Download Periodontal diseases

Libyan International Medical University
2nd Year
First Semester
D Caroline Piske de A. Mohamed
Objectives
 Learning issues and objectives:
 What is meant by periodontium? What are its various
components?
 Describe the functions of periodontium and how they are
performed.
PERIODONTIUM
Cementum
Pulp cavity
Enamel
Dentin
PDL
Gingiva
Alveolar bone
Sharpey's fibers
Attachment
organ
Cementum
Periodontal
ligament
Root canal
Alveolar bone
Apical foramen
Alveolar vessels
& nerves
FUNCTIONS OF PDL
 SUPPORT: PDL supports teeth in their socket. It
prevents loosening of teeth.
 MASTICATORY LOAD: PDL permits teeth to
withstand the considerable forces of mastication.
 SENSORY: PDL is supplied by abundant receptors
and nerves that sense the movement when teeth
are in function. Helps in the proper positioning of the
jaws during normal function.
 NUTRITIVE: Blood vessels of ligament provide
essential nutrients for the ligament’s vitality and hard
tissue of cementum and alveolar bone.
 Fibroblasts, osteoblasts, cementoblasts, and even
resorptive osteoclasts and macrophages require
nutrition.
 CLINICAL CORRELATION:
 Bone, PDL, and the cementum together form a functional
unit of special importance when the orthodontic tooth
movement is undertaken. Orthodontic forces causes
compression and constriction of blood vessels, soft
tissue changes occur.
 Hence loss of alveolar bone occurs, now blood flow
occurs in the spaces. And the mesenchymal cells of PDL
repair the tissues.
 MAINTAINENCE: Tissues are maintained under the
influence of heavy masticatory forces.
 ADAPTIVE ROLE
 SHOCK ABSORBER: It absorbs the shock of
chewing.
PRINCIPAL FIBER BUNDLES OF PDL
1.
THE ALVEOLAR
CREST GROUP
These are attached
to the cementum just
below the
cementoenamel
junction and running
downward and
outward to insert into
the rim of the
alveolus.
2.THE HORIZONTAL GROUP
 These are just apical
to the alveolar crest
fibers and running at
right angles to the
long axis of the tooth
from the cementum
to the bone below
the alveolar crest.
3.
THE OBLIQUE GROUP
 They are the most
numerous in the PDL
and running from the
cementum in an
oblique direction to
insert into the bone
coronally
4.THE APICAL GROUP:
 These are radiating
from the cementum
around the apex of
the root to the bone
forming the base of
the socket.
5.THE INTERADICULAR GROUP
 Found
only in the
multi-rooted teeth and
running
from
the
cementum into the
bone forming the
crest
of
the
Interradicular septum.
TEETH IN-SITU
TYPES OF CEMENTUM
 CEMENTUM is classified
according to the presence or
absence of cells within its
matrix.
 CELLULAR CEMENTUM,
which has an adaptive role in
response to tooth wear and
movement and is associated
with repair of periodontal
disease.
 ACELLULAR CEMENTUM,
which provides attachment for
the tooth.
A- CELLULAR CEMENTUM
B-ACELLULAR CEMENTUM
Materia alba
Bacterial
aggregations,
leucocytes
and
desquamated oral epithelial cells accumulating at
the surface of plaque and teeth, but lacking the
regular internal structure observed in dental
plaque. ( mouth rinse can desegregate it)
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Dental plaque
 Dental plaque is the soft, nonmineralized bacterial deposit
which forms on teeth and dental protheses that are not
adequately cleaned. LÖe 1965
 Microscopically, plaque is simply confluent colonies of
microorganisms connected by a matrix consisting
predominantly of bacterial and salivary polymers. These
accumulations subject the teeth and gingival tissues to high
concentrations of bacterial metabolites, which result in
dental disease.
 The dominant bacterial species in dental plaque are
Streptococcus sanguis and Streptococcus mutans,
both of which are considered responsible for plaque.
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Differences between materia alba, plaque and calculus
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Major sites of plaque accumulation
 Fissures of molar teeth
 Supragingival: on the tooth surface above the
gingiva
 Subgingival: in the area bounded by the margin of
the gum and the tooth
 Interproximal: between adjacent teeth
Plaque formation
•Plaque formation is initiated by a weak attachment of the
streptococcal cells to salivary glycoproteins forming a
pellicle on the surface of the teeth.
• Bacteria adhere to the pellicle, and pellicle coats the
enamel.
• The specific type of bacteria/pellicle adherence is
determined by the innate characteristic of the bacteria and
the pellicle.
• Gram positive rods and cocci are laid down in the first
hour.
Time elapsed 1 hour
 The initial bacteria are called pioneer
colonizer, because
they are hardy and
successfully compete with other members of the
oral flora for a place on the tooth surface.
Primary colonizers
 Generally the primary colonizers are not in sufficiet
number to be pathogenic.
 Overwhelming cocci, specially streptococci and short
rods.
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• Gram-positive facultatively anaerobic
• Streptococcus sanguis is most dominant first to
appear followed later by S. Mutans.
• Actinomyces spp. are also found in 24h plaque.
• Gram-positive cocci and rods co-aggregate and multiply.
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• This is followed by a stronger attachment by means of
extracellular sticky polymers of glucose (glucans) which
are synthesized by the bacteria from dietary sugars
(principally sucrose).
• An enzyme on the cell surface of Streptococcus mutans,
glycosyl transferase, is
the bacterial cells to
conversion of sucrose
which
involved in initial attachment of
the tooth surface and in the
to dextran polymers (glucans)
form
plaque.
 Bacteria adhere, multiply and increase in mass and thickness
and form mini – colonies in layers upon the pellicle (plaque
formed by rod and cocci only).
Time elapsed 24-48 hours
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 Within a short time, the tooth surface adjacent to the
gingiva is covered by intermeshed bacteria.
 New bacteria derived from saliva or surrounding
mucous attach by a bonding interaction to bacteria
already attached to the plaque. All this activity occurs
within the first 2 days of plaque development and, for
description purposes, is called phase I of plaque
formation.
 In phase II of plaque development, the outer
surface of the plaque is covered by gram-positive tall
rods.
 There is a dramatic increase in plaque thickness 3
and 4 days compared to the first two days.
Secondary colonizers
• Adhere to bacteria already in the plaque mass.
• Surface receptors on the Gram-positive facultative
cocci and rods allow the subsequent adherence of
Gram-negative organisms, which have a poor ability
to directly adhere to the pellicle.
Fn: Fusobacterium nucleatum.
BI: Prevotella intermedia.
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 Any area where the plaque has not been removed,
either because of no home care or ineffective
techniques, the bacteria mass continues to grow with a
more complicated mixture of bacteria ( fusobacteria
and filamentous).
 As the plaque thickens at the cervical area, the deeper
layers incorporate more filaments and fusiforms,
eventually turning gram negative. The coronal plaque
is a more simple early arrangement of rods and cocci.
Time elaped 4-7 days
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Micro-colonies
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Microcolonies
coalescing
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 In phase III, 4 to 7 days after initiation, plaque
begins to migrate subgingivally, and bacteria and
their products permeate and circulate in the
pocket.
 The heterogeneity increases as plaque ages and
matures. As a result of ecologic changes, more
Gram-negative strictly anaerobic bacteria
(fusobacteria, veillonellae) colonize secondarily
and contribute to an increased pathogenicity of
the biofilm.
 In phase IV, 7 to 11 days after initiation of
plaque development, the diversity of the flora
increases to comprise motile bacteria
including spirochetes and vibrios as well as
fusiforms and white blood cells appear.
 The plaque becomes more gram negative and
anaerobic in the deeper layers, the gums
become slightly inflamed.
Time elapsed 7-14 days
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 Vibrios and spiroquetes continue to multiply. The
bacteria in the dental plaque become highly
organized, filamentous, are perpendicular to the
tooth surface, and pulsate in a palisade fashion. The
signs of inflamed gums are obvious.
Time elapsed 14-21 days
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The increasing thickness of the plaque limits the
diffusion of oxigen to the entrapped original oxigentolerant populations, as a result the organisms that
survive in the deeper parts of the plaque are either
facultative or obligate anaerobes as fusobacteria
and
veillonese
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Filamentous
bacteria
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“corn-cob”
associations
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 This mature plaque is now so packed with diverse
bacteria that an exogenous species would have great
difficulty becoming established in the overcrowded
habitat.
 With time, more bacteria migrate subgingivally, and
the process continues more aggressively.
Clean
substratum
Molecular
adsorption
(Phase 1)
Single
organisms Multiplication
(Phase 2) (Phase 3)
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Sequential
adsorption
of organisms
(Phase 4)
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Mature dental plaque
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Calculus
Composition
 1. inorganic content 70-90% of calcium phosphate,
calcium carbonate, magnesium phosphate
 2.organic content protein-polysaccharide,
desquamated epithelial cells, leukocytes,
microorganisms
Calculus formation
 Calculus is dental plaque that has undergone
miniralization
 Soft plaque.......precipitation of miniral salts between
1st and 14 days
 Saliva is the source of miniralization
 Gingival Cervicular Fluid (GCF)
Health
Gingivitis
Periodontitis
Normal dental plaque: coccis, filaments, epithelial
cell, little motility
Gingivitis plaque: spirochetes and great motility
 The critical locus of activity is the subgingival space
(periodontal pocket).
 The bacteria residing in the pocket and the host cells
that defend it determine the clinical outcome.
 The diseased periodontal pocket harbors both attached
subgingival plaque biofilms and nonattaching, motile
subgingival microflora (spirochetes, vibrios, and
straight rods with flagella).
 Orland
et al (1954) demonstrated germ-free
animals do not develop caries.
 In humans, when bacteria are allowed to
accumulate in plaque on the tooth surfaces,
enamel caries and gingivitis develop within 2 or
3 weeks.
Periodontal Disease
How do we know there is a
problem??
DIAGNOSIS
 Individual complaine
 Clinical examinations
 Radiographic examination
Individual complaine
 Bleeding gums
 Red gums
 Blood on my pilo
 Bad taste
 Bad smell (halitosis)
 Smokers ....less bleeding
Clinical examinations
 Plaque index
 Gingival index
 Pocket measurment
 Furcation
 Tooth mobility
Plaque Index
Plaque Scoring System for Quigley and Hein
Score
no plaque
0
flecks of stain at the gingival margin
1
definite line of plaque at the gingival
margin
2
gingival third of surface
3
two thirds of surface
4
greater than two thirds of surface
5
total score =
= SUM(scores for all faal and lingual surfaces)
index =
= (total score) / (number of surfaces examined)
Gingival Index
Löe & Silness 1963
Score 0
Score 1
Score 2
Score 3
Gingival Index: GI
0
1
2
3
Gingival Index Löe & Silness 1963
Appearance
Bleeding
Inflammation
Points
normal
slight change in
color and mild
edema with slight
change in texture
redness,
hypertrophy,
edema and
glazing
marked redness,
hypertrophy,
edema,
ulceration
no bleeding
no bleeding
none
mild
0
1
bleeding on
probing/pres
sure
moderate
2
spontaneous
bleeding
severe
3
Gingival Index
Löe & Silness 1963
Teeth examined:
 (1) maxillary right first molar
 (2) maxillary right lateral incisor
 (3) maxillary left first bicuspid
 (4) mandibular left first molar
 (5) mandibular left lateral incisor
 (6) mandibular right first bicuspid
Gingival Index
Löe & Silness 1963
Surfaces examined on each tooth:
 (1) buccal
 (2) lingual
 (3) mesial
 (4) distal
Gingival Index
Löe & Silness 1963
Average Gingival Index Interpretation
2.1 - 3.0
severe inflammation
1.1 - 2.0
moderate inflammation
0.1 - 1.0
mild inflammation
< 0.1
no inflammation
Sign the worse score
Choose the worse score