Occlusion and Periodontitis
by Dinh X. Bui, D.D.S., M.S.

Occlusion and Periodontitis
Occlusion has been one of the most controversial factors in determining the cause of periodontitis in the area of manifestation. Traumatic occlusion, a pathological state of occlusion, has been theorized that the situation could lead to migration of epithelial cuff, localized bone loss, and ultimately the result is pocket deepening. Many researches and studies have aimed to disprove this theory since periodontitis is believed of bacterial etiology. This paper will explore the concept of occlusion, more specifically occlusal trauma, and how it manifests in the etiology and treatment of Periodontal disease.

Jens Waerhaug and Erik Randers Hansen studies the periodontal changes incident to prolonged occlusal overload in monkeys. His study was designed to establish the extent of damage that can be caused by prolonged and repeated occlusal overload in the adult monkey. The site of interest is lower left first molar. Gold crown with high occlusion was fabricated and thus caused an opening of the bite of about five millimeters between the upper and lower incisors. As a result, a combination of vertical and lateral forces was introduced into the lower left first molar and its antagonist from the other arch. Plaque was controlled by brushing every day as to eliminate it as a variable to the outcome. During the course, the crown and its antagonist first was intruded and became very mobile while the occlusal relationship was reestablished. The crown was then removed and the teeth allowed to extrude and the experiment then is repeated. The animal would be sacrifice and the histology was performed in the area of traumatic occlusion to determine its effect and the extent of damage. Three scenarios were examined: histology done with the crown in place, histology performed after crown had been removed for sometimes, and histology in the antagonist tooth.

In the case of high occlusion (crown in place), histology showed that there is bone necrosis and osteoclastic resorption in the compressive side, followed by establishment of periodontal membrane apical to necrotic area. Thus constructive repair occured. There is no apical migration of epithelial cuff. In the case of crown had been removed for sometime prior to histology performed, repair again occured. Teeth extrude and adjust to normal occlusion, periodontal membrane regenerated, bone regenerated, apical migration seen on the pressure side but there is no different from the control. Plaque was seen in the area of apical migration of epithelial cuff. In the case of antagonist, the situation similar to that of the high occlusion occur. However, there was no necrotic tissue observed, with bone apposition and regeneration of periodontal membrane was observed. In all three cases, plaque was seen when is pocket deepening. Bone resorption in the compressive side and regenerated when the pressure was taken off (crown removed). In one of the monkey of which pregnancy occured, (introducing a systemic involvement as a variable), pathologic pocket occured. Jens Waerhaug and Erik Hansen concluded that extreme occlusal overload in combination with highly unfavourable systemic conditions may reduce the resistance to local bacterial factors and also ease the progress of these constituents. Periodontal lesion develop as the result of bacterial plaque accumulation. Occlusion alone will not cause Periodontal disease. However, with plaque and bacterial accumulation, occlusion will exacerbate the process of bone resorption due to bacterial etiology.


Kronfeld examined the morphology and physiology of human periodontal tissues under normal and abnormal functional conditions. He have shown that the gingival tissue can appear normal even though the tooth was in end to end occlusion and was worn flat. In this case, the circumferential bone is thick, and the periodontal membrane is of even width around the root, with strongly developed fiber bundles running from cementum to bone. There are no crevice present, and the gingival epithelium is intact. On the area of tensile stress (the lingual area), the fiber organized horizontally from tooth to bone, stabilized the tooth against lateral displacement, and especially to counteract any attempt to force or tip the crown in the buccal direction. In the apical area where there is a lot of compression, apical fibers of the periodontal membrane served as a cushion when the tooth is pressed down into the socket, and prevented lateral displacement of the apex when the crown is moved under stress. In the tooth without occlusion, Kronfeld reported that the periodontal membrane is thin, atrophic; only a few fiber bundle present, and they are separated by wide areas of loose indefinite fibers. He further described the width of PDL space as from .21mm in young individuals to .18 or.15mm in adult (Coolidge reported of 1100 human measurement.) Coolidge also reported that the thickness of PDL varied between functioning (.22mm) and nonfunctioning teeth (.13mm). He also reported that age is of significance concerning the width of PDL. In the teeth which subjected to abnormal occlusion, when the supporting apparatus can adapt to this condition Kronfeld showed that there is a very strong fiber bundles run horizontally from bone to tooth and there is repair in the supporting apparatus to make adjustment to the existing occlusal condition. On the other hand, if the malocclusion was so profound that the supporting apparatus failed to adapt, Kronfeld reported of loss of PDL space and root resorption occured. PDL is crushed, especially in the case of excessive lateral force. In other word, if the malocclusion is not so great such that the equilibrium between occlusal stress and tissue reaction is preserved, the supporting apparatus will adapt with an establishment of strong fibers surrounding the tooth. In the case of the equilibrium is disrupted, changes to the PDL, the fibers, root resorption occured. However, these changes have the tendency to be repaired and damaged tissue become regenrate when the excessive force subsided (Coolidge, Organ, Stuteville). The periodontal membrane and the supporting bone of human teeth have a wide range of adaptability to changing functional conditions, adjusting to the variety of abnormal and unfavorable occlusal relations and to maintain such relations successfully over a long period of time. Charles A. Kohler reported of periodontal reaction to functional occlusal stress in his study on 15 human teeth. The most stable strucute in regard to functional changes, as reported, is the Sharpey’s fibers entering the cementum and the periodontal fibers coronallly to the margin of the alveolar crest. Most of the adaptation of the periodontal fibers to change in functional demand seemingly takes place at the surface of the alveolar bone and the middle zone of the periodontal membrane. When the tooth is no longer under traumatic occlusion or there is a decrease in occlusal stress, the atrophy of functionally oriented periodontal fibers in adult is a slow process. He further emphasizes that loss of posterior teeth may lead to traumatic occlusion with such sequalae as resorption of the surface of the root extending into dentin, and resorption of the alveolar bone with perforation of the labial wall of the alveolar process. Finally, remodeling and partial rebuilding of the alveolar process in response to changes in functional stress occurred in all of the patients regardless of the variation in age from 16 to 68 years. Overall, the stability of Sharpey fibers inserted into the cementum and the persistence of the alveolar crest fibers in the presence of great changes in the periodontal structure were the two most striking observations in the study.

It has been shown conclusively that occlusal trauma is not capable of initiating marginal inflammation or pocket formation in the absence of bacterial plaque, nor will it aggravate gingivitis. Jens Waerhaug have shown that abnormal occlusion may lead to sterile necrosis within the periodontal membrane and this necrosis cause little inflammation and it is hardly likely to produce an inflammation in the gingival margin. Under extremely unfavorable conditions, a deepening of the clinical pocket below cementoenamel junction can be produced by undue occlusal stress. This unfavorable conditions usually involved inflammatory process surrounding the tooth due to plaque/bacterial accumulation. The downgrowth of epithelium can hardly take place as long as the periodontal membrane is necrotic, and must occur during the healing period after the necrotic tissue is resorbed and before new periodontal fibers have been formed. He also reported that there is a 1 mm wide area between the alveolar crest and the deepest line of the epithelial cuff represents a safety zone which follows the movement of the tooth and is not injured by occlusal overload. This zone prevents damage, done to the periodontal membrane within the alveolus, from spreading to the marginal gingiva. The damage done to the cementum, periodontal membrane, the alveolar bone will be repaired when the tooth readjusts itself in a new position, whereas the downgrowth of the epithelium is permanent damage.

Balint Orban in his article about traumatic occlusion and gum inflammation reported the traumatic changes to the periodontium on the compressive pressure and tensile pressure. The compressive pressure leads to necrosis of periodontal membrane at the alveolar margin, following by resorption of the bony alveolar crest. On the tensile side, widening of periodontal ligament space can be observed but there is no tears with extensive bone forming process taking place. He emphasized that traumatic occlusion and gum inflammation presents different pathological pictures that these conditions must be separated during analysis. A patient with periodontal disease and traumatic occlusion must be treated with two separated condition. The local factors in periodontal disease must be removed. Occlusal disharmony must be erradicated after evaluation.

Abnormal occlusal relationship could damage the periodontium in two different ways: through abnormal or subnormal occlusal stress during mastication or other functional movements or bruxism or other nonfunctional movement, and through disturbances of normal function affecting hygienic condition of the mouth or the efficiency of masticatory system. Investigations have shown that abnormal stress acting on an intact periodontium does produce damage to the periodontal tissue, but the damage is limited to the intraalveolar part of the periodontium. Occlusal trauma is an entity of itself and alone does not lead to periodontal disease. The damage to the intraalveolar periodontal tissues is generally completely repaired, provided the tissue is given resting periods. This may not be the case if persistent parafunctions prevail. Crewcock and Ballard in 1954 reported that occlusal disharmonies may induce parafunctions. Secondary abnormal occlusal stress may be an important aggravating factor in established periodontal diseases and must not be ignored in the treatment of these cases.

How would occlusal trauma affect the periodontally compromising tooth of which there is a reduced bone support? Svanberg and Linhdhe reported that the jiggling type of force induces a series of adaptive alterations within the periodontal tissue in normal or overt gingivitis case. The jiggling force produces the traumatic phase which the tooth demonstrated increasing tooth motility, and the post traumatic phase of which there is a permanent increased of tooth mobility. The traumatic phase characterized by widening of PDL, osteoclastic alveolar bone resorption, and increasing number of vessels exhibiting enhanced permeability to plasma and leukocyte. In the post traumatic phase, the vascularity returned to normal. There is no obvious retention of leukocytes within the periodontal ligaments, nor are there sign of increased osteoclastic activity. In 1974, Lindhe and Svanberg reported that jiggling force on the periodontally compromise patient may cause an increased rate of apical downgrowth of pocket epithelium and infrabony pocket formation. Glickman also reported that peridontal tissue at the pressure side of teeth subjected to periodontitis and trauma from occlusion could be consistently characterized by the presence of angular bony defects and infrabony pockets. Glickman further stated that when the chronic inflammatory lesion produced by the bacterial plaque reaches the major supporting tissue, trauma from occlusion may become a co-destructive factor in periodontitis. Glickman and Smulow also reported the microscopic observation in his experiment with six adult male rhesus monkeys using crown to produce abnormal functional relationship. They found that the pathway of inflammation from the gingiva into the underlying periodontal tissues is affected by the direction and severity of occlusal forces. The pathway of inflammation was not affected by excessive tension. The periodontal membrane did not undergo destructive changes. The tissue of the periodontium are more susceptible to injury from the excessive pressure than from excessive tension. In the presence of excessive pressure, the natural barrier provided by the periodontal fibers is impaired, the bone undergoes resorption and angular remodeling, and the inflammation penetrates into the periodontal membrane. Injury to the periodontium induced by artificial alterations in the occlusion is reversible. Periodontal injuries induced by attrition tends to persist.

Jan Lindhe and Ingvar Ericsson examined the influence of trauma from occlusion on reduced but healthy periodontal tissues in dogs. Periodontal lesion were created five dogs on day 0. After 180 days, trauma from occlusion were introduced which involved a jiggling force. On day 280 periodontal pockets were eliminated and trauma from occlusion deleted on the control side. From day 280 to termination the teeth are subjected to careful mechanical cleaning twice a day. Experiment terminated on day 370. The results showed that gingival condition and the amount of plaque accumulation is as anticipated, i.e. with deterioration without oral hygiene and restored to health with oral hygiene (day 280 to termination). Tooth mobility increases significantly after 6 months. After introduction of trauma occlusion on day 180, mobility increase very pronounced. Upon removal of traumatic occlusion on the control side, the mobility return to normal (at the end there was not a significant difference). On the tested teeth, there was a further increase towards the end of study. Alveolar bone exhibit widening of PDL space, especially around mesial root. On the control side, removal of malocclusion restored the PDL space back to normal and there is the presence of a distinct and radiopaque marginal termination of the alveolar bone. On the tested side, PDL space appear markedly widen in the marginal and also the apical regions. Histology finding showed that tested teeth demonstrated increased vascular units but no leukocyte infiltrates occured. The resulted demonstrated that, provided the plaque and inflamed periodontal tissues were removed and a proper oral hygiene regimen was esttablished, healing also occurred in case where jiggling force were acting on hypermobile teeth. Microbial plaque is always a main causative factor in defining the etiology of periodontal disease. In the tested site, tissue alterations caused by trauma from occlusion do not interfere with regeneration and the reorganization of the epithelial and connective tissue component of the gingiva. The distance between the apical cells of the JE and the alveolar crest was the same to both the test and the control teeth. Once the plaque and the the chronically inflamed periodontal tissue had been removed and provided the dentitions were kept up to a proper standard of oral hygiene, normal healing of periodontal tissue always occurred, even around teeth which subjected to jiggling force.

Bruce L. Pihlstrom and Karl A. Anderson evaluate the association between signs of trauma from occlusion, severity of periodontitis and radiographic record of bone support. The maxillary first molars of 300 individuals (20 to 40 years of age) were independently evaluated by two examiners for signs of trauma from occlusion, pattern of occlusal contacts and severity of periodontitis. Each site was also evaluated radiographically by an independent third examiner. The results indicated that: teeth with either bidigital mobility, functional mobility, a widened periodontal ligament space or the presence of radiographically visible calculus had deeper probing depth, more loss of clinical attachment and less radiographic osseous support than teeth without these findings, teeth with occlusal contacts in centric relation, working, nonworking or protrusive positions did not exhibit any greater severity of periodontitis than teeth without these contacts, (3) teeth with both functional mobility and a radiographically widened periodontal ligament space had deeper probing depth, more clinical attachment loss and less radiographic osseous support than teeth without these findings and (4) given equal clinical attachment levels, teeth with evidence of functional mobility and a widened periodontal ligament space had less radiographic osseous support than teeth without these findings.

In summary, occlusion will never play a role in etiology of Periodontal disease. However, if there is an inflammatory process occuring around the tooth with pathologic occlusion, bone resorption will occur at a much faster rate. Patient plaque control and his or her oral hygiene habit will dictate the majority of the success of therapy. By removing the bacterial factor, patient may relapse into the adaptive, physiologic occlusion from the pathologic occlusion. Thus occlusal therapy should be delivered after the hygienic phase has been provided, unless the occlusal trauma introduced a jiggling force or parafunctions and prevented the proper healing of the treated sites.

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References


1. Bruce L. Pihlstrom, Karl A. Anderson, Dorothy A. Association between signs of trauma from occlusion and periodontitis. Journal of Periodontology : 1986;1.

2. Orban, B. Traumatic occlusion and gum inflammation. Journal of Periodontology, 1939: 39: 10.

3. Posselt U., Emslie, RD. Occlusal disharmonies and their effect on periodontal disease. Int. Dent. J. 1959: 9: 367.

4. Lindhe, J., Svanberg, G. Influence of trauma from occlusion on progression of experimental periodontitis in beagle dog. J. of Clin. Periodont. 1974: 1: 3.

5. Glickman, I., Smullow, JB. Alteration in the pathway of gingival inflammation into the underlying tissues induced by excessive occlusal forces. J. Periodont. 1962: 33: 7.

6. Kronfeld, R. The physiology of the human periodontal tissues under normal and abnormal occlusal conditions. Illinois Dent. J. 1939:8:13.

7. Muhleman HR. Ten years of tooth mobility measurements. J. of Periodontology. 1960: 31: 110.

8. Lindhe, Ericsson, I. The influence of trauma from occlusion on reduced, but healthy periodontal tissues in dogs. J. of Clinical Periodont. 1976: 3: 110.

9. Waerhaug J., Hansen, ER. Periodontal changes incidental to prolonged occlusal overload in monkeys. Acta. Odont. Scand. 1966: 24: 91.

10. Ramfjord SP., Kohler C. Periodontal Reaction to functional occlusal stress. J. Periodont. 1959: 30: 95.

11. Ramfjord, Ash. Occlusion. Third edition. W.B. Saunders Company, 1983.

12. Waerhaug, J.: Pathogenesis of pocket formation in traumatic occlusion. J. of Periodontology:1958:29,87.

13. Glickman, I., Smulow. Further observations on the effects of trauma from occlusion in humans. Journal of Periodontology: 1967:38, 280.

14. Waerhaug, Jens. The Infrabony Pocket and its Relationship to Trauma from Occlusion and Subgingival Plaque, Journal of Periodont, 1979, 355-365.