Trauma from occlusion
 Every
tissue in the human body has got the ability
to adapt according to the functional, physiologic
and environmental changes occurring in and
around it or to it. This adaptive capacity of a tissue
creates a range so that when the tissue is stressed
to its limit or within the limit, still functions
without any pathology occurring in it. But when
this range or limit is crossed or over stressed –
tissue injury or pathology occurs. The adaptive
capacity or the range forms an inherent margin of
safety for that particular tissue.
.
E.g.
 Skin, Mucosa → Stress → Keratinization → Still
increased stress/irritation leads to → Malignant
change
 Just
like any other tissue in the body even the
periodontal tissue has got an inherent margin of
safety to occlulsal forces, but when these forces
exceed the adaptive capacity of the periodontium
tissue injury results. This tissue injury is referred to
as trauma from occlusion and the occlusion which
produces/causes such an injury is known as
traumatic occlusion
 WHO
1978:
 Damage in the periodontium caused by stress on
the teeth produced directly or indirectly by teeth of
opposing jaw.
 AAP 1986:
 An injury to the attachment apparatus as a result of
excessive force.
classification
1
2
a) Acute
b) Chronic
a) Primary
b) Secondary
Criteria:
The main criteria that determines whether the
occlusion is traumatic or not is not how the teeth
occlude.
 Any occlusion that produces injury is traumatic
 An occlusion esthetically and anatomically
acceptable might be functionally traumatic and
other hand highly mal occlusion might be nontraumatic.

All the terms describe the effect of occlusion on
periodontium, not the position of the teeth. As
trauma from occlusion describe tissue injury to the
periodontium rather than to the occlusion .An
increased occlusal force is not traumatic to the
periodontium if it can accommodate it.
Acute
 This
results from an abrupt change
occlusion/occlusal force such as produced by
Biting on hard object
Over hang
Over filling
Faculty restoration/prosthesis
in
 The
teeth might exhibit signs of acute trauma.
pain,
sensitivity to percussion,
mobility etc.
 The injury/ mobility heals after removal of the
irritant, removal of overfilling/prosthesis. If the
condition is not treated then the condition might
worsen and might lead to a chronic lesion.
Sometimes cemental tears have also been found to
occur with acute trauma.
Chronic
 Chronic
trauma from occlusion is the more
common form and is of great significance.
 Chronic trauma from occlusion is produced over a
period of time by tooth wear, migration, extrusion
of teeth etc. compounded with habits such as
bruxism and clenching.
Primary Trauma from Occlusion
 Primary
form includes a tissue reaction or damage
elicited around a tooth with normal height of
periodontium.
 The changes in the periodontium are because of
changing occlusal forces and the local alterations
to which a tooth is subjected from occlusion. :
For example
1 High filling.
2 Improper prosthesis.
3 Drifting of teeth into areas of missing teeth.
4Orthodontic movement of teeth into functional
unacceptable positions.

there is no alteration in the connective tissue
attach level and do not initiate pocket formation.
Secondary Trauma from Occlusion
 Secondary
form is related to situations in which
occlusal forces cause injury in a periodontium of a
reduced height. This occurs when the adaptive
capacity of the periodontium to withstand occlusal
forces is impaired by bone loss resulting from
marginal inflammation.
The result is that there is more force/Unit area of
attachment. Thus the periodontium becomes
vulnerable to injury and previously well tolerated
forces become traumatic.
Trauma From Occlusion and
Plaque Associated Periodontitis
 Way
back in 1901 Karolyi postulated that an
interaction existed between trauma from occlusion
and alveolar pyorrhea. Various opinions have been
postulated for and against the same, over the years.
 Box and Stone (1938) in experiments done on
monkeys and sheep they showed that TFO is and
etiologic factor in a variety of periodontal disease
in which there is vertical bone loss in associated
teeth
 Presently
there are 2 main concepts on the
relationship between TFO and periodontal disease
given by:
Glickman (1965, 1967) and
2. Waerhaug’s (1979) these concepts were based on
studies done on human autopsy material.
1.
 In
studies done on human autopsy material they
assessed:
1. Lesions histopathologically
2. The presence and apical extensions of the
microbial plaque
3. Mobility of teeth involved and
4 Occlusal scrutiny of the sites involved
GLICKMAN’S CONCEPTS 1965,
1967:
 We
know that the normal path of progression of
periodontal diseases is:
 Gingiva → Alveolar bone → PDL
 He said that trauma altered this path of spread of
infection to:
 Gingiva → PDL → Alveolar bone
 This
said that the spread of infection and tissue
destruction in a traumatized tooth was different
than for a non-traumatized tooth.
 Instead
of even destruction of alveolar bone and
PDL with suprabony pockets, with horizontal bone
loss, the regions exposed to trauma developangular defects and infrabony pockets.
In order to understand this we divide
periodontium into 2 parts:
Zone of irritation
2. Zone of co-destruction
1.
the
Zone of irritation:
 This
includes the marginal and inter-dental
gingiva. The soft tissue is bordered only one side
by hard tissue i.e. the tooth and is not effected by
the forces of occlusion.
 This means that TFO does not cause gingivitis.
 Gingivitis is because of the plaque and its products
 The paths of destruction in a non-traumatic tooth
remain as
 Tooth → Bone → PDL Horizontal bone loss
Zone of Co-destruction:
 This
zone includes the PDL, alveolar bone and root
cementum.
 This zone is separated from the zone of irritation
by the the supracrestal fibres.
 This tissue is the seat of a lesion caused by TFO
 The fibre bundles which separate the zones of Codestruction from zone of irritation can be affected
in 2 directions:
1.
2.


.
From the microbial plaque inflammatory lesion
From trauma induced changes in zone of Codestruction
Because of the action of the injurious agents
from 2 different direction the fibres get oriented
in a direction parallel to root surface.
This facilitates the spread of infection from zone
of irritation to directly into the PDL space rather
than through alveolar bone.
 This
alteration in “Normal” pathway leads to
spread of plaque associated inflammatory lesion
and development of angular defects
WAERHAUG’S CONCEPT (1979):
study was similar to Glickman’s but he also
measured the distance between the subginginval
plaque and
1. Periphery of the associated inflammatory cell
infiltrate in the gingiva
2. Surface of the alveolar bone
 This
 From
this study he concluded that angular bony
defects and infrabony pockets occur equally often
at periodontal sites of teeth which are not affected
by TFO as in traumatized teeth.
refutes the Glickman’s concept that TFO has
a role in spreads of infection in the zone of codestruction.
 This
 The
resorption of bone and pocketing are only
because of plaque and its microbial effect.
 This said that infrabony pockets occurred when the
subgingival plaque reached an area apical to than
the adjacent tooth and the volume of the alveolar
bone surrounding the root is large.
Response of the Periodontium to
Increased External Forces
 When
the periodontium is stressed to its limits, the
tissue response occurs in 3 stages:
1.
Injury
2.
Repair
3.
Adaptive remodeling of the periodontium

Tissue injury is produced by excessive occlusal forces, the
tissue then attempts to repair and restore the periodontium.
This occurs if the forces are diminished or the tooth drifts
away from the traumatizing forces.

If the offending force is chronic, the periodontium is
remodeled to cushion its impact. The ligament is widened
at the expense of the bone resulting in angular defects
without periodontal pockets and the tooth becomes mobile.

Under these forces the tooth moves around an axis of
rotation, which is located, in single rooted teeth at the
junction between middle and apical 1/3rd of the
clinical root, which creates different degrees of
pressure and tension and depend upon the type of the
forces.

The furcation areas are the areas most susceptible to
injury
 As
a result of tissue injury there is a temporary
depression in the mitotic activity and the rate of
proliferation and differentiation of fibroblasts in
collagen formation and in bone formation.
 Once
the forces are removed the tissues return to
normal.
2. Repair: Repair is constantly occurring in normal
periodontium and trauma stimulates the reparative
activity. The damaged tissues are removed and
new connective tissue cells, bone, fibres and
cementum are formed in an attempt to restore the
injured periodontium.
 The forces remain traumatic only as long as the
damage produced exceeds the reparative capacity
of the tissues.
3. Adaptive Remodeling of the Periodontium:
Force → Injury → Repair,
 are at an equilibrium the active tissue injury will be
at bay. But if the reparative capacity cannot keep
up with the destruction caused by occlusion, the
periodontium is remodeled in an effort to create a
structural relationship in which the forces are no
longer injurious.
 This
leads to:
1. Thickening of PDL which is funnel shaped at the
crest.
2. Angular bone defects without pocketing
3. The involved teeth become mobile
4 Increased vascularization has also been reported
Mechanism
 To
understand the changes taking place within the
periodontal tissues various experiments were
carried out in different animal models.
1. Slightly excessive pressure

At sites of pressure:

There
is
increased
vascularity
→
Increased
permeability → Thrombosis → Disorganisation of
cells and collagen fibres → If this is within limits then
the vitality of the cells is maintained → Osteoclasts
appear and resorb the bone. This is known as direct
bone resorption.
At the sites of tension:
Stretching of the periodontal ligament fibres
↓
Engorgement of vessels
↓
Increased blood flow
↓
Apposition of bone
2. Greater pressure:
At sites of pressure:
 There is compression of the fibres →
De-composition of fibres and death of cells →
Necrosis of ligament.
 Vascular changes in 30 mins. → Stasis of flow after 23 hrs. → Packing of RBC’s and fragmentation of
RBC’s → (1-7 days) Disintegration of the vessel wall
→ release of contents into surrounding tissues.

 Necrosis
and hyalinization of the ligament →
Osteoclasts appear from adjacent areas → Resorb
bone. This is known as indirect resorption or
Undermining resorption.

Areas of tension:
 Tearing
of fibres → Hemorrhage → Resorption of
bone instead of formation.

Severe pressure:

Causes the root to appose against the bone – leads to
necrosis of the PDL and bone. When bone is resorbed by
excessive occlusal forces the body tries to compensate for
this by formation of bone and this compensatory
mechanism is known as buttressing bone formation.

Bone is resorbed by the viable cells from the adjacent
healthy PDL area and marrow spaces by undermining
resorption/indirect resorption.
 Pressure
and Tension → hypermobility of teeth →
tilting of teeth → escape from forces →
nullification → adaptation → stabilization of tooth.
 The
buttressing bone formation is an important
feature of reparative phase associated with TFO.
Also seen in osteolytic tumors and carcinomas.
 This
buttressing formation can be either –
1 Central
2 Peripheral
 In
central buttressing the endosteal cells deposit
new bone, which restores the bony trabeculae
and reduces the size of marrow spaces.
 Peripheral buttressing occurs on buccal and
lingual surfaces- “Lipping”
 Some times cartilage like material is also
deposited.
JIGGLING TYPE OF TRAUMA:
 The
fact that in humans like in other animals the
trauma is not unilateral, the kind of direction of
forces in humans has been described as JIGGLING
type. This indicates forces acting from all sides
something like torquing/shearing forces
Clinical and Radiographic Features
Clinical:
1.
Increased mobility – injury stage - destruction of PDL
fibres and because of widening of PDL space after
remodeling – This mobility because of adaptation is
normal and is not pathologic because it is an adaptation
and not a disease, but if it becomes progressively mobile
then it is considered to be pathologic.
2.
Pain in acute cases.
3 Fremitus test – This is the clinical test done to
check the presence of trauma in the anterior
region.

Test: Place the moist finger on the labial surface
of the upper anterior teeth and instruct the patient
to bite with his back teeth. Feel for any vibrations
on the finger.
 Grading:
– When only vibration is felt and there is no
mobility.
 II – When the mobility of the teeth is felt but not
clinically visible.
 III – When there is overt, clinically visible
mobility present.
 To evaluate the TFO in posterior region it is
advisable to do a cast mounting on an articulator.
I
Radiographic:
i)
Increased width of PDL space.
ii) Thickening of lamina dura.
iii) Vertical bone loss.
iv) Root resorption.
Treatment:
1.
2.
Coronoplasty
Splinting
conclusion
Trauma from occlusion does not initiate gingivitis or
periodontal pockets, but it may act as an additional
risk factor for the progression and severity of the
disease.