Inflammation and histopathogenesis of periodontal disease
Plan
-introduction
1- Reminder on health and periodontal disease
2-Etiology of periodontal diseases
3-Definitions
-Inflammation
-Pathogenesis
-Histopathogeny
-Histopathology
4-Progression of periodontal disease
5-Essential phenomena of the inflammatory process
-acute inflammation: vascular reaction
Cellular reaction
-chronic inflammation: humoral-mediated reaction
cell-mediated reaction
6-Histopathology and pathogenesis: initial, early, established, advanced lesions.
Conclusion
Bibliography
Inflammation and histopathogenesis of periodontal disease
Introduction : When a tissue of the body is damaged by an aggression of physical origin (heat, cold, ionizing radiation, electricity), mechanical (trauma), chemical or infectious (bacterial, viral or parasitic) and there is cell death, this leads to the initiation of vascular, cellular and humoral phenomena which result in the repair of the damaged tissue. All of these phenomena constitute inflammation. They result either in a restitution of the damaged tissue (when the latter is capable of regenerating) or in the replacement of the affected area by a fibrous scar (when the lesion is extensive or the affected tissue cannot regenerate). Whatever the type of tissue repair obtained, it is always the result of an acute inflammatory reaction, however, when the aggressive agent persists, chronic inflammation develops resulting in tissue fibrosis.
Periodontitis begins with gingivitis and if the inflammatory process is allowed to continue, it will gradually invade deeper periodontal tissues in most patients.
The inflammatory process itself carries the potential to stimulate periodontal tissue resorption and periodontal pocket formation.
1-Reminder
Periodontal health : It can be defined as a stable state over time of all 04 periodontal tissues (gums, cementum, alveolar bone and periodontal ligament) that adhere and/or attach to the entire surface of the dental root. The most coronal part of this attachment is at the enamel-mound junction.
-From a strictly clinical point of view , healthy gingiva is firmly attached to the underlying structures, pale pink in appearance, pitted with orange peel and does not bleed when brushing, chewing, spontaneously and/or when probing with a force of approximately 50 g.
-Radiologically , a retro-alveolar image, taken under optimal conditions of exposure and development, reveals intact deep interproximal periodontal structures (particularly alveolar bone) with a bony crest located approximately 2 mm from the enamel-mound junction (space reserved for epithelioconnective tissue attachment). Some authors admit that the presence of lamina dura (white line highlighting the outline of the roots on the periphery of the alveolus) is synonymous with periodontal health, while its disappearance or absence would be a sign of disease.
Healthy periodontal tissues showing little or no signs of inflammation and connective tissues are infiltrated mainly by neutrophils and lymphocytes.
The supra- and subgingival microbial flora compatible with periodontal health consists essentially of aerobic Gram-positive cocci and filaments in relatively low numbers, and with little or no mobility.
Periodontal disease : Periodontal disease is characterized by gingival inflammation, formation of periodontal pockets, destruction of the periodontal ligament and alveolar bone, and progressive mobilization of teeth.
-Clinical signs of periodontal disease: the gum is generally chronically inflamed, its color varies from red to blue, its consistency varies from soft and collapsed (edematous) to firm (fibrous), its pitting is less marked, its contour is rounded at the level of the marginal gingiva and the interdental papillae are blunted, its volume is increased. Bleeding is generally observed by instrumental examination. The depth of the pockets is increased. Pressure on the pocket often causes a purulent exudate to flow. Tooth mobility may be noted.
Radiographic signs of periodontal disease:
-the alveolar bone crest is located more than 2 or 3 mm apically to the enamel-cementum junction, indicating loss of alveolar bone.
-the crest of the alveolar bone appears blurred, and the crestal lamina dura is not well defined.
– bifurcation and trifurcation areas of the roots of the molars showing radio transparencies significant of inter-radicular bone loss.
-there is a decrease in the density of the interdental bone.
2-Etiology of periodontal diseases : the main etiological agent incriminated in the succession of inflammatory and immunological stimulations of periodontopathies is the bacterial component of dental plaque.
3-Definitions:
Inflammation : inflammation is the set of reactions of the organism caused by an attack of whatever nature (microbe, yeast, virus, toxic agent, trauma, etc.) the attack causes a lesion around which the inflammatory process is formed.
Pathogenesis: This is the mechanism by which the etiology results in the onset of the disease.
Histopathogenesis : is the microscopic study of inflammatory tissue variations of the periodontium following colonization of the sulcus by periodontopathogenic flora.
Histopathology: this is the histological study of cells and tissues affected by a multitude of anomalies, tumoral, inflammatory, degenerative
4-Progression of periodontal disease : the plurality of tissues and the complexity of the method of attachment of the tooth to its supporting tissues make the gingivodental region a particularly vulnerable area to pathogenic mechanisms. The substances secreted by the microorganisms of dental plaque infiltrate along the epithelium forming the wall of the gingivodental sulcus and cause lysis of the gingival fibers near their cementary attachment, ulceration, exposure of the connective tissue resulting in spontaneous or induced bleeding. The inflammation then spreads into the alveolar bone following the vestibular and lingual pathways. This results in proliferation of the epithelial-connective attachment in the apical direction.
5-The essential phenomena of the inflammatory process:
The acute inflammatory reaction can be considered as the first line of tissue defense occurring after irritation or aggression, while the so-called chronic inflammatory reaction can be considered as the second line of defense.
Acute inflammation : the acute inflammatory reaction appears within the connective tissue following an aggression (microbial, chemical, thermal or mechanical). The inflammatory reaction is characterized by the appearance of vascular and cellular changes that result in a transient or permanent deterioration of normal tissue constituents, this causes an alteration or loss of the normal function of the affected tissue. The aim of the local inflammatory reaction is the protection of exposed tissues against the penetration of harmful substances as well as to establish favorable conditions for the repair or regeneration of damaged structures.
Inflammation and histopathogenesis of periodontal disease
Therefore the local inflammatory reaction should be considered beneficial for the body in the sense that it isolates pathogenic substances, thus protecting the more distant parts of the body.
Vascular reaction : The vascular reaction develops rapidly after the aggression, its purpose is
- to supply the damaged area
-in plasma proteins
-and in fluid necessary for the rapid isolation of the irritant and damaged tissue.
- to deliver antibacterial substances and mediators of the inflammatory process to the site of injury.
The vascular reaction is characterized by:
– Vascular dilation
-Decreased blood flow rate in the affected part of the tissue
-Increased permeability of vessels following retraction of endothelial cells.
These changes are responsible for the passage into the damaged area of a fluid called edema or exudate, consisting of water, electrolytes of nutrients and a high concentration of plasma proteins.
The clinical manifestations of acute inflammation are redness, warmth, pain and swelling.
Cellular reaction : leukocytes, neutrophilic granulocytes and monocytes migrate out of the vascular system and enter the adjacent connective tissue. This diapedesis is induced by chemotactic stimulation. Neutrophilic granulocytes are responsible for phagocytosis of foreign particles, harmful substances, microorganisms. They contain in their cytoplasm numerous granules (lysosomes) that contain enzymes and antibacterial substances as well as inflammatory mediators. Lysosomal enzymes released by neutrophils during phagocytosis can cause significant tissue destruction.
Monocytes and their transmuted form, macrophages (which appear when monocytes are stimulated during the local inflammatory reaction) are cells that have functions similar to those of neutrophil granulocytes .
Macrophages contain a large number of lysosomes and participate in the phagocytosis of microorganisms and harmful material.
After phagocytosis and elimination of the irritant, healing begins, during which substances are released that cause an increase in the proliferation of fibroblasts and their metabolic activity.
Chronic inflammation or immune reaction : the immune response is triggered when the local inflammatory reaction is insufficient to eliminate the infectious material (antigen). The transition to chronicity results in the establishment of a state of balance between the phenomena of destruction and tissue repair, this state can last for years. The main purpose of the immune response is to identify and bind the harmful agent (antigen) as well as to activate phagocytes. Immune reactions have two major functions:
-the production of antibodies (immune reaction)
-the participation of certain lymphocytes (cell-mediated reaction)
In most situations, both reactions occur simultaneously, but one or the other may predominate depending on the character of the antigen.
Humorally mediated reaction :
- Antibodies: Antibodies are produced by plasma cells that differentiate from lymphocytes. Antibodies are released either into the tissues at the site of the reaction or into the lymph node from where they enter the circulation. The antibody and antigen molecules bind to form an immune complex. The antigen is thus fixed and its biological effect is in many cases neutralized.
- Complement : Activation of the complement system is a very important consequence of the formation of immune complexes. The complement system consists of a series of at least 9 different proteins present in the plasma. Activation of complement results in the formation of mediators of the local inflammatory reaction. Factors released by activation of the third complement component, C3, induce an increase in vascular permeability and amplify phagocytosis carried out by neutrophil granulocytes and macrophages.
The immune complex is eliminated by the acute inflammatory reaction (exudation and phagocytosis) triggered and maintained by activated complement components.
Cell-mediated immune response : The cell-mediated immune response is conducted by cells belonging to the T lymphocyte series. T lymphocytes release lymphokines when they come into contact with an antigen.
Lymphokines are involved in host defense against bacteria and foreign cells and have the power to mediate the different phases of the local inflammatory reaction.
Many immune processes involve a combination of B and T cell responses.
6-Histopathology and pathogenesis: four anatomopathological stages of the development of periodontal lesions have been described: the first corresponds to the healthy state, stages 2 and 3 to gingivitis and the last stage is periodontitis.
– initial lesion (or macroscopically healthy gingiva): occurs within 2 to 4 days after the start of plaque accumulation. The characteristics of the initial lesion are:
-Hyper vascularization near the junctional epithelium associated with increased vascular permeability.
-Increased flow of gingival fluid
-Movement of leukocytes to the junctional epithelium and gingival sulcus
-Plasma defense proteins (complement and immunoglobulins) are found in the gingival fluid.
-Alteration of the coronal parts of the junctional epithelium
-disorganization of collagen fibers surrounding blood vessels.
Inflammation and histopathogenesis of periodontal disease
-Early (beginning) lesion (gingivitis): between the 4th and 7th day . It is marked by the exaggeration of the signs of the initial lesion:
-formation and maintenance of a dense inflammatory infiltrate rich in T lymphocytes within the gingival connective tissue.
– alteration of the cytoplasmic components of fibroblasts
-greater destruction of gingival collagen fibers (the dentogingival and circular connective fibers which support the junctional epithelium are the most degraded).
-proliferation of basal cells of the junctional epithelium and the sulcular epithelium.
– Established lesion or established gingivitis : approximately 3 weeks after stopping brushing, the signs of acute inflammation persist:
– continuous destruction of collagen fibers
-the junctional epithelium is no longer functional, the intercellular spaces open with rupture of the intercellular desmosomes and the basement membrane is destroyed in certain places.
-proliferation and apical migration of the junctional epithelium
-the underlying vascular network proliferates and forms vascular loops which are separated from the sulcular space by only one or two cell layers, which explains the gingival bleeding found in patients.
Fluid exudate increases and gingival edema increases leading to the formation of false pockets.
-predominance of plasma cells in the inflammatory infiltrate.
-accumulation of immunoglobulins and antigen-antibody complexes in connective tissue.
-Advanced lesion or periodontitis : it is typical of periodontitis and characterized by:
– continuation of signs of established injury
-the spread of the lesion in the alveolar bone and the periodontal ligament, leading to bone destruction
-loss of collagen fibers adjacent to the pocket epithelium
-fibrosis in peripheral areas
-presence of altered plasma cells
-formation of a periodontal pocket
– phases of exacerbations and phases of very low pathological activity
-the transformation of bone marrow into fibrous connective tissue
Conclusion : from the various immunological and bacteriological data we can deduce that the enzymes produced by bacteria can trigger the entire cascade of immune phenomena. All of these phenomena are dependent on the bacterial mass and the regulation of colonization. Self-destructive phenomena within the periodontal tissues can also be triggered. Given the complexity of the mechanisms, our attitude will be essentially preventive by supra and subgingival scaling, as well as root planing, and educating our patient in rigorous hygiene.
Inflammation and histopathogenesis of periodontal disease
Bibliography:
-EA PAWLAK and Ph.M.HOAG manual of periodontology Masson Paris Barcelona Milan Mexico 1988
-J..A.Charon, F.Joachim, Ph.Sandel, orange CD
-Jan Lindhe manual of clinical periodontology cdp edition.
-Joël ITIC Francois ALCOUFFE current interpretation of pathogenic mechanisms in periodontology Question 3rd cycle SEID Paris Editor.
-JMMEGARBANE JFTECUCIANU bacterial pathogenesis of periodontal disease EMC 22030 A 20 6-1976.
-Bercy Tenenbaum periodontology from diagnosis to practice De Boeck-University.
-Philipe Bouchard periodontology implant dentistry volume 1 periodontal medicine
-P. Fréneaux, AHU. Department of Anatomy and Pathological Cytology of Prof. J. Amouroux, Avicenne Hospital, Bobigny Inflammation
Inflammation and histopathogenesis of periodontal disease
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