occlusion basic

1. Basic Concepts Of Occlusion

2. CONTENTS
 INTRODUCTION
 TERMINOLOGIES
 MASTICATORY SYSTEM
 TYPES OF OCCLUSION
 FORCES OF OCCLUSION
 BRUXISM
 PATHOLOGICAL TOOTH MIGRATION
 TRAUMA FROM OCCLUSION
 CONCLUSION
 REFERENCES

3. INTRODUCTION
 Ramjford and Ash
 Latin word
Occ—up
Clusion—closing
Meaning :
Contact relationship of teeth resulting from neuromuscular
control of masticatory system

4. Evidence based decision making
Nunn and Harrell 2001—retrospective study
---periodontitis patients
---loss of attachment---presence/absence of occlusal
interferences
---Result
positive influence of occlusal correction on
surgical/non-surgical outcome

5.  Occlusal forces----broad spectrum
 Biological basis of occlusal function
 Consider components as a functional unit—not in
isolation

6. TERMINOLOGIES
 Maximum intercuspation(centric occlusion and intercuspal
position)
 Centric relation
 Initial contact in centric
 Excursive movement
 Laterotrusion
 Working side
 Non-working side ( balancing side )
 Protrusion
 Retrusion
 Guidance

7. MASTICATORY SYSTEM
1
4
2
3
5

9. 2
4
3
1
DYNAMICS OF EQUILIBRIUM

10.  Primary requirements of a successful occlusal
therapy
1. Comfortable and stable TMJ’S
2. Anterior teeth in harmony with the envelope of
function
3. Non –interfering posterior teeth

11.  Formula for a perfected
occlusion
1. Simultaneous equal
intensity contacts on all
teeth---condyle disk
assembly completely
seated
2. “Dots in back,lines in
front”

12. 3. Posterior teeth ---centric and eccentric
4. Anterior guidance + condyles---disclussion of
posteriors
 REASON
 Elevator muscles shut off---reduce forces on TMJ
and anterior teeth
 Bruxers

13. TYPES OF OCCLUSION

14.  FUNCTIONAL CLASSIFICATION OF OCCLUSION
Physiologic occlusion—is present when no signs of
dysfunction or disease are present and no treatment is
indicated
Non-physiologic(or traumatic) occlusion—is associated
with dysfunction or disease caused by tissue injury, and
treatment maybe indicated.(criteria—whether it contributes
to tissue injury,not how teeth occlude)
Therapeutic occlusion—is the result of specific
interventions designed to treat dysfunction or disease.It is
an occlusal scheme employed in restoring or replacing

15. ORGANISATION OF OCCLUSION
1)Bilateral balanced occlusion: works of Von Spee and
Monson
 Maximum number of teeth contact in all excursive
movements
 Concept :distribution of stresses
 Complete denture--non-working side contacts—
tipping prevented
 Demerit :excessive frictional wear of teeth

16. Unilateral balanced occlusion(group function): Shyyler et al
 Concept :Natural teeth –cross-arch balance not necessary
--Elimination of non-working contacts
 Restorative dentistry
 Lateral excursions---working side—all teeth in contact
 Group function of teeth on working side distributes the occlusal
load
 Absence of non-working side contacts prevents the those teeth
from being subjected to obliquely directed forces found in non-
working interferences

17. Mutually Protected Occlusion (canine protected occlusion or
“organic occlusion” ): D’Amico, Stuart, Stallard et al
Concept :Observation
Posterior teeth contact—centric relation only
Incisor contact –protrusion only
Canine contact—lateral excursions
Why canine?????
--greater no of pressurecoeptors/mechanorecptors
--good crown-root ratio
--position in the arch

18.  Cases its not possible

19. FORCES OF OCCLUSION
1. Antagonistic forces: muscle of mastication and
counteracting oral musculature
2. Inclined planes of the teeth and the anterior component
of force Closure of the mandible
Force Distribution by
inclined planes
Resultant occlusal forces –
anterior force
Tend to move teeth mesially
ANTERIOR COMPONENT
OF FORCE(ACF)
ACF –pushes
teeth mesially in
their sockets
---release of
force
---previous
position
--proximal
contact flatenned
by wear
--physiological
mesial migration
--overall
reduction of
0.5cm in length

20. 3. Proximal contacts: malpositioned contacts(cervico incisal or
faciolingual)----deflect forces of occlusion---dispacement of teeth
and create abnormal forces on the periodontium
4. Design and inclination of teeth: Maxillary central incisor—inclined
mesially—provide maximim efficiency of cutting edge—in function—
driven mesially—root shaped—greater areas of attachment on the
palatal and distal side—counteracts tendency towards facial and
mesial displacement during function.
Molars –inclined mesially---to transmit component of vertical
occlusal forces to premolars and canines
5. Atmospheric equilibrium during breathing and swallowing

21.  Intraoral Occlusal Evaluation
Identification
of occlusal
contacts in
max
intercuspation
Guidance in
excursive
movements
Initial contact
in centric-
relation
closure arc
Tooth mobility Attrition

22. BRUXISM

23.  Bruxism :
Definition:An oral habit consisting of involuntary rhythmic or
spasmodic non-functional gnashing, grinding, or clenching of
teeth, in other than chewing movements of the mandible, which
may lead to occlusal trauma
(Glossary Of Prosthodontic
Terms)
 Clenching :

25.  Evaluation :
Bite guard

26.  Etiology :
OCCLUSAL INTERFERENCES :
 1901 Karolyi—postulated that occlusal interference in
combination with psychic stresses---important factor
 Also without stress
Premature contacts---activate high levels of muscle activity
 1961 Ramfjord
 Ramfjord and Ash 1983, Williamson 1983—EMG studies
Result : “marked reduction in muscle tonus and harmonious
integration of muscle action follows the elimination of
occlusal disharmony”

27.  Trigger parafunctional jaw movement which were not
present earlier to interference
 “Erasure mechanism”
Coarse food of premodern man---abrasive enough to
wear away interfering cusps and inclines when the
bruxism mechanism was triggered and adjust
occlusion within tolerable limits
 Modern diet

28.  Rugh and Solberg 1975
 Habitual nocturnal bruxism continued despite removal of
occlusal interferences.
 EMG recordings---same masticatory muscle contraction
before and after occlusal correction
 Equally in children as in adults

29.  Satoh and Harada 1971
Nocturnal bruxism---from a deeper stage of sleep to a lighter
stage
REM stage---most damaging
 Olkinuora 1972 divided bruxers
1)Stress associated 2)Non-associated with stress
Conclusion :heriditary bruxism more common in the non-
stress group
 Stress –bruxers-----more muscular symptoms and more
emotionally disturbed
 Stress causing stimuli—directly correlated with time of
muscle contraction
 Clenching(increased muscle tonus) –physical

30. Bruxism Clenching
•Severe attrition, Split
teeth
•Hypermobility
•Ulcer associated
sometimes
•Adaptive changes in
TMJ—flattening of
condyles,gradual loss
of convexity of
ementiae
•Fractured fillings
•screeching ,grating
sound at night
•Masseter muscle
enlarged
•Lateral pterygoid
tender
Occluso-muscle pain
Tooth wear not
common
Linea alba seen
sometimes
Lateral indentations on
tongue
Temporalis affected

31.  Evaluation :
 EMG
 Bite strip
0-No sleep bruxism—less than
40 events
1-Mild sleep bruxism—40-74
events
2-Moderate sleep bruxism—75-
124 events
3-Severe sleep bruxism—125
or more events

32. PATHOLOGICAL TOOTH
MIGRATION

33.  Definition :
Tooth displacement that results when the balance among
the factors that maintain physiologic tooth position is
disturbed by periodontal disease.
 May be an early sign of disease and associated with
gingival inflammation and pocket formation
 Anteriors > Posteriors
 Any direction---Associated with mobilty and rotation

34.  In occlusal/incisal direction termed as extrusion
 Prevalence :
Martinez-Canut et al 1997  55.8%
Towfighi et al 1997  30.03%

35. Etiologic factors for pathologic migration
A. Destruction of periodontal supporting tissues
B. Occlusal factors
C. Soft tissue pressure of the tongue, cheek and lips
D. Periodontal and periapical inflammation
E. Extrusive forces
F. Habits

36. Destruction of periodontal supporting tissues
Selwyn S 1973
Bone loss in 30 patients with periodontitis + incisal
migration v/s no migration
Conclusion: more bone loss in PTM teeth
Martinez-Canut et al 1997
852 periodontitis patients
Conclusion: Bone loss, tooth loss and gingival
inflammation :
PTM 2.95 to 7.97

37.  Role of transseptal fibres
Moss and Picton 1982
 Abnormal proximal contacts---Anterior component
of force
Wedging force

38. Occlusal factors
1. Posterior bite collapse –unreplaced first molars
2. Arch integrity  Interproximal contacts destroyed during
tooth loss, dental caries, faulty restorations & severe
attrition
3. Class II malocclusion  Selwyn 1973, class II
malocclusion 17/30 PTM pts

39. 4. Occlusal interferences supracontacts --Thielman’s law
Occlusal factors may become more destructive in
patients who have lost significant alveolar bone

40. Protrusive pattern of mastication
 Yaffe et al 1992
27/131 patients had protrusive mastication
16/27 patients---anterior attrition and flaring of
incisors
Conclusion: etiologic factor for anterior PTM

41. Soft tissue pressure of the tongue, cheek, and lips
 Can move teeth especially after loss of periodontal support---
long duration
 Light forces even1.0 gm by facial muscles at rest—initiate
displacement of incisors
 Stable dentition is the result of an equilibrium between tongue
and cheek pressures is disproven
 Proffit stated that the forces of the tongue, cheek, and lips
together with the forces of the periodontal tissues are the
(Proffit W et al. 1975)

42. Periodontal and periapical inflammation
 Hirschfeld 1933--PTM of teeth is due to pressure of
inflammatory tissue
 Movement occurs in a direction opposite to the deepest
part of the pockets
 Sutton P (1985)  Hydrodynamic and hydrostatic forces
within the blood vessels and inflamed tissues in the pocket
 Spontaneous correction following periodontal treatment
Verendra kumar SC ,Anita S, SN
Thomas 2009

43. Extrusive forces
 Eruption forces are 2 to 10 gms and present
throughout life
 No direct association links eruptive forces to PTM
 Extrusion of incisors is very common, eruptive forces
can be said to be a contributing factor

44. Habits
 Lip and tongue habits, fingernail biting, thumb
sucking, pipe smoking, bruxism
 Martinez et al ---no association between oral habits
and PTM
Out of 475 PTM cases only 11% had oral habits
 Duration of force more imp. than magnitude (Proffit
1973)

46. Basic Concepts Of Occlusion

47. CONTENTS
 INTRODUCTION
 TERMINOLOGIES
 MASTICATORY SYSTEM
 TYPES OF OCCLUSION
 FORCES OF OCCLUSION
 BRUXISM
 PATHOLOGICAL TOOTH MIGRATION
 TRAUMA FROM OCCLUSION
 CONCLUSION
 REFERENCES

48. TRAUMA FROM OCCLUSION
 Introduction
 Historical perspective
 Definitions
 Classification
 Clinical and radiographic signs
 Stages of tissue response to increased occlusal forces
 Reversibility of traumatic lesions
 Influence on progression of marginal periodontitis
 Clinical and animal experiments

49. INTRODUCTION
MAGNITUDE DIRECTION DURATION FREQUENCY

50. Increase in the magnitude of occlusal force
Widening of the periodontal ligament space
Number and width of periodontal ligament fibers
Density of alveolar bone

51.  Changing the direction of occlusal forces causes a re-
orientation of the stresses and strains within the periodontium.
 Principal fibers- arranged--accommodate occlusal force—long
axis of tooth
 Lateral (horizontal) forces and torque (rotational)
forces…..INJURY
 Duration and frequency of occlusal forces affect response of
alveolar bone.

52. HISTORICAL PERSPECTIVE
In 1901, Karolyi indicated that there appeared to be a
correlation between excessive occlusal forces and
periodontal destruction.
“Karolyi effect”

53.  In 1917 and 1926, Stillman stated that excessive occlusal
forces were the primary cause of periodontal disease and
that occlusal therapy was mandatory for the control of
periodontal disease.
 Orban & Weinman, in 1933, used the histologic
observation of human autopsy material
Occlusal forces did not have a major effect on periodontal
destruction and gingival inflammation

54. Definition:-
Trauma from occlusion refers to a condition
where injury results to the supporting structures of teeth by the
act of bringing jaws into a closed position.
STILLMAN
(1917)
Trauma from occlusion is defined as damage in periodontium
caused by stress on teeth produced directly or indirectly by
teeth of opposing jaw.
WHO
(1978)
Occlusal trauma was defined as an injury to the attachment
apparatus as a result of excessive occlusal force.

55. Trauma from occlusion is defined as when occlusal forces
exceed the adaptive capacity of tissue, tissue injury
results. This injury is termed trauma from occlusion.
(CARRANZA)
Other terms
1. Traumatizing occlusion.
2. Occlusal trauma.
3. Traumatogenic.
4. Periodontal traumatism.

56.  Traumatic occlusion
An occlusion that produces such injury is called as a
traumatic occlusion.
Other terms
1. Occlusal disharmony.
2. Functional imbalance.
3. Occlusal Dystrophy.

57. CLASSIFICATION
1)Acute trauma from occlusion
2)Chronic trauma from occlusion
1)Primary trauma from occlusion
2)Secondary trauma from occlusion

58. ACUTE TRAUMA FROM
OCCLUSION
CHRONIC TRAUMA
FROM OCCLUSION
Less common More common
Definition:- Result from abrupt change in
occlusal force
Result from gradual change
in occlusion
Cause:- ●Biting on a hard object
●Restoration
●Prosthetic appliances
●Tooth wear
●Drifting movement with
Parafunctional activity
Clinical Features:- ●Tooth pain
●Sensitivity to percussion
●Increased tooth mobility
●Cementum tears.
●Tooth mobility
Management:- ●Dissipate the force by shift in
the position of tooth
●By wearing away or correction
of restoration.
●Removal of cause

59. PRIMARY TRAUMA FROM
OCCLUSION
SECONDARY TRAUMA
FROM OCCLUSION
Definition:- Result of alterations in occlusal
forces.
Results from reduced ability of
periodontium to resist
occlusal forces.
Etiology:- ●Insertion of high filling
●insertion of prosthetic
replacement
●Drifting movement or extrusion
of teeth into spaces created
by unreplaced missing teeth.
●Orthodontic movement of teeth
into functionally
unacceptable position.
●Bone loss resulting from
marginal inflammation.
Reduction PDL attachment area
Alteration of leverage on
remaining tissue
www.rxdentistry.blogspot.com

60. CLINICAL SIGNS OF OCCLUSAL TRAUMA
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) Thermal sensitivity

61. RADIOGRAPHIC SIGNS OF TFO
 Increased width of the periodontal ligament space, with
thickening of the lamina dura along the
 lateral aspect of the root,
 in the apical region, and
 in bifurcation areas
 A “vertical” rather than “horizontal” destruction of the
interdental septum.
 Radiolucency and condensation of the alveolar bone.
 Root resorption

62. Increased width of the PDL space
Increased density of alveolar bone
Radiographic signs of TFO

63. Tissue response occur in 3 stages:-
1) Injury
2) Repair
3) Adaptive remodeling of the
periodontium
STAGES OF TISSUE RESPONSE WHEN
OCCLUSAL FORCE IS INCREASED

64. Stage I: Injury.
• Tissue injury ….. excessive occlusal forces.
• The body then attempts to repair the injury and restore the
periodontium….. if the forces are diminished or if the tooth
drifts away from them.
• Force is chronic, the periodontium is remodelled to cushion
its impact.
• The ligament is widened at the expense of the bone,
• Angular bone defects without periodontal pockets,
• Tooth becomes loose.

65. Stage I: Injury
• Slight excessive pressure-- Resorption of alveolar
bone(direct bone resorption)
• Widening of periodontal ligament space
• -- Blood vessels numerous and reduced in size
• Slight excessive tension-- Elongation of periodontal
ligament fibers…apposition of bone
• -- blood vessels --Enlarged

66. Greater pressure
Compression of PDL fibers Areas of hyalinization
Fibroblasts & other connective tissue cells
necrosis
Vascular changes Impairment & stasis of blood flow
Fragmentation of RBCsDisintegration of bv
Increased resorption of alveolar bone
Stage I: Injury
1-7 days
30 mins 2-3 hours

67. Stage I: Injury
Widening of the periodontal ligament
Tearing of the periodontal ligament
Severe tension
Thrombosis, hemorrhage
Resorption of alveolar bone

68. Stage I: Injury
 Furcation most susceptible to injury
 Injury to the periodontium produces a temporary
depression
in mitotic activity and the rate of proliferation and
differentiation of fibroblasts,
in collagen formation,
in bone formation
 These return to normal levels after dissipation of the
forces.

69. Stage II: Repair
 TFO stimulates increased reparative activity.
Damaged tissues are removed, and new connective tissue
cells and fibers, bone, and cementum are formed to restore
the periodontium
Forces remain traumatic only as long as the damage
produced exceeds the reparative capacity of the tissues.

70. Stage II: Repair
 Excessive occlusal forces…. resorption of bone…. Body
reinforces the thinned bony trabeculae with new bone…
Buttressing bone formation
Central buttressing
Endosteal cells deposit
new bone ,
Restores bony trabeculae &
reduces the size of marrow spaces
Peripheral buttressing
Shelf like thickening of
the alveolar margin…
Lipping-bulge in the
contour of facial/lingual
bone

71. Stage III: Adaptive Remodeling of the Periodontium.
 Periodontium is remodeled in an effort to create a structural
relationship in which the forces are no longer injurious to the
tissues.
 Thickened periodontal ligament, which is funnel shaped at
the crest
 Angular defects in the bone, with no pocket formation.

72. Carranza FA1970

73. Reversibility of traumatic lesions
 Trauma from occlusion is reversible.
 When the impact of the artificially created force is relieved,
the tissues undergo repair
 It does not correct itself..not always temporary
 Presence of inflammation may impair the reversibility
 Injurious forces relieved for repair to occur--if not periodontal
damage persists & worsens
Polson M
1976

74. • Thinning of the periodontal ligament
• Atrophy of the fibers
• Osteoporosis of the alveolar bone
• Reduction in bone height
Effects Of Insufficient Occlusal Force

75. Effect on progression of marginal periodontitis
Blood supply of marginal gingiva—not affected

76.  Important to eliminate the marginal inflammatory component
in cases of trauma from occlusion because the presence of
inflammation affects bone regeneration after the removal of
the traumatizing contacts.

77. Glickman’s concept
 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.
 Plaque-associated lesions…suprabony pockets &
horizontal bone loss.
 Sites also exposed to abnormal occlusal force…angular
bony defects & infrabony pockets

78. Zone of irritation
Zone of co-destruction
Glickman (1967), “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

79. Waerhaug’s concept
 Waerhaug (1979) examined autopsy specimens similar
to Glickman’s.
 Measured in addition the distance between the
subgingival plaque and
1. Periphery of the associated inflammatory cell
infiltrate in the gingiva and
2. The surface of the adjacent bone
Refuted the hypothesis that TFO played role in the
spread of a gingival lesion into the “zone of co-
destruction”.

80.  Loss of connective tissue attachment & the resorption of
bone around teeth are, exclusively the result of
inflammatory lesions associated with subgingival plaque.
 Relationship of the plaque level between adjacent teeth
(either at the same of different apico-coronal levels)
would yield either horizontal or vertical interproximal bone
loss.

81.  Excessive occlusal forces had no relationship to the
underlying bony defect and that vertical defects were
found equally around traumatized and non-traumatized
teeth.
 Bone loss was always associated with the down growth
of plaque and there was no relationship between
excessive occlusal forces and vertical bone loss.

82.  Conclusion :
Angular defects and 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

83. Trauma-induced areas
favorable environment
plaque and calculus
development of deeper lesions
Sottosanti JS.
Theories of trauma and inflammat
Other theories of trauma and inflammation

84. Orthodontic tooth movement Drifting into edentulous space
Transformation of suprabony pocket into infrabony
Supragingival plaque
Subgingival plaque
Ericsson I
Theories of trauma and inflammat

85. Increased tooth mobility
pumping effect on plaque metabolites
Increasing their diffusion
Vollmer WH
Theories of trauma and inflammat

86. Clinical and Animal Trials

87. EASTMAN DENTAL CENTER GROUP-ROCHESTER NY---SQUIRREL MONKEYS
REPITITIVE INTERDENTAL WEDGING
MILD TO MODERATE GINGIVAL INFLAMMATION
UPTO 10 WEEKS
RESULT:PRESENCE OF TRAUMA DID NOT INCREASE LOSS OF ATTACHMENT
INDUCED BY PERIODONTITIS

88. UNIVERSITY OF GOTHENBURG GROUP IN SWEDEN—BEAGLE DOGS
CAP SPLINTS AND ORTHODONTIC APPLIANCES
MILD TO MODERATE GINGIVAL INFLAMMATION
UPTO 1 YEAR
RESULT:PRESENCE OF TRAUMA INCREASED PERIODONTAL DESTRUCTION
INDUCED BY PERIODONTITIS

89.  Rosling et al. (1976)… “infrabony pocket located at
hypermobile teeth exhibited the same degree of healing
as those adjacent to firm teeth”.
 Fleszar et al. (1980)… “pockets of clinically mobile teeth
do not respond as well to periodontal treatment as do
those of firm teeth exhibiting the same disease severity”.
 Burgett et al. (1992)… Probing attachment gain was on
the average about 0.5mm larger in patients who received
the combined treatment, i.e. scaling and occlusal
adjustment.

90. Orthodontic type traumaTipping movement

91. JIGGLING- TYPE TRAUMA
Healthy periodontium with normal height

92. Healthy periodontium with reduced height

93. Suprabony pockets and advanced bone loss

94. Infrabony pocket and advanced bone loss

95. The conclusions of these studies are as follows:
1) Occlusal trauma does not initiate gingival inflammation.
2) In the absence of inflammation, a traumatogenic occlusion will
result in
increased mobility, widened PDL, loss of crestal bone height and
bone
volume, but no attachment loss.

96. 3) In the presence of gingival inflammation, excessive
jiggling forces did not cause accelerated attachment loss in
squirrel monkeys but increasing occlusal forces may
accelerate attachment loss in beagle dogs.
4) Treating the gingival inflammation in the presence of
continuing
mobility or jiggling trauma will result in decreased mobility

97. CONCLUSION

98. References
 Functional occlusion :From TMJ to Smile design : Peter
Dawson
 Ramfjord and Ash. Occlusion. 3rd edition.
 Clinical Periodontology – Carranza 8th ,10th,11th Edition
 Clinical update-Trauma from occlusion: a
review;Commander R. “Dave” Rupprecht, DC, USN 2004

99.  Clinical Periodontology and Implant Dentistry – Jan
Lindhe 4th Edition.
 Pathologic tooth migration;Brunsvold 2008

100. Thank
u!!!!!