Gingival Crevicular Fluid, Brill

1. Our Team
Style
PRESENTED BY- SK AZIZ IKBAL
GINGIVAL
CREVICULAR
FLUID

2. CONTENTS
INTRODUCTION
HISTORY
MECHANISM OF GCF
PRODUCTION
COMPOSITION
CLINICAL SIGNIFICANCE
CONCLUSION
GINGIVALCREVICULARFLUID

3. J Waerhaug
The pioneer research of J
Waerhaug (1950) was focused on
the anatomy of the sulcus and its
transformation into a gingival
pocket during the course of
periodontitis.
GINGIVALCREVICULARFLUID

4. HISTORY
Waerhaug,
1950
Focused on the
anatomy of the
sulcus and its
transform into a
gingival pocket
during periodontitis
Loe et al.
1965
GCF:
indicator of
periodontal
disease
Sueda, Bang,
Cimasoni, 1971,
1974
Presence &
functions of
proteins and
enzyme in
GCF
Brill et al.
1958
Egelberg,
1966
Physiology of
GCF
formation and
its
composition
Gingival
vasculature,
permeability
to GCF
GINGIVALCREVICULARFLUID

5.  “GCF is an exudate of varying composition found in
the sulcus/periodontal pocket between the tooth and
marginal gingiva” (Cimasoni G, 1983; Embery G
1994)
 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)
GINGIVALCREVICULARFLUID

6. Mechanisms of GCF production
There are 2 theories that suggest the formation of GCF
Theory-1 (Brill & Egelberg)
Increase permeability of vessel
Seepage of fluids in sulcus
Formation of GCF
GINGIVALCREVICULARFLUID

7. Theory-2
Loe H et al. (1965) demonstrated that GCF is
inflammatory exudate and not a common transudate.
GINGIVALCREVICULARFLUID Mechanisms of GCF production

8. Krasse
Brill N, Krasse B, 1958, applied filter
paper to the gingival sulci of dogs that
had previously been injected i.m. with
fluorescein, within 3 mins, the
fluorescent material was recovered on
the paper strips.
 This indicated the passage of fluid
from the bloodstream through the
tissues and the exiting of fluid via the
gingival sulcus.
 Flow of gingival fluid increased
markedly following stimulation of the
gingiva by tooth brushing, chewing,
after intravenous injection of
histamine or development of
inflammation.
GINGIVALCREVICULARFLUID Mechanisms of GCF production

9. Egelberg
Egelberg (1966) continued to analyze
GCF and focused his studies on the
dentogingival blood vessels and their
permeability as they relate to GCF flow.
GINGIVALCREVICULARFLUID Mechanisms of GCF production

10. Alfano
Hypothesis of Alfano
(1974)
GINGIVALCREVICULARFLUID
Very early or pre-inflammatory
flow of gingival fluid is osmotically
mediated
This osmotically modulated fluid
is a transudate
Later, on stimulation, it may
progress to a secondary
inflammatory exudate
Mechanisms of GCF production

11. Pashley
Pashley Model (1976)
 Based on STARLING
HYPOTHESIS governing fluid
distribution across capillaries.
 The model proposed by Pashley,
predicted that GCF production is
governed by-
• Capillary Filtration
• Lymphatic Uptake
GINGIVALCREVICULARFLUID Mechanisms of GCF production

12. i) In healthy condition, the
majority of interstitial fluid is
drained by lymphatic system and
only small amount leak into
gingival crevice forming
transudate. ii) During periodontal
disease, the amount of leaked
fluid from blood vessels is
beyond the drainage capacity of
lymphatics, leading to formation
of inflammatory exudate.
GINGIVALCREVICULARFLUID Mechanisms of GCF production

13. Cimasoni
 Presence and functions of proteins
and enzymes in GCF were first
explored by Sueda, Bang, Cimasoni
(1974)
 It was soon understood that enzymes
released from damaged periodontal
tissue has an enormous potential for
periodontal diagnosis.
GINGIVALCREVICULARFLUID Mechanisms of GCF production

14. 01
02
03
ABSORBING PAPER STRIP
PRE WEIGHED
TWISTED THREADS
MICROPIPETTES
INTRACREVICULAR
WASHINGS
METHODS OF COLLECTION
04
GINGIVAL CREVICULAR FLUID

15. 1. ABSORBENT FILTER PAPER STRIP
01
02
INTRACREVICULAR
EXTRACREVICULAR
These strips are placed within the sulcus (Intrasulcular method) or
at its entrance (Extrasulcular method).
GINGIVALCREVICULARFLUID Methods of collection

16. 1a. Intrasulcular Method
GINGIVALCREVICULARFLUID Methods of collection

17. 1b. Extrasulcular Method
he paper strip is adapted on the gingiva & the hard
tissue of the tooth.
GINGIVALCREVICULARFLUID Methods of collection
T

18. Evaluation of amount of fluid collected
a) Appreciation by Direct Viewing/Staining:
- 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
GINGIVALCREVICULARFLUID Methods of collection

19. The stained area can then be measured with:-
 An ordinary transparent ruler. (Egelberg in 1964)
 Sliding caliper. (Bjorn in 1965)
 Calibrated magnifying glass. (Oliver in 1969)
 Microscope with an eyepiece. (Wilson in 1971)
Golub,1971; Egelberg & Attstrom, 1973
GINGIVALCREVICULARFLUID Methods of collection

20. Evaluation of amount of fluid collected
b) Weighing the Strips
Golub,1971; Egelberg & Attstrom, 1973
Weight the sample (the strips are weighed
before and immediately after collection).
• Valazza, 1972
GINGIVALCREVICULARFLUID Methods of collection

21. Evaluation of amount of fluid collected
c) Use of Periotron
Golub,1971; Egelberg & Attstrom, 1973
GINGIVALCREVICULARFLUID Methods of collection
Types- 600,6000,8000
Harco Electronics, Canada

22. Measures Showing Periotron Indices in Respect to Gingival Disease
Ref:-Brochure from the original Periotron A 600 Loe H, Holm Mann et al.
Periotron reading Gingival Health Gingival Index
0-20 Healthy 0
21-40 Mild Inflammation 1
41-80 Moderate Inflammation 2
81-100 Severe Inflammation 3
GINGIVALCREVICULARFLUID Methods of collection

23. 2. PRE WEIGHED TWISTED THREADS
GINGIVALCREVICULARFLUID Methods of collection

24. 3. CAPILLARY TUBING OR MICROPIPETTES
 he use of micropipettes allows the
collection of fluid by capillarity action.
 Capillary tubes of standardized length and
diameter are placed in the pocket and their
content is later centrifuged and analyzed.
T
GINGIVALCREVICULARFLUID Methods of collection

25. echnique proposed by: Kaslick in 1968.
Following the isolation and drying of a site, capillary tubes of known internal
diameter and length are inserted into the entrance of the gingival crevice.
GCF from the crevice migrates into the tube by capillary action.
Since, the internal diameter of the capillary is known, the volume of fluid
collected can be determined accurately by measuring the distance which
the GCF has migrated.
Sueda T, Bang J, Cimasoni G. Collection of gingival fluid for quantitative
analysis. J Dent Res 1969: 48: 159
Evaluation of the Amount of Fluid Collected
GINGIVALCREVICULARFLUID
T
Methods of collection

26. he Method Of Skapski And Lehner:
 Simpler technique to obtain crevicular washings from gingival crevice
 Installation and re-aspiration of 10ml of Hanks BSS at the interdental
papilla.
 Repeated 12 times to allow through mixing of the transport solution and
GCF
T
GINGIVALCREVICULARFLUID Methods of collection
Intracrevicular Washings

27. 4. INTRACREVICULAR WASHINGS
he 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.
T
GINGIVALCREVICULARFLUID Methods of collection

28. GINGIVALCREVICULARFLUID Methods of collection
Intracrevicular Washings

29. Problems associated
with GCF collection
• Contamination
• Small sample size
• Sampling time
• Volume determination
• Difference in quality of paper strips
GINGIVAL CREVICULAR FLUID

30. End of 1st Part
T H A N K Y O U
GINGIVALCREVICULARFLUID

31. Mechanisms of GCF production
COMPOSITION OF GCF
Cellular
elements
Inorganic
components
Organic
Compounds
Bacterial
products
Enzymes
Bacteria,
desquamated
epithelial
cells, PMNs,
lymphocytes,
monocytes/
macrophage
Potassium,
Sodium,
Calcium,
Phosphate,
Magnesium
Carbohydrate,
Proteins,
Lipids,
Albumin,
Immunoglobul
in
Endotoxins,
Trypsin like
enzyme
Acid
phosphatase ,
Alkaline
phosphatase ,
Prostaglandin
E2,
Collagenase ,
Lysozyme ,
Lactoferrin
GINGIVALCREVICULARFLUID

32. GCF-AS A DIAGNOSTIC MARKER
 An extensive research has been made for GCF components that
might serve as potential diagnostic or prognostic markers for the
progression of periodontitis.
Curtis et al. stated that "markers of disease" might encompass three
separate categories:
1)Indicators of current disease activity;
2)Predictors of future disease progression;
3)Predictors of future disease initiation at currently healthy sites.
GINGIVALCREVICULARFLUID

33. CLASSIFICATION OF GCF BIOMARKERS
Host-derived enzymes and
their inhibitors
Tissue breakdown products
Inflammatory mediator and
host response modifiers
• Aspartate aminotransferase
• Alkaline phosphatase
• Acid phosphatase
• β-Glucuronidase
• Elastase
• Elastase inhibitors
α2 – Macroglobulin
α1 - Antitrypsin
• Cathepsins
• Serine proteinase (G)
• Cathepsin D
• Glycosaminoglycans
Chondroitin-4-sulfate
Chondroitin-6-sulfate
• Hyaluronic acid
• Hydroxyproline
• Fibronectin 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

34.  The oral sulcular epithelium and junctional epithelium are
constantly renewing and the shed cells are found in the
GCF .
 Two different types of cells originating from the junctional
epithelium can be seen depending on their location:-
1. At the sulcus bottom - cells are well preserved, contains
lysosome like bodies.
2. Coronal to the sulcus bottom - cells show progressive
necrosis.
EPITHELIAL CELLS
• Lange and Schroeder in 1971

35. LEUKOCYTES
 In 1960, Sharry & Krasse determined that 47% of all cells
obtained from the gingival sulcus were leukocytes.
 Attstrom in 1970, was one of the first to study the numbers
of leukocytic cells in GCF.

36. GCF PERIPHERAL
BLOOD
Neutrophil 95 – 97 % 60%
Monocyte 2-3% 5-10%
Lymphocyte 1 – 2 % 20-30%
-Attstrom in 1970

37. GCF PERIPHERAL
BLOOD
T cells 24% 50-75%
B cells 58% 15-30%
Mononuclear
phagocyte
18%
T : B 1 : 2.7 3 : 1
-Wilton et al. 1976
Mononuclear Cells:

38.  The first quantitative study has been performed by Matsue in
1967.
Healthy gingiva: 158 mEq of sodium/L.
Inflamed gingiva: 207 - 222 mEq of sodium/L.
 The GCF contains a significantly higher amount of sodium than
serum.
 Sodium concentration tends to increase in cases of more severe
inflammation.
Sodium Concentration
Electrolytes

39. Potassium Concentration
 The potassium content of GCF is also generally more than
that of serum. Values as high as 69 mEg/lit. from the
inflamed areas. Nature (1967).
 The potassium content of crevicular exudate tended to
increase in cases showing more severe periodontitis.

40. Kaslick in 1970 presented that:-
 Sodium and potassium contents follow a circadian periodicity
 Sodium concentration is lower at noon than in the morning
 Potassium values are higher towards the middle of the day.

41. Sodium : Potassium Ratio
 As suggested by Krasse & Egelberg (1962) the fluid passes
through damaged tissues a decrease sodium : Potassium ratio
would be found because of the accumulation of intracellular
potassium from the disrupt cells.
 They showed a sodium: potassium ratio of 3.9:1 in gingival
fluid, which is much lower than the ratio of 28:1 normally found
in extracellular fluid.

42. ORGANIC COMPOUNDS
Carbohydrates
 Glucose, hexosamine and hexuronic acid.
 In inflamed gingiva, Glucose : GCF > serum (3-4:1)
 Increased in:
 Inflammation
 Diabetes
 Hexosamine & Hexuronic acid – no correlation with
variation in gingival inflammation
Hara K, Loe H. Carbohydrate component of gingival exudate. J Periodont Res
1969:4;202-07

43. Proteins
 In healthy gingiva, concentration of proteins in GCF is as low as
1:10 of that of serum. (Brill and Bronnestam,1960)
 Histochemically, it was determined that crevicular exudate contains
proteins similar to those found in serum. [Sueda et al, 1966]
 Albumin, fibrinogen, ceruloplasmin, ß-lipoproteins, transferrin
(Mann & Stoffer, 1964), bradykinin (Rodin et al 1973)
 The average fluid protein concentration was 6.83g/100 ml. (Bang
and Cimasoni, 1971)

44. Lactic Acid
 Its concentration in GCF was reported to be positively
correlated with clinical degree of gingival inflammation and
intensity of gingival fluid flow. (Hasegawa,1967)
METABOLIC AND BACTERIAL PRODUCT
Prostaglandins
 Inflamed gingiva were shown to contain more PGE-2 than
healthy gingiva (El Attar,1976).

45. Urea & pH of Gingival Fluid
 Biswas in 1977 confirmed that urea concentration in crevicular
fluid seems to decrease when gingival inflammation increases.
 Urea could be responsible for the elevation of pH of gingival sulcus,
through the production of ammonia by microorganisms. (Klienberg
and Hall in 1969)

46. HOST DERIVED ENZYMES AND THEIR INHIBITORS
Alkaline Phosphatase (ALP)
 It probably plays a role in calcification. The concentration of ALP in
GCF three times more than that in serum.
 ALP is released from-
 PMNs (During inflammation)
 Osteoblasts (During bone formation)
 Periodontal ligament fibroblast (During periodontal
regeneration)
 The concentration of this enzyme in GCF was found to be
significantly correlated with pocket depth. (Ishikawa and Cimasoni
in 1970)
 Gilbert in 2003 predicted alkaline phosphatase (ALP) as an
indicator for the future periodontal breakdown.

47.  The decrease of ALP in GCF at 15 days corresponded to a
decrease in clinical signs of inflammation; in contrast, the increase
of ALP activity in GCF at 60 days seemed to be related to
subclinical recurrent inflammation or further healing/remodeling of
the periodontal tissue. (Perinetti et al 2008)
 Therefore concentration of ALP in GCF gives use clue about
the short-term periodontal healing or recurrent inflammation
phases in chronic periodontitis patients.

48. Aspartate aminotransferase (AST)
 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 published.

49. β-glucoronidase
 This enzyme concentration is found to be positively correlated with the
mean percentage of bone loss.
 Even in same patient, its concentration is more in active site than in
inactive site.
 Conc. of β-glucuronidase, collagenase and elastase have been
detected significantly higher compared to well-controlled diabetic
patients  Indicating correlation with periodontitis in poorly controlled
diabetic patients.
 In gingival inflammation, its concentration in GCF is 10 times higher
than in serum. Bang et al, 1970

50. Cathepsin-D
 It is one of the chief acid enzymes in lysosomes, present at high
concentration in inflamed tissues.
 This enzyme is considered to be involved in breakdown of
extracellular matrix.
 During periodontal destruction, Its concentration in GCF was found
to be 10 times higher compared to GCF in healthy sulcus.
(Cimasoni et al, 1979).

51. Cathepsin-B
 Main source- Marcophage (Kennett CN, 1997)
 Good indicator of periodontal disease activity because it degrades
extracellular matrix proteins such as collagens.
 Concentration of Cathepsin B in GCF were found to be elevated in
patients with periodontal disease but lower in patients with gingivitis.
 Significant correlation b/w GCF levels of cathepsin B and clinical
parameters before and after periodontal treatment, suggesting that
this enzyme can be used to assess treatment outcomes. (Loss BG
et al, 2005)

52. Elastase
 Potent proteolytic enzyme found in lysozymal granules.
 Amounts of GCF elastase are greater in periodontitis patients than
healthy controls. (Ohlsson K, Olsson I, Tynelius- Bratthall G. Acta
OdontolScand.1973).
 Levels of elastase in GCF during experimental gingivitis are elevated,
which are reduced when plaque removal are reinstituted. ( Eley BM,
1996).
 Increased elastase in GCF denotes increased neutrophil activity and is
predictive of periodontal attachment loss.

53. Elastase Inhibitor
 Activity of protease enzymes are restricted by elastase inhibitors.
 Produced locally or derived from plasma
 In plasma primarily- α2- macroglobulin and α1-antitrypsin are
responsible for more than 90% of anti-protease activity
 Concentration of α2- macroglobulin and α1-antitrypsin in GCF found
three-fourth of their serum concentration.
 α2- macroglobulin in inflamed site were twice as compared to the
samples collected after periodontal treatment from the same sites
(Schenkein HA, 1977).

54. Matrix metalloproteinases (MMPs)
 Proteolytic enzymes involved in the degradation of a variety of
extracellular matrix macromolecules such as collagens, fibronectin,
laminin and proteoglycan.
 MMP-8 (collagenase-2) and MMP-9 (gelatinase-B) are main collagen
degrading enzymes in GCF.
 Some Studies shown that levels of MMP-8, MMP-3 and MMP-13 are
associated with periodontal disease progression.

55.  Collagenase-2(MMP-8)
 Increased levels of MMP-8 in GCF is associated with severity
of periodontitis.
 It is released from PMNs.
 Increased levels of MMP-8 signify conversion of gingivitis into
periodontitis.
 It is found that 18-fold increase of MMP-8 in patients
experiencing active periodontal tissue destruction as compared
with patients under stable condition. (Mancini S, 1999)

56.  Gelatinase(MMP-9)
 Produced by neutrophils and degrades collagen extracellular
ground substance.
 There is 2-fold increase in mean MMP-9 levels is reported in
patients with recurrent attachment loss.

57.  Collagenase-3(MMP-13)
 MMP-13 is expressed by sulcular epithelial cells, endothelial
cells, macrophage-like cells, fibroblasts, plasma cells and
osteoblasts.
 MMP-13 has also been implicated in peri-implantitis.
 Elevated levels of both MMP-13 and MMP-8 are correlated with
irreversible peri-implant vertical bone loss and loosening dental
implants.

58. TISSUE BREAKDOWN PRODUCTS
Hydroxyproline
Since hydroxyproline is the major breakdown product of collagen, Hara
and Takahashi in 1975 compared its concentration in samples of serum
and GCF before and after various types of periodontal surgery.
In both medium, the hydroxyproline concentration increased for 1 month
after surgery and returned to baseline levels after 6 months.
Akalin et al. (1993) investigated raised level of hydroxyproline in GCF of
juvenile, rapidly progressive and adult periodontitis patients.

59. Glycosaminoglycans(GAGs)
 Level of GAGs in GCF is good indicator of underlying tissue turnover.
 Elevated in GCF during inflammation. (Giannobile WV, 1993)
 A study showed higher levels of Chondroitin-4-sulfate at diseased site
prior to the treatment which correlated with increased pocket depth
or attachment level. (Smith AJ, 1997)

60. Yan, 2000

61.  Osteocalcin is non collagenous protein. It is predominately present in
mineralized tissues. It is produced by osteoblasts, help in bone
remodeling.
 Increased levels of osteocalcin are associated with rapid bone
remodeling.
 The levels of osteocalcin remain unchanged in patients with
gingivitis. Osteocalcin levels are increased in Periodontitis.
(Nakashima K et al.)
Osteocalcin

62. INFLAMMATORY MEDIATORS
Cytokines
 Various cytokines detected in GCF and can be used as biomarkers
for periodontal disease progression.
 These cytokines includes Prostaglandin E2, Thromboxane B, IL-1,-
2,-6 and -8, TNF (tumor necrosis factor) etc.

63.  IL-1α :Do not correlate with probing pocket depth
 IL-1β: Associated with progression of attachment loss (Liu CM, 1996)
 IL-2 : Might predict and associate with progressive attachment loss
due to activation of T-lymphocytes in periodontium (Pilon M,1991)
 IL-6: Produced more in refractory sites.

64. INFLAMMATORY MEDIATORS
 IL-8: Good indicator of periodontal disease progression. Some
studies found higher level of IL-8 in diseased sites compared to
healthy sites. (Mathur A 1996)
Whereas others reported an adverse relationship between PMNs
recruitment responsible for periodontal status and IL-8 levels in
GCF. (Chung RM, 1997)

65. Interferon-α (IFN- α)
 Its level in GCF are indicative of Cell- mediated immune response.
 Reduced level of IFN- α at a site may signify a lowered cell-
mediated immune response.
 Mathur A, 1996 concluded that the combination of decreased IL-8
and decreased IFN-α concentrations in GCF at diseased sites may
reflect the reduced anti-bacterial host defence activity.

66. Plasminogen activator
 Hidaka et al (1981) found that the concentration of
plasminogen activators in human gingival fluid seems to
increase as a function of the severity of periodontitis.

67. COMMERCIAL DIAGNOSTIC KITS BASED ON GCF PROTEOLYTIC
AND HYDROLYTIC ENZYME LEVELS
Kit Name Made By Diagnoses
BANA
periodontal test
Ora Tec Corporation Manassas
(USA)
bacterial trypsin like
proteases
Periocheck CollaGenex Pharmaceuticals,
Newtown, PA
neutral proteinases i.e.
Collagenase
Perioscan Oral B Laboratories enzymatic activity of Aggregatibacter actinomycetemcomitans, T.
forsythus, P. gingivalis
Evalusite Kodak Eastman Company
(Switzerland)
Immunological detection of antigens of Aggregatibacter
actinomycetemcomitans, P. intermedia, P. gingivalis using antibodies
(ELISA).
Prognostic Dentsply serine proteinases and elastases
Biolise SLT-Lab instruments, Crailsheim,
Germany
elastase
Periogard Colgate AST
Pocket watch SteriOss®, San Diego, CA, USA Aspartate aminotransferase through
colorimetric detection
TOPAS Affinity Labelling Technologies
(USA)
Detects toxins derived from anaerobic metabolism and measures GCF
protein level

68. CLINICAL SIGNIFICANCE
 The amount of GCF is greater when inflammation is present and it is
sometimes proportional to the severity of inflammation.
 GCF production is not increased by TFO
 But it is increased by coarse foods, toothbrushing and gingival massage,
ovulation, oral contraceptives, prosthetic appliances, and smoking
 Other Factors that influence the amount of GCF are circadian periodicity
and periodontal therapy.

69. Circadian Periodicity
Conflicting results have been reported concerning the possibility of a
circadian pattern in the flow of crevicular fluid.
I. One group of investigators found that the average flow was greater in
the evening and minimal in early morning. (Bissada et al.,1967).
According to them there is gradual increase in GCF amount from 6 AM
to 10 PM and decrease afterword.
II. A second group did not find any systemic differences between the flow
of the fluid measured at 9 a.m. and that of the fluid collected at 3 p.m.
(Suppipat et al.,1977)

70. Gingival Fluid flow and Sex Hormones
 During pregnancy (Loe in 1965), menstrual cycle (Muhlemann in
1948) and at puberty (Sutcliffe in 1972), there is an exacerbation of
gingivitis and therefore, increased levels of GCF is seen.
 According to Lindhe et al in 1969, female sex hormones cause an
increase in gingival vascular permeability.

71. Gingival Fluid in Diabetic Patient
 According to Ringelberg et al.in 1977, higher flow rate of gingival
fluid in diabetic patients were reported when compared to the flow
rate of healthy patients.
 Investigators agree that the exudates collected from diabetic
patients contain significantly more glucose than the exudates
collected from healthy individuals.

72. Periodontal Therapy and Crevicular Fluid
 The effect of repeated prophylaxis on plaque accumulation and
gingival fluid flow were studied by Gwinnett et al in 1978.
 They found that the fluid flow decreased 1 week after the first
prophylaxis and then slowly returned to pre-treatment values.
 After a second prophylaxis the lower levels of fluid were
sustained for longer periods of time.
 Scaling and curettage caused a decrease of gingival fluid
collection to a minimum at 14 days after treatment. (Suppipat
et al in 1977).

73. Drugs in GCF
 Drugs that are excreted through the GCF may be used
advantageously in periodontal therapy.
 Bader and Goldhaber (1966) demonstrated in dogs that
tetracyclines are excreted through the GCF.
 Other drugs that are present in GCF are-
Minocycline(Ciancio et al,1980)
Metronidazole(Eisenberg,1991)

74. CONCLUSION
 Extensive research has been done on GCF in search of reliable
markers for monitoring periodontal disease activity
 Various components of GCF have been investigated to detect the
present status of the periodontal condition and the probable future
status
 Analysis of GCF in health and periodontal disease may be extremely
useful to monitor periodontal disease because GCF can be easily
obtained with non invasive methods.

75. THANK YOU