MICROBIOLOGY OF
PERIODONTAL DISEASES
Dr. Saleem Shaikh
TERMINOLOGY
Dental Plaque
 It is defined clinically as structured , resilient ,yellow grayish
substance that adheres tenaciously to the intra-oral hard surfaces ,
including removable and fixed restorations.
 It is primarily composed of bacteria in a matrix of salivary
 glycoproteins and extracellular polysaccharides.
Materia alba
 Refers to soft accumulations of bacteria and tissue cells that lack the
organized structure of dental plaque.
Calculus
 Is a hard deposit that forms by mineralization of dental plaque
INTRODUCTION
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The term periodontal diseases embraces a number of conditions in which
the supporting tissues of the teeth are compromised.
In periodontal diseases the junctional epithelium at the base of the gingival
crevice migrates down the root of the tooth to form a periodontal pocket.
This is partly due to the direct action by the microorganisms or may be
indirectly due to the side effects of de-regulated inflammatory response due
to plaque accumulation.
The ecology of the gingival sulcus is different from the other areas of the
oral cavity, it is more anareobic. In disease [ when the sulcus is converted to
pocket] the flow of GCF increases many fold this also results in increase the
amount of proteins and glycoproteins that serve as nutrients for bacterial
metabolism.
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Unlike dental caries many of the bacteria associated with periodontal
diseases are asaccharolytic and proteolytic. This proteolysis increases the
pH of the pocket which inturn increases the growth and enzyme activity of
some of the pathogens [porphyromonas gingivalis].
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While attempting to determine the microflora of a periodontal pocket, the
sample should be taken from the base of the pocket near the advancing
front of the lesion.
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The healthy gingival crevice contains large proportions of gram positive
facultative anaerobes such as streptococcus and actinomyces species, with
some anaerobes [prevotella melaninogenica]. A number of spirochaetes like
Treponema vincentii, T. denticola, T maltophilum are also seen
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Koch postulates
Must be routinely isolated from diseased individuals
Must be grown in pure culture
Must produce a similar disease when inoculated into susceptible laboratory
animals .
Must be recovered from lesions in a diseased laboratory animal
Sigmund socransky’s crieria of identifying periodontal pathogens:
Must be associated with disease , as evident by increases in number of
organisms at diseased sites.
Must be eliminated or decreased in sites that demonstrate clinical resolution
of disease with treatment.
Must demonstrate host response, in the form of an alteration in the host
Cellular or humoural response.
Must be capable of causing a disease in experimental animal models
Must demonstrate virulence factors responsible for enabling the microrganism
to cause destruction of periodontal tissues.
GINGIVITIS
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It is usually a non specific reversible inflammatory response to dental
plaque resulting from proliferation of normal gingival sulcus microflora.
No single of group of microorganisms have been found to predominate in
gingivitis and many studies have reported a diverse group of microbes.
50% gram +ve and 50% gram –ve organisms
S.sanguis, S.mitis, S.intermedius, S.oralis, A.viscosus A.naesulundi are most
frequently seen.
Not all forms of gingivitis progress to periodontitis but it is accepted that
gingivitis must precede periodontitis.
Environmental conditions which develop during gingivitis [bleeding and
increased flow of GCF] may favour the growth of species implicated in
periodontitis.
CHRONIC PERIODONTITIS
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This is the most common form of periodontitis affecting the general
population.
This can be localized or generalized
The cultivable microflora is diverse and is composed of large number of
obligatory anaerobic gram negative rod and filament shaped bacteria which
are proteolytic
Many of the bacteria from deep pockets are motile – camphylobacter
rectus, selemonas and treponema species.
Many of the studies have identified five groups of bacteria in the pockets
The red group is found in the deep pockets
The red is preceded by the orange groups.
The members of the yellow green and purple group are seen in more healthy
tissues.
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S.mitis
S.oralis
S.sanguis
Streptococcus sps
S.gorondi,
S.intermedius
CLOSELY ASSOCIATED
V.parvula
COMPLEXES IN THE ORAL
A.odontolyticus
CAVITY
C.rectus
P.intermedia
P.nigrescens
P.micros
F.nucleatum
E.nodatum
P.gingivalis
T.forsythus
T.denticola
C.showae
E.corrodens
Capnocytophaga sps
A.actinomycetocomitans
LATE COLONIZERS
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Chronic periodontitis appears to be result from the activity of mixtures of
interacting bacteria and therefore is said to be of polymicrobial etiology.
The ecology of the microorganisms also undergo change to enable lowlevels
of microorganisms to reach clinically significant proportions.
This may be due to host inflammatory response and increased flow of GCF
which favors the growth of proteolytic bacteria.
NECTROIZING PERIODONTAL DISEASES
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Necrotizing ulcerative gingivitis [NUG] and necrotizing ulcerative
periodontitis [NUP] are included in this category.
NUG is also called as vincent’s disease, trench mouth or ANUG. This is a
true infection unlike gingivitis.
It is caused by a combination of spirochaetes and fusiform bacteria.
Spirochaetes are in very high number [treponema species]; the
fusobacterium species are low in number and prevotella intermedia are also
in high proportions.
Metronidazole is effective in these cases.
NUP is a painful condition seen in HIV positive patients.
Bulleida extructa, dialster, fusobacterium, selenomonas are seen
Some of the more common organisms seen in periodontal lesions of HIV
negative patients [ P. gingivalis ] are not seen.
AGGRESSIVE PERIODONTITIS
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Localized juveline periodontitis; generalized juveline periodontitis; early
onset periodontitis.
Two forms of the disease localized and generalized.
In localized there is a distinct pattern of bone loss in first permanent molars
and incisor teeth. In generalized more teeth are affected
Majority of the patients have functional abnormalities of neutrophils –
reduced chemotaxsis and phagocytosis.
Presence of relatively high number of Aggregatibacter (actinobacillus)
actinomycetecomitans. The microflora of the plaque in these patients is
relatively sparse.
In contrast to other forms of periodontal disease this occurs due to activity
of a specific microflora.
Tetracycline is effective in eliminating A. actinomycetemcomitans from the
pockets.
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PREGNANCY GINGIVITIS: the exaggerated form of gingivitis is possibly due to
the increased level of steroid hormones in GCF. An increased proportion of a
black pigmented anaerobe P. intermedia is seen.
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ACUTE HERPETIC GINGIVITIS: although most of the cases of gingivitis are
caused by bacteria ocassionally viral causes may be seen. The commonest is
caused by herpes simplex virus – type 1. Usually seen in children and is very
painful.
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Diabetes mellitus associated gingivitis: the relation is bi-directional. Diabetes
stimulates the release of pro inflammatory cytokines that have direct effect
on periodontal tissues. Periodontal pathogens also increase the release of
proinflammatory cytokines which will increase the insulin resistance
Capnocytophaga and P.gingivalis are seen in higher proportions.