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THE PERIODONTAL POCKET

DENT 471 3/11/2013

Dr. Hisham Al-Shorman

Introduction
Pathologically deepened gingival sulcus
Periodontal pocket formation & alveolar bone destruction
Neutrophils constantly release granules containing acid hydrolases and neutral proteases (elastase & collagenase) These degrade collagen, proteoglycans & fibrinogen

Granulocytes present in large #s


Burst release large quantities of enzymes

Classification
Gingival Pocket Periodontal Pocket
Suprabony: (supracrestal/supra alveolar):

the bottom of the pocket is coronal to the underlying alveolar bone the bottom of the pocket is apical to the level of the adjacent alveolar bone. The lateral pocket wall lies between the tooth surface and the alveolar bone

Intrabony (infrabony):

Suprabony

Intrabony

Pocket base is coronal to level of alveolar bone


Bone destruction pattern is horizontal Intreproximally, transeptal fibers are arranged horizontally in the space between the base of the pocket and the alveolar bone

Pocket base is apical to crest of alveolar bone


Bone destruction pattern is vertical Intreproximally, transeptal fibers are oblique rather than horizontal. They extend from the cementum beneath the base of the pocket along the bone and over the crest to the cementum of the adjacent tooth On the facial and lingual surfaces, the periodontal ligament fibres follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join the outer periosteum

On the facial and lingual surfaces, the periodontal ligament fibres beneath the pocket follow their normal horizontal-oblique course between the tooth and the bone

Clinical Features
Bluish-red, thickened marginal gingiva

Bluish-red vertical zone form gingival margin to alveolar mucosa


Gingival bleeding

Suppuration
Tooth mobility Diastema formation Localized pain

Pathogenesis

Inflammation in CT of gingival sulcus Degradation of CT Apical to JE collagen is destroyed, so area is occupied by inflammatory cells and edema Collagen loss occurs due to:
Collagenases and other enzymes (matrix metalloproteinases) produced by different cells Fibroblasts phagocytize collagen fibers

Pathogenesis
Therefore, apical cells of JE proliferate along the root & the coronal portion of JE detach from the root More PMNs invade the coronal portion of JE Sulcus deepening

Bacterial Invasion

Some bacteria have been shown to be able to invade the periodontal tissues: Porphyromonas gingivalis Aggrigatibacter actinomycetemcomitans Prevotella Intermedia

Microtopography of the Gingival Wall


1. Area of relative quiescence
2. Area of bacterial accumulation 3. Areas of leukocyte emergence 4. Areas of leukocyte interaction 5. Areas of epithelial desquamation 6. Areas of ulceration

7. Areas of hemorrhage

Healing Pockets

Edematous gingiva Fibrotic gingiva

Root Surface Wall


With deepening of pocket, collagen fibers embedded in the root are destroyed
Cementum becomes exposed to oral environment Sharpeys fibers undergo degeneration Bacteria penetrates root

Fragmentation and necrosis of cementum

Morphology of tooth wall


Cementum covered by calculus
Attached plaque Un-attached plaque Junctional epithelium Partially lysed CT

Intact CT

Periodontal Disease Activity

Period of exacerbation Period of quiescence

Attachment Loss and Pocket Depth


Pocket depth is the distance between the base of the pocket and crest of the gingival margin Attachment loss depends on location of the base of the pocket on the root surface

BONE LOSS & PATTERNS OF BONE DESTRUCTION


DENT 471 3/11/2013

Dr. Hisham Al-Shorman

Bone is a dynamic tissue The height and density of alveolar bone are maintained by an equilibrium, regulated by local and systemic influences, between:

Destruction Caused By Inflammation


The most common cause of bone destruction in periodontal disease is the extension of inflammation from the marginal gingiva into the supporting periodontal tissues The inflammatory invasion of bone mark the transition from gingivitis to periodontitis Periodontitis is always preceded by gingivitis, but not all gingivitis progresses to periodontitis

Factors responsible for the conversion of gingivitis to periodontitis are not known at this time

Bone Destruction in Periodontal Disease is Caused by :

Extension of gingival inflammation.


Trauma from occlusion.

Systemic disorders.
Combination.

Bone Destruction Caused by Extension of Gingival Inflammation:


The main cause of bone destruction in periodontal disease. The transition from gingivitis to periodontitis is associated with changes in the composition of bacterial plaque: Number of motile organisms and spirochetes Number of coccoid rods and straight rods

The cellular composition of the infiltrated connective tissue also changes with increasing severity of the lesion. Fibroblasts and lymphocytes predominate in stage I gingivitis, whereas the number of plasma cells and blast cells increases gradually as the disease progresses. contained gingivitis: T lymphocytes are preponderant. As the lesion becomes a B-lymphocyte lesion, it becomes progressively destructive.

Spread of Inflammation from the Gingiva into the Supporting Periodontal Tissues: A- Interproximally;
* (1) From the gingiva into the bone * (2) From the bone into the periodontal ligament * (3) From the gingiva into the periodontal ligament

B- Facially and lingually;


* (1) From the gingiva along the outer periosteum * (2) From the periosteum into the bone through vessel channels * (3) From the gingiva into the periodontal ligament

Is bone destruction in periodontal disease a process of bone necrosis?


No!

It involves the activity of living cells along viable bone


When tissue necrosis and pus are present in periodontal disease, they occur in the soft tissue walls of periodontal pockets, not along the resorbing margin of the underlying bone

Rate of Bone Loss


Loss of attachment precedes loss of bone by about 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 0.1 to 1 mm ~ 81 % of individuals had moderately progressive periodontal disease, with a yearly loss of attachment of 0.05 to 0.5 mm The remaining 11 % of persons had minimal or no progression of destructive disease (0.05 to 0.09 mm yearly)

Periods of Destruction

Periodontal destruction occurs in an episodic, intermittent manner, with periods of inactivity or quiescence

The destructive periods result in loss of collagen and alveolar bone with deepening of the periodontal pocket

Mechanisms of Bone Destruction


1. Direct Bacterial Destruction:
Bacterial products:

Induce the differentiation of bone progenitor cells into osteoclasts


Stimulate gingival cells to release mediators that have the same effect Act directly on osteoblasts or their progenitors, inhibiting their action and reducing their number.

Mechanisms of Bone Destruction


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 periodontal disease.

These include
o prostaglandins and their precursors o interleukins (ILl and IL-1) o tumor necrosis factor alpha (TNF- )
o prostaglandin E2 (PGE2)

Bone Destruction Caused by Occlusal Trauma


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 and resorption of bone and tooth structure These changes are reversible and can be repaired if the offending forces are removed

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

Normal Variations in Alveolar Bone


The anatomic features that include;
The thickness, width, and crestal angulation of the interdental septa The thickness of the facial and lingual alveolar plates radicular bone The presence of fenestrations, dehiscences, or both The alignment of the teeth Root and root trunk anatomy Root position within the alveolar process Proximity with another tooth surface

Normal Variations in Alveolar Bone

A, Lower incisor with thin labial bone - bone loss can become vertical only when it reaches thicker bone in apical areas B, Upper molars with thin facial bone, where only horizontal bone loss can occur C, Upper molar with a thick facial bone, allowing for vertical bone loss

Exostoses

Exostoses are outgrowths of bon of varied sizes and shapes Palatal exostoses have been found in 40 % of human skulls
They can occur as small nodules, large nodules, sharp ridges, spike-like projections, or any combination of these

Buttressing of Bone Lipping


In an attempt to buttress bony trabeculae weakened by resorption When it occurs within the jaw, it is termed: central buttressing bone formation When it occurs on the external surface, it is referred to as: peripheral buttressing bone formation It may cause bulging of the bone contour, termed lipping, which sometimes accompanies the production of osseous craters and angular defects

Bone Deformities Osseous Defects

Different types of bone deformities can result from periodontal disease Their presence may be seen on radiographs
However, careful probing and surgical exposure of the areas is required to determine their exact conformation and dimensions

Horizontal Bone Loss


Horizontal bone loss is the most common pattern in periodontal disease The bone is reduced in height, but the bone margin remains roughly perpendicular to the tooth surface The interdental septa and facial and lingual plates are affected, but not necessarily to an equal degree around the same tooth

Vertical Bone Loss


Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root The base of the defect is located apical to the surrounding bone In most instances, angular defects have accompanying infrabony pockets

Classification of Osseous Defects


Angular defects are classified on the basis of the number of remaining osseous walls They may have one, two, or three walls

Osseous Craters
Osseous craters are concavities in the crest of the interdental bone confined within the facial and lingual walls

Reversed Architecture
Produced by loss of interdental bone, including the facial plates, lingual plates, or both, without concomitant loss of radicular bone, thereby reversing the normal architecture (- ve architecture) More common in the maxilla

Ledges

Ledges are plateau-like bone margins caused by


resorption of thickened bony plates

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