DOI: 10.1111/prd.
12251
REVIEW ARTICLE
Role of occlusion in periodontal disease
Euloir Passanezi | Adriana Campos Passanezi Sant'Ana
Division of Periodontics, School of Dentistry at Bauru, University of São Paulo, Bauru, Brazil
Correspondence
Euloir Passanezi, Division of Periodontics, School of Dentistry at Bauru, University of São Paulo, Bauru, Brazil.
Email: epperio@fob.usp.br
1 |  I NTRO D U C TI O N
Although more than a century has elapsed since the first publication
of Karolyi,1 which implicated the forces of occlusion in the behavior of
periodontal tissues, deep-­rooted controversy about the role of occlu-
sion in the development/progression of marginal inflammatory infec-
tious periodontal disease—gingivitis and periodontitis—still remains.
Some studies propose that traumatogenic occlusal forces are related to
2–8
the initiation and/or progression of periodontal disease. Conversely,
other studies find no association between trauma from occlusion and
periodontal disease.9,10 These contradictory arguments have led to
widespread disagreement in the literature in relation to the role of oc-
clusion in the pathogenesis of periodontal disease, inspiring much Latin
American research.2,3,11–20 Accordingly, a detailed and comprehensive
presentation of important clinical and scientific evidence to shed light
on the role of occlusion in chronic periodontal disease is required.
2 |  A H I S TO R I C A L PE R S PEC TI V E
The role of trauma from occlusion in the etiology of periodontal dis-
ease has been discussed since the early 1900s. Historically, the first
evidence for a role of trauma from occlusion in periodontal disease
came from research performed in animals21 and human cadavers.3
These studies suggested that trauma from occlusion was related
to the development of infrabony pockets, possibly consequent to
ischemia of periodontal ligament and depletion in gingival blood
supply. 21
Further research2 suggested that trauma from occlusion resulted
in disorganization of periodontal tissues, impairing their normal re-
pair function. Besides that, the alterations produced by trauma from
occlusion might contribute to the deepening of periodontal pockets,
2,22
favoring the spread of inflammation to neighboring tissues.
By this time, other studies performed in animals showed no caus-
ative association between trauma from occlusion and periodontal
Periodontology 2000. 2019;79:129–150. wileyonlinelibrary.com/journal/prd   © 2019 John Wiley & Sons A/S. |  129
disease, indicating little to no correlation between trauma from
occlusion and periodontal disease. 23–25 Bhaskar and Orban26 failed
to observe the development of gingivitis or periodontitis in animals
subjected to trauma from occlusion but not affected by plaque-­
related chronic periodontitis. Polson27 and coworkers9,28 did not find
a positive correlation between occlusal trauma and gingival inflam-
mation or pocket development.
However, these studies, although performed under controlled
experimental conditions, used animal models, which do not deliver
reliable data on the role of occlusion in humans because teeth in an-
imals are designed for defense and attack, as well as for mastication,
and respond very well to different occlusal stimuli. In addition, the
envelope of mandibular motion in animals is quite different from that
in humans, with no opposing directions resulting from the lateral dis-
tribution of occlusal forces. This is probably one of the reasons why
jiggling forces are needed in animals to achieve a periodontal injury
compatible with that induced by traumatogenic occlusion in humans,
with a particular exception for primates.4,9,28–30
During the 1960s and early 1970s, Glickman7,31 and cowork-
ers5,6,17,18,32–35 proposed that occlusal trauma acted as a co-­
destructive zone, influencing the spread of inflammatory gingival
exudate directly to the periodontal ligament, eliciting a combined
lesion of trauma from occlusion and periodontitis. The final result
could be the development of infrabony periodontal pockets, as sug-
gested by other studies,15,22,25 indicating an association of trauma
from occlusion with periodontitis.
However, the possible coexistence of trauma from occlusion and
inflammation without the formation of infrabony pockets cannot be
ruled out, meaning that these conditions are not pathognomonic of
trauma from occlusion.6 Moreover, suprabony pockets and horizon-
tal bone loss could result from the association between trauma from
occlusion and inflammation, under certain circumstances yet to be
determined.
The type of periodontal pocket that develops in response to the
association between trauma from occlusion and chronic periodontitis
Published by John Wiley & Sons Ltd
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130       PASSANEZI and SANT'ANA
is related to the thickness of the bony wall: the thicker the bone wall,
the more probable is the development of an infrabony pocket; the
thinner the bone wall, the more probable is the development of a
suprabony pocket. In areas with suprabony pockets superimposed
by trauma from occlusion, a deeper pocket is expected to develop.
Consequently, areas with different depths of suprabony pockets
could denote the influence of traumatogenic occlusion. In addition,
trauma from occlusion could induce changes in the architectural
structure of alveolar bone, making existing suprabony pockets more
16
prone to conversion to infrabony pockets.
These theories were substantiated in a series of experiments
performed in beagle dogs,4,8,36,37 supporting the relationship be-
tween excessive occlusal forces and the pathway of gingival inflam-
mation seen in animal models and autopsied human jaws.6
In human autopsy material, dental plaque was detected in the
deepest “front” of infrabony periodontal pockets. Hence, it could
not be inferred that infrabony pockets were related to the partici-
pation of traumatogenic occlusal forces, which means that it can not
be assumed that infrabony pockets were related to the incidence
of traumatogenic forces.38,39 The development of infrabony peri-
odontal pockets in animals as a consequence of an alteration in the
pathway of dental biofilm-­related gingival exudate spread to the
supporting tissues only occurred in the presence of forces of high
magnitude. So, the infrabony pocket would be the result of intru-
sion of the tooth, rather than dislodgement of inflammatory exudate
directly into the periodontal ligament space in which destructive al-
terations directly associated with the occlusal trauma were taking
place. 29
Therefore, many contradictory concepts are being challenged by
the same group of authors, making the role of occlusion a cloudy
matter in dentistry. Besides, it is paramount to bear in mind that na-
ture provided occlusion as a vital source of human survival, mean-
ing that deviations from normal occlusion might have a tremendous
deleterious effect. Despite extensive research over many decades,
one such defying question relates to the role of occlusion in the eti-
ology and pathogenesis of chronic periodontitis, which is still not
completely understood.
Recently, the distinction between primary and secondary occlu-
sal trauma has been questioned because the pathological changes
that occur in the periodontium are similar in both types of trauma, ir-
respective of the initial level of periodontal attachment at the onset
40
of injury. By analyzing data from the literature, several points were
stressed by the authors, including:
• There is no scientific evidence to show that trauma from occlu-
sion causes gingivitis or periodontitis or accelerates the progres-
sion of gingivitis to periodontitis.
• The periodontal ligament physiologically adapts to increased oc-
clusal loading by resorption of the alveolar crestal bone, resulting
in increased tooth mobility. This is occlusal trauma and is revers-
ible if the occlusal force is reduced.
• Occlusal trauma may be a cofactor which can increase the rate of
progression of an existing periodontal disease.
• There is a place for occlusal therapy in the management of peri-
odontitis, especially when related to the patient's comfort and
function.
• Occlusal therapy is not a substitute for conventional methods of
resolving plaque-induced inflammation.
Therefore, Davies et al. proposed that occlusion of periodontally
compromised teeth should be designed to reduce the forces to be
within the adaptive capabilities of the damaged periodontium.
Currently, the discussion on the role of trauma from occlusion in
periodontal disease relies on the belief that excessive occlusal forces
do not initiate destructive chronic periodontitis but are capable of
causing periodontal injury.41 Thereby, “the crux of the remaining ar-
gument is this: Can occlusal forces exacerbate the progression of
periodontitis, and is eliminating occlusal discrepancies appropriate
or necessary in the treatment of the disease?”
As many of the studies investigating the role of occlusion in
periodontal tissues and indicating that occlusal forces may not be
a factor in the progression of periodontal disease are performed in
animals, some questions remain unanswered because:
…naturally occurring periodontal disease is virtually
unknown in monkeys, and it usually occurs only in
much older dogs than those used in the studies of
occlusion. Furthermore, in humans, most periodontal
destruction resulting in attachment and bone loss oc-
curs relatively slowly over a much longer period than
that used in the animal studies. Both the use of an-
imal models and the relatively short duration of the
studies leave questions concerning the application of
these results to periodontal destruction occurring in
humans. (Harrel et al.42)
3 | PH YS I O LO G I C A L RO LE O F
TR AU M ATO G E N I C O CC LU S I O N I N TH E
PE R I O D O NTA L S U PP O RTI N G TI S S U E S
CO M PA RTM E NT
Physical forces exert a basic role in regulating the form and func-
tion of periodontal ligament, the fundamental importance of which
is underlined by its functional and biological features, its basic role
in development and maintenance of the periodontium, and its core
function in periodontal wound healing. The periodontal support-
ing compartment is unique among the various ligament and tendon
systems of the body because it harbors two different types of hard
tissue (bone and cementum) and periodontal ligament fibers are at-
tached to both, assuming the feature of Sharpey's fibers. As a biolog-
ical system exposed to repetitive biomechanical strains, periodontal
ligament has special metabolic requirements and an architectural
tissue design that facilitates its function. Therefore, the homeostatic
mechanism of the periodontal supporting compartment seems to
PASSANEZI and SANT'ANA
be engaged with different tissue domains, requiring coordinated ac-
43
tions among the different cell populations involved.
Accordingly, the role played by transfer of the stimulus to the
cells is paramount. It is mediated by, for instance, integrin-­matrix
linkages, which elicit activation of the appropriate cell-­signaling cas-
cades. These cascades then trigger physiological responses to that
stimulus, according to the phenotype of the activated cell. Several
other extracellular matrix components have been mentioned, such
as collagen types V and VI, chondroitin sulfate, proteoglycans, fi-
bronectin, tenascin, and undulin. Periodontal ligament cells are ca-
pable of synthesizing important, locally acting molecule regulators
of cell function, such as cytokines and growth factors, allowing bio-
logical mechanisms that tightly regulate the metabolism and spatial
locations of the cell populations involved in the formation of bone,
cementum, and periodontal ligament to be activated.42,43
The existence of an arborizing network of oxytalan fibers is also
important as it seems to control the influx of blood to the tissue.
Interestingly, periodontal ligament is a highly vascularized tissue,
which allows a hydrodynamic damping to applied forces, coupled
with high plasma transudation rates to nourish the tissue. Therefore,
it can be extrapolated that occlusion or any other function gener-
ating physical forces upon the teeth elicits a complex interplay be-
tween biological molecules of different compositions and functions
and the various cells of the different tissue domains of the periodon-
tal supporting compartment. In other words, it can be assumed that
occlusion is the main factor engaged in the homeostatic behavior of
the supporting periodontal compartment.43
The integrity of all periodontal supporting tissues (cementum, al-
veolar bone, and periodontal ligament) seems to be, at least in part,
coordinated through the expression of periostin, a key molecule
released under the action of occlusal forces in mice. Interestingly,
while periodontal defects were observed in periostin-­null mice after
tooth eruption, contrariwise removal of masticatory forces under
this condition rescued the periodontal defects. Periostin expression
seems to be controlled by activation of transforming growth factor-­
beta in response to mechanical strain, leading to the conclusion
that mechanical loading maintains sufficient expression of periostin
to ensure the integrity of the periodontium in response to occlusal
load.44
Nevertheless, all these observations strongly suggest a poten-
tial role of occlusion in the homeostatic behavior of the periodontal
supporting apparatus, so that deviations of the physiologic occlusal
function should be assumed as risk factors that might jeopardize the
maintenance of a healthy functioning periodontium.
4 | TH E RO LE O F O CC LU S I O N I N TH E
I N J U RY O F PE R I O D O NTA L S U PP O RTI N G
TI S S U E S
Several aspects must be addressed to understand the role of trauma-
togenic in Dentistry (and more specifically in Periodontology). The
term “traumatogenic occlusion” is used to define the conditions
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generating the stressful occlusal forces, while “occlusal trauma” is
aimed to identify the injury produced in the tissues by the incidence
of forces.
The development of traumatogenic occlusion requires the inter-
action of factors related to the occlusal force itself and the adapa-
tibility of subject's tissue,45 so that the pressure surpasses the
threshold of tolerance of the periodontal tissues. The periodontium
attempts to accommodate the forces exerted on a tooth in an adap-
tion mechanism that varies from person to person and also varies in
the same person at different times.46
4.1 | Primary and secondary trauma from occlusion
According to the behavior of tissues in response to the action of
traumatogenic forces, trauma from occlusion would develop in three
sequential stages4,6,16,31,33,37,47–52:
• The active tissue-destruction stage under the action of traumato-
genic occlusal forces, which is characterized by typical features of
trauma from occlusion. During this phase, clinical and histopatho-
logical signs of trauma from occlusion are present, indicating the
fragility of tissues and suggesting their inability to resist the ac-
tion of other aggressive agents.
• The tissue-adaptive stage, during which the structural tissue or-
ganization is reestablished, almost completely restoring the bio-
logical characteristics related to the homeostatic behavior of the
periodontal supporting compartment and tissue resistance ability,
although perhaps at the expense of enlargement of periodontal
ligament, depending on the change of tooth position.
• The tissue-remodeling stage, processed thereafter to achieve
the homeostatic requirements of periodontal supporting tissues
through establishing the final structural and architectural char-
acteristics of cementum, periodontal ligament, and alveolar bone,
with functional reorientation of periodontal ligament fibers and
bone trabeculae, according to the new functional requirements of
the area. This remodeling stage seems to occur when the adaptive
stage cannot be achieved, 5 or when the involved teeth achieve a
new position to avoid the offending occlusal contact.
Trauma from occlusion can be initiated when the intensity of forces
surpasses the adaptive threshold of periodontal supporting tissues
(primary trauma from occlusion) or when the tissue-­adaptive threshold
is weakened to the point that the remaining supporting tissues are un-
able to withstand the physiological occlusal forces (secondary trauma
from occlusion).53 However, pathological changes that characterize
trauma from occlusion are exactly the same in both situations.
In most cases, loss of adaptability in periodontal supporting tis-
sues occurs in the presence of intra-­alveolar bone height loss, with
a significant reduction in the number of principal periodontal liga-
ment fibers per unit of volume of the root, which is critical if we
consider that the reduction occurs in the cervical-­to-­apical direction.
However, loss of periodontal attachment may also occur from the
apical-­to-­coronal direction, as in the case of an apicoectomy, apical
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132       PASSANEZI and SANT'ANA
root resorption, or root fracture. This traumatogenic picture, occur-
ring after application of forces of physiological magnitude to teeth,
which subsequently display significant loss of periodontal support, is
defined as a secondary trauma from occlusion.
4.2 | Tissue-­destructive changes induced by trauma
from occlusion
Several publications have described the periodontal tissue changes
produced by traumatogenic occlusal forces. 3,9,14,16,26,27,33,51,52,54–57
The magnitude, direction, duration, and frequency of force appli-
cation are all factors that may turn a force into traumatogenic. As
a rule, when the magnitude of occlusal forces is increased, peri-
odontal tissues respond with widening of the periodontal ligament
space, an increase in the number and width of periodontal ligament
fibers, and an increase in the density of alveolar bone. When the
direction of occlusal forces is changed, stresses and strains of the
periodontium are reoriented. Principal fibers of periodontal liga-
ment are arranged to accommodate occlusal forces along the long
axis of the tooth. The incidence of nonaxial forces (lateral or hori-
zontal, and torque or rotational) tends to cause injury to periodon-
tal tissues.46 These alterations are more critical in pressure areas
than in tension areas, although no differences in the depth of peri-
odontal pockets were observed between these areas in humans. 3
The response of alveolar bone is also affected by the duration and
frequency of occlusal forces. Constant pressure on the bone is
more deleterious than intermittent forces. The more frequent the
application of an intermittent force, the more injurious is the force
to the periodontium.46
Trauma from occlusion produced by jiggling forces is character-
ized by widening of the socket at the cervical area, resulting in the
development of a funnel-­shaped bone defect with no distinction be-
tween pressure and tension sites, which means that both can occur
at the same place alternatively by a “back-­and-­forth” mechanism, in
such a way that pressure and tension are processed alternatively at
all directions of tooth movement.58
When the tooth is subjected to a lateral force, a rotational move-
ment is established around the geometric center of the alveoli (ful-
crum), resulting in the establishment of two diametrically opposed
pressure areas at cervical and apical thirds and two corresponding
tension areas at opposing regions,46 as the tooth is suspended in
the alveolar socket, developing an intra-­alveolar power arm and an
extra-­alveolar resistance arm. When a lateral force is applied to the
tooth, a critical pressure is exerted at the cervical region, creating
different effects depending on force intensity, as demonstrated by
59,60 32,61
photoelasticity and finite element studies and illustrated in
Figure 1. The findings of these and other studies in which the effects
of force application are investigated, by Latin American researchers,
in periodontal tissues and roots in vitro, are summarized in Table 1.
Frontal resorption of cortical alveolar bone begins from the
area of periodontal ligament compression and proceeds toward
the spongy bone tissue, leading to an almost immediate widening
of the periodontal ligament space after force application. The result
F I G U R E   1   Photoelastic model, evidencing that stress is
concentrated at the level of the buccal bone crest (red arrow)
when a lateral force is applied by the incisal edge of the mandibular
incisor. Internal stress shows greater concentration at the
subcervical region than at the apex [Colour figure can be viewed at
wileyonlinelibrary.com]
is a clinical increase in tooth mobility, observed 24-­38 hours later.
Simultaneously, circulatory changes in lymphatic and blood vessels
modify the cellular metabolism as a result of impaired oxygenation
and consequent hypoxia of compressed periodontal ligament,62 re-
sulting in ischemic changes that cause partial derangement of peri-
odontal ligament, but without cell necrosis. In instances of slightly
excessive occlusal forces, hypoxia could be radically reversed by the
invasion of injured sites by proliferating blood vessels,63 explaining
why no significant changes in the organization of cementoblasts,
which do not possess surface receptors for inflammatory mediators,
are seen.64 This phenomenon would account for failure of cemen-
tum resorption when traumatogenic forces do not exceed the tissue
adaptive threshold at a rate sufficent to produce hyalinization of
periodontal ligament.
On the other hand, heavier occlusal forces cause a more intense
ischemia, leading to cellular necrosis, thrombosis, hemorrhage, and
hyalinization of the periodontal ligament at pressure sites.46 Under
these conditions, periodontal ligament interstitial fluid is moved
into the marrow spaces via alveolar foramina, where an increase in
hydrostatic pressure develops. As a result, osteoclastic stimulation
is produced away from the periodontal ligament, and bone resorp-
tion occurs inside marrow spaces 46,58 toward the periodontal liga-
ment area. No significant mobility is produced until bone resorption
reaches periodontal ligament. When this happens, a sudden and
abrupt increase in tooth mobility occurs. Early activation of os-
teoclasts is observed in the damaged tissues, which corresponds
with the osteoclastic bone resorption observed at the tension side
48 hours after intensive pressure.65
PASSANEZI and SANT'ANA
TA B L E   1   Summary of Latin American in vitro studies investigating the role of occlusion in periodontal disease
Reference Objectives
59
Alves et al To investigate force distribution in bridges with mesial
and distal cantilevers placed on normal-­length and
short-­length roots under 2 types of force: uniformly
distributed; or centered at the pontics
Campos Jr To analyze two types of occlusion: cusp to fossa
et al123 versus cusp to marginal crest
Chiapinotto To investigate periodontal distribution of internal
et al124 tensions at hemisected lower first molars, simulating
a furcation lesion with normal and reduced support
at marginal area
Poiate et al61 To evaluate stress distribution by finite element
analysis in a PDL in three-­dimensional models of
upper central incisors at three different load
conditions: 100 N at 45° (model 1: masticatory load);
500 N at the incisal edge at 45° (model 2: parafunc-
tional habit); and 800 N at the buccal surface at 90°
(model 3: trauma)
PDL, periodontal ligament.
The furcation area of rat molars experimentally submitted to oc-
clusal trauma, associated or not with inflammatory reactions induced
by injection of lipopolysaccharide, showed hyaline degeneration of
periodontal tissue and an irregular bone surface, with osteoclasts
appearing 5 days after force application. These tissue changes were
spontaneously reversed at 10 days, when slight hyaline degenera-
tion of periodontal tissue and no irregular bone surface were seen.67
When hyalinization of the periodontal ligament occurs, cemen-
toblasts also disappear from the scenario, leaving the cementum
surface exposed and amenable to resorption by cementoclasts.
To investigate hyalinization of periodontal ligament with time and
in association with root resorption during orthodontic movement,
premolars indicated for extraction for orthodontic reasons, from
56 adolescents, were submitted to buccally oriented orthodontic
movement of approximately 50 g for a time period of 1-­7 weeks.
Histologic analysis showed increased compression and necrosis of
periodontal ligament and formation of hyalinized areas in 33 (59%)
experimental teeth and 2 (4%) controls. Hyalinization occurred as
early as 1 week after force application and was located mainly at
buccal cervical and lingual apical areas, corresponding to pressure
sites. Root resorption was observed in 93% of experimental teeth
and in 54% of controls. The hyalinized areas (43%) in the experimen-
tal group were close to resorption cavities coronal or apical to re-
68
sorption lacunae.
These findings were also described in a previous study69 per-
formed in animals. An orthodontic appliance was placed on the
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Study design Results
Photoelasticity Mesial cantilevered bridges neutralized occlusal
forces more effectively than did distal cantilevers,
independently of the type of force applied; long
roots supported greater forces than did short roots;
cantilevered bridges generated lateral forces in the
periodontium, regardless of the size and root
anatomy of the abutments
Photoelasticity Both types of occlusion are similar mechanically and
related to axial distribution of tensions through the
periodontium
Photoelasticity In models with normal periodontium, force was
transmitted to the apical region and more concen-
trated at the mesial root. In models with reduced
periodontium, force was distributed mainly to apical
regions and more concentrated at the mesial root,
but lesser force was necessary to produce it. After
splinting of the separated roots at the coronal level,
force distribution was similar to that observed with
normal periodontium.
Finite element The most harmful values of tensile and compressive
stresses were observed in models 2 and 3, with
similarly distinct patterns of stress distributions
along the PDL. Tensile stresses were observed along
internal and external aspects of the PDL, mostly at
cervical and middle thirds.
mandibular second premolar and first molar of Beagle dogs to exert
a continuous and constant reciprocal force of 25 cN for 1, 4, 20, 40,
and 80 days. During the experiment, tooth movement was recorded
weekly. After 24 hours, osteoclastic and osteoblastic activity had
increased at pressure and tension sides, respectively, with some
samples showing hyalinization. When teeth moved quickly, areas of
direct bone resorption at the pressure side and deposition of trabec-
ular bone at the tension side were found. In the periodontal ligament
of teeth showing little movement, small patches of hyalinization
were found at the pressure side, mostly located buccally or lingually
to the mesiodistal plane, which could explain individual differences
in the rate of tooth movement.
Crespo Vázquez et al. 65 investigated root resorption in ex-
tracted teeth showing one-­third to two-­thirds of alveolar bone
loss (Group 2) and more than two-­thirds of alveolar bone loss
(Group 3), with and without antagonists. Teeth showing a greater
amount of alveolar bone loss with antagonists exhibited the great-
est percentage of root resorption, suggesting that the incidence of
forces in a reduced periodontium favors the development of root
resorption.
A recent publication70 indicated that diffuse distribution of
forces applied to periodontal tissues during tooth movement tends
not to promote either extensive areas of hyalinization or significant
death of cementoblasts. However, when concentrated in a limited
area, forces, even if of low intensity, are associated with extensive
areas of hyalinization and focal death of cementoblasts, which are
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134       PASSANEZI and SANT'ANA
commonly associated with root resorption, as observed in the apex
of roots submitted to tipping movements.
As occlusal trauma produces concentration of forces at com-
pression sides, root resorption was investigated in premolars of 12
adolescents submitted to 4 weeks of occlusal trauma by light curing
glass-­ionomer cement to occlusal surfaces before tooth extraction.
Samples were examined by microcomputed tomography and the
results were analyzed using software for volumetric measurements
of resorption craters; significant differences were observed in the
amount of root resorption in traumatized versus nontraumatized
teeth.71
In addition, injury to the periodontium produces a temporary
depression in mitotic activity and in the rate of proliferation and dif-
ferentiation of fibroblasts, both in collagen formation and in bone
formation, which returns to normal levels after force dissipation.45,72
4.3 | Molecular mechanisms of bone resorption
induced by force application
Traumatogenic occlusal forces that slightly surpass the threshold of
tissue adaption produce very rapid circulatory changes in the peri-
53,73
odontal ligament (probably within minutes), resulting in platelet
aggregation and release of prostaglandins, thereby activating osteo-
clasts of the periodontal ligament.74
Mechanical forces can also induce the production of interleu-
kin-­1, a proinflammatory cytokine, and the isoenzyme cyclooxygen-
ase-­2, both involved in prostaglandin synthesis.43 During orthodontic
tooth movement in 10 patients, a significant increase in the levels of
interleukin-­1 and prostaglandin E2 in gingival crevicular fluid were
75
observed at test teeth, which returned to baseline within 7 days. A sion is yet to be determined.
previous study74 suggest that mechanical stress induced in periodon-
tal ligament of cats results in an increase in the levels of interleukin-­1
and prostaglandin E2. Additionally, when mechanically stimulated
periodontal ligament cells were cultivated in preconditioned medium
containing interleukin-­1, greater bone resorption was observed.
Mechanical stimuli on teeth generate free proteins within peri-
odontal ligament, induced either by compression and mechanical
stress of cells or by cellular destruction and collagen fiber disor-
ganization following collapse of blood vessels.17 These proteins
cause degranulation of mast cells present in periodontal ligament,
releasing histamine and free nerve endings neuropeptides. These
processes result in contraction, vasodilatation, and increased vas-
cular permeability of endothelial cells, leading to leukocyte leak-
age from blood vessels through interendothelial cell junctions.
It takes approximately 90 minutes after force application to the
periodontal ligament until an inflammatory infiltrate develops,
eliciting an acid pH that favors the attraction and accumulation of
osteoclasts. Several enzymes in this inflammatory exudate render
the mineralized bone surface unprotected, allowing osteoclasts to
become established. Osteoclastic bone resorption may then pro-
ceed at a rate of 100 μm/d.77
Interestingly, bone resorption occurred 12 hours after the ap-
plication of orthodontic force, reaching a maximum peak 48 hours
after the initiation of orthodontic movement, but these observations
require further confirmation. As the number of osteoclasts started
to increase only 20 hours from initiation of orthodontic movement,
reaching a peak after 60 hours, bone resorption could not be asso-
ciated with the higher number of osteoclasts, suggesting that there
may be quiescent osteoclasts at the site or that an osteocyte-­related
osteolysis could initiate bone resorption.78,79
Furthermore, expression of RANKL on endothelial cells, inflam-
matory cells, and periodontal ligament cells is clearly related to in-
flammatory bone resorption. The distribution of RANKL-­expressing
cells in rat periodontium after injection of lipopolysaccharide to
induce inflammation associated with occlusal trauma showed that
expression of RANKL on endothelial, inflammatory, and periodon-
tal ligament cells was higher than that observed in nontraumatized
teeth, suggesting that the increase in osteoclasts caused by occlusal
trauma is related to expression of RANKL.80
In a hyperocclusion mouse model, it was demonstrated that
traumatogenic occlusion resulted in increased expression of both
RANKL and osteopontin, probably related to the increase in number
of activated osteoclasts. It was also suggested that the maintenance
of a physiological occlusal state is achieved primarily by inhibition
of bone apposition in response to the occlusal forces, rather than
the equilibrium between continuous deposition of apical tissue and
the corresponding resorption of bone tissue. Inhibition of alveolar
bone apposition by occlusal forces was considered to be an import-
ant mechanism for controlling occlusal height, which might work in
synergy with RANKL-­induced bone resorption to maintain normal
occlusion.81 According to Passos et al,82 the precise role of osteo-
pontin and RANKL in bone resorption related to trauma from occlu-
The interrelationship between chemokine expression and os-
teoclastogenesis was further evaluated in hyperocclusion models
in vitro and in vivo.83 The in vitro model showed that intermittent
stretching-­induced mechanical stress upregulated the expression of
C-­C motif chemokine ligand 2, C-­C motif chemokine ligand 3, and
C-­C motif chemokine ligand 5 in periodontal ligament cells. The
in vivo rodent model revealed that expression levels of C-­C motif
chemokine ligand 2 in periodontal ligament tissues, its receptor C-­C
motif chemokine receptor 2 in preosteoclasts, and tartrate-­resistant
acid-­phosphatase-­positive cells in alveolar bone were significantly
up-­regulated 4-­7 days after excessive mechanical stress during hy-
perocclusion. Hyperocclusion predominantly induced C-­
C motif
chemokine ligand 2 expression in periodontal ligament tissues and
promoted chemotaxis and osteoclastogenesis, probably establishing
the link by which the mechanical stress-­dependent alveolar bone de-
struction occurs during occlusal traumatism.
Bone and cementum portray structurally and histologically similar
characteristics. Histomorphometric analysis of root resorption lacu-
nae during orthodontic movement in rats, in which the findings were
assessed and confirmed by RT-­PCR, showed a significant increase
in expression of the osteopontin gene in the test group compared
with the control group.82 Densitometric analysis revealed increased
background levels of osteopontin in the resorptive lacunae of roots
PASSANEZI and SANT'ANA
in the test group, suggesting that increased expression of osteopon-
tin is associated with root resorption induced by orthodontic tooth
movement. As trauma from occlusion can elicit the same response as
orthodontic tooth movement, it can be assumed that the resorptive
processes of roots in teeth under traumatogenic occlusion could be
84
mediated through the same mechanism.
4.4 | Adaption of periodontal supporting tissues to
traumatogenic occlusion
Whether traumatogenic forces are of low or high intensity, moderate
to severe widening of periodontal ligament space is produced as a
result of degenerative processes. This is accompanied by a radio-
graphic smoky aspect or disappearance of lamina dura. The extent
of periodontal ligament space widening is dependent on how much
dental displacement occlusal prematurity is able to produce, as the
destructive process ceases as soon as tooth displacement releases
excessive pressure in periodontal tissues. This adaptive behavior
probably results from activation of osteoclasts following the binding
of inflammatory mediators to specific receptors on the osteoblast
surface, thereby mediating bone resorption.64 A funnel-­shaped bone
defect bordering the cervical area of the periodontal ligament then
6,9,16,51
develops, but without formation of a periodontal pocket.
Before tooth displacement, widening of periodontal ligament
space increases the range of tooth movement in the socket up to the
point where the tension of periodontal ligament fibers could result
in fiber breakdown and cleavage of cementum fragments. Severe
tension could result in tearing of the periodontal ligament and re-
sorption of alveolar bone.46,66 This is mostly produced by interfer-
ence contacts rather than by premature occlusal deflective contact,
as tooth displacement is greater as is the extent of functional tooth
contact during mandibular excursion. Moreover, as the cusp-­
to-­
fossa is the stabilizing tooth contact, the teeth involved with occlusal
interference cannot escape from the offending contact. Accordingly,
periodontal damage may persist and worsen.46
Stable contacts are established in the maximal intercuspal habit-
85
ual position, which is mostly characterized by a cusp-­to-­fossa inter-
relationship. When the mandible is guided in the hinge axis position,
the cusp-­to-­fossa relationship is lost, giving rise to an occlusal con-
tact that embraces a cusp-­to-­slope or a slope-­to-­slope relationship,
which occurs before the vertical dimension of occlusion is achieved.
This position is unstable, resulting in premature deflective occlusal
contact in the centric segment of the mandibular arch of closure.
The difference between the first occlusal contact in the hinge axis
movement of mandibular closure and the maximal intercuspal habit-
86
ual position characterizes the mandibular “slide in centric.”
The extent of lateral tooth displacement under trauma induced
by premature deflective occlusal contacts seems to be limited.
Excessive pressure on periodontal supporting tissues ceases soon
after the corresponding widening of periodontal ligament space. The
tooth become mobile, and a new cusp-­to-­fossa relationship is estab-
lished at the maximal intercuspal habitual position, allowing recon-
struction of the periodontal supporting apparatus and termination
|
      135
of generation of excessive compression of the periodontal ligament
against alveolar bone.46
When traumatogenic forces are generated in the skeletal arc
of mandibular closure or in the habitual arch (eg, by placing a res-
toration in premature occlusal contact), changes in the occlusal
program are produced, leading to the development of different be-
havioral effects on the masticatory system to compensate for occlu-
sal imbalance. First of all, the proprioceptive neuromuscular system
coordinated by the periodontal ligament stimulates the jaw to seek
another stable occlusal position, escaping from the older maximal in-
tercuspal habitual position and developing a new one. This results in
removal of traumatogenic occlusion.85 In the new stable maximal in-
tercuspal habitual position, occlusal contacts may be of the cusp-­to-­
slope type, producing instability of tooth position. In such cases, the
decomposition of occlusal forces leads to the formation of horizontal
components, additionally to the axial component, which mobilize the
tooth laterally within its socket by widening the periodontal ligament
space. Thus, the firm strength of the occlusal contact—which is de-
pendent on the physiological mobility of the tooth—is lost, affecting
the stability of the tooth position also in the vertical plane, thus al-
lowing expression of the active eruption force probably generated
by the continuous renewal of periodontal ligament fibers.86
Antagonist teeth are then subjected to horizontal and vertical
displacement forces, directing the teeth in accordance with the res-
toration of a stable dental relationship cusp-­to-­fossa. When this re-
lationship is achieved, the adaptive remodeling of the periodontal
supporting apparatus consolidates a new stable tooth position. This
is the reason why the jaw may develop different maximal intercus-
pal habitual positions along the years and still maintain the dental
relationship cusp-­to-­fossa, in spite of the existence of other factors
influencing tooth position.46 These periodontal behaviors show that
occlusal stability involves not only the positional stability of the jaw
but also that of the teeth themselves, fulfilling the requirements of
orthopedic stability, dictated by seating both mandibular condyles
in centric relation in their respective glenoid fossae while opposing
teeth maintain the maximal intercuspal position.87
As can be seen, the periodontal adaption to traumatogenic oc-
clusion can involve the widening of the periodontal ligament space
and/or change in tooth position to another stable cusp-­to-­fossa, or
even cusp-­to-­slope, occlusal relationship. During the stages of peri-
odontal adaptive responses, periodontal supporting apparatuses ex-
perience appositional formation of cementum, periodontal ligament,
and alveolar bone,46 thereby reestablishing the biological and meta-
bolic requirements that govern the maintenance of teeth. However,
new scientific observations are needed to assess this behavior,
specifically in cases of generation of occlusal interferences during
mandibular excursions, when teeth are almost unable to escape from
prematurity.
4.5 | Remodeling phase of trauma from occlusion
As described before,45,64,86 as an adaption mechanism to avoid injury
by traumatogenic forces, widening of the periodontal ligament space
 |
136       PASSANEZI and SANT'ANA
allows bone to withstand physiological pressure. The physiological
3
width of periodontal ligament should be regarded as vital space or
minimal essential width. Periodontal ligament exhibits adaptability
to rapidly changing applied force levels and capacity to maintain its
width at constant dimensions throughout its lifetime; this is an im-
portant measure of periodontal ligament homeostasis and gives in-
sight into the function of biological mechanisms that tightly regulate
the metabolism and spatial locations of the cell populations involved
in the formation of bone, cementum, and periodontal ligament.43
The remodeling phase occurs when the tooth cannot escape from
the traumatogenic occlusion, so the periodontal supporting struc-
tures need to remodel in order to overcome the offending forces;
they do so by increasing the minimal essential width through widen-
ing of the periodontal ligament space.
The remodeling capacity of periodontal tissues under the action
of traumatogenic forces, and their clinical implications, are sup-
ported by results obtained in experimental studies performed in
48 50
dogs and monkeys, which showed that facial tipping movements
produce dehiscence defects not necessarily accompanied by at-
tachment loss, in the absence of plaque. Moving these teeth back to
their original positions results in the re-­formation of bone at buccal
48
surfaces. Jiggling forces are able to produce dehiscence defects,
leaving within them a soft tissue layer that, if removed, prevents the
re-­formation of alveolar bone, which suggests that bone resorption
by jiggling forces leaves a supracrestal component capable of form-
50
ing new bone.
Periodontal changes induced by traumatogenic occlusion are re-
stricted to areas in which tooth displacement produces compression
of periodontal ligament against the bone wall, without the develop-
ment of a periodontal pocket in the absence of plaque-­related in-
flammation.4,11,14,16,23,33 The probable reason is that the periodontal
protective compartment (comprising biologic width plus keratinized
gingiva) is not subjected to compressive forces, as the soft tissue
is moved away in the direction of tooth movement. Circulatory
changes in periodontal ligament caused by traumatogenic occlusion
did not produce significant deleterious changes in gingival tissues,
probably because its main source of vascularization is supraperios-
89
teal blood vessels.
5 |  RO LE O F TR AU M A FRO M O CC LU S I O N
I N PE R I O D O NTA L D I S E A S E S
Although there is general agreement that trauma from occlusion
does not initiate chronic periodontitis, the role of trauma from oc-
clusion in periodontal disease is still controversial. According to
the American Academy of Periodontology,90 the lesion of trauma
from occlusion may occur in conjunction with, or independent of,
inflammatory periodontal diseases. The elimination of alveolar bone
inorganic matrix at the cervical area by traumatogenic occlusion ren-
ders the tissue more fragile, facilitating the apical spread of dental
biofilm-­related inflammatory exudate and resulting in direct invasion
of the injured periodontal ligament.5,6,47,55
Similarly to trauma from occlusion, periodontal disease pro-
gresses in episodes of acute destruction followed by periods of
adaptation or stabilization90,91 in which no active destruction of
periodontal tissues exists. When the apical spread of dental biofilm-­
related inflammatory exudate occurs along with trauma from
occlusion-­related inflammatory degenerative changes produced in
the periodontal ligament and zone of bone co-­destruction,6,22,34,35
an association of periodontitis plus trauma from occlusion could be
established (Figure 1). This peculiar condition—“the combined lesion
periodontitis plus trauma from occlusion”— is responsible for the
controversies in the literature.
When (i) occlusal trauma is in the stage of adaption or remodel-
ing and periodontitis is in the phase of activity or (ii) occlusal trauma
is in the active destructive stage and periodontitis is in the remission
phase, the combined lesion trauma from occlusion and periodonti-
tis will not develop. Therefore, traumatogenic occlusion and den-
tal biofilm may be occurring simultaneously, but not producing the
combined lesion, supporting the concept that suprabony pockets
and horizontal bone loss around teeth in instances of trauma might
coexist.6 On the other hand, the interaction of tooth-­tilting forces
and gingival inflammation requires a long period of time to induce
an infrabony lesion.92 Thus, the development of combined injuries is
critical, as the destructive process occurs quickly over a short period
of time, while adaptive phases occur over a fairly long period of time,
which might explain why some studies fail to reproduce the com-
bined lesion.9,10,23,27,28
Progressive stages of trauma from occlusion and periodontitis
are variable. The existence of both lesions at destructive stages is
required to establish the combined (periodontitis plus trauma from
occlusion) lesion. However, an effective association between both
lesions is characterized by overlap of the adaption/remodeling
phases of trauma from occlusion and the remission/acute phases
of chronic periodontitis. In these instances, the sequel produced by
the combined lesion remains, but no other typical changes of the
association between trauma from occlusion and chronic periodon-
titis occur, unless another acute destructive episode of both lesions
develops simultaneously. Jiggling forces can accelerate the rate of
attachment loss, which requires an extremely intense force that
does not allow the tooth to adapt or migrate from offending forces.
Accordingly, few clinical cases would end up with a traumatogenic
condition. Therefore, it could be suggested that adaption to exces-
sive forces takes place in most cases, without affecting the spread of
inflammation deep into periodontal tissues.14
5.1 | Evidence for the role of occlusion in
periodontal parameters
Controversy on the role of occlusion in periodontal diseases may be
attributed to the lack of properly designed methodology to evalu-
ate the border between both conditions, responsible for producing
the combined lesion.92 Even in accordance with the requirements
of evidence-­based science, clearly none of the research intended to
elucidate the role of trauma from occlusion in periodontal diseases
PASSANEZI and SANT'ANA
has properly investigated the initiation and/or progression of dental
biofilm-­related periodontal inflammation simultaneously with the
destructive phase of traumatogenic occlusion. Rather, the meth-
odologies were mainly based on the independent initiation or pro-
gression of chronic periodontitis and the initiation of traumatogenic
occlusion. Therefore, there was no combination of the destructive
phases of trauma from occlusion and chronic periodontitis. Until
that, theories on the association between trauma from occlusion and
periodontitis will rely on evidence arising from case reports or ret-
rospective and short-­term prospective studies in humans. Previous
studies investigating the role of occlusion in periodontal disease
are mainly based on photoelastic or finite element studies, animal
models, or cadavers, which cannot be considered as ideal models to
investigate the causal relationship between traumatogenic occlusion
and periodontal breakdown. Attachment and bone loss in humans
occur slowly, over a much longer period of time than that used in
animal studies, posing a question on the applicability of results from
animal studies on the incidence of traumatogenic forces to perio-
dontal destruction in humans.42
In the following sections, the influence of traumatogenic occlu-
sion on periodontal parameters investigated in animal and human
studies is described and discussed. Latin American research per-
formed to investigate the relationship between traumatogenic
occlusion and periodontal disease is emphasized, with a summary
of the main investigations in animals and humans in Tables 2 and
3. Table 4 summarizes narrative and systematic reviews published
by Latin American authors on the role of occlusion in periodontal
disease.
5.1.1 | Formation or deepening of
periodontal pockets
Most studies agree that traumatogenic forces are not able to pro-
duce a periodontal pocket in the absence of plaque-­related peri-
odontal inflammation but facilitate the spread of inflammatory
exudate toward periodontal supporting structures.6,22,26,33,35,47 The
deepening of existing periodontal pockets is accelerated and angular
bone loss develops in the presence of trauma from occlusion in teeth
with chronic periodontitis.6,31,34,47,94
In teeth subjected to traumatogenic forces, the migration of in-
flammatory exudate toward the bone crest seems to be facilitated
by the resorption of inorganic matrix from alveolar bone at cervi-
cal areas, resulting in the formation of deeper infrabony or supra-
bony pockets, compared with nontraumatized teeth; this suggests
that dental biofilm-­related inflammatory exudate progresses more
8,29,37
rapidly in teeth subjected to traumatogenic forces. A faster
deepening of periodontal pockets under the influence of trauma
from occlusion could also be ascribed to traumatogenic occlusion-­
95 96
induced resorption bays or cracks in the cervical cementum. This
would create a suitable environment for the apical migration of junc-
tional epithelium, and biofilm-­related inflammatory exsudate; new
layers of plaque and calculus are deposited, soon after exposure of
|
      137
junctional epithelium to the outer environment. Therefore, the de-
velopment of deeper periodontal pockets would be favored.94
Studies in animals
The effect of trauma superimposed upon existing intrabony pock-
ets was investigated in monkeys by the surgical creation of localized
infrabony pockets at mesial and distal surfaces of the mandibular
bicuspids. Samples from 2 squirrel monkeys were obtained after
10 weeks. In 4 other monkeys, 10 weeks after inducing periodon-
tal disease, a mesiodistal jiggling movement was established, which
was continued for another 10 weeks. Four additional monkeys were
not subjected to traumatogenic forces and were used as controls.
Biopsies were obtained from these groups at 20 weeks. Gingival
inflammation and increased mobility of the mandibular bicuspids
were observed in all groups after induction of periodontitis. After
the introduction of jiggling forces, greater mobility of the mandibu-
lar bicuspids was observed in the test group, including in vertical
directions. These teeth showed significantly increased bone loss
(P < 0.01), measured as the distance from the alveolar bone crest
to the cementoenamel junction, and a significantly (P < 0.01) lower
percentage of osseous tissue at interproximal sites. Additionally,
marked differences in osseous morphology were found between
test and control groups, but without affecting connective tissue at-
tachment.10 Histologic examination of the specimens showed an ini-
tial phase of intense resorptive activity associated with the coronal
alveolar bone, and the morphology of this bone eventually consisted
of osseous islands surrounded by a loosely arranged, highly vascular
and cellular connective tissue. These findings suggest that trauma
from occlusion is not able to induce the formation of periodontal
pockets, although does produce alterations in marginal bone mor-
phology and crestal bone loss at interproximal sites.9
Orthodontic tooth movement promoted a shift in supragingival
plaque to a subgingival position. The mesial-­to-­apical movement
of teeth with plaque accumulation resulted in the formation of in-
frabony pockets. In 4 out of 5 beagle dogs, displacement of the
plaque-­infected tooth resulted in an apical shift of the connective
tissue attachment. When similar orthodontic forces were applied to
plaque-­free teeth, tilting movement did not result in the formation
of infrabony pockets, and loss of connective tissue attachment was
observed in only 2 of the dogs.4
These results were later confirmed in a similar study in beagle
dogs, in which plaque-­associated marginal periodontitis was devel-
oped, followed by the application of jiggling forces 60 days after
plaque accumulation. The dogs were killed at 360 days; histologic
analysis showed that the application of jiggling forces enhanced the
rate of destruction of the periodontium. 29
In Long-­Evans rats with arteriosclerosis induced by a hypercho-
lesterolic diet that were submitted to occlusal disorders for 6 weeks,
hyperfunction was established by a high restoration in the first
mandibular molars and hypofunction was achieved by removing the
antagonist. A marked increase in the number of inflammatory cells,
as well as deepening of the gingival pocket was observed in one-­
third of arteriosclerosis-­induced rats during the 6-­week treatment
 |
138       PASSANEZI and SANT'ANA
TA B L E   2   Summary of Latin American studies investigating the role of occlusion in periodontal disease in animal models
Reference Objectives
101
de Oliveira Diniz et al To evaluate the influence of DM
on bone response in the
furcation areas of teeth
subjected to OT in the presence
or absence of EP in a rat model
Dotto et al54 To study the effect of trauma
from occlusion on an increase or
positional change of periodontal
blood vessels in rats
Dotto et al16 To evaluate the effects of
experimental trauma from
occlusion in the periodontal
tissues of rats
Study design
32 Wistar rats were assigned to 4
groups:
G1: DM + OT + EP (n = 8)
G2: DM + OT (n = 8)
G3: OT + EP (n = 8)
G4: OT (n = 8).
Rats were euthanized 35 d after
induction of DM
36 male Wistar rats were divided
into 6 groups according to the
duration of the OT: 3 d (n = 5);
7 d (n = 5); 21 d (n = 8); 60 d
(n = 5); 120 d (n = 8); and not
submitted to trauma from
occlusion (n = 5). The histochem-
ical technique of Wachstein and
Meisel for measuring ATP
activity was used to demon-
strate the blood vessels after
15 min of incubation.
22 adult Wistar rats were
submitted to traumatogenic
occlusion for periods of 60 d
(n = 9) and 120 d (n = 13).
Histological sections were
obtained and stained with HE.
Results
Teeth subjected to OT showed
increased alveolar bone loss at
furcation region, while
contralateral teeth showed
preservation of normal width of
PL space and no evidence of
bone loss, for all groups
(P < 0.0001). Rats in G1 and G3
(periodontal inflammation)
showed greater bone loss than
rats in G2 and G4 (periodontal
health), with no differences
between diabetic and nondia-
betic rats subjected to OT. These
findings highlight the role of
trauma from occlusion in the
development and aggravation of
alveolar bone loss.
The results showed a statistically
significant increase of the
vasculature only after 21 d of
OT, which persisted up to the
final period. Blood vessels were
normally closer to the bone
surface in the control specimens
and soon after the 3-­d period
gradually showed a displacement
toward the cemental surface.
In the cervical area of the alveolar
buccal bone there was a
widening of PL and the
formation of a plateau or ledge
of bone. Bone resorption and
long connective tissue attach-
ment was evidenced toward PL.
The outer aspect was undergo-
ing bone formation. Deposition
of cementum could also be
found. The main changes in
alveolar crest were found at the
tension side. The remodeling
phase of trauma initiated 60 d
after induction of trauma. After
120 d, there was adaption of PL
to functional demands, with
persistence of a widened PL
space at the tension side, with a
formation of a plateau of crestal
bone and cementum at the
buccal area.
(Continues)
PASSANEZI and SANT'ANA
TA B L E   2   (Continued)
Reference Objectives
72
Itoiz et al To develop a method for the
production of OT in rats
Nascimento and Sallum126 To investigate changes in
periodontal supporting tissues of
lower canine and premolar of
marmosets under traumatogenic
forces
Nogueira Filho et al127 To investigate the effects of
nicotine on alveolar bone
changes induced by OT
Study design
Induction of OT in the upper third
molars of 45 male Wistar rats
according to 3 methods:Method
I: amalgam restorations (n = 19),
with periods of sacrifice ranging
from 1 d to 4 wk; Method II:
head pins (n = 6), with sacrifice
after 1-­7 dMethod III: stainless
steel arch wire (n = 20), with
sacrifice after 1 d to 4 wk
An extracoronal arch wire was
fixed into occlusal perforations
of upper third premolars and
first molars on both sides of the
maxilla in 8 marmosets. The
marmosets were sacrificed after
7, 14, 21, and 28 d, and
specimens were processed for
histological examination.
30 male rats were randomly
assigned to the following 3
groups:
Group A: injection of nicotine
solution and occlusal overload
Group B: injection of saline
solution and occlusal overload
Group C: injection of saline
solution
|
      139
Results
Bone resorption was detected
earlier in rats treated using
methods II and III. Intense
inflammatory infiltrate invaded
the PL. Migration of the
epithelial attachment and
gingival inflammation associated
with debris present in the pocket
was seen in some species, as well
as rear resorption. Although PL
changes and bone resorption
were still predominant after
4 wk, few osteoclasts were seen.
Cementum resorption could also
be detected. Traumatizing forces
acted directly on the PL and the
compression or stretching of the
fiber bundles produced bone
changes. No pocket formation
was found to be associated with
OT.
Areas of tension showed
stretched periodontal fibers in
the distal region of the canine
and areas of pressure showed
osseous and radicular resorption
in the mesial region of the first
premolar. At the end of the
experiment, newly formed bone
was observed on the interdental
crest, with transseptal fibers
presenting features of normal
orientation and density. No
inflammatory cells were found at
PL. There was no apical
migration of epithelial attach-
ment or pocket formation. These
findings suggest adaption of
periodontal tissues, new bone
formation in tension areas, and
bone, cementum, and dentin
resorption at compression areas.
Nicotine enhanced bone loss
induced by OT in teeth with EP
(Continues)
 |
140       PASSANEZI and SANT'ANA

TA B L E   2   (Continued)

Reference Objectives Study design Results

79
Otero et al To analyze the initiation and
development of bone resorption
and increase in the number of
osteoclasts induced by
orthodontic movement
300 rats were used. A specially
designed orthodontic appliance
was placed between the 2 upper
first molars, without interfering
with occlusion
Signs of gingival inflammation
were found without migration of
epithelial attachment or pocket
formation. Within the first 12 h,
it was possible to distinguish
areas of pressure (resorption)
and tension (stretched) sides.
Areas of resorption started to
increase after 12 h and reached
a maximum after 48 h. The
number of osteoclasts started to
increase 20 h after initiation of
orthodontic forces attaining a
maximum at 60 h. These findings
suggest that the initiation of
bone resorption is not associated
with an increase in the number
of osteoclasts.

DM, diabetes mellitus; EP, experimental periodontitis; HE, hematoxylin and eosin; OT, occlusal trauma; PL, periodontal ligament.

with occlusal disorders (P < 0.05), along with degenerative changes
in connective tissue, and diminished apposition and increased os-
teoclastic resorption of alveolar bone, suggesting superimposition
of inflammation as a result of the lipidic-­rich diet and trauma from
occlusion.97
Studies in humans
A historical study performed in 1939 by Erausquin and Carranza3
in humans suggested that suprabony pockets were related to areas
of normal occlusion or hypofunction (100%) and that a smaller per-
centage (57%) were present in areas of hyperfunction. Infrabony
pockets, in all cases, were related to teeth presenting trauma from
occlusion. Additionally, the mean probing depth at sites of unbal-
anced occlusion (excessive or no function) was twice as deep as that
observed at areas of normal occlusion (2.5 mm vs 1.2 mm, respec-
tively). Moreover, pocket deepening appeared to be strongly influ-
enced by the masticatory function, being minimal in teeth under
normal occlusion, 2-­fold greater in teeth out of occlusion for a long
period of time, and 3-­fold greater in teeth under excessive function.
In a series of studies investigating the causal relationship be-
tween occlusal discrepancies and periodontal disease, clinical re-
cords of patients attending a private practice were included in a
database containing records from medical and dental histories,
complete periodontal examinations, and annotations of occlusal
discrepancies at a minimum interval between examinations of
1 year. Untreated patients (n = 30) were included for comparisons
with partially treated (nonsurgical therapy; n = 18) and completely
treated (nonsurgical + surgical therapy; n = 41) patients. Occlusal
therapy was performed in 17 (39%) patients of the complete treat-
ment group and in 9 (50%) of the partially treated group. Thirty
patients showing occlusal discrepancies were not treated for
these conditions (5 in the partially treated group and 25 in the
untreated group). Teeth with initial occlusal discrepancies showed
deeper probing depths (5.53 ± 1.51 mm) than teeth without oc-
clusal discrepancies (4.77 ± 1.31 mm), even after adjustment for
other confounders (P < 0.0001). Worse initial prognosis (fair to
poor; poor; hopeless) was attributed to teeth showing occlusal
discrepancies (13%) compared with teeth with no occlusal discrep-
ancies (<5%). Mobility10,58,77 was observed in 23% of teeth with
no occlusal discrepancies and in 31% of teeth with occlusal dis-
crepancies (P = 0.03). No significant association between clinical
mobility and occlusal discrepancies was found, although the risk
of teeth with occlusal discrepancies to present clinical mobility
was approximately 1.2 times greater. These findings suggest that
occlusal discrepancies could be considered as an independent risk
factor for periodontal disease.93,98 Teeth with untreated occlusal
discrepancies showed an overall worsening in prognosis over time
compared with teeth with no occlusal discrepancies or teeth with
treated occlusal problems, as well as a greater deepening in peri-
odontal pockets per year.93
More recently, a further analysis of 85 patients with 2219 teeth
presenting prematurity in centric relation (20%) or in maximal in-
tercuspal habitual position (57%), working (32%), and balancing
(11%) contacts during lateral movement showed that teeth with
centric prematurities had 0.9 mm greater probing depth than did
teeth without centric prematurities (P < 0.0001). Anterior teeth
with contact on protrusive movement had a decrease of 0.18 mm
in probing depth compared with anterior teeth without contact on
protrusive movement (P = 0.0076), and posterior teeth with contact
on protrusive movement had an increase of 0.51 mm in probing
depth compared with posterior teeth without contact on protrusive
movement (P < 0.0001). Teeth with working contacts only did not
have significantly different probing depths from teeth without any
contacts except for maximal intercuspal habitual position (P = 0.55).
Teeth with balancing contacts, with or without working contacts,
had 1.1 mm (P < 0.0001) to 1.0 mm (P < 0.0001) greater probing
 PASSANEZI and SANT'ANA |
      141

depth, respectively, compared with teeth with no contacts outside

OA results in improved response to surgical

The prevalence and severity of periodontal

the maximal intercuspal habitual position. Slides in centric of any

diminished after periodontal treatment.

The impact of oral health on mastication

The number of teeth had considerable

disease increases in tooth that do not

vertical distance were associated with over three times the proba-
and nonsurgical periodontal therapy bility of having an initial prognosis less than “good.” The greater the

importance in the perception of

vertical slide (2-­3 mm), the smaller the probability of having an initial
prognosis of “good,” a result in agreement with previous reports of
the study group.99

CAL, clinical attachment loss; MWF, modified Widman flap; OA, occlusal adjustment; OIDP, Oral Impacts on Daily Performance; PD, probing depth; SRP, scaling and root planing.
The association of dynamic occlusal contacts (contacts at
balancing and working sides during lateral excursive movements

mastication.
Conclusion

or posterior contacts during protrusive movements) and probing

occlude
depth and attachment loss were investigated in 2980 patients
aged 20-­79 years. Contacts in balancing sides during lateral move-
ments were significantly associated with greater probing depth
the number of teeth and difficulty in eating
treated; OA did not influence initial pocket

(P < 0.0001) and attachment loss (P < 0.0001). Contacts in balanc-

Absence of occlusal contacts was observed
attachment level in patients who received

before and after treatment was observed.

A significant negative correlation between

more severe periodontal disease and oral

Probing depth had a positive relationship
periodontal disease did not influence the

in 27.82% of teeth. These teeth showed

OA at sites surgically and nonsurgically

ing and working sides in the same tooth were significantly asso-
There was significantly greater gain of

depth or tooth mobility. Severity of

with OIDP score before treatment.

ciated with probing depth only (P = 0.004) in a regression model.

Other factors associated with probing depth and attachment loss
were tilted teeth and restored surfaces, besides elongated teeth
and tooth type.100
response to OA.

5.1.2 | Bone loss
TA B L E   3   Summary of Latin American studies investigating the role of occlusion in periodontal disease in humans

hygiene.

In the presence of a thick bony septum subjected to trauma from

Results

occlusion, the bone matrix alteration may be confined to the peri-

odontal ligament environment, allowing a faster spread of inflam-
matory exudate and formation of an infrabony periodontal pocket.
months after OA, patients were assigned

system was used to determine activity in

periodontitis were randomly assigned to

A clinical examination was performed to

mastication muscles and bite force. PD
50 patients with moderate-­to-­advanced

hygiene levels and periodontal disease

to MWF or SRP (split-­mouth). Patients

The existence of infrabony pockets in areas of thick bone septa is

28 patients were evaluated before and
OA (n = 22) or no OA (control; n = 28)

questionnaire. An electromyographic
after hygienic phase treatment. Two

were maintained every 3 mo for 2 y.

and tooth mobility were registered

suggestive, yet not pathognomonic, of the participation of trauma-

investigate occlusal contacts, oral
after treatment using the OIDP

togenic occlusion in the spread of the inflammatory exudate. In areas

of thin bone septa subjected to trauma from occlusion, the entire
bone may be converted into bone matrix.48,50 Under these condi-
tions, the spread of inflammatory exudate would result in loss of
the entire bone septum, characterizing a horizontal bone loss with
Study design

the formation of a deeper suprabony pocket. The inequality of su-

prabony pocket depths may be an indication of the possible role of
trauma from occlusion in the progression of the inflammatory ex-
udate. Additionally, the change in alveolar crest shape to a funnel
association with periodontal therapy on

profile seems to favor the development of dental biofilm infrabony

To investigate periodontal disease and

pockets, supporting the proposal of a bone co-­destructive zone.6,55

To assess the impact of conventional
To investigate the influence of OA in

periodontitis on the perception of

oral hygiene in disoccluding teeth

periodontal treatment of chronic

Studies in animals
CAL, PD, and tooth mobility

Studies have shown that repeated trauma at interproximal bone

by jiggling forces results in alveolar bone loss and, when combined
with periodontitis, an increased amount of bone loss was observed
when compared with periodontitis alone.9,28 Changes resulting from
mastication
Objectives

traumatogenic forces are reversible when the force is discontinued

or when the tooth moves away from the force in an adaption mech-
anism.93 When the offending forces were removed, a reduction in
the distance from the alveolar crest to the cementoenamel junction
118

Pereira et al128

and a greater percentage of interproximal bone were observed only

Burgett et al
Reference

Vázquez

at traumatized teeth, together with reduction in clinical mobility. In

et al129
Sotres

teeth subjected to jiggling forces and periodontitis, no significant

differences were observed in the distance of the bone crest to the
 |
142       PASSANEZI and SANT'ANA

TA B L E   4   Summary of Latin American narrative and systematic reviews investigating the role of occlusion in periodontal disease

Reference Objectives Methods Main findings

11
Albertini et al To review concepts that deal with
periodontal trauma from occlusion
Gélvez Vera To establish the role of traumato-
et al19 genic occlusion in the development
and progression of gingival
recession
Foz et al119 To identify and analyze the studies
investigating the effects of OA,
associated with periodontal
therapy, on periodontal parameters
and GCF markers
Furlaneto et al17 To investigate the role of traumato-
genic occlusion in aggravation of
periodontal disease, as well as to
investigate the possible advantages
of associating occlusal therapy and
periodontal therapy
Passos et al82 To review current literature on the
role of osteopontin and RANKL on
trauma from occlusion and
periodontitis lesions
Narrative review
Systematic review. Literature
search conducted at
MEDLINE, Ebscohost,
OVID, Science Direct,
Scopus and Proquest.
Systematic review. Literature
search conducted at
MEDLINE, Cochrane
Central Register of
Controlled Trials, and
EMBASE.
Narrative review
Narrative review
Trauma from occlusion is not related to the etiology of
periodontal disease and does not develop attach-
ment loss or periodontal pocket; there are character-
istic signs and symptoms of trauma from occlusion
that dictates its treatment as an independent
condition; its development requires the presence of
occlusal alterations that result in an unequal force
distribution; diagnoses and treatment of trauma from
occlusion require a multidisciplinary approach
directed to a favorable occlusal condition
The role of trauma from occlusion in the etiology of
gingival recession remains as a clinical opinion and it
is convenient to control occlusion as a risk factor to
any type of periodontal lesion
Although the selected studies (n = 4) suggest an
association between OA and improvement in
periodontal parameters, there is a need for new trials
for a better understanding of the efficacy of OA in
reducing the progression of periodontal disease
OA, when indicated, must be routinely performed
during periodontal treatment. Further studies are
necessary for a better understanding of the
association of trauma from occlusion and periodontal
tissues
Different results were found in laboratory and clinical
studies. These differences could be related to
differences in methodologies, which are not always
adequate as related to resistance and/or force
intensity. Based on current literature, the precise
mechanism of periodontal breakdown under
traumatogenic forces induced by osteopontin and
RANKL is yet to be determined.

GCF, gingival crevicular fluid; OA, occlusal adjustment.

cementoenamel junction, in the percentage of interproximal bone,
and in reduction of clinical mobility. Consequently, it can be sug-
gested that primary trauma from occlusion (without periodontal in-
flammation) results in no loss of attachment, with preservation of a
bone matrix that is able to regenerate in the absence of traumato-
genic forces. However, when periodontal inflammation is superim-
posed with trauma from occlusion, alterations in alveolar bone height
and volume are not reverted by elimination of traumatogenic forces,
30
with persistence of clinical mobility and gingival inflammation.
The extent of alveolar bone loss was also analyzed in the furcation
area of teeth exposed to trauma from occlusion in the presence or
absence of experimental periodontitis in 32 Wistar rats with or with-
out diabetes mellitus. The rats were assigned to four groups: (Group
1) diabetes mellitus + occlusal trauma + experimental periodontitis
(n = 8); (Group 2) diabetes mellitus + occlusal trauma (n = 8); (Group
3) occlusal trauma + experimental periodontitis (n = 8); and (Group
4) occlusal trauma (n = 8). Histomorphometric analysis showed that
teeth subjected to trauma from occlusion displayed significantly
greater alveolar bone loss at the furcation region compared with
nontraumatized teeth (P < 0.0001). Groups with experimental peri-
odontitis (1 and 3) showed greater bone loss, with no differences
between diabetic and nondiabetic rats subjected to trauma from
occlusion. The results highlight the role of trauma from occlusion
in the aggravation of alveolar bone loss and suggest that diabetes
mellitus enhances bone loss in the presence of occlusal trauma and
experimental periodontitis.101
Campos et al102 recently investigated the influence of short-­term
cigarette smoke inhalation on interradicular alveolar bone loss induced
by primary occlusal trauma in 48 Wistar rats. Occlusal trauma was in-
duced by bonding an orthodontic wire to the occlusal surface of the
lower first molar. The rats were exposed to cigarette smoke inhalation
in a cigarette smoking chamber for 8 minutes, 3 times a day, during the
experimental period. Smoke was produced by 10 cigarettes containing
1.3 mg of nicotine, 16.5 mg of tar, and 15.2 mg of carbon monoxide. The
rats were randomly assigned to the groups occlusal trauma + cigarette
smoke inhalation (n = 16), occlusal trauma (n = 16), or negative control
PASSANEZI and SANT'ANA
(no occlusal trauma, no cigarette smoke inhalation; n = 16). At intra-
group analysis, a significant increase of interradicular bone loss area
was observed over time in occlusal trauma + cigarette smoke inhalation
(P < 0.0005) and occlusal trauma (P = 0.0182) groups. No interradicular
bone loss was observed in rats of the negative control group (P = 0.99).
Rats from the occlusal trauma + cigarette smoke inhalation group
2
showed a greater (P = 0.0022) area of bone loss (0.54 ± 0.20 mm ) than
rats of the negative control group (0.3 ± 0.29 mm2) at 7 days, but no
significant differences were observed between occlusal trauma + cig-
2
arette smoke inhalation and occlusal trauma (0.42 ± 0.15 mm ) groups
in this period. After 14 days, significant differences (P < 0.05) in mean
interradicular bone loss area were observed between the occlusal
trauma + cigarette smoke inhalation group (0.93 ± 0.16 mm2) vs the
2
occlusal trauma group (0.62 ± 0.14 mm ) or vs the negative control
group (0.29 ± 0.02 mm2). Also, significant differences were observed
between occlusal trauma and negative control groups. The furcation
region of teeth submitted to occlusal trauma showed hyalinization
and cementum resorption (62.5% and 75% in occlusal trauma + cigar-
rete smoke inhalation after 7 and 14 days, respectively; 37.5% after
7 and 14 days in occlusal trauma), which were not observed in rats
of the negative control group. An increase in the number of tartrase-­
resistant acid phosphatase-­positive cells/mm was observed on days 7
(P < 0.0001) and 14 (P = 0.0099) in rats from the occlusal trauma + cig-
arette smoke inhalation group. These findings suggest that short-­term
cigarette smoke inhalation could increase bone damage in the nonin-
fectious periodontal lesion of primary occlusal trauma, suggesting its
possible role in inducing tissue changes and bone loss in smokers.
Studies in humans
The association between signs of trauma from occlusion and peri-
odontitis was evaluated in maxillary first molars of 300 individuals.
Teeth with bidigital mobility, functional mobility, widened periodon-
tal ligament space, or visible calculus on radiography had deeper
probing depth, greater loss of clinical attachment, and less radio-
graphic osseous support than teeth without these findings. Teeth
with occlusal contacts in centric relation, in working, nonworking,
or protrusive positions, did not exhibit any greater severity of peri-
odontitis than teeth without such contacts. Those teeth showing
functional mobility and widened periodontal ligament space showed
deeper probing depth, greater loss of clinical attachment, and less
osseous support than teeth without these findings. Finally, given
equal clinical attachment levels, teeth with evidence of functional
mobility and widened periodontal ligament space showed less radio-
graphic osseous support. These findings suggest that no association
between trauma from occlusion and chronic periodontitis exists.103
5.1.3 | Attachment loss
Studies in animals
The effect on periodontal disease induced by positioning of ligatures
and incidence of jiggling forces after its elimination were inves-
tigated in beagle dogs. Ligatures were positioned to induce peri-
odontal disease in mandibular premolars and removed 90 days later.
|
      143
Trauma from occlusion was induced by jiggling forces for 90 days,
then jiggling forces were stopped in the test group, resulting in a
decrease in clinical mobility. Loss of connective tissue attachment
on day 360 was similar in test and control sites, suggesting that the
height of supporting periodontal tissue was similar in traumatized
teeth before and after force removal.104
A recent study performed in Lewis rats investigated the effects
of occlusal trauma on periodontal destruction, particularly loss of
attachment at the onset of periodontitis. Forty-­eight rats were im-
munized with intraperitoneal injections of Escherichia coli lipopoly-
saccharide suspended in phosphate-­buffered saline. Twenty-­eight
days later, rats were assigned to one of the following groups: trauma,
induced by bonding a high metal wire to the occlusal surface of man-
dibular first molars; inflammation, induced by topical application
of E. coli lipopolysaccharide in phosphate-­buffered saline into the
palatal gingival sulcus of maxillary right first molars; trauma + in-
flammation; or phosphate-­buffered saline (negative control). The
trauma group and the negative control group also received topical
application of phosphate-­buffered saline into the gingival sulcus.
Additionally, 12 nonimmunized rats were treated as described for
the trauma + inflammation group. At 5 days, trauma and negative
control groups showed no loss of attachment. The inflammation
group showed slight loss of attachment, while the trauma + inflam-
mation group showed loss of attachment and inflammatory infiltrate
at the junctional epithelium and connective tissue in all specimens.
In the nonimmunized trauma + inflammation group, loss of attach-
ment was not detected. However, the inflammatory infiltrate was
greater in this group than in negative control and trauma groups at
5 and 10 days. The histometric analysis showed significantly greater
loss of attachment at 10 days than at 5 days for inflammation and
trauma + inflammation groups. Significant differences were ob-
served among groups at 5 and 10 days, with greater attachment loss
for the inflammation and trauma + inflammation groups. Tartrase-­
resistant acid phosphatase-­positive cells were not observed in neg-
ative control, trauma , or the nonimmunized trauma + inflammation
groups, while the inflammation group showed few tartrase-­resistant
acid phosphatase-­positive cells at the edge of palatal alveolar bone
on days 5 and 10, and the trauma + inflammation group showed
many at 10 days. Trauma groups exhibited fewer collagen fibers at-
tached to the roots compared with the other groups. The greater dis-
persion of immune complexes in the trauma + inflammation group
may explain the mechanism of acceleration of attachment loss in-
duced by occlusal trauma.67
Studies in humans
To investigate if trauma from occlusion combined with periodontal
pockets would promote a change in biofilm composition and there-
fore increase loss of attachment, 4-­5 mm interproximal bone defects
were surgically created in Beagle dogs. Trauma from occlusion was
produced by the placement of 1 incisor crown overbuilt by 3 mm,
creating a premature contact, 4 weeks later. Nontraumatized con-
tralateral incisors were used as controls. Samples of biofilm were
collected at baseline, and at weeks 1-­3 (Phase 1: development of
 |
144       PASSANEZI and SANT'ANA
A percentages of motile bacteria, although baseline levels were not
B gain a clearer understanding of the role of trauma from occlusion
C premolars (3P3; Group BII). Ligatures were removed after 120 days
F I G U R E   2   A, Panoramic X-­ray of a 57-­y-­old female patient
showing mesial inclination of the lower-­left second molar and distal
migration of both lower-­left bicuspids. The lower-­left second molar
depicts a periodontal infrabony lesion measuring 7.0 and 5.0 mm
on mesiolingual and lingual surfaces, respectively. B, Advanced loss
of periodontal supporting tissues at the lower-­left second molar;
C, 13 mo after treatment, showing recovery of the periodontal
supporting tissues, which resulted in probing depths of 2.0 mm on
mesiolingual and lingual sites
periodontal pockets) and weeks 5-­16 (Phase 2: trauma from occlu-
sion + periodontal pockets). Significantly greater mobility (P < 0.05)
was observed in teeth with trauma from occlusion and periodon-
tal pockets (test) than in teeth with periodontal pockets only (con-
trols). Test teeth also showed significantly greater loss of attachment
(P < 0.05) than nontraumatized teeth with pockets. At baseline, cocci
(65%-­75%) and small amounts of motile bacteria (12%-­15%), includ-
ing 3%-­4% of spirochetes, were observed. At 4 weeks, a small re-
duction (to 42%-­45%) in the percentage of cocci, and increases in
the percentages of motile bacteria (to 37%-­43%) and spirochetes
(to 24%-­27%), were observed. After scaling and root planing, there
was an increase in the percentages of cocci and a decrease in the
reached, and there were no significant differences between trauma-
tized and non-­traumatized teeth, suggesting that the greater attach-
ment loss observed in the test group was related to the influence of
traumatogenic forces.105
5.1.4 | Gingival inflammation
Studies in animals
Biancu et al36 performed a study in beagle dogs to investigate
which tissue changes may occur in the zone of co-­destruction to
in additional attachment loss and to investigate changes in the peri-
odontal ligament tissue when an inflammatory lesion approaches
the periodontal ligament space. In Group A, a buccolingual jiggling-­
type movement was induced by an orthodontic elastic resulting in
increased tooth mobility at P3, under plaque control. Biopsies were
obtained on day 90 for Group A. Dogs allocated to Group B were
subdivided into two groups: BI (n = 5) and BII (n = 5). On day 0, a
4-­month period of experimental periodontal tissue breakdown was
initiated by placing cotton floss ligatures submarginally around man-
dibular fourth premolars (Group BI) and around mandibular third
and biopsies were retrieved from dogs in Group BI, while dogs in
Group BII were submitted to supragingival debridement followed
by plaque accumulation up to day 225. The histologic and histo-
morphometric analyses showed that the most coronal portion of
periodontal ligament of teeth with increased mobility presented a
widened width, reduced collagen tissue volume, and increased vol-
ume of vascular structures and number of leukocytes. The number
of osteoclasts bordering this portion of alveolar bone was increased
and the number of collagen fibers inserting into the root cementum
and the alveolar bone was decreased. In teeth with normal mobil-
ity, the position of gingival inflammatory connective tissue failed to
influence the composition of the tissue within the coronal portion of
periodontal ligament.
5.1.5 | Severity of periodontal disease
Studies in humans
To understand the role of traumatogenic occlusion on the pro-
gression of periodontal disease, Branschofsky et al106 conducted
a study to correlate the quality and quantity of secondary trauma
from occlusion with the extent and severity of periodontal disease
in 288 subjects with chronic periodontitis and 93 healthy subjects.
Inclusion criteria were for patients to display premature and balance
contacts in habitual intercuspation and to show lateral or protrusive
movements of the mandible. Trauma from occlusion was detected
in 64.3% of all patients. Most patients presenting slight periodonti-
tis did not display trauma from occlusion (n = 36); and most patients
presenting moderate and severe periodontitis displayed, respec-
tively, ≤3 (n = 69) and >3 (n = 42) teeth with trauma from occlusion.
Significant differences were found among groups, including the
PASSANEZI and SANT'ANA
control group versus patients with slight periodontitis. Trauma from
occlusion was positively correlated with the severity of attachment
loss. These findings suggest that trauma from occlusion influences
the severity of chronic periodontitis.4,8,12,49
When diagnosis of occlusal trauma was based on the trauma from
occlusion index, which takes into account the combination of func-
tional mobility of the tooth and the presence of a widened periodontal
ligament space, there was significantly greater probing depth (P < 0.01),
attachment loss (P < 0.01), bone loss (P < 0.01), gingival bleeding and
inflammation (P < 0.05), and plaque index (P < 0.05) in teeth positively
diagnosed than those negatively diagnosed. Considering the same
attachment level, teeth positively identified according to the trauma
from occlusion index showed more bone loss than teeth negatively
identified. Conversely, teeth positively diagnosed according to the
adaptability index (occlusal wear + thickened lamina dura) showed less
attachment loss and greater bone support than teeth negatively iden-
tified according to the adaptability index. No differences were found
in probing depth, attachment loss, bone loss, bleeding index, gingival
index, and plaque index between teeth identified with premature
contacts, balancing side contacts during lateral movements, posterior
contacts during protrusive movements, and premature contacts at an-
terior teeth and teeth without contacts. These findings suggest that
the effects of heavy forces on the periodontium should be investigated
according to the capacity of adaption of involved teeth.107
5.1.6 | Gingival recession
Studies in humans
Kleber and Schenk108 reported that one-­third (1039 of 4022) of pa-
tients seeking periodontal care showed gingival recession. Gingival
recession was present mainly in young (20-­
25 years) patients
(44.4%), who showed functional disturbances during occlusal excur-
sions (79% at first bicuspids and 72% at second bicuspids).
Although it has been speculated that the elimination of trauma
by occlusal adjustment, relieving the incidence of excessive occlusal
force on teeth showing gingival cleft formation, resulted in sponta-
neous remission of gingival recession, with no additional treatment
109,110
performed, this has never been documented by other research.
Furthermore, no relationship was found between the existence of
occlusal discrepancies, whether treated or not, and changes in kera-
tinized gingiva width, as described by Harrel and Nunn111 in a regres-
sion analysis of 91 patients divided into untreated (n = 30), partially
treated (n = 20), and completely treated (n = 41) groups. Occlusal
discrepancies were found in 56 (61.53%) subjects and were more
prevalent in younger patients (50.4 ± 11.6 years vs 57.9 ± 12.3 years;
P = 0.005), and the mean width of keratinized gingiva was 3.28 mm
in patients without occlusal discrepancies and 3.33 mm in patients
with occlusal discrepancies, at initial examination.
An investigation on the nature of occlusal contacts in maximum
intercuspation, protrusive, lateroprotrusive, and lateral excursive
movements was performed in 50 subjects with gingival recession
and 10 subjects with gingival clefts. Gingival recession was more re-
lated to group function than to mutual protected occlusion. Nearly
|
      145
all subjects showed interferences in protrusive, lateroprotrusive,
and lateral excursive movements on teeth showing gingival reces-
sion and gingival clefts. Occlusal wear was present on all teeth with
gingival clefts and on almost all teeth with gingival recession. These
results suggest that occlusal interferences in maximal intercuspation
and eccentric movements and the absence of mutually protected oc-
clusion can contribute to gingival recessions and clefts.112 It should
be mentioned that in many of the aforementioned studies the oral
hygiene habits of the patient, as well as other possible influencing
factors, presently recognized, have not been considered.
A recent systematic review to investigate the role of traumatic
occlusion in the initiation and progression of gingival recessions was
performed, in an attempt to gain a clearer understanding of the role
of occlusion in these lesions. After searching 20 databases, 3577 ref-
erences were found. After considering inclusion and exclusion crite-
ria, 51 references were selected for screening, from which 32 were
excluded. After assessing the quality and validity of the studies ac-
cording to Journal of the American Medicine Association parameters,
7 articles were selected, just 1 of which specifically addressed the
relationship between traumatic occlusion and gingival recession. It
could be concluded that the relationship between the conditions re-
mains as “a clinical opinion” and that it seemed convenient to control
occlusal factor in clinical practice because it can be considered as an
independent risk factor for periodontal disease.18
5.1.7 | Tooth mobility
Studies in animals
Studies performed in Macaca monkeys, in which a dysfunctional
occlusal relationship was created by inserting occlusal splints in
the maxilla, raising the vertical occlusal dimension by 3-­4 mm, and
incorporating interferences in the occlusion at test teeth, showed
evidence of acute trauma from occlusion, development of wear fac-
ets, and significant increases in tooth mobility and gingival index.
Radiographically, signs of breakdown of marginal and interradicular
alveolar bone were observed. One of the monkeys developed peri-
odontal pockets of 4-­5 mm at the test side. Tooth mobility, gingival
index, and plaque index remained elevated, but no clinical or radio-
graphic evidence of further bone loss or increase in pocket depth
was seen. Analysis of cortisol plasma and urine levels showed a sig-
nificant increase in the 24-­hour urinary cortisol excretion rate and
plasma concentration, which showed a decrease to basal values at 6
and 12 weeks, suggesting that a dysfunctional occlusal relationship
may also result in bruxism associated with emotional stress.113,114
6 | C LI N I C A L A N D R A D I O G R A PH I C S I G N S
A N D S Y M P TO M S O F TR AU M A FRO M
O CC LU S I O N
Diagnosis of occlusal trauma can be made by evaluating signs and
symptoms of the injury. Although not pathognomonic of the condi-
tions, signs and symptoms of trauma from occlusion, according to
 |
146       PASSANEZI and SANT'ANA
the American Academy of Periodontology,90 include: tooth mobility;
tooth migration; pain or discomfort on chewing or percussion tests;
widening of periodontal ligament space; disruption of the lamina
dura; furcation or vital tooth apex radiolucencies; root resorption;
tenderness on masticatory muscles or other signs and symptoms of
temporomandibular junction dysfunction; presence of wear facets;
enamel fractures; and fremitus.
Figure 2 presents the radiographic image of a 57-­year-­old patient
with an acceptable periodontal status, except for the lower left sec-
ond molar. Mesial and lingual pockets, of 7.0 and 5.0 mm depth, re-
spectively, were present. A heavy occlusal balancing interference, high
enough to produce disclusion of all other posterior teeth at working
and balancing sides, was detected. In addition, there was a premature
contact in the centric arch of closure between the outer surface of
the distal marginal ridge of the lower-­left second molar and the mesial
slope of the palatal cusp of the extruded upper-­left second molar, pro-
ducing anterior sliding of the mandible. Dental biofilm was detected at
the affected site, suggesting a role in the etiology of the periodontal
lesion. Treatment was accomplished by oral hygiene measures, scaling
and root planing, professional prophylaxis, and selective occlusal ad-
justment, resulting in complete remission of the periodontal pocket.
This case may provide clinical evidence of a cause-­and-­effect relation-
ship between periodontitis and trauma from occlusion.
7 |  TR E ATM E NT CO N S I D E R ATI O N S
Although trauma from occlusion may occur concurrently, the con-
ditions may be treated separately, with specific and independent
treatment goals and end points. The goals of the treatment of oc-
clusal traumatism may be described as: elimination or reduction of
tooth mobility; establishment or maintenance of a stable and repro-
ducible maximal intercuspal habitual position; provision of efficient
masticatory function and a comfortable occlusion with acceptable
phonation and esthetics; and elimination or modification of par-
afunctional habits.90
Treatment of occlusal trauma may be performed at any phase
of periodontal therapy. For chronic periodontitis, treatment efforts
are directed toward elimination or minimization of excessive forces,
and occlusal therapy may be accomplished through several different
approaches, including: occlusal adjustment; management of para-
functional habits; temporary, provisional, or long-­term stabilization
of mobile teeth; orthodontic tooth movement; and occlusal recon-
struction or extraction of selected teeth, depending on the case.
After completion, desired outcomes should be90: reduction or elim-
ination of tooth mobility; absence of further tooth migration; stable
functional physiologic occlusion, compatible with periodontal health
and esthetically acceptable; reduction or elimination of radiographic
signs and symptoms (eg, widening of periodontal ligament); relief of
pain and improved patient comfort; and elimination of premature
contacts, fremitus, and occlusal interferences.
Occlusal therapy is able to reduce the long-­term progression
of periodontal disease, and could be considered as an important
adjunctive therapy in the treatment of periodontal disease.93,99 A
cohort study was performed115 to investigate the relationship be-
tween biting ability and progression of periodontal disease in 194
patients monitored for 3 years during the maintenance phase of
periodontal therapy. Patients who showed progression of periodon-
tal disease during the follow-­up period, defined by the presence of
at least 2 teeth showing interproximal loss of attachment of ≥3 mm
or tooth loss, were included in the progress group (n = 83), while
subjects not showing progression of periodontal disease according
to these criteria were included in the nonprogress group (n = 111).
High occlusal forces were defined as >500 N in men and >370 N in
women. A logistic regression analysis showed that progression of
periodontal disease was significantly associated with attachment
loss of ≥7 mm (odds ratio = 2.397; 95% confidence interval: 1.273-­
4.346; P = 0.005) and low occlusal forces (odds ratio = 2.352; 95%
confidence interval: 1.273-­4.346; P = 0.006), suggesting that in the
presence of severe loss of attachment, even forces of low magnitude
influence the progression of periodontal disease.
Treatment of primary or secondary trauma from occlusion re-
quires controlling marginal inflammation and restoring normal
occlusal function.41,116 Remission of primary trauma from occlu-
sion proceeds uneventfully if periodontal pockets are successfully
treated.9,10,23 Considering that, treatment of primary trauma from
occlusion should basically address the occlusal adjustment to re-
direct occlusal forces, allowing reversibility of the lesion. In cases
in which periodontitis and trauma from occlusion coexist without
producing a combined lesion, treatment should be directed to the
independent treatment of both conditions as two distinct patholog-
ical entities.
According to Bhola et al,116 once periodontal health is estab-
lished, occlusal therapy can be performed, if indicated, to help re-
duce mobility when such a condition is associated with a widened
periodontal ligament space. Redirection of occlusal forces and re-
duction of tooth mobility to physiological levels may influence long-­
term bone regeneration and connective tissue attachment. A total
of 82 patients and 1974 teeth were examined according to pocket
depth, attachment level, and tooth mobility, at baseline and yearly
up to 8 years of follow-­up. Treatment consisted of scaling, oral hy-
giene instruction, occlusal adjustment, and periodontal surgery
(curettage, modified Widman, or pocket elimination), followed by
prophylaxis every 3 months. Tooth mobility was scored as 1 to 3,
with scores being related to changes in attachment levels for three
grades of severity of periodontal disease, based on initial pocket
depth (1-­3 mm; 4-­6 mm; ≥7 mm). The results obtained indicated that
there was a statistically significant relationship between mobility at
baseline and the change in attachment level after treatment. Pockets
of clinically mobile teeth did not respond to periodontal treatment
as well as did firm teeth, when the same initial disease severity was
present. However, mobile teeth could be successfully treated and
well maintained by supportive periodontal treatment.117
The influence of occlusal adjustment in association with peri-
odontal therapy on attachment levels, pocket depth, and tooth
mobility, its significance in nonsurgical periodontal treatment, and
PASSANEZI and SANT'ANA
the influence of initial tooth mobility or disease severity in post-­
treatment attachment levels after occlusal adjustment, were in-
vestigated in 50 patients randomly assigned to occlusal adjustment
therapy (n = 22) or no occlusal adjustment therapy (n = 28). A signifi-
cantly greater gain of clinical periodontal attachment was observed
in patients who received occlusal adjustment compared with those
who did not. Both surgically and nonsurgically treated sites in a split-­
mouth design responded similarly to occlusal adjustment. No effect
of occlusal adjustment was observed on the response in pocket
depth, nor did initial tooth mobility or initial severity of periodontal
disease influence the response to occlusal adjustment.118
A recent systematic review119 of 4 studies, investigating the ef-
fects of occlusal adjustment in the reduction of periodontal disease
progression, demonstrated that occlusal adjustment to eliminate
occlusal interferences in centric relationships, protrusion or lateral
excursions, mandibular eccentric movements, and contacts at bal-
ancing sides, resulted in improvement of periodontal parameters.
However, considering the great heterogeneity of methodologies,
it could be concluded that further studies are necessary to gain a
clearer understanding of the benefits of occlusal adjustment in peri-
odontal treatment.
120
Santamaria et al described a clinical case of a 13 mm pocket
probing depth on the mesial surface of a lower-­right second molar,
with Grade 2 clinical mobility and bleeding upon toothbrushing. The
patient was submitted to nonsurgical periodontal therapy, including
scaling and root planing and occlusal adjustment of an overt protru-
sive interference. After 6 months, reductions in bleeding on probing,
tooth mobility, and pocket probing depth to 4 mm were observed.
These findings suggest that minimizing occlusal interferences along
with appropriate periodontal treatment result in improvement in
periodontal parameters, and clinicians should carefully investigate
excessive occlusal forces.
Occlusal adjustment should be performed, when indicated, 30-­
45 days prior to periodontal surgery in order to allow rebuilding of
existent bone matrix and prevent its loss during surgical debride-
ment of periodontal defects.
8 | FI N A L CO M M E NT S
In the field of periodontics, it seems crucial to prevent, treat, and
maintain the periodontal supporting apparatus, which is respon-
sible for the long-­term stability of teeth. Accepting this concept,
periodontal treatment should be directed at the preservation of
periodontal supporting tissues, the homeostatic behavior of which
may be dependent on the proper distribution and neutralization of
applied mechanical forces.43
Two main factors may challenge the integrity of periodontal sup-
porting tissues: dental biofilm; and trauma from occlusion. Dental
biofilm affects the integrity of the periodontal protective compart-
ment. Hence, the primary goal in the treatment of inflammatory peri-
odontal disease should be to control factors that may jeopardize the
function of this protective compartment, represented by the tissues
|
      147
included in the biologic width.121 An ideal goal is the conversion of a
pathologic periodontal pocket to a healthy one.38,39,122,123
Occlusion is the main factor affecting the behavior of the sup-
portive periodontium. Although no consensus exists on the role of
occlusion in periodontal disease, analysis of the reports described
in this chapter suggest that traumatogenic forces may facilitate api-
cal spread of dental biofilm and inflammatory exudates, resulting in
pocket deepening, and attachment and bone loss. The establishment
of a periodontitis plus trauma from occlusion lesion is very difficult
to reproduce, and consequently to investigate, because for this type
of lesion to occur, it is necessary for both conditions to manifest at
the same time in their destructive phase. This might explain the dif-
ficulty in establishing a causal relationship between traumatogenic
forces and periodontal disease.
Finally, systematic reviews failed to find a causal relationship
between periodontitis and trauma from occlusion, but these pub-
lications exclude case reports, case series, and uncontrolled clinical
trials from analysis, and do not consider many other important re-
sults described in the literature. Mainly, the outcomes investigated
in systematic reviews are based on research performed according
to similar methodologies, but without considering the results of
treatment performed in patients. Most of the research to investigate
the role of occlusion in periodontics has been performed in animal
models or cadavers and hence does not reflect the real influence of
trauma from occlusion in humans. As a consequence, aggravation
of plaque-­related inflammatory periodontal disease by trauma from
occlusion is still under question, and further investigations are nec-
essary to elucidate such an association.
REFERENCES
1. Karolyi M. Beobachtungen über Pyorrhea alveolaris: Österr-­Ung
Vierteljahrschr Zahnheik. 1901;17:279‐283.
2. Carranza F. Un enfoque racional del problema etiológico de la pa-
radentosis. Rev Asoc Odontol Argent. 1957;45:143-147.
3. Erausquin R, Carranza FA. Primeros hallazgos paradentosicos. Rev
Odontol. 1939;27:485-513.
4. Ericsson I. The effects of plaque and physical stress on periodontal
tissues. J Clin Periodontol. 1986;13(10):918-922.
5. Glickman I, Carranza FA Jr. Glickman's Clinical Periodontology, 5th
edn. Philadelphia, PA: Saunders; 1979:275-293, 455-488.
6. Glickman I, Smulow JB. The combined effects of inflamma-
tion and trauma from occlusion in periodontitis. Int Dent J.
1969;19(3):393-407.
7. Glickman I. Clinical significance of trauma from occlusion. J Am
Dent Assoc. 1965;70:607-618.
8. Nyman S, Lindhe J, Ericsson I. The effect of progressive tooth
mobility on destructive periodontitis in the dog. J Clin Periodontol.
1978;5(3):213-225.
9. Polson AM, Meitner SW, Zander HA. Trauma and progression
of marginal periodontitis in squirrel monkeys. III. Adaption of in-
terproximal alveolar bone to repetitive injury. J Periodontal Res.
1976;11(5):279-289.
10. Polson AM. The relative importance of plaque and occlusion in
periodontal disease. J Clin Periodontol. 1986;13(10):923-927.
11. Albertini G, Bechelli D, Capusotto A. The importance of diagnosis
and muldisciplinary treatment of periodontal trauma from occlu-
sion. Rev Asoc Odontol Argent. 2007;95:157-171 [In Spanish].
 |
148       PASSANEZI and SANT'ANA
12. Alves RV, Sallum EA, Sallum WA, Lopes JCA. The relation between
occlusal trauma and periodontal disease. J Bras Clin Odontol Int.
2004;8(46):330-333 [In Portuguese].
13. Andrade RA, Beloti AM, Cézar Zampaio JE, Hidalgo de Andrade LE,
Kina S. Occlusal trauma. Concept and etiology. Part I: review of the
literature. Rev Fed Odontol Colomb. 2001;60:19-23 [In Portuguese].
14. Caffesse RG. El factor oclusal en la enfermedad periodontal. Rev
Asoc Odontol Argent. 1980;68:294-299.
15. Caffesse RG. Management of periodontal disease in patients with
occlusal abnormalities. Dent Clin North Am. 1980;24(2):215-230.
16. Dotto CA, Carranza FA, Itoiz ME. Efectos mediatos del trauma ex-
perimental en ratas. Rev Asoc Odontol Argent. 1966;54(1):48-51.
17. Furlaneto FAC, Melo LGN, Nagata MJH, et al. Occlusion and peri-
odontics: a critical analysis of literature. Rev Sul-­Brasil Odontol.
2009;6(1):85-93 [In Portuguese].
18. Gélvez Vera MA, Martínez Cañón MV, Ferro Camargo MB, Velosa
Porras J. Relación de la oclusión traumática con las recesiones
gingivales: revisión sistemática de la literatura. Univ Odontol.
2009;28(61):101-117.
19. Reyes E, Hildebolt C, Langenwalter E, Miley D. Abfractions and at-
tachment loss in teeth with premature contacts in centric relation:
clinical observations. J Periodontol. 2009;80(12):1955-1962.
20. Ribeiro LLG, Kina JR, Bosco JMD, Lopes AM. Os efeitos do trauma
oclusal na patogênese da doença periodontal. Rev Paul Odontol.
2003;25(1):19-21.
21. Stones HH. An experimental investigation into the association
of traumatic occlusion with periodontal disease. Proc R Soc Med.
1938;31(5):479-495.
22. Glickman I, Weiss L. Role of trauma from occlusion in initia-
tion of periodontal pocket formation in experimental animals. J
Periodontol. 1955;26(1):14-20.
23. Comar M, Kollar J, Gargiulo A. Local irritation and occlusal trauma
as co-­factors in the periodontal disease process. J Periodontol.
1969;40(4):193-200.
24. Ewen S, Stahl S. The response of the periodontium to chronic gin-
gival irritation and long term tilting forces in adult dogs. Oral Surg
Oral Med Oral Pathol. 1962;15(12):1426-1433.
25. Macapanpan LC, Weinman JP. The influence of injury to the peri-
odontal membrane on the spread of gingival inflammation. J Dent
Res. 1954;33(2):263-272.
26. Bhaskar SN, Orban B. Experimental occlusal trauma. J Periodontol.
1955;26(4):270-284.
27. Polson AM. Trauma and progression of marginal periodontitis in
squirrel monkeys. II. Co-­destructive factors of periodontitis and
mechanically produced injury. J Periodontal Res. 1974;9(2):108-113.
28. Polson AM, Zander HA. Effect of periodontal trauma upon intra-
bony pockets. J Periodontol. 1983;54(10):586-591.
29. Ericsson I, Lindhe J. Effect of longstanding jiggling on experimen-
tal marginal periodontitis in the beagle dog. J Clin Periodontol.
1982;9(6):497-503.
30. Polson AM, Meitner SW, Zander HA. Trauma and progression
of marginal periodontitis in squirrel monkeys. IV. Reversibility of
bone loss due to trauma alone and trauma superimposed upon
periodontitis. J Periodontal Res. 1976;11(5):290-298.
31. Glickman I. Occlusion and the periodontium. J Dent Res.
1967;46(Suppl 1):53-59.
32. Geramy A, Faghihi S. Secondary trauma from occlusion: three-­
dimensional analysis using the finite element method. Quintessence
Int. 2004;35(10):835-843.
33. Glickman I, Smulow JB. Adaptive alterations in the periodontium of
the rhesus monkey in chronic trauma from occlusion. J Periodontol.
1968;39(2):101-105.
34. Glickman I, Smulow JB. Alterations in the pathway of gingival in-
flammation to the underlying tissues induced by excessive occlusal
forces. J Periodontol. 1962;33(1):7-13.
35. Glickman I, Smulow JB. Effect of excessive occlusal forces upon
the pathway of gingival inflammation in humans. J Periodontol.
1965;36(2):141-147.
36. Biancu S, Ericsson I, Lindhe J. Periodontal ligament tissue reac-
tions to trauma and gingival inflammation. An experimental study
in the beagle dog. J Clin Periodontol. 1995;22(10):772-779.
37. Lindhe J, Nyman S, Ericsson I. Trauma from occlusion. In: Lindhe
J, ed. Textbook of Clinical Periodontology, 2nd edn. Copenhagen:
Munksgaard; 1990:219-234.
38. Waerhaug J. The angular bone defect and its relationship to
trauma from occlusion and downgrowth of subgingival plaque. J
Clin Periodontol. 1979;6(2):61-82.
39. Waerhaug J. The infrabony pocket and its relationship to
trauma from occlusion and subgingival plaque. J Periodontol.
1979;50(7):355-365.
40. Davies SJ, Gray RJM, Linden GJ, James JA. Occlusal consider-
ations in periodontics. Br Dent J. 2001;191(11):597-604.
41. Deas DE, Mealey BL. Is there an association between oc-
clusion and periodontal destruction? J Am Dent Assoc.
2006;137(10):1381-1389.
42. Harrel SK, Nunn ME, Hallmon WW. Is there an association be-
tween occlusion and periodontal destruction? Yes—occlusal
forces can contribute to periodontal destruction. J Am Dent Assoc.
2006;137(10):1380-1392.
43. McCulloch CAG, Lekic P, McKee MD. Role of physical forces in
regulating the form and function of the periodontal ligament.
Periodontol 2000. 2000;24(1):56-72.
44. Rios HF, Ma D, Xie Y, et al. Periostin is essential for the integrity
and function of the periodontal ligament during occlusal loading in
mice. J Periodontol. 2008;79(8):1480-1490.
45. Goldman HM, Cohen DW. Periodontal Therapy, 6th edn. Saint
Louis, MO: Mosby; 1980:239-261.
46. Carranza FA. Periodontal responses to external forces. In: Newman
MG, Takei HH, Klokkevold PR, Carranza FA, eds. Carranza's Clinical
Periodontology, 10th edn. Saint Louis, MO: Saunders Elsevier;
2006:467-479.
47. Glickman I. Inflammation and trauma from occlusion, co-­
destructive factors in chronic periodontal disease. J Periodontol.
1963;34(1):5-10.
48. Karring T, Nyman S, Thilander B, Magnusson I. Bone regenera-
tion in orthodontically produced alveolar bone dehiscences. J
Periodontal Res. 1982;17(3):309-315.
49. Lindhe J, Nyman S. Occlusal therapy. In: Lindhe J, ed. Textbook
of Clinical Periodontology, 2nd edn. Copenhagen: Munksgaard;
1990:451-465.
50. Nyman S, Karring T, Bergenholtz G. Bone regeneration in alveolar
bone dehiscences produced by jiggling forces. J Periodontal Res.
1982;17(3):316-322.
51. Sallum AW, Nascimento A, Bozzo L, Toledo S. The effect of dexa-
methasone in traumatic changes of the periodontium of marmo-
sets (Callithrix jacchus). J Periodontol. 1976;47(2):63-66.
52. Sallum AW. A study on the participation of trauma from occlu-
sion in the evolution of periodontal disease in rats. Associated
Professor [Thesis]. Piracicaba: UNICAMP-FOP, 1982.
53. American Academy of Periodontology. Glossary of Periodontal
Terms, 4th edn. Chicago, IL: American Academy of Periodontology;
2001 (Special Issue): 1-45.
54. Dotto CA, Carranza FA Jr, Cabrini RL, Itoiz ME. Vascular
changes in experimental trauma from occlusion. J Periodontol.
1967;38(3):183-188.
55. Glickman I. The new practice of dentistry. Midwest Dent.
1972;48(1):16-18.
56. Passanezi E, Sant'ana ACP, Greghi SLA, Rezende MLR, Janson
WA. Traumatogenic occlusion in periodontics and implant den-
tistry. In: Santos Pantaleón D, Passanezi E, eds. Clinical Dentistry.
PASSANEZI and SANT'ANA
Contemporary Practice, Vol. 2. São Paulo: Artes Médicas – Latino
America; 2004:205-250 [In Spanish].
57. Passanezi E, Santana ACP. The role of traumatogenic occlusion
in periodontics and implant dentistry. In: Tunes U, Rapp GE, eds.
Actualization in Periodontics and Implant Dentistry. São Paulo: Artes
Médicas; 1999:253-293 [In Portuguese].
58. Abrams L, Potashnic SR, Rosenberg ES, Evian CI. Role of occlusion
in periodontal therapy. In: Rose LF, Mealey BL, Genco RJ, Cohen
DW, eds. Periodontics: Medicine, Surgery, and Implants. Saint Louis,
MO: Elsevier Mosby; 2004:745-771.
59. Alves ME, Askar EM, Randolph R, Passanezi E. A photoelastic
study of three-­unit mandibular posterior cantilever bridges. Int J
Periodontics Restorative Dent. 1990;10(2):152-167.
60. Asckar EM, Passanezi E. Periodontal distribution of internal ten-
sion produced by occlusal forces exerted on free-­end partial fixed
prosthesis. Rev Assoc Paul Cir Dent. 1980;3454:20 [Em português].
61. Poiate IAVP, Vasconcelos AB, Santana RB, Poiate E Jr. Three-­
dimensional stress distribution in the human periodontal ligament
in masticatory, parafunctional, and trauma loads: finite element
analysis. J Periodontol. 2009;80(11):1859-1867.
62. Shapiro IM, Golub EE, Haselgrove J, Chance B, Frasca P.
Initiation of endochondral calcification is related to changes in
the redox state of hyperthrofic chondrocytes. Science. 1982;217
(4563):950-952.
63. Tuncay OC, Ho D, Barker MK. Oxygen tension regulates osteoblast
function. Am J Orthod Dentofac Orthop. 1994;105(5):457-463.
64. Consolaro A. Biology of tooth movement: basic principles applied
to the clinics. In: Interlandi S, ed. Orthodontics – Basis for Initiation,
4th edn. São Paulo: Artes Médicas; 1999:435-449 [In Portuguese].
65. Crespo Vázquez E, Crespo Abelleira A, Suárez Quintanilla JM,
Rodriguez Cobos MA. Correlation between occlusal contact and
root resorption in teeth with periodontal disease. J Periodontal Res.
2011;46(1):82-88.
66. Hine MK. Periodontal traumatism. J Dent Res. 1962;41(Suppl
1):290-297.
67. Nakatsu S, Yoshinaga Y, Kuramoto A, et al. Occlusal trauma accel-
erates attachment loss at the onset of experimental periodontitis
in rats. J Periodontal Res. 2014;49(3):314-322.
68. Kurol J, Owman-Moll P. Hyalinization and root resorption during
early orthodontic tooth movement in adolescents. Angle Orthod.
1998;68(2):161-165.
69. von Böhl M, Maltha JC, Von Den Hoff JW, Kuijpers-Jagtman AM.
Focal hyalinization during experimental tooth movement in beagle
dogs. Am J Orthod Dentofacial Orthop. 2004;125(5):615-623.
70. Consolaro A. Force distribution is more important than its inten-
sity! Dental Press J Orthod. 2014;19(1):5-7.
71. Cakmak F, Turk T, Karadeniz EI Elekdag-Turk S, Darendeliler MA.
Physical properties of root cementum: Part 24. Root resorption of
the first premolars after 4 weeks of occlusal trauma. Am J Orthod
Dentofacial Orthop. 2014;145(5):617-625.
72. Itoiz ME, Carranza FA Jr, Cabrini RL. Histologic and histomet-
ric study of experimental occlusal trauma in rats. J Periodontol.
1963;34(4):305-314.
73. Van Böhl M, Kuijpers-Jagtman AM. Hyalinization during orthodon-
tic tooth movement: a systematic review on tissue reactions. Eur J
Orthod. 2009;31(1):30-36.
74. Hausmann E. Potential pathways for bone resorption in human
periodontal disease. J Periodontol. 1974;45(5P2):338-343.
75. Grieve WG, Johnson GK, Moore RN, Reinhardt RA, DuBois LM.
Prostaglandin E (PGE) and interleukin-­1B (IL-­1B) levels in gingival
crevicular fluid during human orthodontic tooth movement. Am J
Orthod Dentofacial Orthop. 1994;105(4):369-374.
76. Saito M, Saito S, Ngan PW, Shanfeld J, Davidovitch Z. Interleukin
1 beta and prostaglandin E are involved in the response of
|
      149
periodontal cells to mechanical stress in vivo and in vitro. Am J
Orthod Dentofacial Orthop. 1991;99(3):226-240.
77. Albrektsson T. Bone tissue response. In: Bränemark PI, Zarb GA,
Albrektsson T, eds. Tissue Integrated Prostheses: Osseointegration in
Clinical Dentistry. Chicago, IL: Quintessence; 1985:129-143.
78. Lobregad HP. Occlusion trauma and periodontal disease. An Esp
Odontoestomatol. 1976;35(5):341-358 [In Spanish].
79. Otero RL, Parodi RJ, Ubios AM, Carranza FA Jr, Cabrini RL.
Histologic and histometric study of bone resorption after tooth
movement in rats. J Periodontal Res. 1973;8(5):327-333.
80. Yoshinaga Y, Ukai T, Abe Y, Hara Y. Expression of receptor activa-
tor of nuclear factor kappa B ligand relates to inflammatory bone
resorption, with or without occlusal trauma, in rats. J Periodontal
Res. 2007;42(5):402-409.
81. Walker CG, Ito Y, Dangaria S, Luan X, Diekwisch TGH. RANKL, os-
teopontin, and osteoclast homeostasis in a hyper-­occlusion mouse
model. Eur J Oral Sci. 2008;116(4):312-318.
82. Passos SP, Zamboni SC, Takahashi FE, Macedo NL. Occlusal trauma
x periodontal tissue: action of the osteopontin and receptor acti-
vator of nuclear factor Kappa B ligand. Periodontia. 2009;19(1):75-
81 [In Portuguese].
83. Goto KT, Kajiya H, Nemoto T, et al. Hyperocclusion stim-
ulates osteoclastogenesis via CCL2 expression. J Dent Res.
2011;90(6):793-798.
84. Seifi M, Jessri M, Vahid-Dastjerdi E. Identification of a novel root
resorptive function of osteopontin gene. J Dent. 2008;5:142-149.
85. Beyron H. Optimal occlusion. Dent Clin North Am.
1969;13(3):537-554.
86. Guichet NF. Occlusion – A Teaching Manual, 2nd edn. Anaheim:
DENAR; 1977:1-7.
87. Thomas NR. Collagen as the generator of tooth eruption. In: Poole
DFG, Stack MV, eds. The Eruption and Occlusion of Teeth. London:
Butterworths; 1976:290-301.
88. McDevitt MJ. Masticatory system disorders. In: Newman MG,
Takei HH, Klokkevold PR, Carranza FA, eds. Carranza's Clinical
Periodontology, 10th edn. Philadelphia, PA: Saunders Elsevier;
2006:480-493.
89. Goldman HM. Gingival vascular supply in induced occlusal trauma-
tism. Oral Surg Oral Med Oral Pathol. 1956;9(9):939-941.
90. American Academy of Periodontology. Parameter on occlusal
traumatism in patients with chronic periodontitis. J Periodontol.
2000;71(Suppl 5):873-875.
91. Goodson JM, Tanner AC, Haffajee AD, Sornberger GC, Socransky
SS. Patterns of progression and regression of advanced destruc-
tive periodontal disease. J Clin Periodontol. 1982;9(6):472-481.
92. Heijl L, Rifkin BR, Zander HA. Conversion of chronic gin-
givitis to periodontitis in squirrel monkeys. J Periodontol.
1976;47(12):710-716.
93. Harrel SK, Nunn ME. The effect of occlusal discrepancies on peri-
odontitis. II. Relationship of occlusal treatment to the progression
of periodontal disease. J Periodontol 2001;72(4):495-505.
94. Zander HA, Polson AM. Present status of occlusion and occlusal
therapy in periodontitis. J Periodontol. 1977;48(9):540-544.
95. Sottosanti JS. A possible relationship between occlusion, root re-
sorption, and the progression of periodontal disease. J West Soc
Periodontol Periodontal Abstr. 1977;25(2):69-74.
96. Noma N, Kakigawa H, Kozono Y, Yokota M. Cementum crack forma-
tion by repeated loading in vitro. J Periodontol. 2007;78(4):764-769.
97. Lassila V, Koivumaa KK. Periodontium and occlusal disorders in
rats with experimental arteriosclerosis. A histological study. Acta
Odontol Scand. 1982;40(2):97-101.
98. Nunn ME, Harrel SK. The effect of occlusal discrepancies on peri-
odontitis. I. Relationship of initial occlusal discrepancies to initial
clinical parameters. J Periodontol 2001;72(4):485-494.
 |
150       PASSANEZI and SANT'ANA
99. Harrel SK, Nunn ME. The association of occlusal contacts with the
presence of increased periodontal probing depth. J Clin Periodontol.
2009;36(12):1035-1042.
100. Bernhardt O, Gesch D, Look JO, et al. The influence of dynamic
occlusal interferences on probing depth and attachment level:
results of the study of Health in Pomerania (SHIP). J Periodontol.
2006;77(3):506-516.
101. de Oliveira Diniz CK, Corrêa MG, Casati MZ, et al. Diabetes melli-
tus may increase bone loss after occlusal trauma and experimental
periodontitis. J Periodontol. 2012;83(10):1297-1303.
102. Campos MLG, Correa MG, Nociti FH Jr, Casati MZ, Sallum EA,
Sallum AW. Cigarette smoke inhalation increases the alveolar bone
loss caused by primary occlusal trauma in a rat model. J Periodontal
Res. 2014;49(2):179-185.
103. Pihlstrom BL, Anderson KA, Aeppli D, Schaffer EM. Association
between signs of trauma from occlusion and periodontitis. J
Periodontol. 1986;57(1):1-6.
104. Lindhe J, Ericsson I. The effect of elimination of jiggling forces
on periodontally exposed teeth in the dog. J Periodontol.
1982;53(9):562-567.
105. Kaufman H, Carranza FA, Endres B, Newman MG, Murphy N. The
influence of trauma from occlusion on the bacterial repopulation
of periodontal pockets in dogs. J Periodontol. 1984;55(2):86-92.
106. Branschofsky M, Beikler T, Schäfer R, Flemming TF, Lang H.
Secondary trauma from occlusion and periodontitis. Quintessence
Int. 2011;42(6):515-522.
107. Jin LJ, Cao CF. Clinical diagnosis of trauma from occlusion and
its relation with severity of periodontitis. J Clin Periodontol.
1992;19(2):92-97.
108. Kleber BM, Schenk HJ. Etiology of gingival recession. Dtsch
Zahnarztl Z. 1989;44(11):845-848 [In German].
109. Solnit A, Curnette DC. Occlusal Correction. Principles and Practice.
Chicago, IL: Quintessence; 1988:365-381.
110. Solnit A, Stambaugh RV. Treatment of gingival defects by occlusal
therapy. Int J Periodontics Restorative Dent. 1983;3(3):38-55.
111. Harrel SK, Nunn ME. The effect of occlusal discrepancies on gingi-
val width. J Periodontol. 2004;75(1):98-105.
112. Krishna Prasad D, Sridhar Shetty N, Solomon EG. The influence of
occlusal trauma on gingival recession and gingival clefts. J Indian
Prosthodont Soc. 2013;13(1):7-12.
113. Budtz-Jorgensen E. A 3-­month study in monkeys of occlusal dys-
function and stress. Scand J Dent Res. 1980;88(3):171-180.
114. Budtz-Jorgensen E. Bruxism and trauma from occlusion: an experimen-
tal model in Macaca monkeys. J Clin Periodontol. 1980;7(2):149-162.
115. Takeuchi N, Ekuni D, Yamamoto T, Morita M. Relationship be-
tween the prognosis of periodontitis and occlusal force during the
maintenance phase-­a cohort study. J Periodontal Res. 2010;45(5):
612-617.
116. Bhola M, Cabanilla L, Kolhatkar S. Dental occlusion and peri-
odontal disease: what is the real relationship? J Calif Dent Assoc.
2008;36(12):925-930.
117. Fleszar TJ, Knowles JW, Morrison E, Burgett F, Nizlle R, Ramfjord
SP. Tooth mobility and periodontal therapy. J Clin Periodontol.
1980;7(6):495-505.
118. Burgett F, Ramfjord S, Nissle R, Morrison E, Charbeneau T, Caffesse
R. A randomized trial of occlusal adjustment in the treatment of
periodontitis patients. J Clin Periodontol. 1992;19(6):381-387.
119. Foz AM, Artese HPC, Horliana ACRT, Pannuti CM, Romito GA.
Occlusal adjustment associated with periodontal therapy – a sys-
tematic review. J Dent. 2012;40(12):1025-1035.
120. Santamaria MP, Cerqueira MROV, Feitosa DS, et al. Relationship
between trauma from occlusion and periodontal disease. Case re-
port. PerioNews 2009;3(1):25-29 [In Portuguese].
121. Passanezi E, Sant'Ana ACP, Rezende MLR, Greghi SLA, Janson WA.
Periodontal Biological Width – Principles for Periodontal, Prosthetic
and Esthetic Reconstruction. São Paulo: Artes Médicas; 2011 [In
Portuguese].
122. Waerhaug J. Discussion of Dr. Davies paper. In: Shanley D, ed.
Efficacy of Treatment Procedures in Periodontics. Chicago, IL:
Quintessence; 1980:94-95.
123. Waerhaug J. Discussion of Dr. Ellegaard paper. In: Shanley D,
ed. Efficacy of Treatment Procedures in Periodontics. Chicago, IL:
Quintessence; 1980:142-147.
124. Campos A Jr, Passanezi E, Nahás D, Chiapinotto GA, Lopes ES.
Effect of occlusion in the periodontium: comparative photoelas-
tic analysis of two types of occlusion (tooth-­to-­tooth and one
tooth-­to-­two teeth). I. Normal periodontium. RGO (Porto Alegre).
1989;37(2):335-338 [In Portuguese].
125. Chiapinotto GA, Passanezi E, Campos A Jr, Nahás D, Janson WA.
Periodontal photoelastic distribution of internal stress after sec-
tioning of the mandibular first molar. Estomatol Cult. 1986;16(1):26-
31 [In Portuguese].
126. Nascimento A, Sallum AW. Periodontal changes in dis-
tant teeth due to trauma from occlusion. J Periodontal Res.
1975;10(1):42-48.
127. Nogueira Filho GR, Fróes Neto EB, Casati MZ, et al. Nicotine
effects on alveolar bone changes induced by occlusal trauma: a
histometric study in rats. J Periodontol 2004;75(3):348-352.
128. Pereira LJ, Gazolla CM, Magalhães IB, et al. Treatment of chronic
periodontitis and its impact on mastication. J Periodontol.
2011;82(2):243-250.
129. SotresVázquez JW, López EG, Ruiz AOB, García LOR, Fundora DR.
A study on periodontal disease and oral hygiene in non-­occluding
teeth. Rev Cubana Estomatol 2005;42(3): Available at: http://scielo.
sld.cu/pdf/est/v42n3/est03305.pdf. [In Spanish].
How to cite this article: Passanezi E, Sant'Ana ACP. Role of
occlusion in periodontal disease. Periodontol 2000.
2019;79:129–150. https://doi.org/10.1111/prd.12251