Pathogenesis of periodontitis
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A presentation on the Pathogenesis of Periodontitis
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Pathogenesis of periodontitis
- 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. 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. 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. THEORIES
- 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
- 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. 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. 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. STAGES OF PERIODONTAL DISEASE • Four stages - Page and Shroeder (1976), • Initial • Early • Established • Advanced
- 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. 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
- 14. 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
- 15. 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.
- 17. HOST RESPONSE • How an individual responds to the bacterial attack, greatly determines the disease progression. Host Innate Defense Adaptive Defense
- 18. 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
- 19. • The immune system generally elicits a vigorous inflammation response against pathogens aimed at eliminating them, whereas it normally tolerates commensals.
- 20. 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
- 21. • Cells involved: • Plasma cells • B cells • T helper cels • T cytotoxic cells • PolyMorphonuclear leucocytes • Macrophages Antigen presenting Cells also play a role
- 22. MODIFYING FACTORS • Diabetes, • Puberty, Pregnancy and Menopause • Tobacco smoking • Drugs
- 23. 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
- 24. 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
- 25. 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
- 26. 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
- 27. 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
- 28. 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
- 29. 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:
- 30. 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
- 31. In periodontitis, what is actually occurring in a periodontal pocket…
- 32. Periodontal Pathogens has invaded: • Periodontal pocket • Cementum • Gingival tissue In a patient susceptible to periodontitis, how does the body react?
- 33. 1. Epithelial Cells produce IL-8 and ICAM-1 in response to bacteria & antigens IL-8/ICAM-1
- 34. 2. IL-8 and ICAM-1 are chemotactic signals for neutrophils, which are recruited to the sulcus Neutrophils Bacteria/Antigen s
- 35. 3. Neutrophils control bacterial assault by phagocytosis but also secrete matrix metalloproteinases or collagenases (MMP-8) which results in collagen degradation MMP-8
- 36. 4. Interaction of antigens with B cells lead to production of antibodies and complements, which contribute to phagocytosis B-cell Plasma Cell T-cell
- 37. 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
- 38. 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
- 39. Higher amounts of IL-1, TNF-, PGE2, MMPs Disease Health Lower amounts of IL-10, TGF-, IL- 1ra, TIMPs Major Mediators • Proinflammatory • Destructive
- 40. Lower amounts of IL-1, TNF-, PGE2, MMPs Disease Health Higher amounts of IL-10, TGF-, IL- 1ra, TIMPs • Anti-inflammatory • Protective
- 41. • Thanks
- 42. 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.
Editor's Notes
- The association of bacteria within mixed biofilms is not random, rather there are specific associations among bacterial species. Socransky et al. (1998) examined over 13 000 subgingival plaque samples from 185 adult subjects. YELLOW GREEN PURPLE= EARLY COLONIZERS RED & ORANGE= MAJOR ETIOLOGIC AGENTS OF PERIODONTAL DISEASES.
- Microbial invasion – the invasion of dentogingival complex by spirochetes was documented by lisgarten. (1965) Enzymes- micro org produce a variety of enzymes that may digest EC host proteins and other molecules and thereby produce nutrients for bacterial growth. E.g. proteases – are capable of digesting collagen, elastin, fibronectin, filbrin and other components of ECM. Leukotocin Endotoxin- (lipopolygaccharides= LPS) of gram – ve microorgs are capable of invoking both the inflammatory and immune responses as they interact with Host cells. Stimulate cytokine release Activate complement system Affects bld coagulation
- Increased Flow GCF Dilutes noxious microbial subs in the crevice Flush away microbial subs from the crevice Presence of antib in GCF
- Basal cells of junction and sulcular epith proliferate. This represents an attempt by the body to enhance mechanical barrier protection to plaque bact. Biofilm may now form The early lesion may persist for long periods and the variability in time required to produce and established lesion may reflect variance in susceptibility between subjects.
- Lactoferrin is highly bactericidal. May bind iron, change the local environment and hence prevent microbial proliferation. Complement (in GCF) can kill bacterial directly or together with Abs, can bring PMNs to the region via chemotaxis and thereby initiate and facilitate the process of phagocytosis. Toll-like receptors are structuress evolved to detect bacterial challenge and are present on all human cells and may bind microbial cell molecules such as LPS, microbial fimbriae and lipoteichoic acid. The “bar code”hypothesis of innate recognition of microbes involve a process where TLRs read a “bar code”on microbes which is then decoded intracellularly to tailor the appropriate type of innate response
- The presentation of the processed antigen and its interaction with TCRs → production of cytokines. Cytokines produced by T helper cells regulate most fxns within the adaptive defence system in p’tal tissue. The cells occur as Th1 and Th-2 cells. Both Th-1 and Th – 2 cells express the CD8 markers but produce different cytokines. Th-1 Produces – IL-2, IFN – 8 and TNF. Theses cytokines activate other T cells including cytotoxic T cells to express the CD8 marker and serve as guards against microorganisms that are capable of invading host cells (ie viruses and invasive bacterial). The antigen in the infected host cells binds to MHC class 1 molecule to carry the antigen/peptide to the surface of the infected host cell. The Tc cells has the ability to recognise this alteration in the MHC class 1 molecules and destroys the membrane of the infected cells. It is established that CD8+Ve cells are found in smaller numbers in gingivis/ periodontitis than CD4 + Ve cells (yamazaki). Hence viruses and invasive microbes do not play a major role in p’tis. The Th-2 produces IL-4, IL-5, IL-6, IL-10, IL-13 and activates the humoral immune response by activing B cells to produce plasma cells → antibodies formation. The activation and differentiation of B cells require the presence of cytokines IL -4, IL-5 and IL-6 that are mainly produced by Th-2 cells. This → formation of plasma cells. Plasma cells produce antibiodies representing the final stage in B celss proliferation
- Uncontrolled DM – decreased salivary flow, Hyperglycemia- increase microbe proliferation, Periodontal attachment loss in moderate and poorly controlled diabetic patients, than in those under good control (Westfelt et al. 1996) Reduced PMN function (Marhoffer et al. 1992) and defective chemotaxis in uncontrolled DM impairs host defenses and progression of infection Estrogen affects salivary proxidases, stimulates collagen metabolism, progesterone +estrogen modulate vascular responses, menopause=osteoporosis higher prevalence of acute necrotizing ulcerative gingivitis, a finding that was confirmed in many subsequent studies of this condition (Fig. 12-10) (Pindborg 1949; Kowolik & Nisbet 1983; Johnson & Engel 1986)