TMKARPISKI

ISSN: 2084-3577

PUBLISHER

Journal of Biology
and Earth Sciences

MEDICINE

REVIEW

Microbiology of chronic periodontitis

Anna K. Szkaradkiewicz1 , Tomasz M. Karpiski 2
1University

of Medical Sciences in Pozna, Department of Conservative Dentistry and Periodontology, Pozna, Poland
2University

of Medical Sciences in Pozna, Department of Medical Microbiology, Pozna, Poland

ABSTRACT

Chronic periodontitis is an oral infection that results into destruction involving the gums, cementum,
periodontium and alveolar process bone. The major etiology of periodontitis is bacterial plaque, which
harbors a variety of pathogenic bacteria known as periopathogens or periodontopathogens. The most
important periopathogens are anaerobic bacteria: Porphyromonas gingivalis, Prevotella intermedia,
Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum and the relative anaerobe
Aggregatibacter actinomycetemcomitans. Periopathogens can affect the immune system cells,
stimulating them to produce inflammatory mediators. The development of inflammatory lesions in
chronic periodontitis may restrict oral lactobacilli.

Key words: Chronic periodontitis; Periopathogens;

Aggregatibacter actinomycetemcomitans.

Porphyromonas gingivalis; Prevotella intermedia;

J Biol Earth Sci 201 3; 3(1 ): M1 4-M20

Corresponding author:

M.D., Ph.D. Anna K. Szkaradkiewicz

University of Medical Sciences in Pozna
Department of Conservative Dentistry and
Periodontology
Bukowska 70, str., 60-81 2 Pozna, Poland
e-mail: aniaszk@op.pl
Original Submission: 21 January 201 3; Revised Submission: 1 7 February 201 3; Accepted: 1 9 February 201 3
Copyright 201 3 Author(s). Journal of Biology and Earth Sciences 201 3 Tomasz M. Karpiski. This is an open-access article
distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction
in any medium, provided the original work is properly cited.

http://www.journals.tmkarpinski.com/index.php/jbes or http://jbes.strefa.pl
e-mail: jbes@interia.eu
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Szkaradkiewicz & Karpiski Microbiology of chronic periodontitis

INTRODUCTION
Chronic periodontitis is an oral infection that
results into destruction involving the gums,
cementum, periodontium and alveolar process
bone. Chronic periodontitis is characterized by
moderate or severe clinical course, and can occur
in different age groups, but most commonly in
adults. The incidence and severity of periodontitis
increase with age [1 ]. The main clinical features of
chronic periodontitis are: loss of connective tissue
attachment, alveolar bone loss, the presence of
periodontal pockets and gingival inflammation.
Additional symptoms of this disease are: the
occurrence of supra- and subgingival calculus,
swelling or gum recession, bleeding, furcation
exposure, mobility of the teeth, a bad taste, and
halitosis [2-5].
Severity of periodontitis is determined on the basis
of the following criteria:
1 ) in moderate periodontitis:
- Gingival Index GI > 0
- Sulcus Bleeding Index SBI > 0
- Clinical Attachment Loss CAL: 3-4 mm
- at least 2 teeth with depth of pockets PPD > 4 mm
2) in severe periodontitis:
- Gingival Index GI > 0
- Sulcus Bleeding Index SBI > 0
- Clinical Attachment Loss CAL > 5 mm
- pockets with a depth > 5 mm [6-8].

REVIEW
The main etiological agent of chronic
periodontitis is bacterial plaque. It may cause
damage to host tissues directly or via proinflammatory mediators. Plaque bacteria have
harmful effects on fibroblasts, epithelial and
endothelial cells and extracellular matrix
components. They can also affect the immune
system cells, stimulating them to produce
inflammatory mediators. Patients with periodontitis
display higher concentrations of various cytokines
including TNF-a, IL-1 b, IL-6, IL-1 7, IL-23, and matrix
metalloproteinase (MMP)-8 and MMP-9 in their
GCF. Consequently, analysis of GCF samples may
provide valuable information regarding the
pathophysiologic processes associated with
periodontitis [9-1 8].
The major etiology of periodontitis is bacterial
plaque, which harbors a variety of pathogenic

bacteria known
as periopathogens or
periodontopathogens. The most important
periopathogens
are
anaerobic
bacteria:
Porphyromonas gingivalis, Prevotella intermedia,
Tannerella
forsythia,
Treponema
denticola,
Fusobacterium nucleatum and the relative
anaerobe Aggregatibacter actinomycetemcomitans.
These organisms express a number of potential
virulence factors and induce host inflammatory
mediators, eventually leading to connective tissue
breakdown and alveolar bone resorption [1 9-23].
In a recent studies, using 1 6S ribosomal cloning
and sequencing, it was demonstrated that in
periodontitis may occur many bacterial genera both
culturable and unculturable. Associated with
periodontitis are several genera, many of them
uncultivated, including Peptostreptococcus and
Filifactor. In periodontitis are elevated amounts of
the genera Megasphaera and Desulfobulbus, and
several species or phylotypes of Campylobacter,
Selenomonas, Deferribacteres, Dialister, Catonella,
Tannerella, Streptococcus, Atopobium, Eubacterium
and Treponema [24-26].
Currently, based on the research of Socransky
team stands out specific groups of bacteria (called
complexes) with particular importance in the
pathogenesis of periodontitis. Porphyromonas
gingivalis creates with the species: Tannerella
forsythia and Treponema denticola so called red
complex, which appears to be associated with
disease symptoms in adult periodontitis. The
second important group of bacteria forms orange
complex, comprising 1 3 species, including
Fusobacterium
nucleatum
and Prevotella
intermedia. Orange complex bacteria are an
essential link in allowing the colonization of
periodontal tissue by a red complex. A separate
group of bacteria forms green complex, which
includes species: Capnocytophaga sputigena, C.
gingivalis, and Eikenella corrodens. These species
are also associated with disease symptoms in adult
periodontitis, but with a milder clinical course in
contrast to the red complex [27-29]. There is cooccurrence of green group and yellow complex,
mainly consisting of the oral streptococci, group
"Mitis" (S. mitis, S. oralis, S. gordonii, S. sanguinis)
and connected to this complex Parvimonas micra
belonging to dominant periopathogens [30].
Porphyromonas gingivalis
Porphyromonas gingivalis

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(Fig. 1 ) is a clinically

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Szkaradkiewicz & Karpiski Microbiology of chronic periodontitis

reduced binding of P. gingivalis to PMN and

inhibited phagocytosis. Lipopolysaccharide (LPS)
present in the cell wall plays the role of the antigen
and activates cytokines [40, 41 ].

Fig. 1. Porphyromonas gingivalis

in Gram staining.

important species observed as more than 40%

of patients with periodontitis. [31 ] Strains of
P. gingivalis have fimbriae with numerous adhesins
which ensure adherence of the bacteria to the
periodontal tissues and allow co-aggregation with
other species, and also induce pro-inflammatory
cytokine response.
Different proteinases,
particularly cysteine proteinases (gingipains), are
considered the prominent virulence factor of the
pathogen. These proteinases are responsible for
the high proteolytic activity of the bacterium. On the
basis of substrate specificity gingipains were
divided into arginine-specific called arg-gingipains
(RgpA and RgpB) and lysine-specific KGP, known
as lys-gingipain [32-35]. Gingipains have a strong
influence on the immune system by regulating the
activity of cytokines [36, 37].
P. gingivalis strongly induces the production of
pro-inflammatory cytokines IL-1 , IL-6, IL-8 and TNFalpha by neutrophils, monocytes and macrophages.
It has been shown that arg-gingipain destroys C3
related with opsonization, so that P. gingivalis is
resistant to phagocytosis by neutrophils. In turn, lysgingipain degrades C5, releasing C5a component
and therefore stimulates inflammation. Proteases
damage also the extracellular matrix proteins
[36, 38, 39]. The fermentation end products of
P. gingivalis, such as acetic acid, propionic acid and
butyric acid, and volatile sulfur compounds
produced in large quantities can affect cytotoxic the
host cells. Most P. gingivalis strains are able to
produce capsular polysaccharides. This results in

Fig. 2. Prevotella intermedia

in Gram staining.

Prevotella intermedia
Prevotella intermedia

(Fig. 2) is characterized by
hemolytic activity. Proteases produced by Prevotella
are capable of destroying a number of proteins
including collagen and fibronectin. Has been shown
that proteases possess trypsin-like properties
characteristic for cysteine proteinases and are
capable of antibodies damaging, in particular IgG
and fibrinogen, what reduces the effectiveness of
the host immune and inflammatory defense [42, 43].
LPS produced by Prevotella may participate in the
periodontal destruction and alveolar bone loss
through the osteoclastogenesis stimulation, as well
as reduce bone formation [44].
Aggregatibacter actinomycetemcomitans
Aggregatibacter actinomycetemcomitans (Fig.

3)
is now considered to be the dominant etiologic
factor in the early beginning periodontal disease,
and may be associated with the red complex [45].
Strains of this species are relatively anaerobic,
capnophilic bacteria with microcapsule and bunch
of fimbriae (BF) with the ability to adhere to
the periodontal tissues and autoaggregation.
Strains of A. actinomycetemcomitans produce
leukotoxin (LtxA), which is cytotoxic to neutrophils

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Szkaradkiewicz & Karpiski Microbiology of chronic periodontitis

Treponema denticola
Strains of the Treponema denticola

species
belong to the spiral bacteria, characterized by an
active movement. [54] These spirochetes have the
ability to migrate and penetrate into undamaged
periodontal tissue. At the same time, an important
virulence factors are produced enzymes: trypsin,
chymotrypsin, esterase and alkaline phosphatase,
allowing synergistic effects of T. denticola strains
with the other two species of red complex [55, 56].
Fusobacterium nucleatum
Fusobacterium nucleatum

Fig. 3. Aggregatibacter actinomycetemcomitans

staining.

in Gram

and monocytes/ macrophages. LtxA toxin damages

cell membranes and by apoptosis causes lysis of
polymorpho-nuclear leukocytes, monocytes and T
cells [46-48]. The second major toxin of A.
actinomycetemcomitans is CDT toxin (cytolethal
distending toxin) which, by blocking the cell cycle in
G2 phase in T cells induces apoptosis in these
cells. Cells infected by A. actinomycetemcomitans
undergo apoptosis, which may be the cause of the
development of periodontal disease [49, 50].
Lipopolysaccharide (LPS) of A. actinomycetem
comitans can induce tolerant response in
macrophages which secrete TNF-alpha, IL-1 beta
and methylproteinase-9 enzyme that degrades
tissue. This process may play an important role in
the modulation of the host inflammatory response
and progression of periodontitis [51 ].
Tannerella forsythia
Tannerella forsythia

have over the outer

membrane an additional protective structure - S
surface layer formed by regularly arranged two
protein subunits. Experimental studies show that
the layer S of T. forsythia strains may provide their
adherence to host cells, and invasiveness. At the
same time, an important factors for their
pathogenicity are produced enzymes: trypsin-like
protease (PrtH), and glycosidases. The end
products of the fermentation of T. forsythia, such as
acetic acid, propionic acid and butyric acid can
affect cytotoxic on host cells [52, 53].

produces DNase, an
enzyme that degrades DNA. F. nucleatum
generates also butyric acid, metabolic end products,
and irritates the fibroblast of the gum, leading to
necrotic lesions, abscesses and periodontal disease
[57]. By scavenging oxygen and oxidative free
radicals from dental plaque, F. nucleatum helps to
maintain and support the conditions for major
anaerobic periodontal pathogens [58].
Recently it has been demonstrated that different
strains of Lactobacillus spp. (including L. reuteri,
L. acidophilus, L. brevis) may be of importance in
prevention against progress of chronic periodontitis
[59-65]. Oral lactobacilli may restrict development of
inflammatory lesions in chronic periodontitis. It has
been shown that H 2O 2-producing oral lactobacilli
may prevent against progress of chronic
periodontitis, most probably restricting secretory
activity of Th1 7 cells and growth of
periodontopathogens [1 6].

CONCLUSIONS
Periodontitis as a chronic oral infection can lead
to rapid destruction of periodontal tissues. On the
development of the disease have an impact many
bacteria, in particular anaerobic bacteria which act
on fibroblasts, epithelial and endothelial cells and
extracellular matrix components. They can also
affect the immune cells, stimulating them to produce
inflammatory mediators.

TRANSPARENCY DECLARATION
The authors declare no conflicts of interest.

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