PERIODONTAL

RESPONSE TO EXTERNAL
FORCES
 DEFINITION: When occlusal forces exceed
the adaptive capacity of the periodontal
tissues, tissue injury results. This resultant
injury is termed as trauma from occlusion.

 WHO in 1978 defined trauma from occlusion

as “damage in the periodontium caused by,
stress on the teeth produced directly or
indirectly by the teeth of the opposing jaw”.

Thus trauma from occlusion refers to the tissue

injury & not the occlusal force.
 Magnitude : When it increases, the periodontium
responds with a thickening of the periodontal ligament,
an increase in the number and width of periodontal
ligament fibers and an increase in the density of the
alveolar bone.

 Direction: changes in the direction causes a

reorientation of the stresses and strains within the
periodontium (lateral or horizontal forces, torque or
rotational forces are more likely to injure the
periodontium).

 Duration: constant pressure on the bone is more

injurious than intermittent forces.

 Frequency: the more frequent the application of an

intermittent force, the more injurious it is to the
periodontium.
 Types:

 Depending on the onset and duration.

 Depending on the cause

 Acute trauma from occlusion: Results from
the abrupt changes in the occlusal forces, such
as that produced by biting on a hard object, in
addition, could also be due to iatrogenic factor
(faulty restorations/ prosthetic appliance).
 Chronic trauma from occlusion: As a result
of the gradual changes produced in the
periodontium due to the tooth wear, drifting
movement, extrusion of the teeth combined
with para functional habits such as bruxism
and clenching.
Primary Trauma from occlusion Secondary Trauma from occlusion
Is a tissue injury, which is elicited Is related to situations in which
around a tooth with normal height occlusal forces cause injury in a
of periodontium. periodontium of reduced height.
E.g.: insertion of high fillings, E.g.: periodontitis.
insertion of the prosthetic
replacement, orthodontic
movement in functionally
unacceptable positions.
 Clinical signs and symptoms
 Excessive tooth pain, tenderness on percussion, increased tooth
mobility (hyper mobility) is seen. In severe cases periodontal
abscess formation and cemental tears can be seen. Others such
as presence of infrabony pockets, furcation involvement,
attrition, pathologic migration may also be present.
 Fremitus test is positive.

 Radiographic changes
 Increase in the width of the periodontal ligament space often with
thickening of the lamina dura along the lateral borders of the root,
apical and bifurcation areas.
 “Vertical” rather than horizontal destruction of the interdental
septum.
 Radiolucency and condensation of the alveolar bone
 Root resorption.
Tissue Response
 Stage 1: Injury:

When a tooth is exposed to excessive occlusal forces,

the periodontal tissues are unable to withstand and
hence they distribute, while maintaining the stability of
the tooth. This may lead to certain well-defined
reactions in the periodontal ligament and alveolar
bone, eventually resulting in adaptation of the
periodontal structures to altered functional demand.
When the tooth is subjected to horizontal forces the
tooth rotates or tilts in the direction of force. This tilting
results in the pressure and tension zones, within the
marginal and apical parts of the periodontium.
Depending on the types of forces there can be,
 Slightly excessive pressure :
 Widening of the periodontal ligament.
 Resorption of alveolar bone called as direct bone
resorption.
 The number of blood vessels are increased but the
size is reduced.

 Slightly excessive tension

 Elongation of periodontal ligament fibres.
 Apposition of alveolar bone
 Blood vessels are enlarged & less.
 Greater pressure:
 Compression of fibres producing areas of the
hyalinization,
 Injury to the cells like fibroblasts and other connective
tissue cells leading to necrosis of areas of the
ligament.
 Changes in the blood vessels -breaking of vessel wall.
 Increased resorption of alveolar bone.
 Resorption of tooth surface.

 Greater/severe tension:
 Causes widening of the periodontal ligament,
thrombosis, hemorrhage, tearing of periodontal
ligament.
 Resorption of alveolar bone.
 Pressure severe enough to force the root
against bone
causes necrosis of periodontal ligament and
bone. The bone is resorbed from viable
periodontal ligament adjacent to necrotic areas
and from marrow spaces, a process called
undermining resorption or indirect bone
resorption takes place. The furcation is the
most susceptible area to injury due to
excessive occlusal forces.
 Stage 2: Repair:

 TFO stimulates increased reparative activity.

 When bone is resorbed by excessive occlusal forces,

the body attempts to reinforce the thinned bony
trabeculae with new bone. This attempt to
compensate for lost bone is called buttressing bone
formation which is an important feature of reparative
process associated with trauma from occlusion (also
occurs during inflammation or tumors)

 Buttressing bone formation can occur within the

jaw called central buttressing and on the bone
surface called as peripheral buttressing. It usually
occurs on the facial and lingual plates of the alveolar
bone. If it produces a shelf like thickening of alveolar
bone it is referred as lipping.
 Stage 3: Adaptive remodelling of the
periodontium:

If the repair process cannot keep pace with the

destruction caused by occlusion, the periodontium
may get remodelled in order to maintain the
structural relationship. This may result in thickened
periodontal ligament, angular defects in the bone
with no pocket formation, loose teeth and
increased vascularization.
 Effect of insufficient occlusal force:
 It may also be injurious to periodontal tissues which results in
the thinning of the periodontal ligament, atrophy of the fibres,
osteoporosis of alveolar bone and reduction in alveolar bone
height. Hypofunction can result from an open bite relationship,
absence of functional antagonists, or unilateral chewing
habits.

 Reversibility of traumatic lesion:

 Trauma from occlusion is reversible. When the injurious force
is removed, the repair occurs. The presence of inflammation in
the periodontium as a result of plaque accumulation may
impair the reversibility of traumatic lesions.

 Effect of the increased occlusal forces on pulp:

 The effects on the pulp have not been established.
Role of the trauma form occlusion in the progression
of periodontal disease:

 Glickman’s concept had claimed that the pathway of the spread of

plaque associated gingival lesion could be the forces of an abnormal
magnitude are acting on teeth harboring subgingival plaque. He has
explained that, teeth which are non-traumatized exhibit suprabony
pockets and horizontal bone loss, where as teeth with trauma exhibit
angular bony defects and infra bony pockets.

○ The zone of irritation includes the marginal and inter-dental gingiva, which
is affected only by plaque, where the inflammation spreads in an apical
direction, first involving the alveolar bone and later the periodontal ligament
area. Hence there is an horizontal bone loss.
○ The zone of co-destruction includes the periodontal ligament, cementum
and alveolar bone, which are coronally demarcated by the trans-septal and
the dento alveolar collagen fibres. Here the spread of inflammation is from
the zone of irritation directly down into the periodontal ligament and hence
angular bony defects with infra bony pockets are seen.
 Role of the trauma form occlusion in the
progression of periodontal disease:

Waerhaug’s concept: From his similar studies he

concluded that angular defects and infra bony pockets
occur often at periodontal sites of teeth not affected by
trauma from occlusion. In other words, he refuted the
hypothesis that trauma from occlusion played a role in
the spread of a gingival lesion into the zone of co-
destruction. The loss of periodontium was as a result
of inflammatory lesions associated with sub gingival
plaque. He concluded that angular defect occur, when
the sub gingival plaque of one tooth has reached a
more apical level than the micro biota on the
neighboring tooth, and when the volume of the
alveolar bone surrounding the roots is comparatively
large.
 In conclusion, four possibilities can occur when a
tooth with gingival inflammation is exposed to
trauma.
 Trauma from occlusion may alter the pathway of extension of
gingival inflammation to the underlying tissues. Inflammation may
proceed to the periodontal ligament rather than to the alveolar
bone & the resulting bone loss would be angular with infrabony
pockets.
 It may favor the environment for the formation and attachment of
plaque and calculus and may be responsible for development of
deeper lesions.
 Supragingival plaque can become sub gingival if the tooth is tilted
orthodontically or migrates into an edentulous area, resulting in
the transformation of a suprabony pocket into an infra bony
pocket.
 Increased tooth mobility associated with trauma to the
periodontium may have a pumping effect on plaque metabolites
increasing their diffusion.
Treatment
 Proposed by AAP (1996)
1. Reduce/eliminate tooth mobility
2. Eliminate occlusal prematurities &
fremitus
3. Eliminate parafunctional habits
4. Prevent further tooth migration
5. Decrease/stabilize radiographic changes
Therapy
 Primary Occlusal Trauma:
Selective grinding
Habit control
Orthodontic movement
Night guard

 Secondary Occlusal Trauma:

Splinting
Selective grinding
Orthodontic movement
 In summary, trauma from occlusion does not
initiate gingivitis or periodontal pockets, but it
may constitute an additional risk factor for
the progression and severity of the disease.
An understanding of the effect of trauma
from occlusion on the periodontium is useful
in the clinical management of periodontal
problems.
 Pathologic migration refers to tooth
displacement that results when the balance
among the factors that maintain physiologic
tooth position is disturbed by periodontal
disease.

Pathologic migration is relatively common

and may be an early sign of disease
or
It may occur in association with gingival
inflammation and pocket formation as the
disease progresses.
•Pathologic migration occurs most frequently in the
anterior region, but posterior teeth may also be affected.

•The teeth may move in any direction, and the migration

is usually accompanied by mobility and rotation.

•Pathologic migration in the occlusal or incisal direction is

termed extrusion.

•Even in the early stage, some degree of bone loss occurs.

•It is important to detect it in its early stages and prevent more

serious involvement by eliminating the causative factors.
 Pathogenesis
Two major factors play a role in maintaining the normal position of
teeth:

1.The health and normal height of the periodontium

2.The forces exerted on the teeth.

The latter includes:

2.a.The forces of occlusion and
2.b.Pressure from the lips, cheeks, and tongue.

The following factors are important in relation to the forces of occlusion:

 tooth morphologic features and cuspal inclination;
 the presence of a full complement of teeth;
 a physiologic tendency toward mesial migration,
 the nature and location of contact point relationships;
 proximal, incisal, and occlusal attrition,
 the axial inclination of the teeth.
Alterations in any of these factors start an
interrelated sequence of changes in the
environment of a single tooth or group of teeth
that results in pathologic migration.

Thus pathologic migration occurs under

conditions that weaken the periodontal support,
increase or modify the forces exerted on the
teeth, or both.
WEAKENED PERIODONTAL SUPPORT
 It is important to understand that the
abnormality in pathologic migration rests with
the weakened periodontium.
 The force itself need not be abnormal.
 Forces that are acceptable to an intact
periodontium become injurious when
periodontal support is reduced.
 An example of this is the tooth with abnormal proximal
contacts. Abnormally located proximal contacts convert
the normal anterior component of force to a wedging
force that moves the tooth occlusally or incisally.

 The wedging force, which can be withstood by the intact

periodontium, causes the tooth to extrude when the
periodontal support is weakened by disease.

 As its position changes, the tooth is subjected to

abnormal occlusal forces, which aggravate the
periodontal destruction and the tooth migration.

 Pathologic migration may continue after a tooth no

longer contacts its antagonist. Pressures from the
tongue, the food bolus during mastication, and
proliferating granulation tissue provide the force.
CHANGES IN THE FORCES EXERTED ON THE
TEETH

 Changes in the magnitude, direction, or frequency

of the forces exerted on the teeth can induce
pathologic migration of a tooth or group of teeth.
 These forces do not have to be abnormal to cause
migration if the periodontium is sufficiently
weakened.
 Changes in the forces may occur as a result of
unreplaced missing teeth, failure to replace first
molars, or other causes.
DRIFTING
 Drifting of teeth into the spaces created by
unreplaced missing teeth often occurs.
 Drifting differs from pathologic migration in
that it does not result from destruction of
the periodontal tissues.
 However, it usually creates conditions that
lead to periodontal disease, and thus the
initial tooth movement is aggravated by loss

of periodontal support.
DRIFTING:CAUSING
CONDITIONS
FAVOURING PERIODONTAL
DESTRUCTION

MAY NOT OCCUR IN

SOME CASES
PATHOLOGICAL MIGRATION
PATHOLOGICAL MIGRATION
PHYSIOLOGIC MOBILITY

PRINCIPALLY IN HORIZONTAL DIRECTION

MORE IN: LESS IN:
 Morning due to slight  Waking hours due to
extrusion of teeth in occlusal contacts in
socket. function.
 Healthy periodontium.  Bruxers,disease
 Single rooted teeth. periodontium.
 Multi-rooted teeth.
STAGES OF
MOBILITY
INITIAL OR INTRA- SECONDARY
SOCKET STAGE. STAGE.
 WITH FORCES  WITH FORCES
AROUND 100 lbs. AROUND 500 lbs.
 MOVEMENT OF  MOVEMENT

50-100 MICRONS. VARIES FOR EACH

 WITHIN CONFINES TOOTH.
 ELASTIC
OF PERIODONTAL
LIGAMENT. DEFORMATION OF
ALVEOLAR BONE.
SECONDARY MOBILITY
FOR FORCES OF 500 lbs AND MORE
THE DISPLACEMENT IS:

 100 to 200 microns for incisors

 50 to 90 microns for canines
 8 to 10 microns for premolars
 40 to 80 microns for molars
MECHANISM OF INITIAL
MOBILITY

 The tooth moves within the confines of

the periodontal ligament.
 This is associated with viscoelastic
distortion of the ligament and
redistribution of the periodontal fluids,
interbundle content, and fibers.
ON DISCONTINUATION OF FORCE
APPLICATION,
TOOTH RETURNS TO ITS NORMAL
POSITION IN TWO STAGES:
 The first is an immediate, spring like elastic
recoil
 The second is a slow, asymptomatic recovery
movement.
(The recovery movement is pulsating and is
apparently associated with the normal
pulsation
of the periodontal vessels, which occurs in
synchrony with the cardiac cycle.)
GRADING THE MOBILITY
STANDARDIZATON OF GRADING
MOBILITY IS IMPORTANT :
 TO DIAGNOSE THE STAGE OF THE
DISEASE.
 TO EVALUATE THE TREATMENT
OUTCOME.
 CAN BE DONE :
 MANUALLY, USING HANDLES OF TWO HAND
INSTRUMENTS.
OR
 MECHANICAL OR ELECTRONIC DEVICES FOR
THE PRECISE MEASUREMENT.
(THOUGH STANDARD, THESE INSTRUMENTS ARE NOT
WIDELY USED.) e.g. PERIOTEST
HOW TO
CHECK THE
MOBILITY?
 Mobility is graded according to the ease and
extent of tooth movement as follows:

 Normal mobility
 Grade I: Slightly more than normal.
 Grade II: Moderately more than normal.
 Grade III: Severe mobility facio-lingually
and/or mesiodistally, combined with vertical
displacement.
PATHOLOGIC MOBILITY

 Mobility beyond the physiologic range is

termed abnormal or pathologic.
 It is pathologic in that it exceeds the
limits of normal mobility values.
 The periodontium is not necessarily
diseased at the time of examination.
CAUSES OF MOBILITY

1. Loss of tooth support (bone loss) can

result in mobility. The amount of mobility
depends on the severity and distribution
of bone loss at individual root surfaces,
the length and shape of the roots, and
the root size compared with that of the
crown.
2. Trauma from occlusion (i.e., injury produced
by excessive occlusal forces or incurred
because of abnormal occlusal habits such as
bruxism and clenching) is a common cause
of tooth mobility.
Mobility is also increased by hypofunction.

3. Extension of inflammation from the gingiva

or from the periapex into the periodontal
ligament results in changes that increase
mobility.
4.Periodontal surgery temporarily increases
tooth mobility
5.Tooth mobility is increased in pregnancy and
is sometimes associated with the menstrual
cycle or the use of hormonal contraceptives.
6.Pathologic processes of the jaws that destroy
the alveolar bone and/or the roots o f the
teeth.
7.Teeth with pockets that harbor higher
proportions of Campylobacter rectus and
Peptostreptococcus micros, and possibly of
Porphyromonas gingivalis than nonmobile
teeth. This hypothesis needs further
verification.