Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
DEFENCE MECHANISMS OF THE GINGIVA Introduction The gingival tissue is constantly subjected to mechanical and bacterial aggregations The following substances play a major role in providing resistance against these insults 1)Epithelial surface 2)Sulcular fluid 3)Leucocytes 4)Saliva Epithelial surface 1)Outer epithelium Keratinocytes Langerhan cells 2)Sulcular epithelium Acts as a semipermeable membrane through which injurious bacterial products pass in to gingival tissue and fluid from gingiva seeps into the sulcus. 3)Junctional epithelium Firmly attached to the tooth Forms a barrier against plaque bacteria Allows access to GCF and components of host defence Sulcular fluid known as Gingival Crevicular Fluid GCF is a serum like exudate which bathes the gingival sulcus or periodontal pocket and which follows an osmotic gradient with local tissues. In strictly normal gingiva little or no fluid can be collected. As this fluid traverses from host microcirculation, through inflammed tissues, into the periodontal pocket, it captures mediators involved in the destructive host responses and by products of local tissue metabolism. Composition of GCF The compounds can be host derived or produced by bacteria in the gingival crevices Cellular elements: Bacteria Desquamated epithelial cells Leucocytes Electrolytes: Potassium Sodium Calcium Organic compounds: Glucose concentration of GCF is 3 to 4 times greater than that of serum It may be due to 1)Metabolic activity of adjacent tissues 2)Function of local microbial flora Total protein content is much less than that of serum Other organic compounds include Hexuronic acid, Lactic acid, Urea, Hydroxyproline, Endotoxins, Cytotoxic substances, Hydrogen sulphide, Antibacterial factors etc Enzymes: Acid phosphatase Alkaline phosphatase Aspartate aminotransferase Chondroitin suphate Citric acid Cytokines Contd.. Endopeptidases Exopeptidases Immunoglobulins Lactoferrin Lactate dehydrogenase Lactic acid Lysozyme Prostaglandin Transferrin Thromboxane Methods of collection Absorbing paper strips Twisted threads placed around and into the sulcus Micropipettes Intracrevicular washings Absorbing paper strips Intrasulcular method (Brill technique) The filter paper is inserted into the pocket until resistance is encountered. It may cause a degree of irritation to the sulcular epithelium and can itself trigger the flow of fluid Extrasulcular method (Loe and Holm-Pederson)1965 The strip is placed at the entrance of the pocket Only the fluid seeping out is picked by the strip. Preweighed twisted threads The threads were placed in the gingival crevice around the tooth and amount of fluid collected was estimated by weighing the sample thread Micropipettes It permits collection of fluid by capillarity Capillary tubes of standardized length and diameter are placed in the pocket and their content is centrifuged and analysed Crevicular washings Used to study GCF of clinically normal gingiva. Methods: Uses an appliance consisting of a hard acrylic plate covering the maxilla with soft borders and a groove following the gingival margins. It is connected to four collection tubes and washings are collected by rinsing the crevicular areas from one side to another using a peristaltic pump. Two injection needles fitted one within the other such that during sampling the inside (ejection) needle is at the bottom of the pocket and the outside (collection) needle is at the gingival margin. Evaluation of amount of GCF Methods 1)Staining method Wetted area can be made more visible by staining with ninhydrin It is then measured planimetrically on an enlarged photograph, with a magnifying glass or with a microscope. 2)Electronic method Measures fluid collected on a blotter (Periopaper) and employs an electronic transducer (Periotron). The wetness of the paper strip affects the flow of an electronic current and gives a digital readout. Cellular and humoral activity of GCF Cellular immune response includes appearance of cytokines in GCF Function of IL 1 α and β Increase binding of PMNLs, monocytes, macrophages to endothelial cells Stimulate production of PGE2 Release of lysozymal enzymes Stimulate bone resorption Interferon γ has the ability to inhibit bone resorption Antibodies play a protective role for the periodontium In periodontal disease the reduction in antibody response is detrimental Clinical Significance Amount of GCF is greater in inflammation Increased during mastication of coarse food, tooth brushing, gingival massage, ovulation, smoking and during healing after periodontal surgery. Circadian periodicity:Increases from 6AM to 10 Pm and decreases afterwards Not increased by trauma from occlusion Drugs in GCF:Tetracycline, Metronidazole Saliva Exerts a major influence on plaque by mechanical cleansing of exposed oral surfaces Buffers acids produced by bacteria Controls bacterial activity. Function Salivary component Glycoproteins Probable mechanism Coats similar to gastric mucin Physical protection Glycoproteins Coats similar to gastric mucin Cleansing Physical flow Clearance of debris and bacteria Lubrication Buffering Bicarbonate Antacid phosphate Tooth integrity/ Minerals Maturation maintenece Glycoprotein Remineralisation pellicle Mechanical protection Antibacterial action IgA Lysozyme Lctoperoxid ase Control of colonization Breaks bacterial cell wall Oxidation of susceptible bacteria Leucocytes Differential count in clinically healthy gingival sulcus PMNL: 91.2 % - 91.5% Mononuclear cells: 8.5% - 8.8% B Lymphocytes: 58% T Lymphocytes: 24% Macrophages : 18 % Ratio of T lymphocytes to B lymphocytes is 1:3 in GCF PMNL: First line of defence against pathogens Releases elastase and serine protease which cause tissue breakdown Cytokines are involved in the communication between leucocytes and other cells of immune process Transendothelial Migration Phagocytes kill bacteria through two broad categories of killing mechanism: Oxidative mechanism Non oxidative mechanism Proinflammatory cytokines Production of PGE2 Acts on fibroblasts and osteoclasts Induces matrix metalloproteinases Causes periodontal destruction Lymphocytes: Humoral immunity Cell mediated immunity Conclusion Thank You