TARRSON FAMILY ENDOWED CHAIR IN PERIODONTICS

UCLA SCHOOL OF DENTISTRY

Presents
Dr. E. Barrie Kenney
Professor & Chairman
Section of Periodontics
E. Barrie Kenney B.D.Sc., D.D.S., M.S.,
F.R.A.C.D.S.

Tarrson Family Endowed Chair in Periodontics.

Professor and Chairman Division of Associated

Clinical Specialties UCLA School of Dentistry
Many clinicians believe Traumatic
occlusion causes Intrabony
Periodontal defects but this is not so.
This defect is caused by dental plaque
with accentuation due to the open
contact region and poor subgingival
margin of Restoration.
Histology of Intrabony defect due
to plaque induced Periodontitis.
Arrows show sub gingival plaque
on root surface
Irritation factors are plaque that
induces Gingivitis which
progresses to Periodontitis.
Traumatizing factors from
occlusion cause tissue changes in
periodontal ligament space.
Zone of co-destruction occurs when
plaque induced Periodontitis occurs in
a tooth that also has Traumatic
Occlusion resulting in more severe
bone loss than that seen with
Periodontitis alone.
Host parasite reaction between
bacterial plaque and host
inflammatory response is the cause
of pocket depth and attachment loss.
The presence of Traumatic occlusion
can accentuate the damage when
Periodontitis proceeds apically into
the Periodontal Ligament Space.
 The first reaction to increased
Tissue Changes Due to occlusal loading is increased
vascularity in the Periodontal
Traumatic Occlusion
ligament space. No changes
are seen in gingival tissues.
Normal Periodontal ligament
with normal occlusal forces
showing dense collagen fibers
attached to bone and
cementum with minimal
vascularity.
With excessive occlusal
loading the collagen fibers lose
their connections between
cementum and bone ,and
blood vessels proliferate.
This initial increased
vascularity results in a more
compressible periodontal
ligament and increased clinical
mobility.
Changes in the apical
periodontal ligament vascular
patterns can also result in
increased vasodilation of the
pulp with increased sensitivity
and pain to Hot and Cold
stimuli secondary to Traumatic
Occlusion.
In Traumatic Occlusion after
the initial change of increased
vascularity, there is a
stimulation of osteoclasts
which cause bone loss and a
widened periodontal ligament
space. This also causes
increased tooth mobility.
Further effects of Traumatic
Occlusion are seen with loss of Loss of Density of
density of collagen and Collagen
absence of a functional fiber
arrangement.
High power view. No collagen
fibers adjacent to bone and
loss of functional support of
Periodontium.
Advanced Traumatic Occlusion
with minimal Periodontal
ligament tissue. An advancing
plaque induced Periodontitis
can rapidly spread apically in
this situation.
Normal Periodontium Result of Traumatic
Occlusion
Periodontal ligament tissues
can respond with Traumatic These changes are called
Occlusion changes when a Primary Occlusal Trauma or
normal periodontium is Primary Trauma from
affected by increased occlusal occlusion.
loading due to bruxing
clenching or a high restoration
In teeth with bone loss due to
periodontal disease previously
well tolerated occlusal loading
can become traumatic and
cause changes in the
periodontal ligament tissues.
These changes are called
secondary occlusal trauma or
secondary trauma from
occlusion.
Coronal portion of plaque
induced Periodontitis with
pocket formulation
Region of crestal bone showing
intrabony pocket due to
plaque this is blending with
Traumatic Occlusion induced
Periodontal ligament changes
of loss of collagen and
increased vascularity.
More Apical region with
Traumatic Occlusion changes
seen deep in Periodontal
tissues apical to Periodontitis.
 Apical part of Traumtic
plaque induced occlusion
Periodontitis changes deep in
periodontal
ligament
Radiograph of lower Molar with
Traumatic Occlusion. Widened
Periodontal ligament space on
Mesial all the way around the
apex with beginning bone loss
in furcation (arrows).
There is also thickened lamina
dura and this tooth has
increased mobility.
First molar has traumatic occlusion
causing the bone loss in the furca.
Clinically there is no pocket depth
nor Periodontitis in the furcation
and so the diagnosis is Traumatic
Occlusion and the treatment is
occlusal adjustment to reduce
occlusal loading.
Both premolars have traumatic
occlusion and there is an
addition Periodontitis related
bone loss and pockets on the
mesial of the first premolar.
Gingival recession is not
caused by Traumatic Occlusion
but is related to inadequate
Keratinized Gingiva and
excessive tooth brushing.
Wedge shaped defect in root
of lower first premolar is due
to traumatic toothbrushing
and is not related to Traumatic
Occlusion
“Abfraction” type of root loss
like this has not been shown
to occur clinically in
association with heavy occlusal
forces.
At time of Periodontal surgery
large hyperplastic bone
response to heavy occlusal
load called Buttressing Bone
Buttressing Bone removed
during periodontal surgery to
facilitate normal contour of
gingival tissues.