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The natural history of

periodontal disease
Clinical Histological

1. Pink in color 1. The gingival fiber system well


2. Firm in consistency organized
3. Knife edged contour 2. A few PMNs are found in the
4. Do not bleed on probing junctional epithelium
5. Shallow gingival sulcus 3. Connective tissue contains
isolated inflammatory cells
,mainly lymphocytes and
occasional plasma cells and
macrophages.

Features of gingiva at healthy


state
GINGIVITIS
ETIOLOGY

INFLAMMATION OF GINGIVA OR GINGIVAL SOFT TISSUE.

A reversible & mildest form of periodontal disease


Plaque accumulation is greatest in the interdental region so gingival
inflammation tends to start in the interdental papilla and spreads
from there to the neck of the teeth.
The resultant widening of the spaces between the junctional
epithelial cells during early gingivitis may permit injurious agents
derived from bacteria or bacteria themselves, to gain access to the
connective tissue
ETIOLOGY
Dental plaque

Systemic factors: Puberty, Menstrual Cycle,Pregnancy & DM

Drug induced : gingival enlargements/oral contraceptives

Malnutrition : Ascorbic acid deficency

Bacterial origin : Syphillis, Streptococcal gingivitis

Viral origin

Fungal origin : Linear ginigival erythema,Candidasis,HiV

Genetic origin : Hereditary gingival fibromatosis


STAGES OF GINGIVITIS[Page and
Schroeder 1976]
The sequence of events cumulating in clinically
apparent gingivitis is categorized into:

I) INITIAL LESION

II) EARLY GINGIVITIS

III) ESTABLISHED GINGIVITIS

IV) ADVANCED STAGE


STAGE I GINGIVITIS: THE INITIAL LESION

1. Clinically no visible signs are seen.

2. Increase in GCF.

3. The first manifestations of gingival inflammation are vascular


changes consisting of dilation of capillaries and increased blood
flow.

4. Changes in blood vessel morphologic features occur within 1 week


and sometimes as early as 2 days after plaque has been allowed
to accumulate .

5. Predominant Immune Cells POLYMORPHONUCLEAR


NEUTROPHILS (PMNs)

6. Stage is also called as subclinical gingivitis.


STAGE II GINGIVITIS: THE EARLY
LESION
1. Clinically erythematous gingiva and Bleeding on probing may present.

2. The early lesion evolves from the initial lesion within about 1 week after
the beginning of plaque accumulation.

3. Signs of erythema may appear, mainly because of the proliferation of


capillaries and increased formation of capillary loops between rete pegs .
4. Predominant Immune Cells (T lymphocytes 75%,)

5. 70% of the collagen is destroyed. The main fiber groups affected appear
to be the circular and dentogingival fiber.
STAGE III GINGIVITIS:THE ESTABLISHED
LESION

1. Clinically estimated as moderate to severely inflamed gingiva

2. In chronic gingivitis (stage III), which occurs 2 to 3 weeks after the


beginning of plaque accumulation ,the blood vessels become engorged
and congested, venous return is impaired, and the blood flow
becomes sluggish.

3. The result is localized gingival anoxemia, which superimposes a somewhat


bluish hue on the reddened gingiva.

4. In histological sections, an intense, chronic inflammatory reaction is


observed.

5. A key feature that differentiates the established lesion is the increase


in the number of plasma cells,.
STAGE IV GINGIVITIS: THE ADVANCED LESION

1. Extension of the lesion into alveolar bone characterizes a fourth stage


known as the advanced lesion or phase o f periodontal breakdown.

2. Microscopically, there is fibrosis of the gingiva and widespread


manifestations of inflammatory and immunopathologic tissue damage.

3. Plasma cell presence dominates connective tissue and neutrophils


continue dominating the junctional epithelium.

4. Gingivitis will progress to periodontitis only in individuals who are


susceptible
Figure/ diagram /illustration of
stages of gingivitis
Development of chronic periodontitis
Flowchart depicting PATHOGENESIS OF POCKET
FORMATION
[1] Presence of bacterial plaque on tooth surface

[2] Marginal gingiva becomes inflamed

[3] Gingival sulcus deepens due to edematous enlargement of gingiva


[4] Gingival Pocket


[5] Anaerobic organism tends to colonize the subgingival plaque
[6]The cellular & inflammatory exudates causes the destruction
of gingival fibers.

[7]Apical to junctional epithelium , collagen fibers are destroyed


by two methods

(a) Collagenases (b) Fibroblasts

MMP Phagocytize

Pmn
Macrophages DESTRUCTION OF
Fibroblasts COLLAGEN FIBERS
[8] The epithelial cells degenerate ,separate

[9] Attachment to tooth completely breaks down.

[10] The PMN cells invade the coronal end of JE

[11] The coronal portion of JE detaches from the root when PMN reaches 60%
of volume as a result apical portion migrates. Due to loss of collagen, apical
cells of JE starts proliferating along the root.

[12] Thus the sulcus shifts apically & leading to formation of


Periodontal pocket .

Periodontal pocket is defined as pathologically deepened gingival


sulcus.
.
After the formation of periodontal pocket,
the inflammation spreads in to bone causing
bone loss.

Bone resorption usually starts at


interproximally, then resorption spreads
laterally the entire alveolar crest is resorbed
gradually.
PATHWAYS OF SPREAD OF INFLAMMATION
FROM GINGIVA INTO SUPPORTING
PERIODONTAL TISSUES
Interproximally
a) from gingiva bone

b)from bone periodontal ligament

c) from gingiva periodontal ligament

Facially & Lingually

a)From gingiva periostium bone


b)From gingiva periodontal ligament
BONE DESTRUCTION PATTERNS IN
PERIODONTAL DISEASE

Periodontal disease alters the morphology of bone.


Understanding the alterations is essential for effective
diagnosis & treatment.

Horizontal Bone Loss


Vertical Bone Loss
Osseous Craters
Bulbous Bone Contours
Reverse Architecture
Ledges
Furcation
Horizontal Bone Loss
Most common pattern of bone loss.
The bone is reduced in height
perpendicular to tooth
Vertical Bone Loss
The defect occurs in oblique direction leaving a hollowed out
trough in the bone along side the root.
The base of defect is apical to surrounding bone
Angular defects are classified on the basis of
number of walls present as
One wall defect: One wall is present
Two walled defects : two walls are present
Three walled defect three walls are present
Osseous Craters
They are concavities in the crest of the interdental bone confined with
in the facila and lingual walls.

Most commonly seen in mandibular defects & in posterior teeth.

The following reasons have been cited for formation of craters:

Interdenta areas are more prone to the accumulation of plaque and are more
dificult to clean.
Vascular patterns from the gingiva to the center of the crest may provide a
pathway for inflammation.
Bulbous Bone Contours
They are bony enlargements caused by exostoses or
adaptation to function or butterssing bone formation
Frequenly seen in maxilla
Ledges
They plateau like bone margins caused by
resorption of thickened bone.
Furcation
Furcation refers to invasion of bifurcation
and trifurcation of multirooted teeth .
Classification of
furcation[Glickman]:
Grade I
1. Early stages of furcation
2. Suprabony pocket
3. Increase in probing depth
4. Radiographic changes not seen
Grade II

1. In this, bone is destroyed in one or more aspects of the


furcation, but a portion of the alveolar bone and periodontal
ligament remain intact.
2. Permits only partial penetration of the probe into the
furcation.
3. Radiographs may or may not reveal this type of furcation.
Grade III-
1. The inter-radicular bone is completely lost.

2. The furcation is clinically it is not seen clinically as it is


covered by gingiva on facial & lingual surfaces.

3. It is clearly shown in the radiographs as a radiolucent area in


between the roots, especially in the lower molars.
Grade IV :
1. The gingival tissues recede apically so that
furcation is clearly visible
2. Through and through lesion.
Trauma from occlusion/occlusal
trauma
When occlusal forces exceed the adaptive capacity of the
tissues, it results in tissue injury. The resultant injury is termed
trauma from occlusion.

Thus trauma from occlusion refers to the tissue injury, not


the occlusal forces.
Acute trauma from occlusion

Results from an abrupt occlusal impact,


such as that produced by biting on a hard
object.

In addition, restorations or prosthetic


appliances that interfere with the
direction of occlusal forces on the teeth
may induce acute trauma.
Chronic trauma from occlusion
Is more common than the acute
form and is of greater clinical
significance.

It most often develops from gradual


changes in occlusion produced by
tooth wear,
drifting movement,
extrusion of teeth,
combined with parafunctional habits
such as bruxism and clenching,
Clinical features of TFO
1. Pain on chewing or percussion

2. Mobility (progressive)

3. Periodontal Abscess formation

4. Occlusal prematurity/discrepancies

5. Wear facets in the presence of other clinical


indicators (attrition)Infrabony pockets/ furcation

6. Tooth migration
GINGIVAL RECESSION
Apical movement of the gingival margin leading to exposure root of
the tooth.

Millers Classification:
Class I: Marginal tissue recession which does not extend to the
mucogingival junction (MGJ).
There is no alveolar bone loss or soft tissue loss in the inter-
dental area
NO LOSS OF
INTERDENTAL
TISSUES

MGJ
Class II
Marginal tissue recession which extends to or
beyond the MGJ.
There is no alveolar bone loss or soft tissue loss in
the interdental area
Class III
Marginal tissue recession which extends to or beyond the
MGJ.
Bone or soft tissue loss in the interdental area is present.
Class IV
Marginal tissue recession which extends to or beyond the
MGJ.
There is severe bone or soft tissue loss in the interdental area
Causes of Recession:

1. Anatomical - bulbous roots/ enamel pearls

2. Tooth positioning/crowding

3. Thin labial bone / bony dehiscence

4. Thin biotype gingival tissue

5. Toothbrush trauma

6. Periodontal disease

7. Traumatic occlusion

8. Habitual nail biting / pen chewing / piercing

9. Orthodontic tooth movements


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