Gcf khushbu

GINGIVAL CREVICULAR FLUID
DR. KHUSHBU MISHRA
MDS 1ST YEAR

CONTENTS
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Introduction
Definition
Function
History
Formation

 Permeability of junctional and oral sulcular

epithelium
 Methods of collection
 Problems during collection

 Composition of GCF
 Brief review of pathogenesis of periodontitis
 Use of GCF inflammatory mediators as
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indicators of risk for Periodontal diseases
Commercially available diagnostic kits
Clinical significance
Conclusion
Recent findings in GCF
References

Defence mechanism of oral cavity


Defence mechanism

Specific
1. Humoral immunity
2. cell mediated immunity

Non-specific
1.saliva
2.sulcular fluids
3.Higher tissue turnover
4.Intact epithelial barrier
5.Presence of normal flora
6.Local antibody production
7.Migrating leukocytes

Anatomy of the gingival crevice

The gingival sulcus
is the shallow crevice or
space around the tooth ,
bounded by the surface
of the tooth on one side and
the epithelial lining the
free margin of the
gingiva on the other.

gingival crevicular fluid

Monday, December 02, 2013

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Definition

A fluid occurring in minute amounts in gingival crevice,
belived by some authorities to be an inflammatory exudate
and by others to cleanse material from the crevice,
containing sticky plasma proteins which improve
adhesions of the epithelial attachment, have antimicrobial
properties and exert antibody activity.
(from Jablonski, illustrated Dictionary
of Dentistry, 1982)

Functions :

1) Cleanse material from the sulcus
2) Contain plasma proteins that may improve adhesion of
the epithelium to the tooth.
3) Possess antimicrobial properties.
4) Exert antibody activity in defense of the gingiva.



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Studies on gingival crevice fluid (GCF) extend over a period
of about 50 years
 The pioneer research of Waerhaug (1952) was focused
on ----- the anatomy of the sulcus and its transformation
into a gingival pocket during the course of periodontitis.
 Studies by Brill et al.(1962) laid the foundation for
understanding the physiology of GCF formation and its
composition.
 The studies of Löe et al.(1965) ----- use of GCF as an
indicator of periodontal diseases.



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 Egelberg continued to analyze GCF and focused his

studies on the dentogingival blood vessels and their
permeability as they relate to GCF flow.
 Attstrom R, Egelberg J. presence of leukocytes in
gingival crevice during developing gingivitis in dogs.
JPR 1971 : 6; 110 -114.
 The GCF studies boomed in the 1970s. The rationale for
understanding dentogingival structure and physiology was
created by the outstanding electron microscopic studies of
Schroeder and Listgarten.



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 It was soon understood that enzymes released from

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

damaged periodontal tissue possessed an enormous
potential for periodontal diagnosis.
Presence and functions of proteins – Sueda, Bang and
Cimasoni.
Collagenases and Elastase in GCF are derived from
human cells - Ohlsson, Golub, Uitto.
Goodson thoroughly studied major issues in GCF flow
rate and its method of collection.
Flow rate of GCF may increase about 30 times in
periodontitis patients than compared to healthy sites.
Resting volume also increases with the formation of
pockets.



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In 1974 the first edition of the monograph

 The Crevicular Fluid by Cimasoni was published. This

comprehensive review gave a big boost to GCF studies
and towards the end of the first millennium the research
on GCF increased dramatically.



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Timeline



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Formation of GCF
GCF is formed at the rate of 0.5- 2.4 ml/day.
There are 2 theories that suggest the formation of GCF.
Theory 1 (Brill and Egelberg)

Increase in the permeability of vessels
seepage of fluids in sulcus
Formation of GCF

 Theory 2

 From the work of Alfano (1974) and from the hypothesis

postulated by Pashley (1976) which suggested that the
initial fluid produced could simply represent interstitial
fluid which appears in the crevice as a result of an
osmotic gradient. This initial, pre-inflammatory fluid was
considered to be a transduate and on stimulation, this
changed to become an inflammatory exudate.

 The model proposed by Pashley

predicted that
GCF production is governed by
passage of interstial fluid
from capillaries
tissues
lymphatic system). When the rate of
when capillary filtrate exceeds that of lymphatic
uptake, fluid will accumulate as edema
and/or leave the area as GCF


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 Factors modulating:
 Filtration coefficient of the lymphatic and capillary

endothelium
 Osmotic pressure within the different compartments.
 Therefore, even in health also, if the osmotic pressure of
the sulcular fluid exceeds that of the tissue fluid, (possibly
because of accumulation of plaque derived molecules)
there will be net increase in the flow of GCF.



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PERMEABILITY OF JUNCTIONAL AND
ORAL SULCULAR EPITHELIA
 Substances that have been shown to penetrate the sulcular

epithelium include
albumin, Endotoxins, thymidine, histamine, phenytoin, per
oxidase.
 The main pathway for the transport of substances across

the junctional and sulcular epithelia seems to be the
intercellular spaces which according to Schroeder and
Munzel – Pedrazzoli (1970) form 18% of the total
volume of the junctional epithelium and 12% that of the
oral sulcular epithelium.


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 According to Squier (1973) the degree of permeability of the

oral mucosa does not seem to depend upon its degree of
Keratinization. The mechanisms of penetration through an
intact epithelium were reviewed by Squier and Johnson.
 Three routes have been described:
 Passage Form CT Into The Sulcus:
 Passage From The Sulcus Into The CT:
 Passage Of Substances through

pathological or experimentally
modified gingival sulcus.



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 Brill was also first to show the presence of plasma

proteins in the gingival fluid.
 The fundamental observations of Brill have been confirmed
in other experiments, where it was shown that extraneous
materials such as India Ink, labeled albumin or labeled
fluorescein, tetracycline and saccharated iron oxide could
be seen to pass from the gingival vessels into the gingival
sulcus or pocket



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Absorbent filter paper strips

These strips are placed for 3 mins and GCF sample is
collected by 2 methods.
a) Intrasulcular or Brill technique – within the sulcus
b) Extracellular or Loe & Holm pederson technique- at its
entrance.

Evaluation of amount of fluid collected by paper
strips
1.
2.

Direct viewing and staining
Weighing of the strip

1.


Direct viewing and staining:
Alcoholic solution of ninhydrin (0.2%)
-blue
purple
pink
Measured with – transparent scales, calipers, caliberated
magnifying glass





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 Disadvantages of staining method:
 Cannot be used chair side.
 Inevitable delay in measurement may result in increase

variation due to evaporation of the fluid.
 Staining of the strips for protein labeling prevents
further lab investigations.
2. Weighing of strips
 Sealed micro centrifugation plastic tube.

PERIOTRON

An electronic method has been devised for measuring gingival fluid absorbed on
paper strips by Harco electronics called Periotron (Dental product division
Winnipeg, Manitoba, Canada).

• latest and standard method for measuring gingival fluid
absorbed on paper strips.


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 Developed by Harco electronics
 Principle:- The wetness of the paper strip affects the flow

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of an electronic current
It has 2 metal jaws which acts as the plates of an electrical
condenser.
When a dry strip is placed  zero reading is obtained
A wet paper strip will increase the capacitance in
proportion to the volume of fluid and this can be measured
as an increased value in the readout.
Three models  600, 6000 and 8000.



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Advantages
 Simple procedures, can be viewed directly.
 Quantitative assessment of fluid can be obtained.
 Evaporation is kept minimum.

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Disadvantages
Contamination can occur.
In case of evaporation, has to be repeated many times.
Care should be taken to insert paper strip in standardized
position.
inability to measure the volume of GCF greater than
1.0µl.

Pre-weighed twisted threads

Thread is placed in the gingival crevice around the tooth
and the amount of fluid collected is estimated by weighing
the sample thread.
Used by WEINSTEIN et al.



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Micropipettes/ capillary tubing
 Krasse and Egelberg
 Principle- collection of fluid by capillary action.

After isolation and drying of collection site, capillary
tubes of known diameter are inserted into the entrance
of gingival crevice, GCF migrates into the tube by
capillary action.
As diameter is known, the amount of GCF can be
calculated by measuring the distance which the GCF
has migrated.
And finally, their content is then centrifuged and
analyzed.

Disadvantages
 Collection of fluid is
difficult due to viscosity
of the fluid.
 Recovery of sample is demanding.
 Long collection period.
 May cause trauma as prolonged holding of
pipette is required.

Crevicular washings

 The Method Of Oppenheim:

This method uses an appliance consisting of a hard acrylic
plate covering the maxilla with soft borders and a groove
following the gingival margins, connected to four
collection tubes.

The washings are obtained by rinsing the crevicular
areas from one side to the other, using a peristaltic pump.



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 ADVANTAGES:
 Useful for longitudinal studies.
 Permits collection without disturbing the integrity of

the marginal tissues.
 Contamination is least.
 DISADVANTAGES:
 Complex procedure.
 Represents a dilution of crevicular fluid.



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 The method of Skapski And Lehner:
 This method uses two injection needles fitted one

within the other such that during sampling the
inside, or ejection, needle is at the bottom of the
pocket and the outside, or collecting, one is at the
gingival margin. The collection needle is drained
into a sample tube by continuous suction.



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 ADVANTAGES
 Useful for cases of clinically normal gingiva.
 Useful for studying the number and state of cells and

bacteria form the crevicular area.
 DISADVANTAGES
 Does not permit absolute quantitative assessment as the

dilution factor cannot be determined.



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Problems during GCF collection

 Scarcity of material that can be obtained from sulcus.
 Contamination

The major sources of contamination of GCF sample would
be blood, saliva, or plaque.
 Sampling time
The problem with prolonged collection time is that the
nature of the GCF sample collected is likely to change
with the protein concentration of the initial GCF collected.



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 Volume determination
 Recovery from strips
 Data reporting

Constituents found within GCF samples have either
been reported as absolute amount (mg) or in
concentrations (mg/ml).

Composition of GCF

enzymatic

Host derived

Nonenzymatic
Cellular
component
electrolytes

Bacteria derived

Organic
organic
component

Host derived enzymes
Acid phosphates
Alkaline phosphatase
Alpha 1 antitrypsin
Arylsulphatse
Aspartate aminotransfarase
Chondroition sulphate
Citric acid
Cystatins
B-glucuronidase
Cathepsin
Matrix metalloproteins
Elastase


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Bacteria derived enzymes
 Acid phosphatase
 Alkaline phosphatase
 Collagenase
 Hyaluronidase
 Phospholipse-A
 Phospholipase-C



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Cellular elements
Bacteria
Desquamated epithelial cells
Leucocytes ( PMN’S, monocytes/macrophages)
Electrolytes
Potassium
Calcium
Sodium
Organic compounds
Carbohydrates-Glucosehexosamine
-Hexuronic acid
Proteins


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Metabolic end products
 Lactic acid
 Urea
 Hydroxyproline
 Endotoxins
 Cytotoxic substances
 Hydrogen sulphide



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Electrolytes

 Potassium, sodium, calcium, magnesium and fluoride

have been studied in gingival fluid. Most studies have
shown a positive correlation of calcium and sodium
concentrations as well as sodium to potassium ratio with
inflammation.



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Organic Compounds
 Carbohydrates, proteins and lipids have been investigated.

Glucose hexosamine and hexuronic acid are two of the
compounds found in gingival fluid. Glucose concentration
in gingival fluid is 3-4 times greater than that in serum.
 This is interpreted not only as a result of metabolic

activity of adjacent tissues, but also as a function of the
local microbial flora.



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The total protein content of gingival fluid is much less than
that of serum. No significant correlations have been found
between the concentration of proteins in the gingival fluid
and the severity of gingivitis, pocket depth and extent of
bone loss.
 Proteins
namely
,
,
and
2
1
globulins, transferrin, albumin, immunoglobulins such as
IgG, IgM and IgA, complement components such as
C1, C4, C3, C5 have been reported to be present in GCF.
 Proteins Include: - fibrinogen, ceruloplasmin, lipoprotein, transferrin, 1 – antitrypsin and 2 –
macroglobulin.



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 According to Armitage (2004), more than 65 GCF

constituents have been evaluated as potential diagnostic
markers of periodontal disease progression.

Pathogenesis of periodontal diseases

 Periodontal diseases are caused by a localized

inflammatory reaction in response to a bacterial infection
of the teeth, and are manifested by an alteration of the
integrity of the tissues supporting the teeth.

 studies have brought a paradigm change in periodontal

disease pathogenesis.
 These findings indicate that the microorganisms
associated with disease are also found at healthy or
nonprogressing sites (albeit at lower levels).
 The level of plaque control (oral hygiene) is not
associated with an individual’s disease severity or extent.
 The presence of a certain level of specific pathogens (such
as Porphyromonas gingivalis) makes a statistically
significant but small contribution in multivariate models
of disease.

 The host immune and inflammatory response to the

microbial challenge is a critical determinant of
susceptibility to develop the destructive disease, under the
influence of multiple behavioral, environmental, and
genetic factors.
 Hence, although disease progression is episodic in nature

on a tooth site level, the risk of developing periodontal
disease is principally patient-based rather than site-based.

 As plaque matures, becoming more pathogenic, in

parallel, host inflammatory response evolves from an
acute to a chronic one.
 Gram negative periodontal pathogens can evade the host

clearance mechanisms (complement, antibodies and
neutrophils), while shedding vesicles containing microbial
toxins, proteases and endotoxins( Lipopolysachcharides).

 LPS(Lipopolysachcharides)
penetrates

tissues
stimulates

monocytes
secretes

mediators of inflammation( PGE2, thromboxane B2,
IL-1, 6 & 8, TNF and
collagenases)

Mediators of inflammation
activate

vascular smooth muscles,
fibroblasts,
more monocytes,
and osteoclasts
to produce

MMPS
Stimulates
bone resorption

 This inflammatory cascade produces

clinical inflammation,
attachment loss,
pocket formation,
bone loss.
 Along side monocytic synthesis of inflammatory
mediators
antigen presentation also
occurs.
 This arm of host response triggers adaptive immune
response with an initial (T helper type1 ) response.
 T – helper type 1 response consists of proinflammatory
IL-2, TNF α, Interferon γ.

 T – helper type 1 response later shifts to T – helper type 2

dominant response consisting of antiinflammatory, ILs –
4,5,6,10,13 and production of immunoglobulins.
 This is consistent with a shift from T- helper type 1 to T-

helper type 2 between transitions from gingivitis to
periodontitis as described by Seymour and Gemmal
(1994).
 However other studies indicate that in active periodontal

disease progression, there is dominant T- helper type 1
response versus T – helper type 2 which being consistent
with periodontal disease stability (non progression).

 So, inflammatory cytokines can be detected within GCF

and serve as an indicator of local immunoregulatory and
inflammatory status.
 In addition, collagen breakdown products such as

Hydroxyproline and Pyridinoline cross- linked carboxyterminal telopeptide fragments of type 1 collagen are
found in GCF that serves as direct measure indicator of
connective tissue catabolism for both soft and hard tissues.

 Elevated GCF levels of neutrophil markers i.e.

neutrophil elastase, β-glucuronidase and leukotriene B4
reflects
Acute episodes of localized tissue destruction
 Taken together, these monocytic and neutrophilic mediator

levels in the GCF may also give an indication of quality of
the host response, and of the level of risk for the
individual to develop periodontal disease.

Prostaglandin E2 (PGE2 ):
 PGE2 was first identified in GCF by Goodson et al. in

1974.
 PGE2 is a product of the cyclooxygenase pathway.
Elevated levels of PGE2 in GCF were found in patients
with periodontitis compared to patients with gingivitis.
PGE2 levels were three times higher in patients with
juvenile periodontitis compared to adult periodontitis.

 Offenbacher et al (1986) showed that there were

differences in the GCF concentration of PGE2 in patients
with gingivitis compared with periodontitis.
Subsequently, it was found that there was a correlation
between increased PGE2 concentration and clinical
attachment loss in patients who were diagnosed with
moderate to severe periodontitis.



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Cytokines
 Cytokines are potent local mediators of inflammation

that are produced by variety of cells. Cytokines that are
present in GCF and have been investigated as potential
diagnostic makers for periodontal disease include:
 interleukin - 1 , 1 ,
 interleukin – 6,
 interleukin – 8 and
 tumor necrosis factor (TNF - ).
 Both IL - 1 and IL - 1 have pro-inflammatory effects
and depending on a variety of factors can stimulate
either bone resorption or formation.

 It has also been reported that in adult periodontitis patients,

a higher percentage of sites are positive for IL - 1 (87%)
and IL - 1 (56%) IL-6 has also been associated with bone
resorption. GCF from sites with progressing periodontitis
contains elevated amounts of IL-6.
 IL-8 was formerly called monocyte-derived neutrophil

chemotactic factor. GCF from sites with periodontitis
contains significantly more total IL-8 than GCF from
healthy sites

 Proinflammatory cytokines in particular IL-1, may play

an integral role in the aetiology of periodontal disease.
 Lieu et al (1996) demonstrated that with an increase in

gingival index and probing, there was a corresponding
increase in IL-1 in both the gingival tissue and GCF.
 Engebretson et al through a longitudinal study suggested

that GCF IL-1 expression is genetically influenced and
not solely a result of local clinical parameters. Also, a
GCF level of IL8 was found to be higher in periodontal
diseases and was influenced by local IL-1 activities.



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Total Protein
 Several reports suggest that, compared to periodontal

healthy controls, GCF from sites with periodontitis has
significantly elevated levels of total protein.
 Some study has reported that GCF from inflamed sites in

patients with periodontitis have significantly lower protein
concentrations than GCF from inflamed sites in patients
with gingivitis alone

Host – Derived Enzymes
(a) Aspartate Aminotransferase:
 Aspartate aminotransferase enzyme (AST) is one of the
components of GCF that is released and can be detected as
a result of cell death.
 Significant associations between GCF levels of AST and
clinical measurements have been determined, and a test
system, the PeriogardTM periodontal tissue monitors
(PTM), has been developed (Persson et al. 1990.

 The commercial chair side test do not have the ability to

reliably distinguish between progressing sites and those
that are inflamed but not progressing.

Alkaline phosphatase

 In the periodontium, alkaline phosphatase is a very

important enzyme as it is part of the normal turnover of
periodontal ligament, root cement formation and
maintenance, and bone homeostasis.
 It is produced by many cells, including fibroblasts,

osteoblasts and osteoclasts, but the main source of alkaline
phosphatase in gingival crevice fluid is neutrophils.



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 Similar levels of alkaline phosphatase in GCF have been

found in gingival health and experimental gingivitis, but a
longitudinal study demonstrated that elevated alkaline
phosphatase levels preceded clinical attachment loss and
that the total amount of alkaline phosphatase in GCF was
significantly higher in active sites (Nakashima 1996).

Beta – glucuronidase
 Beta-glucuronidase is a lysosomal enzyme that is active in

the hydrolysis of glycosyl bonds of intercellular ground
substances.
 It is highly conceivable and periodontal disease activity is
associated with increased levels of beta-glucuronidase in
gingival crevice fluid



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 ß glucuronidase is a glycoprotein of about 3,32,000 dalton.

It is a homo tetramer comprised of four identical subunits. It
has high sensitivity and specificity when related to
occurrence of clinical attachment loss. This enzyme also
proved to be a good predictor of the response to treatment
and the risk for future periodontal breakdown (Lamster et al
1998).
 Subjects without active disease did not have elevated betaglucuronidase in gingival crevice fluid. In relation to
attachment loss, they observed beta-glucuronidase to have a
sensitivity and specificity of 89% and 89%, respectively.

Elastase
 Neutrophil elastase, sometimes referred to as

granulocyte elastase, is an abundant proteinase
released from the azurophilic granules of neutrophils
and as such is an indicator of neutrophil activity.
 Neutrophil elastase is a serine proteinase, active in the
degradation of microbiological components in
conjunction with, or without, phagocytosis. At the
same time, when released extracellularly, this enzyme
can degrade host intercellular matrix components,
including elastin, fibronectin, and collagen.


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 Elastase levels in GCF increase with induction of

experimental gingivitis, and decrease when plaque removal
is reinstituted.
 In a longitudinal study, Eley and Cox (1996) demonstrated
that increased elastase in GCF was predictive of periodontal
attachment loss. Long-term observation of adult patients
with periodontitis undergoing supportive periodontal
therapy showed a positive correlation of elastase in GCF
with clinical attachment loss.
 Smokers display higher levels of elastase than nonsmokers.Soder B(2002)

Cathepsin B
 Cathepsin B is an enzyme active in proteolysis; it belongs

to the class of cysteine proteinases. The cellular source of
cathepsin B in gingival crevice fluid seems to be mainly
macrophages.
 Cathepsin B activity has been found in gingival crevice
fluid in adult periodontitis. It seems to be increased in
periodontitis but is not increased in gingivitis, even though
the flow of gingival crevice fluid is more or less equal in
these two periodontal conditions.



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 Kunimatsu et al (1990) observed that levels of

cathepsin B were increased in periodontitis when
compared to gingivitis, despite similar GCF flow.
 Furthermore, GCF levels of cathepsin correlate
significantly with clinical parameter before and after
periodontal treatment suggesting a use for this enzyme
in assessment of treatment outcomes. Cathepsin G may
contribute to periodontal tissue destruction directly and
indirectly, via proteolytic activation of latent neutrophil
procollagenase (promatrix metalloproteinase-8).
 Eley & Cox have further investigated cathepsin B and
evaluated its use as a predictor of attachment loss.

(g) Collagenases/ Gelatinases/ Neutral
proteinases/ stromelysins:
 GCF from sites with adult or juvenile forms of periodontitis

exhibit significantly elevated collagenolytic activities
compared to GCF from healthy or gingivitis sites.
 In ligature-induced periodontitis in the beagle dog, GCF
collagenase activity increased to maximum values within
weeks after ligature placement, active collagenase was
elevated during active periodontitis and active collagenase
was strongly correlated with attachment loss. Latent
collagenase and collagenase inhibitors were prominent
during gingivitis.

(3) Tissue Breakdown Products:
(a) Glycosaminoglycans (GAG’s):
 The GAG’s in GCF that have been most examined as

possible diagnostic markers for periodontal diseases
are:
 Chondroitin – 4 – sulfate,
 chondroitin – 6 – sulfate and
 hyaluronic acid.
 The appearance of C-4-S in GCF has been suggested
as a marker for bone resorption associated with
periodontal disease or orthodontic tooth movement.
But no studies have been conducted to determine its
role in the progression of periodontitis.

(b) Hydroxyproline:



It is a prominent aminoacid of collagen and its
appearance in GCF has been preliminary investigated as a
marker for the destruction of periodontal connective tissue.
Data from one cross-sectional study in humans indicate that
GCF hydroxy proline levels cannot distinguish between
sites with gingivitis or periodontitis. Because of this it is not
an attractive candidate as a potential marker for the
progression of periodontitis.

(c) Fibronectin:
These are a large group of heterogeneous glycoprotein
present in blood and connective tissues. Data from most
studies indicate that GCF fibronectin is not a promising
diagnostic marker.

(d) Connective Tissue Proteins:

 Increased GCF levels of the amino terminal propertied

of type I collagen have been reported at periodontitis
sites. On a concentration basis, the amount of
osteocalcin in GCF does not appear to be different at
sites with gingivitis or periodontitis.
 Osteonectin another non-collagenous protein of bone
and a variety of other tissues, has been reported to be
elevated in GCF at sites with severe periodontitis.
Neither Osteocalcin nor Osteonectin levels in GCF
have been systematically evaluated as diagnostic
markers for periodontitis.

MARKERS FROM MICROBIAL PLAQUE
It is evident that since periodontal disease is associated
mainly with the presence of certain bacteria which are
recognized as the principal etiological agents, then factors
derived from such bacteria may be useful indicators of
their presence and metabolic activity.

Lipopolysaccharides (Endotoxins)
 These molecules are found in the outer membrane of

the cell wall of Gram-negative bacteria. The presence
of endotoxins has been positively correlated with
gingival inflammation (Simonet al, 1971)
 when measured in GCF and in combination with
clinical and histological studies. The level of endotoxin
is related to the number of Gram-negative bacteria.
 Lipopolysaccharides (LPS) vary in their structure
depending on bacterial source.

Bacterial Enzymes

 Perhaps bulk of the work on bacterial enzymes has been

carried out on proteolytic enzymes or proteinases.
 The most studied would be the trypsin-like proteinase of
P.gingivalis.

 Similar trypsin-like enzymes are also associated with

Treponema denticola (Makinin et al, 1987).
 Bacterial collagenases are also identified with Clostridium

histolyticum and Streptococcus mutans.
 The presence of such enzymes in GCF correlates with the

levels of these bacteria in the periodontal pocket and also
with the severity of the attachment loss.

Enzymes Associated with Tissue Destruction
Lactoferrin
 This is an antimicrobial agent with distribution in PMNs

and secretory fluids similar to that of Lysozyme. The
antibacterial properties of Lactoferrin are due to its high
affinity for iron, thus locking available sources required
for bacterial growth.
 Lactoferrin showed better correlation with clinical indices
than PMNs (Adonogianaki et al, 1993).

Friedman et al (1983) found that Lactoferrin increased two
fold in GCF in sites showing gingivitis periodontitis, and
localized juvenile periodontitis. It has also been reported
that the ratio of Lactoferrin to Lysozyme may be more
representative and a useful diagnostic assay of periodontal
inflammation.

Myeloperoxidase

This enzyme has also been shown to give good correlation
with an inflammatory response where it is found in the
primary granules of PMN (Smith et al, 1986).

 Several products show potential benefit, particularly those

directly from specific regions of the periodontium which
give a clue as to which tissue components are at risk. It is
clear that no single marker will fulfill all the criteria
necessary for assessment of the clinical state of the
periodontium, and future research should be directed at
the production of "marker packages". The development of
a wide spectrum of marker factors will be a primary goal
of periodontal research.

 COMMERCIALY AVAILABLE

DIAGNOSTIC KIT
 Periocheck - Neutral Proteinases - Approved by FDA
 Periogard - AST
 Prognostik- Elastase - Not Approved by FDA and ADA
 Biolise - Elastase
 Pocket watch - AST
 TOPAS – Toxicity Pre-screening assay (bacterial toxins

and proteases
 MMP dipstick method - MMPs
 Under development, for B - glucornidase and
proteinases


86

 The components of gingival crevice fluid are analyzed






with regard to their potential utility in fulfilling the
following aims: (BRUNO G. LOOS & STANLEY T JOA)
AIM 1: To detect a case of periodontitis i.e., to distinguish
periodontitis from health and gingivitis
AIM 2: To classify a case of periodontitis, i.e., chronic
periodontitis or aggressive periodontitis
AIM 3: To plan treatment for the patient on the basis of
the level of disease activity
AIM 4: To monitor the treated patient based on the level
of disease activity



88



89

Clinical significance
 Circadian Periodicity:

There is a gradual increase in gingival fluid amount from
6:00AM to 10:00PM and a decrease afterward.



90

 GCF and sex hormones

Clinical investigations have shown an exacerbation of
gingivitis during pregnancy (loe 1965), during menstrual
cycle (------Lemann 1948) and at puberty (Sutcliffe 1972).
Female sex hormones increase the gingival fluid
flow, probably because they enhance vascular
permeability.

Pregnancy, ovulation and hormonal contraceptives all
increase gingival fluid production.



91

 GCF and drugs

Drugs that are excreted through the gingival fluid may be
used advantageously in periodontal therapy. Bader and
Goldhaber demonstrated that intravenously administered
tetracycline in dogs rapidly emerges within the sulcus.



92

 Ciancio et al (1976) measured the concentration of

tetracycline in blood and gingival fluid of 5 adult patients
with advanced periodontitis, who were given 1g of
tetracycline HCL daily for 2 weeks and 0.5g for 10 weeks.
The concentration of the drug in gingival fluid was 1/10 of
that found in serum.
 In a second study from the same laboratory the

concentrations of the drug were found to be 5 times higher
in samples of gingival fluid as compared to the
concentrations in blood.



93

 Stephen et al (1980) measured the conc. of ampicillin,

cephalexin, tetracycline, erythromycin, clindamycin and
rifampicin in serum, saliva and GCF after a single dose
administration. Except on one occasion, individual GCF
antibiotic conc. were equal to or considerably greater than
those found in saliva. But they were, however, always
much lower than the concentration found in serum.
 Metronidazole is another antibiotic that has been detected

in human GCF. (Eiserbeng et-al 1991).



94

 GCF in diabetic patients

Ringelberg et al in 1977 described a higher flow rate of
gingival fluid in a group of diabetic children, when
compared to the flow rate measured in a group of children
without diabetes.
In healthy individuals Hara and Löe found exudate
glucose values up to 6 times those of serum. Kjellman
(1970) reported glucose values much lower in gingival
fluid when compared to serum, this being true for both
healthy and diabetic patients.



95

 Periodontal therapy and GCF
There is an increase in gingival fluid production during the
healing period after periodontal surgery. According to
Arnold et al 1966 this increase was probably the result of
the inflammatory reaction from gingival trauma and the
loss of an intact epithelial barrier, especially considering
the fact that fluid had been collected by deep
intracrevicular technique.
Suppipat et al in 1978 sampled gingival fluid 14, 21, 28
and 35 days after gingivectomy and found an increase in
gingival fluid flow during the first 2 weeks after surgery
followed by a gradual decrease. This decrease was same
when using mechanical or chemical plaque control.


96

 Influence of mechanical stimulation
Chewing and vigorous gingival brushing stimulate the
oozing of gingival fluid. Even the minor stimuli
represented by Intrasulcular placement of paper strips
increase the production of fluid.



97

 Smoking and GCF
Smoking produces as immediate transient but marked
increase in the gingival fluid flow.
Mcluaghlin WS et al 1993



98

CONCLUSION
In conclusion one can say that the origin, the composition
and the clinical significance of gingival fluid are now
known with more precision and have significantly helped
our understanding of the pathogenesis of periodontal
disease. Up to now, for instance, none of the multiple
components analyzed in the fluid has improved clinical
judgment of the rate of progress of gingivitis and
periodontitis or of the rate of repair of these conditions.

Recent findings in GCF

 GCF resistin level as a potential inflammatory marker for

periodontitis with type2 diabetes mellitus.(Gokhale NH et
al.2013).
 OPG concentrations in GCF decreases proportionally

with the progression of periodontal disease, that is
gingival inflammation and clinical attatchment loss
(CAL) (Bandari P et al. 2012).

 IL-23 level in GCF is directly proportional to the severity

of periodontal affliction suggesting its possible role in
periodontal inflammation. (Himani GS 2013).

 Periodontal treatment downregulates protease-activated

receptor2. (VTE Alves 2013)

References
 CARRANZA,s Clinical Periodontology. 10th edition.
 Griffiths. Formation, collection and significance of GCF.

Periodontal 2000 2003; 31:32 – 42.
 J. Max Goodson. Gingival crevicular fluid. Periodontal

2000 2003;31:43 – 54.
 Catherine M.E. et al. Potential for gingival crevice fluid
measures as predictors of risk for Periodontal disease.
Periodontology 2000 2003;31:167-80.
 BRUNO G. LOOS & STANLEY T JOA. Host-derived
diagnostic markers for periodontitis: do they exist in
gingival crevice fluid? Periodontology 2000 2005;39: 53–
72.

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