1. Dental plaque is a biofilm that develops on teeth and comprises living and dead bacteria and their products embedded in an organic matrix. The microbial composition of plaque varies between individuals and locations in the mouth. 2. Gingivitis is a reversible form of periodontal disease caused by dental plaque. It involves inflammation of the gingiva without loss of attachment to the tooth. The gingiva become red, swollen and bleed easily but are not painful. Early plaque is dominated by streptococci while established lesions contain increased levels of anaerobic bacteria like Porphyromonas and Prevotella. 3. Dental caries is caused by acid-producing plaque bacteria metabolizing ferment

1. Dental caries
and
Periodontal diseases:
Gingivitis
and
chronic periodontitis
Chapter 20

2. Dental plaque
Dental plaque is a microbial community which develops on soft and hard-tissue
surfaces of the mouth, comprising living, dead and dying bacteria and their
extracellular products, together with host compounds mainly derived from
saliva.
Composition
The organisms in dental plaque are surrounded by an organic matrix which
comprises about 30% of the total plaque volume. The matrix is derived from the
products of both the host and plaque constituents. In the gingival area, proteins
from the crevicular exudate become incorporated into the plaque. This matrix
acts as a food reserve and as a cement, binding organisms both to each other
and to various surfaces. The microbial composition of dental plaque can vary
widely between individuals; some people are rapid plaque formers, others slow.
bacteria extracellular products Saliva products
organisms organic matrix
the host
plaque
food reserve
cement
binding
surfaces
bacteria
30%
bac
rapid plaque formers
others slow
living, dead and dying
people
microbial composition of dental plaque varies

3. Further, there are large variations in plaque composition within an
individual, for example:
• at different sites on the same tooth
• at the same site on different teeth
• at different times on the same tooth site

4. organisms in dental plaque are surrounded by an organic matrix

5. Distribution
Plaque biofilm is found on dental surfaces and appliances especially
in the absence of oral hygiene. In general it is found in anatomical
areas protected from the host defences, e.g. occlusal fissures,
interproximally or around the gingival crevice. Plaque samples are
described in relation to their site of origin and are categorized as:
- supragingival:
• fissure plaque - mainly in molar fissures
• approximal plaque - at contact points of teeth
• smooth surface - e.g. buccal and palatal surfaces
- subgingival, or appliance-associated:
• full and partial dentures (denture plaque)
• orthodontic appliance-related plaque.
occlusal fissures,
interproximally or
around the gingival crevice.

7. 1- Dental caries
Dental caries is a chronic endogenous infection caused by the normal
flora of the mouth. The carious lesion is the result of
demineralization of enamel - and later of dentine by acids
produced by plaque microorganisms as they metabolize dietary
carbohydrates. However, the initial process of enamel
demineralization is usually followed by
remineralization, and
cavitation occurs when the former process overtakes the latter.
Once the surface layer of enamel has been lost, the infection
invariably progresses to dentine, with the pulp becoming firstly
inflamed and then necrotic.
enamel dentine pulp
inflamed and then
necrotic
demineralization by acids
Caries is defined as localized destruction of the tissues of
the tooth by acid produced by bacterial fermentation of
dietary carbohydrates.
rem

8. EPIDEMIOLOGY
Dental caries (with periodontal disease) is one of the most
common human diseases and affects the vast majority of
individuals.
In the developed world caries prevalence is falling due to the
- Increasing awareness of cariogenic food sources and the
- general improvement in oral hygiene and the
- dental care delivery systems.
In the developing world a remarkable upsurge in caries
occurred due to the ready and cheap availability of fermentable
carbohydrates.

9. CLASSIFICATION of Dental caries
Dental caries can be classified with respect to the site of
the lesion:
• pit or fissure caries (seen in molars, premolars and the lingual
surface of maxillary incisors)
• smooth-surface caries (Occlusal caries)(seen mainly on
approximal tooth surfaces just below the contact point)
• root surface caries (seen on cementum or dentine when the root
is exposed to the oral environment)
• recurrent caries (associated with an existing restoration).

10. 3-root surface
caries
4-recurrent caries
D: Dentine
E: Enamel
P: Pulp
1
2
3
4
CLASSIFICATION of Dental caries
Occlusal caries
just below the
contact point
enamel
dentine
pulp

11. CLINICAL PRESENTATION
The primary lesion of caries is a well-demarcated, chalky white
lesion in which the surface continuity of enamel has not been
breached. This 'white-spot' lesion can heal or remineralize and
this stage of the disease is therefore reversible.
However, as the lesion develops, the surface becomes roughened
and cavitation occurs. If the lesion is not treated the cavitation
spreads into dentine and eventually may destroy the dental
pulp, finally leading to the development of a periapical abscess
and purulent infection.
primary lesion chalky white lesion
the surface continuity of enamel has not been breached
can heal or remineralize
reversible
roughened and cavitation occurs. not treated dentine dental pulp
periapical abscess and purulent infection
enamel

12. 1
2
4
periapical abscess and
purulent infection
primary lesion
chalky white lesion
reversible
the surface continuity of enamel
has not been breached
roughened and cavitation occurs
3

13. Plaque
2- Dental decay
Enamel
Dentine
3- Pulp
periapical abscess and
purulent infection
1- Enamel

14. Pulb involved

15. Purulent infection
Periapical abscess

19. The major factors involved in the aetiology of caries are:
• host factors (tooth, saliva)
Tooth structure
Flow rate and composition of saliva:
mineral content (especially fluoride)).
Removes food debris
Removes unattached oral microorganisms
a high buffering capacity neutralize acids
supersaturated with calcium and phosphorus ions
mechanical
washing
which are important in the remineralization
of white-spot lesions
acts as a delivery vehicle for fluoride
• Plaque
• diet

20. The major factors involved in the aetiology of caries are:
• host factors (tooth, saliva)
Tooth structure
The structure of enamel, and of dentine in root caries, is important:
some areas of the same tooth are much more susceptible to carious
attack than others, possibly because of differences in mineral
content (especially fluoride).
Flow rate and composition of saliva: The mechanical washing
action of saliva is a very effective mechanism in the removal of
food debris and unattached oral microorganisms. It has a high
buffering capacity which tends to neutralize acids produced by
plaque bacteria on tooth surfaces, and it is supersaturated with
calcium and phosphorus ions, which are important in the
remineralization of white-spot lesions. Saliva also acts as a
delivery vehicle for fluoride.
mineral content (especially fluoride)).
host factors diet plaque microorganisms

21. The 'ecological plaque hypothesis' of caries
According to this proposal, cariogenic flora found in natural
plaque are weakly competitive and comprise only a minority of
the total community. With a conventional diet, levels of such
potential cariogenic bacteria are clinically insignificant, and
the processes of remineralization and demineralization are in
equilibrium.
If, however, the frequency of intake of fermentable carbohydrates
increases, then the plaque pH level falls and remains low for
prolonged periods, promoting the growth of acid tolerant
(aciduric) bacteria while gradually eliminating the acid-labile
bacteria. . This process would turn the balance in the plaque
community in favour of mutans streptococci and lactobacilli
Prolonged low-pH conditions also initiate demineralization

22. • diet ( intake of fermentable carbohydrates)
There is a direct relationship between dental caries and
the intake of carbohydrates. The frequency of sugar
intake rather than the total amount of sugar consumed
appears to be of decisive importance. Carbohydrates
other than sucrose, e.g. glucose and fructose, are also
cariogenic, but less so than sucrose.
• plaque microorganisms (i.e. supragingival plaque).
Microorganisms in the form of dental plaque are a
prerequisite for the development of dental caries.
dental caries carbohydrate intake
relation
frequency
Not quantity
sucrose,
glucose and
fructose
cariogenic
plaque is prerequisite dental caries

23. Plaque
Dental decay Dental caries prerequisite
Enamel
2- Dentine
3- Pulp

24. The current evidence implies that some bacteria
(Mutans streptococci, Lactobacillus spp. and Actinomyces spp.)
may be more important than others in the initial as well as
subsequent events leading to both
- enamel and root surface caries.
Streptococcus mutans' is a loosely applied group name for a
collection of seven different species:
S. mutans, S. sobrinus,
S. cricetus, S. ferus,
S. rattus, S. macacae and S. downei
root surface caries
enamel
- Mutans streptococci,
- Lactobacillus spp. and
- Actinomyces spp

25. Management of dental caries
The conventional approach to the treatment of dental caries was to
remove and replace diseased tissue with an inert restoration. This
approach made no attempt to cure the disease and the patient often
returned some months later requiring further fillings due to new or
recurrent caries.
In contrast, the modern philosophy in caries management highlights:
• early detection
• the importance of accurate diagnosis
• minimal cavity preparation techniques
• active prevention.
remove
and
Replace
with inert
restoration

26. Prevention of dental caries
The major approaches to prevention of caries are:
• stopping or reducing between-meal consumption of carbohydrates,
or substituting non-cariogenic artificial sweetener (sugar substitutes), e.g.
sorbitol, xylitol or lycasin
• making the tooth structure less soluble to acid attack by using fluorides
• using sealants to protect susceptible areas of the tooth (e.g. pits and
fissures) that cannot easily be kept plaque free by routine oral hygiene
measures
• reducing cariogenic flora
• replacement of cariogenic bacteria. (Probiotics or Probiotic therapy)
between-meal sugars sweetners Fluoride use sealants reducing cariogenic flora
Probiotic therapy
stopping or reducing non-cariogenic less soluble
pits
fissures
susceptible
areas
replacement of cariogenic
bacteria

27. • reducing cariogenic flora so that even in the presence of sucrose, acid
production will be minimal (e.g. oral hygiene aids, antimicrobial
agents: Chlorhexidine as a 0.2% mouthwash is by far the most
effective antimicrobial in plaque control. and possibly
immunization) Unfortunately, because of the problems of tooth
staining and unpleasant taste, chlorhexidine is normally only used
for short-term therapy. Passive immunization. Experimental studies
indicate that when the natural levels of oral mutans streptococci are
suppressed by chlorhexidine, topical application of monoclonal
antibodies against antigen of mutans streptococci prevents
recolonization by the organisms.
• replacement of cariogenic bacteria by organisms with low or no
cariogenic potential. (Probiotics or Probiotic therapy)
oral hygiene Chlorhexidine Passive immunization: Mon-Abs against stept Ags
Probiotics or Probiotic therapy Replace: organisms with low or no cariogenic potential

28. Replacement therapy
Experimental studies indicate that genetically engineered, low-virulence
mutants of mutans streptococci that are deficient in (metabolic
enzymes) glucosyl transferase or deficient in lactate dehydrogenase
activity can be 'seeded' into the oral environment. These organisms can
replace their more virulent counterparts and prevent their re-emergence.
The term probiotic therapy or probiotics is now used for approaches
where the offending pathogen is replaced artificially by innocuous
commensals that are allowed to obtain a permanent foothold in the locale
(e.g. oral cavity, intestines, vagina).
- oral cavity
- intestines
- vagina
genetically engineered mutans streptococci
lacking enzymes
offending pathogen is
replaced artificially by
innocuous commensals
probiotic therapy
Places of probiotic
glucosyl transferase
lactate dehydrogenase

29. 2- Periodontal diseases
Everyone suffers from various degrees of periodontal disease at some point,
and it is one of the major diseases afflicting humankind. However, in most
people the common chronic inflammatory diseases involving the
periodontal tissues can be controlled, using
mechanical cleansing techniques and good oral hygiene.
A minority experience rapid progressive disease which requires assessment
and management by periodontist. Periodontal disease can be broadly
categorized into gingivitis and chronic periodontitis. Both are caused by
certain bacteria in the dental plaque.
gingivitis and chronic periodontitis
- gingivae
- periodontal ligament
- supporting alveolar bone
Periodontal diseases can be defined as disorders of supporting structures of the teeth,
including the gingivae, periodontal ligament and supporting alveolar bone.

30. gingivae
Periodontal
ligament
alveolar
bone
Periodontal diseases Disorders of supporting structures of the teeth
and supporting alveolar bone
gingivae,
periodontal ligament

31. 2.1- Chronic marginal gingivitis:
There is marked inflammatory infiltrate of polymorphonuclear leukocytes,
lymphocytes and plasma cells in the connective tissue that lies immediately
adjacent to the epithelium lining the gingival crevice and attached to the tooth.
Collagen is lost from the inflamed connective tissue. No direct invasion of the
gingival tissues by large number of bacteria at least in the early stage of the
disease.
It has been suggested that tissue destruction is mediated by bacterial substances
that pass through the epithelial barrier and cause either direct or indirect injury.
1. Direct injury: by toxins such as endotoxins and leukotoxins and
enzymes such as hyluronidase and collagenase.
2. Indirect injury: include initiation of inflammatory response with excessive release
of the lysosomal content from polymorphonuclear leukocytes, actitation of
complement, (magnifies imflamatoty response), and the development of host
humoral and cell-mediated immune response (also magnify inflammatory
reaction and lead to tissue destruction.

32. Marked inflammatory
infiltrate of
polymorphonuclear leukocytes
lymphocytes
plasma cells
in the
connective tissue
that attached
to the tooth.
Collagen is lost also
Tissue destruction
is mediated by
bacterial substances
that pass through the
epithelial barrier and
cause either
direct
or
indirect injury.
Direct: by
Indirect : initiation of
inflammatory response
from
polymorphonuclear
leukocytes,
(magnifies inflammatoty response)
(also magnify
inflammatory reaction
and lead to tissue
destruction
such as endotoxins and leukotoxins
the lysosomal content
activation of complement
humoral
and
CMI response
toxins
as hyluronidase and collagenase Bac.
enzymes
and

34. Plaque is the origin of the bacteria so the disease continue to
progress unless the dental plaque is removed and the involved
tooth is kept plaque-free. If these measures are taken gingivitis
resolve completely and tissue return to normal. (Reversible)
(Reversible)
gingivitis resolve completely
If dental plaque is removed
hidden from body defenses
The causative
bacteria
remains out side
the gingival tissue
supra- and subgingival plaque
in the and

35. Gingivitis Healthy gingivae
- The gingivae are red and
- swollen, with rounded edges;
- bleeding gums and halitosis are common.
However, pain, discomfort and unpleasant taste are uncommon

36. Clinical presentation
- The gingivae are red and
- swollen, with rounded edges;
- bleeding gums and halitosis are common.
.
However, pain, discomfort and unpleasant taste are uncommon

37. Microbiology
In the initial stage, Gram-positive and facultative organisms
predominate, including streptococci.
In the early lesion, Actinomyces spp. increase together with proportions of
capnophilic species such as Capnocytophaga spp. and obligately
anaerobic Gram-negative bacteria. For example, in one study, in the
initial stage (of non-bleeding gingivitis) proportions of Actinomyces
israelii and A. naeslundii almost doubled. When the disease progresses
to the established lesion
In the established lesion, where bleeding is seen, the flora further
changes and levels of black-pigmented anaerobes such as
Porphyromonas gingivalis and Prevotella intermedia
increase quantitatively (e.g. 0.1-0.2% of total plaque flora), together with
spirochaetes.

38. Actinomyces spp
Capnocytophaga spp
Anaerobic Gram-negative bacteria
In the early lesion
For eg.
initial stage
in one study
proportions of
Actinomyces israelii
A. naeslundii
almost
doubled
non-bleeding gingivitis
1
the initial stage
Gram-positive organisms and
facultative organisms predominate, including
streptococci

39. established lesion
bleeding is seen
the flora further changes
levels of
black-pigmented
anaerobes
such as
Porphyromonas gingivalis
Prevotella intermedia
increase
quantitatively
e.g. 0.1-0.2% of
total plaque flora
spirochaetes
2

40. Treatment
Treatment is by thorough:
-removal of plaque and
-calculus deposits, all plaque-retentive factors, and the
-introduction of good oral hygiene.

41. Chronic marginal gingivitis may be present for up to 10 years
in some individuals before progressing to periodontitis.
This transition may be due to one or a combination of the following:
• selective overgrowth of one or more plaque species due to
impairment of the host defenses
• infection and proliferation of a newly arrived pathogen in the
gingival area
• activation of tissue-destructive immune processes.
Chronic
marginal gingivitis
present for up to
10 years
progressing to
periodontitis
The transition from gingivitis to periodontitis

42. 2.2 Chronic periodontitis (formerly adult periodontitis):
Chronic periodontitis is by far the most prevalent disease globally.
Morbidity
About 70-80% of all adults suffer from this universal disease,
and chronic periodontitis comprises 95% of all periodontal diseases.
Prevalence and severity increase with age.
periodontal diseases

43. Clinical presentation
All the following features:
• gross gingival inflammation, fibrosis and some shrinkage
• bleeding pockets of more than 3 mm
• tooth mobility and migration
• irregular alveolar bone loss around the teeth
• gingival recession
• halitosis and offensive taste
• usually little or no pain
• may or may not be associated with systemic disease.

44. Pathogenesis
The main processes that produce loss of attachment and
pocket formation are:
1. The apical spread of subgingival plaque causes the junctional
epithelium to separate from the tooth surface
(i.e. a new 'pocket' epithelium is created).
2. Inflammatory tissue reactions below the pocket epithelium
result in:
- destruction of the gingival connective tissue,
- periodontal membrane and
- alveolar bone.
3. Apical proliferation of the junctional epithelium results
in migration of the epithelial attachment.

45. 4. The rate of tissue destruction is not constant but episodic. A number
of patterns of disease activity can occur, ranging from :- - slowly
progressive destruction to
- brief bursts of episodic activity which may vary in intensity and
duration in different sites in the same mouth. This makes
microbiological sampling for disease activity extremely difficult.
5. More severe destruction in molar areas and in anterior segments.

46. Microbiology
The depth of the periodontal pocket creates a
highly anaerobic locale with a shift from neutral to basic pH
(7.4-7.8). The protein-rich fluid in the pocket encourages the
growth of anaerobes, which possess many .
The subgingival plaque has two distinct zones:
1- a zone of Gram-positive cocci and bacilli close to the tooth
surface, and
2- a zone of Gram-negative organisms next. In active pockets:
-Porphyromonas gingivalis, (G-ve coccobacilli. anaerobe)
-Actinobacillus actinomycetemcomitans,
-Prevotella intermedia and
-Fusobacterium nucleatum may be present.
Proteolytic enzymes
(G-ve bacilli. anaerobe)
(G-ve cigar-shape. anaerobe)
(G-ve bacilli. anaerobe)

47. The End