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