Fosfataza Alcalina Determinare

Journal of Indian Society of Periodontology - Vol 16, Issue 4, Oct-Dec 2012 513
Original Article
Address for
correspondence:
Dr. Pallavi Agrawal,
Department of
Periodontics, KLE V.K
Institute of Dental Science,
KLE University, Belgaum,
Karnataka, India.
E-mail: pallavi_07@
hotmail.com
Submission: 14-07-2011
Accepted: 30-08-2012
Department of
Periodontics, KLE
V. K. Institute of Dental
Science, KLE University,
Belgaum, Karnataka,
India
Gingival crevicular fuid alkaline
phosphatase as a potential diagnostic
marker of periodontal disease
Sheetal Sanikop, Suvarna Patil,

Pallavi Agrawal
Abstract:
Background: Alkaline phosphatase (ALP) enzyme is involved in the destruction of the human periodontium.
The present study was conducted to determine the presence and levels of ALP activity in gingival crevicular
fuid (GCF) in periodontal health, gingivitis, and chronic periodontitis. Materials and Methods: GCF samples
were collected from 45 sites which were divided into three equal groups of healthy samples and gingivitis and
chronic periodontitis samples. Various clinical parameters were evaluated and the levels of ALP were estimated
using a semiautoanalyzer. Analysis of variance was employed to compare the ALP levels in different groups.
Pearsons correlation coeffcient was utilized to fnd the correlation between ALP levels and various clinical
parameters. Results: Difference in the mean ALP levels between healthy and gingivitis groups was found to be
nonsignifcant (P>0.05) and that between the chronic periodontitis group and healthy as well as gingivitis groups
was found to be highly signifcant (P<0.001). Signifcant correlations existed between ALP levels and gingival
index, probing depths, as well as clinical attachment levels. Conclusion: The fnding of the present study confrms
the relationship between ALP level and periodontal disease, thus indicating that GCF ALP levels can be used as
potential biochemical markers for the detection and progression of periodontal disease.
Key words:
Alkaline phosphatase, chronic periodontitis, gingival crevicular fuid, gingivitis
INTRODUCTION
P
eriodontitis is a chronic infammatory disease
characterized by gingival inflammation,
periodontal ligament destruction, and alveolar
bone resorption.
[1]
A diagnosis of periodontal disease is made
after analyzing the information collected
from a periodontal examination.
[2]
Traditional
periodontal diagnostic parameters used
clinically include probing depths, bleeding
on probing, clinical attachment levels, Plaque
index and radiographs assessing alveolar bone
level.
[3]
The goal of periodontal diagnostic procedures
is to provide useful information to the
clinician regarding the present periodontal
disease type, location, and severity which
serve as a basis for treatment planning and
provide essential data during periodontal
maintenance and disease-monitoring phases
of treatment. Traditional diagnostic procedures
are inherently limited, in that only disease
history, not current disease status, can be
assessed. Advances in diagnostic research in
oral and periodontal disease are moving toward
methods whereby periodontal risk can be
identifed and quantifed by objective measures
(e.g., biomarkers).
[4]
The response of an organism to periodontal
infection includes production of several enzymes
released from stromal, epithelial, infammatory,
or bacterial cells. These intracellular enzymes
are released increasingly from the damaged
cells of periodontal tissues into the gingival
crevicular fluid (GCF) and saliva. Several
enzymes that are evaluated for the early
diagnosis of periodontal disease are aspartate
and alanine aminotransferases (AST and ALT),
lactate dehydrogenase (LDH), gamma-glutamyl
transferase (GGT), creatine kinase (CK), alkaline
phosphatase (ALP), and acid phosphatase
(ACP).
[5]
ALP is a calcium- and phosphate-binding
protein and a phosphor-hydrolytic enzyme.
[6]
It
is a membrane-bound glycoprotein produced by
many cells such as polymorphonuclear leukocytes
(PMNLs), osteoblasts, macrophages, and
fbroblasts within the area of the periodontium
and gingival crevice.
[7]
ALP is considered to be an important indicator
of bone formation and is a phenotypic marker
for osteoblast cells. ALP is detected in the
parotid, submandibular, and minor salivary
glands, as well as in desquamated epithelial cells,
leukocytes, and bacteria from dental plaque. The
presence of ALP in the saliva and GCF is usually
indicative of infammation and/or destruction of
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Sanikop, et al.: ALP as a diagnostic marker of periodontal disease
514 Journal of Indian Society of Periodontology - Vol 16, Issue 4, Oct-Dec 2012
the periodontal tissues. The level of ALP is positively correlated
with the severity of the periodontal disease.
[6]
GCF is an inflammatory exudate that seeps into gingival
crevices or periodontal pockets around teeth with infamed
gingiva.
[8]
It represents serum components overlaid with
products from local physiologic phenomena, such as connective
tissue destruction and bone loss, and has diagnostic value. It
is a convenient, noninvasive, and effcient means to sample
biomarkers of infammation and bone resorption in the oral
cavity. Although individual GCF samples have the possibility
of describing the infammatory events occurring at the site,
pooled samples from a small number of sites may characterize
the overall vulnerability to periodontitis and allow periodic
assessment during periodontal treatment or maintenance.
[9]
Thus the current study aimed at determining the ALP enzyme
levels in GCF in periodontal health, gingivitis, and chronic
periodontitis and estimating its possible cross-sectional
relationship with various clinical parameters.
MATERIALS AND METHODS
Subject selection
The study was conducted at the Department of Periodontology,
KLE VK Institute of Dental Sciences, KLE University, Belgaum,
Karnataka, India. Ethical clearance was obtained from the
ethical committee of the institute, and a written informed
consent was obtained from all the participants prior to the
study. The study sample consisted of 45 sites. The subjects
included belonged to both sexes (male and female) and the
age ranged from 20 to 65 years. The mesiofacial, distofacial, or
midfacial surface of the tooth was considered as a site. The sites
were divided into three groups of 15 each: Group 1 (control
group), group 2 (gingivitis group), and group 3 (chronic
periodontitis group) [Figure 1].
Group 1: Sites with clinically healthy gingiva or marginal
gingiva was pink, frm, visually free of infammation, and did
not bleed on probing. Sulcus depth was 3 mm.
Group 2: Plaque-associated gingivitis or marginal gingiva was
erythematous and edematous with bleeding on probing. Sulcus
depth was 3 mm. There was no clinical loss of attachment
and gingival index score (Loe and Silness, 1963) was 2.0.
Group 3: Sites from patients diagnosed with chronic
periodontitis with a probing depth of >4 mm.
Exclusion criteria included patients with systemic disease/
illness or with any oral mucosal inflammatory condition
(e.g., aphthous ulcers, lichen planus, leukoplakia, oral cancer)
and who had taken anti-inflammatory drugs, antibiotics,
nutritional supplements, or any other drugs over the past six
months. Patients with a history of smoking and/or alcoholism
and those who had undergone any periodontal treatment over
the past six months and women who were in menstruation
period, had received hormonal treatment or oral contraceptives,
or were pregnant or lactating were excluded from the study.
Clinical examination
Gingival index (Loe and Silness, 1963) and Plaque index (Silness
and Loe, 1964) were recorded for each site by one examiner
before the collection of GCF. Probing pocket depth (PD) and
clinical attachment level were measured using a Williams
graduated periodontal probe.
GCF collection
The subjects were seated comfortably in an upright position
in the dental chair, with adequate lighting condition. The sites
were chosen from maxillary teeth to avoid contamination
with saliva. Supra gingival plaque and calculus were
removed with hand instrumentation prior to the collection
of GCF. Care was taken not to touch the gingival margin
to prevent stimulation. The calibrated microcapillary tubes
(05 L range) were placed extracrevicular at the mesiofacial,
distofacial, or midfacial surface of the tooth. A standardized
volume of 5 L of GCF was collected. The entire volume
was collected from one site only. Test sites which did not
express adequate volume of fuid or microcapillary tubes
contaminated with blood were discarded. The collected GCF
was immediately transferred to the sterilized microcentrifuge
(Eppendorff) tubes that contained 45 L of normal saline.
The tubes were then transported for analysis which was
done within two hours of collection of the crevicular
fuid.
Enzyme assay
A diagnostic kit was used for the estimation of ALP. The kit
consisted of two reagents:
Reagent 1
1. p-Nitrophenyl phosphate
2. Magnesium ion (Mg
[2]+
)
3. Tris/carbonate buffer (pH 10.20.2 at 25C)
Reagent 2 (Aqua-4)
1. Distilled water
The GCF (5 L) was diluted 10 times with 45 L of normal
saline, to make 50 L of sample. The diluted GCF was
then centrifuged for 35 minutes at 35004500 rotations
per minute (rpm) in a microcentrifuge; 10 L of the
clear supernatant was utilized for the analysis of ALP
activity.
Figure 1: Criteria for group division
Group 1 (Control group)
Sites with clinically healthy gingiva
Marginal gingiva was pink, firm, visually free of inflammation
and did not bleed on probing
Sulcus depth was 3mm
Group 2 (Gingivitis group)
Plaque-associated gingivitis
Marginal gingiva was erythematous and edematous with
bleeding on probing
Sulcus depth was 3mm
No clinical loss of attachment
Gingival index score (Loe and Silness, 1963) 2.0
Group 3 (Chronic Periodontitis group)
Sites from patients diagnosed with chronic periodontitis with
probing depth of >4mm
The working agent was prepared by adding 2.2 mL of distilled
water to reagent 1.
Then, 500 L of the prepared reagent was taken in a
microcentrifuge (Eppendorff tube) and 10 L of the sample
was added to it. The enzyme activity was recorded using a
semi-autoanalyzer and the result was obtained in the form of
a digital readout.
Principle of the reaction [Figure 2]
p - Nitrophenyl phosphate + H
2
O p- Nitrophenol + phosphate
ALP
Mg
2+
Statistical analysis
The mean and the standard deviation with regard to the level
of ALP, age, gingival index, Plaque index, pocket probing
depth, and clinical attachment level were calculated. The mean
values of the measured clinical parameters and ALP levels were
assessed by oneway ANOVA. The pairwise comparison was
done using the posthoc Scheffes test. Pearsons correlation
coeffcient was utilized to fnd the correlation between ALP
levels and various clinical parameters.
RESULTS
The mean and the standard deviation with regard to level of
ALP, age, gingival index, Plaque index, pocket probing depth,
and clinical attachment level are demonstrated in Table 1.
The clinical parameters recorded in groups 1-3 were compared
with each other [Figure 3]. The difference in gingival index and
Plaque index was found to be highly signifcant (P<0.001) when
groups 1 & 2 and groups 1 & 3 were compared. No statistically
signifcant difference was found when groups 2 and 3 were
compared. The probing pocket depth and attachment levels
showed signifcant difference between groups 2 & 3 and 3 & 1
and no statistical difference between groups 1 and 2 [Table 2].
Difference in the mean ALP levels between group 1 and 2
was found to be nonsignifcant (P>0.05) and that between the
groups 2 and 3 as well as groups 3 and 1 was found to be highly
signifcant (P<0.001) [Table 2].
DISCUSSION
The processes responsible for the destruction of the human
periodontium are highly complex and the vast range of
biological substances involved have their own relevance to
specifc aspects of different disease types.
[10]
A biomarker or biologic marker is a substance that is objectively
measured and evaluated as an indicator of normal biologic
processes, pathogenic processes, or pharmacologic responses
to a therapeutic intervention (Biomarkers Defnitions Working
Group. Biomarkers and surrogate endpoints: Preferred
defnitions and conceptual framework 2001).
[4]
One of the most active areas in periodontal research has been
the search for a biochemical marker of the progression of
periodontitis in GCF.
The potential of ALP as an important biochemical marker of
GCF was identifed by Ishikawa and Cimasoni.
[11]
ALP has the
peculiarity of being involved in infammation
[11,12]
as well as
regeneration.
[13]
In this present study, the ALP levels in GCF in health, gingivitis,
and chronic periodontitis were estimated. Moreover, the
clinical parameters namely gingival index score, Plaque index,
probing pocket depth, and clinical attachment level of the site
correlated with the ALP levels in group 1 (healthy), group 2
(gingivitis), and group 3 (chronic periodontitis) [Table 3].
Figure 2: Principle of the reaction
Figure 3: Comparison of various clinical parameters in the three groups
Table 1: Mean ALP levels, age, and the various clinical parameters of the three groups
Groups ALP Levels (in
IU/L) MeanSD
Mean age
(in years)
Gingival index
MeanSD
Plaque index
MeanSD
Probing depth (in mm)
MeanSD
Clinical attachment
level (in mm) MeanSD
Healthy 170.3370.01 37.00 0.000.00 0.460.63 1.260.45 1.400.50
Gingivitis 271.26107.96 41.53 2.130.63 2.730.45 2.200.67 1.930.70
Chronic periodontitis 732.06414.93 47.20 2.400.73 2.460.51 6.131.46 7.071.44
ALP Alkaline phosphatase; SD Standard deviation

+ H
3
PO
4

OH

+ H
2
O
NO
2

NO
2
Alkaline
Phosphatase

p-nitrophenyl phosphate
(Colorless in alkaline and acid
medium)

p-nitrophenol
(Colorless in acid medium,
yellow in alkaline medium)

OPO
3
H
2
0
1
2
3
4
5
6
7
8
Gingival
Index
Plaque
Index
Probing
Depth
Clinical
Attachment Level
Healthy
Gingivitis
Chronic Periodontitis
The sites were chosen from the maxillary arch, due to lesser
chances of contamination from saliva. A single site was chosen
for collection because of the known site specifcity of the
periodontal diseases as shown by Chapple et al.
[14]
The mean ALP levels of group 1 (healthy) were found to
be lower than other two groups (gingivitis and chronic
periodontitis) [Figure 4]. In support of this finding,
Lilja, Lindskog, and Hammarstrom (1984) have shown
through histochemical techniques that ALP is present
in the normal periodontal membrane in rats.
[15]
Lindhe
(1996) showed that even in healthy gingiva, certain
leukocytes (neutrophils) can be seen in the junctional
epithelium.
[16]
Four out of 15 sites showed increased levels of ALP as
compared to the remaining 11 sites refecting the subclinical
difference in inflammatory status despite the sites being
clinically identical. This indicates the difference in the amount
of enzyme produced locally within the periodontal tissues.
It was noticed that GCF ALP levels were detectable before
increase in gingival indices and thus it appears to be a better
marker of gingival infammation.
In group 2 (gingivitis), the increase in the mean level of ALP
can be due to tissue alteration as a result of host-parasite
reaction or host-bacterial interplay, as gingivitis is an
infammatory process. During progression of the disease,
enzymes are released from dead and dying cells of the
periodontium, PMNLs, inflammatory, epithelial, and
connective tissue cells of the affected sites.
[17]
As PMNLs
are the major source of ALP, they could have contributed
to the increased levels of ALP in GCF through secondary
granule release.
[14]
Micro-organisms like Prevotella intermedia
and Streptococcus sanguis are thought to be important in the
initiation and progression of gingivitis and are known to
show high ALP activity.
[18]
Thus the increase in ALP level in
gingivitis could be due to the increased number of crevicular
PMLs (CPMNLs) and bacteria.
Among the three groups, the mean values of ALP levels were
highest in group 3. Periodontal pockets are chronic infammatory
lesions and are constantly undergoing repair. The condition
of the soft tissue wall of the periodontal pocket results from
the interplay of destructive and constructive tissue changes.
Complete healing does not occur because of the persistence of
local irritants. These irritants continue to stimulate fuid and
cellular exudates, which in turn causes degeneration of the
new tissue elements found in the continuous effort at repair.
At some period following the initial attack on the periodontal
connective tissue, as a result of host defence mechanism or
other changes in the local environment, the lesion begins to
undergo remission.
[19,20]
There is an increase in the number of
CPMNLs which play a vital role in pathogenesis of periodontal
lesions (Genco et al. 1990) by migrating into the sulcus.
[21]

Among various periodontopathic bacteria, P. intermedia and
Porphyromonas gingivalis are known to have high ALP activity
and Aggregatibacter actinomycetomcomitans show very low ALP
activity.
[18]
In periodontitis, one of the mechanisms of collagen
loss is that the fbroblasts phagocytize collagen fbers. The
increase in the fbroblast activity contributes to the total ALP
level. Both histochemical and biochemical studies have shown
that periodontal cells have intense ALP activity, unlike gingival
fbroblasts.
[17]
The increased ALP in the 11 sites out of 15 in group 3 could
be due to increased CPMNLs, periodontopathic bacteria, and
Table 2: Comparison of the various clinical parameters
and ALP levels between the three groups
Clinical parameter Groups P value Signifcance
GI III <0.001 HS
IIIII 0.447 NS
IIII <0.001 HS
PI III <0.001 HS
IIIII 0.808 NS
IIII <0.001 HS
PD III 0.127 NS
IIIII <0.001 HS
IIII <0.001 HS
CAL III 0.331 NS
IIIII <0.001 HS
IIII <0.001 HS
ALP III 0.5 NS
IIIII <0.001 HS
IIII <0.001 HS
HS Highly signifcant; S Signifcant; NS Nonsignifcant; GI Gingival
index; PI Plaque index; PD Pocket depth; CAL Clinical attachment
level; ALP Alkaline phosphatase
Table 3: Correlation of the mean ALP levels with the
various clinical parameters in the three groups
Clinical parameter Groups P value Signifcance
GI I - -
II 0.000 HS
III 0.001 HS
PI I 0.120 NS
II 0.140 NS
III 0.296 NS
PD I 0.093 NS
II 0.011 S
III 0.007 S
CAL I 0.093 NS
II 0.025 S
III 0.011 S
HS Highly signifcant; S Signifcant; NS Nonsignifcant; GI Gingival
index; PI Plaque index; PD Pocket depth; CAL Clinical attachment level;
ALP Alkaline phosphatase
Figure 4: Comparison of mean GCF ALP levels (IU/L) in the three groups
0
100
200
300
400
500
600
700
800
Healthy Gingivitis Chronic
periodontitis
M
e
a
n

A
L
P

l
e
v
e
s

(
I
U
/
L
)

increased fbroblast activity. The remaining four sites had the
highest ALP levels as compared to all sites in the sample size.
This could be because these sites were undergoing remission.
Remission means healing and there is increased osteoblastic
activity which stimulates bone formation by mineralization.
ALP is an enzyme of osteoblasts and serum levels of ALP are
often elevated when bone formation is increased.
[22,23]
ALP
plays a major role in bone mineralization.
[17]
Robinsons ALP
theory formulated in 1923 suggested that in mineralization,
a possible function of ALP is to raise the local concentration
of inorganic phosphate ions and thus cause the precipitation
of calcium phosphate. ALP is responsible for the liberation of
free phosphate from phosphate esters. The ALP yields high
concentrations of inorganic phosphate salts that get deposited
locally to form bone.
ALP might also promote mineralization by hydrolyzing
inorganic pyrophosphate, a potent inhibitor of hydroxyapatite
crystal formation and dissolution, within the extracellular
calcifying matrix vesicles.
[24]
Signifcant correlation was found between ALP levels and
gingival index which is in agreement with Chapple et al.
[10]

and Nakashima et al.
[25]
The increase in gingival index denotes
infammation as a result of which the number of PMNLs
increases. Plaque scores and ALP levels were not signifcantly
correlating which is in favor of studies done by Binder et al.
[26]

and Chapple et al.
[14]
Signifcant correlations existed between
ALP levels and probing depths as well as clinical attachment
levels except in the healthy group. These findings were
consistent with the results of the study done by Ishikawa and
Cimasoni
[11]
and Binder et al.
[26]
respectively.
Thus the fndings of this study state that ALP levels in GCF
could differentiate between health, gingivitis, and periodontitis
appreciably. Various other studies have shown a remarkably
increased activity of ALP in the acute phase of periodontal
disease, and after the periodontal therapy, the activity of
these enzymes were restored to values as found with healthy
individuals.
[27]
Change in ALP in GCF, saliva, and serum has
been used as an infammatory marker of periodontium as well
as of bone metabolism.
[7,17,28,29]
Studies have shown that ALP is involved in gingivitis
[14]
and
periodontitis
[11,30]
with an increase seen in GCF ALP activity.
Increased GCF ALP activity has been shown to have predictive
value in terms of attachment loss that is signifcantly more
accurate than the use of clinical parameters.
[26,17]
GCF ALP is also
shown to refect the shortterm periodontal healing/recurrent
infammation phases in patients with chronic periodontitis.
[31]
This results of this study also showed that a significant
difference exists in ALP levels in GCF between health
and chronic periodontitis as well as gingivitis and chronic
periodontitis. Thus ALP promises to be a potential biochemical
marker for the detection and progression of periodontal
disease. With the advent of novel technologies such as
labonachip, microfuidic devices, and rapid pointofcare
oral diagnostics, the generation of a periodontal disease
biomarker report appears promising for future application to
diagnose periodontal diseases and to prognosticate treatment
outcomes of periodontal disease.
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crevicular fuid alkaline phosphatase as a potential diagnostic marker
of periodontal disease. J Indian Soc Periodontol 2012;16:513-8.
Source of Support: Nil, Confict of Interest: None declared.
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Journal of Indian Society of Periodontology - Vol 16, Issue 4, Oct-Dec 2012 513

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