Periodontology 2000, Vol.
34, 2004, 151±164 Copyright # Blackwell Munksgaard 2004
Printed in Denmark. All rights reserved
Occlusal analysis, diagnosis and
management in the practice of
periodontics
William W. Hallmon & Stephen K. Harrel
Occlusal trauma is de®ned as injury resulting in tissue
changes within the periodontal attachment apparatus
as a result of occlusal forces (1). The controversy that
surrounds this condition including recognition, diag-
nosis, effects, and management, has been widely
debated since the early part of the 20th century (8,
48, 97, 98). Since occlusal trauma can only be con-
®rmed histologically, the clinician is challenged to
use clinical and radiographic surrogate indicators in
an attempt to facilitate and assist in its diagnosis.
This chapter will focus on the role of occlusal
analysis, tooth mobility and occlusal therapy in the
clinical practice of periodontics. Diagnostic and ther-
apeutic approaches and effects on treatment out-
comes will be reviewed and discussed. In an
attempt to facilitate this process, the following ques-
tions will be addressed:
 What is occlusal trauma?
 What is the role of occlusion in the pathogenesis of
periodontitis?
 How is occlusal trauma detected clinically?
 What is abfraction and are there data to support a
role for occlusion in its development?
 What methods are used to detect hypermobility of
teeth? Of what value are assessments of tooth mobi-
lity in the management of periodontitis patients?
 Under what clinical circumstances is occlusal
adjustment indicated? Following occlusal adjust-
ment, what clinical outcomes are expected and
how are they evaluated?
What is occlusal trauma?
The International Workshop for a Classi®cation of
Periodontal Diseases and Conditions in 1999 evalu-
ated the available materials relating to the effects of
PERIODONTOLOGY 2000
occlusion on the periodontium and the role that
occlusion may play in periodontal disease. The con-
sensus report of the International Workshop group
evaluating occlusion adopted the following working
de®nitions for occlusal trauma. These de®nitions are
critical to the clinical evaluation, diagnosis, and
treatment of occlusion in periodontal disease (1).
Occlusal trauma ± Injury resulting in tissue
changes within the attachment apparatus as a result
of occlusal force (s).
Primary occlusal trauma ± Injury resulting in tissue
changes from excessive occlusal forces applied to a
tooth or teeth with normal support (Fig. 1). It occurs
in the presence of: 1) normal bone levels, 2) normal
attachment levels, and 3) excessive occlusal force (s)
(Fig. 1).
Secondary occlusal trauma ± Injury resulting in
tissue changes from normal or excessive occlusal
forces applied to a tooth or teeth with reduced sup-
port (Fig. 2). It occurs in the presence of: 1) bone loss,
2) attachment loss, and 3) normal/excessive occlusal
force (s) (Fig. 2).
What is the role of occlusion in the
pathogenesis of periodontal
disease?
Occlusal trauma has been associated with periodon-
tal disease for over 100 years. In 1901, Karolyi (48)
reported an apparent association between excessive
occlusal forces and periodontal destruction. In 1917
and 1926, Stillman (96, 97) indicated that excessive
occlusal force was the primary cause of periodontal
disease. Stillman felt that occlusal forces must be
controlled in order to prevent and treat periodontal
151
Hallmon & Harrel
Fig. 1. Primary occlusal trauma results from excessive
occlusal forces applied to a tooth with normal support.
Note that the center of rotation is near the middle of the
root. (From: T. G. Wilson Jr. et al. Advances in periodontics,
1992. Printed with permission, Quintessence Publishing
Co., Inc.).
Fig. 2. Secondary occlusal trauma results from excessive
occlusal forces applied to a tooth with reduced support.
Note that the center of rotation is in the apical third of the
root. (From: T. G. Wilson Jr. et al. Advances in periodontics,
1992. Printed with permission, Quintessence Publishing
Co., Inc.).
152
disease. These early reports created a background for
controversy that continues to this day:
 Is there an association between excessive occlusal
forces and the progression of periodontal disease?
 How are occlusal forces evaluated in a clinical
setting and at what point does an occlusal force
become ``excessive''?
 When an occlusal force is detected and the deter-
mination is made that it is excessive, when should
treatment be initiated and how should this treat-
ment be accomplished?
To effectively evaluate the role of occlusal trauma
in periodontal disease, it is necessary to review stu-
dies that have used human autopsy material or ani-
mal models. As previously stated, several early
authors felt that occlusal forces were the initiating
factor in periodontal disease and led to the ongoing
progression of the periodontal lesion. The associa-
tion between occlusion and periodontal disease was
based on clinical observation as opposed to scienti®c
evaluation. In an attempt to demonstrate this rela-
tionship, several animal studies on sheep and mon-
keys were conducted. These studies were an attempt
to determine the response of the periodontium to
occlusal forces both clinically and histologically (8,
98). The authors of these studies felt that their ®nd-
ings showed that excessive occlusal forces were a
contributing factor in the progression of periodontal
disease. By the end of the 1930's, many practitioners
felt that excessive occlusal forces (occlusal trauma)
were a causative factor in periodontal disease, that
occlusal adjustment was a necessary part of period-
ontal treatment, and that occlusal discrepancies
should be prophylactically treated to prevent period-
ontal disease (9, 60).
The role of excessive occlusal forces in the patho-
physiology of periodontal disease has been disputed
by several researchers. Orban & Weinmann in 1933
(70) and Weinmann in 1941 (109), using human
autopsy material, evaluated the effect of excessive
occlusal forces on the periodontium. They concluded
that there was no relationship between occlusal
forces and periodontal destruction and suggested
that occlusal forces played no part in periodontal
destruction. Instead, they indicated that gingival
in¯ammation extending into the supporting bone
was the cause of periodontal destruction.
During the 1950's and 1960's, further animal
research using rats, monkeys, and dogs evaluated
the effect of occlusal forces on the periodontium
(13, 20, 59, 73, 110). The designs of these studies were
more controlled than most of the earlier investiga-
tions. The results from these studies did not support

the concept that excessive occlusal force was a cau-
sative agent of periodontal destruction. Further,
many of the studies showed no obvious association
between occlusal forces and periodontal disease.
In contrast to the above noted studies, at approxi-
mately the same time Glickman and co-workers pub-
lished studies based on animal models and human
autopsy material. Animal studies using a heavy
occlusal contact created by placing a ``high'' restora-
tion were performed utilizing dogs and monkeys (30,
33). While these studies showed no evidence of initia-
tion of periodontal disease by occlusal contacts, the
authors felt that a study using rhesus monkeys
demonstrated a phenomenon described as an
``altered pathway of destruction'' when excessive
occlusal forces were present (31). This altered path-
way of destruction was described as a change in the
orientation of the periodontal and gingival ®bers
which occurred in the presence of excessive occlusal
forces, allowing gingival in¯ammation to extend
along the periodontal ligament. The altered pathway
of destruction was postulated to cause vertical bony
defects due to in¯ammation and bony destruction
following the periodontal ligament. Another animal
study (34) showed that bone in bifurcation areas was
stressed by excessive occlusal force and that bone
loss in the furcation area was related to these forces.
Glickman and coworkers also reported evidence of
an altered pathway of destruction in studies utilizing
human autopsy material (30).
From these studies, Glickman and co-workers con-
cluded that excessive occlusal forces in the presence
of plaque-associated in¯ammation caused a change
in the alignment of the periodontal ligaments, allow-
ing an altered pathway of in¯ammation/destruction,
resulting in vertical bony defects. Because there were
two separate pathologic processes working together
to cause bone loss, the process was termed a ``co-
destructive'' effect. Glickman and coworkers sum-
marized their work in a series of review articles (25,
27±29, 32). These papers indicated that excessive
occlusal forces (trauma from occlusion) were a co-
destructive force in the presence of gingival in¯am-
mation and could lead to vertical osseous defects.
Based on these observations, the use of occlusal
adjustment was advocated as part of the treatment
for existing periodontal disease. Because no evidence
existed that excessive occlusal forces initiated peri-
odontal disease, occlusal adjustment to prevent per-
iodontitis was not advocated.
Waerhaug (103±105) evaluated a large number of
human autopsy specimens to determine the relation-
ship of subgingival plaque to the morphology of oss-
Occlusal analysis, diagnosis and management in periodontics
eous defects and any associations with the presence
or absence of excessive occlusal forces. He found that
the ``plaque front'' (i.e. the apical border of the sub-
gingival plaque) was always in very close approxima-
tion to the epithelial attachment level and always
followed the morphology of the bony defect. In addi-
tion, the relationship of the plaque level between
adjacent teeth (either at the same or different apico-
coronal levels) was associated with either horizontal
or vertical interproximal bone loss. He also observed
that excessive occlusal forces bore no relationship to
the underlying bony defect and that vertical defects
were found equally around traumatized and non-
traumatized teeth. Waerhaug concluded that bone
loss was always associated with the downgrowth of
plaque and there was no relationship between exces-
sive occlusal forces and vertical bone loss.
The use of human autopsy material to study the
effect of occlusal forces has the inherent problem
that rarely if ever is there a true understanding of
the patient's occlusal relationship that existed in life.
Some knowledge can be obtained by studying the
wear patterns on the teeth but there is no assurance
that the teeth actually occluded in the assumed man-
ner or that wear facets represent current and active
occlusal trauma. Therefore, any conclusion or obser-
vations based on autopsy material concerning the
role that occlusal forces may or may not have on
the progression of periodontal disease has to be
questioned. A single histologic study (95) evaluated
the occlusal relationships of four patients prior to the
removal of their jaws for cancer therapy. This study
did not show a relationship between occlusal forces
and periodontal disease. However, it is unclear if
excessive occlusal forces existed in these patients.
Two extensive animal studies were performed in
the 1970s. These studies evaluated the effect of pla-
que and excessive occlusal forces in the animal mod-
els utilized. Unlike most of the earlier investigations,
stringent scienti®c controls and designs were used.
One series of studies were conducted by Polson and
co-workers (47, 71, 76±83) and a different series of
studies was performed by Lindhe and co-workers
(17±19, 55±57, 67, 68, 100±102). Polson's group used
squirrel monkeys and mesial±distal compression
forces comparable to orthodontic forces whereas
Lindhe's group used beagle dogs and applied buc-
cal±lingual forces using a high occlusal contact and a
®nger spring. Both groups investigated excessive
occlusal forces in the presence and absence of pla-
que.
These studies yielded similar results despite the
different animal models and the different excessive
153
Hallmon & Harrel
occlusal forces used. Excessive occlusal forces in the
absence of plaque were found to cause loss of bone
density and mobility of the affected tooth but no
evidence was found that the occlusal forces alone
could cause attachment loss. When the excessive
occlusal forces were removed, it was noted that the
loss of bone density was reversible. In the presence of
plaque, in¯ammation of the gingiva and periodontal
supporting structures were noted and in the pre-
sence of excessive occlusal forces and plaque
together there was an indication that more bone
density was lost in both animal models. In the beagle
dog model there was evidence of attachment loss
when plaque and excessive occlusal forces were both
present. These results were not observed in the squir-
rel monkey model.
These two series of studies exhaustively evaluated
the relationship of occlusal forces and plaque in an
animal model. They both concluded that there was
no evidence indicating that excessive occlusal force
alone will cause loss of attachment. The studies on
beagle dogs showed that under speci®c circum-
stances there may be attachment loss when plaque
and excessive occlusal forces are both present. Both
studies agreed that the removal of plaque and the
control of in¯ammation will stop the progression of
periodontal disease whether or not excessive occlusal
forces are present.
Human studies
Only a few studies have evaluated the effects of
excessive occlusal forces in humans. There are many
ethical dif®culties associated with the non-treatment
of diagnosed periodontal disease that complicate
studying the effect of occlusion on the progression
of periodontal disease. The gold standard of clinical
research is the randomized controlled clinical trial.
These studies require prospective comparisons of
different treatment methods on treatment outcomes.
However, in order to compare the combined effects
of excessive occlusal forces and periodontal disease,
it would be necessary to treat one group of patients
while leaving the other group untreated. This creates
an unacceptable ethical dilemma due to the known
deleterious effects of the non-treatment of period-
ontal disease. The World Workshop in Periodontics
stated, ``Prospective studies on the effect of occlusal
forces on the progression of periodontitis are not
ethically acceptable in humans'' (23). As a result,
human studies are limited to retrospective and
observational research.
154
It has been reported that patients who have occlu-
sal discrepancies have no more severe periodontal
destruction than do patients without occlusal discre-
pancies (46, 51, 74, 84, 85, 94). However, it has also
been reported that molars with furcation invasion
and mobility have greater probing depths than
molars that are clinically nonmobile (106). The
increased mobility noted in this study may have been
due to occlusal factors or to greater loss of bony
support associated with the furcation involvement.
Due to the inability to determine whether occlusal
factors or bone loss was initially present, it is impos-
sible to draw a clear relationship between occlusal
discrepancies, mobility, and probing depths from
this study. Other studies reported that patients who
received occlusal adjustment as part of their period-
ontal therapy had greater attachment gain than
patients who did not receive occlusal adjustment
(10, 21). These studies suggest that occlusal adjust-
ment should be performed, where indicated, as a
part of periodontal treatment. A report on risk factors
for periodontal destruction indicated that mobility
and parafunctional habits that are not treated with
a biteguard are associated with increased attachment
loss, worsening prognosis, and tooth loss (61). This
study seems to indicate that untreated (i.e. no bite-
guard) parafunctional habits may contribute to
increased periodontal breakdown. Another study
has shown that mobile teeth treated with regenera-
tive surgery did not respond as well as nonmobile
teeth (14). However, no association was drawn
between mobility and occlusal forces.
In a series of retrospective reports, private practice
patients were evaluated who were diagnosed with
advanced periodontal disease and had a comprehen-
sive treatment plan recommended that included sur-
gical treatment. Occlusal adjustment was
recommended if signi®cant occlusal discrepancies
were detected. Some of these patients self-selected
to not have any periodontal treatment performed
(untreated group). Other patients had only nonsur-
gical periodontal treatment performed (partially
treated group). Others followed through with all
recommended periodontal treatment including sur-
gery (fully treated group). The effect of occlusal dis-
crepancies was studied in each of these groups using
the individual tooth as the experimental unit (40, 41,
66). This means that the progression of periodontal
destruction or the improvement of the periodontium
for each tooth was followed over time. This study
design allowed for the evaluation of teeth with occlu-
sal discrepancies versus teeth without occlusal dis-
crepancies rather than comparing patients with

occlusal discrepancies vs. patients without occlusal
discrepancies. This experimental approach differs
from most past studies where the patient was the
experimental unit and the changes in probing depth
or attachment levels were expressed as the ``patient
mean.'' Using the patient mean may tend to mask
changes that are occurring at the more active sites
and, thereby, give results that do not re¯ect what is
actually occurring during localized disease progres-
sion.
These studies found that teeth with occlusal dis-
crepancies had deeper presenting probing depths
and worse prognoses than those teeth that did not
have occlusal discrepancies. Further, when teeth
with occlusal discrepancies were followed over time,
a signi®cant increase in probing depth and a worsen-
ing of prognosis was noted when compared to teeth
without occlusal discrepancies. Additionally, teeth in
the partially treated group that had received occlusal
adjustment showed a slowing of the progression of
periodontal destruction when compared to teeth
with occlusal discrepancies from the same group that
had not had occlusal adjustment. It was concluded
that occlusal discrepancies appear to be a signi®cant
risk factor that contribute to more rapid periodontal
destruction and that treatment of occlusal discrepan-
cies seemed to slow periodontal destruction. The
authors postulated that the reason for the difference
in their ®ndings and those of previous studies was
the use of the individual tooth as the experimental
unit, which they felt yielded a more accurate assess-
ment of the effect of occlusal discrepancies on the
periodontium (40, 41, 66).
In summary, animal and human studies have indi-
cated some association between occlusal discrepan-
cies/occlusal trauma and changes in the periodontal
supporting structures. Extensive animal studies have
shown that occlusal trauma does have an effect on
the periodontal supporting structure but does not
initiate breakdown of the attachment apparatus with
resulting measurable attachment loss. The human
studies have indicated that treating occlusal discre-
pancies may lead to better results following period-
ontal treatment. A study using a more contemporary
statistical analysis and utilizing individual sites as the
basis for comparison, has shown a strong association
between occlusal discrepancies and deeper pockets
(66).
Furthermore, existing research does not establish a
cause-and-effect relationship between occlusion and
periodontal disease. However, there are strong data
to indicate that occlusion is a potential risk factor
for periodontal breakdown and that controlling this
Occlusal analysis, diagnosis and management in periodontics
risk factor may slow the progression of periodontal
destruction and improve the results of periodontal
treatment outcomes. As is the case with all risk factors
such as smoking, oral hygiene, and systemic factors,
the effect of occlusion on periodontal disease needs
to be minimized by recognizing the risk, diagnosing
the existence of the risk factor, and minimizing the
risk by the use of various treatment modalities such
as selective grinding, orthodontics, and/or occlusal
appliances.
How is occlusal trauma detected
clinically?
Because trauma from occlusion is de®ned and diag-
nosed on the basis of histologic changes in the per-
iodontal supporting structure, a diagnosis of occlusal
trauma is impossible without block section biopsy.
Because this is clearly impractical for the clinical
practice of periodontics, the clinician must rely on
the clinical signs of potential occlusal trauma. The
following discussion is based for the most part on
clinical experience due to the extreme paucity of
written material on the subject.
Most periodontal training programs and the Amer-
ican Board of Periodontology require an analysis of
the patient's occlusal relationship as part of a com-
prehensive periodontal examination. Often the Angle
classi®cation is part of this analysis (5). However, the
Angle classi®cation was designed to quantify the ske-
letal relationship between the maxilla and the mand-
ible. While important in determining the growth
pattern of adolescents and recording a starting point
for orthodontic treatment, the Angle classi®cation
has little bearing on the occlusal relationship that
exists between various cusp surfaces. The relation-
ship between cusps is the most important factor in
the transmittal of occlusal forces to the periodontal
supporting structures. Therefore, it is the relation-
ship between opposing cusps that is the most impor-
tant aspect of occlusion and any role it may play in
the progression of periodontal destruction or the
outcomes of periodontal treatment.
The relationship of opposing cusps is usually deter-
mined by using a composite of means that generate a
list of data that must be correlated by the practitioner.
The compiling of data on the relationship of opposing
cusps usually starts with the detection of occlusal
discrepancies. Typically, the initial contact between
the teeth is detected by gently manipulating the
patient's mandible into a ``retruded'' position (15,
26). There is little agreement as to what is meant by
155
Hallmon & Harrel
Fig. 3. (a) Initial contact in centric relation. (b) Centric
slide between centric relation and centric (acquired cen-
tric; habitual) occlusion. (c) Centric (acquired centric;
a retruded position of the mandible but on a clinical
basis, an attempt is made to guide the mandible into
a position where both right and left condyles are
®rmly placed in the fossa of the temporomandibular
joint. This position is one that is felt by the practi-
tioner rather than con®rmed by any type of device or
instrument and is therefore subjective in nature.
Once the practitioner feels that a retruded position
has been achieved, the patient is asked to close until
the patient feels the ®rst contact between the teeth
(Fig. 3a). This contact point is veri®ed by the exam-
iner either by eye, inked marking paper or ribbon, or
both. This initial contact in a retruded position has
been described as contact in ``centric relation''. Fol-
lowing the establishment of the initial contact, the
patient is asked to continue to close the jaws together
until maximum contact between the teeth is
achieved. The jaw position of maximum tooth con-
tact is often termed ``centric occlusion''. The position
of maximum tooth contact is assumed to be the
position that the patient will naturally move to as
the most comfortable or habitual position (Fig. 3b,c).
The distance that the patient moves between the
retruded initial contact and the point of maximal
tooth contact is termed the slide between the posi-
tions of centric relation and centric occlusion. This
slide is often described as the ``centric relation/cen-
tric occlusion slide'' or ``CR/CO shift''. This slide is
usually recorded as the length of the slide in the
anterior, vertical, and lateral planes (26).
No direct correlation with histologic evidence of
trauma from occlusion has been shown between the
presence of a slide between the contacts in centric
relation and the contacts in centric occlusion. How-
ever, indirect clinical evidence of a more rapid pro-
gression of periodontal destruction as evidenced by
increased probing depths has been shown to occur in
patients with untreated periodontal disease (40, 41,
66). While this ®nding cannot be directly correlated
with animal research showing histologic evidence of
156
habitual) occlusion, demonstrating maximum intercus-
pation or contact of the teeth of the opposing arches.
(Courtesy Dr. J. Y. Cho).
in¯ammation and bone rarefaction in the presence
of experimental occlusal stress and, in beagle dogs,
the loss of attachment when plaque is present in
addition to the experimental occlusal stress, there
is a likelihood that a similar process is occurring in
humans as in the beagle dog model. If this assump-
tion is true, then at least in certain cases the histo-
logic lesion of occlusal trauma is likely to be present
in periodontal patients who have occlusal interfer-
ences.
Other clinical ®ndings that have been associated
with trauma from occlusion are tooth mobility and
wear patterns on the occlusal surface of the teeth
(Table 1). These clinical ®ndings are extremely dif®-
cult to correlate with occlusal contacts. In the case of
mobility, many other factors such as loss of attach-
ment can affect the presence and severity of the mobi-
lity. In the case of occlusal wear patterns, it is often
impossible to determine whether they are caused by
functional or parafunctional habits that are occur-
ring at present or whether they may be associated
with episodes of bruxism that have occurred in the
past. If bruxism has occurred in the past, what if any
part did it play in the current clinical evidence of
periodontal breakdown? The practitioner must eval-
uate and record all of these ®ndings so that a picture
of the occlusal stresses being placed on the period-
ontium can be assessed and to help form an assump-
tion of the occurrence of trauma from occlusion.
Table 1. Clinical indicators of occlusal trauma
Clinical indicators of occlusal trauma may include one
or more of the following:
1. Fremitus
2. Mobility (progressive)
3. Occlusal discrepancies
4. Wear facets in presence of other indicators
5. Tooth migration
6. Fractured tooth/teeth
7. Thermal sensitivity
 Occlusal analysis, diagnosis and management in periodontics

What's abfraction and are there data

to support a role of occlusion in its
development?
Abfraction has been de®ned as the ``pathological loss
of hard tooth substance by biomechanical loading
forces'' (37). The lesions have been described as angu-
lar or wedge-shaped defects that occur at the cemen-
toenamel junction of affected teeth as a result of
¯exure and eventual fatigue of enamel and dentin
(7) (Fig. 4). The prismatic structure of enamel is strong
Fig. 5. Note the generalized loss of cervical tooth sub-
in compression, but vulnerable in areas of tension, stance and accompanying marginal tissue recession. The
accounting for the resultant morphology of the pro- patient admitted (and demonstrated) aggressive horizon-
posed lesion (52). It is further noted that occlusal tal toothbrushing.
loads which generate cervical ¯exure may disrupt
hydroxyapatite crystal bonds, and result in micro-
fracture and eventual loss of associated enamel (53).
Noncarious hard-tissue cervical lesions (NCLs)
have been classi®ed as abrasive, erosive, corrosive,
abfractive or combined (38). In contrast to abfrac-
tion, abrasion represents a pathologic loss of tooth
substance resulting from biomechanical wear and is
exempli®ed by improper or overzealous toothbrush-
ing. This condition is generally accompanied by mar-
ginal tissue recession and may affect one or more
teeth (75) (Fig. 5). Erosion is a chemically induced
loss of tooth substance that occurs primarily through
acid dissolution (44) (Fig. 6). Attrition is de®ned as
the physiologic wearing away of a substance or struc- Fig. 6. The maxillary right central incisor shows erosion as
a result of chemically induced loss of enamel. (Courtesy
ture, such as the teeth (3). This typically affects the
Dr. Terry D. Rees).
occlusal and incisal surfaces of the teeth and may
result from functional or parafunctional wear, man-
ifesting as facets (7). These highly polished surfaces
may appear on marginal, transverse and oblique
Is there evidence for a role of
ridges, and on cusps and restored surfaces (Fig. 7). occlusal loading in the genesis of
noncarious cervical tooth loss?
The presence of lesions consistent with those
described as abfraction have been reported to
increase in size and depth with age of affected indi-
viduals (54). In a study of 913 subjects, 23% pre-
sented with such defects. Sixty-®ve percent of the
affected individuals had con®rmed parafunction as
compared to 35% who did not (35). Another study
reported that 96% of teeth with noncarious cervical
lesions also presented evidence of occlusal discre-
pancies (86). In comparing canine-guidance with
group-function occlusal relationships, abfraction-
like lesions were observed six times more often in
Fig. 4. Maxillary right ®rst premolar presents a well-deli-
the latter group, suggesting that increased occlusal
neated noncarious hard-tissue cervical lesion consistent tooth contact during lateral excursion favored the
with abfraction. occurrence of these lesions (87).

157
Hallmon & Harrel
Fig. 7. The mandibular ®rst molar presents facets on the
mesiobuccal and distobuccal cusps and on the amalgam
restoration at the mesiolingual surface.
In addition to clinical observations, evidence sug-
gesting a role of occlusal loading in development of
abfraction-like lesions comes from various stress and
strain studies. These include articulated study mod-
els, strain-gauge studies, ®nite element stress analy-
sis and photoelastic stress analysis (88). Such studies
have shown that controlled loading (500 N) applied
to inner inclines of the buccal and lingual cusps of
mandibular premolars resulted in stress values
exceeding the failure stress of enamel (89). This load-
ing corresponds to that anticipated during excursive
contacts in group-function occlusal relationships.
These studies are principally in vitro investigations
that fail to take into account the role of the period-
ontal ligament and bone during the course of occlusal
loading. It is important to note that in a strain gauge
study of maxillary incisors in healthy volunteers,
large cervical surface strains were observed (65).
In a clinical investigation of the characteristics and
prevalence of abfraction-like lesions in a U.S. popu-
lation with 103 noncarious cervical lesions, the vast
majority of the lesions were strongly suspected as
being the result of toothbrush abrasion. A small sub-
set (i.e. 15 lesions) was deemed the result of some
other phenomenon. Six (40%) of these teeth mani-
fested premature occlusal contacts. Compared to
control teeth without NCLs, affected teeth did not
signi®cantly differ in terms of wear facets or occlusal
contacts. No NCLs were reported on lingual surfaces.
However, the authors cautioned that teeth with non-
carious wedge-shaped lesions should be carefully
158
evaluated for occlusal correction or bite-splint ther-
apy to address interferences that may contribute to
tooth ¯exure (75). In a separate case study of 52
modern human skulls, occlusal ®ndings failed to
provide evidence for abfraction (43).
There is a strong contention that NCLs represent a
multifactorial phenomenon. It has been proposed that
the presence of occlusal stresses in combination with
acidic substances may result in greater damage than
either alone (39). However, one clinical question
remains ± Why does abfraction occur on the buccal/
facial surfaces, with only rare reports of lingual lesions?
In summary, available evidence suggests a plausi-
ble explanation for abfraction. It is equally apparent
that this diagnosis is not absolute. In cases where the
therapist is confronted with NCLs, toothbrushing
habits and occlusal relationships should be thor-
oughly evaluated. Restorative and/or periodontal
plastic surgical intervention should be preceded by
control of any habits and/or untoward occlusal load-
ing which may adversely affect predictable long-term
treatment outcome.
What methods are used to detect
hypermobility of teeth?
Assessment of tooth mobility constitutes a basic part
of the comprehensive periodontal examination (2, 4).
Hypermobility occurs in response to applied force
and is dependent upon its direction, frequency, mag-
nitude, distribution and type (2, 90, 107). The mobi-
lity status of the dentition has traditionally been
evaluated by visual assessment, using two instrument
handles to apply alternating luxating force orofacially
(Fig. 8). In 1950, Miller (63) described a mobility index
based on this approach (Table 2). Variations and modi-
Fig. 8. One way to assess tooth mobility is by using two
instrument handles applied to the tooth and applying
alternating luxating force orofacially.

Table 2. Miller Mobility Index (63)
1. The first distinguishable sign of movement
greater than normal (physiologic)
2. Movement of the tooth which allows the
crown to move 1 mm from its normal position
in any direction
3. Teeth which may be rotated or depressed in
their alveoli
®cations of this index are used extensively throughout
dentistry, and especially periodontics (11, 20).
Clinical assessments of tooth mobility derived by
this means are somewhat arbitrary and dependent
on examiner subjectivity and interpretation. As a
result, they do not usually discriminate well between
small mobility increments (99). Consequently, a
means of more precise and objective measurement
of tooth mobility has been pursued and includes
mechanical, electronic and optical devices, and laser
Doppler vibrometry (12, 64, 69, 72, 92). Despite
objective approaches striving to standardize tooth
mobility evaluation, such devices by and large have
not been well accepted for use in clinical practice.
More recently, the Periotest1 (Gulden-Medizintech-
nik, Bensheim, Germany), a device resembling a den-
tal handpiece, has gained favor in evaluating and
monitoring tooth mobility and clinical success of
dental implants (6, 93). The instrument is applied
orthoradially to the center of the anatomic crown,
delivering a standardized percussive force. Recorded
values range from 0 to 100, and correspond to time in
milliseconds taken for the supporting structure(s) to
respond to impact deceleration, thus assessing
rebound dynamics and damping characteristics of
the periodontium (42, 58, 91, 108). It is interesting
to note that no signi®cant change in numeric Peri-
otest1 values has been observed when comparing
baseline values with those recorded after the initial
phase of periodontal therapy (16). This would sug-
gest that Periotest1 mobility evaluation relates pri-
marily to the amount of bone loss (i.e. support) about
teeth being evaluated and may not be directly related
to traditional tooth mobility. Contraindications to
use of this instrument include acute in¯ammation,
traumatic subluxation and dental implants in the
initial phases of healing (91).
One of the diagnostic challenges confronting the
clinician is to determine the associative cause of
the observed tooth mobility. It is widely recognized
that some degree of tooth mobility is always present
in the healthy dentition. This has been termed
physiologic (normal) tooth mobility, in contrast to
Occlusal analysis, diagnosis and management in periodontics
pathologic (abnormal) mobility. Factors that have
been associated with tooth mobility include period-
ontal status of the teeth (e.g. in¯ammation, loss of
clinical attachment/bone), periodontal surgery,
occlusal trauma, pregnancy, and pathologic pro-
cesses affecting the jaws/teeth (22, 24, 36, 49, 50).
More recently, it has been proposed that the desig-
nators ``pathologic tooth mobility'' and ``adaptive
tooth mobility'' may be helpful in addressing mobi-
lity status and thus, facilitate management and
maintenance approaches in affected patients (4).
Stability of tooth mobility appears acceptable in
the absence of confounding variables, but progres-
sive mobility is a concern and should be addressed
by controlling in¯ammation, occlusal adjustment
and considering a stabilization appliance or splinting
as indicated. The long-term therapeutic objective is
to maintain the health, stability, comfort and func-
tion of the patient's natural dentition (or implants).
Of what value are assessments of
tooth mobility in the management
of patients with periodontitis?
A limited number of human studies have suggested
that tooth mobility may be associated with greater
attachment loss, probing depth and bone loss when
compared to nonmobile teeth (45, 46, 106). It is dif-
®cult to determine from these studies whether tooth
mobility was a result of the associated periodontal
disease process or if, in some way, it contributed
etiologically. Two studies reported that teeth exhibit-
ing a combination of furcation invasion and tooth
mobility were at risk of sustaining greater attachment
loss as compared to nonmobile teeth or teeth with
furcation invasion alone (45, 106). In a longitudinal
study by McGuire & Nunn (62), tooth mobility was
associated with non-improving prognoses of affected
teeth. Other studies have examined the effects of
tooth mobility on periodontal treatment outcomes.
In an 8-year follow-up study in which patients
received scaling, oral hygiene instruction, occlusal
adjustment, periodontal surgery (subgingival curet-
tage, modi®ed Widman ¯ap or pocket elimination)
and 3-month maintenance, baseline and annual
assessments were made of probing depth, attach-
ment level and tooth mobility. Results indicated that
pockets associated with mobile teeth did not respond
as positively (i.e. clinical attachment level gain) to
therapy as ®rm teeth. This in¯uence was observed
by the end of the ®rst year and became more
pronounced by the second year, with only minor
159
Hallmon & Harrel

changes occurring throughout the duration of the 8- between centric relation and centric occlusion con-
year clinical trial. It should be noted that although tribute to the progression of periodontal destruction
clinically mobile teeth could be effectively treated and that the presence of mobility will negatively
and maintained, better responses (i.e. clinical attach- affect the outcome of periodontal treatment. What
ment level gain) were generally observed in associa- part each of these actually plays in periodontal
tion with ®rm teeth (21). destruction, whether these ®ndings are related to
In a randomly controlled clinical trial examining each other or play separate roles, and whether either
clinical outcomes and postoperative morbidity in or both of these ®ndings are associated with the
regenerative treatment of deep infrabony defects, classic histologic de®nition of occlusal trauma is
tooth mobility was assessed as a covariate. Among unknown. Furthermore, due to ethical considera-
clinical parameters evaluated in the study were clin- tions, it is unlikely that these questions will ever be
ical attachment level, probing depth, recession, tooth satisfactorily answered. However, when periodontal
mobility, full-mouth plaque scores, and full-mouth disease and destruction are present, the currently
bleeding scores. These were assessed immediately, available evidence appears to support the need for
prior to surgery and at 1-year post-treatment. Tooth occlusal treatment that will minimize occlusal inter-
mobility was evaluated with a purpose-built electro- ferences and help decrease tooth mobility.
nic device (Periotest1). Baseline tooth mobility was The treatment of occlusion usually involves either
signi®cantly associated with a reduction in antici- a reversible approach consisting of some type of bite
pated amounts of clinical attachment level gain. appliance (i.e. ``night guard'') and/or the selective
Based on the results of this study, the authors sug- grinding of the occlusal surfaces of the teeth (Fig. 9).
gested that clinicians may want to consider reducing Orthodontic therapy is also an effective method of
tooth mobility prior to attempting periodontal regen- changing occlusal relationships and minimizing
erative therapy to facilitate therapeutic success (14).
Other studies have examined the effect of splinting
on tooth mobility after initial therapy and after oss-
eous surgery. In the initial therapy study, there was a
reduction in tooth mobility over the 17-week period,
but there was no difference between the splinted and
non-splinted sites. The reduction in mobility
observed in both study groups was attributed to
reduction of in¯ammation and occlusal adjustment
accompanying initial therapy (49). No difference was
observed between splinted and non-splinted teeth
receiving osseous surgery, indicating that splinting
had no lasting effect on tooth mobility. Mobility pre-
dictably increased following surgery, but returned to
baseline presurgical levels after 6 months (22).
In summary, although a signi®cant role has been
suggested regarding the effect of tooth mobility on
treatment results, it is clear that controlled interven-
tion studies will be necessary in order to clarify the
effect of reducing baseline tooth mobility on period-
ontal treatment outcomes. Until such studies are
conducted, it would appear prudent, based on avail-
able data, to consider reduction/control of tooth
mobility as an integral part of periodontal therapy.

Under what clinical conditions is
occlusal adjustment indicated?
Based on current knowledge, it seems that research
supports the ®nding that occlusal discrepancies
Fig. 9. (a) Hard acrylic occlusal nightguard in place. As the
patient's jaw moves into a left lateral excursion, note the
disclusion of the teeth in the anterior and right side. (b)
Note the smooth, highly polished occlusal surface and the
presence of ball clasps between the second premolar and
the ®rst molar to facilitate retention.

160
 Occlusal analysis, diagnosis and management in periodontics
occlusal forces between opposing teeth. However,
orthodontics is rarely used during the active phase
References
of periodontal therapy and selective grinding of the
contacting surfaces is usually necessary following
orthodontic therapy. Appliance therapy has the
advantage of causing no permanent changes to the
occlusal surfaces and is therefore fully reversible.
However, appliance therapy is only effective in con-
trolling occlusal forces when the appliance is worn
by the patient. Selective grinding involves the non-
reversible reshaping of occlusal surfaces but has the
advantage of minimizing occlusal forces at all times.
The selection of the treatment modality for treating
occlusal stresses must take into consideration opera-
tor skill and con®dence in selective grinding, the
presence or absence of parafunctional habits, the
presence or absence of muscle splinting, and the
patient's psychological state.
Measurement of the outcomes from occlusal ther-
apy usually cannot be readily achieved. In cases
where the patient is experiencing discomfort from
occlusal contact, the relief of heavy occlusal pressure
by selective grinding may elicit immediate relief of
the patient's symptoms. In most cases, however, the
changes are subtle and can only be measured in
terms of decreased mobility and long-term favorable
results to periodontal therapy. Due to the fact that
other treatments routinely performed during period-
ontal therapy will also tend to improve mobility and
contribute to long-term favorable outcomes, it is dif-
®cult to determine to what extent occlusal treatment
has played a role in any clinical improvements
observed. However, just as periodontal disease
results from a combination of risk factors and con-
tributing causes, long-term favorable outcomes and
decreases in mobility are probably due to the elim-
ination or relief of multiple risk factors. The treat-
ment of periodontal disease consists of attempting to
control the risk factors for the disease such as bac-
terial plaque and the deeper pockets, which harbor
reservoirs of plaque bacteria, ameliorate negative
habits such as smoking, and controllable systemic
factors such as diabetes. The treatment of occlusal
discrepancies/occlusal trauma should also be viewed
in the context of the control of one of the risk factors
contributing to periodontal disease. The successful
treatment of periodontal disease requires the control
of all controllable risk factors. If occlusal discrepan-
cies exist in the presence of periodontal disease, the
occlusal factors should be controlled by the minimi-
zation of the occlusal forces. In other words, occlusal
treatment should be performed, where indicated, as
a routine part of periodontal therapy.
1. American Academy of Periodontology. 1999 International
Workshop for a Classification of Periodontal Diseases and
Conditions. Ann Periodontol 1999: 4: 102±107.
2. American Academy of Periodontology Parameters of care.
J Periodontol 2000: 71 (Suppl): 873±875.
3. American Academy of Periodontology Glossary of Terms,
4th edn. Chicago: American Academy of Periodontology,
2001: 5.
4. Anderegg CR, Metzler DG. Tooth mobility revisited. J Per-
iodontol 2001: 72: 963±967.
5. Angle EH. Malocclusion of the Teeth, 7th edn. Philadelphia:
SS White Dental Manufacturing Co., 1907.
6. Aparicio C. The use of the Periotest value as the initial
success criteria of an implant: 8-year report. Int J Period-
ontics Restorative Dent 1997: 17: 150±161.
7. Boston DW, Al-Bargi H, Bogert M. Abrasion, erosion and
abfraction combined with linear enamel hyperplasia: a
case report. Quintessence Int 1999: 30: 683±687.
8. Box HK. Experimental traumatogenic occlusion in sheep.
Oral Health 1935: 25: 9±15.
9. Bunting R. Oral Hygiene and the Treatment of Periodontal
Diseases. Philadelphia: Lea & Febiger, 1936.
10. Burgett FG, Ramfjord SP, Nissle RR, Morrison EC, Charbe-
neau TD, Caffesse RG. A randomized trial of occlusal ad-
justment in the treatment of periodontitis patients. J Clin
Periodontol 1992: 19: 381±387.
11. Carranza FA Jr, Newman MG. Clinical Periodontology, 8th
edn. Philadelphia: WB Saunders, 1996.
12. Castillini P, Scalise L, Tomasini EP. Teeth mobility mea-
surement: a laser vibrometry approach. J Clin Laser Med
Surg 1998: 15: 269±272.
13. Comar MD, Kollar JA, Gargiulo AW. Local irritation and
occlusal trauma as co-factors in the periodontal disease
process. J Periodontol-Periodontics 1969: 40: 193±200.
14. Cortellini P, Tonetti MS, Lang NP, Suvan JE, Zucchelli G,
Vangsted T, Silvestri M, Rossi R, McClain P, Fonzar A,
Dubravec D, Adriaens P. The simplified papilla preserva-
tion flap in the regenerative treatment of deep intrabony
defects: clinical outcomes and postoperative morbidity.
J Periodontol 2001: 72: 1702±1712.
15. Dawson PE. Evaluation, Diagnosis, and Treatment of Oc-
clusal Problems, 2nd edn. St. Louis: CV Mosby Co., 1989:
28±55.
16. Demirel K, Gu È r H, MericË H, Suvuk CË. Damping character-
istics of teeth with periodontal breakdown: correlation of
mobility meter values with bone and attachment loss.
J Periodontol 1997: 68: 166±171.
17. Ericsson I, Lindhe J. Lack of effect of trauma from occlu-
sion on the recurrence of experimental periodontitis. J Clin
Periodontol 1977: 4: 115±127.
18. Ericsson I, Lindhe J. Effect of longstanding jiggling on
experimental marginal periodontitis in the beagle dog.
J Clin Periodontol 1982: 9: 497±503.
19. Ericsson I, Lindhe J. Lack of significance of increased tooth
mobility in experimental periodontitis. J Periodontol 1984:
55: 447±452.
20. Ewen SJ, Stahl SS. The response of the periodontium
to chronic gingival irritation and long-term tilting forces
in adult dogs. Oral Surg Oral Med Oral Pathol 1962: 15:
1426±1433.
161
Hallmon & Harrel
21. Fleszar TJ, Knowles JW, Morrison EC, Burgett FG, Nissle
RR, Ramfjord SP. Tooth mobility and periodontal therapy.
J Clin Periodontol 1980: 7: 495±505.
22. Galler C, Selipsky H, Phillips C, Ammons WF Jr. The effect
of splinting on tooth mobility. (2) After osseous surgery.
J Clin Periodontol 1979: 6: 317±333.
23. Gher ME. Non-surgical pocket therapy: dental occlusion.
Ann Periodontol 1996: 1: 567±580.
24. Gillespie BR, Chasens AI, Brownstein CN, Alfano MC. The
relationship between the mobility of human teeth and their
supracrestal fiber support. J Periodontol 1979: 50: 120±124.
25. Glickman I. Inflammation and trauma from occlusion, co-
destructive factors in chronic periodontal disease. J Period-
ontol 1963: 34: 5±10.
26. Glickman I. Clinical Periodontology, 3rd edn. Philadelphia:
W.B Saunders Co., 1964: 695±715.
27. Glickman I. Clinical significance of trauma from occlusion.
J Am Dent Assoc 1965: 70: 607±618.
28. Glickman I. Occlusion and the periodontium. J Dent Res
1967: 46: 53±59.
29. Glickman I. Role of occlusion in the etiology and treatment
of periodontal disease. J Dent Res 1971: 50: 199±204.
30. Glickman I, Smulow JB. Alterations in the pathway of gin-
gival inflammation into the underlying tissues induced by
excessive occlusal forces. J Periodontol 1962: 33: 7±13.
31. Glickman I, Smulow J. Adaptive alteration in the period-
ontium of the rhesus monkey in chronic trauma from
occlusion. J Periodontol 1968: 39: 101±105.
32. Glickman I, Smulow J. The combined effects of inflamma-
tion and trauma from occlusion in periodontitis. Int Dent J
1969: 39: 101±105.
33. Glickman I, Weiss L. Role of trauma from occlusion in
initiation of periodontal pocket formation in experimental
animals. J Periodontol 1955: 26: 14±20.
34. Glickman I, Stein R, Smulow J. The effect of increased
functional forces upon the periodontium of splinted and
non-splinted teeth. J Periodontol 1961: 32: 290±300.
35. Graehn G, Berndt C, Staege B. The epidemiology of wedge
shaped defects. Dtsch Stomatol 1991: 41: 210±213.
36. Greenstein G, Polson AM. Understanding tooth mobility.
Compend Contin Educ Dent 1988: 9: 470±479.
37. Grippo JO. Abfraction: A new classification of hard tissues
of teeth. J Esthet Dent 1991: 3:14±19.
38. Grippo JO. Noncarious cervical lesions: the decision to
ignore or restore. J Esthet Dent 1992: 4: 55±64.
39. Grippo JO, Masi JV. Role of biodental engineering factors
(BEF) in the etiology of root caries. J Esthet Dent 1991: 3:
71±76.
40. Harrel SK, Nunn ME. The effect of occlusal discrepancies
on treated and untreated periodontitis. II. Relationship of
occlusal treatment to the progression of periodontal dis-
ease. J Periodontol 2001: 72: 495±505.
41. Harrel SK, Nunn ME. Longitudinal comparison of the per-
iodontal status of patients with moderate to severe period-
ontal disease receiving no treatment, non-surgical
treatment, and surgical treatment utilizing individual sites
for analysis. J Periodontol 2001: 72: 1509±1519.
42. d'Hoedt B, Lukas D, MuÈlbrandt L Scholz F, Schulte W, Quante
F, Topkaya A. The Periotest1 methods ± development and
clinical trials. Dtsch ZahnaÈrztl Z 1985: 40: 113±125.
43. Horning GM, Cohen ME, Neils TA. Buccal alveolar exo-
stoses: Prevalence, characteristics and evidence of buttres-
sing bone formation. J Periodontol 2000: 71: 1032±1042.
162
44. Imfeld T. Dental erosion. Definition, classification and
links. Eur J Oral Sci 1996: 104: 151±155.
45. Ismail AI, Morrison ED, Burt BA, Caffessee RG, Kavanaugh
MT. Natural history of periodontal disease in adults: Find-
ings from the Tecumseh periodontal disease study. J Dent
Res 1990: 69: 430±435.
46. Jin LJ, Cao CF. Clinical diagnosis of trauma from occlusion
and its relation with severity of periodontitis. J Clin Period-
ontol 1992: 19: 92±97.
47. Kantor M, Polson AM, Zander HA. Alveolar bone regenera-
tion after removal of inflammatory and traumatic factors.
J Periodontol 1976: 47: 687±685.
48. Karolyi M. Beobachtungen uÈber Pyorrhea alveolaris. OÈst
Ung Vierteljschr Zahnheilk 1901: 17: 279±283.
49. Kegel W, Selipsky H, Phillips C. The effect of splinting on
tooth mobility. I. During initial therapy. J Clin Periodontol
1979: 6: 45±58.
50. Kerry GJ, Morrison EC, Ramfjord SP, Hill RW, Caffesse RG,
Nissle RR, Appleberry EA. The effect of periodontal treat-
ment on tooth mobility. J Periodontol 1982: 53: 635±638.
51. Knowles JW. Occlusal interferences and loss of periodontal
attachment. J Dent Res (IADR Abstracts) 1967: 46: 168 (Ab-
stract #517).
52. Lambert RL, Lindenmuth JS. Abfraction ± a new name for
an old entity. J Colo Dent Assoc 1994: 72: 31±33.
53. Lee WC, Eakle WS. Possible role of tensile stress in the
etiology of cervical erosion lesions of teeth. J Prosthet Dent
1984: 52: 374±380.
54. Levitch LC, Bader JD, Shugars Da, Heymann HO. Noncar-
ious cervical lesions. J Dent 1994: 22: 195±207.
55. Lindhe J, Ericsson I. Influence of trauma from occlusion on
reduced but healthy periodontal tissues in dogs. J Clin
Periodontol 1976: 3: 110±122.
56. Lindhe J, Ericsson I. The effect of elimination of jiggling
forces on periodontally exposed teeth in the dog. J Period-
ontol 1982: 53: 562±567.
57. Lindhe J, Svanberg G. Influence of trauma from occlusion
on progression of experimental periodontitis in the beagle
dog. J Clin Periodontol 1974: 1: 3±14.
58. Lukas D, Schulte W. Periotest - a dynamic procedure for
the diagnosis of the human periodontium. Clin Phys Phy-
siol Meas 1990: 11: 65±75.
59. Macapanpan LC, Weinmann JP. The influence of injury to
the periodontal membrane on the spread of gingival in-
flammation. J Dent Res 1954: 33: 263±272.
60. McCall JO. Traumatic occlusion. J Am Dent Assoc 1939: 26:
519±526.
61. McGuire MK, Nunn ME. Prognosis versus actual out-
come. III. The effectiveness of clinical parameters in ac-
curately predicting tooth survival. J Periodontol 1996: 67:
666±674.
62. McGuire MK, Nunn ME. Prognosis versus actual outcome.
II. The effectiveness of commonly taught clinical para-
meters in developing an accurate prognosis. J Periodontol
1996: 67: 658±665.
63. Miller SC. Textbook of Periodontia (Oral Medicine), 2nd
edn. Philadelphia: The Blakiston Co., 1943: 103.
64. Mu È hlemann HR. Tooth mobility: a review of clinical as-
pects and research findings. J Periodontol 1967: 38: 686±
708.
65. Nohl FS, Setchell DJ. Surface strains induced by measured
loads on teeth in vivo: a methodologic study. Eur J Prostho-
dont Restor Dent 2000: 8: 27±31.

66. Nunn M, Harrel SK. The effect of occlusal discrepancies on
treated and untreated periodontitis: I. Relationship of in-
itial occlusal discrepancies to initial clinical parameters.
J Periodontol 2001: 72: 485±494.
67. Nyman S, Lindhe J, Ericsson I. The effect of progressive
tooth mobility on destructive periodontitis in the dog. J Clin
Periodontol 1978: 5: 213±225.
68. Nyman S, Karring T, Bergenholtz G. Bone regeneration in
alveolar bone dehiscences produced by juggling forces.
J Periodont Res 1982: 17: 316±322.
69. O'Leary TJ, Rudd KD. An instrument for measuring hor-
izontal tooth mobility. Periodontics 1963: 1: 249±254.
70. Orban B, Weinmann J. Signs of traumatic occlusion in
average human jaws. J Dent Res 1933: 13: 216 (Abstract).
71. Perrier M, Polson A. The effect of progressive and in-
creasing tooth hypermobility on reduced but healthy
periodontal supporting tissue. J Periodontol 1982: 53:
152±157.
72. Persson R, Svensson A. Assessment of tooth mobility using
small loads. I. Technical devices and calculations of tooth
mobility in periodontal health and disease. J Clin Period-
ontol 1980: 7: 259±275.
73. Pihlstrom BL, Ramfjord SP. Periodontal effect of nonfunc-
tion in monkeys. J Periodontol 1971: 42: 748±756.
74. Pihlstrom BL, Anderson KA, Aeppli D, Schaffer EM. Asso-
ciation between signs of trauma from occlusion and per-
iodontitis. J Periodontol 1986: 57: 1±6.
75. Piotrowski BT, Gillette WB, Hancock EB. Examining the
prevalence and characteristics of abfractionlike cervical
lesions in a population of U.S. veterans. J Am Dent Assoc
2001: 132: 1694±1701.
76. Polson AM. Trauma and progression of marginal period-
ontitis in squirrel monkeys. II. Co-destructive factors of
periodontitis and mechanically produced injury. J Period-
ont Res 1974: 9: 108±113.
77. Polson AM. The relative importance of plaque and occlu-
sion in periodontal disease. J Clin Periodontol 1986: 13:
923±927.
78. Polson AM, Zander HA. Effects of periodontal trauma on
intrabony pockets. J Periodontol 1983: 54: 586±591.
79. Polson AM, Kennedy JE, Zander HA. Trauma and progres-
sion of periodontitis in squirrel monkeys. I. Co-destructive
factors of periodontitis and thermally produced injury.
J Periodont Res 1974: 9: 100±107.
80. Polson AM, Meitner SW, Zander HA. Trauma and progres-
sion of marginal periodontitis in squirrel monkeys. III.
Adaptation of interproximal alveolar bone to repetitive in-
jury. J Periodont Res 1976: 11: 279±289.
81. Polson AM, Meitner SW, Zander HA. Trauma and progres-
sion of marginal periodontitis in squirrel monkeys IV. Re-
versibility of bone loss due to trauma alone and trauma
superimposed upon periodontitis. J Periodont Res 1976: 11:
290±297.
82. Polson AM, Kantor ME, Zander HA. Periodontal repair
after reduction of inflammation. J Periodont Res 1979: 14:
520±525.
83. Polson AM, Adams RA, Zander HA. Osseous repair in the
presence of active tooth hypermobility. J Clin Periodontol
1983: 10: 370±379.
84. Ramfjord SP, Ash MM Jr. Significance of occlusion in the
etiology and treatment of early, moderate and advanced
periodontitis. J Periodontol 1981: 52: 511±517.
Occlusal analysis, diagnosis and management in periodontics
85. Ramfjord SP, Kohler CA. Periodontal reaction to functional
occlusal stress. J Periodontol 1959: 30: 95±112.
86. Radentz W, Barnes GP, Cutright DE. A survey of factors
possibly associated with cervical abrasion of tooth sur-
faces. J Periodontol 1976: 47: 148±154.
87. Rees JS. The role of cuspal flexure in the development of
abfraction lesions: a finite element study. Eur J Oral Sci
1998: 106: 1028±1032.
88. Rees JS. A review of the biomechanics of abfraction. Eur J
Prosthodont Restor Dent 2000: 8: 139±144.
89. Rees JS. The effect of variation in occlusal loading on the
development of abfraction lesions: a finite element study.
J Oral Rehabil 2002: 29: 188±193.
90. Ross IF, D'Onofrio ED, Roman JS. Occlusal contacts and
tooth mobility. Females, aged 18-30. J Periodontol 1972: 43:
760±764.
91. Schulte W. The new Periotest method. Compend Contin
Educ Dent 1989: 10 (Suppl. 12): S410±S417.
92. Schulte W, d'Hoedt B, Lucas D, MuÈhlbrandt L, Scholz F,
Bretschi J, Frei D, Gudat H, Knig M, Markl M, Quante F,
Schief D, Topkaya A. Periotest ± ein neues Verfahren und
GeraÈt zur Messung der Funktion des Parodontiums. Zah-
narztl Mitt 1983: 73: 1229±1240.
93. Schulte W, d'Hoedt B, Lucas D, Maunz M, Steppeler M.
Periotest for measuring periodontal characteristics ± Cor-
relation with periodontal bone loss. J Periodont Res 1992:
27: 184±190.
94. Shefter GJ, McFall WT Jr. Occlusal relations and period-
ontal status in human adults. J Periodontol 1984: 55: 368±
374.
95. Stahl SS. The responses of the periodontium to combined
gingival inflammation and occluso-functional stresses
in four human surgical specimens. Periodontics 1968: 6:
14±22.
96. Stillman PR. The management of pyorrhea. Dent Cosmos
1917: 59: 405±414.
97. Stillman PR. What is traumatic occlusion and how can it
diagnosed and corrected. J Am Dent Assoc 1926: 12: 1330±
1338.
98. Stones HH. An experimental investigation into the associa-
tion of traumatic occlusion with periodontal disease. Proc
R Soc Med (Odontol Sec) 1938: 31: 479±495.
99. Stoller NH, Laudenbach KW. Clinical standardization of
horizontal tooth mobility. J Clin Periodontol 1980: 7:
242±250.
100. Svanberg G. Influence of trauma from occlusion on the
periodontium of dogs with normal or inflamed gingiva.
Odontol Revy 1974: 25: 165±178.
101. Svanberg G, Lindhe J. Experimental tooth hypermobility in
the dog. Odontol Revy 1973: 24: 269±282.
102. Svanberg G, Lindhe J. Vascular reactions in the periodontal
ligament incident to trauma from occlusion. J Clin Period-
ontol 1974: 1: 58±69.
103. Waerhaug J. Subgingival plaque and loss of attachment in
periodontosis as observed in autopsy material. J Period-
ontol 1976: 47: 636±642.
104. Waerhaug J. The angular bone defect and its relationship
to trauma from occlusion and downgrowth of subgingival
plaque. J Clin Periodontol 1979: 6: 61±82.
105. Waerhaug J. The infrabony pocket and its relationship to
trauma from occlusion and subgingival plaque. J Period-
ontol 1979: 50: 355±365.
163
Hallmon & Harrel
106. Wang H-L, Burgett FG, Shyr Y, Ramfjord SP. The influence
of molar furcation involvement and mobility on future
clinical periodontal attachment loss. J Periodontol 1994:
65: 25±29.
107. Weatherford T. Tooth mobility: mechanisms and treat-
ment. Ala J Med Sci 1977: 14: 32±38.
108. Webber RL. Some candid observations and reflections on
the results of an in vitro test of the Siemens Periotest
164
device. Compend Contin Educ Dent 1988: 9 (Suppl. 12):
S438±S441.
109. Weinmann JP. Progress of gingival inflammation into the
supporting structures of the teeth. J Periodontol 1941: 12:
71±82.
110. Wentz FM, Jarabak J, Orban B. Experimental occlusal trau-
ma imitating cuspal interferences. J Periodontol 1958: 29:
117±127.