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Original Article
Effect of Orthodontic Tooth Movement on Gingival
Crevicular Fluid Infiltration; a Preliminary Investigation
A. Dannan 1~, MA. Darwish 2, MN. Sawan 3
1
Assistant Clinical Specialist, Department of Periodontology, School of Dentistry, Witten/Herdecke University, Witten, Germany
Professor, Department of Periodontology, School of Dentistry, Damascus University, Damascus, Syria
3
Professor, Department of Orthodontics, School of Dentistry, Damascus University, Damascus, Syria
2
Abstract:
~
Corresponding author:
A. Dannan, Department of Periodontology, School of Dentistry, Witten/Herdecke University, Witten, Germany.
[email protected]
Received: 25 August 2008
Accepted: 31 December 2008
Objective: The gingival crevicular fluid (GCF) is an inflammatory exudate found in the
gingival sulcus. The forces exerted during orthodontic treatment cause distortion of the
periodontal ligament (PDL) extra-cellular matrix, resulting in some biological features that
can lead to modification of both GCF volume and its components. The present study investigated the effect of orthodontic tooth movements, specifically canine retraction, on the
volume of GCF exudate.
Materials and Methods: Fourteen upper and lower canines of patients with different Angle classifications were selected for the study. After extraction of the first premolars, the
canines were subjected to orthodontic distal retraction. GCF was sampled from mesial and
distal gingival crevices of each canine separately at baseline, 1 hour, 7 days, 14 days, 21
days, and 28 days after the application of the orthodontic distal retraction. GCF volume
was determined by means of an electronic device.
Results: GCF volume at tension sites was slightly greater after 21 and 28 days compared
to other observation time points. At pressure sites, GCF volume was slightly greater after
28 days compared to other observation time points. None of the observed differences,
however, was statistically significant (P>0.05).
Conclusion: Orthodontic tooth movement, namely canine retraction, does not significantly increase the volume of GCF exudate. The slight increase in GCF volume could be
due to a slight degree of gingival inflammation.
Key Words: Gingival Crevicular Fluid; Periodontal Ligament; Tooth Movement
Journal of Dentistry, Tehran University of Medical Sciences, Tehran, Iran (2009; Vol. 6, No.3)
INTRODUCTION
The gingival crevicular fluid (GCF) is an osmotically mediated inflammatory exudate
found in the gingival sulcus. As an exudate, it
tends to increase in volume with inflammation
and capillary permeability.
Serum is the main source of the aqueous component of the GCF. The composition of GCF,
however, can be modified by the gingival tissue through which the fluid passes, as well as
bacteria both in tissues and the gingival crevice [1,2]. Consequently, the constituents of this
2009; Vol. 6, No. 3
fluid vary according to the condition of the
periodontal tissues. Generally, cells, immunoglobulins, microorganisms, toxins, and lysosomal enzymes can all be found in the GCF.
It has been shown that GCF flow rate is a reliable indicator of gingivitis development in experimentally induced gingivitis [3]. Moreover,
the levels of some of the GCF components like
alkaline phosphatase, β-glucoronidase, aspartate aminotransferase, prostaglandins, immunoglobulin G4, interleukin-1 (IL-1) and others
correlate specifically with the actual clinical
109
Journal of Dentistry, Tehran University of Medical Sciences
measurements of periodontal disease progression [4-13].
The forces exerted during orthodontic treatment cause distortion of the periodontal ligament (PDL) extra-cellular matrix, resulting in
some biological features that can lead to cellular activation by changing membrane polarity
and ion channel activity. In addition, as the
capillaries are stretched or compressed excessively, tissue damage may occur. Such events
and interactions lead to the synthesis and secretion of extracellular matrix components,
tissue-degrading enzymes, acids, and local factors; induce cellular proliferation and differentiation; and promote wound healing and tissue
remodeling. In vivo studies suggest that as biologic reactions progress at varying rates and
intensities during different periods of treatment, alternate combinations of biochemical
molecules come into play. These combinations
are dependent on alveolar remodeling dynamics, the cycles of injury and healing, and the
composition of the PDL cell population at
each period [14-16].
More recently, Rhee et al [17] conducted a
study to provide a better understanding of both
the dynamics and the metabolic stages of orthodontic tooth movement in terms of Cystatins and Cathepsin B relationships in GCF.
They showed that the balance between enzyme
and inhibitor might reflect the clinical status of
orthodontic tooth movement and provide valuable information for the assessment of recall
intervals and retention procedures [17].
Such changes in the deeper periodontal tissues
during orthodontic treatment can lead to modification of both the GCF volume and its components.
Dannan et al.
The present study was undertaken to investigate the effects of one type of orthodontic
tooth movements, specifically canine retraction, on the secretion of GCF from retracted
teeth, and to consider any implications of such
findings for clinical orthodontic procedures.
MATERIALS AND METHODS
Study Population
The samples were selected from the patients
referred to Department of Orthodontics, Faculty of Dental Medicine, Damascus University. To be eligible for the study, the patients
had to meet the following criteria: good general health; lack of antibiotic therapy during
the previous six months; absence of antiinflammatory drug administration in the month
preceding the study; and periodontal health
with generalized probing depths ≤ 3 mm and
no radiographic evidence of periodontal bone
loss. They also required upper and/or lower
first premolars extraction and canine distal
tooth movement as part of orthodontic treatment plan. Based on these criteria seven orthodontic patients comprising four females,
(mean age 16.5 years, SD=1.5) and three
males (mean age 17.6 years SD=2.5) were selected.
An oral approval to be subjected to the study
was obtained from the patients or from the
parents of patients under 18 years of age, prior
to the commencement of the study. One week
before the baseline examination, all patients
underwent a session of supra- and sub-gingival
ultrasonic scaling.
Experimental Design
Based on complete orthodontic treatment
Table 1. Mean and standard deviation (SD) of the clinical parameters used in the study.
Baseline
Day 28
Mean (SD)
Mean (SD)
0.24 (0.13)
0.19 (0.10)
Plaque Index
1.6 (0.51)
1.5 (0.45)
Probing Depth (mm)
0.23 (0.20)
0.30 (0.28)
Gingival Index
ANOVA Test
NS
NS
NS
NS= Not statistically Significant
110
2009; Vol. 6, No. 3
Dannan et al.
plans, six upper and eight lower first premolars
were extracted for all of the patients as the first
step. Three weeks after the extraction of the
first premolars, the canines next to the extraction areas were moved in a distal direction using 90g forces for mandibular and 115g forces
for maxillary canines. These teeth comprised
six upper canines (four canines in two female
patients and two canines in one male patient)
and eight lower canines (four canines in two
female patients and four canines in two male
patients). The forces were exerted by means of
an archwire using a retraction spring. The
amount of forces was verified using a calibrated orthodontic force gauge, which was adjusted for each case separately.
Clinical Monitoring
The status of the periodontal tissues was determined by clinical periodontal assessments
including plaque index (PI) [18], gingival index (GI) [19] and probing depth (PD). These
clinical parameters were assessed twice: at
baseline (prior to orthodontic appliance
placement) and on day 28.
GCF Samples Collection
GCF samples from each tooth was collected
separately from the mesial and distal gingival
crevices of each canine where the orthodontic
forces were applied at baseline (before the application of the orthodontic force) and one
Tooth Movement and Gingival Crevicular Fluid
hour, 7 days, 14 days, 21 days and 28 days after the application of the orthodontic force.
Gingival crevicular fluid was sampled from
the mesial and distal gingival crevices of each
canine, where the orthodontic forces were applied, using the method described by Offenbacher et al [20]. The area was isolated with
cotton rolls and the teeth and adjacent marginal gingival were dried with air to minimize
saliva contamination. Then a paper strip
(Roeko Inc®, Germany) was inserted into the
crevice to a level of one millimeter below the
gingival margin for 60 seconds. After removing the first strip and waiting for one minute, a
second strip was placed at the same site for
another 60 seconds in order to obtain a sufficient (measurable) amount of GCF since using
one strip might not be sufficient. Strips contaminated by saliva or blood were excluded.
GCF volume was measured with a calibrated
electronic device (Periotron® 8000, Ora Flow,
USA). We then used a software program
(Mlconvert.exe, Ora Flow, USA) to convert
the measurements to microliters [21].
Data Processing
The data was analyzed using SPSS (version
11, SPSS Inc., USA). One-way ANOVA test
served for statistical analysis. The measurements of GCF volume were expressed as the
overall volume for each experimental group
considering the tooth itself as the statistical
Table 2. Mean and standard deviation of GCF volumes at mesial (tension) and distal (pressure) sites of the 14
retracted canines.
GCF Volume (µL)
Time
at Mesial Sites
at Distal Sites
Mean (SD)
Mean (SD)
0.46 (0.15)
0.50 (0.15)
Baseline
0.50 (0.15)
0.50 (0.08)
One-hour
0.47 (0.14)
0.44 (0.09)
Day 7
0.46 (0.10)
0.47 (0.10)
Day 14
0.53 (0.12)
0.50 (0.11)
Day 21
0.55 (0.15)
0.56 (0.17)
Day 28
NS
NS
ANOVA Test
NS= Not statistically Significant
2009; Vol. 6, No. 3
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Journal of Dentistry, Tehran University of Medical Sciences
unit. A probability of P<0.05 was accepted for
rejection of the null hypothesis and to state
that with a 95% level of confidence that the
two parameters are not the same.
RESULTS
At the baseline, the clinical indices, expressed
as the mean, were recorded as follows: 0.24
mm (SD=0.13), 1.6 mm (SD=0.51), and 0.23
(SD=0.2) for PI, PD and GI, respectively. The
corresponding figures after 28 days were 0.19
mm (SD=0.1), 1.5 mm (SD=0.45) and 0.30
(SD=0.28), respectively. No statistically significant difference of pairwise comparisons
over the two time points was found (Table 1).
No sign of periodontal destruction was observed in any subject.
GCF volume at tension sites was slightly
greater after 21 and 28 days compared to other
observation time points (Table 2). At pressure
sites, GCF volume was slightly greater after 28
days compared to other observation time
points. None of the observed differences, however, was statistically significant (P>0.05).
DISCUSSION
The present study investigated the effect of
orthodontic canine retraction on GCF volume
in a sample of seven orthodontic patients. According to the results, no statistically significant increase occurred in GCF volume during
orthodontic tooth movement.
In periodontal tissues, orthodontic tooth
movement produces a biological process previously described as a continuous phenomenon, leading to bone resorption in pressure
sites and bone deposition in tension sites [2225]. Histological animal research has shown
that both bone deposition and resorption occur
in both tension and pressure sites in the alveolar bone undergoing mechanical stress through
tooth movement [26]. Based on these data,
first a wave of resorption occurs in 3 to 5 days.
This early wave is followed by its reversal in 5
to 7 days. Then a late wave of bone formation
112
Dannan et al.
lasting for 7 to 14 days occurs. This process
can be detected on both compression and tension sides of the alveolar wall [26]. This model
is marked out by a preliminary asynchronous
period in which bone resorption is greater than
bone deposition, while, at later times, resorption and deposition may become synchronous.
It is supposed that all those histological actions, which take place during orthodontic
treatments, may affect the flow rate of the
GCF of the related teeth.
It has been shown that the placement of fixed
orthodontic appliances has a significant impact
on microbial and periodontal clinical variables
including GCF’s flow and contents [27-29].
Baldwin et al [30] reported that the increase in
GCF flow induced by orthodontic tooth
movement begins earlier than the pronounced
changes in GCF components. This finding
suggests an immediate effect of orthodontic
force on the blood vessels, rather than induction of biochemical changes in the extracellular matrix. In contrast, Uematsu et al [31] reported that the volume of fluid around the experimental tooth during orthodontic movement
was similar to the fluid around healthy teeth.
Corroborating evidence was produced by Miyajima et al [32] who found no significant differences in GCF volume between treatment,
retention, and control groups, although the
mean value of the retention group was smaller
than that of the other groups.
Tersin [33] reported an increase in GCF production during orthodontic treatment, in both a
group receiving oral hygiene instruction and
supervision, and a group not receiving these
interventions, while a recent study [34] found
no significant difference between teeth undergoing orthodontic treatment and untreated contralateral teeth.
In the present study, a slight increase in the
volume of GCF occurred at the mesial sites
one hour after the force had been started. After
one week, all the values of GCF volume decreased. These values increased gradually after
2009; Vol. 6, No. 3
Dannan et al.
21 and 28 days. However, none of these
changes was statistically significant.
Many studies have reported a significant correlation between plaque accumulation, gingival
inflammation, and the volume of gingival exudate [1]. This may account for the contradictory evidence, as the additional effect of orthodontic treatment itself on gingival fluid
flow rate cannot be determined unless such
influences are eliminated. However, some
studies considering gingival status reported
that significant increase in GCF flow rate during orthodontic treatment is partly unrelated to
the presence of significantly more severe gingival inflammation [35-37]. Later, Pender et al
[38] reported that the GCF tended to increase
at both non-inflamed and moderately inflamed
sites, compared to similar sites before treatment. Last et al [36] demonstrated an increased GCF flow rate at early stages of retention compared to an untreated control group.
The slight insignificant increase in GCF volumes in the present study might be due to a
slight gingival inflammation existed after 28
days. However, this gingival inflammation did
not reach – at any time – destructive values.
CONCLUSION
According to the results obtained, and within
the limitations of the study, it could be stated
that GCF volume was not significantly affected by the orthodontic movements and the
forces applied.
However, the slight increase in GCF volume,
although not statistically significant, could be
due to slight degree of gingival inflammation,
which is normally found during any orthodontic treatment.
Further studies are needed to establish procedures useful for clinical monitoring of biologic
processes in the deeper periodontal tissues and
the GCF during orthodontic tooth movement
in human beings. The association between
clinical parameters and tissue remodeling represented by GCF alterations can be clinically
2009; Vol. 6, No. 3
Tooth Movement and Gingival Crevicular Fluid
useful to biologically monitor and predict orthodontic treatment.
For future studies in this field, we suggest the
use of cephalometric analysis in order to control the tooth movement more precisely.
ACKNOWLEDGMENTS
The Authors are thankful to Dr. Ramadan
Darwish for his contribution regarding the statistical analysis
REFERENCES
1- Cimasoni G. Crevicular fluid updated. In: Myers
HM, editors. Monographs in Oral Science. Basel:
Karger; 1983. pp. 259-78.
2- Tollefsen T, Saltvedt E. Comparative analysis of
gingival fluid and plasma by crossed immunoelectrophoresis. J Periodontal Res 1980 Jan;15(1):96106.
3- Brecx MC, Schlegel K, Gehr P, Lang NP. Comparison between histological and clinical parameters during human experimental gingivitis. J Periodontal Res 1987 Jan;22(1):50-7.
4- Ishihara Y, Nishihara T, Kuroyanagi T, Shirozu
N, Yamagishi E, Ohguchi M, et al. Gingival crevicular interleukin-1 and interleukin-1 receptor antagonist levels in periodontally healthy and diseased sites. J Periodontal Res 1997 Aug;32(6):5249.
5- Kamma J, Mombelli A, Tsinidou K, Vasdekis V,
Giannopoulou C. Cytokines in gingival crevicular
fluid of adolescents and young adults. Oral Microbiol Immunol 2009 Feb;24(1):7-10.
6- Dutzan N, Vernal R, Hernandez M, Dezerega A,
Rivera O, Silva N, et al. Levels of InterferonGamma and Transcription Factor T-Bet in Progressive Periodontal Lesions in Patients With Chronic
Periodontitis. J Periodontol2009 Feb;80(2):290-6.
7- Lamster IB, Hartley LJ, Oshrain RL, Gordon
JM. Evaluation and modification of spectrophotometric procedures for analysis of lactate dehydrogenase, beta-glucuronidase and arylsulphatase
in human gingival crevicular fluid collected with
filter-paper strips. Arch Oral Biol 1985;30(3):23542.
113
Journal of Dentistry, Tehran University of Medical Sciences
8- Lamster IB, Holmes LG, Gross KB, Oshrain RL,
Cohen DW, Rose LF, et al. The relationship of
beta-glucuronidase activity in crevicular fluid to
clinical parameters of periodontal disease. Findings
from a multicenter study. J Clin Periodontol 1994
Feb;21(2):118-27.
9- Lamster IB, Mandella RD, Gordon JM. Lactate
dehydrogenase activity in gingival crevicular fluid
collected with filter paper strips: analysis in subjects with non-inflamed and mildly inflamed gingiva. J Clin Periodontol 1985 Feb;12(2):153-61.
10-Lamster IB, Vogel RI, Hartley LJ, DeGeorge
CA, Gordon JM. Lactate dehydrogenase, betaglucuronidase and arylsulfatase activity in gingival
crevicular fluid associated with experimental gingivitis in man. J Periodontol 1985 Mar;56(3):13947.
11-Offenbacher S, Odle BM, Van Dyke TE. The
use of crevicular fluid prostaglandin E2 levels as a
predictor of periodontal attachment loss. J Periodontal Res 1986 Mar;21(2):101-12.
12-Page RC. Host response tests for diagnosing
periodontal diseases. J Periodontol 1992 Apr;63(4
Suppl):356-66.
13-Reinhardt RA, McDonald TL, Bolton RW,
DuBois LM, Kaldahl WB. IgG subclasses in gingival crevicular fluid from active versus stable
periodontal sites. J Periodontol 1989 Jan;60(1):4450.
14-Davidovitch Z. Cell biology associated with
orthodontic tooth movement. In: Berkovitz BJM,
Newman HN, editors. The Periodontal Ligament in
Health and Disease. 2nd ed. St Louis: Elsevier Science Health; 1995.
15-Hill PA. Bone remodelling. Br J Orthod 1998
May;25(2):101-7.
16-Sandy JR, Farndale RW, Meikle MC. Recent
advances in understanding mechanically induced
bone remodeling and their relevance to orthodontic
theory and practice. Am J Orthod Dentofacial Orthop 1993 Mar;103(3):212-22.
17-Rhee SH, Kang J, Nahm DS. Cystatins and
cathepsin B during orthodontic tooth movement.
Am J Orthod Dentofacial Orthop 2009
Jan;135(1):99-105.
114
Dannan et al.
18-Silness J, Loee H. Periodontal Disease in Pregnancy. Ii. Correlation between Oral Hygiene and
Periodontal Condtion. Acta Odontol Scand 1964
Feb;22:121-35.
19-Loee H, Silness J. Periodontal Disease in Pregnancy. I. Prevalence and Severity. Acta Odontol
Scand 1963 Dec;21:533-51.
20-Offenbacher S, Odle BM, Van Dyke TE. The
use of crevicular fluid prostaglandin E2 levels as a
predictor of periodontal attachment loss. Journal of
Periodontal Research 1986;21(2):101-12.
21-Deinzer R, Mossanen BS, Herforth A. Methodological considerations in the assessment of gingival crevicular fluid volume. Journal of Clinical
Periodontology 2000;27(7):481-8.
22-Chapple IL, Garner I, Saxby MS, Moscrop H,
Matthews JB. Prediction and diagnosis of attachment loss by enhanced chemiluminescent assay of
crevicular fluid alkaline phosphatase levels. J Clin
Periodontol 1999 Mar;26(3):190-8.
23-Rygh P. Ultrastructural vascular changes in
pressure zones of rat molar periodontium incident
to orthodontic movement. Scand J Dent Res
1972;80(4):307-21.
24-Rygh P. Ultrastructural changes in tension
zones of rat molar periodontium incident to orthodontic tooth movement. Am J Orthod 1976
Sep;70(3):269-81.
25-Storey E. The nature of tooth movement. Am J
Orthod 1973 Mar;63(3):292-314.
26-Keeling SD, King GJ, McCoy EA, Valdez M.
Serum and alveolar bone phosphatase changes reflect bone turnover during orthodontic tooth
movement. Am J Orthod Dentofacial Orthop 1993
Apr;103(4):320-6.
27-van Gastel J, Quirynen M, Teughels W, Coucke
W, Carels C. Longitudinal changes in microbiology and clinical periodontal variables after placement of fixed orthodontic appliances. J Periodontol
2008 Nov;79(11):2078-86.
28-Tzannetou S, Efstratiadis S, Nicolay O, Grbic J,
Lamster I. Comparison of levels of inflammatory
mediators IL-1beta and betaG in gingival crevicular fluid from molars, premolars, and incisors during rapid palatal expansion. Am J Orthod Dentofa-
2009; Vol. 6, No. 3
Dannan et al.
cial Orthop 2008 May;133(5):699-707.
29-Giannopoulou C, Mombelli A, Tsinidou K,
Vasdekis V, Kamma J. Detection of gingival
crevicular fluid cytokines in children and adolescents with and without fixed orthodontic appliances. Acta Odontol Scand 2008 Jun;66(3):169-73.
30-Baldwin PD, Pender N, Last KS. Effects on
tooth movement of force delivery from nickeltitanium archwires. Eur J Orthod 1999 Oct;21(5):
481-9.
31-Uematsu S, Mogi M, Deguchi T. Interleukin
(IL)-1 beta, IL-6, tumor necrosis factor-alpha, epidermal growth factor, and beta 2-microglobulin
levels are elevated in gingival crevicular fluid during human orthodontic tooth movement. J Dent
Res 1996 Jan;75(1):562-7.
32-Miyajima K, Ohno Y, Iwata T, Tanida K, Iizuka T. The lactic acid and citric acid content in
the gingival fluid of orthodontic patients. Aichi
Gakuin Dent Sci 1991;4:75-82.
33-Tersin J. Studies of gingival conditions in relation to orthodontic treatment. V. A comparison
between the gingival exudation in orthodontically
activated teeth and non-activated teeth. Swed Dent
2009; Vol. 6, No. 3
Tooth Movement and Gingival Crevicular Fluid
J 1978;2(4):137-9.
34-Tersin J. Studies of gingival conditions in relation to orthodontic treatment. IV. The effect of oral
hygiene measures on gingival exudation during the
course of orthodontic treatment. Swed Dent J
1978;2(4):131-6.
35-Griffiths GS, Moulson AM, Petrie A, James IT.
Evaluation of osteocalcin and pyridinium
crosslinks of bone collagen as markers of bone
turnover in gingival crevicular fluid during different stages of orthodontic treatment. J Clin Periodontol 1998 Jun;25(6):492-8.
36-Last KS, Donkin C, Embery G. Glycosaminoglycans in human gingival crevicular fluid during orthodontic movement. Arch Oral Biol
1988;33(12):907-12.
37-Samuels RH, Pender N, Last KS. The effects of
orthodontic tooth movement on the glycosaminoglycan components of gingival crevicular fluid.
J Clin Periodontol 1993 May;20(5):371-7.
38-Pender N, Samuels RH, Last KS. The monitoring of orthodontic tooth movement over a 2-year
period by analysis of gingival crevicular fluid. Eur
J Orthod 1994 Dec;16(6):511-20.
115