*RAMA DENTAL COLLEGE HOSPITAL AND RESEARCH CENTRE DEPARTMENT OF PERIODONTOLOGY TRAUMA FROM OCCLUSION When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results the resultant injury is termed as trauma from occlusion.

1. PERIODONTAL RESPONSE
TO
EXTERNAL FORCES.

2. TRAUMA FROM OCCLUSION.
* When occlusal forces exceed the
adaptive capacity of the tissues,
tissue injury results the resultant
injury is termed as trauma from
occlusion.

3. Excessive occlusal forces also cause-
Painful spasms in masticatory musculature.
Injury to the TMJ.
Excessive tooth wear.

4. Traumatic occlusion
• Any occlusion which produces periodontal
injury is called as Traumatic occlusion.

5. Types of trauma from occlusion.
1). Acute T.F.O.
2). chronic T.F.O
A) Primary T.F.O
B) Secondary T.F.O

6. Acute T.F.O
• It results from an abrupt occlusal impact such
as –biting on hard object, faulty restoration,
faulty prosthesis.
• clinical features,
-Tooth pain,
-Sensitivity to percussion,
-Increased tooth mobility,
-Cementum tears.

7. Chronic T.F.O
• It develops from gradual changes in occlusion
- Due to tooth wear ,
- Drifting movement ,
- Extrusion of tooth ,
- Bruxism & clenching.

8. Causes for T.F.O
1) Alterations in occlusal forces,
2) Reduced capacity of the periodontium to
withstand occlusal forces,
3) Both.

9. Primary T.F.O
It is because of alterations in occlusal forces
which results in T.F.O
• High filling,
• Faulty prosthesis,
• Drifting/extrusion of teeth into spaces of
unreplaced missing teeth,
• Orthodontic tooth movement to functionally
unacceptable positions

10. Secondary T.F.O
 It occurs when the adaptive capacity of the
tissues to withstand occlusal forces is
impaired by bone loss resulting from
marginal inflammation, resulting in reduced
periodontal ligament area

11. Excessive occlusal forces can be
superimposed on three different
situations.
1) Normal periodontium with normal height of
bone- Primary T.F.O
2) Normal periodontium with reduced height
of bone- Secondary T.F.O
3) Marginal periodontitis with reduced height
of bone - Secondary T.F.O

13. Stages of tissue response to increased
occlusal forces
Stage i- Injury.
Stage ii- Repair.
.
Stage iii- Adaptive remodelling of the
periodontium.

14. Stage i-Injury
 Slightly excessive pressure- cause widening
of pdl space, stimulates resorption of
alveolar
 Slightly excessive tension- causes elongation
of pdl fibres,apposition of alveolar bone.
 Greater pressure- causes compression of pdl
ligament leading to areas of hyalinization
& necrosis, injury to fibroblasts, increased
resorption of alveolar bone & tooth surface.

15.  Severe tension- Causes widening,
thrombosis, hemorrhage & tearing of
pdl ligament and resorption of
alveolar bone.
 Severe pressure- causes necrosis of
bone & pdl ligament
 Undermining resorption- The bone is
resorbed from viable pdl ligament
adjacent to necrotic areas and from
marrow spaces .

16. Injury produces –
• A temporary depression of mitotic activity.
• Depression in rate of proliferation &
differentiation of fibroblasts.
Furcation areas are more susceptible to
injury due to excessive occlusal forces

17. Stage ii-Repair
 The damaged tissues are removed and new
connective tissue cells ,fibers, bone &
cementum are formed.
 Buttressing bone formation;-
when bone is resorbed by excessive
occlusal forces the body attempts to reinforce
the thinned bony trabeculae with new bone
is known as buttressing bone formation .

18. Types of buttressing bone formation.
 Central buttressing bone formation.- Occurs
within the jaw bone by endosteal cells.
 Peripheral buttressing bone formation.-
Occurs on the facial and lingual surfaces
of the alveolar bone.
 Lipping- Shelf like thickening of alveolar
bone margin.

20. Stage iii- Adaptive remodelling of the
periodontium.
 The periodontium is remodelled in an effort
to create a structural relationship in which
the forces are no longer injurious to the
tissues.
-Thickened pdl ligament,
-Funnel shaped crest,
-Angular bone defect with no pocket
formation.

21. Clinical features of T.F.O
 Increased tooth mobility,
 Vertical destruction of interdental septum,
 Radiographs reveal-increased width of pdl
space, thickening of lamina dura,
 Radiolucency & condensation of the alveolar
bone,
 Root resorption.

22. Effects of insufficient occlusal forces
on the periodontium.
In case of - Openbite,
- Absence of functional antagonist,
- Unilateral chewing habits.
 Thinning of pdl ligament,
Atrophy of pdl fibers,
Osteoporosis of the alveolar bone,
Reduction in bone height.

23. Effect of T.F.O on progression of
marginal periodontitis.
Marginal gingiva is unaffected by T.F.O
because its blood supply is not affected,
As long as inflammation is confined to the
gingiva the inflammatory process is not
affected by occlusal forces,

25. Glikman’s concept
 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 progressive destruction of the periodontium
at a traumatized tooth will be different from
that of non traumatized tooth causing angular
bony defects & infrabony pockets instead of
suprabony pockets & horizontal bone loss.

26. Glikman’s concept
Periodontal structures are divided into two
zones,
1) Zone of irritation- includes marginal gingiva
& interdental gingiva.
2) Zone of co-destruction- includes
periodontal ligament ,root cementum & the
alveolar bone. this zone is seperated by zone
of irritation by trans-septal & dentoalveolar
fiber bundles.

30. • These fiber bundles are affected from two
different directions,
1. From inflammatory lesion due to plaque in zone of
irritation,
2. From trauma induced changes in the zone of
co-destruction,
This may dissolve & / or orient the fibers in
parallel direction to the root surface. hence the
spread of inflammatory lesion from zone of
irritation directly down into the periodontal
ligament not via interdental bone.
- when inflammation extends from gingiva into the
supporting pdl tissues , plaque induced
inflammation enters the zone influenced by
occlusion,this is called as Zone of codistruction,

32. Glikman’s concept
• This alteration of the normal pathway of
plaque associated inflammatory lesion
results in angular bony defects,
• Therefore T.F.O is a etiologic factor
(co-destructive factor) in teeth with
infrabony pockets with angular bony defects.

33. Waerhaug’s concept
• He measured the distance between the
subgingival plaque & 1) the periphery of the
associated inflammatory cell infiltrate in the
gingiva,2) the surface of the adjacent alveolar
bone.
• Found angular bony defects & infrabony
defects occur equally often at periodontal
sites of teeth which are not affected by T.F.O
as in traumatized teeth

34. Waerhaug’s concept
 He concluded that angular bony defects
& infrabony pockets occur when the
subgingival plaque of one tooth has reached
a more apical level than the microbiota on
the neighboring tooth & when the volume of
the alveolar bone surrounding the roots is
comparatively large

36. Proposed theories of interaction of
T.F.O and inflammation
 T.F.O may alter the pathway of extension of
gingival inflammation to the underlying
tissues.
 T.F.O induced root resorption uncovered by gingival
recession favor plaque & calculus formation lead
to development of deeper lesions .
 supragingival plaque can become subgingival if tooth
migrates resulting in transformation of Suprabony
pocket into infrabony pocket .
 Increased tooth mobility due to T.F.O causes
pumping effect on plaque metabolites &
increase their diffusion

37. DIAGNOSIS OF T.FO
Clinically –history, excessive tooth wear,
tooth mobility,
Radiographs,
Occlusal evaluation,
Fremitus test-

39. Fremitus test
N= Normal (no vibration or movement)
+= one degree fremitus- slight vibration can be
felt
++= two degree fremitus-the tooth is clearly
palpable but movement is barely visible
+++= three degree fremitus-movement is
clearly observed visually

40. Management.
• Occlusal adjustment-is the establishment of
functional relationships favorable to the
periodontium by,
* Reshaping of the teeth by grinding,
* Dental restoration,
*Tooth movement,
*Tooth removal / orthognathic surgery

41. Coronoplasty
• It is a selective reduction of occlusal areas.
• Is the mechanical elimination of occlusal
supra contacts involved in function &
parafunction

42. Pathologic tooth migration
 Is a tooth displacement that results when
the balance among the factors that
maintain physiologic tooth position is
disturbed by periodontal disease.
Normal position of teeth are controlled by,
# Health & normal height of the
periodontium.
# Forces exerted on the teeth.

43. Causes of pathologic tooth migration
 Weakened periodontal support,
- Periodontitis- LAP
 Changes in the forces exerted on the teeth. -
Unreplaced missing teeth,
-Failure to replace 1st molar,
-T.F.O
-Pressure from tongue,
-Pressure from the granulation tissue of
pockets.

44. Failure to replace first molars
• Second & third molars tilt, resulting in decrease
in vertical dimension,
• Premolars move distally ,& mandibular incisors
tilt lingually,
• Anterior overbite is increased,
• Mandibular incisors strike maxillary incisors
near the gingiva & traumatize the gingiva,
• Maxillary incisors are pushed labially & laterally,
• Anterior teeth extrude,
• Diastema created between anterior teeth

53. Treatment pathologic migration
• Non surgical & surgical periodontal therapy.
• Orthodontic therapy.
• Prosthodontic therapy.
-Interdisciplinary approach

54. Conclusion.
T.F.O does not initiate gingivitis or
periodontal pockets but it may constitute an
additional risk factor for the progression &
severity of the disease