Microbial Interactions in Periodontal Diseases: Host Response

1. MICROBIAL INTERACTIONS WITH THE HOST IN PERIODONTAL DISEASES

2. TOOTH HOST RESPONSE DENTAL PLAQUE

3. INTRODUCTION • GINGIVITIS and PERIODONTITIS are chronic infectious diseases. • Course and durationInteraction between the microorganism and the host. • Host tissue destruction is result of direct or indirect mechanism of microorganisms

4. GINGIVITIS

5. PERIODONTITIS

6. MICROBIAL ASPECTS OF MICROBIAL-HOST INTERACTION • Specific micro-org found in periodontal diseases are Gram negative facultative/ obligate anaerobes

7. Predominantly • Porphyromonasgingivalis • Aggregatibacteractinomycetemcomitans • Tannerella forsythia • Fusobacteriumnucleatum • Prevotellaintermedia • Campylobacter rectus • Treponema denticola • Peptostreptococcus micros • Eikenellacorrodens

8. Virulence factor

9. Virulence factor • A virulence factor is any microbial component necessary for causing disease in the host. • Define as The property of a microorganism that enables it to cause disease Classified as • Factors which enable bacterial species to colonize and invade host tissues • Factors that enable a bacterial species to cause host tissue damage directly or indirectly

11. Bacterial colonization Bacterial adherence in the periodontal environment: • GCF-bathes the gingival sulcus, or periodontal pocket . • Surfaces Available- Tooth/Root, Tissues, Preexisting plaque mass. e.g.ofvirulance factors - Fimbriae, surface proteins etc.

12. Host Tissue Invasion • Through the ulcerations in the gingival epithelium of the sulcus and the pocket. • Direct penetration of bacteria in to host epithelial or connective tissue cells. Eg-A a comitans,P gingivalis, F nucleatum, T denticola. Localisation of bacteria to the tissues→effectively deliver toxic molecules.

13. Bacterial evasion of host defense mechanism • To survive in the periodontal environment, bacteria must neutralize or evade host defense mechanism For examples • Immunoglobulin degrading proteases. • Leukotoxins, Cytolethal distending toxins-suppress the activity of or kill PMNS. And lymphocytes.(Aa comitans)

14. Microbial mechanisms of Host Damage B’al enzymes species Collagenase- P gingivalis, A a comitans Trypsin like enzyme- P gingivalis , A a comitans Arysulfatase - C rectus Neuraminidase- P gingivalis,T forsythus, Fibronectin degrading enzyme- P gingivalis, P intermedia Phospholipase A- P intermedia

15. Modification of host response • MMP 1 AND 8 • CYTOKINES- IL-1,IL-6,TNF α • PROSTAGLANDINS

16. Virulence factors of Aggregatibactor actinomycetemcomitans

17. Virulence factors • Virulence traits relevant to colonisation:- • Autotransporter proteins - the largest known family of extracellular proteins • Pili - • Fimbriae • O polysaccharide • Phosphorylcholine

19. Virulence factors- contd • Lipopolysaccharides:– (Endotoxin) has a high potential for causing destruction of an array of host cells and tissues, a key factor in periodontal disease. There is resultant necrosis, bone resorption, platelet aggregation and activation of macrophages. • Fc binding proteins:– the organism’s ability to make proteins that bind to the fc receptors, inhibits the ability of opsonising antibodies to bind PMNL, thus reducing phagocytosis.

20. Immunosuppresive factors capable of suppressing the host defense by • downregulates T & B cells to respond to mitogens. • Impairing the ability of leucocytes to respond to mitogens • Impairs IgG & IgM synthesis

21. Extra cellular membrane vesicles – almost all strains of A.a form vesicles • These vesicles often contain leucotoxin,endotoxinand abacteriocinthat mediates bone resorption activity.

22. Virulance factor for P. Gingivalis • Capsule:- considered an important anti- phagocytic virulence factor. • Outer membrane proteins:- plays a major role in coaggregation. • Fimbriae:- arranged in a peritrichous fashion all over the surface of the cell. exhibiting great ability to both bind & invade epithelial cells.

23. Proteinases:- its the most important virulence factors in the progress of Periodontal disease - degrading collagen types I and IV, and ECM proteins (fibrinogen, laminin and adhesion molecules). • The familyof cysteineproteinases:- namely gingipains are trypsin like proteases comprising a group of cysteineendopeptidases.

24. Gingipains It is the product of three genes which code for the proteolytic activity seen in P.gingivalis – these genes encode for 2 cysteine proteases- Arginine- gingipain(RgpA, RgpB) and a Lysine- gingipain(Kgp) . • These cystine proteinases execute various activities - activation of the Kallikrein/ kinin system, blood clotting system, degradation of fibrinogen and fibrin and the disruption of the host defences.

25. In addition to Gingipains, P.gingivalis also produces:- : • Aminopeptidases. • Caseinases. • Collagenase. • Numerous proteolytic enzymes. • Haemagglutinin,

26. Immunologic aspects of the microbial –host interaction • Innate factors – complement, resident leukocytes and mast cells-important role in signaling endothelium, thus initiating inflammation. • Acute inflammatory cells-protect local tissues by controlling the periodontal microbiota within the gingival crevice and junctionsl epithelium.

27. Chronic inflammatory cells- macrophages,lymphocytes protect the Entire host from within the subjacent connective tissues

28. Microbiology and immunology in gingival health • Gram positive facultative organisms- Actinomyces, Streptococcus. • Gram negative species and spirochaetes forms –in small numbers.

29. Microbiology and immunology in gingivitis • Gram positive→gram negative bacteria Pregnancy gingivitis→P intermedia that can substitute progesterone or estradiol for vitamin k as an essential bacterial growth factor.

30. Chronic Periodontitis

31. Necrotizing periodontal diseases • P intermedia, • fusobacterium and • spirochetal microorganisms.

32. Neutrophil disorders • Disorders that affect production or function of leukocytes may results in severe periodontal destruction

33. Neutrophil abnormalities • Neutropenia • Agranulocytosis • Chediak –Higashi Syndrome • Lazy Leukocyte Syndrome • Leukocyte Adhesion Deficiency • Papillon –Lefevre Syndrome • Downs Syndrome • Diabetes

34. Neutropenia • Individual with an ANC less than 1500 cells/microlit • Can be Genetic or drug induced or viral Clinical presentation • Severe periodontitis, • spontaneous bleeding,ulcerations, • rapid spread of infections

36. Agranulocytosis • Characterized by reduction in the number of circulating granulocytes and results in severe infections, ulcerations, necrosis, gingival hemorrage • Absence of notable inflammation due to absence of granulocytes

38. Chediak higashi syndrome • Rare disease affecting phagocytes, platelets and neutrophil • Neutrophil contains giant lysosome that can fuse with phagosome …. But does not release its content….. Unable to kill pathogen • Severe periodontitis(rapidly progressing periodontitis)

40. Lazy leukocyte syndrome Defective chemotactic property, neutropenia

41. Papillon leferve syndrome • Genetic disorder • Syndrome characterised by hyperkeratotic skin lesions, severe destruction of periodontium

45. Downs syndrome • Congenital disease characterised by mental deficiency and growth retardation • Poor chemotaxis and phagocytosis • Oral manifestation • Deep periodontal pocket • Marked recession • Tooth mobility, tooth loss

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