Periodontology Dept. P.U.A.

Chapter 5 ( 15 Pages) 2010

Chronic Periodontitis

Chronic periodontitis occurs as a result of extension of inflammation

from the gingiva into the deeper periodontal tissues. It has recently
been defined as "an infectious disease resulting in inflammation within
the supporting tissues of the teeth, progressive attachment loss and
bone loss."

The Periodontal Pocket

 A sulcus depth up to 3 mm is considered to be normal, provided

the patient can maintain oral hygiene. If it is increased beyond 3
mm it is called as a pocket. The cause for this is mainly extension
of inflammation leading to pathologic deepening of the gingival
sulcus, and, this marks the transition from gingivitis to
periodontitis. Periodontitis is always preceded by gingivitis, but
not all gingivitis progresses to periodontitis.

 "Pocket can be defined as pathologic deepening of the gingival

sulcus."

 If this happens due to coronal migration of the marginal gingiva it

is called as gingival or pseudo-pocket. Deepening due to apical
migration of the junctional epithelium is referred to as "true
pocket."

 The most common form of periodontitis occurs in adults; hence

the term "adult periodontitis" was used. Since this form of the
disease which progresses slowly is also seen in non adults (e.g.
Asst.Prof.Dr. Hala Yassin
Page 1 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

adolescents), the term "chronic periodontitis" is more likely to be

used.

 It was thought that once periodontal disease is initiated in an

individual it would slowly but progress over time if treatment
was not instituted. Recent data suggested that periodontal disease
progression is characterized by remission (quiescence) period and
exacerbation (activity) period that is not uniform for all teeth in a
patient or for all patients.

Clinical Signs

1. Enlarged, bluish-red marginal gingiva with a 'rolled' edge

separated from the tooth surface.
2. A bluish-red vertical zone extending from the gingival margin to
the alveolar mucosa.
3. A break in the faciolingual continuity of the interdental gingiva.
4. Shiny, discolored and puffy gingiva associated with exposed root
surfaces.
5. Gingival bleeding, purulent exudate from the gingival margin.
6. Mobility, extrusion and migration of teeth.
7. The development of diastema where none had existed previously.
Symptoms
1. Localized pain or a sensation of pressure in the gingiva after
eating, which gradually diminishes.
2. A foul taste in localized areas.
3. A tendency to suck material from the interproximal spaces.
4. Radiating pain "deep in the bone."
5. A "gnawing' feeling or feeling of itching in the gums.
6. The urge to dig a pointed instrument into the gums and relief is
obtained from the resultant bleeding.

Asst.Prof.Dr. Hala Yassin

Page 2 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

7. Patient complains that food "sticks between the teeth" or that the
teeth "feel loose" or a preference to "eat on the other side."
8. Sensitivity to heat and cold; toothache in the absence of caries

Remember
 One of the most important features of chronic periodontits is almost total
absence of pain unless acute inflammation is present. This is one of the main
distinctions between periodontal and pulp disease.

• Pulp pathology may be a complication of advanced periodontal disease and

severe pain may then develop.

 The root surface wall of periodontal pockets often undergoes structural changes.
Cementum exposure to oral fluid and bacterial plaque results in proteolysis of
the embedded remnants of sharpey's fibers and the cementum may be softened
and undergo fragmentation and cavitations.
 Involvement of the cementum is followed by bacterial penetration of the
dentinal tubules resulting in destruction of the dentin.
 Caries of the root may lead to pulpitis, sensitivity to sweets and thermal
changes or severe pain.
 Necrotic cementum must be removed by scaling and root planing until firm
tooth surface is reached since it acts as reservoir for bacteria and its products.

 Periodontal pockets contain debris consisting principally of micro-organisms

and other. products (enzymes, endotoxins, and metabolic products), gingival
fluid, desquamated epithelial cells and leukocytes. Plaque covered calculus
usually projects from the tooth surface.

 Purulent exudates consisting of living, degenerated and necrotic leukocytes;

living and dead bacteria and serum may be present. The presence of pus
expressed from the pocket reflects the nature of inflammatory changes in the
pocket wall.

Asst.Prof.Dr. Hala Yassin

Page 3 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

Pathogenesis of pocket formation:

The first event in pocket formation is the laying down of a lawn of

gram-positive bacteria on the supragingival tooth surface and its
extension into the gingival sulcus.

The periodontal pockets are caused by micro organisms and their

products, which produce pathologic changes that lead to the
deepening of the gingival sulcus

As a result of inflammation, the following changes are seen in the

junctional epithelium.
1. The junctional epithelium proliferates along the root in the form
of finger-like projections.
2. The coronal portion of the junctional epithelium detaches from
the root as the apical portion migrates.

These changes occur due to:

a. Enzymes released by bacteria
b. Physical force exerted by rapidly growing bacteria
c. Bacteria may also interfere with growth of junctional epithelial
cells and also with the normal maintenance of the attachment .
d. Exudate associated with the advancing bacteria may also be
important.
Thus the sulcus base migrate apically and this will be replaced by
pocket epithelium.
3. Under normal conditions neutrophils emigrate from the vessels of
the gingival plexus through the junctional epithelium into the
gingival sulcus and oral cavity, the transmigrating cells leave no
trace of their passage and cause no damage. These neutrophils are

Asst.Prof.Dr. Hala Yassin

Page 4 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

the primary and first line of defence around the teeth; the
epithelial barrier is the second.
4. Extension of plaque subgingivally causes an increase in the
number of transmigrating neutrophils, which may be due to the
increased concentration of chemotactic factors and other
inflammation induced substances derived from the bacteria.
These substances cause vasculitis. Neutrophils adhere to the
endothelial lining and migrate into the connective tissue, but they
still do not accumulate there. Instead they rapidly pass through
the junctional or pocket epithelium to form a thick layer that
covers the surface of the subgingival plaque. Upon arrival at the
plaque surface, the neutrophils are viable partly, but not
completely functional. Their role is to limit further extension and
spread of bacteria by phagocytosis and killing.

5. A constant battle occurs at the neutrophil plaque interface.

Usually the normal neutrophil activities are sufficient to limit the
extension of plaque, however increasing growth rate of bacteria,
permits tissue destruction to occur.
6. Assuming the pocket formation proceeds either because of
growth and action of bacteria or because of increasing number of
neutrophils that transmigrate through the junctional epithelium
and pocket epithelium causes open communication between the
pocket and connective tissue (i.e it disrupting the epithelial
barrier.)

7. Ulceration now is the second major event in pocket formation,

now the epithelial barrier is breached

8. As a result the neutrophils no longer have a guidance systems, to

direct them from the vessels through tissues and into the pocket;
they remain in the connective tissue moving randomly. Also
Asst.Prof.Dr. Hala Yassin
Page 5 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

because of the rupture of the epithelial barrier, the connective

tissue become flooded with the bacterial substances, and bacteria
may enter the connective tissue.
9. . If this epithelial barrier barrier is not re established, tissue
destruction continues and alveolar bone is resorbed. A
periodontal pocket is now established

Classification Of Pockets

1-Depending upon its morphology

a. Gingival/false/relative pocket/pseudo pocket.

b. Periodontal/absolute/true pocket.
c. Combined pocket.

2-Depending upon its relationship to crestal bone & the base of periodontal
pockets are further classified as:

a. Suprabony/supracrestal/supra-alveolar pocket.
1. The bottom of the pocket is coronal to the crest of alveolar bone.
2. The pattern of destruction of the underlying bone is horizontal.
3. Interproximally, the transeptal fibers that are restored during
progressive periodontal disease' are arranged horizontally in the
space between the base of the pocket and the alveolar bone.

b. Infrabony/intrabony/ subcrestal/intra-alveolar pocket.

1. The bottom of the pocket is apical to the level of the crest of

Asst.Prof.Dr. Hala Yassin

Page 6 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

2. alveolar bone
3. The bone destructive pattern is vertical (angular).
Interporximally, the transeptal fibers are oblique rather than
horizontal. They extend from the cementum beneath the base
of the pocket along the crest of interdental bone cementum of the
adjacent tooth.

Infrabony pocket can be classified according to:

a-The number of remaining osseous walls into
 One osseous wall Infrabony pocket
 Two osseous walls Infrabony pocket
 Three osseous walls Infrabony pocket
 Combined osseous,where the number of osseous defects in
the apical part is greater than the occlusal part
b-The depth & width of the osseous defect

Narrow Wide

Deep Shallow Deep Shallow

Asst.Prof.Dr. Hala Yassin

Page 7 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

3. Depending upon the number of surfaces involved:

a. Simple pocket-involving one tooth surface.
b. Compound pocket-involving two or more tooth surfaces
c. Complex pocket-where the base of the pocket is not in direct
communication with the gingival margin. It is also known as
spiral pocket.

4. Depending upon the nature of the soft tissue wall of the pocket

a. Edematous pocket.
b. Fibrotic pocket.

5. Depending upon the disease activity

a. Active pocket.
b. Inactive pocket

Determination of Pocket Depth

 Probing depth measurement.

 Clinical detection of attachment loss.
 Clinical detection of suprabony and infrabony pockets.

Clinically, probing depth measurement is recorded from the crest of the

marginal gingiva to the probable depth of the pocket. Whereas

Asst.Prof.Dr. Hala Yassin

Page 8 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

attachment level is measured from cementoenamel junction to the

probable depth of the pocket.

Factors which influence the result of measurement made with a

periodontal probe:

a) The thickness of the probe, a pocket measuring probe must be fine

enough to enter a narrow pocket (0.8mm diameter) but must have
a blunt end so that the tissue is not penetrated.

b) Malposition of the probe due to anatomic features such as the

contour of the tooth surface,
c) The pressure applied on the instrument during probing (the
recommended force should be 25g. Vigorous probing is not only
painful but likely to give an inaccurate reading.( Deposits of
subgingival calculus may keep the probe tip from penetrating to
the depth of the pocket. It is usually possible to work around this
obstacle, so , delicate handling of the probe must be employed to
negotiate subgingival calculus without impaction against the root
surface.)

d) The degree of inflammatory cell infiltration In the soft tissue and

accompanying loss of collagen.

Note:

Asst.Prof.Dr. Hala Yassin

Page 9 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

Since in CAL the reference point is fixed which is the CEl, it is more
reliable assessment than pocket depth.

Although gingival inflammation is a necessary precursor to

periodontitis, obvious manifestations of inflammation may
become less apparent with the progress of periodontitis. Gingival
bleeding has been correlated with periodontitis activity.

Generally increased tooth mobility is produced by:

1- Spread of inflammation from the gingiva into the deeper tissue.
2- Loss of supporting tissue (e.g. periodontal ligament and alveolar
bone)

Mobility which is produced by inflammation is reversible as demonstrated by the reduction

in mobility following scaling; mobility associated with destruction of supporting tissue is
not reversible

The degree of mobility may be graded as follows:

Grade 1: just noticeable < lmm in a horizontal direction
Grade 2: Easily noticeable > lmm in a horizontal direction.
Grade 3: Well marked labiolingual displacement, mobility of the tooth
up and down in axial direction/vertical mobility

Bone Loss and Patterns of Bone Destruction

 Pattern of bone loss is related to the thickness of alveolar bone. i.e.

angular defects cannot form in thin labial or lingual alveolar
Asst.Prof.Dr. Hala Yassin
Page 10 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

plates, which have little or no cancelleous bone between the outer

and inner cortical layers. In such instances the entire crest of the
plate is destroyed and the bone loss is horizontal.

 Pattern of bone loss depends on the distribution of dental plaque

i.e. angular defects interdentally form when dental plaque is
located more apically on a tooth than adjacent one.

 Bone loss also can be seen between roots in furcations. In patients

with advanced periodontitis, bone loss can extend to the apex of
the teeth. There may be a widened periodontal ligament space
and areas of root resorption associated with periodontitis

Furcation Involvement

Furcation involvement refers to commonly occurring conditions in

which the bifurcations and trifurcations of multi-rooted teeth are
invaded by the disease process

Classification of furcation Involvement:

1- Glickman (1958): Horizontal classification

 Grade I: Incipient involvement into furcation with suprabony
pockets and no interradicular bone loss.
 Grade II: Any involvement of the interradicular bone without
through-and through probe ability.
 Grade III: Through-and through loss of interradicular bone but
the facial or lingual surfaces are occluded by gingival tissues.
Therefore, the furcation opening can not be seen clinically, but it
is a through and through tunnel. If the radiographs are taken with

Asst.Prof.Dr. Hala Yassin

Page 11 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

proper angulation and the roots are divergent, the lesion will
appear as a radiolucent area between the roots

 Grade IV: As in grade III lesions, the inter-radicular bone is

completely lost but in grade-IV involvement the gingival tissues
recede apically so that the furcation opening is seen clinically. The
radiographic changes are the same as that of grade-III lesion.

Glickman's classification of furcation involvement.

2- Lindhe (1983): Horizontal Classification

 Grade I (initial): Loss of interradicular bone less than or equal to

one-third.
 Grade II (partial): Loss of interradicular bone greater than one-
third but not through and through.
 Grade III (total): through-and through loss of interradicular bone.

Asst.Prof.Dr. Hala Yassin

Page 12 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

3- Tarnow and Fletcher (1984): Vertical Classification

This Classification presents a subclassification that measures the

probeable vertical depth from the roof of the furca apically

 Grade "A" indicates a probeable vertical depth of 1-3 mm,

 Grade "B" 4-6 mm
 Grade "C" 7 or more mm of probeable depth from the roof of the
furca apically

Radiographic Features

Pattern of bone loss observed in chronic periodontitis may be vertical or

horizontal. When attachment loss and bone loss on one tooth surface is
greater than that on an adjacent surface is referred to as vertical bone
loss and is usually associated with angular bony defects and infrabony
pockets. When attachment loss and bone loss occur at a uniform rate on
majority of tooth surfaces it is called horizontal bone loss and is
generally associated with suprabony pockets.

Asst.Prof.Dr. Hala Yassin

Page 13 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

Disease Distribution

Localized periodontitis:
Periodontitis is considered localized when less than 30 percent of the
sites assessed in the oral cavity demonstrate attachment loss and bone
loss.

Generalized periodontitis:
It is considered generalized when more than 30 percent of the sites
assessed in the oral cavity demonstrate attachment loss and bone loss.

Disease Severity

Periodontal disease were separated into four classes according to

amount of attachment

I-Chronic gingivitis:
 Sulcus depth range from 1-3 mm.
 Bleeding on probing
 Radiographic presentation: no bone loss is seen.

2-Mild chronic adult (Class II) periodontitis:

 4 to 5 mm pocket probing depth.
 2 to 4 mm probing attachment loss.
 Bleeding, suppuration, or other signs of disease activity is present.
 Minimal furcation invasions with little or no mobility are
observed
 Radiographic presentation: bone loss is minimal.

Asst.Prof.Dr. Hala Yassin

Page 14 of 15
 Periodontology Dept. P.U.A. Chapter 5 ( 15 Pages) 2010

3-Moderate chronic adult (Class III) periodontitis:

 5 to 6 mm pocket probing depth.
 4 to 7 mm probing attachment loss.
 Early to moderate furcation invasion.
 Bleeding on probing, suppuration, or other signs of active disease
present with slight to moderate tooth mobility.
 Radiographic presentation: apparent bony destruction (up to
40%).

4- Severe chronic adult (Class IV) periodontitis:

 7 mm pocket probing depth or greater.
 7 mm probing attachment loss or more.
 Furcation invasion ranging from early to through & through.
 Bleeding on probing, suppuration or other signs of disease
activity present.
 Excessive tooth mobility
 both horizontal and angular bony defects are observed

-------------------------------------------------------------------------

Asst.Prof.Dr. Hala Yassin

Page 15 of 15