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Pre-clinical Periodontics

Pre-clinical Periodontics

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Pre-clinical Periodontics

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  1. Pre-clinical Periodontics Dr Jamal Naim PhD in Orthodontics Defense mechanisms of the periodontium

  2. Initiation of periodontal disease • Microorganisms which form the dental biofilm contain or release components which induce gingivitis. • The inflammatory changes may remain confined to the gingival area for several years but at some sites gingivitis eventually shifts to destructive periodontal disease.

  3. Why lesions remain localized to the marginal portion of the gingival tissues, while in others they progress to involve the loss of connective tissue attachment and supporting alveolar bone? Imbalance of the host-microbial relationship is occurring in the destructive lesions!

  4. Normal gingiva vs. clinical healthy gingiva • Pink color, firm consistency and scalloped outline for gingival margin. • The interdental papillae are firm, do not bleed on gentle probing and fill the space below the contact areas. • Can only be established experimentally after super- vised meticulous daily plaque control for several weeks.

  5. Normal gingiva vs. clinical healthy gingiva • the gingivae we would routinely classify as "clinically healthy gingivae" are not as histological perfect as the "normal gingivae“ • Clinically healthy gingivae would be typically that level of health which could be attained by patients regularly practicing a good standard of plaque control.

  6. The oral surface of clinically healthy gingiva consists of keratinized oral epithelium continuous with the JE.

  7. Below the JE is a vascular network which supplies the epithelium with nutrients and defense cells.

  8. Neutrophils and macrophages can be seen in the junctional epithelium of the clinically healthy gingiva

  9. Defence mechanisms of the periodontium Clinically the gingival tissue is able to deal with external challenges without progressing to a diseased state, probably due to several defensive factors:

  10. Host defense processes Host-parasite reactions can be divided into: • Innate (non-specific) response include the inflammatory response • Adaptive (specific) response include immunological responses

  11. Innate (non-specific) response Innate immune mechanisms operate without any previous contact with the disease-causing microorganism. These mechanisms include: • the physical barriersof the oral mucosal epithelial surfaces and • vascularand cellularaspects of the inflammatory responses.

  12. Innate (non-specific) response • Regular shedding of epithelial cells into the oral cavity • Positive fluid flow of the gingival crevice (GCF) which may remove non-attached microorganisms and noxious products • Antimicrobial effect of antibodies • Phagocytic function of neutrophils and macrophages • Detrimental effect of complements on microbes

  13. Innate (non-specific) response • Gingival epithelial cells may form the first barriers of defense against oral bacteria in periodontal tissues. (KE) • Prevention of attachment and colonization: • the washing effect of the saliva and gingival crevicular fluid (GCF), • the constituents of these fluids (antibodies, proteases, complement and lactoferrin) can be bactericidal.

  14. Turnover time of JE • JE has a high turnover (5 days) compared to oral gingival epithelium (8-10 days) • The shedding rate is very high for JE 50-100 > than OGE. • JE-cells that are degenerating and covered by bacteria and or their products are expelled at a fast rate • This also may explain why gingivitis can be a reversible condition, which is considered a defensive mechanism of this tissue`

  15. JE has a rapid turnover rate • JE cells at the base of the Sulcus are covered by microbes and constantly shed into the Sulcus. • Replacement rate of the JE is 5 days (vs 8-10 days for oral gingival epithelium) Tooth surface

  16. JE has impressive antimicrobial systems • Enzyme-rich lysosomes (packages of enzymes in the JE cytoplasm) • e. g. Defensins Antimicrobial peptides

  17. blood vessels in gingiva • JE behaves like a semi-permeable membrane • Small molecules injected intravenously can be detected in sulcus after 1-5 minutes. • Large molecules (eg immunoglobins) take 30-120 minutes to get into sulcus. Tooth surface

  18. JE behaves like a semi-permeable membrane • Bacteria in the sulcus release large quantities of metabolites which diffuse through the JE: • Butyric & propionic acids (toxic to tissues) • Peptides • Lipopolysaccharides (LPS)

  19. JE is part of the immune system Bacteria JE has a sensory function detecting chemical excreted from the bacteria HELP!!!!! we’re under attack

  20. cytokines blood vessels in gingiva • JE is part of the immune system Bacteria JE produces cytokines (IL-8) which recruit PMN from underlying blood vessels in connective tissue, through JE and out into sulcus

  21. blood vessels in gingiva • JE is part of the immune system Bacteria JE produces other cytokines which switch on the inflammatory response in the gingiva. Cytokines

  22. Neutrophils (PMN) • Polymorphonuclear leucocytes Different names for the same cell • Polymorphs • PMN • Neutrophils

  23. PMN = primary periodontal defensive cell • Produced in the bone marrow from stem cells; live for about 4-5 days. • PMN have a rapid turnover rate. • Engulf microbes in sulcus (phagocytosis). • Digest microbes by powerful enzymes contained in cytoplasm.

  24. PMN = primary periodontal defensive cell May blow up in the gingival tissues, releasing destructive enzymes and pro-inflammatory mediators which exacerbates the inflammatory response.

  25. cytokines PMN form a dense layer (pallisade) over plaque & engulf bacteria in sulcus Biofilm Bacterial product stimulates JE cells to produce concentration gradient of chemo-attractant (IL-8) for PMN. Tooth surface blood vessels in gingiva

  26. Transendothelial migration • Defects of the PMN function can reduce host defense capability. • PMN function may be blocked at various sites: • Chemotactic defects • Inadequate adherence • Defective phagocytosis • Impaired ability to digest

  27. Transendothelial migration • Systemic diseases characterized by granulocyte defects are usually accompanied by severe periodontal disease (diabetes mellitus, crohn's disease, down syndrome) • Granulocytes in most patients with LJP or RPP exhibit more or less comprised functions

  28. Gingival crevicular fluid • Gingival Crevicular Fluid transports PMN, antibodies, host enzymes and helps flush out the sulcus • Positive pressure from gingival blood vessels, through JE into sulcus. Tooth surface blood vessels will be discussed later

  29. Non specific antibodies Non-specific: from circulation Specific: against bacteria localized in the gingival tissues This topic will be discussed in more details later

  30. Immune system interactions • PMN • Complement • Antibody interaction

  31. Immune system interactions • The complement systemis a series of 25 proteins manufactured in the liver and are are activated by, and work with, (i.e. complement) antibodies Function of complement: • lysing (bursting) of cells and signal to phagocytes that a cell have to be removed. Complement coated bacterial cells are easier for PMN to phagocytose • binding to bacteria, and when activated, can directly kill them.

  32. Defensive factors All of these factors may operate at the same time to reduce the bacterial load and thus prevent an over-response of the tissue defense systems which could result in the formation of a lesion.

  33. Summary of primary periodontal defenses • Physical barrier • High turnover rate • Large inter-cellular spaces permit PMN progress to sulcus • JE produces cytokines which call to PMN • Crevicular fluid, flushing carries cells + antibodies • Immune system interactions