Periodontitis and gingivitis are inflammatory diseases of bacterial origin. However, pathogenic bacteria alone are not sufficient for their onset and progression. The way the immune system reacts also determines the course of the disease. This post looks at the pathogenesis of periodontal diseases as well as the pathophysiology.

In addition, other local, general, and environmental factors may predispose to their development or influence their severity.

Therefore, periodontal disease is a set of inflammatory conditions that results from the interaction of multiple factors. Individuals are not equal in this regard. Some will experience persistence and moderate inflammation for years, while others will experience rapid tissue destruction.


Destruction of the Periodontal Tissues 


Microorganisms and host response interaction (2)

Not all bacterial species in the mouth are aggressive. Some of them are friendly and help keep the balance.

In periodontal disease, more than 500 species are present, but only a few are pathogenic. Pathogenic bacteria cause the initiation and progression of periodontal disease.

They colonise the different mouth surfaces and form the biofilm, also known as plaque. This environment protects and allows them to act in synergy.

Plaque build-up leads to gingivitis, the early stage of periodontal disease. In contrast, periodontitis is not triggered by the plaque amount but by the presence of specific bacteria with high virulence potential. Virulence factors include:

  • Ability to colonise tissues: Virulent bacteria have adhesion factors that allow them to attach to periodontal tissues and act as a carrier for other bacteria. Some of them can even penetrate inside the tissues, which explains the inefficiency of mechanical debridement sometimes.
  • The ability to evade host defenses: Virulent bacteria have features that allow them to protect themselves against defense mechanisms. These include capsules, immunoglobulin-destroying proteases, and PMN receptor blockers.
  • Ability to produce tissue-destroying substances: Virulent bacteria can destroy periodontal tissue in two ways. The first is through bacterial components (LPS) and metabolic products (proteases, collagenases. phospholipases, and fibrinolysin). Lipopolysaccharides (LPS) are endotoxins found on the outer membrane of Gram-negative bacteria. The second way is indirectly by stimulating the host’s response.


Virulence Factors of A. actinomycetemcomitans

Virulence Factors of A. actinomycetemcomitans (Aa) (2)

The imbalance between the host’s response and bacterial factors leads to the destruction of periodontal tissues.

Different mechanisms are involved in this process:

  1. Bacteria and their products:

After a few days of plaque accumulation, virulent bacteria start to grow. They have the common point of being gram-negative with a high pathogenic potential. They include Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, and Treponema denticola.

LPS, proteases, and enzymes lead to connective tissue breakdown and bone lysis.

Bacteria and their products also stimulate the production of cytokines and inflammatory mediators that are highly involved in tissue damage.


  1. Host response:

The host response protects the periodontium against bacterial aggression. However, large amounts of plaque and highly virulent bacteria can disturb tissue homeostasis, leading to periodontitis.

The immune system sets up two lines of defence to eliminate bacteria.

  • The first line of defence:

When toxins and bacterial components (LPS) diffuse through the junctional epithelium, the first to be involved are polymorphonuclear cells (PMNs). They kill invading bacteria through phagocytosis (a mechanism that involves killing and digesting the microorganisms) and produce substances called cytokines.

Cytokines regulate important immune system functions, including inflammation, cell proliferation, growth, activation, and repair. However, when released in excess, they cause tissue damage.

When plaque accumulates predominantly with gram-negative bacteria, PMNs migration increases by diapedesis. Macrophages enhance phagocytosis and present antigens to T and B cells.

  • The second line of defence:

After the presentation of the antigen, B and T cells are activated. They proliferate and migrate to the infected site through the bloodstream.

B cells then predominate and mature into plasma cells capable of releasing specific antibodies.

This line of defence takes longer to intervene. However, it has a “memory” function that allows it to act quickly and effectively when exposed to the same antigen a second time.

  • Cytokines:

Innate and adaptive immune response during periodontal disease  Innate and adaptive immune response during periodontal disease (1)

The interaction between LPS and immune cells (PMNs and macrophages) stimulates the synthesis of inflammatory mediators and cytokines. While these substances regulate the immune response, they can destroy surrounding tissues. Among them: interleukin-1 (IL1), interleukin-6 (IL6), interleukin-8 (IL8), tumour necrosis factor (TNF), Prostaglandin E2 (PGE2), and natrix metalloproteinases (MMP).

-IL1: It leads to the migration of inflammatory cells, but also the destruction of bone and the stimulation of other inflammatory mediators, such as PGE2 and MMP, which degrade the extracellular matrix proteins.

-IL6: Stimulates the production of antibodies and osteoclasts differentiation, which are responsible for bone destruction.

-IL8: Attracts immune cells, stimulates MMPs, and contributes to the destruction of collagen.

-TNF: It had the same activity as the IL1. It exacerbates the inflammatory response.

-PGE2: Produced by monocytes and fibroblasts, it increases bone resorption and MMP release.

– MMP: Bacteria and their products can directly stimulate cells to produce MMPs, which can destroy the extracellular matrix of connective tissue and bone.


The progression of periodontal disease

Plaque build-up leads to inflammation which is a physiological response.

Inflammation involves different cells and biochemical molecules that trigger complex reactions. This will lead to disease progression from gingivitis to periodontitis.

However, it is important to know that inflammation can stagnate and never lead to periodontitis. It all depends on the individual’s risk factors and how the immune system reacts.


  1. Healthy gums:

Stage 1

         Stage 1 (2)

In healthy gingiva:

-Plaque accumulation is minimal.

-Epithelial attachment, fibroblasts, and collagen fibres are intact.

-The junctional epithelium firmly attaches the gum to the tooth surface.

-No signs of inflammation.


  1. Early lesion:

Stage 2

         Stage 2 (2) 

8 to 14 days after plaque accumulation, bacterial products stimulate epithelial attachment cells and attract PMNs (blue dots). This will send signals to the blood vessels to dilate, leading to inflammation.

As a result, gingival crevicular fluid increases, and PMNs migrate to form a barrier against bacterial plaque.

At this stage, PMNs predominate. Lymphocytes start accumulating under the junctional epithelium (black dots).

There is an initial alteration of fibroblasts, collagen fibres, and junctional epithelium that starts to proliferate laterally.

Clinically, signs of gum inflammation are seen, including redness, swelling and a tendency to bleed.


  1. Established lesion:

Stage 3

         Stage 3 (2)

3 to 4 weeks after plaque accumulation, the previous phenomena intensify. The junctional epithelium retracts in its coronal part, pushed back by the growing plaque, but without causing any attachment loss. This leads to pseudopockets formation.

The lateral proliferation of the junctional epithelium continues to form a barrier against the progressing bacteria.

The inflammatory infiltrate increases with a significant infiltration of plasma cells. The deterioration of fibroblasts and collagen fibres worsens, but the bone is not yet affected.

Clinically, there is a high amount of plaque, pseudo pockets, and pronounced inflammation.

This stage may persist for years without progressing to periodontitis.


  1. Advanced lesion:

Stage 4

         Stage 4 (2)

This is where gingivitis turns into periodontitis. The pocket epithelium proliferates and migrates apically, forming true periodontal pockets. The degeneration of the underlying gingival fibres leads to a loss of connective tissue attachment. The bone is also affected by the inflammatory infiltrate and gradually resorbs.

The inflammatory infiltrate continues to expand with a predominance of plasma cells. Excessive exudation, sometimes purulent, may occur.

This stage refers to the formation of periodontal pockets and the onset of periodontitis.

Untreated periodontitis progresses at different rates, depending on the individual risk factors. Knowing the type of periodontitis is necessary, but it is also essential to identify the pattern of bone loss and the severity of the attachment loss. This allows us to establish the prognosis and estimate the degree of treatment difficulty.

Bone loss progresses in two patterns: horizontal and vertical:

Horizontal vs. vertical bone loss

Horizontal vs. vertical bone loss (2)


Horizontal bone loss:

This is the most common type of bone loss. The bone is reduced in height, and its edge is parallel to the line passing through the cementoenamel junction of the two adjacent teeth.

It occurs especially in chronic periodontitis. Panoramic and retro alveolar radiographs can reveal the extent and severity of the damage.


Vertical bone loss:

When bone loss progresses in an oblique direction or its edge is not parallel to the line joining the cementoenamel junction of the two adjacent teeth, the bone lysis is vertical.

In most cases, vertical bone loss results in infrabony pockets, which means that the bottom of the pocket is in an apical position to the bone.

We distinguish three-wall, two-wall, and one-wall bony defects.

  • Three wall-bony defects: Pockets are bordered by three osseous surfaces.
  • Two wall-bony defects: Pockets are bordered by two osseous surfaces.
  • One-wall bony defect: Pockets are bordered by only one osseous surface (facial or oral), and soft tissue.

Bony defects


Risk factors 

Risk factors are characteristics that, when present, increase the probability of the disease occurrence, and decrease this probability when absent. There are local, general and environmental risk factors.


Local risk factors:

-Oral hygiene: Poor oral hygiene promotes plaque accumulation, an inflammation-inducing factor.

-Tartar: Tartar is a mechanical irritant and promotes further plaque accumulation.

-Anatomical factors: Certain anatomical peculiarities, especially in the furcation, insufficient keratinised gingivae, and dental crowding, facilitate the accumulation of bacterial plaque and make oral hygiene difficult.

-Iatrogenic factors: An ill-fitting filling or crown can affect the periodontal tissues and increase the risk of periodontitis.

-Functional factors: Teeth grinding, occlusal trauma, or mouth breathing can aggravate the periodontal disease and accelerate its progression.

General risk factors:

Factors such as ageing, genetics, systemic diseases, or certain medications can worsen periodontal disease.

Environmental risk factors:

These include all behaviours, habits, and environmental characteristics that may affect the immune response or increase the risk of periodontal disease. Among them are stress, smoking, nutritional deficiency, and low socioeconomic status.



  • Periodontal disease is a set of inflammatory conditions that results from the interaction of multiple factors.
  • In addition to the pathogenic bacteria, the immune response also determines the severity and progression of the disease.
  • Plaque accumulation causes inflammation limited to the gums. This stage refers to gingivitis.
  • When virulent bacteria proliferate associated with a poorly regulated inflammatory response, homeostasis is disrupted, resulting in tissue destruction. Gingivitis then evolves into periodontitis.
  • Other risk factors can be added, aggravating or accelerating the periodontal disease process.

Useful Links & Recommended Reading


  1. Pathogenesis of Periodontal Disease. In: Yussif, N. M. A. , editor. Periodontal Disease – Diagnostic and Adjunctive Non-surgical Considerations [Internet]. London: IntechOpen; 2019 [cited 2022 Nov 28]. Available from: doi: 10.5772/intechopen.86548
  2. H.F. Wolf,  E.M. Rateitschak, K.H. Rateitschak & T.M. Hassell. Color atlas of dental medicine: Periodontology.
  3. Ramadan DE, Hariyani N, Indrawati R, Ridwan RD, Diyatri I. Cytokines and Chemokines in Periodontitis. Eur J Dent. 2020 Jul;14(3):483-495. doi: 10.1055/s-0040-1712718. Epub 2020 Jun 23. PMID: 32575137; PMCID: PMC7440949.


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I have just finished my internship at the Faculty of Dentistry. Currently, I am working on my thesis for a DMD degree. I have also started a blog on oral health (just on my personal site), hoping it could become an invaluable resource for anyone interested in dental science and oral health.


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