Inflammatory and immune reaction of the periodontium

Inflammatory and immune reaction of the periodontium

Introduction  :

  The body is constantly under threat of external aggression, in order to fight against these aggressions, the body is equipped with a defense system which is the immune system.

  In the oral cavity, the aggressive elements are constantly present but there is self-regulation between the different germs of the oral cavity. The triggering of inflammation occurs when there is:

• Disruption of the balance between the germs of the oral flora.
• Decreased host resistance.
• Introduction of a pathogenic germ.

I- Definition  :

1. Inflammation :

It is the body’s first reaction to an external attack, whether biological (virus, bacteria, parasite, etc.), chemical (acid, venom, etc.) or physical (wounds, bites, etc.).

It is expressed by the cardinal signs which are: redness, heat, swelling, pain.

2. Immunity:

It is the set of tissue and humoral modifications produced in an organism by any attack on its integrity. 

II- The actors of inflammation  :

1. Non-specific immune cells:
2. Platelets  : have contractile and secretory properties (histamine, serotonin), possess receptors for IgG and IgE.
3. Mast cells  : found in connective tissue, are the first to intervene in the inflammatory reaction; their cytoplasm is filled with granules containing mediators.
4. Polymorphonuclear cells  : play an essential role in inflammation, there are 3 types:

• PN neutrophils: participate in phagocytosis and secrete mediators.
• PN eosinophils: phagocytes the Ag-Ac complex, intervene in allergic phenomena.
• Basophilic PN: contain receptors for IgE.

4. Macrophages  : key cells of inflammation, present Ag to lymphocytes, secrete prostaglandins.

2. Cells of specific immunity:
3. T lymphocytes  : mature in the thymus and are responsible for the secretion of lymphokines.

• LT ₈ or LT _C   (cytotoxic): they release cytokines that attract macrophages and read target cells.
• LT _S (suppressor): reduce and regulate the immune response, by inhibiting the proliferation of LT and LB.
• LT _M  (memory): able to recognize the antigen years later.
• LT ₄ or LT _H (helper): combine with LB and secrete interleukin II.

2. B lymphocytes: mature in the marrow and spleen, they transform into plasma cells which produce antibodies.
3. Mediators of inflammation: 

These are chemical substances present in the plasma in an inactive state or secreted by cells whose role is:

– Increased capillary permeability.

– Chemotaxis.

– Amplifies inflammation.

– Painful symptoms.

• Messengers of immunity:

• Interleukin I  : This is a chemical substance synthesized by macrophages in the presence of Ag and is used to transfer the message to lymphocytes.
• Interleukin II  : it is a lymphokine released by lymphocytes in the presence of interleukin I, it stimulates the production and differentiation of B lymphocytes into plasma cells in order to produce antibodies.

4. The antigen: 

Any substance that, introduced into an organism, provokes an immune reaction is called Ag.

5. The antibody: (or immunoglobulin)

It is a plasma protein formed by an organism in response to the introduction of an Ag. There are 5 Ig classes (GAMED).

6. The supplement: 

The complement system consists of a series of at least 9 different proteins present in plasma (from C1 to C9). 

The components of the complement system can be compared to enzymes that would be activated according to a predetermined sequence.

The complement cascade is initiated in 2 ways:

– Classical route: from C1 to C9 via the Ag-Ac complex.

– Alternate pathway: from C3 to C9 by enzymes of bacterial origin.

It has a triple role: bacterial lysis, chemotaxis and opsonization. 

Inflammatory and immune reaction of the periodontium

Inflammatory and immune reaction of the periodontium

FIG.1: The complement activation cascade with its two pathways.

III- Acute inflammation  :

  Following an aggression or irritation, an acute inflammatory reaction appears, it is characterized by a vascular and cellular reaction. The main objective of this acute reaction is to protect the exposed tissue, as well as to establish favorable conditions for regeneration. 

1. Vascular reaction:

It is characterized by:

• Vascular vasodilation.
• Decreased blood flow velocity.
• Increased vascular permeability induced by chemical mediators (histamine, serotonin)

This permeability will allow water and electrolyte molecules to leave the bloodstream towards the injured site (edema)

2. Cellular reaction:

This is an extravascular migration of defense cells under the dependence of chemical mediators. This phenomenon occurs as follows:

• Margination: this is the adhesion of phagocytic cells along the vascular wall.
• Diapedesis  : this is the crossing of the vascular wall by the defense cell which deforms to insinuate itself into the intercellular spaces. 
• Chemotaxis  : this is the phenomenon by which phagocytic cells are attracted to the inflammatory site, thanks to chemical mediators.
• Phagocytosis  : this is the purpose of migration, the cells will ingest and attempt to reabsorb the bacteria using lysosomes. Once the foreign body is identified, there is adhesion between the phagocyte and the antigen, then emission of pseudopodia which result in its inclusion in a vacuole or phagosome.

Inflammatory and immune reaction of the periodontium

FIG.1: Cellular reactions during acute inflammation

3. Healing:

Once the pathogen and necrotic tissue are eliminated by phagocytes, fibroblasts colonize the wound to form scar tissue which will gradually lead to wound closure.

• This is the usual evolution of any acute lesion, however it happens that acute inflammation becomes chronic when the antigen is still present, in which case specific immunity will intervene.

IV- Chronic inflammation  :

  When the acute inflammatory reaction is insufficient to eliminate the irritant, an immune response is triggered, its goals being:

• Identify the harmful agent.
• Activate phagocytes.
• Antibody secretion.

Whether the immune reaction is cellular (T lymphocyte) or humoral (B lymphocyte), both involve a phase preceding them which is the identification of the antigen. The macrophages will present the antigen to the lymphocytes which will recognize it and differentiate.  

1. Cell-mediated reaction:

Once the antigen is known, comes the action of the T lymphocytes.

• Lymphokines will cause:

– Increased vascular permeability and cellular diapedesis.

– Cytotoxicity towards fibroblasts.

– Chemoattractant activity and stimulation of macrophages.

– Activation of osteoclasts (which explains the transition from gingivitis to periodontitis)

2. Humorally mediated reaction:

When LBs are stimulated they transform into plasma cells which will produce Ig antibodies (GAMED). This transformation requires the participation of LT ₄ which promote it and LT _S which slow it down. 

Once secreted the antibodies are released into the site of the reaction.  

Antigen and antibody molecules bind to form an immune complex, which can be neutralized but often activates complement, which leads to either lysis of the bacteria or stimulation of phagocytes.

3. Non-specific reaction:

The non-specific reaction involves monocytes and macrophages; once the causal agent has been eliminated by the body’s defenses, the phagocytic cells will regroup at the inflammatory site to clean it and allow healing.

• Noticed  :

Acute inflammation quickly results in healing, sometimes with after-effects; chronic inflammation is a process that could evolve in a prolonged or even indefinite manner (worsening).

V- Study of clinical signs of inflammation at the level of the periodontium  :

1. Erythema: (this is the change in color of the gum)

It begins with a simple redness appearing at the level of the gum, in the case of acute inflammation the erythema will be bright red, and in the chronic case the erythema begins with redness then passes through shades varying from reddish blue to dark blue.

According to GLICKMAN: it is through a dilation of the capillaries and an increase in blood flow that the initial erythema occurs, the increase in redness corresponds to the proliferation of the capillaries.

As the inflammation becomes chronic, the blood vessels become congested and congested, venous return is impaired and blood flow slows down, tissue anoxemia (absence of oxygen) then occurs which adds a bluish component to the already red gum.

2. Edema:

The increase in vascular permeability will allow the passage of fluids rich in water, electrolytes, albumin and fibrinogen within the connective tissue, causing bloating responsible for edema. 

Clinically the gum increases slightly in volume, the appearance is smooth and shiny, the consistency is soft with a positive Godet sign.

3. Bleeding:

It is caused by the introduction of a blunt-tipped periodontal probe into the sulcus.

Following inflammation, the sulcular epithelium undergoes varying degrees of ulceration and degeneration. As a result, the capillaries are brought closer to the surface and are therefore less protected. Consequently, stimuli that are usually harmless cause the capillaries to rupture and gingival bleeding to occur.

4. The fake pocket:

This is the deepening of the SGD by increase in gingival volume, without migration of the epithelial attachment.

5. The real pocket:

This is the deepening of the SGD by migration of the epithelial attachment.

6. Suppuration:

Pus forms in a cavity formed by tissue disintegration. Clinically it can be demonstrated by probing or digital pressure.

Pus is a common feature of periodontal disease, it can form in both shallow and deep pockets, but for some authors (CHARON) it represents a sign of periodontal disease activity.

 Conclusion  :

  The inflammatory reaction involves a whole range of specific and non-specific reactions, the aim of which is to defend the body.

  However, when it increases in an uncontrolled manner, the inflammatory reaction leads to pathological manifestations.

Inflammatory and immune reaction of the periodontium

  Cracked teeth can be healed with modern techniques.
Gum disease can be prevented with proper brushing.
Dental implants integrate with the bone for a long-lasting solution.
Yellowed teeth can be brightened with professional whitening.
Dental X-rays reveal problems that are invisible to the naked eye.
Sensitive teeth benefit from specific toothpastes.
A diet low in sugar protects against cavities.
 

Inflammatory and immune reaction of the periodontium