Periodontal microbiology

Periodontal diseases are the infections resulting from the microorganisms that colonize on the tooth surface. About 500 different microbial species are known to be capable of colonizing in the oral cavity. But out of these only a few organisms are responsible for the periodontal distruction.

Need for understanding microbial etiology of periodontal diseases:

  • For understanding etiopathogenesis of periodontal diseases.
  • For the prevention of periodontal diseases.
  • For the selection of appropriate treatment approach.

Difficulties in studying periodontal microbiology:

Periodontal microbiology is difficult to study because of multiple reasons. Haffajee and Socransky have enumerated the reasons for the difficulties in pinpointing specific periodontal pathogens:

Difficulties related to microbial sampling and culturing:

  • Obtaining a sample from a periodontal pocket
  • Some organisms are difficult to cultivate
  • Periodontal pocket contains a large number of pathogens
  • Opportunistic species are also present in the periodontal pockets along with the pathogens.

Difficulties related to the nature of periodontal diseases themselves:

  • periodontal disease is a collection of different diseases and is not just a single disease.
  • Periodontal diseases have periods of disease activity and inactivity .
  • Variation in disease activity in different sites within an individual.
  • Variation in individual host response.

Requirements for a microorganism to be a dental pathogen:

To cause disease, a pathogen must possess some characteristic features. Initially they were identified by Kotch (kown as kotch’s postulates). Because multiple bacteria are involved in periodontal infections, Socransky proposed following postulates for a microorganism to be a periodontal pathogen,

Socransky’s postulates:

  • The organism must be present in higher numbers in the disease active sites as compared their number in the disease inactive sites.
  • The organism should possess virulence factors relevant to the periodontal disease.
  • The organism should initiate a cellular or humoral immune response.
  • The organism must mimic the similar pathogenic properties in an appropriate animal model.
  • The progression of the disease should arrest and clinical improvement should be seen after the elimination of the organism.

Mechanisms of pathogenicity:

a) By attaching to one or more of the available host surfaces. This is done by following mechanisms:

  • Adhesins: Various studies demonstrated the specificity of bacterial adhesions. There are one or more specific receptor molecules present on the host cell to which specific adhesion molecules of the bacteria may get attached. Receptors on the tissue surface mainly includes galactosyl residues, proline rich proteins, sialic acid residues, TYPE I or IV collagen. Adhesions on the surface of subgingival bacterial species mainly includes fimbriae, cell associated proteins. 
  • Coaggrigation: Coaggrigation is the phenomenon of attachment of bacteria to another bacteria which are attached to the host surfaces. Thus in coaggrigation bacteria doesnot attach directly to the host surface. The process of attachment of different bacterial species shows specificity and are mediated by specific receptor-adhesin interation. These interactions are mainly based on the attachment of specific protein on the surface of one species to a specific carbohydrate on the surface of other. Thus, this interaction is lecithin-like. Non-coaggregating bacterial species may show aggregation due to the cellular constituents of a third species

b) By multiplying:

Subgingival microorganisms mainly receives their nutrition from three sources:

  1. Diet
  2. Host
  3. Other bacterial species in that area.

c) By producing factors that damage the host tissue:

This damage to the host tissue con be done either directly by these factors or these factors lead to the host tissue damaging itself.

d) By overcoming the defence mechanism of the host. 

e) By competing successfully with the other species in that habitat. 

Microorganisms associated with periodontal health:

Not all the bacterial species present in the host are damaging to the periodontium. Infact, some species shows negative effect on the progression of the disease by:

Preventing the colonization of pathogenic microorganisms.

Degrading the virulence factors produced by these pathogenic bacteria.

Micro-organisms beneficial to the periodontal health are as following:






Micro-organisms associated with periodontal diseases (periodontal pathogens):

Actinobacillus actinomycetemcomitans:

  • They are gram –ve bacteria.
  • They are small, non-motile, rod shaped.
  • Colonies: on blood agar plates, it forms small, convex colonies with a star shaped center.
  • They show very strong association with destructive periodontal diseases.
  • They are found in higher numbers in:
  1. Localized juvenile periodontitis.
  2. Pre-pubertal or adolescent periodontal disease.
  3. Some adult periodontal lesions.
  •  Their number is very negligible in
      1. Healthy periodontium.
      2. Gingivitis.
      3. Edentulous sites.
  • Virulence factors found in A. actinomycetemcomitans include: Leukotoxin, endotoxin, collagenase, epitheliotoxin, bone resorption inducing factor, fibroblast inhibitory factor.
  • Modes of action of virulence factors:

Modification of neutrophil function, induction of cytokine production from macrophages, degradation of immunoglobulins, induces apoptotic cell death.

  • Host response to these changes:

Antibodies are elevated in serum or saliva of patients suffering from localized juvenile periodontitis or chronic periodontitis.

  • Local antibody titers at the LJP sites is also elevated.
  • Their elimination is indicative of successful periodontal therapy.
  • Recurrent lesions again harbor the bacterial species.

Porphyromonas gingivalis:

These are black pigmented bacteriods. The strains of black pigmented bacteriods that ferment carbohydrates are placed in genus provetela while other strains that are asaccharolytic are placed under genus porphyromonas. The taxonomic position of weakly saccharolytic bacteriods like bacteroides levii and bacteroides macacae is still uncertain.

  • They are anaerobic, gram –ve, non-motile, asaccharolytic and has shapes that varies from coccal to short rods.
  • Colonies: on blood agar medium, it forms brown to black colonies.
  • They are found in higher numbers in:
    1. In periodontitis.
    2. In actively progressing periodontal disease.
  •  Their number is negligible in:
    1. Healthy periodontium.
    2. Gingivitis.
    3. Edentulous sites.
  • Virulence factors related to P. gingivalis include: collagenase, endotoxin, fibrinolysin, hemolysin, phospholipase A, fibroblast inhibitory factor, bone resorption inducing factor.
  • Host response to these factors:

Antibody levels in serum or saliva is elevated in case of the patients suffering from various forms of periodontitis. Local antibody titer is also altered at the sites with periodontitis.

  • Their eradication from the diseased site leads to the successful therapy.

Bacteroides forsythus:

  • It was first described as fusiform bacteroides by Tanner et al. in 1979.
  • This organism is a gram –ve, anaerobic, highly pleomorphic, spindle-shaped rod.
  • Culture: This bacterial species is highly difficult to grow. Even for minute colonies to grow, it requires about 7 to 14 days.
  • Factors enhancing its growth: 
    1. Co-cultivation with F. Nucleatum.
    2. Inclusion of  N- acetylmuramic acid into the culture media.
  • Studies using monocolonal antibodies have shown that elevated number of this bacterial species were very much related to the pocket depth.
  • Studies also showed that levels of B. Forsythus are much greater in subgingival plaque as compared to the supragingival plaque.
  • It is clear from double-labelling experiments that B. Forsythus was present both on and in the epithelial cells of the periodontal pocket. This clearly proves the ability of this species to invade connective tissue and cells.
  •  Number of this microorganism is higher in case of destructive periodontal disease, periodontal abscess and refractory periodontitis as compared to their number in case of healthy periodontium or gingivitis. Also, the chances of attachment loss, alveolar bone loss and tooth loss are greater in patients who harbored B. Forsythus than the patients in whom B. Forsythus is not found.
  • Virulence factors:

Endotoxin, fatty acid and methylglyoxal production.

  • This bacteria produces Trypsin-like proteolytic activity by enzymes and induces apoptotic cell death.
  • Its eradication leads to the successful periodontal therapy.

Prevotella intermedia:

  • They are black –pigmented bacteroides.
  • They are short, gram –ve, round-ended, strict anaerobic and rod shaped.
  • They ferment carbohydrates.
  • They are elevated in:
  1. Acute necrotizing ulcerative gingivitis.
  2. In progression sites in chronic periodontitis.
  3. Rapidly ptogressive periodontitis.


  • They are gram –ve, anaerobic and helical-shaped micro-organisms.
  • They are highly motile.
  • They are found to be associated with acute necrotizing ulcerative gingivitis. There role in other periodontal diseases is less clear.
  • Healthy sites have a few,if any,spirochetes.
  • Sites with gingivitis have low to moderate level of spirochetes in them.
  • Sites with deep pockets have large number of these organisms.
  • Individual species of spirochetes are difficult to distinguish, thus making it difficult to define the role of spirochetes in various periodontal diseases. Recent studies have shown that specific species of spirochetes are related to periodontal distruction. Treponema dentocola was found more common in the sites of periodontal distruction than in the healthy sites. Also, it was found  more common in subgingival plaque than in supragingival plaque.

Virulent factors produced by various periodontal pathogens and their actions

Virulent factorsActions
Aggregatibactor actinomyce-


Capsular antigen

Cytolethal distending toxin (CDT)

Fc-binding protein



Kills neutrophils, lymphocytes and monocytes

Host cell cytotoxicity

Deactivation of Ig’s

Disintegration of collegen

Potent stimulator of IL-1, PGE-2 and TNF-α

Cleavage of Ig’s.
Host cell cytotoxicity
P. GingivalisPill


Capsular antigen
Proteases (gingipains)



Volatile sulfur


Degradation of Ig, complement factors.

Potent stimulator of IL-1, PGE-2 and TNF-α

Causes agglutination and lysis of erytherocytes.

Host cell cytotoxicity

Host cell cytotoxicity

Host cell cytotoxicity
P. IntermediaBacterial surface adhesinsProteases


Degrade matrix components, host cell receptors and Ig’s

Lysis of RBC’s

Potent stimulator of IL-1, IL-6 and IL-8 release. Causes periodontal tissue destruction and alveolar bone resorption.
T. DenticolaMajor surface protein (MSP)

Fibronectin-binding adhesins



Major surface protein (MSP)

Phospholipase C (PLC)

H2S and methyl mercaptan
Potent stimulator of IL-1, PGE-2 and TNF-α

Degradation of extracellular matrix

Pleiotropic effects. Crucial for the virulence of T.denticola

Cytotoxic for a wide variety of cells

Directly or indirectly damages tissue by hydrolysis of membrane phospholipids

Cytotoxic effects that is primarily due to inhibition of cytochrome oxidases.
T. ForsythiaS-layer (TfsA and TfsB)

Leucine-rich-repeat protein (BspA)
Lipoproteins (BfLP)

Leucine-rich-repeat protein (BspA)
Activates gingival fibroblasts to produce elevated levels of interleukin-6 and TNF-α.

Causes release of pro-inflammatory cytokines from monocytes and chemokines from osteoblasts

Microbial complexes:

A landmark study done by Socransky et al. (1998) 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 DNA-DNA hybridization.

Subgingival microbial complexes

1st complex (Red complex) – Bacteroides forsythus. Porphvromonas gingivalis and Treponema denticola.

2nd complex (Orange complex) Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis.

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.


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