DEN

DEN TAL
TAL PLAQUE
PLAQUE
The
The oral
oral micro-ecological
micro-ecological system
system
 PLAQUE
PLAQUE FORMATION
FORMATION
The organism enharbour many billions of
bacteria on its surfaces. Nevertheless the
desquamation of the epithelial cells
anticipates the long lasting bacterial
coexistence in the body.

In the oral cavity the non shedding

surfaces, like enamel, root cementum,
restorations can promote permanent, long
lasting bacterial adhesion and survival on
the surfaces.
 PLAQUE
PLAQUE FORMATION
FORMATION
dental plaque is a bacterial aggregation that are
teanaciously attached to the teeth and other non seddign
features
9
One mm 3-dental plaque contains more than 10
microrganisms.
 PLAQUE
PLAQUE FORMATION
FORMATION
Löe - experimental gingivitis model (1965), proved that
plaque accumulation can lead to gingivitis, and its
removal can reverse the disease.

Similarly experimentally was proven that plaque

accumulation can cause peri-implantalis
3 kifejlődése
(Pontoriero 1994). Pontoriero R, Tonelli MP, Carnevale G,
Mombelli A, Nyman SR Land NP.
Experimentally induced periimplant
mucositis. A clinical study in humans.
ii
Clinical Oral Implants Research 5 254-
259. 1994.
 PLAQUE FORMATION

N on-specific plaque theory (Theilade 1986)

9

Only the quantity of bacteria mass is important, and the

abundant amount of plaque cab cause disease.
There are no individual differences
3 between plaques and
the healthy and diseased sites show only8 differences in
the quantity of the plaque and not in its composition.

Theilade E. The non-specific theory in microbial etiology of inflammatory

periodontal disease. J Clin Periodontol 1986;13: 905-911.
 PLAQUE FORMATION
It was difficult to explain:

Why some patients have plaque and calculus

accumulation for several years, but they develop only
gingivitis without any attachment loss?
Others show severe attachment loss with relatively good
oral hygiene.

Why the severity and speed of progression differ from

tooth to tooth in the same individual or even show
different pattern around different surface at the same
tooth?
 PLAQUE
PLAQUE FORMATION
FORMATION
Longitudinal studies showed that the presence of
certain bacterial strains in the dental plaque show good
correlation with the disease activity and the magnitude of
attachment loss. The total eradication of those9 bacteria
can ensure long lasting therapeutic results.

The massive mixed bacterial colony 3 has minimal

pathogenic potential to initiate attachment8loss.
Only certain members of those colony should be
eradicate to anticipate the attachment loss.
 Those
Those early
early studies
studies established
established aa
base
base of
of the
the so
so called
called specific
specific plaque
plaque
theory
theory (Loesche
(Loesche 1979).
1979).
Gingivitis/periodonitis are true infections

But this infection is not a classic infection in terms of

the Koch's postulates

Loesche WJ, Clinical and microbiological

aspects of chemotherapeutical agents
used according to the specific plaque
theory . J. Dentr Res. 56: 2404- 2414.
1979.
 PLAQUE
PLAQUE FORMATION
FORMATION
Gingivitis/periodontitis are hardly exogenous infections

The normal indigenous bacterial flora is the9 source of the

"endogenous " infection.

It is a true opportunistic infection

3

8
 PLAQUE FORMATION
To day only a couple of bacterial strains are known that
are not detectable in healthy oral environment or they only
9
occur in a very-very low rate. (ie. Porphyromonas
gingivalis, Actinobacillus Actinomycetemcomitans)

They are very numerous in diseased

3 periodontal pockets.
8

Those so called "periodonto-pathogenic microorganisms"

can only be considered and true exogenous agents.
 DEN
DEN TAL
TAL PLAQUE
PLAQUE
The
The oral
oral micro-ecological
micro-ecological system
system
 PLAQUE
PLAQUE FORMATION
FORMATION
Dental plaque accumulation starts supragingivally but
later the bacteria spread into the gingival sulcus and into
the pathologically deepened sulcus - ie. periodontal
pocket.

The composition and morphology of the subgingival

plaque are totally different from the supragingival one.
 PLAQUE
PLAQUE FORMATION
FORMATION
SUPRAGIN GIVAL PLAQUE

SUBGIN GIVAL PLAQUE

HARD TISSUE ASSOCIATED

EPITHELIAL ASSOCIATED
DISPERSED
INVASIVE
 THE
THE MECHAN
MECHAN ISM
ISM OF
OF PLAQUE
PLAQUE
ACCUMULATION
ACCUMULATION

Dental plaque or certain specific bacterial components

are necessary but not sufficient etiologic factors
9 for
the development of destructive periodontitis.

The complex equilibrium between 3the oral bacterial

ecosystem and the host defensive mechanisms 8 will
determine the nature of the disease and the character of
its progression.
THE
THE MECHAN
MECHAN ISM
ISM OF
OF PLAQUE
PLAQUE
ACCUMULATION
ACCUMULATION
As soon as the cleaned and polished tooth surface is
moisturized by saliva a monomolecular protein layer will
cover all the surfaces. It binds to enamel by ionic,
hydrophobic and van der Waals forces
This protein layer is called as " acquired pellicle"

The main component of acquired pellicle is salivary

glycoprotein (mucin), and in a lesser extent some
salivary immuno globulins
Its thickens is less than 1um
Early pellicle is bacteria free
 Plaque distribution after 12 hours of no
oral hygiene
Approximal Facial/Oral
100% 100%
Upper Upper

DISTAL 0% FACIAL 0%
Lower Lower
100% 100%

100% 100%
Upper Upper

MESIAL 0% ORAL 0%

Lower Lower

100% 100%
M P C I C P M

PL 1 = 0 PL 1 = 1 PL 1 =2

Lang et al. 1973

 THE MECHAN ISM OF PLAQUE
ACCUMULATION
ACCUMULATION
Initially bacteria binds to pellicle by physico-chemical forces
( ionic bonds, Van der Waals force). Later bacteria bind to
pellicle by protein-protein and protein - carbohydrate
interactions.

Several virulence factors can enhance their adhesion. The

natural bacterial glycoprotein coat (glycocalix), contains a
great amount of polysaccharides that many times organized
in surface fibrils.

Certain bacteria can synthesize extracellular polysaccharides

by glycosyl transferase enzyme.

De Jong HP, DeBoer P, Busscher HJ et al.: Surface free energy changes of

human enamel during pellicle formation: an in vivo study Caries Res 18: 408-
415. 1984.
THE
THE MECHAN
MECHAN ISM
ISM OF
OF PLAQUE
PLAQUE
ACCUMULATION
ACCUMULATION
The non-soluble extracellular polysaccharides form the
interbacterial matrix of the dental plaque while the
soluble part serves as energy reservoir.

The attached bacterial mass grows very rapidly partly

by cell division partly bacterial coagreagation
THE MECHAN ISM OF PLAQUE
ACCUMULATION
As the bacterial plaque gets thicker the oxygen cannot
reach the deepest bacterial layers partly because of simple
physico-chemical rules, partly because of the oxygen
consumption of the superficial bacteria

In this way an oxygen gradient is to form from the surface

to the depth with decreasing oxygen concentration.
This eventually will reorganize the composition of the
bacteria in the depth and shifting towards the anaerobes.
THE
THE MECHAN
MECHAN ISM
ISM OF
OF PLAQUE
PLAQUE
ACCUMULATION
ACCUMULATION
In the depth - anaerobes
on the surface - aerobe or facultative anaerobes

In the depth bacteria cannot utilize nutrients

originating from the saliva they use the sulcular fluid
and blood as energy source.

In the depth of the sulcus no saccharolytic bacteria

occur.
THE
THE MECHAN
MECHAN ISM
ISM OF
OF PLAQUE
PLAQUE
ACCUMULATION
ACCUMULATION
day 0
sterile dental pellicle

1 Gram+ cocci

3 Gram+ rods, actinomyces

6 Gram - bacteria

21 anaerobes, Gram - majority

 Dental
Dental plaque
plaque as
as aa biofilm
biofilm
Biofilm is a well organized bacterial coating on the
non- shedding hard surfaces
In the depth of the biofilm the microorganisms are
densely packed embedded into sticky polysaccharide
matrix.
Periodontal diseases
are bacterial infections
Specific bacterial
pathogens are the
primary etiologic agents
These bacteria form a
biofilm above and
below gingival margin

Plaque is natural and might exist in harmony
with the host
•NO OVERT INFLAMMATORY REACTION
•OR
•INFLAMMATION
Disease is the consequence of breaking down
this balanced relationship
• The magnitude or nature of the microbial challenge
• Nature of the host response
•(Socransky et al. 1998).
DENTAL PLAQUE IS A NECESSARY BUT NOT
SUFFICIENT ETIOLOGIC FACTOR OF
DESTRUCTIVE PERIODONTAL DISEASE

DENTAL PLAQUE

RISK FACTORS
GENETIC GINGIVITIS
SYSTEMIC

BEHAVIORAL
PERIODONTITIS

DESTRUCTIVE PERIODONTITIS
 RISK FACTORS
Oral hygiene
Local plaque retentive factors
bacterial specificity
systemic immune status
Diabetes mellitus
Tobbaco smoking
Osteoporosis
Ethnic background
Age
Diet
Genetics
Stress
Socio-economics
Supragingival
irregularities
 crowding,
 calculus
 rough restorations

enhance the retention

of the supragingival
biofilm
protect organisms
from the action of oral
hygiene measures.
 LOCAL PLAQUE RETENTIVE
FACTORS
 1 ANATOMICAL
ETIOLOGIC
FACTORS

 2 IATROGENIC
ETIOLOGIC
FACTORS
 1 ANATOMICAL ETIOLOGIC
FACTORS

 a) Palatine sulcus of upper incisors.

 b) Furcation areas.
 c) Cervical enamel projections
 d) Enamel pearls
 e) Crowding of the teeth in the dental arch.
 f) Mucogingival deformities .
 g) Occlusal anomalies.
 a) Palatine sulcus of upper incisors.

 palatine sulcus which

starts from the palatine
tubercle of the lingual
surface accumulates
dental plaque, and
enhances the pocket
formation.

Lee K. et al.: Palato-gingival grooves in

maxillary incisors. Br. Dent. J. 124:14,
1968.
 b) Furcation areas
 The anatomy of the
furcation :
 favors retention of
bacterial deposit
 makes periodontal
debridement,
 oral hygiene
procedures difficult.

Hirschfeld L, Wasserman B. A long-term survey of tooth loss in 600

treated periodontal patients. J Periodontol 1978: 49: 225–237
 b) Furcation areas
 Furcations are
difficult to
instrument
because of their
gothic arch
configuration
 b) Furcation areas
 The dental plaque
accumulates in that
region and causes
faster periodontal
destruction of the
molars and
premolars,
PSEUDOFURCATION
(BUCCAL GROOVES)
ON THE ROOTS OF
CENTRAL INCISIORS
FURCATION LESIONS ARE ALSO THE
CONSEQUENCE OF PERIODONTAL
ATTACHMENT LOSS AND
PERIODONTAL RESECTIVE SURGERY
 c) Cervical enamel projections
 Ectopic deposits of
enamel apical to the
level of the normal
cementoenamel
junction
 Connective tissue
does not attach to
cervical enamel
projections
 they can lead to
furcation defects.
 c) Cervical enamel projections
 82.5% of molars with cervical enamel
projections, exhibited furcation involvement,
 while only 17.5% of molars without cervical
enamel projections had furcation involvement

Hou G-L, Tsai C-C. Relationship between periodontal furcation involvement and
molar cervical enamel projections. J Periodontol 1987: 58: 715–721
 d) Enamel pearls
 Enamel pearls can lead
to furcation involvements

 The prevalence of
enamel pearls are
reported between 1.1–
9.7%.
 Nearly three-quarters of
enamel pearls are found
on maxillary third molars.

Moskow BS, Canut PM. Studies on root

enamel. (2) Enamel pearls. A review of their
morphology, localization, nomenclature,
occurrence, classification, histogenesis and
incidence. J Clin Periodontol 1990: 17:
Cervical enamel pearl on
the maxillary first molar
Alveolar bone loss
associated with this
anomaly

That is not present in the

contralateral tooth and no
bone loss either
 e) Crowding of the teeth in the
dental arch.
 the close convergence of
the roots of neighboring
teeth promotes the plaque
accumulation resulting in
faster periodontal
destruction, is important due
to the difficulty of removing
dental plaque.

Ainamo J. Relationship between malalignment of the teeth and periodontal
disease. Scand J Dent Res 1972: 80: 104–110
Geiger AM, Wasserman BH, Turgeon LR. Relationship of occlusion and periodontal
disease. Part VIII. Relationship of crowding and spacing to periodontal destruction
and gingival inflammation. J Periodontol 1974: 45: 43–49
 f) Mucogingival lesions
 The clinical impression is
that the attached gingiva
will provide a protective
barrier against
inflammation and
attachment loss.
 Several studies have
challenged the view that a
wide zone of attached
gingiva is a more effective
barrier against recession
 f) Mucogingival lesions
 It has been
demonstrated that in
the absence of
attached gingiva,
gingival health and
attachment levels can
be maintained
Dorfman HS, Kennedy JE, Bird WC. Longitudinal evaluation of free autogoneous
gingival grafts. J Clin Periodontol 1980: 7: 316–324
Wennström J, Lindhe J. Role of attached gingiva for maintenance of periodontal
health. Healing following excisional and grafting procedures in dogs. J Clin
Periodontol 1983: 10: 206–211
Wennström J, Lindhe J, Nyman S. Role of keratinized gingiva for gingival health.
Clinical and histologic study of normal and regenerated gingival tissues in dogs. . J
Clin Periodontol 1981: 8: 311–328
 f) Mucogingival lesions
 High frenum and
muscle attachments,
 can cause the
detachment of the
free gingiva,
 promotes the spread
of the dental plaque
inside the gingival
sulcus
f) Mucogingival lesions
 g) Occlusal anomalies.

 Occlusal anomalies had been considered as

causative factor for periodontal disease
(Ramfjord et al. 1966 ).
 It has been proven by long term animal studies (
Lindhe & Svanberg 1974 ), that the traumatic
occlusion can not be regarded as an etiologic
factor for periodontal disease
 it does not cause pocket or attachment loss

Lindhe J., Svanberg G.: Influence of trauma from occlusion on progression of

experimental periodontitis in the beagle dog. J. Clin. Period. 1:3, 1974
 g) Occlusal anomalies.
 Occlusal traumatism can cause degenerative changes
in the deep periodontal structures
 Inflammatory process in the gingiva is allowed to
spread apically more rapidly and result in more severe
periodontal destruction.
 g) Occlusal anomalies.
 Missing teeth can
lead to mesial drifting,
tilting and extrusion of
teeth.
 These alterations
can result in
increased plaque
retention, food
impaction and
vertical bony defect
 2 IATROGENIC ETIOLOGIC
FACTORS
 a) Dental caries
 b) Dental calculus
 c) Dental materials and plaque retention.
 d) Effect of bad restoration quality on periodontal health.
 e) The effect of the position of the crown margin to the
periodontium.
 f) Pontic design and the edentulous mucosal area.
 g) Overconturing of restorations.
 h) Temporary restorations and their effect on the
periodontium.
 a) Dental caries
 Dental caries
enhance plaque
retention - promoting
periodontal disease.
 Ainamo (1970) first
noted a strong
relation between the
GI value and
untreated dental
caries,.
Ainamo J.: Concominant periodontal disease and dental caries in young
adult males. Suomen Hammaslaakariseuran Toimituksa 66:303, 1970
 a) Dental caries
Secondary caries in restored teeth and the relationship
of its incidence to the location of the preparation margin

5 years follow-up study:

 15.4% of the supragingivally
located amalgam-restoration
 30.4% of the subgingivally
located amalgam-restoration
exhibited secondary caries

Hammer and Hotz

 b) Dental calculus
The calculus per se is not a primary etiologic factor.

 In the practice calculus is

always an important factor in
the development of
periodontitis.
 It is a plaque retentive factor.
 Its surface is always covered
by fresh bacterial plaque
 it can also guide the plaque
bacteria subgingivally
Patient’s and dentist’s negligence
 c) Dental materials and plaque
retention.
 Dental materials posses a
greater capacity to
accumulate and retain
plaque than do either
enamel or dentin.
 Polymethyl-methacrylate
accumulates plaque
faster than gold and
porcelain,
Dental gold, porcelain and
composites irritate tissues
hardly if at all.

Porosity contribute to the

plaque retentive potentials.
 c) Dental materials and plaque
retention.
 Especially the transition zone
at restoration margins
represents a predilection site
for plaque accumulation.
 The "cement line" associated
with seated crowns may
approach several square
millimeters.
 Histological investigations by
Waerhaug have shown that the
subgingival cement roughness
enhances plaque accumulation
in the gingival sulcus
 d) Effect of bad restoration quality
on periodontal health.
 The World Workshop
in Periodontics (1966)
reported that the
overhanging at the
margins of a
restoration are local
plaque retentive
factors promoting
periodontitis.
 d) Effect of bad restoration quality
on periodontal health.
 Teeth with inadequate
restorations had significantly
more plaque, gingivitis and
periodontal pocket formation
than adequately restored
teeth.
 For both amalgam and crown
restorations, the health of the
periodontium is adversely
affected by the presence of a
restoration.

Grosso E. J. et al.: Effect of restoration quality on periodontal health. J. Prosthetic

Dentristy. 1985; 53: 14-19.
 d) Effect of bad restoration quality
on periodontal health.
 Björn et al. reported a
generally poor
marginal fit in
retainers for fixed
partial dentures.
 Eighty percent of the
radiographically
studied restorations
exhibited marginal
defects on the
proximal surfaces.
 d) Effect of bad restoration quality
on periodontal health.
 In a German survey, only 18.2% of crown
margins were clinically perfect.
 Margins that were open by more than 0.2mm
were always associated with alveolar bone
loss.

Lange D.: Attitudes and behaviour with respect to oral hygiene and periodontal
treatment need in selected group in West Germany. Ín: Frandsen A. Public
health aspects of periodontal disease. Berlin: Quintessence, 1984: 83-97
 Incidence of bad restorations
Reference Diagnostic method for detection % restored surfaces with
overhangs
(n = number of subjects)
subjects)

Gilmore & Sheiham, 1971 Bitewing radiographs 25% (n = 1976)

Burch et al., 1976 Bitewing radiographs 30% (n = 825)
Hakkrainen & Ainamo, Orthopantograms 50% (n = 85)
1980
Than et al., 1982 Calculus probe 60% (n = 240)
Lervik & Riordan, 1984 Bitewing radiographs, 25% (n = 175)
microscope
Keszthelyi & Szabo, 1984 Bitewing radiographs, 86% (n = 176)
microscope
Coxhead, 1985 Bitewing radiographs, 76% (n = 50)
mirror, probe
Claman et al., 1986 Bitewing radiographs 27% (n = 826)
Jansson et al., 1994 Bitewing radiographs 18 % (n = 162)
 d) Effect of bad restoration quality
on periodontal health.
 overhanging restorations
disturb the ecological
balance in the gingival
sulcus
 allow the growth of a
group of disease
associated
microorganisms.

Lang PN, Kiel AR, Anderhalden : Clinical and microbiological effects of subgingival
restorations with overhangings or clinically perfect margins. J. Clin Periodontol 1983; 10: 563-
578
 d) Effect of bad restoration quality
on periodontal health.
 Even an adequately restored
tooth can lead to gingivitis
and periodontal pocket
formation.
 the larger the number of
restorations, the more
important the plaque control
is

Grosso E. J. et al.: Effect of restoration quality on periodontal health. J. Prosthetic

Dentristy. 1985; 53: 14-19.
 OVERCONTOURED
CROWN MARGIN
WITH SEVERE
OVERGANG

THE WHOLE DENTAL PROBE

CAN BE PUT UNDER THE
CROWN MARGINE!!!!!!
 OVERCONTOURED
CROWN MARGIN
WITH SEVERE
OVERGANG

CLASS TWO FURCATION

LAESION TOTALLY
COVERED BY
OVERHANGING CROWN
MARGIN
 d) Effect of bad restoration quality
on periodontal health.
 The early detection of
overhanging dental
restorations is an
important part of
preventive dental care
 The removal of
overhanging margins
should be part of
initial periodontal
therapy
BRAND NEW FULL ARCH BRIDGE WITH SEVERE OVERHANGS AND
OVERCOUNTURED CROWNS AND PONTICS
 The effect of the position of the
crown margin to the periodontium.
 In the past, Black's theory
dominated dentistry for
decades
 The concept of "extension
for prevention" by Black
(1908).
 It postulates that the
cervical margins of all
reconstructions should be
placed subgingivaly.
 The effect of the position of the
crown margin to the periodontium.
 Bodecker and Applebaum (1934) where the first
to question Black's theory about extension of the
cavity boarders in the gingival sulcus.
 Waerhaug (1967, 1968), stated that there is
scientific proof that subgingival crown margins
create periodontal destruction due to plaque
retention.
 Loe (1968), Zander and Kennedy (1970)
supported the position of the crown margins
above the free gingiva
 The effect of the position of the
crown margin to the periodontium.
 Follow-up
examinations of fixed
reconstructions have
demonstrated :
 crown margins
positioned
subgingivally were
associated with the
highest
 and supragingival
crown margins with the
lowest GI values.

Silness J.: Periodontal conditions in patients treated with dental bridges. J. Periodont Res.
1970; 5:225-229.
 The effect of the position of the
crown margin to the periodontium.
 102 patients with 108 bridges were studied over
15 years.

 Loss of the periodontal supporting apparatus was

significantly higher around teeth with
subgingivally located crown margins
 than around teeth with crown margins located
supragingivally.
Valderhaug J., Birkland JM: Perodontal conditions in patients 5 years following
insertion of fixed prosthesis. Pocket depth and loss of attachment. J. Oral Rehab.
1976; 3(3)
Valderhaug J.: Periodontal conditions and carious lesions following the insertion of
fixed prosthesis: a 10-year follow up study. Int. Dent. J. 1980;30
 The effect of the position of the
crown margin to the periodontium.
 A follow-up survey of 423 crown margins

 Gingival tissues tended to bleed 2.42 times more

frequently with subgingival margins
 had a 2.65 times higher chance of gingival
recession
 Crowns with supragingival margins did not differ
significantly compared with the contra-lateral
tooth,
Orkin DA, Reddy J. & Bradshaw D.: The relationship of the position of the crown
margin to gingival health. J. Prosthetic Dentristy. 1987; 4: 421-424.
 The effect of the position of the crown
margin to the periodontium.
 From a caries
preventive point of
view, the location
of crown margins
does not seem to NO CARIUOUS LEASIONG AFTER 12 YEARS
be of great
importance if
patients maintain
a satisfactory oral
hygiene.
Valderhaug J, Loe H: Oral hygiene in a group of supervised patients with fixed
prosthesis. J. Periodontol. 1977; 48:221- 224
 The effect of the position of the
crown margin to the periodontium.
 Subgingival margins
can also lead to
gingival recession as
a possible
consequence of
chronic irritation and
the violation of
biologic width

Valderhaug J, Loe H: Oral hygiene in a group of supervised patients with fixed

prosthesis. J. Periodontol. 1977; 48:221- 224
f) Pontic design and the edentulous
mucosal area
 Badly designed
pontics are very
frequently the cause
of tissue damage,
gingival infammation,
hyperplasia of the
underlying mucosa
and bone resorption.
 .
f) Pontic design and the edentulous
mucosal area
 The distribution of
P.gingivalis,
P.intermedia
T. forsythia
under the pontics
adjacent to healthy
and inflammed
mucosa is different
.
Wang JC, Lai CH, Listgarten M A: Porphyromonas gingivalis, Prevotella
intermedia and Bacteroides forsythus in plaque subjacent bridge pontics.
J. Clin Periodontol 1998 ; 25: 330-333
g) Overconturing of restorations.
 Oral hygiene
practices may be
severely hampered
by overconturing
restorations.
 it is more difficult for
the patient to
effectively clean the
area
 g) Overcontouring of restorations.
 Interdental space should
be kept wide,
 for the normal
development of the
gingival papilla,
 to make access to
hygienic oral devices.
 access to interdental
spaces is one of the most
important factors for a
long-time expectancy
h) Temporary restorations and their
effect on the periodontium
THE QUALITY AND THE MARGINAL ADAPTATION
OF A PROVISIONAL RESTORATION SHOULD
ALSO BE CORRECT
Quality of restorations
 From a periodontal point of view, a supragingival position
of the crown margin is the most favorable.
Morman W. et al.: Gingival reaction to well fitted subgingival proximal gold inlays. J. Clin
Periodontol. 1:120, 1974.
 The most expensive
techniques and
materal can cause
severe periodontal
disease if the quality
is questionable