Download Plaque and Calculus

Plaque and Calculus
Composition, Development, and It’s
Relationship to Disease
What Is Plaque?
• An invisible layer of microorganisms growing
in a colony on the teeth
• Specific bacteria in the colony are the etiology
of dental caries and periodontal diseases
• Plaque begins to form immediately on a freshly
polished tooth, but it takes approximately 21
days for plaque to completely mature
• If plaque is disturbed (brushed away) when it
begins to form, it does not mature
What Is Plaque’s Composition?
Plaque is composed of:
• Components of saliva (glycoproteins)
• Various bacterium including gram + and
gram -; aerobic, facultative, and anaerobic;
saccharolytic (metabolize sugars) and
asaccharolytic (don’t require sugars)
• Bacteria metabolism products
• Minerals and their ions (ca+, PO4¯, F ¯)
Is This Plaque?
Is This Plaque?
Arrow points to visible
material so its not plaque, it’s
materia alba
Materia alba is food debris,
dead cells, bacteria
plaque is underneath
materia alba
What Damage Plaque Can Do
• Plaque requires stain
to be seen because it is
invisible
THIS IS PLAQUE!
From healthy
To localized
(30% or less)
To generalized
(75% or more)
1
More Damage
TOOTH
GINGIVA
CEJ
BONE
From treatable--
PDL
To hopeless
A Freshly Polished Molar
SULCUS
SULCULAR EPITHELIUM
ATTACHMENT
LAMINA PROPRIA
(Connective tissue)
• In minutes salivary
glycoproteins form the
acquired pellicle on ALL
teeth. (It’s that “slick”
f li on your teeth)
feeling
t th)
• The part of pellicle that
attaches to tooth
irregularities is called
“subsurface pellicle”
• Pellicle itself is acellular
PDL
BONE
A Molar Within 24 Hours That
Is Not Brushed
• In 24 hours aerobic,
gram + bacteria
(primary colonizers)
such as streptococcus
sanguis,
i s. mutans,
t
Rothia, Actinomycosis
begin growing in pellicle
• Neisseria, gram –
facultative anaerobe also
primary colonizer
Stem cells in bone marrow
produce inflammation
and immunity cells and
send them to body tissues
blood
for later use
Stem cell
Thymus
T Lymphocyte
blood
Lymph tissue
PMN
Monocyte
B
Lymphocyte
Macrophage
In
tissue
Initial gingivitis
2
A Molar Not Brushed For 24 Hours
• If bacteria are allowed to
grow, there is an
immediate subclinical
inflammatory response
(
(can’t
’t b
be seen clinically)
li i ll )
PMN’s (neutrophils)
enter lamina propria
pmn pmn
pmn
Initial gingivitis
A Molar Not Brushed in 2-3 Days
• Secondary colonizers such
as Provetella, intermedia,
capnocytophaga series,
fusobacterium nucleatum,
and bacteriodes
i
forsyth
f
such as begin growing
• Inflammation still acute
and subclinical but blood
vessels beginning to dilate,
macrophages appear,
pmn’s move into junctional
epithelium, sulcus
pmn
pmn
macrophages
pmn
Initial gingivitis
A Molar within 4-6 Days That
Is Not Brushed
• Plaque becoming thicker,
tertiary colonizers such as
A.A., P. gingivalis, treponema
d ti l campylobacter
denticola,
l b t
recta appear
• Endotoxins from gram –
bacteria begin to form)
• Now considered EARLY
(STAGE TWO) GINGIVITIS
A Molar within 4-6 Days That
Is Not Brushed
• ulcers appear in sulcular
epithelium,
• signs of inflammation
may begin to be clinically
apparent (bleeding
apparent,
(bleeding,
slight redness, swelling)
• Lymphocytes become the
most prolific WBC, a sign
of chronic inflammation
lymphocytes
lymphocytes
Early gingivitis
A Molar Not Brushed for 7-14 Days
• Plaque grows apically,
thickens
• Inflammatory
response intensifies
• Crystal nidus’s of
minerals (calcium,
phosphates, etc) grow
together to form
calculus
Early gingivitis
lymphocytes
lymphocytes
macrophages
pmn
A Molar Not Brushed for 14-21 Days
• Piles of bacteria form
“domes”, “corncobs”,
“test tube brushes”
present
• Plasma cells, mast cells,
macrophages
p g increase in
connective tissue
• Plaque has matured
• Bacterial biproducts
(colleganase, protease)
now ready to break
down attachment and
cause it to migrate
apically
Domes
lymphocytes
lymphocytes
Plasma cell
pmn
pmn
pmn
pmn
pmn
Mast cell
macrophage
Established gingivitis
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Plaque and Periodontal Disease
• When attachment
migrates apically, it is no
longer gingivitis but
periodontitis
• Most common form is
chronic periodontitis
• Contributing factors can
alter or intensify process
but it’s pathogenesis
stays the same
Attachment
migrated apically
Plaque and Periodontal Disease
• Unattached plaque has more
motile, gram – bacteria with
many WBC’s
• TISAP has gram -, motile
bacteria that invade tissue
through ulcers in sulcular
epithelium
TOOAP
unattached
TISAP
How Bone and the PDL Are
Destroyed
• The inflammatory process
spreads to PDL.
• Sharpey’s
p y fibers are
destroyed by collagenase
and protease
• Endotoxins are
incorporated into
cementum
Plaque and Periodontal Disease
•
Subgingival plaque is “tooth
associated” (TOOAP),
unattached, and “tissue
associated” (TISAP)
• TOOAP is continuation of
supragingival plaque, has more
gram +, nonmotile bacteria in
coronal 1/3, more gram -, motile
bacteria in apical 1/3
TOOAP
unattached
TISAP
How Bone and the PDL Are
Destroyed
• Gram –bacteria endotoxins
enter lamina propria
through ulcers in
epithelium
• They follow vascular
bundles to bone where they
stimulate osteoclasts to
destroy bone
Different Patterns of Destruction
 Horizontal bone loss
 Vertical bone loss
 Buccal bone loss
4
What is Calculus?
• Calculus is
mineralized plaque
• Calculus is a
contributing factor to
dental diseases
• Calculus provides a
rough surface on
which bacterial plaque
can grow
How Does Calculus Attach?
• Attaches three ways
– Irregularities
– Cohesion
– Acquired pellicle
Supragingival vs Subgingival
Calculus
Supragingival
• Minerals come from
saliva
• Usually whitish in
color
• Found mainly near
salivary ducts
Subgingival
• Minerals come from
sulcular fluids
• Usually black in color
• Found everywhere
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