Trauma From Occlusion (TFO)

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 Trauma from Occlusion:
 Pathologic or adaptive changes which develop in the
periodontium as a result of undue force produced by
the masticatory muscles.
 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 … by the teeth of the opposing jaw.
 AAP (1986): An injury to the attachment apparatus as a
result of excessive occlusal force.
 Trauma from Occlusion
 Primary TfO:
 A tissue reaction, which is elicited around a tooth with
normal height of the periodontium (no attachment
loss!)
 Secondary TfO:
 Related to situations in which occlusal forces cause
damage in a periodontium of reduced height
(attachment loss present)
 Karolyi’s (1901) Hypothesis
 An interaction exists between TfO and alveolar
pyorrhea.
 Stones (1938)
 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
 Pathway of spread of a plaque-
associated gingival lesion can be
changed if abnormally strong
forces are acting on teeth with
subgingival plaque
 Zone of irritation includes
marginal and interproximal
gingiva. Not affected by occlusal
forces. Lesion propagates
apically first by involving the
bone then the periodontal
ligament.
 Zone of co-destruction
includes the ligament,
cementum, bone, and the
transseptal and
dentoalveolar fibers
 Fibers can be affected
from the lesion in the zone
of irritation, or from
trauma-induced changes
in the zone of codestruction
 In teeth not affected by
TfO, inflammatory lesion
can spread into alveolar
bone
 In teeth affected by TFO,
inflammatory lesion
spreads into periodontal
ligament. This will create
an angular bony lesion
combined with an
infrabony pocket.
Angular bony defect and infrabony pocket
distal of premolar
Apical cells of the JE and the subgingival plaque are
at different levels. Crest of marginal bone is slanting.
It follows the location of the JE and plaque.
 Waerhaug measured distance between the
subgingival plaque and
 The perimeter of the associated inflammatory infiltrate
 The surface of the adjacent alveolar bone
 He concluded that angular defects and infrabony
pockets occurred equally frequently in teeth with
TfO and in teeth without TfO
 Waerhaug postulated that loss of attachment and
bone are the result of inflammation induced by
subgingival plaque
T: tension zone
P: pressure zone
Recession or AL can occur at sites of gingivitis when tooth
is moved through the envelope of the alveolar process.
 Combined pressure and
tension zones result from
jiggling
 Zones are characterized by
collagen resorption, bone
resorption, and cementum
resorption.
 Signs of increased vascularity
or exudation.
 Tooth shows progressive
mobility.
 Ligament space
gradually adjusts to new
situation.
 No attachment loss!
 Increased tooth mobility
 Occlusal adjustment
normalizes the width of
the periodontal
ligament.
 Teeth are stabilized and
regain normal mobility.
 Zones of combined pressure
and tension exhibit
 vascular proliferation,
 exudation,
 thrombosis, and
 bone resorption
 A widened periodontal
ligament develops
 Tooth mobility is increasing
progressively
 Ligament space
gradually adjusts to new
situation.
 No attachment loss!
 Increased tooth mobility
 Ligament tissue regains
normal composition
 Supra-alveolar tissue
unaffected
 No further loss of attachment
 Teeth hyper mobile,
surrounded by tissue that
adapted to the new
functional situation
 Occlusal adjustment will
allow the periodontal
ligament to regain its normal
width.
 Can abnormal occlusal forces
influence the spread of the
plaque-associated
periodontal lesion and/or
enhance tissue breakdown?
 In the case presented here,
there is a healthy zone
between inflamed CT and PL
 Pathologic and adaptive
reactions occur in the PL
 A widened periodontal
ligament and increased
tooth mobility will
result
 No further loss of
attachment is observed
result in reduction of
periodontal ligament
width and
 Reduced (not normal!)
tooth mobility
 Presence of infrabony
pocket and infiltrated
connective tissue
 Merging of zones of
“irritation” and “codestruction”
 Jiggling forces lead to
typical vascular and
exudative reaction in
ligament space
 Pathologic reaction may
occur within a zone that
also contains (plaqueinduced) inflammatory
cell infiltrate
 In this situation,
increasing tooth
mobility may also be
associated with an
enhanced loss of
attachment and further
down growth of the most
apical portion of the PE
result in narrowing of the
ligament space, less tooth
mobility
 Regeneration of attachment
cannot be expected
 Loss of attachment is
permanent
 If plaque-induced
inflammation persists, more
attachment loss may occur
 In a healthy periodontium, neither unilateral nor
jiggling forces can result in attachment loss or
pocket formation
 TfO alone cannot induce periodontal tissue
breakdown
 Bone resorption in TfO should be interpreted as an
adaptation of the ligament and bone to the altered
functional requirements
 In plaque-induced inflammation, TfO may
enhance the disease progression
 This series of slides is based on Lindhe et al.’s textbook
“Clinical Periodontology and Implant Dentistry”,
chapter 8.

Trauma From Occlusion (TFO)

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