Trauma from occlusion

Trauma from occlusion
Presented by:
Pallavi Prashar
MDS Student

Introduction
• Occlusal force is a critical factor affecting the
condition and structure of the periodontium.
• In fact, the periodontal ligament and alveolar
bone require mechanical stimulation from
occlusal forces in order to remain structurally
sound.
• When function is insufficient, these tissues
undergoes atrophy, and when occlusal forces
exceed the physiologic adaptive capacity of the
tissues, they are damaged. Such damage is
referred to as trauma from occlusion.

 Other terms often used are:
• traumatizing occlusion,
• occlusal trauma,
• traumatogenic occlusion,
• periodontal traumatism,
• overload.

ADAPTIVE CAPACITY OF THE PERIODONTIUM TO
OCCLUSAL FORCES
varies in different persons and in the same
person at different times and is influenced by
the:
• magnitude,
• direction,
• duration and
• frequency of the force.

MAGNITUDE
↓
Widening of periodontal ligament space,
increase in width of PDL fibres & an increase
in density of alveolar bone.

DIRECTION
↓
Changing the direction of occlusal forces causes
reorientation of stresses within periodontium. The
principal fibers of PDL are arranged so that they
best accommodate occlusal forces . Lateral forces
& torque are more likely to injure the
periodontium.

DURATION AND FREQUENCY OF
OCCLUSAL FORCES
↓
Constant pressure on the bone is more injurious
than intermittent forces. But also, more
frequent the application of intermittent force,
the more injurious is the force to periodontium.

DEFINITIONS:
When occlusal forces exceed the adaptive
capacity of the tissues , tissue injury results.
The resultant injury is termed as trauma from
occlusion’
- Carranza 11th edition
‘A term used to describe pathological
alterations or adaptive changes which develop
in the periodontium as a result of undue force
produced by the masticatory muscles’
-Lindhe 5th edition

A condition where injury results to the supporting
structures of the teeth by the act of bringing the
jaws into a closed position’
-Stillman(1917)
‘Damage in the periodontium caused by stress on
teeth produced directly or indirectly by teeth of
the opposing jaw’
-WHO(1978)
An injury to the attachment apparatus as a result
of excessive occlusal forces’
-Glossary of Periodontal Term (AAP in 1986)

TYPES OF TRAUMA FROMOCCLUSION
• Acute or Chronic
• Primary and Secondary TFO

Acute TFO
Develops from:
• Abrupt occlusal impact such as, by biting on a
hard object.
• Restorations or prosthetic appliances that
interfere with or alter the direction of occlusal
force
Clinical features:
• Tooth pain, sensitivity to percussion, and
increased tooth mobility.

Outcome:
Force dissipated
i. Shift in tooth position heals
ii. Wearing &
iii. Correction of restoration subsides
Or else
Periodontal injury Necrosis+ perio. abscess
or Cementum tears

Chronic TFO
• More common & significant
• Gradual changes by:
- tooth wears
- drifting movement & extrusion
- parafunctional habits
• Malocclusion not necessarily TFO

Primary and Secondary TFO
• Trauma from occlusion may be caused by
– alterations in occlusal forces,
– reduced capacity of the periodontium to withstand
occlusal forces,
– or both.
• When trauma from occlusion is the result of
alterations in occlusal forces, it is called “primary
trauma from occlusion.”
• When it results from reduced ability of the
tissues to resist the occlusal forces, it is known as
“secondary trauma from occlusion.”

Primary TFO
The primary form includes a tissue reaction
(damage), which is elicited around a tooth with
normal height of the periodontium,
Occurs if:
Trauma from occlusion is considered the primary
etiologic factor in periodontal destruction
Occlusion results in the only local alteration of teeth
Parafunctional habits

Examples include periodontal injury
produced around teeth with prevviously
healthy periodontium after:
– Insertion of a “high filling”
– Insertion of a prosthetic replacement that creates
excessive forces on abutment and antagonist teeth.
– Drifting movement or extension of teeth into
spaces created by unreplaced missing teeth, OR
– Orthodontic movement of teeth into functionally
unacceptable positions.
• Changes produced by primary trauma do not
alter the level of connective tissue attachment
and do not initiate pocket formation.

Secondary TFO
• Occurs when the adaptive capacity of the
tissues to withstand occlusal forces is impaired
by bone loss resulting from marginal
inflammation.
• and previously well-tolerated occlusal forces
become traumatic.

Extension of gingival inflammation to alveolar bone
• Gingival inflammation collagen fiber bundles blood
vessels alveolar bone
• Interproximally, through the vessels perforating the crest of
the interdental septum
• Directly into the PDL & from there into the interdental
septum
•Facially & lingually , spreads
along the outer periosteal
surface & penetrates into the
marrow spaces through vessel
channels
•Destroys the transseptal &
gingival fibers on the course

Once bone is reached:
• Spreads into the marrow spaces & replaces
marrow with exudate.
• Bone resorption proceeds from within the marrow
spaces
• Thinning of bony trabeculae & enlargement of the
marrow spaces
• Bone destruction & a reduction in bone height
• Fatty bone marrow replaced with fibrous marrow

GLICKMAN’S CONCEPT
• Concept given in 1965,1967
• The pathway of the spread of a plaque-associated gingival
lesion can be changed if forces of an abnormal magnitude
are acting on teeth harboring subgingival plaque
• It would imply that character of progressive tissue destruction
of periodontium at a “traumatized” tooth different from that in a
“non-traumatized” tooth .
• Instead of an even destruction of the periodontium and alveolar
bone (suprabony pockets and horizontal bone loss), which,
according to Glickman, occurs at sites with uncomplicated
plaque-associated lesions, sites which are also exposed to
abnormal occlusal force will develop angular bony defects and
infrabony pockets.

Periodontal structures divided into two zones:
1. Zone of Irritation
2. Zone of co-destruction

Zone of irritation
• Includes the marginal and interdental gingiva.
• The soft tissue of this zone is bordered by hard
tissue (the tooth) only on one side and is not
affected by forces of occlusion.
• This means that gingival inflammation cannot be
induced by trauma from occlusion but is the result
of irritation from microbial plaque.
• The plaque-associated lesion at a “non-
traumatized” tooth propagates in the apical
direction by first involving the alveolar bone and
only later the periodontal ligament area.
• The progression of this lesion results in an even
(horizontal) bone destruction.

Zone of co-destruction
• Includes PDL, Root cementum & alveolar bone
• Coronally demarcated by the transseptal & the
dentoalveolar collagen fiber bundles
• TFO may cause a lesion here

• The fiber bundles which separate the zone of
codestruction from the zone of irritation can
be affected from two different directions:
1. From the inflammatory lesion maintained by
plaque in the zone of irritation
2. From trauma-induced changes in the zone of
co-destruction.
• Through this exposure from two different
directions the fiber bundles may become
dissolved and/or orientated in a direction
parallel to the root surface.
• The spread of an inflammatory lesion from
the zone of irritation directly down into the
periodontal ligament (i.e. not via the
interdental bone) may hereby be facilitated.
• This alteration of the “normal” pathway of
spread of the plaque-associated inflammatory
lesion results in the development of angular
bony defects.

Waerhaug’s Concept (1979)
• Refuted the hypothesis that trauma from occlusion played a role in
the spread of a gingival lesion into the "zone of co-destruction".
• He measured in addition the distance between the subgingival
plaque and
1. the periphery of the associated inflammatory cell infiltrate in the
gingiva.
2. the surface of the adjacent alveolar bone.
• He concluded that angular defects and infrabony pockets occur
equally frequently in teeth with TFO and in teeth without TFO,
• Waerhaug's observations support findings presented by Prichard
(1965) and Manson (1976)

• The loss of connective attachment and the resorption
of bone around teeth are, according to Waerhaug,
exclusively the result of inflammatory lesions
associated with subgingival plaque.
• Waerhaug concluded that angular bony defects and
infrabony pockets occur when the subgingival plaque
of one tooth has reached a more apical level than the
microbiota on the neighboring tooth, and when the
volume of the alveolar bone surrounding the roots is
comparatively large.

STAGES OF TISSUE RESPONSE TO INCREASED OCCLUSAL FORCES
Tissue response occur in three stages:
– Stage I: Injury.
– Stage II: Repair.
– Stage III: Adaptive Remodeling of periodontium.

STAGEI : INJURY
• Caused by Excessive occlusal forces.
• Under the forces of occlusion or tooth rotates around a
fulcrum which creates pressure and tension on opposite sides
of fulcrum.
• Slightly excessive pressure stimulates resorption of alveolar
bone, with compression of PDL fibres.
• Slightly excessive tension causes elongation of PDL fibers &
apposition of alveolar bone.
• In areas of increased pressure, the blood vessels are numerous
and reduced in size and in increased tension they are enlarged.

GREATER PRESSURE
• Compression of fibres produces hyalinization.
• Injury to fibroblasts and other connective tissue cells
leads to necrosis.
Vascular changes:
• Within 30 min: retardation and stasis of blood flow
• 2-3 hrs: blood vessels paused with erythrocytes which
start to fragment.
• In 1-7 days disintegration of the blood vessel walls and
release of the contents into the surrounding tissue

SEVERE TENSION
• Widening of the periodontal ligament.
• Thrombosis.
• Hemorrhage.
• Tearing of the periodontal ligament.
• Resorption of the alveolar bone.

• The areas of the periodontium most susceptible
to injury from excessive occlusal forces are
the furcations.
• Injury to the periodontium produces a
temporary depression in mitotic activity and
the rate of proliferation of fibroblasts, collagen
and bone formation.
• These return to normal levels after dissipation
of the forces.

Orthodontic type trauma
• In case of orthodontic type of trauma, when
tooth is exposed to unilateral forces of a
magnitude frequency or duration that its
periodontal tissues are unable to withstand and
distribute while maintaining the stability of the
tooth, certain well defined reactions develop in
the periodontal ligament.

• If the magnitude of forces is within certain limits, allowing
the maintenance of the vitality of the periodontal ligament
cells, bone-resorbing osteoclasts soon appear on the bone
surface of the alveolus in the pressure zone. A process of
bone resorption is initiated. This phenomenon is called
“direct bone resorption”.
• If the force applied is of higher magnitude, the result may
be necrosis of the periodontal ligament tissue in the
pressure zone, i.e. decomposition of cells, vessels, matrix,
and fibers (hyalinization). “Direct bone resorption”
therefore cannot occur.
• Instead, osteoclasts appear in marrow spaces within the
adjacent bone tissue where the stress concentration is
lower than in the periodontal ligament and a process of
undermining or “indirect bone resorption” is initiated.

Jiggling type trauma
• Jiggling forces are intermittent type of forces
subjected to tooth or teeth in more than one
direction, such as in case of premature contacts
(crowns/high fillings).
• In conjunction with “jiggling-type trauma” no
clearcut pressure and tension zones can be
identified but rather there is a combination of
pressure and tension on both sides of the
jiggled tooth.

Two mandibular premolars with normal periodontal tissues (a) are exposed to jiggling forces (b) as illustrated
by the two arrows. The combined tension and pressure zones (encircled areas) are characterized by signs of
acute inflammation including collagen resorption, bone resorption, and cementum resorption. As a result of
bone resorption the periodontal ligament space gradually increases in size on both sides of the teeth as well
as in the periapical region. (c) When the effect of the force applied has been compensated for by the
increased width of the periodontal ligament space, the ligament tissue shows no sign of infl ammation. The
supra-alveolar connective tissue is not affected by the jiggling forces and there is no apical downgrowth of
the dentogingival epithelium. (d) After occlusal adjustment the width of the periodontal ligament becomes
normalized and the teeth are stabilized.
Jiggling type of trauma in healthy periodontium with
normal height

Healthy periodontium with reduced height
(a) Two mandibular premolars are surrounded by a healthy periodontium with reduced height. (b) If such
premolars are subjected to traumatizing forces of the jiggling type a series of alterations occurs in the
periodontal ligament tissue. (c) These alterations result in a widened periodontal ligament space and in an
increased tooth mobility but do not lead to further loss of connective tissue attachment. (d) After occlusal
adjustment the width of the periodontal ligament is normalized and the teeth are stabilized.

Plaque associated periodontal disease
a) Two mandibular premolars with supra- and subgingival plaque, advanced bone loss and periodontal
pockets of a suprabony character. Note the connective tissue infi ltrate (shadowed areas) and the uninfl
amed connective tissue between the alveolar bone and the apical portion of the infi ltrate. (b) If these teeth
are subjected to traumatizing forces of the jiggling type, pathologic and adaptive alterations occur within the
periodontal ligament space. (c) These tissue alterations, which include bone resorption, result in a widened
periodontal ligament space and increased tooth mobility but no further loss of connective tissue
attachment. (d) Occlusal adjustment results in a reduction of the width of the periodontal ligament and in
less mobile teeth.

Stage II: Repair
• Repair is constantly occurring in the normal
periodontium and TFO stimulates increased reparative
activity.
• The damaged tissues are removed and new connective
tissue cells, fibers, bone, and cementum are formed in
an attempt to restore the injured periodontium.
• When bone is resorbed by excessive occlusal forces,
the body attempts to reinforce the thinned bone with
new bone. This attempt to compensate for lost bone is
called buttressing bone formation and is an important
feature associated with TFO.

• Buttressing bone formation occurs within the jaw (central
buttressing) and on the bone surface (peripheral
buttressing).
• In central buttressing the endosteal cells deposit new bone,
which restores the bony trabeculae and reduces the size of
the marrow spaces.
• Peripheral buttressing occurs on the facial and lingual
surfaces of the alveolar plate.
• Depending on its severity, peripheral buttressing may
produce a shelflike thickening of the alveolar margin,
referred to as “lipping”, or a pronounced bulge in the
contour of the facial and lingual bone.

Stage III: Adaptive remodeling of the periodontium
• If the repair process cannot keep pace with the
destruction, the periodontium is remodeled in an
effort to create a structured relationship in which
forces are no longer injurious to the tissues.
• This results in a thickened periodontal ligament,
which is funnel- shaped at the crest, and angular
defects in the bone with no pocket formation,
increased mobility and increased vascularisation
(Dutto et al 1967).

REVERSIBILITY OF TRAUMATIC LESIONS
• TFO is reversible, it does not always correct
itself, & therefore it is not always temporary or of
limited clinical significance.
• The injurious force must be relieved for repair to
occur.
• If conditions do not permit the teeth to escape
from or adapt to excessive occlusal force,
periodontal damage persists & worsens.

INTERACTION OF TFO & INFLAMMATION
• Trauma from occlusion may alter the pathway of extension of gingival
inflammation to the underlying tissues. This may be favored by the
reduced collagen density and increased number of leukocytes, osteoclasts,
and blood vessels in the coronal portion of increasingly mobile teeth.
Inflammation then may proceed to the periodontal ligament rather than to
the bone. Resulting bone loss would be angular, and pockets could become
intrabony.
• Trauma-induced areas of root resorption uncovered by apical migration of
the inflamed gingival attachment may offer a favorable environment for
the formation and attachment of plaque and calculus and therefore may be
responsible for the development of deeper lesions.
• Supragingival plaque can become subgingival if the tooth is tilted
orthodontically or migrates into an edentulous area, resulting in the
transformation of a suprabony pocket into an intrabony pocket.
• Increased mobility of traumatically loosened teeth may have a pumping
effect on plaque metabolites, increasing their diffusion

Symptoms of TFO
1. Periodontal pain
• In severe trauma from occlusion, there is localized, sharp pain or
soreness to the tooth.
• In chronic long standing trauma from occlusion, there is little or no
pain.
• The symptoms, if present are those of vague regional discomfort
2. Pulpal pain
• Sensitivity of the teeth, especially to cold, is commonly found .
3. Food impaction
• The plunger cusp effect of occlusal interference may produce a
functional opening of contact between the teeth, leading to food
impaction.
4. TMJ pain
• This is always accompanied by an occlusal disharmony.

Clinical Signs of Trauma from Occlusion
• Increased tooth mobility
– This is a hallmark of trauma from occlusion
– It can be easily measured by blunt ends of two
dental instruments which are placed
approximately at the buccal and lingual heights of
contour of the tooth, and force are applied in the
bucco-lingual direction.
46

MILLER’S MOBILITY INDEX (1950)
• Mobility 1 – First distinguishable sign of
movement greater than normal.
• Mobility 2 – Movement of 1 mm from normal
position in any direction.
• Mobility 3 – Greater than 1 mm and rotation,
or depression.

2. Migration of teeth
• Loss of inter proximal contact and migration of teeth may be seen in
traumatic occlusal relation.
3. Atypical pattern of occlusal wear
• Tooth wear which appears to be greater than one might expect in a
patient of that age, and which cannot be attributed to any special diet
or deficiency in tooth mineralization.
4. Changes in percussion sound
• On percussion, the tooth affected by trauma from occlusion, gives a
dull sound whereas a normal teeth gives a sharp sound.
• This difference could be due to altered width and consistency of
periodontal membrane, and partial resorption of lamina dura.
5. Hypertonicity of masticatory muscles
• Bruxism and hypertonicity makes the periodontium susceptible to
trauma.

Fremitus test/Functional Mobility
• Test to detect trauma from occlusion.
• Fremitus is a measurement of the vibratory pattern of
the teeth when the teeth are placed in contacting
position and movements.
• To measure fremitus ,a dampened index finger is
placed along the buccal and labial surface of the
maxillary teeth. The patient is asked to tap the teeth
together in the maximum intercuspal position and
then grind systematically in the lateral, protrusive,
and lateral-protrusive contacting movements and
positions.
• The teeth that are displaced by the patient in these
jaw positions are then identified.

• Mandibular teeth assessed in edge to edge occlusion
• The following classification system is used :
– Class I fremitus – Mild vibration or movement
detected
– Class II fremitus – Easily palpable vibration but no
visible movement
– Class III fremitus – Movement visible with naked eye
• Fremitus differs from mobility in that fremitus is
tooth displacement created by patient’s own
occlusal force.
• Fremitus is a guide to the ability of the patient to
displace and traumatize the teeth.

• In the posterior teeth TFO can be detected
with help of occlusion rregistration strip/
articulating paper.
• High pressure points can be detected by
pattern of impression made by registration
strip/articulating paper.

Radiographic features of TFO
• Trauma from occlusion produces radiographicaly
detectable changes in the lamina dura, periodontal
ligament spaces, morphology of alveolar crest, and
density of surrounding bone.
• These changes include :
– Increased width of periodontal space, often with
thickening of lamina dura along the lateral aspect of root,
in the apical region and in the bifurcation areas.
– A “vertical” rather than horizontal destruction of
interdental septum.
– Widening of periodontal ligament space at the crest,
giving a funnel-shaped appearance and angular defects
during adaptive remodeling stage.
– Root resorption is seen.

TREATMENT PLANNING
• The decision to treat the patients occlusion either
by adjusting the occlusal surfaces or by the use of
occlusal appliance will be influenced by the
patients symptoms such as:
• tooth sensitivity
• pain on chewing,
• mobility,
• presence of wear facets,
• extent of periodontal destruction,
• patients ability to adequately function.

• If the patient is asymptomatic and does not
have significant periodontal disease, treatment
of occlusion may not be indicated even if
significant occlusal discrepancies are present.
• If the patient has occlusal discrepancies in
addition to periodontal disease, occlusal
treatment can be considered.

• The decision to perform occlusal therapy
should be made after reevaluation of the
patient’s response to nonsurgical treatment
such as oral hygiene instructions and root
planing.
• Mobility and fremitus will often be greatly
reduced by these procedures, and the need for
occlusal treatment may be diminished.

• An exception to this treatment timing would be
when the patient has difficulty chewing or
tooth pain when chewing that appears directly
related to occlusal trauma.
• If a decision is made to begin occlusal
treatment prior to controlling inflammation, it
will probably be necessary to perform further
occlusal treatment following control of
inflammation. The patient should be informed
of this prior to beginning treatment.

Occlusal treatment consists of two basic
approaches:
– The use of bite appliance (bite guard)
– Adjusting the occlusion by altering the occlusal
relationships between the teeth.

• A bite appliance fits over the patients teeth and
creates an artificial occlusal surface for the
opposing dentition to contact.
• A bite appliance is usually made from hard
acrylic, which has the advantage of cushioning
contact forces between the teeth. Heat- or cold-
cured hard acrylic is recommended over a soft
acrylic material

• The use of a maxillary bite appliance is
preferred for most periodontal patients because
it will stabilize potentially loose maxillary
anterior teeth and prevent flaring.
• If a mandibular bite appliance is used against
maxillary teeth with compromised teeth,
flaring of the maxillary teeth is possible.

Selective grinding / Coronoplasty
• Selective grinding is a procedure by which the
occlusal surfaces of teeth are precisely altered
to improve the overall contact pattern. Tooth
structure is selectively removed until the
reshaped teeth contact in such a manner as to
fulfill the treatment goals.

Treatment of increased tooth mobility
Situation I
• Increased mobility of a tooth with increased
width of the periodontal ligament but normal
height of the alveolar bone

Situation II
• Increased mobility of a tooth with increased width
of the periodontal ligament and reduced height of
the alveolar bone
• If the excessive forces are reduced or eliminated by
occlusal adjustment, bone apposition to the
“pretrauma” level will occur, the periodontal ligament
will regain its normal width and the tooth will become
stabilized

Conclusion: situations I and II
• Occlusal adjustment is an effective therapy against
increased tooth mobility when such mobility is
caused by an increased width of the periodontal
ligament.

Situation III
• Increased mobility of a tooth with reduced height
of the alveolar bone and normal width of the
periodontal ligament
• The increased tooth mobility which is the result of a
reduction in height of the alveolar bone without a
concomitant increase in width of the periodontal
membrane cannot be reduced or eliminated by
occlusal adjustment.
• In teeth with normal width of the periodontal
ligament, no further bone apposition on the walls of
the alveoli can occur.

• If such an increased tooth mobility does not
interfere with the patient’s chewing function or
comfort, no treatment is required.
• If the patient experiences the tooth mobility as
disturbing, however, the mobility can only be
reduced in this situation by splinting, i.e. by
joining the mobile tooth/teeth together with other
teeth in the jaw into a fixed unit – a splint.

Situation IV
• Progressive (increasing) mobility of a tooth (teeth)
as a result of gradually increasing width of the
reduced periodontal ligament
• It will only be possible to maintain such teeth by
means of a splint. In such cases a fixed splint has two
objectives:
(1) to stabilize hypermobile teeth and
(2) to replace missing teeth

CONCLUSION
• Occlusal trauma is an important risk factor
which can increase the rate of progression of
an existing periodontal disease.
• There is a place for occlusal therapy in the
management of periodontitis, especially when
related to the patient's comfort and function.
• Occlusal therapy is not a substitute for
conventional methods of resolving plaque-
induced inflammation.

Trauma from occlusion

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