When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. The resultant injury is termed as trauma from occlusion. TFO refers to tissue injury, not the occlusal force. An occlusion that produces such injury is termed as traumatic occlusion.

1. Trauma from
Occlusion
Presented by:-
Raina J.P Khanam
2nd year PG

2. Contents
• Definitions
• Classification
• Acute & Chronic Trauma
• Primary & Secondary Trauma
• Stages of Tissue Response

3. • Influence of Trauma from Occlusion on Marginal Periodontitis
• Clinical Signs & Symptoms
• Radiographic Features
• Therapy, treatment outcomes and prognosis
• Conclusion

4. Definition
 When occlusal forces exceed the adaptive capacity of the tissues, tissue
injury results. The resultant injury is termed as trauma from occlusion.
 TFO refers to tissue injury, not the occlusal force. An occlusion that
produces such injury is termed as traumatic occlusion.

5. Trauma from occlusion was defined by Stillman (1917) as "a condition
where injury results to the supporting structures of the teeth by the act of
bringing the jaws into a closed position".
WHO in 1978 defined trauma from occlusion as "damage in the
periodontium caused by stress on the teeth produced directly or indirectly
by teeth of the opposing jaw".

6. Other terminologies
Traumatic occlusion
Traumatogenic occlusion
Occlusal trauma
Periodontal traumatism
Traumatizing occlusion
Overload

7. Adaptive capacity of periodontium to occlusal
forces
The periodontium attempts to accommodate to the forces exerted on the crown.
This adaptive capacity varies in different persons and in the same person at different
times.
Effect of occlusal forces on periodontium is influenced by
1. Magnitude
2. Direction
3. Duration
4. Frequency of the forces.

8. 1. When the magnitude of occlusal forces is increased, the periodontium responds with a
widening of the periodontal ligament space, an increase in the number and width of
periodontal ligament fibers and an increase in the density of alveolar bone.
2. Changing the direction of occlusal forces causes a re-orientation of the stresses and strains
within the periodontium.
3. Lateral (horizontal) forces and torque (rotational) forces are more likely to injure the
periodontium .
4. The alveolar bone is also affected by the duration and frequency of occlusal forces. Constant
pressure on the bone is more injurious than intermittent forces. The more frequent the
application of an intermittent force, the more injurious is the force to the periodontium.

9. Classification
Based on
duration
Acute
Chronic
Based on
causative factors
Primary
Secondary

10. 1. Acute trauma from occlusion
 It results from an abrupt occlusal impact such as biting on a hard object e.g. olive pit.
 Restorations or prosthetic appliances may alter occlusal forces and induce acute
trauma.
 Acute trauma results in:
1. Tooth pain
2. sensitivity to percussion
3. Increased tooth mobility
 If the force is removed by a shift in the position of the tooth or by wearing away or
correction of the restoration, the injury heals and the symptoms subside.
 Otherwise, periodontal injury may worsen and develop into necrosis, accompanied by
periodontal abscess formation.

11. 2. Chronic trauma from occlusion
It is more common than acute form.
It most often develops from gradual changes in occlusion produced by
1. Tooth wear
2. Drifting movement
3. Extrusion of teeth
4. Combined with para functional habits such as, bruxism and clenching.

12. 3. Primary trauma from occlusion
When trauma from occlusion is the result of alterations in occlusal forces, it is called
primary trauma from occlusion.
Etiologic factors include:
1. Insertion of high filling.
2. Insertion of prosthetic replacement that creates excessive forces on abutment and antagonistic teeth.
3. Drifting movements or extrusion of teeth into spaces created by unreplaced missing teeth.
4. Orthodontic movement of teeth into functionally unacceptable positions.
Primary trauma do not alter the level of connective tissue attachment and do not initiate
pocket formation. This is probably because the supracrestal gingival fibers are not
affected and therefore prevent apical migration of the junctional epithelium.

13. 4. Secondary trauma from occlusion
It occurs when the adaptive capacity of the tissues to withstand occlusal forces is
impaired by bone loss resulting from marginal inflammation.
The periodontium becomes more vulnerable to injury and previously well-tolerated
occlusal forces become traumatic.

14. A. Normal periodontium with normal height of bone.
B. Normal periodontium with reduced height of bone.
C. Marginal periodontitis with reduced height of bone.
The first case is
an example of
primary trauma
from occlusion,
whereas the last
two represent
secondary trauma
from occlusion.

15. Stages of tissue response to increased
occlusal forces
Tissue response occurs in three stages
1. Injury
2. Repair
3. Adaptive remodelling

16. 1. Injury
Tissue injury is produced by excessive occlusal forces.
The ligament is widened at the expense of the bone,
resulting in angular bone loss defects without
periodontal pockets and the tooth becomes loss.

17. Slightly excessive pressure
stimulates resorption of the
alveolar bone, widening of the
periodontal ligament space. Also
the blood vessels are numerous
and reduced in size.
Slightly excessive tension causes
elongation of the periodontal
ligament fibers and apposition of
the alveolar bone. Blood vessels
are enlarged.
Pressure
Tension
Severe tension causes widening of
the periodontal ligament,
thrombosis, hemorrhage, tearing
of the periodontal ligament and
resorption of alveolar bone.

18. 1. Greater pressure produces a gradation of changes in the periodontal ligament, starting with
compression of fibers, which produces areas of hyalinization.
2. Injury to the fibroblast and other connective tissue cells leads to necrosis of areas of the ligament.
3. Vascular changes are produced, within 30 minutes impairment and stasis of blood flow occur.
4. By 2 to 3 hours blood vessels appear to be packed with erythrocytes, which start to fragment.
5. Between 1 to 7 days, there is disintegration of the blood vessel walls and release of the contents into
the surrounding tissue.
6. Also increased resorption of alveolar bone and resorption of the tooth surface occur.
7. The bone is resorbed from viable PDL adjacent to necrotic areas and from marrow spaces, this
process is known as undermining resorption.
Pressure

19. 2. Repair
Repair is constantly occurring in the normal periodontium and trauma
from occlusion stimulates increased reparative activity.
The damaged tissues are removed and new connective tissue cells and
fibers, bone and cementum are formed to restore the injured periodontium.

20.  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 and is an
important feature of the
reparative process in TFO.
Buttressing Bone Formation
Central Buttressing
(within the jaw)
Endosteal cells deposit new
bone, which restores the bony
trabeculae & reduces the size
of the marrow spaces.
Peripheral
Buttressing (on the
bone surface)
It produce a shelflike
thickening of the alveolar
margin referred as
lipping/bulge in the contour
of the facial & lingual bone.

21. BUTTRESSING

22. 3. Adaptive Remodeling of the
Periodontium
The periodontium is remodeled in an effort to create a structural relationship in which the
forces are no longer injurious to the tissues.
This results in a widened periodontal ligament, which is funnel shaped at the crest and
angular defects in the bone, with no pocket formation.
The involved teeth become loose.
Increased vascularization.

23. The injury phase shows an
increase in areas of resorption and
a decrease in bone formation.
The repair phase demonstrates
decreased resorption and increased
bone formation.
After adaptive remodelling of
the periodontium, resorption and
formation return to normal.

24. Association of trauma from occlusion and
periodontal disease
1. Glickman’s concept
 Glickman (1965, 1967) claimed that 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.
 The character of the progressive tissue destruction of the periodontium at a "traumatized tooth"
will be different from that characterizing 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.

25. The periodontal structures can
be divided into two zones:
1. The zone of irritation
2. The zone of co-destruction

26. Zone of irritation:
 This zone consists of marginal &
interdental gingiva.
 The soft tissue is bordered by hard
tissue only on one side (tooth) and is
unaffected by the occlusal forces.
 This means that gingival inflammation
cannot be induced by trauma from
occlusion but is the result of irritation
from microbial plaque.
 Inflammation in the “zone of irritation”
causes horizontal bone loss.

27. Zone of Co-destruction
The zone of co-destruction includes the periodontal ligament, the root cementum and the alveolar bone
and is coronally demarcated by the trans-septal (inter-dental) and the dentoalveolar collagen fiber
bundles.
The tissue in this zone may become the seat of a lesion caused by trauma from occlusion.
The fiber bundles which separate the zone of co-destruction 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.

28.  Through this exposure from two different directions
the fiber bundles may become dissolved and/or oriented
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
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.
 Glickman (1967) in a review paper stated that trauma
from occlusion is an etiologic factor of importance in
situations where angular bony defects combined with
infrabony pockets are found at one or several teeth.

29. 2. waerhaug’s concept
 Waerhaug (1979) measured 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 from his analysis that angular bony defects and infrabony pockets
occur equally often at periodontal sites of teeth which are not affected by trauma
from occlusion as in traumatized teeth.
 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".

30.  According to Waerhaug, the loss of connective attachment and the resorption of bone around
teeth are, 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.
 As a consequence, the conclusions drawn from this field of research have not been generally
accepted.

31. Clinical and radiographic features of
trauma from occlusion
 The most common clinical sign of trauma to the periodontium is increased tooth mobility.
 Increased width of the periodontal ligament space, with thickening of the lamina dura along the
1. lateral aspect of the root
2. in the apical region
3. in bifurcation areas
 A “vertical” rather than “horizontal” destruction of the interdental septum.
 Radiolucency and condensation of the alveolar bone.
 Root resorption

32. Fremitus test
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 dry 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 inter-
cuspal 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.

33. The following classification system is used :
1. Class I fremitus – Mild vibration or movement detected
2. Class II fremitus – Easily palpable vibration but no visible movement
3. 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.
In the posterior teeth TFO can be detected with help of occlusion registration strip/articulating
paper.
High pressure points can be detected by pattern of impression made by registration
strip/articulating paper.

34. Therapy
Primary Occlusal Trauma:
1. Selective grinding
2. Habit control
3. Orthodontic
movement
4. Night guard
Secondary Occlusal Trauma
1. Oral prophylaxis
2. Splinting
3. Selective grinding
4. Orthodontic
movement

35. Unsuccessful Therapy
1. Increasing tooth mobility
2. Progressive tooth migration
3. Continued client discomfort
4. Premature contacts remain
5. No change in radiographs
6. Para functional habits remain
7. TMJ problems remain or worsen

36. 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.