Trauma from occlusion and its treatment

Introduction:

Do abnormal occlusal forces play a significant role in initiation of periodontal diseases? This question has been our focus of attention for many years. It is generally accepted that trauma from occlusion or occlusal traumatism is a separate entity not related to periodontitis. But, when both of the conditions are present simultaneously, it becomes a matter of discussion to designate them entirely non associated, partially associated or completely associated conditions. Although, many studies have been done to evaluate any relation between progressions of gingival inflammation and trauma from occlusion, conflicting results have been encountered. In the following discussion, we shall try to understand our current understanding of trauma from occlusion and its association with inflammatory periodontal diseases.

Definition:

Following definitions are commonly used to describe trauma from occlusion,

  • Carranza: When occlusal forces exceed the adaptive capacity of tissues, tissue injury results. The resultant injury is termed trauma from occlusion 1.
  • According to world health organization (WHO), 1978, trauma from occlusion is “damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw.”
  • Glossary of Periodontal Terms: Injury resulting  in  tissue  changes  within the  attachment  apparatus  as a result  of  occlusal force(s) 2.
  • Trauma from occlusion can be defined as structural and functional changes in the periodontal tissues caused by excessive occlusal forces 3.

Etiology of TFO:

There are many factors involved in etiology of trauma from occlusion. They can be divided into two broad categories: precipitating factors and predisposing factors. In case of TFO the precipitating factor is destructive occlusal forces. The predisposing factors are those which contribute to the development of TFO indirectly. They include intrinsic and extrinsic factors.

Precipitating factor:

As already stated, destructive occlusal forces are the precipitating or primary etiology of trauma from occlusion. The occlusal forces when within normal range can be well adapted by tooth supporting soft tissues. But, when these forces exceed the adaptive capacity of tooth supporting tissues, pathological changes can be seen in the soft tissues. These forces are usually described in terms of magnitude, direction, duration of application and frequency of application.

  • Magnitude of occlusal forces: When the magnitude of occlusal forces exceeds the normal range of forces for a tooth, due to natural adaptive response, some changes can be appreciated in the periodontal ligament. There is widening of periodontal ligament (PDL) space, increase in the number of PDL fibers, increase in the width of PDL fibers and increase in the density of alveolar bone.
  • Direction of force application: The principle fibers of the periodontal ligament play an important role in withstanding the occlusal forces and transferring them to the alveolar bone. Normally, they are oriented in such way that they are best capable of withstanding the occlusal forces. But, if the direction of occlusal forces is changed, these fibers are not able to efficiently bear the forces hence injury results.
  • Duration of force application: If the abnormal occlusal forces are subjected to a tooth for a long duration of time, they cause injury to periodontal tooth supporting structures which can be seen histologically.
  • Frequency of force application: Frequent application of abnormal occlusal forces results in more damage to the periodontal tooth supporting structures than less frequent application.
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Type of occlusal forces:
The abnormal occlusal forces are the primary etiology of trauma from occlusion. The occlusal forces can be divided into various types according to their direction, magnitude, duration and frequency of application. These are as follows,
Normal physiological forces:
These forces are exerted on teeth during chewing and swallowing. These are small magnitude forces and rarely exceed 5N. These are beneficial to the periodontal structures as they provide positive stimulus for the maintenance of the periodontal ligament and alveolar bone in healthy and functional condition.
Impact forces:
These are the forces which are of high magnitude and are exerted on the teeth for a short duration of time. The periodontal ligament has inherent viscoelastic properties to absorb impact forces, but if these forces exceed the viscoelastic buffer capacity of periodontal ligament, injury to the periodontal ligament or the alveolar bone results.
Continuous forces:
These are very low magnitude forces subjected to tooth or teeth for long duration of time such as in orthodontic treatment. These forces are directed in one direction and resulting in remodelling of the alveolar bone moving the teeth in desired direction.
Jiggling forces:
These are intermittent forces subjected to tooth or teeth in more than one direction such as in case of premature contacts (crowns/ high fillings). These are quite deleterious and result in widening of the alveolus and increased mobility.

Predisposing factors:

These can be divided into intrinsic and extrinsic factors,

Intrinsic factors:

  • Orientation of long axis of the teeth in relation to forces to which they are exposed.
  • Morphological characteristics of the roots. The size, shape and the number of the roots determine how occlusal forces are dissipated. In general short, conical, slender or fused roots are more vulnerable to TFO.
  • The morphology of the alveolar process, i.e. the quality and the quantity of the alveolar bone play an important role in absorbing the occlusal forces.

Extrinsic factors:

  • Local factors such as plaque which predisposes to the alveolar bone loss.
  • Fabrication of long span bridges on few teeth, thus overloading them.
  • Injudicious bone resection during surgical periodontal therapy or oral surgical procedures.
  • Parafunctional habits as a result of neurosis.
  • Other factors include: food impaction, overhanging fillings, poorly contoured crowns and bridges and ill fitting partial dentures.
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Is pattern of occlusion of teeth, responsible for TFO?

Trauma from occlusion does not depend upon how the teeth occlude. Any kind of occlusion may result in TFO. An esthetically acceptable occlusion may not be functionally normal. During function, various kinds for forces are exerted onto the teeth and their supporting structures. When a particular tooth or teeth are not able to dissipate the occlusal forces normally, soft tissue injury may result which is totally independent of type of malocclusion.

 

Historical perspective:

The association of excessive occlusal forces and their deleterious effects on tooth and tooth supporting structures has been established for over 100 years now. Karolyi (1901) 4 implied a cause and effect relationship between traumatic occlusion and periodontal disease progression. Since then a lot of research has been done using autopsy studies, animal studies and human studies. Two studies supported Karolyi’s hypothesis 5, 6.

In Box’s study 5, gold crown was placed on lower incisor of sheep in supra-occlusion thereby increasing the crown-root ratio and bucco-lingual dimensions of the tooth. After more than three months, the crowned tooth showed increased mobility, slightly increased pocket depth and greater calculus accumulation as compared to other three incisors. Along with this the pulpal tissue of the crowned tooth showed sub-acute inflammation and surrounding tissue were inflamed. This study has been criticized by many researchers. Regardless the results of the study, Box himself did not claimed any definite relationship between occlusal trauma and periodontal diseases.

In Stone’s study 6, high occlusal restorations were done in monkeys and their histological analysis was done after 43 weeks. About 30% of experimental teeth showed changes similar to gingivitis and periodontitis. These changes were seen in tooth with high filling and its antagonist. Stone concluded that occlusal trauma led to periodontal diseases and that the disease would increase in its severity as long as the trauma was present.

There have been fundamental differences between various research groups working to establish the etiological significance of TFO. Some groups say that specific occlusal forces and specific occlusal contacts are responsible for periodontal disease progression, whereas others assert that occlusal forces are not associated with progression of periodontal diseases. Bhaskar and Orban 7 have contended that the apical migration of epithelial attachment observed by Stone in his study was physiological and not pathological and cannot be considered to be related to occlusal trauma.

Regardless of results of various studies, most authorities believed that occlusal trauma did not initiate gingivitis or periodontitis and that the microbial plaque was responsible for initiation of gingivitis, which in turn is essential for development of periodontitis.

Terminologies which have been used to describe occlusal trauma:

Various researchers who have studied the affect of traumatic occlusal forces on periodontium have used different terms to denote these abnormal forces and associated occlusion. Following is the description of some initial researchers, who used different terminologies to describe abnormal occlusal forces,

  • Stillman 8 used the term “Traumatic occlusion” to describe abnormal stresses capable of producing injury to dental or periodontal tissues.
  • Box 9 used the term “traumatogenic occlusion” to describe these abnormal occlusal stresses and used another term “traumatic occlusion” to describe the functional contact relationship of occlusal surfaces which result due to this trauma.
  • The term “traumatic occlusion” was also used by Ramfjord and Ash 10.
  • Muhlemann 11 used the term “Traumatogenic occlusal situation” to address the factors initiating the abnormal occlusal stresses and “Occlusal trauma” to describe the resulting microscopic lesion.
  • Orban 12 and Prichard 13 gave the term “Periodontal traumatism” to address the tissue injury caused by abnormal occlusal forces and not for the occlusal forces themselves.
  • Glickman 14 used the term “Trauma from occlusion” (TFO) to describe these abnormal occlusal forces. In present discussion we shall use this term to discuss trauma from abnormal occlusal forces.

Review of literature of studies done on association of TFO and spread of inflammation:

Stillman 8, initially started the discussion over the role of occlusion in the progression of periodontal disease by stating that trauma from occlusion was the primary cause of periodontal disease and, as such, occlusal treatment was mandatory for the successful treatment and control of periodontal disease. According to him, all other clinical factors including oral hygiene and the presence of dental plaque were secondary to occlusal forces in the pathogenesis of periodontal disease. To verify these initial findings various autopsy, animal and human studies were done to investigate any association between TFO and inflammatory periodontal diseases.

Autopsy studies:

These observations made by Stillman, set a stage for controversies regarding association of TFO and spread of inflammation in inflammatory periodontal diseases. These findings were opposed by Weinman et al 15-17; in their autopsy studies Weinman et al observed that the spread of inflammation into the underlying bone followed the course of blood vessels. They found no correlation between type of occlusal contact and progression of periodontal inflammation. Later on various researchers published their findings which were both in favour and against the association of TFO and spread of inflammation in inflammatory periodontal diseases. To understand this controversy, we must know about “Glickman’s concept” and “Waerhaug’s concept”.

Glickman’s concept:

Glickman and Smulow 18, 19 in autopsy studies investigated, if TFO could alter the progression of inflammation in underlying soft tissue and bone. According to their investigation occlusal trauma could alter the progression of periodontal destruction. Glickman stated that the pathway of the spread of a plaque-associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harbouring subgingival plaque. Therefore, the periodontium of non-traumatized teeth would present an even destruction (horizontal bone loss), while traumatized teeth would present angular bony defects.

Glickman 20, 21 then proposed the “Theory of Co-destruction” to explain the relationship between occlusion and periodontal disease. This theory suggested that occlusal trauma in the presence of plaque-induced inflammation may result in alteration of the normal pathway of inflammation, and development of angular bony defects with intrabony pockets, but that occlusal trauma, in and of itself, did not cause gingivitis and periodontitis 20, 22-24. This theory suggested presence of a “zone of irritation” (marginal/interdental gingiva; gingival fibers) and “zone of co-destruction” (transseptal/alveolar crest fibers, periodontal ligament, cementum, bone).

Zone of irritation:

This zone consists of marginal and interdental gingiva. This tissue is bordered by hard tissue only on one side i.e. tooth and is unaffected by the occlusal forces. In other words we can say that the gingival inflammation cannot be induced by TFO but is the result of irritation produced by microbial plaque. Inflammation in the “zone of irritation” causes horizontal bone loss.

Zone of co-destruction:

The zone of co-destruction includes transseptal/alveolar crest fibers, periodontal ligament, cementum and alveolar bone. It is coronally demarcated by trans-septal and dento-alveolar fibers. The fiber bundles which separate the zone of irritation from the zone of co-destruction are affected both by inflammatory lesion produced by plaque and trauma induced changes in the zone of co-destruction. As a result of both of these factors, the fiber bundles may get dissolved or may get oriented parallel to the root surface. This may facilitate the direct spread of inflammation from zone of irritation to periodontal ligament without involving the inter-dental bone. Hence, the normal pathway of spread of inflammation in non-traumatized teeth (from zone of irritation to alveolar bone) is altered in case of traumatized teeth (from zone of irritation directly to periodontal ligament). This altered pathway of spread of inflammation causes angular bone loss.

Glickman’s theory of co-destruction

( 1: normal spread of inflammation, 2: spread of inflammation in TFO)

Glickman's concept of Trauma from occlusion

According to Glickman, TFO is an etiological factor particularly in situations where angular bony defects combined with infrabony pockets are found around single or multiple teeth.

Waerhaug’s concept:

In his classical study, Waerhaug disputed Glickman’s concept. Waerhaug measured distance between the subgingival plaque and, the perimeter of the associated inflammatory infiltrate and the surface of the adjacent alveolar bone. Based on large number of human autopsy specimens, he concluded that angular defects and infrabony pockets occurred equally frequently in teeth with TFO and in teeth without TFO. The reduction in alveolar crestal height was related to the presence of subgingival plaque, ranging from 0.5 to 2.7 mm (mean 1.63 mm) from the alveolar crest. He postulated that loss of attachment and bone are the result of inflammation induced by subgingival plaque and not occlusal trauma. Teeth with narrow interproximal bone develop horizontal defects while teeth with wide interproximal bone were more likely to develop angular or vertical defects.

Animal studies:

Rochester Group (Polson and co workers) 25-31 and the Gothenburg group (Lindhe and co workers) 32-38 used primate model and dog model respectively to investigate the effect of occlusal trauma on periodontal disease progression. These groups differed in some of their findings which may be attributed to the differences in study design and the animal model utilized.

The Rochester (Polson and co workers) and Gothenburg group (Lindhe and co workers) animal studies

Rochester Group
Gothenburg Group
In their studies squirrel monkeys were used.In their studies beagle dogs were used.
Duration of experiment was upto 10 weeks.Duration of experiment was upto 1 year.
Studies concluded that occlusal trauma does not influence periodontal disease progression as they found no evidence of attachment loss in the presence of plaque and occlusal forces.Studies concluded that occlusal trauma could accelerate the progression of periodontal disease as they found evidence of attachment loss when plaque and occlusal forces were both present.
They asserted that adaptive changes in response to occlusal trauma can be largely reversible if inflammation is controlled.They concluded that In the presence of reduced healthy periodontium, occlusal trauma will not produce loss of attachment.
Occlusal trauma can cause bone loss.The ability of the periodontium to adapt to occlusal trauma maybe inhibited in the presence of inflammation.

The conclusions of these studies are as follows:

  • Trauma from occlusion alone could not cause attachment loss.
  • Gingival inflammation is not initiated by occlusal trauma.
  • In the absence of inflammation, a traumatogenic occlusion will result in increased mobility, widened PDL, loss of crestal bone height and bone volume, but no attachment loss.
  • The excessive jiggling forces in presence of inflammation did not cause accelerated attachment loss in squirrel monkeys (Rochester Group studies) but accelerated attachment loss in beagle dogs (Gothenburg Group studies).
  • Treating the gingival inflammation in the presence of continuing mobility or jiggling trauma will result in decreased mobility and increased bone density, but no change in attachment level or alveolar bone level.
  • When excessive occlusal forces were removed, loss of bone density was reversible, except in the presence of periodontitis.

Majority of the animal studies concluded that the application of excessive forces on teeth creates areas of pressure and tension around involved tooth/teeth. The early changes seen on the tension side include widening of the periodontal ligament space, stretching or tearing of fibers and thrombosis. On the pressure side, necrosis or disorientation of the periodontal ligament fibers, thrombosis, haemorrhages and undermining bone resorption can be seen. TFO tends to change the shape of the alveolar crest, causing widening of the marginal periodontal ligament space, a narrowing of the interproximal alveolar bone, and a shelf like thickening of the alveolar margin. In the absence of inflammation, tooth/teeth adapt to the increased occlusal forces (explained later), but in presence of inflammation the changes in the shape of the alveolar crest may be conducive to angular bone loss, and existing pockets may become intrabony. The control of plaque and gingival inflammation would stop the periodontal disease progression in the presence or absence of excessive occlusal forces.

If the excessive occlusal forces continue, the tooth tries to move away from the forces. When the tooth is out of abnormal occlusal forces, the repair begins. This period is characterized by formation of new bone and connective tissue. With continued remodelling, the damaged periodontal ligament, cementum and alveolar bone are completely restored.

The major objection raised regarding the design of animal studies was the quality of forces. It was said that the occlusal overloading did not replicate the same jiggling type of forces that are observed in humans. To overcome this objection, studies were designed by placing lingual locks on the crowns which forced the tooth buccally with every occlusal closure. An orthodontic appliance then pulled the tooth back lingually with disocclusion. This arrangement prevented the tooth to move away from the excessive forces. The histological examination revealed that either with or without jiggling trauma, the results are the same except that pressure and tension areas occurred on both buccal and lingual side with jiggling trauma causing widening of periodontal ligament space and lengthening of fibers of periodontal ligament. In both the cases no attachment loss was seen and despite of severe tooth mobility, new bone was being laid down simultaneously with alveolar bone resorption 39, 40

Human trials:

Gold standards for experimental studies are the blinded randomized controlled clinical trials. To study association between TFO and inflammatory periodontal diseases, study should include identified cases of trauma from occlusion with periodontal diseases which need to be followed during long duration of time, which raises serious ethical issues. Therefore, all human studies on TFO have been designed considering the ethical issues which make them less ideal than an ideal clinical controlled trial.

Burgett et al 41 in a randomized clinical trial evaluated the effect of occlusal treatment on the outcome of periodontal therapy. Half of the patients, selected randomly received occlusal treatment as part of their periodontal therapy whereas remaining did not received any occlusal treatment. All the patients were treated with identical non-surgical and surgical periodontal treatment. The patients were then followed for over two years and then were re-evaluated. The results of the study showed that the group of patients who received occlusal therapy along with periodontal treatment, showed a significant improvement in pocket depth in comparison to the group which did not receive occlusal treatment. This study emphasized that occlusal treatment yields a beneficial effect on the outcome of periodontal treatment.

In other investigations 42, 43, the association of occlusal trauma and periodontitis was studied. Results of these studies demonstrated that teeth in patients with occlusal disharmonies (centric relation-centric occlusion, balancing; or protrusive contacts) did not demonstrate any greater severity of periodontitis when compared to teeth without such contacts.

In a study series 44, 45 the effect of parafunctional habits on long term prognosis of teeth was investigated. Authors reviewed the change in prognosis and in the number of teeth lost by patients with periodontal disease who had parafunctional habits. The study concluded that patients with parafunctional habits who were given occlusal appliances showed better prognosis of dentition. In comparison, patients with parafunctional habits that had not been treated with an occlusal appliance, there was no improvement in prognosis despite periodontal therapy.

Occlusal forces during jaw movements:

The forces exerted on the teeth during jaw movements such as chewing, swallowing and the performance of parafunctional habits, including bruxism and clenching, are well tolerated by the tooth supporting structures. During speech the tooth contact is minimal, so there are hardly any forces exerted on teeth. During mastication in normal healthy adults, the mandible typically follows a wide lateral path during closure. The tooth contacts occur on the lateral guiding cusps, typically the cusps of the canines and premolars. The forces exerted on teeth during these contacts are of low magnitude, averaging 81 N lasting during small time period (20-50 ms). At final closure in intercuspal position, the forces are much higher, averaging 262 N for relatively longer duration of time (115 ms). The occlusal forces during swallowing in intercuspal position are averaging around 296 N for duration of about 700 ms 46.

Classification of trauma from occlusion:

The TFO can be classified as,

  • Acute / chronic trauma from occlusion.
  • Primary / secondary trauma from occlusion.

Acute trauma from occlusion:

This type of trauma is caused due to abrupt occlusal impact, such as due to biting on hard object (e.g. biting on olive pit, piece of stone in flalfel). Another cause of acute TFO is high restorations or prosthetic appliances. The clinical signs and symptoms of the condition include, tooth pain and sensitivity to percussion, increased tooth mobility and when the cause is removed, symptoms subside and complete healing takes place. If the cause is not removed, the abnormally high occlusal forces may cause areas of necrosis in tooth supporting tissue, abscess formation and cemental tears. In some cases the patient may become asymptomatic which results in chronic condition.

Chronic trauma from occlusion:

It results from abnormal occlusal forces exerted on the tooth supporting structures during long duration of time. It is more common and is of greater significance than acute condition, because it results in gradual changes in occlusion clinically seen as tooth wear, tooth migration and extrusion of teeth. This condition is usually associated with parafunctional habits such as bruxism and clenching. With duration of time pathological changes are seen in the tooth supporting structures which are discussed in detail later.

Primary trauma from occlusion:

It refers to injury resulting from excessive occlusal forces applied to a tooth or teeth with normal support  47. Examples include high restorations, drifting or extrusion into edentulous spaces, and orthodontic movement. Once the abnormal forces are removed, the tooth returns to complete health. It must be noted that in case of primary TFO, there is no alteration in the connective tissue attachment level and it does not initiate the pocket formation. It may be because; the supra-crestal fibers remain un-affected, preventing the apical migration of connective tissue attachment 27.

Secondary trauma from occlusion:

It refers to the injury resulting from normal occlusal forces applied to a tooth or teeth with inadequate support 47. In other words we can say that even the normal occlusal forces become deleterious to the tooth supporting structures, because the periodontal support is reduced and is not able to withstand the occlusal forces. Due to the loss of tooth supporting structures, the fulcrum of the tooth shifts apically within its alveolus (increased crown root ratio), due to which the functional and parafunctional loads exceed the resistance and the reparative capacity of the periodontium. The most common cause for secondary TFO is periodontitis, causing bone loss. Other causes include injudicious bone resection during surgical periodontal therapy or oral surgery, accidental trauma or from excessive apical resorption associated with endodontic or orthodontic therapy.

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Secondary TFO always has signs of primary TFO:

It must be noted that all teeth suffering from secondary trauma from occlusion show histological signs of primary trauma from occlusion. In other words we can say that when examined histopathologically, the supporting structures of a tooth suffering from secondary trauma from occlusion consistently shows changes which are seen in primary trauma from occlusion.

Although, secondary trauma from occlusion is never present without the manifestations of primary trauma from occlusion, the primary trauma from occlusion may or may not be associated with secondary trauma from occlusion.

 

Stages of tissue response to excessive occlusal forces:

Carranza 48, 49 has described three stages of tissue response to excessive occlusal forces. These are: injury, repair and adaptive remodelling of the periodontium. Following is the description of these stages,

Stage I, Injury:

The immediate result of excessive occlusal forces is soft tissue injury. The occlusal forces may vary in their magnitude, being slightly excessive, greater than slightly excessive or severely high. The center of rotation of single rooted teeth is located at the junction of middle third and apical third of the tooth, whereas the center of rotation of multi-rooted teeth lies near the furcation area. When excessive occlusal forces are subjected to teeth, they rotate around the fulcrum of rotation, thereby moving away from the deleterious forces. Due to this rotation in the tooth socket, areas of pressure and tension are created on the opposite sides of the fulcrum. If the force is unidirectional, these areas are created on the opposite surfaces whereas in case of jiggling forces, these areas may coexist in same area.

Slightly excessive forces:

The slightly excessive forces stimulate bone resorption in the areas of pressure, causing widening of periodontal ligament space. In areas of tension, elongation of periodontal ligament fibers takes place. The blood vessels on the pressure side are numerous and compressed whereas on the tension side they are enlarged 50. In due course of time, slow remodelling of the alveolar socket takes place.

Greater than slightly excessive forces:

Marked changes in the tooth supporting structures are seen in case of greater occlusal forces. The excessive compression of periodontal ligament produces areas of hyalinization 51-53. Areas of necrosis can be seen in periodontal ligament due to excessive trauma to the periodontal ligament fibers and connective tissue cells including fibroblasts. Within 30 minutes of application of such traumatic forces on tooth, vascular changes can be seen. There is impairment and stasis of blood flow within 30 minutes. Within next 2 to 3 hours the blood vessels appear to be packed with erytherocytes which start to fragment. During 1 to 7 days, the disintegration of the blood vessel walls and their content takes place. The defragmented products disperse in the surrounding tissues 54.

Severely high forces:

Severely high occlusal forces result in thrombosis, haemorrhage, tearing of periodontal ligament, widening of periodontal ligament space and alveolar bone resorption. Under severely high forces, on the pressure side, there is disturbance of blood flow in the compressed PDL and cell death in the compressed area of the PDL (hyalinization). The first sign of hyalinization is the presence of pyknotic nuclei in cells, followed by areas of acellularity, or cell-free zones. The resolution of this hyalinized area starts when cellular elements such as macrophages, foreign body giant cells, and osteoclasts from adjacent undamaged areas invade the necrotic tissue. These cells also resorb the underside of bone immediately adjacent to the necrotic PDL area and remove it together with the necrotic tissue. This process is known as undermining resorption 55, 56.

Due to injury caused by occlusal trauma, there is a temporary reduction of mitotic activity of cells including fibroblasts (reducing their rate of proliferation) 57 and osteoblasts (reducing the rate of bone formation) 57, 58 In presence of these excessive occlusal forces, all the above stated changes take place, but if the forces are removed or tooth moves away from the forces and the periodontium is completely restored.

Stage II, Repair:

Repair is a well regulated mechanism in which the damaged tissues are replaced by new connective tissue and cells. The extracellular matrix and certain inflammatory mediators play critical regulatory functions directly or indirectly facilitating the healing process. Although, the reparative activity is always going on in normal periodontium, it is increased during trauma from occlusion.

To withstand the heavy occlusal forces, body tries to reinforce the trabeculae within new bone. This process is known as “buttressing bone formation” 21. When this process occurs within the bone, it is known as ‘central buttressing’ and when it occurs on the facial or lingual surface of the alveolar bone, it is known as ‘peripheral buttressing’. In case of central buttressing, the endosteal cells deposit bone on the trabecular walls thereby reducing the marrow space and strengthening the bone to bear increased occlusal load. In case of peripheral buttressing, shelflike thickening of the bone can be seen on the lingual or the buccal surface of the alveolar bone which is sometimes referred to as “lipping” 18.

Stage III, adaptive remodelling of the periodontium:

If the repair process cannot keep pace with the destruction caused by excessive occlusal forces, adaptive remodelling of the periodontium occurs. In this process of remodelling, a structural relationship is established is such a way that the occlusal forces are no longer harmful to the periodontium. It includes thickening of periodontal ligament, funnel shaped defect in the crestal portion and vertical/angular bone loss. It must be noted that there is no pocket formation during this adaptive response. Because of the above changes, the tooth becomes loose 39. Studies have also reported increased vascularization of the involved area of periodontium 59.

Response of normal and reduced periodontium to normal and increased occlusal forces

Trauma from occlusion

Examination and diagnosis of trauma from occlusion:

Clinical history of the patient and clinical examination are the cornerstones of correct diagnosis of trauma from occlusion.

Signs of trauma from occlusion:

Tooth mobility:

It is one of the earliest signs of trauma from occlusion. As already discussed, the widening of periodontal ligament space and angular bone loss during the adaptive response are the main causes of increased tooth mobility. Although increased tooth mobility is one of the most widely used indicators of occlusal trauma, it may result from bone loss independent of occlusal forces. It may also represent a self-limiting adaptive response of the host periodontium to the sustained application of occlusal forces 39, 60. Progressive mobility may be suggestive of on-going occlusal trauma, but assessments and monitoring at differing points in time are necessary to make this determination 61.

It is important to differentiate pathologic tooth mobility from physiologic tooth mobility. Normal physiological movement is thought to vary between 10 µm and 150 µm and would not be detectable on clinical examination. One common index used to classify tooth mobility is Miller’s Index (1938) 62:

I - up to 1 mm of movement in a horizontal direction

II - greater than 1 mm of movement in a horizontal direction

III - excessive horizontal movement and vertical movement.

For detailed description on tooth mobility read “Tooth mobility”.

Tooth migration:

To avoid excessive occlusal forces, tooth tries to move away from them. Loss of interproximal contacts and migration of tooth from its stable position is one of the signs of trauma from occlusion.

A case of TFO due to cross-bite of incisors with grade II mobility with respect to mandibular incisors

Trauma from occlusion due to cross-bite

Radiographic examination reveals widening of periodontal ligament space

Widening of periodontal ligament space

Wear patterns:

Wear surfaces in the area of interference can be seen. A common reason for formation of wear facets is bruxism. Bruxism causes formation of wear facets on the occlusal/incisal surfaces of teeth which can be identified as shiny and irregular areas. 

Abfraction, especially in premolars:

Due to excessive lateral forces, abfraction can be seen especially in premolars. The wear facets and abfraction appears before gingival recession. So, when these are present, the clinician may conduct a careful periodontal examination and radiographic examination to diagnose trauma from occlusion.

V-shaped or angled gingival recessions:

Trauma from occlusion may promote gingival recession, particularly V-shaped or angled gingival recession. This has been a matter of controversy as many researchers are in favour of this finding 63, 64 and many others are not 65, 66. Researchers who are not in favour of association of TFO with recession claim that recession results from marginal inflammation due to the presence of plaque, whereas researchers in favour of association of recession with TFO claim that V-shaped or angled gingival recessions with a small fissure in their most apical extremity is directly associated with occlusal trauma 64 and is commonly associated with abfraction 63, 67, 68.

Buccal bone dehiscence:

Buccal cortical bone is thin especially in the canine and premolar areas. As already stated, due to occlusal trauma there is widening of periodontal ligament space at the expense of bone resorption. In these areas, a very little resorption on the periodontal face may result in loss of cervical height and V-shaped bone dehiscence over the buccal face of the root that is affected. The detection of these areas is quite difficult and newer diagnostic techniques such as CT scan or CBCT scans can be used to diagnose these bone defects.

With the loss of bone in the marginal area, the periosteum covering the bone persists for indefinite period. Later on, the periosteum due to lack of bone and blood vessels to nourish it, it gets restricted to the bone margins, leaving the root surface exposed to gingival and periodontal connective tissues.

Clinical and radiographic indicators of trauma from occlusion

Clinical indicators of occlusal trauma may include one or more of the following
  • Mobility (progressive)
  • Fremitus
  • Occlusal prematurities
  • Wear facets in presence of other clinical indicators
  • Tooth migration
  • Fractured tooth (teeth)
  • Thermal sensitivity
  • Angled gingival recessions
  • Abfraction, especially in premolars
Radiographic indicators of occlusal trauma may include one or more of the following
  • Discontinuity and thickening of lamina dura
  • Widened PDL space
  • Bone loss (furcation; vertical; circumferential)
  • Root resorption

 

Fremitus test:

This test is used to clinically detect trauma from occlusion. It measures the vibratory pattern of the teeth when the teeth are placed in the contacting positions and movements. In this test dampened index finger is placed along the buccal and labial surfaces of the maxillary teeth and the patient is asked to tap the teeth together in the maximum intercuspal position and then grind systematically in the lateral, protrusive movements and positions. The teeth that are displaced by the patient in these positions are identified and graded. In the posterior teeth trauma from occlusion can be detected with help of occlusion registration strips/articulating paper. High pressure points can be detected by the pattern of impressions made by registration strips/articulating paper.

The following classification system is used:

Class I fremitus : Mild vibration or movements detected.

Class II fremitus : Easily palpable vibration but no visible movements.

Class III fremitus : Movements visible with naked eye.

Symptoms of trauma from occlusion:

Persistent discomfort on eating:

Patient complains of persistent discomfort during eating. Due to excessive occlusal forces on a tooth or group of teeth, patient is not able to satisfactorily chew the food and the teeth under high occlusion cause discomfort.

Thermal sensitivity:

Although, the exact effect of occlusal trauma on dental pulp is still not clear, but studies have demonstrated that there are changes in the vascular supply of the pulp due to excessive occlusal forces 69. It causes increased blood pressure in the pulp and hence tooth becomes sensitive to thermal changes.

Muscle hypertonicity:

The patient complains of tired jaws especially after rising in the morning and at the end of the day. It is because of the occlusal interferences causing muscle spasm and discomfort.

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Effect of insufficient occlusal forces:

Insufficient occlusal forces are also deleterious for the tooth supporting structures. There is thinning of periodontal ligament, atrophy of fibers and osteoporosis of the alveolar bone. The bone height also reduces. The reasons for insufficient occlusal forces include, intentional unilateral chewing habit, open bite or absence of antagonist tooth.

 

Radiographic signs of trauma from occlusion:

The radiographic signs that can be seen in tooth/teeth with trauma from occlusion are,

  • Thickening of the lamina dura.
  • Irregular widening of the periodontal ligament space.
  • Vertical bone loss.
  • Bone sclerosis in the periapical area or in the interdental bone crest.
  • Inflammatory root resorption, more common in advanced stages of occlusal trauma.

Sclerosing osteitis type of increase in periapical bone density around a vital tooth on radiograph and positive clinical signs of trauma from occlusion can guide us to a correct diagnosis and treatment plan.

Is traumatic occlusion reversible?

Although, the injury caused by trauma from occlusion is reversible, there may or may not be complete restoration of the tooth supporting structures. If the excessive occlusal forces are neutralized, healing takes place and there is an attempt to restore the normal periodontal structures. The presence of plaque which results in inflammation may impair the healing, so resolution of inflammation should be done.

Trauma from occlusion around implants:

An osseointegrated implant is in direct contact with surrounding bone. There is no periodontal ligament around dental implants. It has been suggested that functional load on dental implants may enhance osseointegration and does not result in marginal bone loss when the occlusal load is adequately distributed 70. But, occlusal overload adversely affects the implant stability. It has been suggested by animals and humans studies that occlusal overload may cause a loss of osseointegration and early implant failure 71-78. To understand the implant failure due to occlusal overload, we need to understand the bio-mechanics of the implant osseointegrated to the surrounding bone.

One of the key factors controlling the bone remodelling at molecular level is, strain in the surrounding environment. Strain is defined as the change in length divided by the original length. Strain is created when the any object is subjected to external stress. In oral environment, this stress is the occlusal load. The occlusal stresses on the implant prosthesis are transmitted at implant bone interface 79. The mechanoreceptors present in the bone respond to these stresses and initiate bone remodelling. These mechanoreceptors are very sensitive and microstrain levels 100 times less than the ultimate strength of bone may trigger bone remodelling 80. If the implant is subjected to trauma from occlusion, high levels of stress is imposed at the implant bone interface, initiating bone resorption leading to implant failure.

Another important mechanical factor is the modulus of elasticity (stiffness of a material). The modulus conveys the amount of dimensional change in a material for a given stress level. The modulus of elasticity of a tooth is similar that of to cortical bone but the modulus of elasticity of titanium is 5 to 10 times greater than that of cortical bone 81. There is an engineering principle known as “the composite beam analysis”. According to this principle, when two materials of different elastic moduli are placed together with no intervening material and one is loaded, a stress contour increase will be observed where the two materials first come into contact 82. In case of osseointegrated implants these stresses are concentrated at crestal bone level. This observation has been authenticated by photoelastic and 3-dimensional finite element analysis studies where implants were loaded within a bone stimulant 83, 84. This is the reason why crestal bone loss is often observed around implants.

The density of the bone is directly related to the bone strength and modulus of elasticity 85. Denser bone has more strength and modulus of elasticity that a softer bone, hence denser bone can bear more stresses as compared to the softer bone. There is less bone remodelling in denser bone as compared to soft bone under same stress levels 86.

It must be remembered that other factors such as peri-implantitis, the microgap position of the implant platform and abutment and the biologic width are also equally responsible for crestal bone loss around implants.

Our present understanding of trauma from occlusion:

As we know that normal occlusal forces are required to keep periodontal tissue healthy. In case where the functional demand of the tooth increases, the periodontium accommodates this increased functional demand which is evidenced by thickened lamina dura and reinforcement of bony trabeculae. If the functional demand of the tooth cannot be met by periodontium, tissue injury results. If the noxious stimulus is chronic, there is widening of the periodontal ligament space at the expense of bone resorption. Widening of the periodontal ligament space has a cushioning effect which enables the tooth to bear the excessive occlusal forces.

Inflammation is the primary factor responsible for the destruction of the periodontal tissue. Trauma from occlusion does not cause gingival inflammation. But, it has a definite role in modifying the spread of inflammation. The modification or intensification of the inflammation causes rapid breakdown of the periodontal tissue.   

Treatment of trauma from occlusion:

The treatment of trauma from occlusion involves removal of the excessive occlusal forces and bringing the tooth/teeth in comfortable position. Many treatment modalities have been advised to treat trauma from occlusion 87. These include,

  • Occlusal adjustment
  • Management of parafunctional habits
  • Temporary, provisional or long-term stabilization of mobile teeth with removable or fixed appliances
  • Orthodontic tooth movement
  • Occlusal reconstruction
  • Extraction of selected teeth

Occlusal adjustment:

The reshaping of the occlusal/incisal surfaces of the tooth/teeth or coronoplasty involves selective grinding of the teeth to achieve harmonious relationship of teeth in the opposite arches. There are many controversies regarding the grinding of occlusal surfaces of teeth. These are regarding the extent of selective grinding of teeth and its long term effectiveness. The 1989 World Workshop in Periodontics listed the following indications and contraindications for occlusal adjustment 88:

Indications for Occlusal Adjustment:

  1. To reduce traumatic forces to teeth that exhibit:
    1. Increasing mobility or fremitus to encourage repair within the periodontal attachment apparatus.
    2. Discomfort during occlusal contact or function.
  2. To achieve functional relationships and masticatory efficiency in conjunction with restorative treatment, orthodontic, orthognathic surgery or jaw trauma when indicated.
  3. As adjunctive therapy that may reduce the damage from parafunctional habits.
  4. To reshape teeth contributing to soft tissue injury.
  5. To adjust marginal ridge relationships and cusps that are contributing to food impaction.

Contraindications for Occlusal Adjustment:

  1. Occlusal adjustment without careful pre-treatment study, documentation, and patient education.
  2. Prophylactic adjustment without evidence of the signs and symptoms of occlusal trauma.
  3. As the primary treatment of microbial-induced inflammatory periodontal disease.
  4. Treatment of bruxism based on a patient history without evidence of damage, pathosis, or pain.
  5. When the emotional state of the patient precludes a satisfactory result.
  6. Instances of severe extrusion, mobility or malpositioning of teeth that would not respond to occlusal adjustment alone.

Management of parafunctional habits:

Parafunctional habits like bruxism cause excessive forces on the periodontium causing injury to the periodontium. The correct diagnosis of bruxism should be made by taking history of the patient and associated clinical findings. Night guard is used to treat night grinding of the teeth. It also helps in relaxation of the masticatory muscles.

Splinting of teeth:

Splinting is the mechanism of joining adjacent teeth thereby reducing their mobility and converting them into single unit which is expected to withstand the occlusal forces better than the individual tooth. However, it must be understood that the removal of abnormal occlusal forces should be our primary target. Glickman et al. 89 in a study clearly showed that although fixed splints provide some beneficial distribution of occlusal forces, the ideal way to alleviate excessive occlusal forces that cause tooth or teeth mobility is to remove the destructive occlusal contacts. Following are indications and contraindications for splinting as listed in the 1989 World Workshop in Periodontics 88,

Indications of splinting:

  1. Stabilize teeth with increasing mobility that have not responded to occlusal adjustment and periodontal treatment.
  2. Stabilize teeth with advanced mobility that have not responded to occlusal adjustment and treatment when there is interference with normal function and patient comfort.
  3. Facilitate treatment of extremely mobile teeth by splinting them prior to periodontal instrumentation and occlusal adjustment procedures.
  4. Prevent tipping or drifting of teeth and extrusion of unopposed teeth.
  5. Stabilize teeth, when indicated, following orthodontic movement.
  6. Create adequate occlusal stability when replacing missing teeth.
  7. Splint teeth so that a root can be removed and the crown retained in its place.
  8. Stabilize teeth following acute trauma.

Contraindications for Splinting:

  1. When the treatment of inflammatory periodontal disease has not been addressed.
  2. When occlusal adjustment to reduce trauma and /or interferences has not been previously addressed.
  3. When the sole objective of splinting is to reduce tooth mobility following the removal of the splint.

Stabilization of teeth with splinting

Splinting

Orthodontic tooth movement:

Moving tooth/teeth through orthodontic forces is one of the ideal treatments of trauma from occlusion. But, applications of orthodontic forces also have their own indications and contraindications. A periodontally compromised tooth with little bone support is not a good candidate for orthodontic tooth movement. Moving the tooth in a position which will further compromise its stability and long term prognosis is also not desirable. Tooth movement which shall eliminate abnormal occlusal forces as well as improve its long term prognosis should be our primary goal during application of orthodontic forces on the tooth.

Occlusal reconstruction:

Complete occlusal reconstruction involves redesigning complete occlusal scheme. It is done in cases where, by no other means occlusal equilibration can be achieved. It involves re-designing the occlusal contacts by giving crowns, bridges or implant supported prosthesis. This kind of procedure requires a thorough knowledge of occlusion. It must be remembered that this procedure completely changes the occlusal scheme, so the changed occlusion should be thoroughly studied first on articulated casts and then it should be replicated into the patient’s mouth.

Extraction of selected teeth:

Rarely, a tooth is extracted to correct trauma from occlusion. In certain situations extraction of selected tooth/teeth may be done to correct trauma from occlusion, such as a tooth with extensive periodontal involvement with poor prognosis, extraction of which may improve prognosis of the remaining teeth. During orthodontic treatment also extraction of certain teeth may be indicated for proper final positioning and alignment of teeth.

Conclusion:

Abnormal occlusal forces and their role in progression of periodontal diseases has been studied for over last hundred years. From the above discussion it is clear that trauma from occlusion does not causes gingival inflammation but can modify the spread of inflammation into the underlying connective tissue. The plaque control and proper oral hygiene are the primary factors which are focused to eliminate inflammation of periodontal tissue. Elimination of the abnormal occlusal forces along with stabilization of the involved tooth/teeth is the primary treatments for trauma from occlusion.

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