8.TFO.pptx

• To understand the role of trauma from occlusion in
periodontal disease, it is necessary to understand the
relationship of occlusion to periodontal health.
• Occlusion is the lifeline of the periodontium.
2
ROLE OF OCCLUSION IN THE ETIOLOGY AND TREATMENT OF PERIODONTAL DISEASE
IRVING GLICKMAN J DENT RES SUPPLEMENT NO. 2 VOL 50, 1971
INTRODUCTION

3
• When there is increased functional demand, the
periodontium tries to accommodate it. The
periodontal ligament thickens and becomes more
dense; the bone trabeculae are reinforced.
• If the periodontium cannot adapt to the force, the
tissues are injured,Injury in the periodontium
produced by occlusal forces is "TRAUMA FROM
OCCLUSION“
ROLE OF OCCLUSION IN THE ETIOLOGY AND TREATMENT OF PERIODONTAL DISEASE
IRVING GLICKMAN J DENT RES SUPPLEMENT NO. 2 VOL 50,1971

DEFINITIONS
4
CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY - JAN LINDHE – 5TH EDITION
“An injury to the attachment apparatus as a result of excessive
occlusal force.” American Academy of periodontology -1986
Glickman 1972, “ When occlusal forces exceed the adaptive
capacity of the tissues, tissue injury results. The resultant
injury is termed trauma from occlusion.”

• Trauma from Occlusion is defined as an injury
resulting in tissue changes within the periodontal
attachment apparatus as a result of occlusal force.
Such an occlusion is called truamatic occlusion.
6
ANN PERIODONTOL 1999(4);102-107.
ANN PERIODONTOL 1999(4);102-107.

SYNONYMS
• Traumatic occlusion
• Traumatizing occlusion
• Occlusal trauma
• Traumatogenic occlusion
• Periodontal traumatism
• Overload
• Occlusal dystrophy/disharmony
7

HISTORICAL PERSPECTIVE
• Karolyi (1901) – postulated interaction between TFO &
“alveolar pyrrohea”
• Stillman (1917 & 1926) – advocated use of occlusal
adjustment for treatment of TFO
• Box & Stones (1938’s ) - animal experiments TFO
etiologic factor in periodontal disease
8

Effect of occlusal forces on the periodontium is
influenced by their :-
 Magnitude
 Direction
 Duration
 Frequency
9
CARRANZA’S CLINICAL PERIODONTOLOGY –10TH EDITION

TYPES
TRAUMA FROM
OCCLUSION
ACUTE CHRONIC
TRAUMA FROM
OCCLUSION
PRIMARY SECONDARY
10

ACUTE TFO
• Results from an abrupt change in the occlusal forces,
such as
- that produced by biting on a hard object or
- by restorations or prosthetic appliance.
• Teeth exhibit signs of acute trauma - tooth pain,
- sensitivity to percussion,
- tooth mobility etc.
11

• If the force is dissipated the injury heals and the
symptoms subside.
• If untreated or unresolved it may worsen leading to
necrosis, pdl abscess formation or persist as a
symptom free chronic condition.
• Sometimes cemental tears may occur as a result of
occlusal trauma.
12

CHRONIC TFO
- more common than acute TFO
- greater clinical significance.
• develops from gradual changes in occlusion produced by
- tooth wear,
- drifting movement, and
- extrusion of teeth,
- combined with parafunctional habits such as
bruxism and clenching
13

14
Primary TFO occurs if
• TFO is the primary etiologic factor in periodontal
destruction
• Local alteration to which a tooth is subjected is from
occlusion
Causes -
• Insertion of high filling
• Insertion of a prosthetic replacement
• Drifting / extrusion of teeth into spaces
• Orthodontic movement
Primary TFO
Figure showing primary trauma from occlusion it is caused b
on normal healthy periodontium

• Primary trauma does not alter the level of connective
tissue attachment and does not initiate pocket
formation.
• Supracrestal gingival fibers are not affected ,therefore
prevent apical migration of the Junctional epithelium.
(Polson et al – JPR 1976; 279 )
15

SECONDARY TFO
16
• When the adaptive capacity of the tissues to withstand
occlusal forces is impaired by bone loss resulting from
marginal inflammation.
• Periodontium becomes vulnerable to injury
• Previously well tolerated forces become traumatic.
• Marginal inflammation reduces the periodontal
attachment area
Figure showing secondary trauma from occlusion, which is inj
even to normal occlusal forces because of reduced periodontal su

GLICKMAN’S CONCEPT: (1965, 1967),
17
• Pathway of spread of plaque associated gingival
lesion can be changed if forces of abnormal
magnitude are acting on teeth harboring subgingival
plaque
• Character of progressive tissue destruction different
in:
1. Traumatized tooth
2. Non – traumatized tooth

• Instead of an even destruction of the periodontium and
alveolar bone (suprabony pockets and horizontal bone
loss),sites which are also exposed to abnormal occlusal
force will develop angular bony defects and infrabony
pockets.
18

• The periodontal structures can be divided into two
zones:
• 1. the zone of irritation and
• 2. the zone of co-destruction
19

20
Zone of irritation
Marginal & interdental gingiva
Gingival inflammation not induced by TFO
It results from microbial plaque
Zone of co-destruction
PDL
Root cementum
Alveolar bone
Seat of lesion caused by TFO.

21
Fig. 14-2 The infl ammatory lesion in the zone of irritation can, in teeth not subjected to
trauma, propagate into the alveolar bone (open arrow), while in teeth also subjected to trauma
from occlusion, the infl ammatory infi ltrate spreads directly into periodontal ligament (fi lled
arrow).

• Waerhaug’s concept : 1979
• Waerhaug (1979) examined autopsy specimens,
measured the distance between the subgingival plaque
and
• (1) the periphery of the associated inflammatory cell
infiltrate in the gingiva and
• (2) the surface of the adjacent alveolar bone.
22

• 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.
• 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.
23

• Waerhaug concluded that angular bony defects and
infrabony pockets occur when –
- the subgingival plaque of one tooth has reached
more apical level, and
- when the volume of the alveolar bone
surrounding the roots is comparatively large.
24

25
• Waerhaug's observations support findings presented
by Prichard (1965) and Manson (1976) which imply
that the pattern of loss of supporting structures is the
result of interplay between the form and volume of the
alveolar bone and the apical extension of the microbial
plaque on the adjacent root surfaces.

• Glickman's conclusions that trauma from occlusion is
an aggravating factor in periodontal disease
• Waerhaug's concept, i. e. that there is no relationship
between occlusal trauma and the degree of periodontal
tissue breakdown
26

EFFECT OF PERIODONTAL TISSUES ON ORTHODONTIC TYPE OF
TRAUMA
27

JIGGLING TYPE OF TRAUMA
• Occlusal forces act alternately in one then the opposite
direction
• Such forces – jiggling forces
28

Healthy periodontium with normal height
29

Healthy periodontium with reduced height
30

Plaque-associated periodontal disease
31

Stages of Tissue Response
1. Injury
2. Repair
3. Adaptive remodeling of the periodontium.
TISSUE RESPONSE TO INCREASED OCCLUSAL FORCES
33
CARRANZA’S CLINICAL PERIODONTOLOGY –10TH EDITIONS

STAGE 1 - INJURY
• Excessive occlusal forces  tissue injury.
• Body attempts to repair the injury & restore the
periodontium.
• Occurs if the forces are diminished / tooth drifts away
from them.
• If force is chronic  periodontium is remodeled to
cushion its impact.
34

• Ligament is widened at the expense of the bone
• Angular bone defects occur without periodontal pocket
formation
• Tooth becomes loose.
Under the forces of occlusion :
• A tooth rotates around a fulcrum or axis of rotation
35

• Areas of pressure and tension on opposite sides of the
fulcrum.
• Different lesions are produced by different degrees of
pressure and tension.
• Slightly excessive pressure  resorption of the alveolar
bone  widening of the periodontal ligament space.
• Slightly excessive tension  elongation of the
periodontal ligament fibers  apposition of alveolar
bone.
36

• Histologically : Greater pressure produces gradation of changes in the pdl
Compression..hyalinization
Injury to fibroblasts and C.T …necrosis
Vascular changes… 30 min. stasis…2-3 hrs B.V packed
Disintegration of B.V… increased resorption of alveolar bone and tooth surface
37

Severe tension:
widening of the periodontal ligament
Thrombosis
Hemorrhage
Tearing of the PDL
Resorption of alveolar bone.
Severe pressure :
Force the root against bone
Necrosis of PDL and bone (undermining resorption)
38

• The damaged tissues are removed
• New connective tissue cells and fibers, bone and
cementum are formed attempt to restore the injured
periodontium.
• Forces remain traumatic as long as the damage
produced exceeds the reparative capacity of the tissues.
STAGE II: REPAIR
39

• Thinned bony trabaculae reinforced with new bone
• Important feature of the reparative process associated
with TFO
• Central buttressing ( within the jaws ) and peripheral
buttressing (bone surface).
Lipping
• Peripheral buttressing produce a shelf-like
thickening of the alveolar margin
BUTTRESSING BONE FORMATION
40

• Results in thickened PDL  funnel shaped at the crest
• Angular defects in the bone with no pocket formation.
• Involved teeth become loose.
• ed vascularization also reported.
STAGE III: ADAPTIVE REMODELING OF THE PERIODONTIUM
41

EFFECT OF INSUFFICIENT FORCE
• Insufficient occlusal force may also be injurious to the
supporting periodontal tissues (Cohn 1961).
• Hypofunction can result from
- open bite relationships,
- absence of functional antagonists
- unilateral chewing habits.
42

• Insufficient stimulation causes
• Thinning of PDL
• Atrophy of fibers
• Osteoporosis of alveolar bone
• Reduction in bone height
43

REVERSIBILITY OF TRAUMATIC LESIONS
• Trauma from occlusion is reversible.
• 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 and worsens.
44

If periodontal structures could adapt to the applied force
• Progressive mobility – terminated in few weeks
• Active resorption ceased
• Angular bone destruction persisted
45

If the tissues couldn’t adapt –
• Angular bone destruction was continuous & mobility
remained progressive
• Zone of irritation & co-destruction merged,
dentogingival epithelium proliferated in apical direction
• Increase in width of PDL on both sides
• Teeth hypermobile ( Progressive mobility )
• Angular bony defects – radiographs
46

CHANGES IN OTHER TISSUE
• 1. Gingiva:
• No evidence of gingival changes .
• The accumulation of bacterial plaque that initiates
gingivitis and results in periodontal pocket formation
affects the marginal gingiva, but TFO occurs in the
supporting tissues and does not affect the gingiva.
47
VASCULAR REACTIONS IN THE PERIODONTAL LIGAMENT INCIDENT TO TRAUMA FROM OCCLUSION .
JOURNAL OF CLINICAL PERIODONTOLOGY: 1974: 1: 58

48
VASCULAR REACTIONS IN THE PERIODONTAL LIGAMENT INCIDENT TO TRAUMA FROM OCCLUSION .
JOURNAL OF CLINICAL PERIODONTOLOGY: 1974: 1: 58
• The marginal gingiva is unaffected by TFO as its blood
supply is sufficient to maintain it, even when the vessels of
the periodontal ligament are obliterated by excessive
occlusal forces.

2.Cementum:
• In acute phase, cemental tears and fractures.
• In the chronic phase reparative changes such as
cementum hyperplasia and formation of cementum
spurs may occur. In some cases cementum resorption
may follow.
49
SIGNIFICANCE OF OCCLUSION IN THE ETIOLOGY AND TREATMENT IS EARLY,MODERATE AND ADVANCED
PERIODONTITIS.SIGURD P.RAMFJORD AND MAJOR M.ASH.J PERIODONTOL 1981,511

• 3. Pulp:
• Odontoblastic activity may be stimulated and secondary
dentin may be formed.
• Pulp chamber and canal may become narrower and even
obliterated.
• Pulp stones may be formed. In such cases there may be even
pulpitis and loss of pulp vitality.
50
CARRANZA’S CLINICAL PERIODONTOLOGY – 10TH EDITION

CLINICAL SIGNS
• Increase tooth mobility
• Migration
• Wear facets Vertical impaction of food and wear facets.
• Hypersensitivity
• Abfraction
51
JIN LJ AND CAO CF: CLINICAL DIAGNOSIS OF TRAUMA FROM OCCLUSION AND ITS RELATION WITH
SEVERITY OF PERIODONITIS. J CLIN PERIODONTOL 1992: 19: 92-97

RADIOGRAPHIC CHANGES
• Increased width of periodontal space
• Thickening of lamina dura
• Vertical rather than horizontal bone loss
• Radioluscence and condensation of alveolar bone
• Root resorption
• increased radiodensity due to change in axial forces or
decreased trabecular pattern on side of pressure.
52

ETIOLOGY
• Malocclusion
• TMJ dysfunction
• Faulty restoration
• Faulty orthodontic
treatment
• Parafucntional habits
• Drifting/Extrusion of
teeth
• Dental caries
• Occupational Bruxism
• Restricted unilateral
mastication.
53

• Neuromuscular irritation
• Faulty proprioception
• Altered adaptive capacity of PDL
• Alveolar Bone loss
• Psychic disturbance
54

HOW TO DETECT CLINICALLY
1) Fremitus.
2) Mobility (progressive).
3) Occlusal Discrepancies.
4) Wear facets in the
presence of other
indicators.
5) Tooth migration.
6) Fractured tooth/teeth.
7) Thermal sensitivity.
Clinical diagnosis of trauma from occlusion and its relation with severity of periodonitis. J Clin Periodontol 1992: 19: 92-97

Fremitus test
Classified into 3 classes
 Class I : Mild vibration or
movements detected.
 Class II : Easily palpable vibration
but no visible movements.
 Class III : Movements visible with
naked eye.
DIAGNOSIS OF OCCLUSAL TRAUMA
7/18/2023 56
Occlusal strips
Auditory test for TFO
Tactile Method
Histologic studies
Radiographs
Clinical diagnosis of trauma from occlusion and its relation with severity of periodonitis. J Clin Periodontol 1992: 19: 92-97

HALL –CRITICAL DECESSIONS IN PERIODONTOLOGY- 4TH EDITION. 57

HALL –CRITICAL DECESSIONS IN PERIODONTOLOGY- 4TH EDITION.
58

TREATMENT OF TFO
• Occlusal equilibration
• Splinting
• Orthodontic treatment
• Restorative options like onlays
• Prosthetic replacement
59
Significance of occlusion in the etiology and treatment is early,moderate and advanced periodontitis.Sigurd p.Ramfjord and
major m.Ash.J periodontol 1981,511

• CORONOPLASTY - STEPS
• Step 1 : Remove retrusive
prematurities and eliminate
the deflective shift from RCP
to ICP
61

• STEP 2 :adjustment of the ICP
 To achieve a stable ICP and to
refine occlusal anatomic
relationships
 The posterior teeth are adjusted
first, followed by conservative
adjustment of the anterior teeth
if necessary.
62

• Step 3: test for excessive contact on the incisor teeth in
icp
The incisor teeth should be slightly out of contact or in
light contact over the maximum number of teeth.
Mylar occlusal strip should be held with a hemostat
and contacts should be checked.
Any supracontacts detected are reduced.
63

• STEP 4: remove posterior
protrusive supracontacts and
establish contacts that are
bilaterally distributed on the
anterior teeth.
64

• Step 5 : remove (or) lessen (balancing) supracontacts
MEDIOTRUSIVE
SUPRACONTACTS Grooving
65

• Step 6 : reduce supracontacts on the laterotrusive
(working) side
66
CARRANZA’S CLINICAL PERIODONTOLOGY –
8TH EDITION

• Step 7: eliminate undesirable gross occlusal features
• Step 8 : Recheck tooth contact relationship
• Step 9 : Polish all rough tooth surfaces.
67

ROTATED, MALPOSED OR TILTED TEETH
Plunger cusp
Facets Flat Occlusal wear
Uneven marginal
ridges 68

CONCLUSION
• There is no scientific evidence that TFO causes
gingivitis or periodontitis
• It is reversible if forces reduced leading to a reduction
tooth mobility and physiologic adaptation
• May be a co-factor in pathogenesis of periodontal
disease
69

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