Periodontal Pocket & Bone Loss and Pattern of Bone Destruction

8/13/2019 Periodontal Pocket & Bone Loss and Pattern of Bone Destruction

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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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Periodontal Pocket & Bone Loss and Pattern of Bone Destruction

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