 What is periodontitits?

 Periodontal pocket
 Bone loss and patterns of bone
destruction
 Pathologic tooth migration
 Chronic periodontitis
 The role of dental calculus
 Periodontitis is an
inflammatory
condition of the teeth
and their supporting
structures
 It’s response of the
tissue to the bacterial
biofilm insult, resulting
in the destruction of
periodontal ligament
fibers and bone loss
 The periodontal pocket is pathologically
deepened gingival sulcus which is one of
the most important clinical features of
periodontal disease
 Same histopathological features (tissue
changes, mechanisms of destruction,
healing) but different in etiology, natural
history, progression, and response to
therapy
 2 types of pockets:
- Gingival
- Periodontal: suprabony
and intrabony
 Pockets can involve
one or more tooth
surfaces, and can be
of different depths
and types on different
surfaces of the same
tooth
 Gingival (pseudo) due to
gingival enlargment withput
destruction of periodontal
tissue
 Periodontal pocket is formed
because of destruction of
supporting periodontal
tissues which leads to
looseining of the teeth
 Suprabony the bottom of the
pocket is coronal to the
underlying alveolar bone
 Intrabony the bottom of the
pocket is apical to the level
of the adjacent alveolar
bone.
 Clinical signs of periodontal pockets:
a bluish red thickened marginal gingiva,
gingival bleeding and suppuration,
tooth mobility,
diastema formation,
pain “deep in the bone.”
 Reliable method of locating periodontal
pockets and determining their extent is
careful probing of the gingival margin
along each tooth surface.
 Lesion in the development of periodontitis is
the inflammation of the gingiva in response
to a bacteria
 Initially it was assumed that after the
bacterial attack, periodontal tissue
destruction continued to be linked to
bacterial action but we found out that
person’s immune response to bacteria
unleashes mechanisms that lead to
collagen and bone destruction (cytokines,
monocytes, etc)
 Bacterial invasion of the apical and
lateral areas of the pocket wall has been
described in human chronic periodontitis
 The inflammatory response triggered by
bacterial plaque unleashes a complex
cascade of events aimed at destroying
and removing bacteria and necrotic
cells
 Periodontal pockets are chronic
inflammatory lesions and thus are
constantly undergoing repair.
 Complete healing does not occur
because of the persistence of the
bacterial attack, which continues to
stimulate an inflammatory response
 Soft tissue wall has destructive and constructive
tissue and it’s changes determine clinical
features of such as color, consistency, and
surface texture of the pocket wall
 If the inflammatory fluid and cellular exudate
predominate, the pocket wall is bluish red, soft,
spongy, and friable, with a smooth, shiny
surface (edematous pocket wall)
 If there is a relative predominance of newly
formed connective tissue cells and fibers, the
pocket wall is more firm and pink and clinically
referred to as a fibrotic pocket wall.
 Periodontal pockets contain debris that consists of
microorganisms and their products, gingival fluid,
food remnants, salivary mucin, desquamated
epithelial cells, and leukocytes
 Plaque-covered calculus usually projects from the
tooth surface
 Purulent exudate consist of living, degenerated,
and necrotic leukocytes; living and dead bacteria;
serum; and a scant amount of fibrin.
 Pus is a common feature of periodontal disease,
but it is only a secondary sign. It doesnt indicate
depth of pocket or severity of destruction of tissues.
 The root surface wall
of periodontal
undergoes changes
 As the pocket
deepens, collagen
fibers in cementum
are destroyed and
cementum becomes
exposed to the oral
environment – easier
penetration of
bacteria
 The spread of infection from periodontal
pockets may cause pathologic changes in
the pulp – painful symptomes
 A periodontal abscess is a localized
purulent inflammation in the periodontal
tissues
 Abscesses that are localized in the gingiva,
caused by injury to the outer surface of the
gingiva and that do not involve the
supporting structures are called gingival
abscesses
 Location periodontal
abcess classification:
- Abscess in the supporting
periodontal tissues along
the lateral aspect of the
root
- Abscess in the soft-tissue wall
of a deep periodontal
pocket
 Acute abscess becomes a
chronic when it’s purulent
content drains through a
fistula into the outer
gingival surface or into the
periodontal pocket
 Alveolar bone is
maintaned by
balance between
resorption and
formation of the
bone. When
resorption exceeds
formation, both
bone height and
bone density may
be reduced.
 Bone loss is last
conseqence of the
periodontitis
 Existing bone level is
the due to past
pathologic episodes,
changes present in the
soft tissue of the
pocket wall reflect the
presence of the
inflammatory
condition
 Periodontitis is always
preceded by gingivitis
but not all gingivitis
progresses to
periodontitis
 Sometimes it goes
rapidly from gingivitis
to periodontitis and
sometimes it doesnt
proceed further from
gingivitis, meaning the
reason behind it is not
compleatly known
 Gingival
inflammation
extends along the
collagen fiber
bundles and follows
the course of the
blood vessels
through the loosely
arranged tissues
around them into the
alveolar bone.
 Inflammation pathway
from the gingiva
A) Interproximally, from the
gingiva into the bone (1),
from the bone into the
periodontal ligament (2),
and from the gingiva into
the periodontal ligament
(3).
B) facially and lingually, from
the gingiva along the
outer periosteum (1), from
the periosteum into the
bone (2), and from the
gingiva into the
periodontal ligament (3).
 Rate of bone loss averages about 0.2 mm per
year for facial surfaces and about 0.3 mm per
year for proximal surfaces (untreated)
 3 subgroups of bone loss:
1. Approximately 8% of persons had a rapid
progression of periodontal disease that was
characterized by a yearly loss of attachment of 0.1
mm to 1 mm.
2. Approximately 81% of individuals had moderately
progressive periodontal disease with a yearly loss of
attachment of 0.05 mm to 0.5 mm.
3. The remaining 11% of persons had minimal or no
progression of destructive disease with a yearly loss
of attachment of 0.05 mm to 0.09 mm
 Bone destruction factors in periodontal
disease are bacterial and host mediated.
The bacterial biofilm products induce the
differentiation of bone progenitor cells into
osteoclasts and stimulate gingival cells to
release mediators that have the same
effect
 Areas of bone formation are found
immediately adjacent to sites of active
bone resorption The presence of bone
formation in response to inflammation, has
an effect on the outcome of treatment.
 Bone destruction
patterns:
Horizontal bone loss –
most common, bone
reduced in height
 Bone destruction
patterns:
Vertical or Angular
defects – usually in
adults, occur in an
oblique direction,
defects that occur
interdentally can
generally be seen on
the radiograph
 Pathologic migration is relatively
common condition that refers to tooth
displacement which results when the
balance among the factors that
maintain physiologic tooth position is
disturbed by periodontal disease
 It may be an early sign of disease, or it
may occur in association with gingival
inflammation and pocket formation as
the disease progresses
 Mostly affects anterior
teeth but posterior can
be affected as well
 Teeth may move in any
direction, and migration
usually comes with
mobility and rotation
 Migration occurs under
conditions that weaken
the periodontal support,
that increase or modify
the forces exerted on
the teeth or both
 Factors that are important in relation to the
forces of occlusion include the following:
1. tooth morphologic features and cuspal
inclination
2. the presence of a full complement of teeth
3. a physiologic tendency toward mesial
migration
4. the nature and location of contact point
relationships
5. proximal, incisal, and occlusal attrition
6. the axial inclination of the teeth
 The tooth with
weakened support is
unable to maintain its
normal position in the
arch and moves away
from the opposing force
 The drifting of teeth into
the spaces created by
unreplaced missing
teeth often occurs -
tooth movement is
aggravated by a loss of
periodontal support
 Chronic periodontitis is the most
prevalent form of periodontitis, and it
generally shows the characteristics of a
slowly progressing, complex
inflammatory disease
 Systemic or environmental factors
(diabetes mellitus, smoking) modify the
host immune response to the dental
biofilm so that the periodontal
destruction becomes more progressive
 Slow progressing
disease, but in
presence of systemic
conditions or
environmental
factors it progresses
faster
 Mostly found in
adults
 Clinical and etiologic characteristics:
1. microbial biofilm formation (dental
plaque),
2. periodontal inflammation (gingival
swelling, bleeding on probing), and
3. attachment as well as alveolar bone
loss
 General symptoms:
• Supragingival and subgingival plaque (and calculus)
• Gingival swelling, redness, and loss of gingival stippling
• Altered gingival margins (rolled, flattened, cratered
papillae, recessions)
• Pocket formation
• Bleeding on probing
• Attachment loss
• Bone loss (angular/vertical or horizontal)
• Root furcation involvement
• Increased tooth mobility
• Change in tooth position
• Tooth loss
 Chronic periodontitis is classified in:
Localized chronic periodontitis, meaning
that less than 30% of the teeth show
attachment and bone loss
Generalized chronic periodontitis, meaning
that 30% or more of the teeth show
attachment and bone loss.
 The progression rate of chronic
periodontitis is slow, so that symptoms of
the disease appear around the age of
40 or later in life
 Not all sites in the mouth are equally
prone to chronic periodontitis, and it
exhibits site specificity. Interproximal sites,
in general, are more prone to
periodontal destruction, compared to
buccal/facial sites.
 Risk factors:
Microbial – bad oral
hygiene, plaque
Local – calculus,
restorations
overhangs
Systemic – HIV/AIDS,
osteoporosis
Environmental -
smoking
 Treatment by a
systematic
periodontal therapy
that includes optimal
long-term plaque
control,
debridement of soft
and hard deposits, or
surgical pocket
reduction
 The primary cause of gingival
inflammation is bacterial plaque
 Other factors include calculus, faulty
restorations, complications associated
with orthodontic therapy, self-inflicted
injuries, and the use of tobacco.
 Calculus consists of
mineralized bacterial
plaque that forms on
the surfaces of
natural teeth and
dental prostheses.
 Supragingival calculus:
- located coronal to the
gingival margin
- whitish/yellow, clay like
consistency
- can be generalized in the
entire mouth
- easily detached from
tooth surface
- commonly found in
buccal surfaces of
maxillary molars and
lingual surfaces of
anterior teeth
 Subgingival calculus:
- Located below crest of
marginal gingiva
- location and extend of
calculus may be
evaluated by tactile
perception using an
explorer
- hard and dense, dark
brown or greenish black
in colour
- firmly attached to tooth
surface