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THE PERIODONTALPOCKETDENT 471
3/11/2013
Dr. Hisham Al-Shorman
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Introduction
Pathologically deepened gingivalsulcus
Periodontal pocket formation &alveolar bone destruction
Neutrophils constantly releasegranules containing acidhydrolases and neutral proteases(elastase & collagenase)
These degrade collagen,proteoglycans & fibrinogen
Granulocytes present in large #s
Burstrelease large quantitiesof enzymes
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Classification
Gingival Pocket
Periodontal Pocket
Suprabony: (supracrestal/supra
alveolar): the bottom of the pocket is
coronal to the underlying alveolarbone
Intrabony (infrabony):
the bottom of the pocket is apicalto the level of the adjacentalveolar bone.
The lateral pocket wall liesbetween the tooth surface and the
alveolar bone
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Suprabony Intrabony
Pocket base is coronal to level ofalveolar bone
Pocket base is apical to crest ofalveolar bone
Bone destruction pattern ishorizontal
Bone destruction pattern is vertical
Intreproximally, transeptal fibersare arranged horizontally in thespace between the base of the
pocket and the alveolar bone
Intreproximally, transeptal fibers areoblique rather than horizontal. Theyextend from the cementum beneath
the base of the pocket along thebone and over the crest to thecementum of the adjacent tooth
On the facial and lingual surfaces,the periodontal ligament fibresbeneath the pocket follow theirnormal horizontal-oblique coursebetween the tooth and the bone
On the facial and lingual surfaces,the periodontal ligament fibresfollow the angular pattern of theadjacent bone. They extend from thecementum beneath the base of thepocket along the bone and over the
crest to join the outer periosteum
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Clinical Features
Bluish-red, thickened marginal gingiva
Bluish-red vertical zone form gingival margin toalveolar mucosa
Gingival bleeding
Suppuration
Tooth mobility
Diastema formation
Localized pain
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Pathogenesis
Inflammation in CT of gingival sulcus
Degradation of CT
Apical to JE collagen is destroyed, so area isoccupied by inflammatory cells and edema
Collagen loss occurs due to:
Collagenases and other enzymes (matrixmetalloproteinases) produced by different cells
Fibroblasts phagocytize collagen fibers
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Pathogenesis
Therefore, apical cells ofJE proliferate along theroot & the coronal
portion of JE detachfrom the root
More PMNs invade the
coronal portion of JE
Sulcus deepening
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Bacterial Invasion
Some bacteria have been shown to be able toinvade the periodontal tissues:
Porphyromonas gingivalis
Aggrigatibacter actinomycetemcomitansPrevotella Intermedia
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Microtopography of the Gingival Wall
1. Area of relativequiescence
2. Area of bacterialaccumulation
3. Areas of leukocyteemergence
4. Areas of leukocyteinteraction
5. Areas of epithelialdesquamation
6. Areas of ulceration
7. Areas of hemorrhage
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Healing Pockets
Edematous gingiva
Fibrotic gingiva
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Root Surface Wall
With deepening of pocket, collagen fibersembedded in the root are destroyed
Cementum becomes exposed to oralenvironment
Sharpeys fibers undergo degeneration
Bacteria penetrates rootFragmentation and necrosis of cementum
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Morphology of tooth wall
Cementum covered by calculus
Attached plaque
Un-attached plaque
Junctional epithelium
Partially lysed CT
Intact CT
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Periodontal Disease Activity
Period of exacerbation
Period of quiescence
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Attachment Loss and PocketDepth
Pocket depth is the distancebetween the base of the
pocket and crest of thegingival margin
Attachment loss depends onlocation of the base of thepocket on the root surface
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Bone is a dynamic tissue
The height and density of alveolar boneare maintained by an equilibrium,regulated by local and systemicinfluences, between:
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Destruction Caused ByInflammation
The most common cause of bone destruction inperiodontal disease is the extension ofinflammation from the marginal gingiva into the
supporting periodontal tissues
The inflammatory invasion of bone mark thetransition from gingivitis to periodontitis
Periodontitis is always preceded by gingivitis, butnot all gingivitis progresses to periodontitis
Factors responsible for the conversion of gingivitisto periodontitis are not known at this time
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Bone Destruction in Periodontal
Disease is Caused by :
Extension of gingival inflammation.
Trauma from occlusion.
Systemic disorders.
Combination.
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Spread of Inflammation from theGingiva into the SupportingPeriodontal Tissues:
A- Interproximally;
* (1) From the gingiva into the bone* (2) From the bone into the periodontalligament* (3) From the gingiva into theperiodontal ligament
B- Facially and lingually;
* (1) From the gingiva along theouter periosteum* (2) From the periosteum into the bonethrough vessel channels* (3) From the gingiva into the
periodontal ligament
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No!
It involves the activity of living cells alongviable bone
When tissue necrosis and pus are present
in periodontal disease, they occur in thesoft tissue walls of periodontal pockets,not along the resorbing margin of theunderlying bone
Is bone destruction in periodontaldisease a process of bone necrosis?
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Rate of Bone Loss
Loss of attachment precedes loss of bone byabout 6 to 8 months.
Patterns of bone loss RATE (Loe and co-workers): ~ 8 % of persons had rapid progression,
characterized by a yearly loss of attachment of 0.1to 1 mm
~ 81 % of individuals had moderately progressive
periodontal disease, with a yearly loss ofattachment of 0.05 to 0.5 mm
The remaining 11 % of persons had minimal or noprogression of destructive disease (0.05 to 0.09 mmyearly)
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Mechanisms of Bone Destruction
1. Direct Bacterial Destruction:
Bacterial products:
Induce the differentiation of bone progenitorcells into osteoclasts
Stimulate gingival cells to release mediators thathave the same effect
Act directly on osteoblasts or their progenitors,inhibiting their action and reducing theirnumber.
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2. Host-mediated Destruction:
Several host factors released by inflammatory
cells are capable of inducing bone resorption
in vitro and can play a role in periodontaldisease.
These include
o
prostaglandins and their precursorso interleukins (ILl and IL-1)
o tumor necrosis factor alpha (TNF- )
o prostaglandin E2 (PGE2)
Mechanisms of Bone Destruction
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Bone Destruction Caused by OcclusalTrauma
Trauma from occlusion can produce bone destruction in
absence or presence of inflammation
In the absence o f inflammation, the changes caused by
trauma from occlusion vary from; Increased compression and tension of the
periodontal ligament and increased osteoclasis of
alveolar bone
To necrosis of the periodontal ligament and bone andresorption of bone and tooth structure
These changes are reversible and can be repaired if the
offending forces are removed
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Examples of Systemic Disorders
Osteoporosis
Periodontitis and osteoporosis share a
number of risk factors; aging, smoking,
diseases, and medications that interfere with
healing
Hyperparathyroidism
Leukemia
Langerhans' cell histiocytosis
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Horizontal Bone Loss
Horizontal bone loss is the most common pattern inperiodontal disease
The bone is reduced in height, but the bone marginremains roughly perpendicular to the tooth surface
The interdental septa and facial and lingual platesare affected, but not necessarily to an equal degreearound the same tooth
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Classification of Osseous Defects
Angular defects are classified on the basis of thenumber of remaining osseous walls
They may have one, two, or three walls
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Osseous Craters
Osseous craters are concavities in the crestof the interdental bone confined within the
facial and lingual walls
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Reversed Architecture
Produced by loss of interdental bone, including thefacial plates, lingual plates, or both, withoutconcomitant loss of radicular bone, therebyreversing the normal architecture (- ve architecture)
More common in the maxilla
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Ledges
Ledges are plateau-like bone margins caused byresorption of thickened bony plates
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