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3/8/2015 Microbiology of periodontal diseases
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Microbiology of periodontal diseases
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1) Introduction:
Bacterial biofilm in the gingival sulcus around tooth is the most important cause of periodontal
diseases. Bacterial biofilm is defined as a structured community of bacterial cells enclosed in a self
produced polymeric matrix 1 . Although more than 500 different species are present in subgingival
microbiota 2 only very few of these species are actually involved in the initiation and progression of
the periodontal disease process. Although recent studies have suggested a role for environmental 3,
behavioral 45, and genetic 6 risk factors in periodontal disease progression, most, if not all, forms of
periodontitis should be viewed as infectious diseases.
2) Historical aspect:
As already described during discussion of plaque as biofilm, the period from 1880 to 1930 was called
the golden age of microbiology 7. Using the techniques available at that time (wet mounts or stained
smear microscopy), scientists identified four different groups of potential etiologic agents for
periodontal diseases. Amoebae, spirochetes, fusiforms and streptococci were isolated from patients
with periodontal diseases and, therefore, suggested as possible etiologies. Researchers suggested a
specific plaque hypothesis based upon these findings.
Studies conducted between 1930 to 1970 failed to identify a specific organism as the etiologic agent
of periodontal diseases. Nonspecific plaque hypothesis was proposed according to which gross
accumulation of dental plaque would be necessary and sufficient to cause periodontitis.
With the advancements in the field of microbiology and immunology numerous studies have
concluded a putative pathogenic role of a dozen bacteria, mainly Gramnegative species. These
species include Actinobacillus actinomicetemcomitans, Bacteroides forsythus, Porphyromonas
gingivalis, Prevotella intermedia, Campylobacter rectus, Fusobacterium nucleatum, and Treponema
denticola. Virulent factors produced by these microorganisms have been identified and their role in
periodontal destruction is well established. These findings led to return to specificity in microbial
etiology of periodontal diseases.
3) Microbiology in periodontal health:
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3/8/2015 Microbiology of periodontal diseases
Various microorganisms are involved in pathogenesis of periodontal diseases. But along with them
many microorganisms are beneficial also as they promote periodontal health known as commensals.
So, the presence of pathogens and absence of commensal bacterial species in periodontal arena
initiates the periodontal disease process. One of the most important characteristics of commensal
bacteria is their ability to prevent the host immune system from being activated. One proposed
mechanism is the development of tolerance 8, which includes the generation of suppressive T
lymphocytes and the presence of inhibitory cytokines, mainly transforming growth factorβ and
interleukin (IL)10.
Most of the microorganisms in periodontal health exist in a symbiotic capacity, maintaining
relationships with the host that are based on mutual benefits 9. Microorganisms which are present in
healthy oral cavity include: Streptococcus, Actinomyces, Veillonella, Fusobacterium, Porphromonas,
Prevotella, Treponema, Nisseria, Haemophilis, Eubacteria, Lactobacterium, Capnocytophaga,
Eikenella, Leptotrichia, Peptostreptococcus, Staphylococcus, and Propionibacterium 1011. These
bacteria contribute to periodontal health probably by following mechanisms 12 ,
Occupying niches passively, thereby preventing pathogens to colonise.
Preventing growth of pathogens.
Preventing pathogens from producing virulent factors.
By degrading virulence factors produced by pathogens.
4) Microbiology in periodontal diseases:
Many microorganisms are presently identified as periodontal pathogens, but what are criteria to
classify an organism as periodontal pathogen? We must understand Socransky’s postulates first before
read about periodontal pathogens.
Socransky’s postulates:
Periodontal diseases are not caused by single organism; the cornerstone of Koch’s postulates. Indeed,
these disease entities are the result of mixed infections. To better identify periodontopathic bacterial
candidates, Koch’s postulates were replaced with Socransky’s postulates (1992) 13. These include the
following:
1. The organism must be found in relatively high numbers in proximity to the periodontal lesion;
2. The organism must be absent, or present in much smaller numbers in periodontally healthy
subjects or in subjects with other forms of periodontal disease;
3. The organism must have high levels of serum, salivary and gingival crevicular fluid antibody
developed against it in periodontally diseased subjects;
4. The organism must be found to produce virulence factors in vitro which can be correlated with
clinical histopathology;
5. The organism must mimic similar pathogenic properties in an appropriate animal model;
6. Clinical improvement following treatment must eliminate the putative pathogen from the
periodontal lesion.
Pathogens implicated for periodontal breakdown:
A. actinomycetemcomitans.
T. forsythus.
E. corrodens.
F. nucleatum.
P. micros.
P. gingivalis.
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3/8/2015 Microbiology of periodontal diseases
P. intermedia.
C. rectus.
Selenomonas sp.
Eubacterium sp.
Spirochetes
5) Subgingival microbial complexes:
A landmark study done by Socransky et al. (1998) 14 examined over 13,000 subgingival plaque
samples from 185 adult subjects and used DNA hybridization methodology and community ordination
techniques to demonstrate the presence of specific microbial groups within dental plaque. The
presence and levels of 40 subgingival taxa were determined in plaque samples using whole genomic
DNA probes and checkerboard DNADNA hybridization.
1st complex (Red complex) – Bacteroides forsythus (presently named as Tannerella
forsythia), Porphvromonas gingivalis and Treponema denticola.
3rd complex (Yellow complex) – Streptococcus sanguis. S. oralis, S. mitis, S. gordonii and S.
intermedius.
4th complex (Green complex) Campylobacter concisus, Eikenella corrodens and Actinobacillus
actinomycetemcomitans serotype a.
5th complex (purple complex) – Veillonella parvula and Actitwmyces odontotylicus.
A. actinotnycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2
(A. viscosus) were outliers with little relation to each other and the 5 major complexes.
Out of these groups of species the actinomyces species, yellow, green and purple complexes are early
colonizers of the tooth surface whose growth usually precedes the multiplication of the predominantly
gramnegative orange and red complexes. The remaining two complexes i.e. orange and red
complexes are comprised of the species thought to be the major etiologic agents of periodontal
diseases.
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3/8/2015 Microbiology of periodontal diseases
6) Virulence of periodontal pathogens:
Virulence provides a quantitative measure of the pathogenicity or the likelihood of causing disease.
Virulence factors refer to the properties (i.e., gene products) that enable a microorganism to establish
itself on or within a host of a particular species and enhance its potential to cause disease. Virulence
factors help bacteria to (1) invade the host, (2) cause disease, and (3) evade host defenses. The
following are types of virulence factors:
Adherence Factors: Colonization of bacteria on mucosal sites is facilitated by pili (fimbriae) which
help them to adhere to cells.
Invasion Factors: Surface components that allow the bacterium to invade host cells can be encoded
on plasmids, but more often are on the chromosome. Hyaluronidase, lecithinase, and phospholipase
etc.
Capsules: Many bacteria are surrounded by capsules that protect them from opsonization and
phagocytosis.
Endotoxins: These are lipopolysaccharide endotoxins produced by Gramnegative bacteria that cause
fever, changes in blood pressure, inflammation, lethal shock, and many other toxic events.
Exotoxins: Exotoxins include several types of protein toxins and enzymes produced and/or secreted
from pathogenic bacteria. Major categories include cytotoxins, neurotoxins, and enterotoxins.
The attachment of bacteria to dental pellicle exhibits a great deal of specificity and appears to involve
specific receptors on the bacterial and pellicle surfaces. Plaque accumulation may be mediated by
bacterial extracellular polysaccharides, salivary components as well as direct celltocell binding.
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3/8/2015 Microbiology of periodontal diseases
Salivary components play a dual role in plaque formation. They can mediate bacterial attachment to
the pellicle or plaque periphery, but by binding to unattached bacteria they can also diminish the
attachment of such bacteria. As the plaque matures, bacterial coaggregation can be seen.
Coaggregationprevalent among bacteria isolated from the human oral cavity and was first reported by
Gibbons and Nygaard in 1970 15. For Adherence, Colonization, and Growth of microorganisms in
dental plaque please read “Plaque as Biofilm and ecological plaque hypothesis.”
Virulent factors produced by various periodontal pathogens and their actions
Adhesion/ Virulent
Microorganism Actions
Colonization factors
Collagenases Disintegration of collegen
LPS Potent stimulator of IL1, PGE2 and TNFα
Proteases Cleavage of Ig’s.
Host cell cytotoxicity
Ammonia
Host cell cytotoxicity
Indole
Host cell cytotoxicity
Phospholipase
C (PLC) Directly or indirectly damages tissue by
hydrolysis of membrane phospholipids
H2S and
methyl Cytotoxic effects that is primarily due to
mercaptan inhibition of cytochrome oxidases.
7) Interactions between various microorganisms:
The behaviour of bacteria is different in a biofilm as compared to planktonic form. Streptococcus
gordonii assists in minimizing dental plaque due to its production of hydrogen peroxide, which can
kill many oral bacteria. Recent studies have demonstrated that S. gordonii and Actinomyces
naeslundii, two bacterial species that are highly represented in early oral biofilms, in coaggregate
cultures A. naeslundii allowed S. gordonii to grow in the absence of arginine and removed hydrogen
peroxide, decreasing protein oxidation in S. gordonii. Conversely, hydrogen peroxide produced by S.
gordonii inhibited growth of A. Naeslundii 16.
Fusobacterium nucleatum can aggregate with a large range of bacterial species and can bind to host
tissues and immunoglobulin A, allowing F. nucleatum to invade epithelial cells and participate in
biofilm formation 17. That is why Fusobacterium nucleatum is often called as nucleus of plaque
development. Streptococcus, Actinomyces, and Lactobacillus generate an acidic pH, thus inhibiting
growth of a variety of bacterial species 18.
8) Microorganisms implicated for various periodontal diseases:
Specific microorganisms have been implicated for various periodontal conditions by various studies.
These genera include, but are not limited to, Treponema, Bacteroides, Porphyromonas, Prevotella,
Capnocytophaga, Peptostreptococcus, Fusobacterium, Actinobacillus, and Eikenella. For example,
Porphyromonas gingivalis has been implicated in chronic adult periodontitis and severe adult
periodontitis19 Actinobacillus actinomycetemcomitansin localized aggressive periodontitis 2021, and
Prevotella intermedius and Treponema denticola (intermediatesized oral treponemes) in acute
necrotizing ulcerative gingivitis 2223 in juvenile diabetes cases Capnocytophaga spp. appear to play
an important role 24. Along with these Wolinella recta, Eikenella corrodens, andf B.forsythus also
play a major role in the progression of periodontal disease 2528 .
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3/8/2015 Microbiology of periodontal diseases
Microbiology of various periodontal conditions2930
Chronic
Periodontal Health Gingivitis Aggressive periodontitis
periodontitis
9) Conclusion:
To understand the microbiology of periodontal health and disease various technical tools are being
developed for facilitating sequencing of microbial communities and data analysis. The microbiology
of periodontal health and diseases is complex and a lot of research at molecular level is required to
understand the etiopathogenesis of periodontal diseases.
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Clonal types in pathogenesis of periodontal diseases:
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3/8/2015 Microbiology of periodontal diseases
The first step in the pathogenesis of periodontal disease is the adherence of bacteria to
periodontal tissue. Various clonal types of microorganisms have been implicated for their
pathogenesis, for example the role of bacterial fimbriae of Porphyromonas
gingivalis. Amano and coworkers have reported that both diseaseassociated and non disease
associated genotypes exist in P. gingivalis, suggesting that there is a significant predominance
of P. gingivalis with type II fimA in periodontitis patients 31. Highly leukotoxic clones of
Actinobacillus actinomycetemcomitans have been identified 32 Other studies have
demonstrated the production of leukotoxin from A. actinomycetemcomitans is regulated in part
by environmental factors, such as atmosphere, nutrition supply, and pH 3335. The optimal pH
for the growth of A. actinomycetemcomitans is reported to be in the range of 7.0–8.0 36. These
findings suggest that particular clonal types of a bacterial species are involved in pathogenesis
of disease.
Renaming and Reclassification of periodontal pathogens 3740:
Renaming and re classification of these bacteria has been done due to advances in bacterial
identification techniques.
Previous Classification New Classification Reference
References:
Please contact author for references
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