The aetiology of periodontal diseases - aspects of host defence Flashcards
Role of saliva in defence of periodontal diseases
Contains IgA Contains antibacterial substances -lactoferrin -thiocynate -hydrogen peroxide
Role of epithelium
- Surface epithelium shed together with any attached bacteria
- Permeability barrier
- JE may be more permeable than oral epithelium
- Epithelium can stimulate inflammatory and immune response by releasing cytokines e.g. IL-1
The inflammatory response
Crevicular fluid Tissue damage > blood flow Oedema Neutrophils, macrophages
Crevicular fluid
Inflammatory exudate
Contains complement: C1-9
May contain antibodies which act as an ‘opsonin’ & aid phagocytosis
Contains clotting cascade and kininogens
Complement C3a, C5a, C9
- C3a & C5a: vascular changes, stimulate histamine release, promote formation of leukotrienes and prostaglandins; attract phagocytes and aid phagocytosis
- C9: membrane attack complex, destroys micro-organisms
Clotting cascade
Fibrin forms a barrier to spread of infection
-thrombin and Hageman factor promote the inflammatory response
Kininogens
Converted to kinins by proteases
Bradykinin - similar to histamine, promotes inflammatory response
What happens to crevicular fluid in the crevice
Becomes modified
Bacteria in plaque can metabolise some components
Complement, immunoglobulin and other components partly consumed and degraded in crevice
Up to 1ml fluid may be lost per day
Functions of neutrophils
Production of NETS - neutrophil extracellular traps
Kill microbes by antimicrobial peptides
Neutrophils themselves die in the process
Functions of macrophages
Phagocytosis
Antigen presentation - simulate immune response
Growth factors
-stimulation of fibroblasts and endothelial cells to promote healing
Cytokines and chemokines attract inflammatory cells and regulate inflammatory response
-IL-1 & TNF important
The inflammatory response: neutrophils
Neutrophils cannot phagocytose - secrete enzymes and NETS
Kill bacteria and solublizes plaque
Washed out by crevicular fluid
Some neutrophils inhibited
Evidence that neutrophils are important
Pxs with < neutrophils have > periodontal destruction e.g. cyclic neutropenia
Pxs with defective neutrophil function have > periodontal destruction e.g. Papillon Lefevre syndrome
Impaired neutrophil function may contribute to periodontitis in diabetes and Downs’ syndrome
What are macrophages derived from?
Blood monocyte
+IFN-γ T cells
The inflammatory response: macrophages
Stimulate immune response
Release cytokines
Phagocytose
Stimulate healing
Humoral immunity
B cells
Production of antibody by plasma cells
Cell mediated immunity
T cells
Immune regulation and cytotoxic T cell killing of virally infected and neoplastic cells
What leads to IgA being secreted in saliva?
Bacteria swallowed and antigens recognised in gut MALT
What does IgA secretion lead to?
Antigen penetrates epithelium
Carried to lymph nodes
Initiates immune response
Antibody secreted in plasma
Antibody enters crevice in crevicular fluid
Some antibody produced locally in tissues by plasma cells
Role of antibody in defence
Bind to bacteria -acts as opsonin -activates neutrophil enzyme secretion -prevents bacterial attachment -activates complement -directly inhibits bacterial metabolism Bind to soluble factors -neutralises toxins -inhibits enzymes
Chronic marginal gingivitis
Bleeding on probing
False pocketing
What is the cause of the tissue damage and bone loss in periodontal disease?
Bacterial products
Host response
Bacterial products
Endotoxins
-may damage epithelium, fibroblasts
Bacterial enzymes e.g. collagenase, hyaluronidase
-break down CT
LPS, capsular material, peptidoglycans, muramyl dipeptide, proteases
-may cause resorption
Host products
Release of enzymes from neutrophils
Complement
Production on IL-1, IL-6 by macrophages
-stimulates bone resorption and epithelial proliferation
Inflammatory mediators
-prostaglandins, other cytokines, leukotrienes also stimulate bone resorption
Summary of tissue destruction
Some caused by bacteria but effects are limited by host response
Some due to host response - so called bystander cell damage
-IL-1 may be particularly important
Inflammation results in disturbance of normal tissue turnover
Mostly periodontal disease is stable, with tissue damage = repair
Progression when balance altered by host response or bacterial factors
