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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
OUTLINE
• Introduction
• Theories
• Biofilm
• Complexes
• Microbial Virulence
• Clinically Healthy GINGIVA
• Stages of Per...
PERIODONTITIS
• Periodontitis, also known as pyorrhea, is a set of
inflammatory diseases affecting the periodontium, i.e.,...
THEORIES
BIOFILM
• Cooperating community of various types of microorganisms
• Microorganisms are arranged in microcolonies with cha...
MICROBIAL COMPLEXES
• Multiple bacterial spp are implicated at various stages of
disease.
• Bacterial species relevant at a stage of the disea...
MICROBIAL VIRULENCE
• Microbial invasion
• Enzymes- Protease
• Endotoxin – lipopolysaccharide
• Microbes and their product...
CLINICALLY HEALTHY GINGIVA
• Clinically healthy gingiva is associated with small
infiltrate of inflammatory cells that inv...
STAGES OF PERIODONTAL DISEASE
• Four stages - Page and Shroeder (1976),
• Initial
• Early
• Established
• Advanced
INITIAL
• 24hrs of plaque accumulation changes in
dentogingival plexus
• Increased blood flow (vascular dilatation)
• Incr...
EARLY LESION
• There is marginal redness of the gingiva- characteristic
clinical symptom.
• Lymphocytes and PMNs are predo...
ESTABLISHED LESION
• Exposure to plaque continues leading to enhancement of the
inflammatory response of the gingiva
• Pla...
ADVANCED LESION
• As the pocket deepens, the biofilm continues its apical
down growth and flourishes in this anaerobic eco...
HOST RESPONSE
• How an individual responds to the bacterial attack,
greatly determines the disease progression.
Host Inna...
INNATE DEFENSE SYSTEMS
Does not require any previous contact with the micro-
organism
Includes: Barrier function of oral e...
• The immune system generally elicits a vigorous
inflammation response against pathogens aimed at
eliminating them, wherea...
ADAPTIVE DEFENSE SYSTEMS
• Adaptive response unlike Innate, utilizes features like
recognition, memory and binding to supp...
• Cells involved:
• Plasma cells
• B cells
• T helper cels
• T cytotoxic cells
• PolyMorphonuclear leucocytes
• Macrophage...
MODIFYING FACTORS
• Diabetes,
• Puberty, Pregnancy and Menopause
• Tobacco smoking
• Drugs
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
tissue and bone
metabolism
Clinical signs of
disease ini...
Pathogenesis of Periodontitis
Microbial
Challenge
Host Immuno-
inflammatory
response
Clinical signs of
disease initiation
...
Microbial
Challenge
Host Immuno-
inflammatory
response
Clinical signs of
disease initiation
and progression
Page, Ann Peri...
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
tissue and bone
metabolism
Clinical signs of
disease ini...
In Patient A, who is NOT
susceptible to periodontitis:
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
t...
In Patient B, who is susceptible
to periodontitis:
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
tissu...
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
tissue and bone
metabolism
Clinical signs of
disease ini...
Microbial
Challenge
Host Immuno-
inflammatory
response
Connective
tissue and bone
metabolism
Clinical signs of
disease ini...
In periodontitis, what is actually
occurring in a periodontal
pocket…
Periodontal Pathogens
has invaded:
• Periodontal pocket
• Cementum
• Gingival tissue
In a patient susceptible to periodont...
1. Epithelial Cells produce
IL-8 and ICAM-1 in
response to bacteria &
antigens
IL-8/ICAM-1
2. IL-8 and ICAM-1 are
chemotactic signals for
neutrophils, which are
recruited to the sulcus
Neutrophils
Bacteria/Antigen...
3. Neutrophils control
bacterial assault by
phagocytosis but also secrete
matrix metalloproteinases or
collagenases (MMP-8...
4. Interaction of antigens with B cells
lead to production of antibodies and
complements, which contribute to
phagocytosis...
5. In response to bacterial LPS,
various cells produce IL-1, TNF-,
and PGE2
Activate
d B-Cell
LPS
Macrophage
Fibroblast
...
Activate
d B-Cell
Macrophage
Fibroblast
IL-1
TNF-
Osteoclas
t
activation
PGE2
6. Production of IL-1, TNF-, and PGE2
le...
Higher amounts
of IL-1, TNF-,
PGE2, MMPs
Disease Health
Lower amounts of
IL-10, TGF-, IL-
1ra, TIMPs
Major Mediators
• ...
Lower amounts
of IL-1, TNF-,
PGE2, MMPs
Disease Health
Higher amounts of
IL-10, TGF-, IL-
1ra, TIMPs
• Anti-inflammator...
• Thanks
1. Karring T., Lang NP., Lindhe J., Clinical periodontology
and Implant dentistry, (2008) 5th ED.
2. Pathogenesis of Perio...
Pathogenesis of periodontitis
Pathogenesis of periodontitis
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Pathogenesis of periodontitis

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A presentation on the Pathogenesis of Periodontitis

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Pathogenesis of periodontitis

  1. 1. 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
  2. 2. OUTLINE • Introduction • Theories • Biofilm • Complexes • Microbial Virulence • Clinically Healthy GINGIVA • Stages of Periodontitis • HOST RESPONSE • Host Innate Defense • Adaptive Defense • Modifying Factors • Summary • References
  3. 3. 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.
  4. 4. THEORIES
  5. 5. 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
  6. 6. MICROBIAL COMPLEXES
  7. 7. • 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
  8. 8. 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
  9. 9. 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
  10. 10. STAGES OF PERIODONTAL DISEASE • Four stages - Page and Shroeder (1976), • Initial • Early • Established • Advanced
  11. 11. 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 PMN Within 2-4 days of days of plaque, there is an established response but gingiva still looks healthy clinically
  12. 12. 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
  13. 13. 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
  14. 14. 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.
  15. 15. HOST RESPONSE • How an individual responds to the bacterial attack, greatly determines the disease progression. Host Innate Defense Adaptive Defense
  16. 16. INNATE DEFENSE SYSTEMS Does not require any previous contact with the micro- organism Includes: Barrier function of oral epithelium Vascular and Cellular aspects of inflammatory response Mechanical washing effects of Saliva and GCF Antibodies, proteases, complement, cytokines, salivary lactoferrin found in saliva and GCF Toll-like receptors
  17. 17. • The immune system generally elicits a vigorous inflammation response against pathogens aimed at eliminating them, whereas it normally tolerates commensals.
  18. 18. 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
  19. 19. • Cells involved: • Plasma cells • B cells • T helper cels • T cytotoxic cells • PolyMorphonuclear leucocytes • Macrophages Antigen presenting Cells also play a role
  20. 20. MODIFYING FACTORS • Diabetes, • Puberty, Pregnancy and Menopause • Tobacco smoking • Drugs
  21. 21. 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
  22. 22. 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
  23. 23. 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
  24. 24. 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
  25. 25. 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
  26. 26. 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
  27. 27. 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:
  28. 28. 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
  29. 29. In periodontitis, what is actually occurring in a periodontal pocket…
  30. 30. Periodontal Pathogens has invaded: • Periodontal pocket • Cementum • Gingival tissue In a patient susceptible to periodontitis, how does the body react?
  31. 31. 1. Epithelial Cells produce IL-8 and ICAM-1 in response to bacteria & antigens IL-8/ICAM-1
  32. 32. 2. IL-8 and ICAM-1 are chemotactic signals for neutrophils, which are recruited to the sulcus Neutrophils Bacteria/Antigen s
  33. 33. 3. Neutrophils control bacterial assault by phagocytosis but also secrete matrix metalloproteinases or collagenases (MMP-8) which results in collagen degradation MMP-8
  34. 34. 4. Interaction of antigens with B cells lead to production of antibodies and complements, which contribute to phagocytosis B-cell Plasma Cell T-cell
  35. 35. 5. In response to bacterial LPS, various cells produce IL-1, TNF-, and PGE2 Activate d B-Cell LPS Macrophage Fibroblast IL-1 TNF- PGE2
  36. 36. Activate d B-Cell Macrophage Fibroblast IL-1 TNF- Osteoclas t activation PGE2 6. Production of IL-1, TNF-, and PGE2 leads to osteoclast activation, proliferation and differentiation
  37. 37. Higher amounts of IL-1, TNF-, PGE2, MMPs Disease Health Lower amounts of IL-10, TGF-, IL- 1ra, TIMPs Major Mediators • Proinflammatory • Destructive
  38. 38. Lower amounts of IL-1, TNF-, PGE2, MMPs Disease Health Higher amounts of IL-10, TGF-, IL- 1ra, TIMPs • Anti-inflammatory • Protective
  39. 39. • Thanks
  40. 40. 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.

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