Вы находитесь на странице: 1из 12

VOLUME 44 NUMBEP 2 FEBPUAPY 2013 137

QUI NTESSENCE I NTERNATI ONAL


IMPLANTOLOGY
clinical parameters such as bleeding on
probing (BoP) and probing doptn (PD), as
well as radiographic evaluations.
4,5
Apart
from iatrogenic factors such as inadequate
rostorations, inoomploto romoval o oomon-
tum in tno suloular rogion, inadoquato
implant positioning, and surgioal oomplioa-
tions, oarly oolonization o oxposod implant
suraoos plays an important rolo in tno
development of peri-implant diseases.
6-8

Many studios roportod tnat Gram-nogativo
anaerobes are the predominant bacterial
species
7,9,10
and induoo a proinhammatory
nost rosponso onaraotorizod by tno roloaso
o intorloukin-1 (L-1) and tumor noorosis
aotor alpna (TNF-alpna). Tnoso modiators,
or oxamplo, stimulato hbroblasts to pro-
Pori-implant disoasos aro onaraotorizod by
an inhammatory rosponso most oommonly
induood by plaquo aooumulation
1
in asso-
ciation with bone loss around the implant.
2,3

Pori-implantitis is diagnosod on tno basis o
1
Head, Center for Dental Specialities - Periodontology, German
Armed Forces Hospital, Ulm, Germany.
2
Head, Center for Dental Specialities - Periodontology, German
Armed Forces Central Hospital, Koblenz, Germany.
Correspondence: Dr Ren Thierbach, Center for Dental
Specialities - Periodontology, German Armed Forces Hospital,
Oberer Eselsberg 40, 89081 Ulm, Germany. Email: renethierbach@
bundeswehr.org
This article represents the opinion of the authors and does not neces-
sarily reect the opinions of the Medical Service of the German Armed
Forces, the German Armed Forces, or the German Ministry of Defense.
Clinical outcome of a nonsurgical and
surgical treatment protocol in different types
of peri-implantitis: A case series
Ren Thierbach, Dr Med Dent
1
/ Thomas Eger, Dr Med Dent
2
Objective: The replacement of missing teeth with dental implants has been standard prac-
tioo in dontistry or many yoars. Tno suoooss o dontal implants doponds on many aotors,
among wnion tno diagnosis, olinioal sovority, and troatmont o pori-implant disoasos play
a koy rolo. n tnis prospootivo oaso sorios, tno inhuonoo o oumulativo troatmont modali-
ties on peri-implantitis with and without pus formation on clinical outcome was assessed.
Method and Materials: During 2010, 28 pationts woro roorrod or pori-implantitis troat-
mont. Tnoy prosontod two dioront typos o pori-implant disoasos: pori-implantitis witn (17
implants) or witnout pus ormation (33 implants). Ator miorobiologio diagnosis, all pationts
woro troatod at basolino witn ull-moutn soaling and root planing. Two montns lator, urtnor
ull-moutn soaling and root planing and additional antimiorobial pnotodynamio tnorapy
(aPDT) was appliod. Four montns ator basolino, pationts witn pus ormation addition-
ally undorwont aoooss hap surgory. Aotivo numan matrix motalloprotoinaso-8 (aMMP-8)
levels were measured in eluates before and after all treatment modalities and 7 months
after baseline. Results: Clinioal paramotors (probing doptn, blooding on probing) and
aMMP-8-lovols improvod in botn groups ator troatmont and tno hnal oxamination. n pori-
implantitis pationts witnout pus ormation, all paramotors dooroasod ator ull-moutn soal-
ing and root planing and tno additional aPDT and no surgory was nooossary to improvo
tno paramotors. n pationts witn pus ormation, tno paramotors dooroasod only ator
aoooss hap surgory. Conclusion: The presence of pus inuences the clinical outcome of
the treatment of peri-implant diseases. Whereas peri-implantitis cases without pus forma-
tion oan bo suooossully managod nonsurgioally, pori-implantitis witn pus ormation oan
bo oootivoly troatod ator an additional obsorvation timo o 3 montns postoporativoly only
witn additional hap surgory. (Quintessence Int 2013;44:137148)
Key words: matrix motalloprotoinaso, miorobiology, nonsurgioal troatmont, pori-
implantitis, pus, surgioal troatmont
138 VOLUME 44 NUMBEP 2 FEBPUAPY 2013
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
duoo prostaglandins (PGE-2) and matrix
motalloprotoinasos (MMPs), wnion oauso
alvoolar bono loss. For tnis roason, tno
treatment of peri-implantitis consists of rig-
orous inootion oontrol by romoving biohlms
and urtnor anti-inhammatory moasuros
suon as ad|uvant antibiotio tnorapy.
11,12
As a
rosult o tno morpnology o implant suraoos
and tno possibility o supraorostal oxposuro
o tnroadod portions o an implant, oonsor-
vative nonsurgical treatment of peri-implan-
titis may navo limitod valuo to oontrol
disease progression.
13
In a literature review
by Ponvort ot al,
12
no dohnito ovidonoo o
the effectiveness of nonsurgical treatment
for peri-implantitis was found. Some authors
recommended surgical intervention with or
without regenerative procedures to com-
plotoly romovo biohlms rom implant sur-
aoos, ospooially in pationts witn ma|or
bone defects.
14,15
Tno aim o tnis study was to invostigato
two dioront typos o pori-implantitis and
assess the inuence of different treatment
measures on clinical parameters in an
attempt to establish a treatment concept for
peri-implant diseases.
METHOD AND MATERIALS
Patients
Twonty-oignt partially odontulous pationts
witn oonhrmod pori-implantitis
4
took part in
tno study. Tno pationt population oonsistod
o our womon and twonty-our mon witn a
moan ago o 50.6 9.41 yoars). Tnoro woro
104 sorow implants, 62 o wnion snowod
peri-implant soft tissue changes indicative
o muoositis. Pori-implant bono struoturos
woro aootod at 50 implant sitos.
Inclusion criteria for participation in this
study woro tno prosonoo o at loast ono
sorow implant witn a probing doptn > 5mm
and intraossoous bono loss > 3mm as ovi-
donood by olinioal and radiograpnio oxami-
nations, satisaotory implant rostorations,
good oral nygiono as ovidonood by a
plaquo oontrol rooord < 30%, no ooolusal
ovorload, no systomio disoasos (og, diabo-
tos witn HbA1o > 6.5%), and no bispnos-
phonate treatment. Informed consent was
obtained from all subjects. The research
was conducted according to the principles
outlinod in tno Doolaration o Holsinki on
oxporimontation involving numan sub|oots.
Parameters
Ator tnorougn nistory taking and inormod
oonsont, all pationts undorwont poriodontal
diagnostio proooduros. PDs, muoosal
rooossions (MP), olinioal attaonmont lovols
(CALs), and BoP sooros woro dooumontod
at six sitos por implant. Panoramio dontal
radiograpns (Sirona, Ortnopnos XGplus)
and nonstandardizod singlo-tootn radio-
grapns (Sirona, Holiodont DS) o tno implant
rogion woro takon. n addition, miorobio-
logio tosts (ParoCnook20, GroinorBioOno)
woro porormod to onaraotorizo tno baoto-
rial ora. Samples were obtained from the
sitos wnoro tno groatost PDs woro moa-
surod. Tno samplo sitos woro driod, and
supragingival plaque was removed. Sterile
paper points were inserted down to the
baso o tno pookots or 15 sooonds. Tno
individual samples were then placed in
transportation tubos. Baotoria woro idonti-
hod and spooihod using polymoraso onain
roaotion (PCP) assays targoting and ampli-
ying DNA ooding or 16S rPNA. Tno dotoo-
tion tnrosnold was 10
3
copies of a bacterial
gonomo. Aotivo numan matrix motallopro-
toinaso-8 (aMMP-8) lovols woro moasurod
in peri-implant uid for an evaluation of peri-
implant tissue destruction.
16
For this pur-
poso, tno sitos to bo samplod woro driod.
Gingival orovioular huid (GCF) samplos
woro tnon oollootod on ono storilo GCF/PSF
(pori-implant sulous huid) oollootion strip
that was inserted into the deepest peri-
implantitis sulous or 10 sooonds. Tno sam-
ples were placed in special transportation
tubos. Analysis was porormod by immuno-
ahnity onromatograpny (Dontognostios).
At basolino and ator 2 montns (T1), 4
montns (T2), and 7 montns (T3), a poriodon-
tal probo (PCP-11, Hu-Friody) was usod to
assoss olinioal paramotors inoluding PD as
measured from the mucosal margin to the
baso o tno pookot, MP as moasurod rom
tno implant snouldor to tno muoosal margin,
and CAL as moasurod rom tno implant
snouldor to tno baso o tno pookot (Fig 1).
All valuos woro rooordod to tno noarost mil-
limotor. Furtnormoro, BoP was assossod.
VOLUME 44 NUMBEP 2 FEBPUAPY 2013 139
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
Fig 2 Peri-implantitis with pus formation.
Stage of
treatment
Time point
After baseline
Baseline (BL) 0 months
14 days
Clinical examination: PD, MP, CAL, BoP, aMMP-8, L-1, radio-
grapnio assossmont, miorobiologioal tosts
Treatment: Subgingival dobridomont, antibiotios (wnoro appro-
priato), CHX
Clinical examination: PD, MP, CAL, BoP, aMMP-8
Treatment: Subgingival dobridomont, aPDT, CHX
Clinical examination: PD, MP, CAL, BoP, aMMP-8
Treatment: Supragingival debridement
Pori-implantitis and pus ormation: aoooss hap surgory, CHX
Clinical examination: PD, MP, CAL, BoP, aMMP-8
Treatment: 7 months Supragingival debridement
T1 2 months
T2 4 months
T3 7 months
aMMP-8, aotivo numan matrix motalloprotoinaso-8, aPDT, antimiorobial pnotodynamio tnorapy, BoP, blooding on
probing, CAL, olinioal attaonmont lovol, CHX, onlornoxidino digluoonato, MP, muoosal rooossion, PD, pookot doptns.
Fig 1 Diagnostic and therapeutic procedures
Sitos woro oonsidorod positivo or BoP
wnon blooding was obsorvod witnin 20 soo-
onds after probing.
All moasuromonts woro porormod by a
oalibratod oxaminor. During tno oalibration
proooduro, tno oxaminor moasurod PDs
and CALs in oignt pationts at two timo
points soparatod by an intorval o 48 nours.
Calibration was considered successful
wnon at loast 90% o tno moasurod valuos
were in agreement.
Apart rom olinioal moasuromonts,
microbiological and genetic tests were per-
ormod at basolino. n addition, oluatos
were collected at this time point for the
dotormination o aMMP-8 lovols.
At initial prosontation, oaon pationt was
plaood in ono o two groups:
1. Pori-implantitis witn positivo ovidonoo o
pus ormation: 7 pationts witn 17 implants
(7.15 4.09 yoars in plaoo) (Fig 2)
140 VOLUME 44 NUMBEP 2 FEBPUAPY 2013
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
2. Pori-implantitis witnout ovidonoo o pus:
21 pationts witn 33 implants (6.13 3.24
yoars in plaoo).
Radiographic evaluation
Prior to pori-implantitis tnorapy, singlo-tootn
radiograpns (Sirona, Holiodont DS) or pan-
oramio radiograpns (Sirona, Ortnopnos
XGplus) woro obtainod o oaon pationt. All
radiographs were viewed in a darkened
room. Polativo bono loss rom tno viowablo
affected most apical radiologic part of the
bony dooot to tno apioal position o tno
abutment at the implant was assessed at
tno poriodontally most aootod sito o tno
implants. A Sonoi rulor
17
was usod. All
radiographic assessments were performed
by ono oxaminor.
At basolino, tno moan rolativo radiologio
attaonmont loss at basolino was 29.12%
10.18% and 3.73 1.37 mm (tno attaon-
ment loss from the apical position of the
abutment to the deepest position of the
bony dooot): pori-implantitis witn pus or-
mation, 34.29% 10.38% and 4.40 1.33
mm, pori-implantitis witnout pus ormation,
27.02% 9.34% and 3.42 1.28 mm.
Treatment
At basolino, supragingival plaquo was
romovod in all pationts. Fourtoon days lator,
subgingival debridement (full-mouth scaling
and root planing) o all patnologioally doop-
ened pockets was performed under local
anesthesia in all four quadrants of all patients
in accordance with the principles of full-
mouth disinfection
7,18,19
with ultrasonic
(SonioFlox, Kavo) and nand instrumonts
and applioation o onlornoxidino digluoonato
(0.12%) (Paroox, Sunstar).
20
Ad|uvant antibi-
otio troatmont witn motronidazolo 400g (1-1-
1) was porormod or 10 days in pationts
(n=24) in wnom tno prosonoo o anaorobio
baotoria (>10%) was dotootod.
21-24

Fig 3 Clinical situation after mucoperiosteal fap
preparation. The defect shows a circular bone
resorption with buccal dehiscence and maintenance
of the lingual compacta.
Fig 4 Clinical situation after implantoplasty.
VOLUME 44 NUMBEP 2 FEBPUAPY 2013 141
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
Fig 5 Radiologic situation before treatment. Fig 6 Radiologic situation after resective treat-
ment.
Fig 7 Clinical situation before treatment. Fig 8 Operating site. Circular bone resorption and
maintenance of the buccal and lingual compacta.
Eignt wooks ator basolino, all pationts
woro ro-oxaminod (PD, CAL, BoP and
aMMP-8). Pationts witn porsisting patno-
logioally dooponod pookots again undor-
wont subgingival dobridomont. n addition,
all patients with a peri-implant disease
undorwont antimiorobial pnotodynamio
tnorapy (aPDT) using a low-intonsity lasor
troatmont (LLT) lasor (TnoraLito lasor,
Holbo Pnotodynamios Systoms). For tnis
purposo, a pnotosonsitizor (pnonotniazino
onlorido, Holbo Bluo, Holbo Pnotodynamios
Systoms) was insortod into all patnologioal-
ly dooponod pookots and romovod witn
saline solution after 3 minutes. The defects
woro tnon oxposod to lasor lignt witn a
wavolongtn o 660nm or 10 sooonds using
hbor optios. Lignt was dolivorod to six sitos
per implant or tooth.
25
Four montns ator basolino, tno pationts
were reassessed. On the basis of the clini-
oal rosults, pationts witn pori-implantitis and
no pus (33 implants) undorwont supragingi-
val dobridomont. Pationts witn pori-implant-
itis and pus ormation (17 implants) roooivod
surgioal troatmont. An intororovioular inoi-
sion was mado undor looal anostnosia, and
a mucoperiosteal ap was raised in the
vostibular and oral dirootions. Granulation
tissuo was oomplotoly romovod, and implant
surfaces were cleaned with plastic curettes
(Univorsal mplant Doplaquor, Hawo) and
sterile saline solution. Supracrestal portions
of implant screws were smoothed and pol-
isnod (implantoplasty) (Figs 3 and 4).
Autologous bono matorial was narvostod
rom a rotromolar sito (Saosorapor twist,
Mota) and insortod into tno dooots. Tno
entire defect area was then covered with a
biorosorbablo poroino mombrano (Goistlion
BioGido, Goistlion Biomatorials) and olosod
witn tno muooporiostoal hap, wnion was
ooronally positionod and soourod in pos-
ition by mattross suturos (Prolono 5-0,
142 VOLUME 44 NUMBEP 2 FEBPUAPY 2013
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
Fig 13 Radiologic situation before regenerative
treatment.
Fig 14 Radiologic situation after regenerative
treatment.
Fig 9 Defect confguration after removal of granu-
lation tissue.
Fig 11 Wound closure with mattress sutures.
Fig 10 Operating site. Placement of autologous
bone material and coverage with a bioresorbable
porcine membrane.
Fig 12 Clinical situation 10 days after treatment
and suture removal.
Etnioon) (Figs 5 to 14). All proooduros woro
porormod by tno samo dontal surgoon
(P.T.). Postoporativoly, tno pationts woro
advised to use mouthwash containing
onlornoxidino digluoonato (0.12%) (Paroox,
Sunstar) twioo a day or 14 days (soo Fig 1).
Suturos woro romovod ator 10 days.
Final oxaminations woro oonduotod 7
months after baseline.
Statistical analysis
Statistioal analysis was porormod using tno
SPSS 19.0 (BM). Moans and standard
doviations woro oaloulatod. Data woro tost-
ed for normal distribution using the
Kolmogorov-Smirnov tost. Tno analysis o
varianoo (ANOvA) tost witn Bonorroni oor-
rootion was usod to idontiy dioronoos
VOLUME 44 NUMBEP 2 FEBPUAPY 2013 143
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
between groups. P < .01 was oonsidorod
statistioally signihoant.
RESULTS
Clinical parameters
During tno study poriod, no oomplioations
suon as allorgio roaotions, modioation intol-
oranoo, or inootions woro obsorvod in
either group. Table 1 gives an overview of
the mean values obtained at all tested time
poriods. At basolino, no signihoant dior-
ences were observed between the two
groups in maximum PD and CAL (P > .01).
By oontrast, tnoro woro signihoant dior-
onoos in BoP sooros and aMMP-8 lovols (P
< .01).
Microbiologic fndings
All miorobiologioal tosts woro nogativo or
Aggregatibacter actinomycetemcomitans in
botn groups. Anaorobio baotoria, nowovor,
Table 1 Means and standard deviations for clinical parameters and differences
BL T1 Difference P value T2 Difference P value T3 Difference P value
PDmax (mm)
With pus 8.57 0.97 7.14 1.77 1.43 1.27 <.01 8.00 1.00 0.57 0.78 <.01 5.2 1.09 3.6 1.6 <.01
Without pus 7.23 1.22 5.55 1.27 1.70 1.83 <.01 4.90 1.29 2.30 1.45 <.01 4.47 0.77 2.58 1.3 <.01
PD (mm)
With pus 2.97 0.86 2.65 0.94 0.32 0.11 >.01 2.56 0.83 0.41 0.08 >.01 2.53 0.76 0.43 0.1 >.01
Without pus 4.02 1.03 3.05 0.76 0.97 0.42 >.01 3.01 0.65 1.01 0.16 >.01 2.89 0.81 1.13 0.17 >.01
CAL (mm)
With pus 5.82 1.07 3.93 0.73 1.87 0.56 <.01 4.67 1.09 1.12 1.38 >.01 4.03 0.94 1.79 0.36 <.01
Without pus 4.57 0.95 3.78 0.84 0.71 0.99 <.01 3.45 0.84 1.06 0.83 <.01 3.07 0.52 1.30 0.93 <.01
BoP (%)
With pus 96.19 7.12 42.44 24.72 53.75 24.42 <.01 55.87 24.40 41.75 21.07 <.01 10.41 10.21 85.91 11.53 <.01
Without pus 68.32 26.62 32.71 28.16 34.04 34.08 <.01 15.07 20.73 51.40 27.84 <.01 10.00 12.89 54.98 28.19 <.01
aMMP-8 (ng/mL)
With pus 188.09 101.41 93.86 73.57 94.23 140.57 <.01 108.43 76.8 79.66 147.7 <.01 25.20 31.07 162.89 111.82 <.01
Without pus 45.48 62.41 24.89 41.74 11.33 67.59 >.01 20.35 34.46 34.95 64.67 >.01 11.89 14.91 23.47 55.89 >.01
were detected in the cultures of both
groups. Table 2 gives the mean percent-
ages for detected bacterial species. The
results show marked contamination of the
peri-implant region with Fusobacterium
nucleatum (24.38% 18.62%), Tannerella
forsythia (16.82% 12.33%), Treponema
denticola (13.04% 11.49%), and
Porphyromonas gingivalis (7.18%6.83%).
The distribution of periodontal pathogens
26

in patients with peri-implantitis and pus for-
mation showed a higher contamination with
rod oomplox spooios tnan pationts witn
peri-implantitis and no pus.
Treatment outcome in patients
with peri-implantitis and no pus
formation
At T1, T2, and T3, tno moan valuos or
maximum PD, CAL, and BoP woro signih-
oantly roduood (P < .01) (Tablo 1). Moan
aMMP-8 lovols woro also lowor but witnout
signihoant dioronoos (P > .01). Maximum
PD valuos dooroasod rom 7.231.22mm)
at basolino to 4.47 0.77 mm ator 7
144 VOLUME 44 NUMBEP 2 FEBPUAPY 2013
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
montns. Tno dioronoo was 2.581.30mm
(P<.01). CAL valuos also dooroasod oon-
tinuously rom 4.57 0.95 mm at basolino
to 3.070.52mm at T3 (P < .01). Tno di-
oronoo was 1.30 0.93mm (P<.01). BoP
sooros dooroasod oonsidorably rom
68.32% 26.62% at basolino to 32.71%
28.16% at T1 (P<.0001). Similar valuos
woro notod ator 4 montns (15.07%20.73%)
and 7 montns (10.00%12.89%). aMMP-8
lovols dooroasod rom 45.4862.41ng/mL
at basolino to 11.89 14.91 ng/mL at T3.
Tno dioronoo o 23.4755.89ng/mL was
not signihoant (P>.01).
Treatment outcome in patients
with peri-implantitis and pus
formation
Wnon oomparod witn basolino, tno moan
valuos or maximum PD, CAL, BoP, and
aMMP-8 dooroasod during tno poriod undor
invostigation (Tablo 1). Tno roduotion in
CAL valuos was signihoant (P < .01). Tno
difference between baseline and T3 was
1.79 0.36 mm. Likowiso, BoP valuos
dooroasod signiioantly by 85.91%
11.53% rom basolino to T3. t snould bo
notod, nowovor, tnat all paramotors
decreased from baseline to T2 but increased
rom T1 to T2. For oxamplo, tnoro was a
CAL inoroaso o 0.740.46mm rom T1 to
T2. BoP sooros inoroasod by 13.43%
7.62%. Tno dioronoo in maximum PD
was -0.86 0.77 mm. From T1 to T2,
Table 2 List of detected bacterial species as percentages. Peri-implantitis with
pus formation showed a higher contamination with red complex species
than patients with peri-implantitis and no pus
Total (%)
Peri-implantitis with
pus formation (%)
Peri-implantitis without
pus formation (%)
Aggregatibacter actinomycetemcomitans 0 0 0
Porphyromonas gingivalis 7.18 12.04 5.39
Tannerella forsythia 16.82 16.91 16.78
Treponema denticola 13.04 19.17 10.79
Campylobacter gracilis 3.7 2.02 4.32
Campylobacter rectus 2.11 2.29 2.04
Eubacterium nodatum 0.16 0.29 0.11
Fusobacterium nucleatum nucleatum 24.38 20.00 26.00
Prevotella intermedia 3.32 4.26 2.96
Prevotella nigrescens 6.67 2.19 8.31
Peptostreptococcus micros 5.11 4.64 5.29
Streptococcus constellatus 0.96 0.53 1.12
Streptococcus mitis 2.85 3.91 2.46
Streptococcus gordonii 1.31 0.63 1.57
Eikenella corrodens 0.63 0.50 0.67
Capnocytophaga species 2.57 4.16 1.98
Campylobacter concisus 0.21 0.03 0.28
Veillonella parvula 6.86 4.73 7.65
Actinomyces odontolyticus 1.31 1.68 1.18
Actinomyces naeslundi (=viscosus) 0.79 0.22 1.00
Tno oolors roprosont tno dioront patnogon-oomploxos o poriodontitis, aooording to tno Amorioan Aoadomy o
Poriodontology Worksnop (1996).
VOLUME 44 NUMBEP 2 FEBPUAPY 2013 145
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
aMMP-8 lovols inoroasod by a moan o
14.57 57.39 ng/mL (P < .01). Ator sur-
gory, tnoro was again a signihoant dooroaso
in maximum PD, BoP, and aMMP-8 rom T2
to T3 (3 montns). During tnis poriod, moan
CAL valuos also dooroasod, but tno dior-
onoo did not roaon statistioal signihoanoo
(P> .01). Botwoon basolino and T3 (ator 7
montns), maximum PD valuos dooroasod
on avorago by 3.6 1.6 mm and aMMP-8
lovols by 162.89111.82ng/mL.
DISCUSSION
Wo invostigatod dioront typos o pori-
implantitis on tno basis o a varioty o olini-
cal parameters. Our data suggest that a
distinction between peri-implant diseases
witn and witnout pus ormation plays a koy
role in the success of different treatments.
Availablo studios do not distinguisn
between peri-implantitis with or without pus
ormation, so tnoy oan bo oomparod witn
our study only to a limitod oxtont. n a num-
bor o oaso roports,
11,27-30
subgingival clean-
ing and antiseptic mouthwash led to a
reduction in probing depth and an improve-
ment in bleeding indices. Mombelli et al.
31

achieved a reduction in clinical parameters
with the adjunctive use of local antibiotics
(totraoyolino hbor tnorapy). Two pationts
woro oxoludod during tno study (n = 25)
booauso tnoy nad porsisting aotivo pori-
implantitis with pus formation which did not
show an improvement in clinical parameters
dospito anti-inootivo tnorapy. Our oaso
sorios snowod similar olinioal hndings. Anti-
inootivo tnorapy (ull-moutn soaling and
root planing and applioation o onlornoxi-
dino digluoonato) oombinod witn systomio
antibiotio troatmont, or oxamplo, lod to
short-term improvement in clinical parame-
ters also in patients with peri-implantitis and
pus formation but recurrence occurred after
our montns (T2). Popoatod subgingival
debridement and the additional use of
aPDT (T2) did not navo a positivo ooot in
pationts witn pus ormation. Nonsurgioal
treatment consisting of subgingival debride-
mont oombinod witn systomio antibiotio
tnorapy and aPDT was suooossul only in
patients with peri-implantitis and no pus
formation. The effectiveness of laser treat-
ment in patients with peri-implantitis and no
pus was also roportod by otnor autnors
32

wno, it snould bo notod, usod an Er:YAG
lasor and not a low-intonsity lasor and wno
too oxoludod pationts witn porsisting pus
ormation. Tno positivo ooots on maximum
PD, BoP, and CAL ator surgioal troatmont
were also reported in earlier studies.
33

mplantoplasty was also ound to bo ooo-
tivo in a study on 38 implants.
34

Sonwarz ot al
15
were able to show in a
study witn applioation o a natural bono
mineral in combination with a collagen
membrane that the outcome of regenerative
tnorapios was inhuonood by tno typo o
bone defect. Cases with pus formation were
oxoludod by tnoso autnors. n our study, wo
inoludod all typos o dooots. Only pationts
with peri-implantitis and pus formation
underwent regenerative treatment with
autologous bone and a collagen mem-
brane. Supracrestal portions of implant
screws were smoothed and polished during
implantoplasty or provontion o baotorial
rooolonization.
The inuence of implant surface charac-
teristics on the outcome of surgical treat-
ment of peri-implantitis was described in a
rooontly publisnod study.
35
Further studies
must be conducted to investigate whether
regeneration is more successful with smooth
supracrestal implant surfaces than with
tnroadod suraoos. Altnougn pationts witn
peri-implantitis and no pus formation showed
improvomonts in all olinioal paramotors, sur-
gory was not oonsidorod to bo nooossary.
Tno long-torm suoooss o tnis typo o troat-
mont snould bo oxaminod in studios tnat
cover a longer period of observation.
Poriodontal nistory and smoking nabits
did not dior in our study botwoon tno di-
oront pori-implatitis typos, altnougn Lovin
et al
36
snowod in a largo oonort study witn
736 patients that peridodontal status and
smoking aro signihoant risk aotors or
implant failure.
Charalampakis et al
37
were able to follow
up 245 pationts ator troatmont or 9 montns
to 13 yoars. Smoking was ound to bo sig-
nihoantly oorrolatod witn pori-implantitis.
F nucleatum was found to dominate the
baotorial hora. Tno massivo oolonization o
146 VOLUME 44 NUMBEP 2 FEBPUAPY 2013
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
tno implants oan possibly oxplain wny tnoro
was more severe destruction of bone and
surrounding connective tissue than is seen
in poriodontitis. A oomparativo study and
tno assossmont o inhammatory paramotors
suon as PGE-2, MMP-3 and L-1 bota would
provide useful data.
There was no evidence of A actinomy-
cetemcomitans. The predominant bacterial
species were anaerobes. It is not clear to
wnat oxtont provious antibiotio troatmonts
play a rolo in onangos o tno baotorial hora.
Dospito tno uso o systomio antibiotios, or
oxamplo, tno long-torm olimination o anaor-
obic bacterial species was found to be pos-
siblo only in raro oasos.
38
A roduotion o
individual species below the detection
tnrosnold o oommoroially availablo mioro-
biologioal tosts and/or tno dovolopmont o
resistance of periodontal pathogens should
also bo takon into oonsidoration. No baoto-
rial ro-oxamination 7 montns ator basolino
was porormod, booauso all paramotors
decreased with treatment and the applica-
tion o systomio antibiotios. Tno antibiotio
ooot and baotorial rooolonization snould
be evaluated in further studies with longer
maintenance phase. The quantitative detec-
tion o aMMP-8 doos not appoar to play a
relevant role in the diagnosis of peri-implan-
titis. For oxamplo, pori-implantitis pationts
without pus formation and with severe bone
loss woro ound to navo rolativoly low
aMMP-8 lovols. By oontrast, pori-implantitis
witn pus ormation, wnion is assooiatod witn
a nign lovol o aotivity, is oorrolatod witn a
markod inoroaso in aMMP-8 lovols.
Espooially in pationts witn pori-implantitis
and pus ormation, tno roduotion in aMMP-8
levels during treatment shows that quantita-
tivo moasuromonts o aMMP-8 oan play an
important diagnostic role during follow-up.
An inoroaso in aMMP-8 lovols ator troat-
mont would provido oarly ovidonoo o
repeated inammation so that appropriate
measures could be taken to prevent a pos-
sible recurrence. For the institution of thera-
poutio moasuros on tno basis o aMMP-8
lovols, nowovor, it would bo nooossary to
domonstrato a oorrolation botwoon aMMP-8
lovols and bono loss sovority.
The present case series shows a
decrease in the clinical peri-implantitis
parameters as a result of the nonsurgical
and urtnor surgioal tnorapy. Booauso o tno
small oonort population, ospooially in pori-
implantitis oasos witn pus ormation, it doos
not allow a gonoralizod oonolusion. n tno
treatment protocol numerous treatment
modalitios, suon as antibiotios, aPDT, ull-
moutn soaling and root planing, and
onlornoxidino moutnrinso, woro oarriod out.
Booauso o tno snort intorvals o tno various
troatmonts (6 wooks), mutual inhuonoos o
the nonsurgical treatments are possible in
spito o tno aot tnat tnoy woro not suoooss-
ful 6 weeks after nonsurgical treatment. This
should be noticed in further studies of lon-
ger duration.
CONCLUSION
The present case series suggests that the
presence of pus is a clinical parameter that
inuences the outcome of surgical and non-
surgical treatment of peri-implantitis.
Whereas nonsurgical treatment was effec-
tive in managing peri-implantitis without pus
ormation, suooossul troatmont o pori-
implantitis with pus formation required a
combination of surgical and regenerative
procedures. Further studies should be con-
ducted to investigate the usefulness of dif-
ferent treatment approaches for different
lovols o sovority o pori-implantitis.
ACKNOWLEDGMENTS
The authors declare that there are no conficts of inter-
est in this study. No external funding, apart from the
support of the authors institution, was available for
this study. The study was approved by the Ministry of
Defense, Medical Service Staf I.3. This article represents
the opinion of the authors and does not necessarily
refect the opinions of the Medical Service of the German
Armed Forces, the German Armed Forces, or the German
Ministry of Defence.
VOLUME 44 NUMBEP 2 FEBPUAPY 2013 147
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
REFERENCES
1. Leonhardt A, Berglundh T, Ericsson I, Dahln
G. Putative periodontal pathogens on titanium
implants and teeth in experimental gingivitis and
periodontitis in beagle dogs. Clin Oral Implants Res
1992;3:112-119.
2. Albrektsson TO, Johansson CB, Sennerby L. Biological
aspects of implant dentistry: Osseointegration. J
Periodontol 1994;4:58-73.
3. Lindhe J, Meyle J. Peri-implant diseases: Consensus
report of the sixth European Workshop on peri-
odontology. J Clin Periodontol 2008;35:282-285.
4. Heitz-Mayfeld LJA. Peri-implant diseases: Diagnosis
and risk indicators. J Clin Periodontol 2008;35:292-304.
5. Lang NP, Berglundh T. Peri-implant diseases: Where
are we now? Consensus of the Seventh European
Workshop on Periodontology. J Clin Periodontol
2011;38:178-181.
6. van Winkelhof AJ, Goene RJ, Benschop C, Folmer
T. Early colonization of dental implants by puta-
tive periodontal pathogens in partially edentulous
patients. Clin Oral Implants Res 2000;11:511-520.
7. Quirynen M, Vogels R, Peeters W, van Steenberghe
D, Naert I, Hafajee A. Dynamics of initial subgingi-
val colonization of pristine peri-implant pockets.
Clin Oral Implants Res 2006;17:25-37.
8. Salvi GE, Persson R, Heitz-Mayfeld LJA, Frei M, Lang
NP. Adjunctive local antibiotic therapy in the treat-
ment of peri-implantitis. II: Clinical and radiographic
outcomes. Clin Oral Implants Res 2007;18:281-285.
9. Leonhardt A, Renvert S, Dahln G. Microbial fnd-
ings at failing implants. Clin Oral Implants Res
1999;10:339-345.
10. Quirynen M, De Soete M, Van Steenberghe D.
Infectious risks for oral implants: A review of the
literature. Clin Oral Implants Res 2002;13:1-19.
11. Mombelli A, Lang NP. Antimicrobial treatment
of peri-implant infections. Clin Oral Implants Res
1992;3:162-168.
12. Renvert S, Roos-Jansaker AM, Clafey N. Nonsurgical
treatment of peri-implant mucositis and peri-
implantitis: A literature review. J Clin Periodontol
2008;35:305-315.
13. Renvert S, Polyzois I, Clafey N. How do implant sur-
face characteristics infuence peri-implant disease?
J Clin Periodontol 2011;38:214-222.
14. Clafey N, Clarke E, Polyzois I, Renvert S. Surgical
treatment of peri-implantitis. J Clin Periodontol
2008;35:316-332.
15. Schwarz F, Sahm N, Biehling K, Becker J. Surgical
regenerative treatment of peri-implantitis lesions
using a nanocrystalline hydroxyapatite or a natural
bone mineral in combination with a collagen mem-
brane: A four-year clinical follow-up report. J Clin
Periodontol 2009;36:807-814.
16. Xu L, Yu Z, Lee HM, et al. Characteristics of col-
lagenase-2 from gingival crevicular fuid and
peri-implant sulcular fuid in periodontitis and
peri-implantitis patients: Pilot study. Acta Odontol
Scand 2008;66:219-224.
17. Schei O, Warhaug J, Lovdal A, Arno A. Alveolar
bone loss as related to oral hygiene and age. J
Periodontol 1959;30:7-16.
18. Mongardini C, van Steenberghe D, Dekeyser C,
Quirynen M. One stage full- versus partial-mouth
disinfection in the treatment of chronic adult or
generalized early-onset periodontitis. I. Long term
clinical observations. J Periodontol 1999;70:632-645.
19. Quirynen M, Mongardini C, de Soete M, et al. The
role of chlorhexidine in the one-stage full-mouth
disinfection treatment of patients with advanced
adult periodontitis. Long term clinical and
microbiological observations. J Clin Periodontol
2000;27:578-589.
20. Eick S, Goltz S, Nietzsche S, Jentsch H, Pfster W.
Efcacy of chlorhexidine digluconate-contain-
ing formulations and other mouthrinses against
periopathogenetic microorganisms. Quintessence
Int 2011;42:687-700.
21. Winkel EG, van Winkelhof AJ, Timmermann MF,
Vangsted T, van der Felden U. Efects of metronida-
zole in patients with refractory periodontitis asso-
ciated with Bacteroides forsythus. J Clin Periodontol
1997;24:573-579.
22. Lindhe J, Liljenberg B, Adielson B, Borjesson I. Use of
metronidazole as a probe in the study of human peri-
odontal disease. J Clin Periodontol 1983;10:100-112.
23. Loesche WJ, Syed SA, Morrison EC, Kerry GA,
Higgins T, Stoll J. Metronidazol in periodontitis. I.
Clinical and bacteriological results after 15 to 30
weeks. J Periodontol 1984;55:325-335.
24. Ehmke B, Moter A, Beikler T, Milian E, Flemmig TF.
Adjunctive antimicrobial therapy of periodontitis:
Long-term efects on disease progression and oral
colonization. J Periodontol 2005;76:749-759.
25. Takasaki AA, Aoki A, Mizutani K, et al. Application of
antimicrobial photodynamic therapy in periodon-
tal and peri-implant diseases. Periodontol 2000
2009;51:109-140.
26. American Academy of Periodontology. World
Workshop in Periodontics. Ann Periodontol
1996:926-932.
27. Buchmann R, Khoury F, Hesse T, Mller RF, Lange
DE. Antimikrobielle Therapie der periimplantren
Erkrankung. Z Zahnrztl Implantol 1996;12:152-157.
28. Buchmann R, Khoury F, Mller RF, Lange DE. Die
Therapie der progressiven marginalen Parodontitis
und Periimplantitis. Dtsch Zahnrztl Z 1997;6,421-426.
29. Khoury F, Buchmann R. Surgical therapy of peri-
implant disease: A 3-year follow-up study of cases
treated with 3 diferent techniques of bone regen-
eration. J Periodontol 2001;72:1498-1508.
QUI NTESSENCE I NTERNATI ONAL
Thi erbach et al
30. Nibali L, Donos N. Radiographic bone fll of peri-
implantitis defects following nonsurgical therapy:
Report of three cases. Quintessenz Int 2011;42:
393-397.
31. Mombelli A, Feloutzis E, Brgger U, Lang NP.
Treatment of peri-implantitis by local delivery of
tetracycline. Clinical, microbiological and radiologi-
cal results. Clin Oral Implants Res 2001;12:287-294.
32. Schwarz F, Bieling K, Nuesry E, Sculean A, Becker J.
Clinical and histological healing pattern of peri-implan-
titis lesions following non-surgical treatment with an
Er:YAG laser. Lasers Surg Med 2006;38:663-671.
33. Leonhardt A, Dahln G, Renvert S. Five year clini-
cal, microbiological, and radiological outcome
following treatment of peri-implantitis in man. J
Periodontol 2003;74:1415-1422.
34. Romeo E, Lops D, Chiapasco M, Ghisolf M, Vogel G.
Therapy of peri-implantitis with resective surgery.
A 3-year clinical trial on rough screw-shaped oral
implants. Part II: Radiographic outcome. Clin Oral
Implants Res 2007;18:179-187.
35. Albouy J-P, Abrahamsson I, Persson LG, Berglundh
T. Implant surface characteristics infuence the
outcome of treatment of peri-implantitis: An
experimental study in dogs. J Clin Periodontol
2010;38:58-64.
36. Levin L, Ofec R, Grossmann Y, Anner R. Periodontal
disease as a risk for dental implant failure over
time: A long-term historical cohort study. J Clin
Periodontol 2011;38:732-737.
37. Charalampakis G, Rabe P, Leonhardt A, Dahln G. A
follow-up study of peri-implantitis cases after treat-
ment. J Clin Periodontol 2011;38:864-871.
38. Weyer J, Rist A, Gutsche G, Eger T. Nachweis
von A.a. und P.g. nach Parodontalbehandlung
schwerer Parodontitisformen mit untersttzender
systemischer Antibiose - Fnfahresergebnisse.
Parodontologie 2007;18:377-386.

Вам также может понравиться