TARRSON FAMILY ENDOWED CHAIR IN PERIODONTICS

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TARRSON FAMILY ENDOWED CHAIR IN PERIODONTICS
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UCLA SCHOOL OF DENTISTRY
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Presents
Presents
Dr. E. Barrie KenneyProfessor ChairmanSection
of Periodontics
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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
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• 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.

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• Histology of Intrabony defect due to plaque
  induced Periodontitis. Arrows show sub gingival
  plaque on root surface

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• Irritation factors are plaque that induces
  Gingivitis which progresses to Periodontitis.
  Traumatizing factors from occlusion cause tissue
  changes in periodontal ligament space.

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• 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.

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• 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.

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• The first reaction to increased occlusal loading
  is increased vascularity in the Periodontal
  ligament space. No changes are seen in gingival
  tissues.

Tissue Changes Due to Traumatic Occlusion
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• Normal Periodontal ligament with normal occlusal
  forces showing dense collagen fibers attached to
  bone and cementum with minimal vascularity.

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• With excessive occlusal loading the collagen
  fibers lose their connections between cementum
  and bone ,and blood vessels proliferate.

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• This initial increased vascularity results in a
  more compressible periodontal ligament and
  increased clinical mobility.

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• 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.

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• 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.

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• Further effects of Traumatic Occlusion are seen
  with loss of density of collagen and absence of a
  functional fiber arrangement.

Loss of Density of Collagen
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• High power view. No collagen fibers adjacent to
  bone and loss of functional support of
  Periodontium.

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• Advanced Traumatic Occlusion with minimal
  Periodontal ligament tissue. An advancing plaque
  induced Periodontitis can rapidly spread apically
  in this situation.

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Result of Traumatic Occlusion
Normal Periodontium
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• Periodontal ligament tissues can respond with
  Traumatic Occlusion changes when a normal
  periodontium is affected by increased occlusal
  loading due to bruxing clenching or a high
  restoration

• These changes are called Primary Occlusal Trauma
  or Primary Trauma from occlusion.

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• 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.

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• Coronal portion of plaque induced Periodontitis
  with pocket formulation

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• 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.

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• More Apical region with Traumatic Occlusion
  changes seen deep in Periodontal tissues apical
  to Periodontitis.

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Traumtic occlusion changes deep in periodontal
ligament
Apical part of plaque induced Periodontitis
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• 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).

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• There is also thickened lamina dura and this
  tooth has increased mobility.

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• 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.

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• Both premolars have traumatic occlusion and
  there is an addition Periodontitis related bone
  loss and pockets on the mesial of the first
  premolar.

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• Gingival recession is not caused by Traumatic
  Occlusion but is related to inadequate
  Keratinized Gingiva and excessive tooth brushing.

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• Wedge shaped defect in root of lower first
  premolar is due to traumatic toothbrushing and is
  not related to Traumatic Occlusion

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• Abfraction type of root loss like this has not
  been shown to occur clinically in association
  with heavy occlusal forces.

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• At time of Periodontal surgery large
  hyperplastic bone response to heavy occlusal load
  called Buttressing Bone

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• Buttressing Bone removed during periodontal
  surgery to facilitate normal contour of gingival
  tissues.