MICROBIOLOGY OF

PERIODONTAL DISEASES

Dr Hala Elsabagh
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
■ 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 Gingival Crevicular Fluid GCF increases
many fold this also results in increase the amount of proteins and
glycoproteins that serve as nutrients for bacterial metabolism.
■ 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].

■ 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.

■ 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
■ Koch postulates
1. Must be routinely isolated from diseased individuals
2. Must be grown in pure culture
3. Must produce a similar disease when inoculated into susceptible
laboratory animals .
4. Must be recovered from lesions in a diseased laboratory animal

■ Sigmund socransky’s crieria of identifying periodontal pathogens:

1. Must be associated with disease , as evident by increases in
number of organisms at diseased sites.
2. Must be eliminated or decreased in sites that demonstrate
clinical resolution of disease with treatment.
3. Must demonstrate host response, in the form of an alteration in
the host Cellular or humoural response.
4. Must be capable of causing a disease in experimental animal
models
5. Must demonstrate virulence factors responsible for enabling the
microrganism to cause destruction of periodontal tissues.
 Gingivitis
■ It is usually a non specific reversible inflammatory response
to dental plaque resulting from proliferation of normal
gingival sulcus microflora.
■ No single 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
■ 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
1. The red group is found in the deep pockets
2. The red is preceded by the orange groups.
3. The members of the yellow green and purple group are seen
in more healthy tissues.
E CLOSELY ASSOCIATED
V.parvula
A COMPLEXES IN THE ORAL
A.odontolyticus
R CAVITY
S.mitis
L
S.oralis
Y S.sanguis
C.rectus
C P.intermedia
O Streptococcus sps P.nigrescens P.gingivalis
P.micros E.nodatum
L S.gorondi, T.forsythus
S.intermedius F.nucleatum
O T.denticola
N C.showae
I
Z
E.corrodens LATE COLONIZERS
E
Capnocytophaga sps
R
A.actinomycetocomitans
S
■ 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 low levels 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.
Necrotizing periodontal diseases
■ 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 in HIV
positive patients.
■ Some of the more common organisms [ P. gingivalis ] seen in periodontal
lesions of HIV negative patients.
■ Necrotizing ulcerative gingivitis [NUG]

■ Necrotizing ulcerative periodontitis [NUP]

Aggressive periodontitis
■ 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.
■ 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 Prevotella intermedia [P.
intermedia] is seen.

■ 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.

■ 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.
Summary
■ In general, the putative periodontal pathogens are non-competitive
and remain at low levels; such levels would not be clinically
significant.
■ If plaque is allowed to accumulate, then the host mounts an
inflammatory response. The flow of GCF is increased, and this
introduces components of the host defences but also complex host
molecules (e.g. transferrin, haemoglobin, etc.) that can be
catabolized and used as a nutrient source by the proteolytic Gram
negative anaerobes that predominate in advanced periodontal
lesions.
■ This metabolism leads to an increase in local pH and more
anaerobic. These changes in the local environment will up-regulate
some of the virulence factors associated with these putative
pathogens (e.g. protease activity by P. gingivalis), and favour their
growth at the expense of the species associated with gingival health
(i.e. increase the competitiveness of the potential pathogens).