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Step 1: The birth of biofilm — the skin of our teeth

Let’s start with the best-case scenario: a healthy oral microbiome. Saliva plays a vital role in maintaining this healthy balance. It helps wash away debris, regulates pH, and provides antimicrobial protection through immune components like immunoglobulin A, lysozyme, and lactoferrin.

Saliva also allows microorganisms to adhere to oral surfaces, and supplies the nutrients that support their growth. This is how the first thin layer of biofilm is formed: as a means of protection and structural integrity, microorganisms embed themselves in a matrix that consists of extracellular DNA, polysaccharides and proteins.

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Step 2: Cooperation versus competition

When a biofilm first forms, it is mostly composed of gram-positive bacteria, like Streptococcus. These bacteria can survive with or without much oxygen. However, these bacteria do not act alone. They use a communication system known as quorum sensing to work together, changing how their genes act and how they produce enzymes. As the biofilm grows and thickens, its structure strengthens. This allows many different types of microbes to live there, but it especially favours the survival of anaerobic bacteria in the deeper, oxygen-poor parts of the biofilm.

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Step 3: A turn for the worse

As the biofilm continues to mature, pathogenic bacteria start to thrive:

  • Gram-negative anaerobes begin to dominate and increase virulence potential.
  • Bacterial by-products such as proteases and endotoxins initiate host immune responses.
  • The protective matrix enhances resistance to brushing, antimicrobial agents and immune system attacks.

This transition to dysbiosis sets the stage for oral disease development, particularly periodontal disease and dental caries.

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Step 4: The body fights back and loses

At this point, dysbiosis is fully established, so an inflammatory response is triggered:

  • White blood cells are recruited to neutralise the bacterial invasion.
  • Biofilm-induced immune evasion means the extracellular matrix acts as a shield, making it difficult for white blood cells and antimicrobial agents to eliminate the bacteria effectively. During this battle, tissue-damaging enzymes are released.
  • This chronic inflammation and connective tissue breakdown leads to deepening periodontal pockets.

Rather than eliminating the infection, the immune response contributes to the progression of periodontal disease by exacerbating tissue destruction.

The worst offenders

Unlike dental caries, which result from acidogenic bacteria, periodontitis is driven by polymicrobial synergy rather than a single pathogenic species. Certain bacterial complexes serve as strong indicators of disease:

  • Aggregatibacter actinomycetemcomitans – associated with aggressive periodontitis.
  • Tannerella forsythia and Prevotella spp. – linked to chronic inflammation.
  • Socransky’s famous Red Complex:
    • Porphyromonas gingivalis – immune modulation and connective tissue degradation
    • Tannerella forsythia – epithelial invasion and inflammatory response
    • Treponema denticola – tissue penetration and destruction

These pathogens thrive in mature biofilms, which reinforces the chronic nature of periodontal disease.

Important to remember 

Eubiosis

A stable oral biofilm consists of commensal and symbiotic microorganisms that:

☑Prevent the overgrowth of pathogens
☑Maintain immune homeostasis by modulating inflammatory responses
☑Promote mineralisation and oral tissue repair
☑Contribute to salivary and digestive functions
☑Regulate plaque by forming structured biofilms that inhibit the adhesion of harmful bacteria

Dysbiosis

Dysbiosis occurs when opportunistic pathogens dominate and trigger inflammation. This shift can be caused by:

Poor oral hygiene: Leads to plaque buildup, favouring pathogenic bacteria
☑ Smoking and poor diet: Altered oxygen levels and nutrient availability, favouring anaerobic pathogens
Reduced salivary flow: Saliva washes away debris, neutralises acids, and transports antimicrobial compounds
Stress and systemic disease: Weaken immune regulation, allowing dysbiotic shifts
Antibiotics: Eliminate beneficial bacteria, enabling pathogenic overgrowth

Up next: Oral microbiome in practice: Actionable insights with Dr. Thompson