pathogenesis of periodontitis
TRANSCRIPT
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D R G A B R I E L D O E K E T E M E P I , G C P S I I
PATHOGENESIS OF PERIODONTITIS
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OUTLINE• Introduction• Theories
• Biofilm• Complexes• Microbial Virulence
• Clinically Healthy GINGIVA• Stages of Periodontitis• HOST RESPONSE• Host Innate Defense• Adaptive Defense
• Modifying Factors• Summary• References
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PERIODONTITIS
• Periodontitis, also known as pyorrhea, is a set of inflammatory diseases affecting the periodontium, i.e., the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth.
• Inflammatory and immune reactions to microbial plague are the predominant features of gingivitis and periodontitis.
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THEORIES
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BIOFILM
• Cooperating community of various types of microorganisms
• Microorganisms are arranged in microcolonies with channels between the microcolonies
• Microcolonies are surrounded by protective matrix• Differing environments within the microcolonies in the
biofilm• Microbial gene expression differs when microorganisms
are in a biofilm• Microorganisms have primitive communication system• Microorganisms in biofilm are resistant to antibiotics,
antimicrobials, and host response
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MICROBIAL COMPLEXES
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• Multiple bacterial spp are implicated at various stages of disease.• Bacterial species relevant at a stage of the
disease may not be important at other stages• The pathogenicity of micro-organism relates to
interplay between:• Individuals host innate capability• Adaptive response• Virulence of the bacteria
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MICROBIAL VIRULENCE
• Microbial invasion• Enzymes- Protease• Endotoxin – lipopolysaccharide• Microbes and their products can directly or
indirectly harm the host. However, the main detrimental effect may be the host’s own innate, inflammatory and immune response to the foreign molecules and antigens of the microbe
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CLINICALLY HEALTHY GINGIVA
• Clinically healthy gingiva is associated with small infiltrate of inflammatory cells that involves both junctional epithelium and subjacent Connective Tissue.• Subclinical inflammatory reactions occur in
response to the continuous presence of bacterial pdts in the crevice.• Present in a healthy gingiva are:• Leucocyte; PMN• lymphocyte• Macrophages
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STAGES OF PERIODONTAL DISEASE
• Four stages - Page and Shroeder (1976), • Initial• Early• Established• Advanced
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INITIAL
• 24hrs of plaque accumulation changes in dentogingival plexus• Increased blood flow (vascular dilatation)• Increased hydrostatic pressure• Formation of inter cellular gaps between Endothelial cells• Increased Gingivo crevicular Fluid• Chemotaxis of PMNWithin 2-4 days of days of plaque, there is an established response but gingiva still looks healthy clinically
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EARLY LESION
• There is marginal redness of the gingiva- characteristic clinical symptom.
• Lymphocytes and PMNs are predominant leukocytes in the infiltrate at this stage
• Very few plasma cells• Degeneration of fibroblasts via apoptosis• Breakdown of collagen fibers providing space for
inflammatory cells• Basal cells of junction and sulcular epith proliferate. • Biofilm may now form
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ESTABLISHED LESION
• Exposure to plaque continues leading to enhancement of the inflammatory response of the gingiva
• Plasma cells predominate• Increased proliferation of epithelium and rete pegs
extend deeper into the connective tissue• Junction epithelium is substituted by pocket epithelium.
Enhancing further apical migration of the biofilm• Ulceration of pocket epithelium • 2 types of established lesion appear to exist;• Stable• Progressive
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ADVANCED LESION
• As the pocket deepens, the biofilm continues its apical down growth and flourishes in this anaerobic ecological niche. • There is further loss of connective tissue and
bone• The lesion is not localized to gingiva but extends
apically and laterally into CT with Plasma cells dominant.
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HOST RESPONSE
• How an individual responds to the bacterial attack, greatly determines the disease progression.
Host Innate DefenseAdaptive Defense
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INNATE DEFENSE SYSTEMS
Does not require any previous contact with the micro-organismIncludes: Barrier function of oral epitheliumVascular and Cellular aspects of inflammatory responseMechanical washing effects of Saliva and GCFAntibodies, proteases, complement, cytokines, salivary lactoferrin found in saliva and GCFToll-like receptors
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• The immune system generally elicits a vigorous inflammation response against pathogens aimed at eliminating them, whereas it normally tolerates commensals.
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ADAPTIVE DEFENSE SYSTEMS
• Adaptive response unlike Innate, utilizes features like recognition, memory and binding to support the effector system (via Innate) in the elimination of psthogens.• It is the SECOND line of defense• Hallmarks of adaptive immunity are immune
memory and clonal expansion• Consists of Cell mediated immunity and Humoral
response
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• Cells involved:• Plasma cells• B cells• T helper cels• T cytotoxic cells• PolyMorphonuclear leucocytes• Macrophages
Antigen presenting Cells also play a role
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MODIFYING FACTORS
• Diabetes,
• Puberty, Pregnancy and Menopause
• Tobacco smoking
• Drugs
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Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Environmental and acquired risk factors
Genetic risk factors
Page, Ann Periodontol 1998
Summary of Pathogenesis of Periodontitis
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Pathogenesis of Periodontitis
Microbial Challenge
Host Immuno-inflammatory response
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Bacteria attacking the body• Antigens• Lipopolysaccharides• Other virulence factors
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Microbial Challenge
Host Immuno-inflammatory response
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Bacteria attacking the body• Antigens• Lipopolysaccharides• Other virulence factors
The body defense:• Antibodies• Neutrophils
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Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Inflammatory response releases:• Cytokines• Prostanoids• Matrix Metalloproteinases
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In Patient A, who is NOT susceptible to periodontitis:
Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Tissue and bone repair/healing
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In Patient B, who is susceptible to periodontitis:
Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Tissue destruction and bone loss
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Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Page, Ann Periodontol 1998
Deepening of periodontal pockets, furcation involvement, contaminated cementum…
In Patient B, who is susceptible to periodontitis:
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Microbial Challenge
Host Immuno-inflammatory response
Connective tissue and bone metabolism
Clinical signs of disease initiation and progression
Environmental and acquired risk factors
Genetic risk factors
Page, Ann Periodontol 1998
Pathogenesis of Periodontitis
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In periodontitis, what is actually occurring in a periodontal pocket…
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Periodontal Pathogens has invaded:
• Periodontal pocket• Cementum• Gingival tissue
In a patient susceptible to periodontitis, how does the body react?
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1. Epithelial Cells produce IL-8 and ICAM-1 in response to bacteria & antigens
IL-8/ICAM-1
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2. IL-8 and ICAM-1 are chemotactic signals for neutrophils, which are recruited to the sulcus
Neutrophils
Bacteria/Antigens
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3. Neutrophils control bacterial assault by phagocytosis but also secrete matrix metalloproteinases or collagenases (MMP-8) which results in collagen degradation MMP-
8
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4. Interaction of antigens with B cells lead to production of antibodies and complements, which contribute to phagocytosis
B-cell
Plasma Cell
T-cell
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5. In response to bacterial LPS, various cells produce IL-1, TNF-, and PGE2
Activated B-Cell
LPSMacrophage
Fibroblast
IL-1TNF-
PGE2
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Activated B-Cell
Macrophage
Fibroblast
IL-1TNF-
Osteoclast activation
PGE2
6. Production of IL-1, TNF-, and PGE2 leads to osteoclast activation, proliferation and differentiation
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Higher amounts of IL-
1, TNF-, PGE2, MMPs
Disease Health
Lower amounts of IL-10, TGF-, IL-1ra, TIMPs
Major Mediators
• Proinflammatory• Destructive
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Lower amounts of IL-
1, TNF-, PGE2, MMPs
Disease Health
Higher amounts of IL-10, TGF-, IL-1ra, TIMPs
• Anti-inflammatory• Protective
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• Thanks
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1. Karring T., Lang NP., Lindhe J., Clinical periodontology and Implant dentistry, (2008) 5th ED.
2. Pathogenesis of Periodontitis, Lecture notes, School of Medicine and Dentistry, University of Ghana.
3. Pathogenesis of Periodontitis, Lecture notes, University of Toronto
4. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr., Microbial complexes in subgingival plaque. J Clin Periodontol. 1998 Feb;25(2):134-44.