Introduction to the Microbiology of Periodontal Disease

The bacteria involved in causing periodontal disease are numerous, with associations with over 400 bacterial species in a pocket! The microbial composition changes between gingival health and disease. A few bacteria are specifically associated with periodontal disease; the pathogenic bacteria form the Red Complex. 

Properties of Bacteria Involved

For the bacteria to cause damage to the periodontium, they must be able to;

• Colonise and survive effectively 
  • This requires the bacterium to be able to adhere to the host surface, or bridging species (such as Fusobacterium) to allow them to indirectly adhere 
  • Have and use the nutrients available to replicate
  • Compete against existing microorganisms
  • Defend itself against protective host mechanisms
• Produce factors that damage the host tissue through direct or indirect methods
• Spread!!

The microbial composition of plaque varies depending on the location. As plaque accumulates, the inflammatory response is triggered. The inflammation causes changes to the gingival environment; changes which favour the growth of the pathogenic bacteria. This shift allows for bacteria to survive in the new conditions of the biofilm. 

The table below highlights the differences in biofilms. 

The Bacterial Shift

In healthy gingivae, gram +ve bacteria such as Streptococci, Actinomyces, and Neisseria species dominate. 

As gingivitis develops and plaque accumulates, there is a decrease in the number of Gram +ve cocci present during this stage. Instead, the number of gram -ve anaerobic bacteria increases; such as Fusobacterium and Actinomyces. Additional species which can be present include spirochetes and motile bacilli. 

An important note to make at this stage is the requirement for Fusobacterium spp. Fusobacterium is a bridging species which means anaerobic gram -ve bacteria can adhere and colonise host tissue, which they previously were unable to do. This means removing bridging species through brushing can prevent the potential progression from gingivitis to periodontitis!

During periodontitis however, the microflora is predominantly anaerobic gram-ve motile rods and spirochetes. The species present as this stage include several key periodontal pathogens, such as Aggregatibacter Actinomycetemcomitans (Aa for short!), Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia. The red complex, as previously mentioned consists of 3 bacteria which are most commonly associated with periodontal disease. These bacteria and their characteristics can be found below. 

Red Complex

Treponema denticola

• Gram -ve 
• Obligate anaerobe
• Spirochete
• Virulence Factors:
  • Able to adhere to epithelial cells and fibroblasts to release damaging enzymes into their ECM

Tannerella forsythia

• Gram -ve 
• Obligate anaerobe
• Spirilla (spindle shaped)
• Virulence Factors:
  • Cell surface proteolytic enzymes

Porphyromonas gingivalis

• Gram -ve
• Rod shaped
• Anaerobe
• Virulence Factors: 
  • Produces a collagenase enzyme which breaks down the collagen in periodontal tissues 
  • Degrade haemoglobin which results in the release of Iron, therefore preventing iron transport 

Additional Bacteria to be aware of with relevance to Periodontal Disease include Fusobacterium nucleatum and Aa .

Fusobacterium nucleatum 

• Gram -ve
• Anaerobic
• Non motile 
• Cigarette shaped bacilli with sharply pointed ends 
• Virulence;
  • Adhesin A – these adhesion molecules allow for other species to adhere and colonise a region of host tissue they otherwise couldn’t colonise 
  • Endotoxin 

Aggregatibacter actinomycetemcomitans (AA).

This bacterium is found in high numbers in patients with Aggressive periodontitis. Please note however, Aggressive periodontitis is no longer a diagnosis based on the BSP guidelines.

• Gram -ve 
• Capnophilic 
• Coccobacillus (appears circular however actually rod shaped) 
• Important virulence:  
  • Produces leukotoxin which can kill various WBCs including monocytes and granulocytes 
    • Leukotoxin works by embedding itself in the cell membranes of WBC’s which forms pores. This therefore causes the WBC’s contents to be released.