone flexes and bends. Electric signals that might initiate tooth movement initially were thought to be piezo-electric.
Piezo electricity is a phenomenon observed in many crystalline materials in which a deformation of the crystal structure produces flow of electric current as electrons are displaced from one part of the crystal lattice to another. Not only is bone mineral a crystal structure with piezoelectric properties, collagen itself is piezoelectric, and stress-generated potentials in dried bone specimens can be attributed to piezoelectricity. When a force is applied to a crystalline structure (like bone or collagen), a flow of current is produced that quickly dies away. When the force is released, an opposite current flow is observed. This can be explained by the migration of electrons within the crystal lattice as it is distorted by pressure resulting in an electric charge. As long as the force is maintained, the crystal structure is stable and no further electric events are observed. When the force is released, however, the crystal returns to its original shape, and a reverse flow of electrons is seen. Ions in the fluids that bathe living bone interact with the complex electric field generated when the bone bends, causing temperature changes as well as electric signals. The small voltages that are observed are called the “streaming potential.” There is no longer any doubt that stress-generated signals are important in the general maintenance of the skeleton. The type of sustained force used to induce orthodontic tooth movement does not produce prominent stress generated signals. When the force is applied, a brief signal is created; when it is removed, a reverse signal appears. As long as the force is sustained, however, nothing happens. If stress-generated signals were important in producing the bone remodeling associated with orthodontic tooth movement, a vibrating application of pressure would be advantageous. Experiments indicate little or no advantage in vibrating over sustained force for the movement of teeth7, 8.
Thus, it appears the stress-generated signals, important as they may be for normal skeletal function, probably have little if anything to do with the response to orthodontic tooth movement. Perhaps a fair conclusion is that even though stress-generated signals do not explain tooth movement, electric and electromagnetic influences can modify the bony remodeling on which tooth movement depends and may yet prove useful therapeutically.
This 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 entirely alter blood flow9. The pressure tension theory, the classic theory of tooth movement relies on chemical rather than electric signals as the stimulus for cellular differentiation and ultimately tooth movement occurs.
In this theory, an alteration in blood flow within the periodontal ligament is produced by the sustained pressure that causes the tooth to shift position within the periodontal ligament space, compressing the ligament in some areas while stretching it in others. Blood flow is decreased where the periodontal ligament is compressed, while it usually is maintained or increased where the periodontal ligament is under tension.
Alteration in blood flow quickly creates changes in the chemical environment. These chemical changes, acting either directly or by stimulating the release of other biologically active agents that would stimulate cellular differentiation and activity. In essence, this view of tooth movement shows three stages:
1. Alteration in blood flow associated with pressure within the periodontal ligament.
2. The formation and / or release of chemical messengers. (Cyclic adenosine monophosphate, prostaglandins).
3. Activation of cells.
The two theories are neither incompatible nor mutually exclusive. From a contemporary perspective, it appears that both mechanisms may play a part in the biologic control of tooth movement.
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 blood vessels are totally collapsed and no further blood flows.
This theoretic sequence actually occurs and has been demonstrated in animal experiments, in which increasing the force against a tooth causes decreasing, perfusion of the PDL on the compression side9.
illustration not visible in this excerpt
Optimum forces for orthodontic tooth movement
illustration not visible in this excerpt
In clinical orthodontic it is difficult to avoid pressure that produces at least some avascular area 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. Animal experiments support this hypothesis10.Because of its histological appearance as the cells disappear, an avascular area in the periodontal ligament traditionally has been referred to as hyalinized. Despite the name, the process has nothing to do with the formation of hyaline connective tissue but 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 periodontal ligament 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 periodontal ligament area. This process is appropriately described as "undermining resorption", since the attack is from the underside of the lamina dura. When hyalinization and undermining resorption occurs, an inevitable delay in tooth movement occurs. So, it is apparent that optimum force levels for orthodontic movement should be just high enough to stimulate cellular activity without completely occluding blood vessels in the periodontal ligament area. Both the amount of force delivered to a tooth and also the area after periodontal ligament over which that force is distributed are important in determining the biologic effect.
The periodontal ligament response is determined not by force alone, but by force per unit area, or pressure. Since the distribution of force within the periodontal ligament, and therefore the pressure, differs with different types of tooth movement, it is necessary to specify the types of tooth movement as well as the amount of force in discussing optimum force levels for orthodontic purposes.
The gingiva is composed of epithelium and underlying connective tissue that is attached to the external part of the alveolar bone and the supracrestal region of the tooth. Collagen fibers are the main structural component in the extra cellular matrix (ECM) of the gingiva. They account for about 60% of total tissue protein12.
Healthy gingiva contains:
Interstitial collagen type I - 90%
Interstitial collagen type III - 8%
Interstitial collagen type IV, V, VI, VIII - 2%13-16
There are two patterns of gingival collagen arrangement13:
1. Large thick, mostly parallel collagen type - I fibers interconnected by thin fibrils17. This arrangement of the collagen fibers confers strength and rigidity to this tissue, which sustains heavy masticatory forces.
2. Short and thin fibers in a fine reticular net work located mainly under the epithelial basement membrane and around blood vessels.
Apart from the collagen network, the gingiva also contains a network of elastic fibers, comprising 6% of the total human gingival protein. This net work composed of 3 different types of fibers, namely elastin, elaunin, and oxytalan fibers, which provide the gingiva with the elastic properties needed to oppose pressure18.
Gross gingival changes are observed after closure of an extraction site on rotation movement or excessive labial tooth movement. Adjacent to an extraction site, the teeth that approximated resulted in an accumulation of gingival tissue and enlargement of the interdental papilla19. The tissue accumulation is the result of both retraction and compression. The gingiva retracts together with the tooth movement, although at a less distance19. At the mesial surface of orthodontically retracted tooth, a triangular patch of red tissue appears20. This red patch is considered to Reduced Enamel Epithelium (REE) that has been peeled off the tooth surface20.
Adjacent to the accumulated gingival tissue, vertical invaginations or cleft of both the epithelium and the connective tissue are formed on the buccal and lingual aspects. Many of these deformities persist for years after treatment21, 22. Extensive rotational movement causes the rotational gingiva to be compressed in the interdental area at the direction of rotation; the gingiva rotates both to the same degree and in the same direction as the tooth23.
The assumption that the observed tooth relapse is associated with clinical changes in the gingiva led to histologic studies being carried out in order to investigate micro structural nature of these changes.
Histologically , discontinuation of the transeptal fibers is seen after a tooth has been extracted. During healing of the extraction site, newly formed collagen fibers bring about a reestablishment of continuity of the transeptal fibers, thus creating a fibrous bridge connecting the seperated teeth24.
The orthodontic approximation is accompanied by papillary hyperplasia25. The newly formed transeptal fibers are coiled and compressed26, and have a ''foot ball' shaped appearance27. The New transeptal fibers have a normal morphologic appearance after closure of the extraction site22. In the transeptal region, distant to the alveolar crest, significant increase in oxytalan fibers22 as well as increased level of GAG has been described28. This elevates the elastic proportion of the tissue at the extraction sites. In rotational movement, an increase in oxytalan fibers and reorientation ("Stretching") of the gingival collagen fibers has been reported23, 29. The clinical instability of the rotated tooth, which almost always relapse has been attributed to these stretched collagen fibers. It has been reported that proline uptake of the newly formed collagen increased significantly in both the lamina propria and transeptal region thus suggesting that orthodontic force stimulates collagen production in the gingiva30.
The effect of orthodontic tooth movement on both collagen and elastin in the gingiva has been investigated also by ultra structural analysis31. The diameter of collagen fibers is significantly increased in both pressure and tension aspects when compared to untreated controls. In some areas with in the compressed papilla, degraded collagen fibers have been longitudinally split and without the typical bonding pattern.
On the pressure aspect of the gingiva, a slight increase in the number and size of elastic fibers has been seen. On the tension aspect, however, only few elastic fibers have been observed. A similar gingival response to force has been found following rotational movement in the dog17.
The effect of mechanical force on gene transcription of collagen type I and tissue collagenase (MMP I, Matrix metalloproteinase - I) has been studied on gingival fibroblasts in vitro using the reverse transcriptase polymerase chain reaction (RT - PCR) 32
Under these observations the transcription level of collagen type I has been significantly increased whereas that of collagenase has been significantly decreased. These changes indicate disturbed equilibrium between collagen synthesis and degradation required to maintain adequate tissue stability at the pretranslational level.
Unlike bone and periodontal ligament, the gingival tissue is not resorbed after orthodontic treatment, but it is compressed and consequently retracts. The fact that orthodontic force does not bring about gingival resorption prevents the formation of periodontal pockets and subsequent detachment of the tooth from the gingiva. The clinically observed gingival changes after tooth movement are accompanied by a significant increase in the relative amount of both interstitial collagen and elastin. As for the clinically manifested relapse of teeth after rotation movement, an ultra structural study showed that it cannot be attributed to "Stretched" collagen fibers17. Unlike normal gingiva there is also an increase in the number of elastic fibers in the compressed gingiva after rotation17. It is these increased elastic fibers that exert pressure on the tooth leading to relapse after release of retention.
For many years it was thought that the root structure of teeth was not remodeled in the same way as bone. Research has made it evident that when orthodontic forces are applied, it resorbs similar to bone. It appears that cementum (and dentin if the resorption penetrates through the cementum), is removed from the root surface while active force is present and is then restored during periods of relative quiescence. Repair becomes impossible only in cases where islands at cementum or debris have been cut totally free from the root surface. This is primarily observed at the apex.
Maxillary central incisor and lateral incisors, mandibular, incisors and first molars are more prone for root resorption.
RELATIONSHIP BETWEEN ALTERED TOOTH POSITION AND PERIODONTAL HEALTH AND DISEASE
An “ideal” occlusion is exemplified by a normal mesiodistal relation and interdigitation of the cusps of the posterior teeth, with an acceptable overbite, overjet, and incisal guidance of anterior teeth in well-developed and well-aligned dental arches. This type of occlusion has been regarded as “Normal” and most compatible with periodontal health. Unfortunately, normal occlusion is found in only a small percentage of the population. Because great pains are taken in orthodontics to achieve a normal occlusion, it would be desirable to show that this small percentage of the population has a greater predisposition to periodontal health and significantly less periodontal disease than does the remainder of the population.
It has always been thought that an ideal, “good” uncrowded arch form would be more conducive to the maintenance of good oral hygiene by the patient. Food impactions, both vertical and lateral, may be reduced or eliminated by the creation of proper arch form. For example, when crowded anterior teeth are unraveled, oral hygiene is more easily maintained and food impaction is significantly decreased. Placing uneven adjacent marginal ridges at the same height alters the proximal tooth contact and reduces food impaction. If teeth are placed in their correct axial inclinations, forces will be directed in the long axis of these teeth. In this position, most of the principal periodontal fibers are stretched and there is minimum compressed fibers, which then provides the greatest resistance to tooth displacement. The anatomic structure of the periodontium is, therefore, developed so that it can best withstand stresses placed in the long axis of the tooth33.
Malposed or rotated teeth maybe predisposed to more rapid breakdown of the periodontium when the roots are too close to one another, resulting in a thin interproximal septum. A rotated tooth may have a portion of the root out of the alveolar housing. There is a great possibility of such a tooth having a dehiscence or fenestration and more readily succumbing to periodontal insults.
When tooth position, as represented by centric occlusion, is compatible with centric relation, the possibility of trauma is thought to be greatly reduced. A severe disparity between centric occlusion and centric relation may not be amenable to alleviation by occlusal adjustment and correction may necessitate the intervention of orthodontic therapy.
Alignment of malposed teeth can help the patient in maintaining good oral hygiene. Patient finds it easier to keep the mouth clean, thereby reducing the amount of food debris and plaque which is shown to be the more important factor in the development of gingivitis and subsequent periodontitis. If left uncorrected, periodontitis can progress leading even to mobility and pathologic migration of teeth.
Variation studies have emphasized the role of malocclusion in periodontitis. Protruded maxillary anterior teeth can cause loss of lip seal. This is usually a common cause for gingivitis. If the teeth are retracted orthodontically, lip seal is attained back and the gingivitis subsides.
Drifted teeth with abnormal proximal inclination is another example. Oral hygiene maintenance is extremely difficult and this can lead to periodontal break down. Correction by orthodontics has shown to be beneficial. Progressive tipping of teeth with periodontitis and trauma from occlusion accelerates periodontal break down.
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