Download defence mechanisms of the gingiva

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
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