email antarleenasengupta@gmail.com for full seminar

1. Gingival
Crevicular
Fluid
Dr. Antarleena Sengupta
I Year PG, Deptt. Of Periodontology,
MCODS Mangalore
2019-22

2. JensMartensson
Contents• INTRODUCTION
• HISTORY
• GINGIVAL VASCULATURE AND
PERMEABILITY
• MECHANISMS OF GCF PRODUCTION
• ASSESSMENT OF GCF
• COMPOSITION
• GCF as a diagnostic marker
• ANALYSIS OF COMPONENTS
• COMMERCIAL DIAGNOSTIC KITS
• CLINICAL SIGNIFICANCE
• CONCLUSION
• REFERENCES
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Introduction
Anatomy of the gingival crevice
• The gingival sulcus is the shallow
crevice or space around the tooth,
bound by surface of the tooth on
one side and the epithelial lining
the free gingival margin on the
other.
• V-shaped; depth as determined
via histological sections is 2.1± 0.2
mm.
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Sections show presence of 3 types
of epithelium,
1. The oral or keratinized epithelium
covering the gingival tissue in
continuation with
2. The sulcular epithelium, which is
not keratinized. It forms the soft
tissue wall of the gingival sulcus and
the
3. Junctional epithelium is in
continuation with the oral and
sulcular epithelium. It is formed by
few strata of cells, with long flat
basal layer and a very small
desquamating surface that forms the
base of the gingival sulcus. 4

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Definition
• GCF is an exudate that can be harvested from the gingival
crevice or periodontal pocket using either filter paper strips or
micropipettes. (Manson & Eley, 2000)
• GCF is a serum-like exudate that bathes the gingival sulcus and
follows an osmotic gradient within the local tissues. (Per
Axelsson, 2002)

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Definition
Gingival crevicular fluid (GCF) is
defined as a specific serum
originating biologic fluid – found in
periodontal microenvironment and
can be harvested from the gingival
sulcus of natural teeth
Bulkacz J, Carranza FA. Defense mechanisms of the gingiva. In: Newman MG, Takei HH, Carranza FA, eds.
Carranza’s Clinical Periodontology, 11th ed. Los Angeles: Saunders: 2012:66 – 70.

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History
Studies on gingival crevicular fluid (GCF) extend over a period of more than
50 years
Egelberg (1966)
Gingival vasculature &
permeability
Waerhaug (1952)
Sulcus periodontitis gingival pocket
Cimasoni
(1969)
Presence and func. of proteins
in GCF
Brill et al (1962)
Physiology and composition
Loe & Holm-Pederson
(1965)
Indicator of periodontal
diseases
Schroeder (1969),
Listgarten (1966)
Dentogingival structure

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MECHANISMS OF GCF PRODUCTION
• Existence of GCF – over 100 years (Black, GV. 1899)
• BRILL & KRASSE, 1958
• BRILL & BJORN, 1959
• EGELBERG, 1966
Production of fluid is
related to an
inflammatory-related
increased permeability
of vessels underlying the
sulcular & junctional
epithelium

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MECHANISMS OF GCF PRODUCTION
• Existence of GCF – over 100 years (Black, GV. 1899)
EXUDATE
TRANSUDATE

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GCF: EXUDATE v/s
TRANSUDATE
• Very early or pre-inflammatory flow of
gingival fluid is osmotically mediated.
• This osmostically mediated fluid is a
TRANSUDATE.
• Later, on stimulation, it may progress to
a secondary inflammatory exudate.
• Thus, even in health, if osmotic pressure
>>tissue fluid due to accumulation of
plaque → increased flow of GCF
ALFANO (1974)

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GCF: EXUDATE v/s
TRANSUDATE PASHLEY (1976)
• Based on STARLING HYPOTHESIS
governing fluid distribution across
capillaries.
• Model proposed by Pashley
predicted that GCF production is
governed by
• CAPILLARY FILTRATION
• LYMPHATIC UPTAKE
• When the rate of capillary filtrate
exceeds that of lymphatic uptake,
fluid will accumulate as edema
and/or leave the area as GCF.

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• According to Alfano and Pashley, the initial fluid produced could simply
represent interstitial fluid which appears in the crevice as a result of an
osmotic gradient.
• Whereas, the work of both Brill in 1962 and Egelberg in 1974 seemed to
suggest that the production of GCF was primarily a result of an inflammatory
increase in the permeability of the vessels underlying junctional and sulcular
epithelium.
GCF: EXUDATE v/s
TRANSUDATE
It was concluded that the initial, pre-inflammatory fluid was considered
to be a transudate, and, on stimulation and inflammation, this changed
to become an inflammatory exudate.
Bickel et al,
1985

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Functions of GCF
Cleanse material from the sulcus
Contain plasma proteins– may improve adhesion of
epithelium to the tooth
Possess antimicrobial properties
Exert antibody activity in defense of the gingiva

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Histamine
Pre-
inflammator
y GCF
Conc. of
protein
Mechanic
al stimuli
Passage of
fluid & PMNMorphology
of JE
Inflammator
y changes of
BM
Factors
affecting
flow of
GCF

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Gingival vasculature & Crevicular
fluid
• Increased vascular permeability plays an important role in the
production of gingival fluid (Brill, 1959)
• Increased permeability of the blood vessels of healthy gingiva by use of 3
different experimental methods (Egelberg, 1966):
• Topical application of histamine
• Gentle massage of the gingiva by means of a ball-ended amalgam
plugger
• Scraping of the gingival crevice by means of a blunted dental explorer.
• A fluid occurring in minute amounts in the gingival crevice, believed 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. (Jablonski, Illustrated Dictionary
of Dentistry, 1982)

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Permeability of Junctional and
Oral Sulcular Epithelia
• Three routes have been
described:
• Passage from CT into the
sulcus
• Passage from the sulcus into
the CT
• Passage of substances through
pathological or experimentally
modified gingival sulcus
(Squier, 1973)

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Absorbent paper strips
Micropipettes
Gingival washings
Plastic strips
Isotope dilution
Pre- weighed twisted threads
Methods
of
collectio
n of GCF

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Extracrevicular method Intracrevicular method ‘superficial’
[Loe & Holm-Pedersen]
Intracrevicular method
‘deep’ [Brill, 1958]

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• This technique appears to be
ideal as it provides an
undiluted sample of ‘native’
GCF whose volume can be
accurately assessed
ADVANTAGE
• Time consumption – 30 min
• Difficulty in removing the
complete sample
DISADVANTAGES
KRASSE & EGELBERG, 1962
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.

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WEINSTEIN et al, 1967
 thread is placed in the gingival crevice around the
tooth and the amount of fluid collected is estimated
by weighing the sample thread.

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Takamori & Oppenheim method (1970)
- customized hard acrylic plate covering the
maxilla with soft borders and a groove along the
gingival margins which is connected to 4 plastic
tubes; 4-6mL – 15 min – peristaltic pump
Skapski & Lehner method (1976)
ADVANTAGES
• Useful for longitudinal
studies
• Permits collection
without disturbing the
integrity of the
marginal tissues
• Contamination is
lowest
DISADVANTAGES
• Complex procedure
• Represents a dilution
of crevicular fluid
10 μL Hank’s Balanced Salt Solution (HBSS) are ejected
and reaspirated 12 times by resting the point of a
needle of a 50 μL microsyringe interdentally on the
buccal surface of the teeth, just above the interdental
papilla
DISADVANTAGES
• Does not permit absolute
quantitative assessments
• Dilution factor cannot be
determined

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• GINS and MATTIG, 1941
• ATTSTROM, 1970
• RENGGLI and REGOLATI, 1972; LANGE, 1973
• Transparent strips are placed along long axis of the tooth
• Pressure applied on the gingiva
• Drying → staining → mounting in cedar oil →observed under
microscope

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• CHALLACOMBE, 1980
• Isotope dilution method
• Anteriors = 0.24 - 0.43 μL per tooth; Posteriors= 0.43 – 1.56 μL per tooth
• Suggested that the total volume of GCF secreted in the human mouth
per day = 0.5 – 2.4 mL of fluid

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METHODS OF ESTIMATING GCF VOLUME
COLLECTED
• Strip can be directly viewed under a microscope.
OR
• Area of the wetted surface can be made visible by staining
with an alcoholic solution of NINHYDRIN
GOLUB, 1971; EGELBERG & ATTSTROM, 1973
1. Direct viewing/ Staining:
The stained area can then be measured with :
• Ordinary transparent ruler (EGELBERG, 1964)
• Sliding calliper (BJORN, 1965)
• Calibrated magnifying glass (OLIVER, 1969)
• Microscope with an eyepiece (WILSON, 1971)
• Specially designed, inexpensive paper strip viewer (WILSON, 1978)

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• Pre- weighed twisted threads (WEINSTEIN, 1967)
• Weigh the sample – the strips are weighed before and immediately
after collection (VALAZZA, 1972)
The time of collection was measured with a chronometer and
this enabled the investigator to express the flow of fluid in
mg/min.
2. Weighing the strips

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3. Use of Periotron
PERIOTRON 600
PERIOTRON 6000
PERIOTRON 8000
 Considerably sensitive to
qualitative differences in fluid
 Relatively unaffected by
qualitative differences in
fluids.
 Ability to quantitatively
measure the gingival
crevicular fluid without
permanently altering it
(Chapple et al, 1995)
 differences in calibration fluid
composition (e.g. protein content) are
reflected in the Periotron scores
 calibration of the Periotron 8000 seems
to be consistent over a 1-wk interval.
(Ciantar et al, 1998)

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Periotron reading Level of gingival
inflammation
Gingival Index
0-20 Healthy 0
21-40 Mild 1
41-80 Moderate 2
81-200 Severe 3
Translation of Periotron values to clinical conditions and
Gingival index with which they may be associated

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COMPOSITION OF
GCF
NON-ENZYMATIC
COMPONENTS
CELLULAR
ELEMENTS
ELECTROLYTES
ORGANIC
COMPOUNDS
ENZYMATIC
COMPONENTS
BACTERIA-
DERIVED
PRODUCTS
HOST-DERIVED
PRODUCTS

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Epithelial cells – Lange & Schroeder, 1971
Cells of the sulcular epithelium
• Flattened
• Cytoplasmic filaments
Cells originating from the junctional epithelium
• Found at the bottom of the sulcus
Role of inflammation
• Rate of renewal
• Structural characteristics of desquamating cells
• Reduction in acid phosphatase activity (Cornaz et al., 1974)
Epithelial cells, leukocytes and bacteria
• CELLULAR ELEMENTS

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GCF Peripheral blood
Neutrophil 95- 97% 60%
Monocyte 2- 3% 5- 10%
Lymphocyte 1- 2% 20-30%
T- cells 24% 50-75%
B- cells 58% 15- 30%
Mononuclear phagocyte 18%
T : B 1 : 2.7 3 : 1
 Differential leukocyte count in the sulcus
Leukocytes
 Role of inflammation:
↑number
(EGELBERG, 1963)
 Phagocytic function
of PMNs: AgP < CP
Poor correlation to severity of gingival inflammation and depth of pocket (KREKELER &
FERCK, 1977)
Bacteria

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• ELECTROLYTES
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SODIUM
• Normal GCF – 158 mEq/L
• Inflammation – 207 to 222
mEq/L
• Follows circadian periodicity
(KASLICK et al, 1970)
• ↑pocket depth →↓Na
concentration
POTASSIUM
• Mean conc. in GCF = 9.54
mEq/L
• GCF >> serum
• Increases towards the middle of
the day
• ↑severity of periodontitis
• ↑pocket depth
SODIUM-POTASSIUM RATIO
• Diseased tissues-- ↓ratio
• Accumulation of intracellular potassium
• GCF < ECF (KRASSE & EGELBERG, 1962)
3.9 28.1

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Other ions
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• Fluoride : GCF = Plasma (WHITFORD et al, 1981)
• Calcium: Normal gingiva – 10mEq/L
Inflamed gingiva – 15.9mEq/L
↑ with inflammation
GCF (30-50x) > Serum (BISWAS et al, 1977)
• iPO4: 4.2 mg/100mL of GCF
• Mg: 0.8 mEq/L
• I: 40% of concentration in saliva

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• ORGANIC COMPOUNDS
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Carbohydrates
Glucose, hexosamine and hexuronic acid (HARA & LOE, 1969)
Glucose: GCF >>> serum
Hexosamine & hexuronic acid – no correlation with variation in gingival
inflammation
Increased in:
• Inflammation
• Diabetes
Lipids
Serum, saliva, bacteria and host tissue
Phospholipids and neutral lipids

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Proteins
 GCF < serum
 IgG, IgA - plasma cells
 Complements → tissue damage (SCHENKEIN & GENCO,1977)
 Chemotactic attraction of PMNs
Release of lysosomal enzymes
Degranulation of mast cells
Albumin , fibrinogen, ceruloplasmin, ß-lipoproteins & transferrin
(MANN & STOFFER, 1964)
Bradykinin (RODIN et al,1973)

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• Metabolic and bacterial products
36
 Lactic acid – inflammation, flow
 Hydroxyproline
 Prostaglandins
 Urea and pH
• Inversely related to severity of inflammation
• GCF > saliva, serum
• pH: 7.54 - 7.89 (BANG AND CIMASONI)

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 Endotoxins
• Lipopolysaccharides(LPS) of cell wall of Gram-ve bacteria
released from autolysing bacteria cells
• Highly toxic to gingival tissues & possible pathogenic
factor in periodontal disease.
• Positive correlation b/w LPS conc. & gingival inflammation
(SHAPIRO, 1972)
 Cytotoxic substances - H2S

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 Antibacterial factors
• Crevicular fluid was found to be as potent as leukocyte extract
in lysing S. aureus, S. faecalis & A.viscosus. S. mutans seemed
more resistant.
• Lysosomal enzymes present in GCF are lytic agents. (SELA et
al, 1980)
• A peroxidase mediated antimicrobial system has also been
shown in human crevicular fluid
• Growth stimulating factors – Lactobacilli ( TAKAMORI,1963)

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CLINICAL
SIGNIFICANCE
OF GCF
CIRCADIAN
PERIODICITY
SEX
HORMONES
DRUGS
DIABETES
MECHANICAL
STIMULATION
PERIODONTAL
THERAPY
SMOKING
gradual increase in
gingival fluid amount
from 6:00AM to
10:00PM and a
decrease afterward.
- Pregnancy
- Menstrual cycle
- Puberty
- Metronidazole
- Tetracycline I.V.
- GCF antibiotic conc.
equal to or
considerably greater
than those found in
saliva.
- Glucose values much
lower in GCF in healthy
& diabetics
- Higher flow rate of
gingival fluid
- Chewing
- Vigorous gingival brushing
- Intrasulcular placement of
paper strips
- ↑GCF production
during healing
period after
periodontal
surgery
- ↑gingival fluid flow
during first 2 weeks
after gingivectomy
followed by a
gradual decrease.
- ↓GCF flow 4 weeks
following root
planing &
curettage
- Lower resting GCF flow
rate
- immediate transient but
marked ↑GCF flow.
- GCF volumes decreased
further immediately
after smoking
- subsequently increased
transiently after 10
minutes.

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PROBLEMS ASSOCIATED WITH GCF
COLLECTION :
CONTAMINATION
SAMPLING
TIME
VOLUME
DETERMINATION
RECOVER
FROM
STRIPS
DATA
REPORTING

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GCF v/s SALIVA: DIAGNOSTIC
BIOMARKERS
41
SALIVA
- Sample contamination with blood from
oral mucosa and periodontal lesions due
to inflammation
- Collection methods are not completely
standardized in terms of different
physiological states and types of
commercial kits
- Most of the biomarker levels in saliva
are lower than that found in the GCF.
- Influenced by the method of collection
and the degree of stimulation of salivary
flow
Pathiyil, Varsha & Udayasankar, Rahul. (2019). Salivary Diagnostics.
10.5772/intechopen.84722.
GCF
- >65 GCF constituents have been evaluated
as potential diagnostic biomarkers of
periodontal disease progression (Armitage
et al, 2004)
- can provide site-specific status of
inflammation without necessitating
histopathological evaluation
- The calculated cut-off values for biomarkers
from GCF gives higher sensitivity,
specificity and predictive values than saliva
samples (Hormdee et al, 2017)
Gupta S, Chhina S, Arora SA. A systematic review of biomarkers of gingival
crevicular fluid: Their predictive role in diagnosis of periodontal disease status.
Journal of oral biology and craniofacial research. 2018 May 1;8(2):98-104.

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CLASSIFICATION OF GCF BIOMARKERS (Gupta, G.
2012)
42
Host-derived enzymes and
their inhibitors
Tissue breakdown products Inflammatory mediators
host response modifiers
• Aspartate aminotransferase
• Alkaline phosphatase
• Acid phosphatase
• β-glucoronidase
• Elastase
• Elastase inhibitors
• α2 – macroglobulin
• α1 – proteinase inhibitor
• Cathepsins
• Cysteine proteinases (B, H,
L)
• Serine proteinase (G)
• Glycosaminoglycans
• Hyaluronidase
• Lactate dehydrogenase
• Chondroitin-4-sulphate
• Chondroitin-6-sulphate
• Dermatan sulphate
• Hydroxyproline
• Fibronectic fragments
• Connective tissue and bone
proteins
• Osteonectin
• Osteocalcin
• Type I collagen peptides
• Osteopontin
• Cytokines
• IL-1 alpha
• IL-1 beta
• IL-2
• Il-6
• IL-8
• TNF alpha
• Interferon alpha
• Leukotriene B4
• Prostaglandin E2
• Transferrin
• Lactoferrin
• Ig- G1, G2, G3, G4, IgM

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• Enzymes and Enzyme Inhibitors
Lysozyme
 Major source : PMNs
 Bactericidal - hydrolyzes β-1,4 glycosidic bonds of peptidoglycans of
bacterial cell wall
 Activity : GCF, saliva > serum (BRANDTZAEG & MANN,1964)
 May contribute to the formation of pocket
 Accelerates release of bacterial enzymes (SELA ,1976)

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β glucoronidase
• Lysozomal enzyme
• Primary granules of PMNs
• Sources : macrophages, fibroblasts, endothelial cells, bacteria
• Plays a role in the catabolism of mucopolysaccharides
Hyaluronidase
 Lysosomal enzyme
 Splits β-1,4–N– acetylglucosaminide links in hyaluronic acid and chondroitin
sulphate
 pH : 3.5 – 4.1
 Increases – Gram positive bacteria, inflammation (TYNELIUS- BRATHALL &
ATTSTROM,1972)

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Acid phosphatase
• Lysosomal enzyme
• Present in azurophil granules
• Sources : PMNs, desquamating epithelial cells
• Associated with connective tissue catabolism
• Can also attack teichoic acid
• Acts at a pH of 4 to 5
Pyrophosphatase
• Role in calculus formation
• Concentration is positively correlated – amount of calculus
Lactate dehydrogenase
 Pyruvate ↔ Lactate
 GCF > blood

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Proteolytic enzymes
 Cathepsin D
 Elastase
 Cathepsin G
 Plasminogen activators
 Collagenase
 Bacterial proteinases (i.e. endo and exopeptidases)
 Lactic dehydrogenase serum proteinase inhibitors such as α2 –
macroglobulin, α1 – antitrypsin, α1 – antichymotrypsin have also
been known to be present in GCF.

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• Host- derived enzymes
47
(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).
(b) Alkaline phosphatase:
• part of the normal turnover of periodontal ligament, root cement formation and maintenance,
and bone homeostasis.
• main source of alkaline phosphatase in gingival crevice fluid is neutrophils.
• 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).

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(c) Cathepsin B
• active in proteolysis
• cellular source of cathepsin B in gingival crevice fluid seems to be mainly macrophages.
• KUNIMATSU et al (1990) observed that levels of cathepsin B were increased in periodontitis when
compared to gingivitis, despite similar GCF flow.
• ELEY & COX have further investigated cathepsin B and evaluated its use as a predictor of
attachment loss.
(d) Neutrophil elastase
• 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, Jin LJ, Wickholm S. Granulocyte elastase, matrix metalloproteinase-8 and prostaglandin E2 in gingival crevicular fluid in matched clinical
sites in smokers and non-smokers with persistent periodontitis. J Clin Periodontol 2002: 29: 384–391

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Prostaglandin E2 (PGE2)
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• First identified in GCF by GOODSON ET AL. in 1974.
• PGE2 is a product of the cyclooxygenase pathway.
• ↑PGE2 in GCF are seen in patients with periodontitis compared to patients with
gingivitis.
• ↑PGE2 levels : patients with juvenile periodontitis >3x adult periodontitis.
• OFFENBACHER ET AL (1986)
• differences in the GCF concentration of PGE2 in patients with gingivitis
compared with periodontitis.
• correlation between ↑PGE2 concentration and clinical attachment loss in
patients who were diagnosed with moderate to severe periodontitis.

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Cytokines
50
 Cytokines are potent local mediators of inflammation that are produced by
variety of cells.
 Cytokines that are present in GCF have potential diagnostic markers for
periodontal disease including:
• interleukin - 1α , 1β ,
• interleukin – 6,
• interleukin – 8 and
• tumor necrosis factor α (TNF -α ).
 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.
 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.
 ↑IL8 in periodontal diseases influenced by local IL-1 activities.

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DIAGNOSIS OF GCF BIOMARKERS

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Analysis of components
52
TESTS COMPONENTS ANALYSED
Fluorometry MMPs
ELISA Enzyme levels and IL-1β
RIA COX derivatives and
procollagen III
HPLC Tinidazole
Direct/Indirect immunodot tests Acute phase proteins

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COMMERCIALLY
AVAILABLE
DIAGNOSTIC KITS

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RECENT FINDINGS IN GCF
54
- IL-29: antiviral IL-29 level was highest in GCF of aggressive periodontitis patients while that
of chronic periodontitis lying in between. After non-surgical therapy, IL-29 levels increased both
in chronic and aggressive periodontitis patients as a potential therapeutic agent in treating
periodontitis. (Shivaprasad BM, Pradeep AR 2013)
- SYSTEMIC DISEASE-RELATED
- PROGRANULIN – Chronic periodontitis & type 2 DM (Pradeep et al, 2013)
- CAPSASE 3 – GCF and the serum concentration of capsase-3 proportionally increases with
the progression of periodontal disease (Pradeep et al, 2014)
- OBESITY RELATED
- CHEMERIN – an adipokine; CP & DM
- LEPTIN – the decreasing leptin level in GCF and gingival tissue was associated with a
deteriorated periodontal status, and smokers also showed reduced GCF leptin levels in
recent studies (Pradeep et al, 2015)

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RECENT FINDINGS IN GCF
55

56. CONCLUSION
The origin, 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. On the other hand, none of the multiple components analysed in
the fluid has improved clinical judgement of the rate of progress of gingivitis and
periodontitis or of the rate of the repair of these conditions.
Through the biomarker discovery process, new therapeutics have been designed
linking therapeutic and diagnostic approaches together leading to more individualized and
targeted treatments for oral health.
Several tests have been developed that are aimed at specifically and sensitively
revealing the metabolic status of periodontal tissues. Some of them have shown good
specificity and sensitivity values as well as potential for predicting disease progression.
Unfortunately only a handful of GCF tests have made their way into clinical practice.
Clinicians are still missing a practical test based on enzymes, tissue degradation products
or cytokines that accurately indicates an initial periodontitis process, active disease
periods or effective healing. This will eventually pave the way for the development of
practical GCF indicators that will aid in the accurate diagnosis and appropriate treatment
of periodontal diseases.

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