Dominique Plagnat

Catherine Giannopoulou
Anne Carrel
Jean-Pierre Bernard
Andrea Mombelli
Urs C. Belser

Authors affiliations
Dominique Plagnat, Catherine Giannopoulou,
Andrea Mombelli, Department of Periodontology,
School of Dental Medicine, University of
Geneva.
Urs C. Belser, Department of Prosthetic
Dentistry, School of Dental Medicine, University
of Geneva.
Anne Carrel, Department of Preventive
Dentistry, School of Dental Medicine, University
of Geneva.
Jean-Pierre Bernard, Department of Stomatology,
School of Dental Medicine, University of
Geneva, Geneva, Switzerland
Correspondence to:
Catherine Giannopoulou
Department of Periodontology
School of Dental Medicine
University of Geneva
19 rue Barthelemy-Menn
1206 Geneva
Switzerland

Date:

Accepted 22 March 2001

To cite this article:

Plagnat D, Giannopoulou C, Carrel A, Bernard JP,

Mombelli A, Belser UC. Elastase, a2-macroglobulin
and alkaline phosphatase in crevicular fluid from
implants with and without periimplantitis
Clin. Oral Impl. Res, 13, 2002; 227233
Copyright C Blackwell Munksgaard 2002
ISSN 0905-7161

Elastase, a2-macroglobulin and

alkaline phosphatase in crevicular fluid
from implants with and without
periimplantitis

Key words: healthy implant, periimplantitis, periimplant crevicular fluid, elastase, alpha 2macroglobulin, alkaline phosphatase
Abstract: The aim of this investigation was to determine the presence of selected enzymes and
enzyme inhibitors in crevicular fluid collected from implants with and without clinical,
radiographic and microbiological signs of periimplantitis. Eleven implants with symptoms of
periimplantitis in eight patients (four men and four women) were compared to eleven implants
in seven subjects (one man and six women) without periimplantitis. Periimplant crevicular fluid
(PICF) was collected at the mesial and distal sites of each implant. Alkaline phosphatase activity
(ALP) was measured by using p-nitrophenyl-phosphate as substrate, elastase activity (EA) by the
use of a low molecular weight fluorogenic substrate, and the inhibitor a2-macroglobulin (a2M)
by ELISA. ALP, EA and a2M were detected in the majority of samples in both groups. In
comparison to the clinically healthy implants, total amounts of each of these substances were
significantly higher in PICF collected around implants with periimplantitis. The mean total
amounts of EA, a2M and ALP in the healthy group were: EA: 1.8 ng, a2M: 3.1 ng, ALP: 24.1 U, and
in the periimplantitis group EA: 23.1 ng, a2M: 25.2 ng and ALP: 142.3 U. In addition, all three
mediators were correlated with the clinical parameters. The results confirm the similarity of the
inflammatory response of tissues surrounding implants and natural teeth, and suggest that ALP
and EA could be promising markers of bone loss around dental implants.

In the last decades, periodontal research

has focused on the analysis of gingival crevicular fluid (GCF) with the aim of identifying potential host markers, which may
permit diagnosis of disease activity and
prognosis of future disease (Genco 1992;
Birkedal-Hansen 1993). An important
number of markers, such as neutrophil
elastase (Giannopoulou et al. 1992; Palcanis et al. 1992), prostaglandin E2, b-glucuronidase, collagenase, alkaline phosphatase (Offenbacher et al. 1986; Nakashima
et al. 1994, 1996), aspartate aminotransferase (Persson & Page 1992) and many
others, have been shown to be associated
with periodontal disease activity. Until
now, only few similar associations have

been reported in relation to periimplantitis

(Kao et al. 1995; Panagakos et al. 1996;
Rhling et al. 1999).
Apse et al. (1989) observed that the volume of GCF did not differ between implant
sites and natural teeth, and that the features
of inflammation seem to be the same
around teeth and implants. In addition, the
histologic arrangement of periimplant soft
tissue resembles that observed around
natural teeth (Berglundh et al. 1991;
Listgarten et al. 1991; Tonetti et al. 1993).
Last et al. (1991, 1995) evaluated the glycosaminoglycan (GAG) content in periimplant crevicular fluid. Two GAG bands,
hyaluronic acid and chondroitin 4-sulphate, were detected. In addition, GCF vol-

227

Plagnat et al . Markers of bone loss in periimplantitis

ume and GAG levels were higher at periimplantitis sites when compared to control sites with healthy tissues. Eley et al.
(1991) evaluated protease activities in periimplant crevicular fluid and reported that
total activity of elastase, cathepsin, dipeptidyl peptidase and trypsin were correlated
positively with Gingival Index and bone resorption. Recently, the analysis of interleukin-1b levels in diseased and healthy periimplant tissues indicated that IL-1b may
provide a means of monitoring the health
status of dental implants (Kao et al. 1995;
Panagakos et al. 1996).
Two enzymes, elastase and alkaline phosphatase, and the inhibitor a2-macroglobulin
were shown to be associated with tissue destruction in periodontitis (Page 1992). Elastase is a serine protease able to degrade several functionally and structurally important
proteins in the periodontium (Janoff 1985).
Increased GCF elastase activity has been
found in periodontitis sites (Gustafsson
et al. 1994; Ingman et al. 1994) and it has
been suggested that elastase activity could
be a predictor of disease progression (Palcanis et al. 1992; Armitage et al. 1994). The
potential clinical value of GCF elastase activity may be reduced by the presence of endogenous inhibitors such as a2-macroglobulin, reported to be present in both gingival
tissue (Kennett et al. 1995) and gingival
fluid (Ichimaru et al. 1992). Finally, alkaline
phosphatase, an enzyme involved in bone
metabolism, has been shown to be significantly elevated in active sites as compared
to inactive sites (Nakashima et al. 1996),
and has been suggested to be a predictor of
current or future disease activity (Chapple
et al. 1999). Since these markers were found
to be associated with periodontitis, it may
be interesting to study their relationship
with periimplantitis. The aim of the present
investigation was therefore to compare
levels of elastase, a2-macroglobulin and alkaline phosphatase in crevicular fluid collected from healthy implants and from implants with periimplantitis, and to establish
whether these parameters could be associated with tissue destruction.

Material and methods

Patient population

The population for this cross-sectional

study consisted of 15 subjects, ten women
and five men, selected from a group of pa-

228 |

tients treated with implants (ITI Dental

Implant System, Institut Straumann, Waldenburg, Switzerland) at the School of Dentistry of the University of Geneva. All fixtures had been placed at least six months
before the examination. Patients were all
in good health, and had not received antibiotics during the six months prior to the
study. Pregnant women, as well as patients
who required premedication, were not included. Eight subjects carried one or several implants with clinical signs of periimplantitis, and seven subjects carried one or
several implants with clinically healthy
periimplant tissues. Patients with both
clinically healthy and diseased periimplant
tissues were not included.
Criteria for healthy and diseased periimplant
tissues

Implants with healthy periimplant tissues

did not show any pockets deeper than
4mm, had no suppuration, no plaque or
gingival inflammation 1, and exhibited
no radiographic evidence of bone loss. Implants with periimplantitis exhibited
pockets deeper than 5mm in at least one
site, showed bleeding on probing and/or
suppuration, and had radiographic evidence of crestal bone loss greater than 20%
in at least one site (mesial or distal) along
the implant.
Clinical examination

The clinical and radiographic evaluations

were performed by one periodontist (D.P).
The clinical examination included assessment of pocket probing depth (PPD), measurement of the Modified Plaque Index
(mPli; Mombelli et al. 1987) and of the
Gingival Index (GI; Le 1967). The presence or absence of suppuration (SI),
bleeding on probing (BOP) and the distance
between implant shoulder and gingival
margin (DIM) were also recorded. Positive
DIM values corresponded to a supragingival location of the implant shoulder. All
measurements were performed at four sites
around each implant and were carried out
to the nearest mm using a Hu-Friedy
PCP12 periodontal probe. The stability of
the implant was assessed by means of the
Periotest electronic device (Siemens AG,
Bensheim, Germany).
Radiographic evaluation was performed
on two radiographs in each subject. The
first radiograph was taken as soon as
possible after placing the implant (Rx 1),

Clin. Oral Impl. Res. , Clinical Oral Implants Research / 227233

the second was taken either during a control visit (healthy group), or when periimplantitis was discovered (diseased group,
Rx 2). After digitalization at a resolution
of 1200bit pixels, the levels of crestal
bone were measured mesially and distally, and compared at the two different
time points.
Crevicular fluid sampling

Periimplant crevicular fluid (PICF) was collected mesially and distally to each implant after assessing the presence or absence of plaque, and before registration of
any other clinical parameters. The implants were isolated with cotton rolls and
dried gently with air. After 3min, standardized paper strips (Periopaper, Pro Flow,
Amityville, NY, USA) were inserted into
the sulci or pockets until slight resistance
was felt, and left in place for 15s. The
amount of fluid was evaluated using the
Periotron 8000 (Pro Flow). Immediately
thereafter, the strips were transferred to
plastic vials and were stored at 20C until the day of analysis.
Biochemical analysis of crevicular fluid

One hundred microliters of phosphate buffered saline (PBS, pH7.2) was added to each
sample. The tubes were vigorously shaken
for 1min and then centrifuged at 2000g for
5min, with the strips kept at the collar of
the tube in order to completely elute PICF
components. After removal of the strip, the
supernate was divided into three aliquots,
one for the determination of each biochemical compound. Elastase activity (EA) was
determined using the fluorogenic substrate Meo-Suc-Ala-Ala-pro-Val/7-amino-4methylcoumarin (MW 627.69) (Bachem,
Bubendorf, Switzerland) (Castillo et al.
1979; Baici 1990).
The inhibitor a2-macroglobulin (a2M)
was determined by ELISA (Giannopoulou
et al. 1992). The activity of alkaline phosphatase (ALP) was measured by using pnitrophenyl phosphate as substrate (Nakashima et al. 1994).
Final results were expressed as total
amounts per 15s samples. Sites with levels
below the limits of assay detectability were
scored as 0ng.
Microbiological sampling

Subgingival plaque samples were collected

from the deepest pocket of each implant
by using paper points. The plaque samples

Plagnat et al . Markers of bone loss in periimplantitis

were placed in 100ml of physiological sterile solution and examined by dark field
microscopy (Listgarten & Hellden 1978).
Immunofluorescence with specific monoclonal antibodies was used for the detection of the following pathogenic bacteria:
Actinobacillus actinomycetemcomitans,
Prevotella intermedia, Porphyromonas
gingivalis, Bacteroides forsythus and

Campylobacter rectus (Gmr et al. 1989).

Results were expressed as percentage of
sites positive to one of the target bacteria.
Statistical analysis

Differences between implants with

healthy or diseased periimplant tissues
were tested for statistical significance
using Wilcoxons rank sum test. A value of

P0.05 was required for statistical significance. Multiple linear regression analysis was used to assess a relationship between the levels of EA, a2M and ALP and
the following clinical parameters: GI, BOP,
PPD and percentage of bone loss.

Results
Patient data and clinical results

Table 1. Profile of patients with periimplantitis

Patient data
Patient no.

Age

Implant data
Sex

Position

Type

Length
(mm)

Time in
place (mo)

46

47

HS

12

53

2
3
3
4
5
6
7
8
8
8

36
43
43
63
53
55
59
62
65
65

M
M
M
M
F
F
F
M
M
M

45
14
16
34
23
46
46
25
23
24

HS
HS
HS
HS
HC
HSus
HSus
S
HS
S

10
12
8
12
10
10
8
8
12
8

84
24
24
84
50
28
6
25
53
53

HS hollow screw, HC hollow cylinder, HSus hollow screw (USA); S solid screw

Table 2. Profile of patients with healthy implants

Patient data
Patient no.

Age

Implant data
Sex

Position

Type

Length
(mm)

Time in
place (mo)

1
2
2
3
3
4
5
5
6
6
7

32
61
61
52
52
27
63
63
54
54
30

F
F
F
F
F
M
F
F
F
F
F

45
45
47
35
36
41
33
36
46
47
47

HS
HS
HS
HS
HS
HC
S
HS
HSus
HSus
HS

8
8
10
10
10
8
10
8
8
8
8

99
74
74
71
71
69
69
69
61
61
27

Radiographic data

As explained in the Methods section, implants in the healthy group lost a mean of
maximum 0.6mm of bone, whereas in the
diseased group, bone loss was greater than
20% in at least one site (mesial or distal)
along the implant (Table4).
Microbiological results

HS hollow screw, HC hollow cylinder, HSus hollow screw (USA), S solid screw

Table 3. Clinical data from healthy and diseased implants

Healthy
PPD (mean SD)

2.2 0.7

Diseased
6.1 2.5

P
0.001

% sites with
mPli 0
gingival inflammation (GI 1)
bleeding on probing (BOP 1)
suppuration (SI 1)
DIM 0
% implants with
Periotest 0

9.1
11.3
47.7
0
35

7.2

Eleven implants in eight patients (four

men and four women) showed signs of periimplantitis (Table1). A second group of 11
implants in seven patients (one man and
six women) with healthy periimplant
tissues were used as controls (Table2). The
implants of the two groups are described in
Tables1 and 2.
Table3 shows the clinical status of each
group including pocket probing depth
(PPD), percentage of sites with plaque accumulation, mucosal inflammation, bleeding on probing and suppuration. In the same
table, the percentage of sites with a positive
DIM value, as well as the percentage of implants with a Periotest value 0, are given
(for the diseased group, Periotest values
could be obtained from only eight implants). Statistically significant differences
between the two groups were observed for
all clinical parameters (P0.001).

36.3
95
79.5
64
52

0.001
0.001
0.002
0.001
0.002

50

0.002

PPD pocket probing depth, mPli plaque accumulation, DIM distance between implant shoulder and gingival
margin

229 |

Dark-field microscopy revealed the presence of coccal and filamentous bacteria in

the healthy group and a flora dominated
by spirochetes and mobile organisms in the
periimplantitis group.
With the exception of one implant, all
samples from the periimplantitis group revealed the presence of at least one target
organism. P.intermedia was detected in
90% of sites, followed by C.rectus and B.
forsythus (85% of sites), P.gingivalis (75%
of sites) and A.actinomycetemcomitans
(20% of sites).
None of these bacteria were detected in
samples from implants with healthy periimplant tissues.

Clin. Oral Impl. Res. , Clinical Oral Implants Research / 227233

Plagnat et al . Markers of bone loss in periimplantitis

Table 4. Bone loss (%) around diseased implants

Patient
No.

Position

Time between
radiographs (mo)

% Bone loss
mesial

distal

1
2

47

40

41.3

36.2

45

81

86.2

65.2

14

19

11

22.6

3
4

16
34

19
80

46.2
23

46.9
32.2

23

48

13

47

18

31.1

46

37.8

46.6

25

24

42.1

78.4

8
8

23
24

40
40

57.7
99.5

87.6
73.9

1.2
36.7

Table 5. Total amounts (SD) of elastase, a2-macroglobulin (a2M) and alkaline phosphatase (ALP) in
healthy and diseased implants

elastase (ng/sample)
a2M (ng/sample)
ALP (U/sample)

Healthy

Diseased

1.8 1.2
3.1 1.1
24.1 6.35

23.1 12.6
25.2 14.6
142.3 51.1

0.001
0.001
0.001

Biochemical analysis of periimplant crevicular

fluid

Elastase and alkaline phosphatase were

regularly recovered from PICF samples collected from both healthy and diseased periimplant tissues. However, a2-macroglobulin was absent from most of the samples
belonging to the healthy group. Table5
shows the mean total amount (SD) of
each biochemical parameter in the healthy
and the periimplantitis groups. Significant
differences at the level of P0.001 were
found between the two groups, for all three
substances.
Figure1 shows the relationship between
PPD and elastase as well as alkaline phosphatase activity. As can be seen, the
healthy group (blue) could be clearly separated from the diseased group (red), using
these parameters. Further, interactions between clinical and biochemical parameters
were explored using stepwise regression
analysis. The final models expressing
levels of biochemical markers with clinical
parameters are shown in Table6. EA was
correlated with PPD and percentage of
bone loss, a2M with GI, and ALP with GI
and percentage of bone loss.

of a pathological process cannot be detected. Biochemical markers in PICF may

indicate periimplantitis earlier, allowing
intervention before substantial amounts of
bone are lost. In order to study the possible
association of their levels with periimplant
health and disease, three biochemical compounds were analyzed in the periimplant
crevicular fluid: elastase, a2-macroglobulin
and alkaline phosphatase. Elastase is one of

the major enzymes of the azurophilic granules of human leukocytes, and during inflammation its release is known to contribute to tissue damage (Baggiolini et al. 1978;
Virca & Schnebli 1984). However, the activity of this protease is modulated by the
presence of inhibitors either produced locally, or circulating in plasma (Travis et al.
1978). Alpha 1-antitrypsin and a2-macroglobulin have been shown to play an important role in the neutralization of proteases released in the gingival crevice, their
amounts increasing significantly in diseased sites as compared with healthy regions (Adonogianaki et al. 1992, 1993). Finally, alkaline phosphatase has often been
measured in serum as possible indicator of
the overall activity of cells responsible for
bone formation (Delmas 1991). Recently,
Chapple et al. (1999) reported that monitoring ALPase activity in human crevicular
fluid permits prediction of periodontal
attachment loss.
In the present cross-sectional study, two
groups of implants were identified by clinical observations, radiographical analysis
and microbiological determinations: a first
group comprising healthy implants and a
second group including fixtures with periimplantitis. Microbiological observations
by immunofluorescence confirmed the
presence of five pathogenic bacteria known

Discussion
Until now, the determination of disease activity around implants has been based on
clinical and radiological observations.
Using this approach, the very early stages

230 |

Fig.1. Pocket probing depth in association with total amounts of elastase and alkaline phosphatase in crevicular
fluid of healthy and diseased implants.

Clin. Oral Impl. Res. , Clinical Oral Implants Research / 227233

Plagnat et al . Markers of bone loss in periimplantitis

Table 6. Multiple linear regression; subset of predictor variables for elastase activity (EA), a2-macroglobulin (a2M) and alkaline phosphatase (ALP)
Marker
EA

Predictor
variable
PPD
% bone loss

Coefficient

SE

1.08

0.001

0.289

0.105

0.01

7.865

a2M

GI

9.996

2.627

0.001

ALP

GI
% bone loss

41.025
0.911

10.435
0.309

0.001
0.005

Le but de cette etude a ete de determiner la presence

denzymes selectionnes et dinhibiteurs denzymes dans
le fluide creviculaire preleve autour dimplants (PICF)
avec ou sans signes de periimplantite clinique, radiographique et microbiologique. Onze implants ayant des
symptomes de periimplantite chez huit patients, quatre
hommes et quatres femmes, ont ete compares a` onze implants chez sept personnes, un homme et six femmes
sans periimplantite. Le PICF a ete preleve dans les sites
mesiaux et distaux de chaque implant. Lactivite de la
phosphatase alcaline (ALP) a ete mesuree en utilisant le

PPD pocket probing depth, GI Gingival Index

to be associated with periodontal disease

and periimplantitis (Mombelli et al. 1987;
Haffajee & Socransky 1994).
Because of the inability to measure extremely small quantities of PICF recovered
from healthy sites, the levels of the biochemical compounds have been reported
as total activity per 15s sample, rather
than as concentrations. This method of reporting biochemical parameters in GCF is
appropriate in view of the findings of
Smith et al. (1992), indicating that total
amounts of GCF compounds per site are
more closely associated with activity of
periodontal disease than concentrations.
One should also point out that saliva contamination of GCF may have a significant
effect on the calculated concentration of an
enzyme. Our study data indicated that elevated total amounts of elastase, a2M and
ALP were associated with implants showing periimplantitis, the levels of the potential markers being 13 times higher for elastase, eight times for a2M and six times for
ALP in the diseased group as compared to
the healthy one. In addition, the present results showed that the total amounts of EA,
a2M and ALP were correlated with the
clinical parameters.
The present results are similar to those
previously reported for gingival fluid collected during periodontitis. So far, very few
studies have been performed on the presence and levels of elastase and the inhibitor
a2M in PICF. To our knowledge, the presence of ALP has never been investigated in
PICF. Significantly higher levels of neutrophil elastase have been detected by Boutros
et al. (1996) in crevicular fluid collected
from moderately to severely inflamed implant sites as compared to mildly or non-inflamed sites, thus suggesting that neutrophil elastase may be used as marker of implant failure. Similarly, Adonogianaki et al.
(1995) found higher total amounts of a2macroglobulin in PICF from inflamed sites,
thus confirming that the inflammatory and

Resume

immune events in the periimplant mucosa

do not differ from those of the gingiva. Several other potential markers have been
examined in an effort to identify molecules
involved in the inflammatory response and
tissue damage in periimplantitis. Inflammatory cytokines, such as interleukin-1b
(Kao et al. 1995; Panagakos et al. 1996;
Curtis et al. 1997; Salcetti et al. 1997) and
interleukin-6 (Salcetti et al. 1997), have
been found in significantly higher amounts
in diseased as compared to healthy periimplant sites. Similar results were found
for myeloperoxidase, b-glucuronidase and
prostaglandin E2 (Boutros et al. 1996; Salcetti et al. 1997). Finally, Teronen et al. (1997)
reported significantly higher collagenase activity in PICF from diseased sites than in
healthy sites, as well as the presence of
MMP-8 only in the diseased sites.
In the present study, the total content in
PICF of elastase, a2M and ALP was much
higher in the presence of periimplantitis.
The difference was particularly high for
elastase, but the significance of this result
remains difficult to interpret, in view of the
parallel increase of the inhibitor a2M
around failing implants. As for ALP, its concentration in biological fluids has been considered as a general marker of bone metabolism. In human crevicular fluid, the
level of this enzyme has been mentioned as
a possible predictor of attachment loss in
periodontitis. Our results show that PICF of
implants with periimplantitis produced as
much as seven times more ALP in comparison to healthy implants. We suggest that
longitudinal monitoring of ALP in PICF
may confirm its possible use as a marker
and/or predictor of implant failure.
Acknowledgements: The authors would
like to thank PD Dr R. Gmr, Institute of
Oral Microbiology and General Immunology, University of Zrich, for kindly providing the monoclonal antibodies for the
detection of the bacterial target organisms.

231 |

p-nitrophenyl-phosphate comme substrat, lactivite de

lelastase (EA) par lutilisation dune substrat de faible
poids moleculaire fluorogenique et linhibiteur alpha 2macroglobuline (alpha 2-M) par ELISA. ALP, EA et alpha
2-M ont ete detectes dans la majorite des echantillons des
deux groupes. En comparaison aux implants cliniquement sains, les quantites totales de chacune de ces
substances etaient significativement superieures dans le
PICF preleveautour des implants avec periimplantite. Les
quantites totales moyennes de EA, alpha 2-M et ALP
dans les groupes sains et avec periimplantite etaient,
respectivement de EA: 1,8 ng, alpha 2-M: 3,1 ng, ALP:
24,1 U et EA: 23,1 ng, alpha 2-M: 25,2 ng, ALP: 142,3 U.
De plus, les trois mediateurs ont ete mis en correlation
avec les parame`tres cliniques. Les resultats confirment la
similarite de la reponse inflammatoire des tissus autour
des dents et des implants, et sugge`rent que ALP et EA
pourraient etre des marqueurs potentiels de la perte osseuse autour des implants dentaires.

Zusammenfassung
Es war das Ziel dieser Untersuchung, zu bestimmen,
ob bestimmte Enzyme und Enzymhemmer der periimplantare Sulkusflssigkeit mit oder ohne klinische, radiologische und mikrobiologische Anzeichen von Periimplantitis vorhanden sind. 11 Implantate bei 8 Patienten (4 mnnliche/4 weibliche) mit Symptomen einer
Periimplantitis wurden mit 11 Implantaten bei 7 Patienten (1 mnnlicher/6 weibliche) ohne Periimplantitis
verglichen. Periimplantre Sulkusflssigkeit (PICF) wurde an den mesialen und distalen Stellen jedes Implantates gesammelt. Die Aktivitt der alkalischen Phosphatase (ALP) wurde mittels p-Nitrophenyl-Phosphat als Substrat gemessen. Die Aktivitt der Elastase (EA) wurde
mit einem fluorogenen Substrat mit einem niedrigen
Molekulargewicht ermittelt und der Hemmer alpha2Makroglobulin (alpha2-M) wurde mit ELISA gemessen.
ALP, EA und alpha2-M wurden bei der Mehrzahl der
Proben beider Gruppen entdeckt. Im Vergleich zu den
klinisch gesunden Implantaten war die total Menge von
jeder dieser Substanzen in der PICF von Implantaten
mit Periimplantitis signifikant grsser. Die mittlere totale Anzahl EA, alpha2-M und ALP betrug in der gesunden Gruppe fr EA: 1.8 ng, alpha2-M: 3.1 ng, ALP 24.1
U und in der Periimplantitis-Gruppe fr EA: 23.1 ng,
alpha2-M: 25.2 ng, ALP: 142.3 U. Zustzlich waren
alle drei Mediatoren mit den klinischen Parametern
korreliert. Die Resultate besttigen die hnlichkeit der
Entzndungsantwort der periimplantren und parodontalen Gewebe. Es wird vermutet, dass ALP und EA
vielversprechende Marker fr periimplantren Knochenverlust um Implantate sein knnten.

Clin. Oral Impl. Res. , Clinical Oral Implants Research / 227233

Plagnat et al . Markers of bone loss in periimplantitis

Resumen
La intencion de esta investigacion fue determinar la presencia de enzimas seleccionadas y enzimas inhibidoras
en el fluido crevicular recogida de implantes con y sin
signos clnicos, radiograficos y microbiologicos de periimplantitis. Se compararon 11 implantes con signos de pe-

a2-M: 25.2, ALP: 142.3, respectivamente. Ademas, los

tres mediadores se correlacionaron con los parametros clnicos. Los resultados confirman la similitud de la respuesta inflamatoria de los tejidos circundando implantes
y dientes naturales, y sugieren que ALP y EA pudieran
ser marcadores prometedores en la perdida de hueso alrededor de los implantes dentales.

riimplantitis en 8 pacientes (4 varones/4 hembras) con 11

implantes, en 7 sujetos (1 macho/6 hembras), sin periimplantitis. Se recogio el fluido crevicular periimplantario
(PICF) en los lugares mesial y distal de cada implante. Se
medio la actividad de la fosfatasa alcalina (ALP) usando
p-nitrofenil-fosfato como sustrato, la actividad de la elastasa (EA) usando un sustrato fluorogenico de bajo peso
molecular y el inhibidor a2-macroglobulin (a2-M) por
medio de ELISA. Se detectaron ALP, EA y a2-M en la
mayora de las muestras en ambos grupos. En comparacion con los implantes clnicamente sanos, las cantidades
totales de estas sustancias fueron significativamente mas
altas en el PICF recogido alrededor de los implantes con
periimplantitis. Las cantidades totales medias de EA, a2M y ALP en los grupos sanos y con periimplantitis fueron: EA: 1.8 ng, a2-M: 3.1 ng, ALP: 24.1 U y EA: 23.1 ng,

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