Definition, types, stages, studies, clinical features, diagnosis and management

1. DR.VIDYA VISHNU
SENIOR LECTURER
MALABAR DENTAL COLLEGE AND RESEARCH CENTRE
1

2. INTRODUCTION
 The periodontium attempts to accommodate the
forces exerted on the crown.
 This adaptive capacity varies in different persons and
in the same person at different times.
2

3.  The effect of occlusal forces on the periodontium →
magnitude
frequency
direction
duration
3

4.  ↑ed Magnitude of occlusal forces :
- widening of the PDL space,
-increase in the number and width of periodontal
ligament fibers, &
-increase in the density of alveolar bone.
4

5.  Changing the direction of occlusal forces:
-reorientation of the stresses & strains within the
periodontium .
 The principal fibers of PDL are arranged so that they
best accommodate occlusal forces along the long axis of
the tooth.
 Lateral (horizontal) & torque (rotational) forces are
more likely to injure the periodontium.
5

6.  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 the force .
6

7. TYPES OF OCCLUSAL FORCES
Physiologically normal occlusal forces in chewing and
swallowing :
 ≤ 5 N.
 positive stimulus to maintaining the periodontium and the
alveolar bone in a healthy and functional condition
Impact forces :
 mainly high magnitude & short duration.
 exceeding the viscoelastic buffer capacities of PDL
 results in injury to PDL/ alveolar bone
9

8. Continuous forces :
 very low magnitude forces, long duration (eg, orthodontic
forces),
 directed in one direction
 Results in remodeling of alveolar bone moving teeth in desired
direction.
Jiggling forces :
 intermittent forces in more than one direction
 premature contacts eg, crowns, high fillings
 result in widening of the alveolus and increased mobility.
10

9. TRAUMA FROM OCCLUSION
 When occlusal forces exceed the adaptive capacity of
the tissues, tissue injury results. The injury: TFO
FORCE
periodontium
11

10.  Tissue injury , not the occlusal force.
 An occlusion that produces such an injury →
Traumatic occlusion
 Any occlusion can produce pdl injury, malocclusion is
not necessary.
 Malocclusions are not necessarily injurious to the
periodontium.
12

11.  Traumatic occlusal relationships are called occlusal
disharmony, functional imbalance, & occlusal
dystrophy.
 Refer to the effect of the occlusion on the
periodontium rather than to the position of the teeth.
 An increased occlusal force is not traumatic if the
periodontium can accommodate it.
13

12.  Stillman ( 1917) : “A condition where injury results to
the supporting structures of the teeth by the act of
bringing the jaws into a closed position".
 WHO (1978) : “Damage in the periodontium caused
by stress on the teeth produced directly or indirectly by
teeth of the opposing jaw".
14

13.  "Glossary of Periodontic Terms" (AAP 1986) : "An injury
to the attachment apparatus as a result of excessive
occlusal force".
 Other terms:
• Traumatizing occlusion,
• Occlusal trauma,
• Traumatogenic occlusion,
• Periodontal traumatism,
• Overload.
15

14.  Excessive occlusal forces may also disrupt the function
of the masticatory musculature & cause painful
spasms, injure the temporomandibular joints, or
produce excessive tooth wear.
 However, TFO is generally used in connection with
injury in the periodontium.
16

15. TRAUMA FROM OCCLUSION
ACUTE TFO CHRONIC TFO
PRIMARY TFO
SECONDARY
TFO
or
or
17

16. ACUTE TFO
 Abrupt occlusal impact like biting on a hard object
 Restorations or prosthetic appliances that interfere
with or alter the direction of occlusal force.
18

17.  SIGNS & SYMPYOMS:
 Tooth pain
 sensitivity to percussion, and
 increased tooth mobility.
 Shift in the position of the tooth or wearing away or
correction of the restoration → force is dissipated →
injury heals, & symptoms subside.
19

18.  Otherwise, periodontal injury may worsen → necrosis
& periodontal abscess formation, or may persist as a
symptom-free chronic condition.
 Cementum tears.
20

19. CHRONIC TFO
 More common, of greater clinical significance.
 Develops from gradual changes in occlusion →
• tooth wear,
• drifting movement,
• extrusion of the teeth in combination with
parafunctional habits (e.g., bruxism, clenching).
21

20. PRIMARY & SECONDARY TFO
 TFO → Alterations in occlusal forces, a reduced
capacity of the periodontium to withstand occlusal
forces, or both.
 Primary TFO: result of alterations in occlusal forces.
 Secondary TFO: reduced ability of the tissues to resist
the occlusal forces.
22

21. PRIMARY TFO
 Eg. periodontal injury produced around
teeth with a previously healthy periodontium
after:
 (1) the insertion of a “high filling”;
 (2) the insertion of a prosthetic replacement
that creates excessive forces on abutment and
antagonistic teeth;
23

22.  (3) the drifting movement or extrusion of the teeth into
spaces created by unreplaced missing teeth; or
 (4) the orthodontic movement of teeth into
functionally unacceptable positions.
24

23.  No alteration in the level of connective tissue
attachment.
 Do not initiate pocket formation.
 Supracrestal gingival fibers are not affected &
therefore prevent the apical migration of the JE.
25

24. SECONDARY TFO
 Occurs when the adaptive capacity of the tissues to
withstand occlusal forces is impaired by bone loss that
results from marginal inflammation.
26

25.  Reduces the periodontal attachment area and alters
the leverage on the remaining tissues.
 The periodontium becomes more vulnerable to injury,
& previously well-tolerated occlusal forces become
traumatic.
27

26. Traumatic forces can occur on :
A, normal periodontium with normal height of bone-
PRIMARY TFO
B, normal periodontium with reduced height of bone; or,
C, marginal periodontitis with reduced height of bone –
SECONDARY TFO 28

27.  It has been found in experimental animals that
systemic disorders can reduce tissue resistance & that
previously tolerable forces may become excessive.
 May represent another mechanism by which tissue
resistance to increased forces is lowered, thereby
resulting in secondary tfo.
29

28. Stages Of Tissue Response To
Increased Occlusal Forces
INJURY REPAIR
ADAPTIVE
REMODELING
30

29. Stage I: Injury
 Produced by excessive occlusal forces.
 The body then attempts to repair the injury & restore
the periodontium.
 This can occur if the forces are diminished or if the
tooth drifts away from them.
 If the offending force is chronic, the periodontium is
remodeled to cushion its impact.
31

30.  The ligament is widened at the expense of the bone,
which results in angular bone defects without
periodontal pockets, and the tooth becomes loose.
32

31.  Under the forces of occlusion, a tooth rotates around a
fulcrum or axis of rotation.
 Single-rooted teeth : junction between the middle
third and the apical third of the clinical root
 Multirooted teeth : middle of the interradicular bone.
33

32.  Creates areas of pressure and tension on opposite
sides of the fulcrum.
 If jiggling forces are exerted, these different lesions
may coexist in the same area.
 Furcations - Most susceptible to injury from excessive
occlusal forces.
34

33.  Slightly excessive pressure :
• resorption of the alveolar bone,
• widening of the periodontal ligament space.
• blood vessels are numerous and reduced in size
 Slightly excessive tension :
• elongation of the periodontal ligament fibers
• apposition of alveolar bone.
• blood vessels are enlarged.
35

34.  Greater pressure : compression of the fibers, which
produces areas of hyalinization.
 Subsequent injury to the fibroblasts and other
connective tissue cells leads to necrosis of areas of the
ligament.
 Increased resorption of alveolar bone and resorption of
the tooth surface.
36

35.  Vascular changes :
• within 30 minutes, impairment and stasis of blood flow
occur;
• at 2 to 3 hours, blood vessels appear to be packed with
erythrocytes, which start to fragment; and
• between 1 and 7 days, disintegration of the blood vessel
walls and release of the contents into the surrounding
tissue occur.
37

36.  Severe tension :
• widening of the periodontal ligament,
• thrombosis, hemorrhage,
• tearing of the periodontal ligament, and
• resorption of alveolar bone.
38

37.  Pressure severe enough to force the root against bone
causes necrosis of the periodontal ligament and bone.
 The bone is resorbed from viable periodontal ligament
adjacent to necrotic areas and from marrow spaces;
this process is called undermining resorption.
39

38. STAGE II: REPAIR
 Occurs constantly in the normal periodontium.
 TFO - increased reparative activity.
 The damaged tissues are removed, new CT cells &
fibers, bone, & cementum are formed to restore the
injured periodontium.
 Forces remain traumatic only as long as the damage
produced exceeds the reparative capacity of the
tissues.
40

39.  When bone is resorbed by excessive occlusal forces,
the body attempts to reinforce the thinned bony
trabeculae with new bone - Buttressing bone
formation.
 An important feature of the reparative process
associated with trauma from occlusion.
 Also occurs when bone is destroyed by inflammation
or osteolytic tumors.
41

40.  Central buttressing- occurs within the jaw;
 The endosteal cells deposit new bone, which restores
the bony trabeculae and reduces the size of the
marrow spaces.
42

41.  Peripheral buttressing- on the bone surface .
 occurs on the facial and lingual surfaces of the alveolar
plate.
 Shelflike thickening of the alveolar margin- lipping, or
a pronounced bulge in the contour of the facial and
lingual bone.
 The formation of crystals from erythrocytes .
43

42. STAGE III: Adaptive Remodeling of
the Periodontium
 If Repair process cannot keep pace with the
destruction caused by the occlusion →
the periodontium is remodeled
in an effort to create a structural relationship in which
the forces are no longer injurious to the tissues.
44

43.  Widened periodontal ligament, which is funnel shaped
at the crest,&
 Angular defects in the bone with no pocket formation.
 Involved teeth become loose.
 Increased vascularization.
45

44.  The injury phase shows an increase in areas of
resorption and a decrease in bone formation, whereas
the repair phase demonstrates decreased resorption
and increased bone formation.
 After adaptive remodeling of the periodontium,
resorption and formation return to normal.
46

45. TFO & PLAQUE-ASSOCIATED PERIODONTAL
DISEASE
 Karolyi (1901) postulated that an interaction may exist
between "trauma from occlusion" and “ alveolar pyrrohea" .
 Orban & Weinman (1933) based on histologic observation
of human autopsy material concluded that occlusal forces
did not have a major effect on periodontal destruction.
 Instead, they interpreted that gingival inflammation
extending into the supporting bone was the cause of
periodontal destruction.
47

46.  Box (1935) and Stones (1938) reported experiments in
sheep and monkeys.
 “TFO is an etiologic factor in the production of that
variety of periodontal disease in which there is vertical
pocket formation associated with one or a varying
number of teeth" (Stones 1938).
 Criticized because they lacked proper controls.
48

47. • During the 1950s and 1960s, rats, monkeys, and dogs to
evaluate the effect of occlusal forces on the periodontium.
• None of these studies supported concept that excessive
occlusal forces were a primary causative agent of periodontal
destruction and many of the studies indicated that there was
little or no correlation between occlusal forces and
periodontal destruction.
49

48. Analysis of human autopsy
material
Glickman's concept (1965, 1967)
 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.
 Character of the progressive tissue destruction of the
periodontium at a "traumatized tooth" will be different
from a “ non-traumatized" tooth.
50

49.  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.
51

50.  The periodontal structures :
1. the zone of irritation & 2. the zone of co-destruction
52

51.  Zone of irritation :
 marginal & interdental gingiva.
 The soft tissue of this zone is bordered by hard tissue
(the tooth) only on one side
 not affected by forces of occlusion.
 Gingival inflammation cannot be induced TFO but is
the result of irritation from microbial plaque.
53

52.  The plaque-associated lesion at a "non-traumatized“
tooth propagates in apical direction by first involving
the alveolar bone and only later the periodontal
ligament area.
 Results in an even (horizontal) bone destruction.
54

53.  Zone of co-destruction
 Periodontal ligament, root cementum & alveolar bone
 coronally demarcated by the transseptal (inter-dental)
and the dentoalveolar collagen fiber bundles.
 This zone may become the seat of a lesion caused by
trauma from occlusion.
55

54.  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.
 Through this exposure from two different directions
the fiber bundles may become dissolved and/or
oriented in a direction parallel to the root surface.
56

55.  The spread of an inflammatory lesion from the zone of
irritation directly down into the periodontal ligament (
i.e. not via the interdental bone) 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.
57

56. 59

57.  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.
 They termed this different progression of periodontal
disease as an “altered pathway of destruction.”
 They termed the combined effects of occlusal trauma
and inflammation as “co-destructive factors” in
periodontal disease. (Glickman & Smulow)
60

58. Waerhaug's concept (PLAQUE
FRONT HYPOTHESIS-1979)
 Examined autopsy specimens similar to Glickman's,
but measured in addition 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.
61

59.  Angular bony defects & infrabony pockets occur
equally often at periodontal sites of teeth which are
not affected by TFO as in traumatized teeth.
 Refuted the hypothesis that trauma from occlusion
played a role in the spread of a gingival lesion into the
"zone of co-destruction".
62

60.  The loss of connective attachment and the resorption
of bone around teeth are exclusively the result of
inflammatory lesions associated with subgingival
plaque.
 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 neighbouring tooth, and when the volume of the
alveolar bone surrounding the roots is comparatively
large.
63

61.  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 an interplay between the form and volume of
the alveolar bone and the apical extension of the
microbial plaque on the adjacent root surfaces.
64

62.  Examinations of autopsy material have a limited value
when "cause effect“ relationships with respect to
trauma and progressive periodontitis are to be
determined.
 The conclusions drawn from this field of research have
not been generally accepted.
65

63. CLINICAL TRIALS
Yuodelis and Mann, 1965
 Relationship between periodontal parameters and
molar nonworking contacts using the records,
radiographs and study models of 54 patients with
periodontal disease.
 Fifty-three percent of molar teeth had nonworking
contacts, and the authors determined that probing
depths and bone loss were greater for those teeth.
66

64. Werner H. Vollmer, Klaus H. Rateitschak (1975)
 The effect of occlusal adjustment by grinding on
marginal inflammation and tooth mobility was
investigated in 43 occlusally traumatized teeth in 29
subjects with gingivitis and marginal periodontitis.
 Consisted of 4 groups with tooth mobility of varying
degrees of severity and bone destruction.
 In all groups increased tooth mobility decreased
subsequent to occlusal adjustment.
 The latter was without effect on sulcus fluid flow rate
or gingivitis scores in either gingivitis or periodontitis
patients.
67

65. Rosling et al. (1976) :
 Patients with advanced periodontal disease associated
with multiple angular bony defects & mobile teeth
were exposed to antimicrobial therapy (i. e.subgingival
scaling after flap elevation).
 Healing was evaluated by probing attachment level
measurements and radiographic monitoring.
 “Infrabony pocket located at hypermobile teeth
exhibited the same degree of healing as those adjacent
to firm teeth".
68

66. Sottosanty (1977)
 A possible relationship between occlusion, root
resorption, and the progression of periodontal disease.
 Resorption bays or cracks in the cervical cementum.
 Faster deepening of pdl pockets.
69

67. Fleszar et al. (1980) :
 Influence of tooth mobility on healing following
periodontal therapy including both root debridement
and occlusal adjustment.
 “Pockets of clinically mobile teeth do not respond as
well to periodontal treatment as do those of firm teeth
exhibiting the same disease severity".
70

68. Pihlstrom et al. 1986
 Association between TFO and periodontitis by
assessing a series of clinical and radiographic features
at maxillary first molars.
 Parameters : probing depth, probing attachment level,
tooth mobility, wear facets, plaque and calculus, bone
height, widened periodontal space, etc.
72

69.  “Teeth with increased mobility and widened
periodontal ligament space had deeper pockets, more
attachment loss and less bone support than teeth
without these symptoms”.
73

70. Burgett et al. (1992)
 Effect of occlusal adjustment in the treatment of
periodontitis.
 Fifty subjects with periodontitis were examined at
baseline and subsequently treated for their periodontal
condition with root debridement ± flap surgery.
 Twenty-two out of the 50 patients, in addition, received
comprehensive occlusal therapy.
74

71.  Reexaminations performed 2 years later disclosed that
probing attachment gain was on the average about 0.5
mm larger in patients who received the combined
treatment, i.e. scaling and occlusal adjustment, than
in patients in whom the occlusal adjustment was not
included.
75

72. Neiderud et al. (1992)
 Demonstrated in a beagle dog study that tissue
alterations which occur at mobile teeth with clinically
healthy gingivae may reduce the resistance offered by
the periodontal tissues to probing.
 The tip of the probe will penetrate 0.5 mm deeper at
the mobile than at the non-mobile tooth.; must be
taken into consideration when the above clinical data
are interpreted.
76

73. Jin and Cao (1992) :
 In patients with moderate-to-advanced periodontitis
to determine the reliability of several selected signs of
occlusal trauma.
 Since the total number of teeth examined is not
included in the article, it is difficult to determine the
percentage of teeth with occlusal discrepancies versus
the number with more objective signs of occlusal
trauma.
77

74.  Reported no significant differences in pocket depths,
attachment levels or alveolar bone height between
teeth with and without various abnormal occlusal
contacts.
78

75. McGuire and Nunn (1996) :
 Reviewed the change in prognosis and in the number of
teeth lost by patients with periodontal disease who had
parafunctional habits.
 In patients with parafunctional habits that had not
been treated with an occlusal appliance, there was no
improvement in prognosis despite periodontal therapy.
79

76.  More teeth were lost in the untreated group than in a
group that received occlusal appliances.
 “In patients with periodontal disease, the treatment of
occlusal trauma improved treatment outcomes and
that the lack of treatment resulted in greater tooth
loss.”
80

77. Nunn and Harrel, 2001 (NEW MILLENIUM CONCEPT):
 Investigated the association between occlusal
discrepancies and periodontitis in a private practice
setting.
 Analysis of individual teeth according to occlusal
discrepancy sets this study apart from most previous
studies that have made comparisons between patients
with and without occlusal trauma.
81

78.  Data entered were regarding 89 patients and 2,147
teeth into the database.
 The patients fell into three groups based on the type of
treatment performed:
o untreated group,
o nonsurgically treated group &
o surgically treated group
82

79.  Compared 41 patients who received all recommended
treatment, including adjustment of occlusal
discrepancies, with 48 patients who received partial
treatment or no treatment.
 56 (62.92 percent) of the 89 total patients & 307 (13.35
percent) of 2,147 teeth had occlusal discrepancies;
these discrepancies were listed as a vertical slide
greater than or equal to 1 millimeter from a premature
contact and balancing contacts in lateral movement.
83

80.  Teeth with an occlusal discrepancy had pocket depths
approximately 1 mm deeper than those of teeth with no
occlusal discrepancy; statistically significant (P ≤ .0001)
and was true regardless of age, sex, smoking status or
other risk factors.
 Teeth with occlusal discrepancies had statistically greater
mobility, as well as a prognosis statistically worse than
that for teeth without occlusal discrepancies.
84

81.  Occlusal discrepancies were a better predictor of pocket
depths, mobility and poor prognosis than were any
other risk factors evaluated, including smoking.
 Teeth with untreated occlusal discrepancies
experienced a significant increase in pocket depth per
year when compared with teeth with no occlusal
discrepancies or teeth with treated occlusal
discrepancies.
85

82.  Occlusal discrepancies were not a factor in the width
of attached gingivae and did not appear to contribute
to recession.
86

83. ANIMAL EXPERIMENTS
ORTHODONTIC TYPE TRAUMA
 Application of forces which were inflicted on teeth in
one direction only.
 Biopsies including tooth and periodontium were
harvested.
87

84. Varying analysis of the tissue sections (Haupl &
Psansky 1938, Reitan 1951, Muhlemann & Herzog
1961, Ewen & Stahl 1962, Waerhaug & Hansen 1966,
Karring et al. 1982) revealed the following:
 when a tooth is exposed to unilateral forces of a
magnitude, frequency or duration that its
periodontal tissues are unable to withstand &
distribute while maintaining the stability of the
tooth, certain well-defined reactions develop in the
PDL, eventually resulting in an adaptation of the pdl
structures to the altered functional demand.
88

85.  If the crown of a tooth is affected by such horizontally
directed forces, the tooth tends to tilt (tip) in the
direction of the force.
 This tilting force results in the development of
pressure and tension zones within the marginal and
apical parts of the periodontium.
89

86. 90

87. PRESSURE ZONE:
 increased vascularization,
 increased vascular permeability,
 vascular thrombosis, and
 disorganization of cells and collagen fiber bundles.
91

88.  If the magnitude of forces is within certain limits,
allowing the maintenance of the vitality of the
periodontal ligament cells, bone-resorbing osteoclasts
soon appear on the bone surface of the alveolus in the
pressure zone.
 A process of bone resorption is initiated- "direct bone
resorption".
92

89.  If the force applied is of higher magnitude, the result
may be necrosis of the periodontal ligament tissue in
the pressure zone, i.e. decomposition of cells, vessels,
matrix and fibers (hyalinization).
 "Direct bone resorption" therefore cannot occur.
93

90.  Instead, osteoclasts appear in marrow spaces within
the adjacent bone tissue where the stress
concentration is lower than in the periodontal
ligament - undermining or “ indirect bone resorption".
 Surrounding bone is resorbed until there is a
breakthrough to the hyalinized tissue within the
pressure zone.
94

91.  This results in a reduction of the stress in this area, &
cells from the neighbouring bone or adjacent areas of
the periodontal ligament can proliferate into the
pressure zone and replace the previously hyalinized
tissue, thereby reestablishing prerequisites for "direct
bone resorption".
 Irrespective of whether the bone resorption is of a
direct or an indirect nature the tooth moves ( tilts)
further in the direction of the force.
95

92. TENSION ZONE:
 Apposition of bone to maintain the normal width of
the periodontal ligament in this area.
 Because of the tissue reactions in the pressure and
tension zones the tooth becomes, temporarily,
hypermobile.
 When the tooth has moved (tilted) to a position where
the effect of the forces is nullified, healing of the
periodontal tissues takes place in both the pressure and
the tension zones and the tooth becomes stable in its
new position.
96

93.  Neither gingival inflammation nor loss of connective
tissue attachment will occur in a healthy periodontium
and – as long as the tooth is not moved through the
envelope of the alveolar process – there is no apical
migration of the dentogingival epithelium.
 Since the supraalveolar connective tissue is only
bordered by hard tissue (the tooth) on one side (in the
direction of the force), this structure remains
unaffected by this type of force.
97

94. `
 These tissue reactions do not differ fundamentally
from those which occur as a consequence of bodily
tooth movement in orthodontic therapy (Reitan 1951).
 The main difference is that the pressure and tension
zones, depending on the direction of the force, are
more extended in an apical-coronal direction along
the root surface than in conjunction with tipping
movement.
98

95.  Neither in conjunction with tipping nor in conjunction
with bodily movements of the tooth is the
supraalveolar connective tissue affected by the force.
 Unilateral forces directed to the crown of teeth,
therefore, will not induce inflammatory reactions in the
gingiva or cause loss of connective tissue attachment.
99

96.  Studies (Steiner et al. 1981, Wennstrom et al. 1987) have
demonstrated, however, that orthodontic forces
producing bodily (or tipping) movement of teeth may
result in gingival recession and loss of connective tissue
attachment.
 This breakdown of the attachment apparatus occurred
at sites with gingivitis when the tooth was moved
through the envelope of the alveolar process.
100

97.  At such sites a bone dehiscence becomes established
and, if the covering soft tissue is thin (in the direction
of the movement of the tooth), recession (attachment
loss) may occur.
 Criticism has been directed at experiments in which
only unilateral trauma is exerted on teeth (Wentz et al.
1958).
101

98. Jiggling-type trauma
 In humans, unlike in the animal experiments
described above, the occlusal forces act alternately in
one and then in the opposite direction, called jiggling
forces.
102

99. Healthy periodontium with normal height
 Traumatic forces were exerted on the crowns of the
teeth, alternately in buccal and lingual or mesial and
distal directions, and in which the teeth were not
allowed to move away from the force (e.g. Wentz et al.
1958, Glickman & Smulow 1968, Svanberg & Lindhe
1973, Meitner 1975, Ericsson & Lindhe 1982).
 There is a combination of pressure and tension on
both sides.
103

100.  The tissue reactions in the PDL were similar, to those
reported for the pressure zone at orthodontically
moved teeth, with the one difference that the PDL
space at jiggling gradually increased in width on both
sides of the tooth.
104

101.  During the phase when the periodontal space
gradually increased in width
(1) inflammatory changes were present in the ligament
tissue,
( 2) active bone resorption occurred, and
(3) the tooth displayed signs of gradually increasing
(progressive) mobility
105

102.  When the effect of the forces applied had been
compensated for by the increased width of the
periodontal ligament space, the ligament tissue
showed no signs of increased vascularity or exudation.
106

103.  The supraalveolar connective tissue was not
influenced by the occlusal forces, because It is
bordered by hard tissue on one side only.
 Gingiva which was non inflamed at the start of the
experiment remained noninflamed, but also that an
overt inflammatory lesion residing in the
supraalveolar connective tissue was not aggravated by
the jiggling forces.
107

104. 108

105. Healthy periodontium with reduced height
 Progressive periodontal disease is characterized by gingival
inflammation and a gradually developing loss of connective
tissue attachment and alveolar bone.
 Treatment of periodontal disease, i.e. removal of plaque and
calculus and elimination of pathologically deepened
pockets, will result in the reestablishment of a healthy
periodontium but with reduced height.
 The question is whether a healthy periodontium with
reduced height has a capacity similar to that of the normal
periodontium to adapt to traumatizing occlusal forces
(secondary occlusal trauma).
109

106.  This problem has also been examined in animal expmts
(Ericsson & Lindhe 1977).
 Destructive periodontal disease was initiated in dogs by
allowing the animals to accumulate plaque and calculus for
a period of 6 months.
 When around 50% o the periodontal tissue support had
been lost, the progressive disease was subjected to
treatment by scaling, root planing and pocket elimination .
 During a subsequent 8-month period, the animals were
enrolled in a careful plaque control program. During this
period certain premolars were exposed to traumatizing
jiggling forces.
110

107.  The periodontal tissues in the combined pressure and
tension zones reacted to the forces by vascular
proliferation, exudation and thrombosis, as well as by bone
resorption.
 In radiographs, widened periodontal ligaments could be
found around the traumatized teeth, which at clinical
examination displayed signs of progressive tooth mobility.
 The gradual increase in the width of the PDL and the
resulting progressive increase in tooth mobility took place
during a period of several weeks but eventually terminated.
111

108.  The active bone resorption ceased and the markedly
widened periodontal ligament tissue regained its
normal composition; healing had occurred.
 The teeth were hypermobile but surrounded by
periodontal structures which had adapted to the
altered functional demands.
112

109.  Supraalveolar connective tissue remained unaffected
by the jiggling forces.
 No further loss of connective tissue attachment and no
further downgrowth of dentogingival epithelium.
 Within certain limits a healthy periodontium with
reduced height has a capacity similar to that of a
periodontium with normal height to adapt to altered
functional demands .
113

110. 114

111. 115

112. Plaque-associated periodontal disease
 Studied in animal experiments (Lindhe & Svanberg
1974, Meitner 1975, Nyman et al. 1978, Ericsson &
Lindhe 1982, Poison & Zander 1983).
 Progressive and destructive periodontal disease was
first initiated in dogs or monkeys by allowing the
animals to accumulate plaque and calculus.
 Teeth were also subjected to trauma from occlusion.
116

113.  "Traumatizing" jiggling forces (Lindhe & Svanberg
1974) were exerted on premolars and were found to
induce certain tissue reactions in the combined
pressure tension zones.
 The periodontal ligament tissue in these zones, within
a few days of the onset of the jiggling forces, displayed
signs of inflammation, had increased numbers of
vessels, showed increased vascular permeability and
exudation, thrombosis, as well as retention of
neutrophils and macrophages.
117

114.  On the adjacent bone surfaces there were a large
number of osteoclasts.
 Since the teeth could not orthodontically move away
from the jiggling forces, the periodontal ligament of
both sides of the tooth gradually increased in width,
the teeth became hypermobile (progressive tooth
mobility) and angular bony defects could be detected
in the radiographs.
 The forces were eventually nullified by the increased
width of the periodontal ligament.
118

115.  If the forces applied were of a magnitude to which the
periodontal structures could adapt, the progressive
increase of the tooth mobility terminated within a few
weeks.
 The active bone resorption ceased but the angular
bone destruction persisted as well as the increased
tooth mobility.
 The periodontal ligament had an increased width but
a normal tissue composition.
119

116.  Histologic examination of biopsies revealed that this
adaptation had occurred with no greater apical
proliferation of the dentogingival epithelium than was
caused by the plaque-associated lesion (Meitner 1975).
 Thus occlusal forces which allow adaptive alterations
to develop in the pressure/ tension zones of the
periodontal ligament will not aggravate a plaque-
associated periodontal disease.
120

117. 121

118.  If the magnitude and direction of the jiggling forces were
such that tissues in the pressure/tension zones could not
become adapted, the injury in the zones of co-destruction
had a more permanent character.
 The periodontal ligament in the pressure/tension zones
displayed for several months signs of inflammation
(vascular proliferation, exudation, thrombosis, retention of
neutrophils and macrophages, collagen destruction).
 Osteoclasts residing on the walls of the alveolus
maintained the bone-resorptive process, which resulted in
a gradual widening of the periodontal ligament in the
pressure/tension zones.
122

119.  As a consequence, the resulting angular bone
destruction was continuous and the mobility of the
teeth remained progressive.
 The plaque-associated lesion in the "zone of irritation"
and the inflammatory lesion in the "zone of co-
destruction" merged;
 The dentogingival epithelium proliferated in an apical
direction and periodontal disease was aggravated
(Lindhe & Svanberg 1974).
123

120. 124

121.  Similar findings were reported from another experiment
in the dog (Ericsson & Lindhe 1982) in which the effect
was assessed of a prolonged period of jiggling force
application on the rate of progression of plaque
associated,marginal periodontitis.
 In dogs with continuing periodontal disease, certain
teeth were exposed to jiggling forces during a period of
10 months.
 Control teeth were not jiggled.
125

122. (a) Periodontal conditions around a tooth which has been exposed to TFO (jiggling
type) for 300 days in combination with plaque-associated experimental periodontitis.
(b), Condition of a control tooth from the same dog in which experimental
periodontitis but no jiggling trauma had been in operation. Note the difference
between (a) and (b) regarding the degree of bone destruction and loss of connective
tissue attachment. Note also in (a) the location of the subgingival plaque at the apex
of the root. From Ericsson & Lindhe ( 1982).
126

123.  More short-term experiments in the monkey (Poison
& Zander 1983), evaluating the effect TFO on teeth
involved in periodontitis, failed to support the findings
by Lindhe & Svanberg (1974) and Ericsson & Lindhe
(1982).
127

124.  Poison & Zander (1983) observed that trauma
superimposed on periodontal lesions associated with
angular bony defects
(1) caused increased loss of alveolar bone but
(2) failed to produce additional loss of connective tissue
attachment.
128

125. ROCHESTER GROUP (Polson & co workers) & GOTHENBURG
GROUP (Lindhe & co workers) animal studies
 The Eastman Dental Center group in Rochester, NY, used
squirrel monkeys, produced trauma by repetitive interdental
wedging, and added mild to moderate gingival inflammation.
 The University of Gothenburg group in Sweden used beagle
dogs, produced trauma by placing cap splints and orthodontic
appliances, and induced severe gingival inflammation.
129

126. ROCHESTER GROUP GOTHENBURG GROUP
Used squirrel monkeys Used beagle dogs
Duration of expt upto 10 wks Duration upto 1 year
Concluded that occlusal trauma doesn’t
influence pdl dse progression. No evidence
of AL in presence of plaque & occlusal
forces.
Concluded that occlusal trauma could
accelerate progression of pdl dse. Evidence
of AL when plaque & occlusal forces both
were present.
Asserted that adaptive changes in response
to occlusal trauma is largely reversible if
inflammation is controlled.
In presence of reduced healthy pdium,
occlusal trauma will not produce loss of
attachment.
Occlusal trauma can cause bone loss Ability of pdium to adapt to occlusal trauma
may be inhibited in presence of
inflammation.
130

127.  When TFO is eliminated, a substantial reversal of
bone loss occurs, except in the presence of
periodontitis; indicates that inflammation inhibits the
potential for bone regeneration.
 TFO does not induce progressive destruction of the
periodontal tissues in regions that are kept healthy
after the elimination of preexisting periodontitis.
131

128.  TFO also tends to change the shape of the alveolar
crest- widening of the marginal periodontal ligament
space, a narrowing of the interproximal alveolar bone,
and a shelflike thickening of the alveolar margin.
 In the absence of inflammation, the response to tfo is
limited to adaptation to the increased forces.
 In the presence of inflammation, the changes in the
shape of the alveolar crest may be conducive to angular
bone loss, & existing pockets may become intrabony.
132

129. Other theories that have been proposed to explain the
interaction of trauma and inflammation include the
following:
 TFO may alter the pathway of the extension of gingival
inflammation to the underlying tissues. This may be
favoured by the reduced collagen density and the increased
number of leukocytes, osteoclasts, and blood vessels in the
coronal portion of increasingly mobile teeth. Inflammation
may then proceed to the periodontal ligament rather than
to the bone. Resulting bone loss would be angular, and
pockets could become intrabony.
133

130.  Trauma-induced areas of root resorption uncovered by
apical migration of the inflamed gingival attachment
may offer a favorable environment for the formation
and attachment of plaque and calculus and therefore
may be responsible for the development of deeper
lesions.
 Supragingival plaque can become subgingival if the
tooth is tilted orthodontically or if it migrates into an
edentulous area, which results in the transformation
of a suprabony pocket into an intrabony pocket.
134

131.  Increased mobility of traumatically loosened teeth
may have a pumping effect on plaque metabolites,
thereby increasing their diffusion.
135

132. Effects of Insufficient
Occlusal Force
 open-bite relationship, an absence of functional
antagonists, or unilateral chewing habits
 May also be injurious to the supporting periodontal
tissues.
 Thinning of the periodontal ligament, atrophy of the
fibers, osteoporosis of the alveolar bone, and a
reduction in bone height.
136

133. Effects of Excessive Occlusal Forces
on Dental Pulp
 Not been established
 Some clinicians report the disappearance of pulpal
symptoms after the correction of excessive occlusal
forces.
 Pulpal reactions have been noted in animals subjected
to increased occlusal forces, but these did not occur
when the forces were minimal and occurred over short
periods.
137

134. REVERSIBILITY OF TRAUMATIC LESIONS
 Reversible.
 When trauma is artificially induced in experimental
animals, the teeth move away or intrude into the jaw.
 When the impact of the artificially created force is
relieved, the tissues undergo repair.
138

135.  If conditions in humans do not permit the teeth to
escape from or adapt to excessive occlusal force,
periodontal damage persists and worsens.
 The presence of inflammation in the periodontium as
a result of plaque accumulation may impair the
reversibility of traumatic lesions.
139

136. CLINICAL SIGNS & SYMPTOMS
1. Mobility (progressive)
2. Pain on chewing or percussion
3. Fremitus
4. Occlusal prematurities/discrepancies
5. Wear facets in the presence of other clinical indicators
6. Tooth migration
7. Chipped or fractured tooth (teeth)
8. Angled gingival recession
9. Abfraction, espy in PMs
10. Thermal sensitivity
11. Muscle/ TMJ pain
12. Muscle hypertonicity
DIAGNOSIS OF TFO
140

137.  Most common & one of the earliest signs.
 “Hallmark” of occlusal trauma
 Due to destruction of periodontal fibers during the
injury stage.
 During the final stage, the accommodation of the
periodontium to increased forces entails a widening of
PDL → ↑ tooth mobility.
TOOTH MOBILITY
141

138.  Tooth mobility greater than nl, but Cannot be
considered pathologic, because it is an adaptation and
not a disease process.
 If it does become progressively worse, it can then be
considered pathologic.
142

139.  PERIOTEST
 commercial device designed to measure periodontal re
action to specific loads on the tooth crown.
 Dynamic device designed to provide objective
measurement of tooth mobility by assessing damping
characteristics of pdium; it doesn’t require a fixed rigid
measuring apparatus on teeth.
 measure initial stability of dental implants.
143

140.  Periotest Value PTV : -8 TO +50
 PTV Mobility grading
 -8 to +9 0
 +10 to +19 I
 +20 to +29 II
 +30 to + 50 III
 Other objective methods:
 Laser diodes, magnetic sensors, Doppler vibrometer,
Muhlemanns periodontometer
144

141. FREMITUS (FUNCTIONAL MOBILITY)
 Used to clinically detect TFO.
 Tooth displacement created by patient’s own occlusal
force.
 Palpable deflection of a tooth either on closure or
during excursive movements.
 Measures the vibratory patterns of the teeth when the
teeth are placed in contacting positions & movements
 Ability of patient to displace & traumatize teeth
 Mobility without fremitus: Probably no Occlusal
Trauma
145

142.  Dampened index finger – buccal & labial surfaces-
maxillary teeth
 Tap the teeth together in the maximum intercuspal
position
 Grind symmetrically in lateral, protrusive & lateral-
protrusive contacting movements
146

143. CLASS I: Mild vibration/ movmts detected
CLASS II: Easily palpable vibration but no visible
movement
CLASS III: Movement visible with the naked eye
147

144. TOOTH MIGRATION
 To avoid excessive occlusal forces, tooth tries to move
away from them.
 Loss of interproximal contacts & migration of tooth
from its stable position.
148

145. WEAR PATTERNS
 wear surfaces in area of interference.
 A common reason for wear facets is bruxism.
 Appear as shiny & irregular areas on incisal & occlusal
surfaces.
149

146. V-SHAPED OR ANGLED GINGIVAL RECESSION
 TFO → V shaped/ angled gingival recession
 Controversial
 Researchers in favour - V shaped/ angled gingival
recession with a small fissure in most apical extremity is
directly associated with tfo & is commonly associated
with abfraction.
 Researchers not in favour- recession results from marginal
inflammation due to plaque.
150

147. ABFRACTION
151

148. BUCCAL BONE DEHISCENCE
 Buccal cortical bone is thin espy in canine & PM
regions.
 TFO leads to widened PDL at expense of bone
resorption.
 In these areas, very little resorption leads to bone
dehiscence over buccal face of root that is affected.
 Diagnosed by CT/ CBCT scans.
152

149. Other clinical changes attributed to TFO
 Food impaction
 Abnormal habits
 Obscure facial pain
 Erosion
 Gingival bleeding
 Cheek biting
 C/c NUG
 Hyperplasia of gingiva
 Pericementitis
153

150.  Bruxism
 Unilateral mastication
 Ltd excursion of mandible (insufft wear)
 Unlimited excursion of mandible (excessive wear)
 Interproximal caries
 Formation of subgingvl calculus & gingivitis
 Epulis formation
 Blanching of gingiva
154

151. Box & Stillman considered trauma to be causative
factor for following signs of incipient pdl dse:
 Traumatic crescent – bluish red zone of gingiva
confined to 1/6th of root circumfrnce
 Congestion, ischemia or hyperemia of marginal
gingiva
 Recession of gingiva which may be asymmetrical,
associated with resorption of alv crest
155

152.  Stillman’s cleft
 McCall’s festoons
 Absence of stippling, evidence of edema secondary to
trauma
 Injection of BVs in marg gingiva
 Sharply demarcated linear deprssn in alv mucosa
parallel to long axis of root
 Distended veins in oral mucosa
156

153. Mc calls festoon
Stillmans cleft
157

154. RADIOGRAPHIC SIGNS
 1. Increased width of the periodontal space
 2. Thickening of the lamina dura along the lateral
aspect of the root, in the apical region, and in
bifurcation areas.
 These changes do not necessarily indicate destructive
changes, because they may result from thickening and
strengthening of PDL & alveolar bone, constituting a
favourable response to increased occlusal forces.
158

155.  3. A “vertical” rather than “horizontal” destruction of
the interdental septum.
 4. Radiolucency and condensation of the alveolar
bone.
 5. Root resorption.
159

156. 160

157. THERAPEUTIC GOALS AND TREATMENT
CONSIDERATIONS
 Maintain the periodontium in comfort and function.
 Includes one or more of the following:
1) Occlusal adjustment
2) Management of parafunctional habits
3) Temporary, provisional or long-term stabilization of
mobile teeth with removable or fixed appliances
4) Orthodontic tooth movement
5) Occlusal reconstruction
6) Extraction of selected teeth
161

158. LOCALIZED GENERALIZED
Pt with Primary occlusal trauma
HIGH
RESTORATION
MALALIGNED
TOOTH
Replace
restoration
SELECTIVE
GRINDING
EXTRACTIONORTHODONTIC
T.M
CLENCHING,
GRINDING
HABITS(BRUXISM)
OCCUPATION
AL BRUXISM
RECREATION
AL BRUXISM
POSTORTHODONTIC
CLENCHING
OCCLUSAL
ADJUSTMENT
Counseling
Bite
guard
Change
job
Stop drug use
Futher ortho RxOCCLUSAL
ADJUSTMENT
Bite
guard
Bite guard
Bite guard Full mouth
reconstruction162

159. LOCALIZED GENERALIZED
Pt with Secondary occlusal trauma
Good adjt
abutment teeth
No Good adjt
abutment teeth
SELECTIVE
GRINDING
Hopeless,
but
maintain or
extract
Consider
whether tooth
is amenable to
GTR
PERMANENT
SPLINT
TEMPORARY SPLINT BITE GUARD EXTRACT
Splint to
those teeth
GTR
candidate
Not a GTR
candidate
ExtractGTR
163

160. LOCALIZED GENERALIZED
Periodontal pt with loose teeth
SELECTIVE
GRINDING
SELECTIVE
GRINDING &
Night guard
SELECTIVE
GRINDING
Adjt teeth
are sound
Most other
teeth are sound
Loose tooth
moderately
involved
Loose tooth
severely
involved
Loose teeth have
little or no bone
loss (Primary TFO)
Loose teeth have
moderate to severe bone
loss (secondary TFO)
SELECTIVE
GRINDING
splint
Most teeth have
moderate to
severe bone loss
(secondary TFO)
Most teeth have
little or no bone
loss (Primary TFO)
Whether tooth is
amenable to GTR
Assess psychogenic
factors
psychogenic
compt
No psychogenic
compt
Consider
whether any
severely involved
teeth are
amenable to GTR
GTR
possible
GTR not
possible
GTR possible GTR not possible
GTR Extract & Bridge
SELECTIVE
GRINDING
SPLINTING164

161. OCCLUSAL ADJUSTMENT OR SELECTIVE GRINDING
 Reshaping of occlusal/incisal surfaces of teeth or
coronoplasty involves selective grinding to create
harmonious contact relationships between of teeth in
opposite arches.
 Controversies regarding extent and long term
effectiveness.
165

162. Indications (1989 World Workshop in Periodontics)
1) To reduce traumatic forces to teeth that exhibit:
Increasing mobility or fremitus to encourage repair
within the periodontal attachment apparatus.
Discomfort during occlusal contact or function.
2) To achieve functional relationships & masticatory
efficiency in conjunction with restorative treatment,
orthodontic, orthognathic surgery or jaw trauma when
indicated.
166

163. 3)As adjunctive therapy that may reduce the damage
from parafunctional habits.
4) To reshape teeth contributing to soft tissue injury.
5) To adjust marginal ridge relationships and cusps that
are contributing to food impaction.
167

164. Contraindications
1) Occlusal adjustment without careful pretreatment
study, documentation, and patient education.
2) Prophylactic adjustment without evidence of the signs
and symptoms of occlusal trauma.
3) As the primary treatment of microbial-induced
inflammatory periodontal disease.
168

165. 4) Treatment of bruxism based on a patient history
without evidence of damage, pathosis, or pain.
5) When the emotional state of the patient precludes a
satisfactory result.
6) Instances of severe extrusion, mobility or
malpositioning of teeth that would not respond to
occlusal adjustment alone.
169

166. THERAPEUTIC OCCLUSION
 One in which arrangement of teeth & their opposing
occlusal surfaces satisfies function & esthetic
requirements while distributing occlusion over as
many teeth during functions of mandible.
 Concepts:
 Fully balanced occlusion
 Unilateral balanced occlusion
 Cusp fossa occlusion
170

167. Steps in coronoplasty
1. Retrusive prematurities are eliminated.
2. Adjust ICP to achieve stable, simultaneous contacts.
3.Test for excessive occlusal contact on the incisors in ICP.
4.Elimination of posterior protrusive contacts.
5.Reduce mediotrusive prematurities.
6. Laterotrusive prematurities
7.Gross occlusal disharmonies
8.Recheck Contact relationships.
9. Polish all depressed surfaces to make the patient feel
comfortable. The occlusal surfaces are smoothened and
polished.
171

168. MANAGEMENT OF PARAFUNCTIONAL HABITS
 Use of night guards
 Also relaxes masticatory muscles
172

169. SPLINTING
 Mechanism of joining adjacent teeth thereby reducing
their mobility & converting them into single unit
which withstands occlusal forces better than
individual tooth.
 But, removal of abnormal occlusal forces must be the
primary target.
173

170. ORTHODONTIC TOOTH MOVEMENT
 Tooth movt which shall eliminate abnl occlusal forces
& improve its long term prognosis – goal.
 One of the ideal Rx of TFO.
 But periodontally compromised tooth with little bone
support – not good candidate.
 Moving tooth in a position which will further
compromise its stability & long term prognosis not
desirable.
174

171. Will orthodontic tooth movement, correct
or reduce occlusal trauma?
Then aim at
elimination of interferences
If yes, then assess the periodontal health
Assess whether the patient has
any comprehensive malocclusion
If no, ortho-therapy not indicated
If yes, then proceed
with comprehensive
orthodontic diagnosis
and treatment plan
Orthodontic
mechanotherapy &
correction of all
functional problems
Assess whether occlusal
trauma has been
eliminated
If yes, then debond and put
on retainers &
maintain periodontal
maintenance therapy
Adult patients with occlusal trauma
If all teeth healthy
175

172. OCCLUSAL RECONSTRUCTION
 Done when occlusal equilibration cant be achieved by
any other means.
 Involves redesigning complete occlusal scheme by
giving crowns, bridges or implant supported
prosthesis.
 Must be thoroughly studied first on articulated casts &
then replicated in pt’s mouth.
176

173. EXTRACTION OF SELECTED TEETH
 Extraction of tooth with extensive pdl involvement
with poor prognosis may improve prognosis of
remaining teeth.
 Also, during orthodontic Rx, extraction of certain
teeth may be indicated for proper final positioning &
aligning of teeth.
177

174. CONCLUSION
178

175.  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.
 The initial treatment of the periodontitis lesion should
focus on control of inflammation by means of patient
oral hygiene and nonsurgical therapy.
179

176.  In situations in which an obvious occlusal discrepancy
is directly related to a clinically and/or radiographically
evident traumatic lesion, it may be appropriate to
adjust the occlusion at this stage.
 Conversely, occlusal discrepancies that are not
accompanied by signs or symptoms of occlusal trauma
generally do not require adjustment.
 After initial therapy, the dentist should re-evaluate the
patient to assess the results.
180

177.  At this time, if indicated by persistent hypermobility or
patient discomfort, further occlusal therapy may be
indicated.
 Thus the treatment of occlusal trauma is directed toward
the specific instances in which occlusal trauma truly exists.
 An understanding of the effect of trauma from occlusion
on the periodontium is useful during the clinical
management of periodontal problems.
181

178. REFERENCES
1. Newman, Takei, Klokkevold, Carranza- Clinical
Periodontology.11thed. Elsevier publication; 2011
2. Jan Lindhe, Niklaus P Lang, Thorkild Karring -Clinical
Periodontology & Implant Dentistry .
3. JD Manson, B M Eley- Outline of Periodontics. 3rd edition
4. Critical decisions in periodontology- Hall. 4th edition
5. Irving Glickman- Clinical Periodontology
6. Dilip G Nayak, Ashita Uppoor, Mahesh C P- Textbook of
Periodontology & Oral Implantology. 1st edition
7. Glickman I. Inflammation and trauma from occlusion, co-
destructive factors in chronic periodontal disease. J
Periodontol 1963 Nov;34(1):5-10.
182

179. 8.Vollmer WH, Rateitschak KM. Influence of occlusal adjustment
by grinding on gingivitis and mobility of traumatized teeth. JCP
1975; 2:1 13.
9.Sottosanti. A possible relationship between occlusion, root
resorption and the progression of periodontal disease, j West Soc.
Periodontol 1977; 25:69.
10.Lindhe J, Ericsson I.The effect of elimination of jiggling forces on
periodontally exposed teeth in the dog. J Periodontol 1982 ; 53(9)
11.Stephen K. Harrel, Martha E. Nunn and William W. Hallmon. Is
there an association between occlusion and periodontal
destruction?: Yes—occlusal forces can contribute to periodontal
destruction. J Am Dent Assoc 2006;137;1380-1392.
12.Commander R. “Dave” Rupprecht. Trauma from occlusion: a
review. Clinical Update 2004;26(1)
13.R. Saravanan, Prajeeth J. Babu, P. Rajakumar. Trauma from
occlusion -An orthodontist’s perspective. JISP 2010; 14(2)
183

180. THANKYOU
184