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INTRODUCTION
TISSUE IMPLANT BIOLOGIC SEAL
THE PERI IMPLANT MUCOSA
BIOLOGIC WIDTH AROUND DENTALIMPLANTS
PROBING THE PERIIMPLANT MUCOSA
COMPARISON OF TISSUES SURROUNDING
NATURAL DENTITION AND ORAL IMPLANTS
FACTORS AFFECTING SOFT TISSUES
AROUND IMPLANTS
BONE LOSS AND SOFT TISSUE HEALTH
PERI IMPLANT MICROBIOLOGY
CONTENTS
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Oral implants pierce through the mucosa, thus establishing the
connection between the oral environment and the underlyingtissues.
The soft tissue connection to the transmucosal part is of crucial
importance as it relates to the stability of the peri implant
tissues and the prevention of the peri implant infection with
subsequent destruction of the periimplant structures.
Hermetic closure of the gingival tissues is important to
minimize the risk of infection and prevent the apical downgrowth of the epithelium.
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REGENERATION OF THE ATTACHED GINGIVA AND ITS ABILITY TO FORM AGINGIVAL SULCUS LINED BY CREVICULAR EPITHELIUM
McKinney et al 1984
SYSTEMATIC SCIENTIFIC STUDY TO INVESTIGATE THE SEAL PHENOMENON
James and Kelln1974, 1981
NECESSITY FOR ATTACHED GINGIVA TO APPROPRIATELY ADAPT TO THEIMPLANT
Lavelle 1981
CONCEPT OF A SEAL AROUND THE DENTAL IMPLANTS
Weinmann 1956
EARLY CIVILIZATIONS LATE 19thand EARLY 20thCENTURIES
Gramm CT (1898) Lewis (1889)
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The concept of the gingival epithelium informing a biological seal is one of great
importance in implant dentistry
PERMUCOSAL PASSAGE A WEAK LINK A zone where initial tissue
breakdown begins that can result in eventual
tissue necrosis and destruction aroundimplants.
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The seal is a physiological barrier to prevent
ingress of bacterial plaque,toxins, oral debris..
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1
INFLAMMATION OF SOFT TISSUES
2 OSTEOCLASTIC ACTIVITY
3 CHRONIC RESORPTION OF SUPPORTING BONE
4 FILL WITH GRANULATION TISSUE
5 IMPLANT MOBILITY
6
PERCOLATION OF BACTERIAL TOXINS AND DEGENERATIVE AGENTS FURTHERINTO THE INTERNAL ENVIRONMENT SURROUNDING THE IMPLANT
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7ACUTE SUPPURATIVE INFLAMMATION
8
EXTENSIVE MOBILITY
9
RENDERING SUPPORT TO PROSTHESIS
IMPRACTICAL
10 IMPLANT TO BE REMOVED
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PERIIMPLANT
MUCOSA
EPITHELIALCOMPONENT
PERIIMPLANT
MUCOSA
CONNECTIVE
TISSUE
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The interface between the epithelial cells and the titanium
surface is characterized by the presence of
hemidesmosomes and a basal lamina.
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EA: Epithelial Attachment, LBI: Lamina Basalis Interna, LBE: Lamina Basalis Externa,
BC: Basal Complex, a junctional epithelium, b sulcular epithelium, c oral
epithelium; T/I : Titanium Implant, LL: Lamina Lucida, LD: Lamina Densa, HD:
Hemidesmosomes, D: Desmosomes
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a junctional epithelium,b sulcular epithelium,
c oral epithelium;
Im : Implant,
Ab: Abutment, MR: Margin of
gingiva, Bo: Bone, A/I :
Abutment/ Implant junction,aAE : apical point of attached
epithelium
1. Implant Crown
2. Vertical alveologingival ct
fibers
3. Circular gingival fibers4. Circular gingival fibers
5. Periosteal gingival ct
fibers
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The connective tissue appears to be in direct contact with the
surface (TiO)of the implant.
The collagen fibers in this connective tissue form bundles which run
PARALLEL to the implant surface.
They can also have a cuff like circular orientation.
Higher amounts of collagen type V and VI were noticed.
Capillary loops under JE and SE
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Moon et al (1999) reported that the attachment tissue close to theimplant contains only few blood vessels but a large number of
fibroblasts that were oriented with their long axes parallel with the
implant surface.
In more lateral compartments, there were fewer fibroblasts but
more collagen fibers and more vascular structures.
Berglundh et al (1994) observed that the vascular system of the peri implant mucosa originates SOLELY from the LARGE
SUPRAPERIOSTEAL BLOOD VESSEL on the outside of the alveolar
ridge.
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B.W.
Epithelialattachment
Supracrestal
connectivetissue zone
3 to 4mm
2mm
1mm
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A MINIMUM DIMENSION OF THE BIOLOGICAL WIDTH IS NEEDED
IN ORDER TO ACCOMMODATE FOR THE SOFT TISSUE HEALING
PROCESS; WHEN THIS DIMENSION IS NOT PRESENT, BONE
RESORPTION MAY OCCUR TO ALLOW FOR AN APPROPRIATE
BIOLOGICAL DIMENSION
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DAY 0: COAGULUM OCCUPIESSPACE BETWEEN MUCOSA ANDIMPLANT SURFACE
DAY 4: GRANULOCYTES INFILTRATECLOT; INITIAL SEAL
1 WEEK: FIBROBLASTS ANDCOLLAGEN FIBERS
2 WEEKS: CONNECTIVE TISSUE RICHIN CELLS AND VASCULARITY;JUNCTIONAL EPI STARTS TO FORM
4 WEEKS: JUNCTIONAL EPITHELIUMFORMS; MATURE CT
MORPHOGENESIS OF
PERI IMPLANT
MUCOSA
(BERGLUNDH et al
2007)
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I n case of an implant probe goesbeyond the sulcus and reaches closer
to the bone
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Ericsson and L indhe (1993)
Probing caused both compression and lateral dislocation of
the per iimplant mucosa, and the average histologic
probing depth was markedly deeper than at the tooth site:
2mm vs 0.7 mm.
The tip of the probe was consistently positioned deep in the
connective tissue/ abutment inter face and apical of thebarr ier epithel ium.
Distance between probe tip and the bone crest was 0.2 mm.
The depth of the probe penetration reveals the thickness ofthe mucoperiosteum through which the abutment/
restoration is emerging rather than a loss of attachment.
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FLEXIBLE PLASTIC
PROBE FOR
PROBING AROUND
IMPLANTS
Recommended to not probe the
implant for at least 3 months following
abutment attachment to avoid disrupting
the permucosal seal
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COMPARISON OF TOOTH AND IMPLANT SUPPORT STRUCTURES
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STRUCTURE TOOTH IMPLANT
Connection Cementum, bone , periodontium Osseointegration , bone functional ankylosi
Junctionalepithelium
Hemidesmosomes and basal lamina (lamina lucida and lucida , lamina
densa zones )
Hemidesmosomes and basal lamina ( lamin, lamina densa and sublamina lucida zones )
Connective
tissue
13 groups : perpendicular to tooth
surfaces
Decreased collagen, increasedfibroblasts
Only 2 groups : parallel and circular fibers .
No attachment to the implant surface and
bone
Increased collagen and decreased fibroblast
Biological
width
2.04 to 2.91 mm 3.08 mm
Vascularity Greater ; supraperiosteal and
periodontal ligament
Less ; periosteal
Probing
depth
3mm in health 2.5 to 5.0mm ( depending on soft tissue
depth )
Bleeding onprobing More reliable Less reliable
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Attachment between the
per iodontal tissue and the
root sur face
Attachment between the
per i-implant tissue and an
implant sur face
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Periotest was originally devised by Dr. Schulte to measure tooth
mobility.
Teerlinck, et al.(1991) used this method to overcome destructive
methods in measuring the implant stability.
Periotest evaluates the damping capacity of the periodontium. It
is designed to identify the damping capacity and the stiffness ofthe natural tooth or implant by measuring the contact time of an
electronically driven and electronically monitored rod after
percussing the test surface.
Periotest value(PTV) is marked from -8(low mobility) to +50(high
mobility). PTV of -8 to -6 is considered good stability.
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Control Box + Probe
PROBE APPLIED
HORIZONTALLY
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MUCOSAL THICKNESS
SURGICAL PROCEDURE
LOADING
TITANIUM SURFACES AND ABUTMENT
MATERIALS
IMPLANT STRUCTURE AND POSITION
IMMEDIATE POST EXTRACTIVE INSERTION
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THIN BIOTYPE
OCHSENBEIN &ROSS
THICK BIOTYPE
DELICATE AND
FRIABLE
REACTS TO INJURY BYRECESSION
AMOUNT OF
KERATINIZED MUCOSA
USUALLY QUITE SMALL
DENSER AND MORE
FIBROTIC GINGIVA
MIMICKING THE
FLATTER AND THICKER
UNDERLYING OSSEOUS
ARCHITECTURE
MORE RESISTANT TO
INJURY
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PROBE VISIBLE THROUGH THE
THIN GINGIVA
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THIN
BIOTYPE
MORE PRONE TOCRESTAL BONERESORPTION
AVOID SUPRACRESTALPLACEMENT
THICK BIOTYPE
LESS CRESTAL BONE
RESORPTION
SUPRACRESTALPLACEMENT
MINIMIZES BONELOSS
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A minimum of 3 mm of periimplant mucosa is required for
a stable epithelial connective tissue attachment to form.
Linkevicious et al in a human study done to compare the
effects of tissue thickness at the time of surgery on crestal
bone changes around non submerged implants after one year
follow up found that positioning an implant 2mm supra
crestally did not prevent crestal bone loss, if THIN GINGIVAL
TISSUES are present at the time of implant placement.
Implants with thin tissue underwent additional bone loss
interproximally than the group with thick tissue pattern which
had significantly less bone loss.
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Initial tissue thickness if less than 2.5 mm leads to an
expected bone loss of 1.45 mm within the first year of
function.
In thick tissues, >2.5 mm or more, marginal bone recession
can be avoided if the implant abutment junction is 2mm or
above the bone level, minimal 0.2 mm
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Thin Biotypes
Thick maintainpapillary height
GINGIVAL
RECESSION
Apical and lingualdirection
Facial plate loss GRAYISH COLOR
ALVEOLAR
BONE
RESORPTION
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PROSTHETIC
DESIGN
CONCAVE ABUTMENT/CROWN PROFILE
IMPLANT DESIGNSMALLER DIAMETER,
PLATFORM SWITCHING
STRAIGHT/ PARALLELWALLED IMPLANT
IMPLANTPOSITION
(PALATAL/APICAL)
ESTHETIC MANAGEMENT TRIAD
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Abrahamsson et al 1996 :
Evaluated the influence of the surgical protocol (one
stage vs. two stage) on the soft tissue healing around
3 different implant systems.Histological results demonstrated similar dimensions
and composition of the epithelial and connective
tissue components.
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Abrahamsson et al 1999
THE SURGICAL PROTOCOL (i.e. one or two stage surgical
protocol) do not influence the dimensions and composition of
the biological width.
It was observed that the mucosa that formed at implants
placed in a submerged or a non submerged procedure hadmany features in common
THE DEEPER THE IMPLANT SHOULDER POSITION IN BONE THE
LONGER THE BIOLOGICAL WIDTH.
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Cochran et al. 1997
Evaluated the dimensions of the implanto gingival junctionaround non submerged loaded and not loaded implants at 3
and 12 months after implant placement.
SD: 0.50 mm
JE: 1.44 mm
CT: 1.01 mm
LOADED
SD: 0.49mm
JE: 1.16 mm
CT: 1.36 mm
UNLOADED
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Abrahamsson et al.
Analyzed soft tissue healing to abutments made of titanium,
gold alloy, dental porcelain and AlOceramic
Failed to form an attachment
Gold alloyand
porcelains
Formed attachment with similar
dimensions and tissue
structures
Titanium andceramic
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Abrahamsson et al. 2002
Demonstrated that surface characteristics (smooth vs
rough titanium surfaces) do not influence thebiologic width dimension.
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ABUTMENT IMPLANT INTERFACE
MICROGAP
LEVELBONE CREST
LEVEL OF THE INTERFACE
SUBMERGED AND NON SUBMERGED
CRESTAL BONE LOSS IN VARIOUS CASES
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SUBMERGED
Implant placed into
the bone and the topof the implant placedat or below the bone
crest
Soft tissues are closedover the bone and
implant therebysubmerging it
NON SUBMERGED
Implant extendscoronally beyond thealveolar crest wherethe soft tissue flap is
placed around theimplant body
Secondintervention not
needed
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Hermann et al 2000Study on 6 types of implants
AC NON SUBMERGED
DF SUBMERGED
A : 6mm R/S at bone crestB: 5mm; R/S 1mm below
A,B: ONE PIECE; No interface
C, D: 4.5 mm interface at bone crest
E,F : 4.5 mm interface 1 mm above
and 1mm below the crest
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MEASUREMENTS:1. Distance between the top of the implant (top) and
first bonetoimplant contact (fBIC) for A and B.
2. Distance between interface (microgap) of the
implant (IF) and fBIC
3. Top and R/S for A and B.
4. IFR/S (for CF).
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TYPE TOP - fBIC R/S - fBIC MICROGAP - fBIC
A 2.98 mm 0.19 mm
B 3.88 mm 0.01 mm
C 1.68 mm 0.39 mm
D 0.28 mm 1.57 mm
E 0.06 mm 2.64 mm
F 0.89 mm 1.25 mm
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GREATEST BONE LOSS
WAS OBSERVED
AROUND TYPE F
(2.25mm)
TYPES C, DF: SEVERE
SIGNS OF CLINICAL
INFLAMMATION
TYPE A AND B : SLIGHT
INFLAMMATION
R/S fBIC
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IN ALL 2 PIECE IMPLANTS, THE LOCATION OF THE
INTERFACE (MICROGAP) WHEN LOCATED AT OR
BELOW THE ALVEOLAR CREST DETERMINES THE
AMOUNT OF BONE RESORPTION
A and B showed minimal signs of clinical
inflammation
C, DF Moderate to Severe signs of disease
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2 piece implants
Abutmentimplant junction:Microgap
Crestal bone resorption
FURTHER BIOLOGICAL WIDTH CHANGES,INCREASED SUBGINGIVAL BACTERIALCOLONIZATION LEADING TO FURTHERBONE LOSS
INEVITABLE
1.5 mm during first
year
0.1 mm in subsequent
years
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The greatest crestal bone loss occurs with 2 piece
implants when the interface located below the crest
rather than at or above the crestal bone level.
Osseous changes influence the location of the gingival
margin and the dimensions of the biologic width.
SIGNIFICANT CRESTAL BONE LOSS OCCURS IN 2PIECE
IMPLANT CONFIGURATIONS EVEN WITH THE
SMALLEST SIZE OF THE MICROGAP (
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Schultes and Gaggl 2001
Compared healing at implants placed in a healed ridge
and implants immediately placed in fresh extractionsockets at 8 months have reported a LARGER
DIMENSION OF SOFT TISSUE BARRIER IN IMPLANTS
PLACED IMMEDIATELY
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P i i l t di t i t f
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Both of these are characterized by an inflammatory reaction in the tissuessurrounding an implant.
Peri-implant mucositis has been described as a disease in which thepresence of inflammation is confined to the soft tissues surrounding adental implant with no signs of loss of supporting bone following initial
bone remodeling during healing.
Peri-implantitishas been characterized by an inflammatory processaround an implant, which includes both soft tissue inflammation and
progressive loss of supporting bone beyond biological bone remodeling
Peri-implant diseases present in two forms
PERI-IMPLANT MUCOSITIS
PERI-IMPLANTITIS
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The term peri-implantitis was introduced in the 1980s
(Mombelli A,1987)
Formerly used terms as implant histoclasia and peri
implantoclasia accepted in the 1963 edition of Current Clinical Dental
Terminology.
Periimplantitis was defined as an inflammatory reaction with loss of
supporting bone in tissues surrounding a functioning implant
Albrektsson T et al, Proceedings of the 1stEuropean Workshop on
Per iodontology, 1994
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While peri-implant mucositis is a reversible inflammatory condition
confined to the peri-implant soft-tissue unit, peri-implantitisis
characterised by progressive inflammatory destruction of the crest
of the alveolar bone supporting the implant, by increased peri-
implant probing depths, and by bleeding and/or suppuration on
probing.
Additionally, peri-implant mucositis may be successfully treated
using non-surgical efforts if detected early, whereas peri-implantitis
usually requires surgical treatment.
Main Diagnostic Differences Between
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Main Diagnostic Differences Between
Peri-implant Mucositis And Peri-
implantitis
Clinical parameter Peri-implant mucositis Peri-implantitis
Increased probing depth +/- +
BOP + +
Suppuration +/- +
Mobility - +/-
Radiographic bone loss - +
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(a)Peri-implant mucositis presenting with
changes in color, form, and texture
(b)Peri-implant mucositis presentsradiographically with no change in crestal
bone
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(a) Peri-implantitis presenting withchanges in color, form, texture, and
associated bone loss resulting inincreased probing depth
(b) Peri implantitis radiographicallydemonstrates crestal bone resorption
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Saucer shaped destruction of the crestal bone or wedge-shaped
defects along the implant.
Bone destruction may proceed without any notable signs of
implant mobility until osseointegration is completely lost.
Vertical bone destruction is associated with the formation of a
peri-implant pocket.
Bleeding after gentle probing with a blunt instrument
There may be suppuration from the pocket.
Tissues may or may not be swollen.
Hyperplasia is frequently seen
Pain is not a typical feature of peri-implantitis.
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MICROBIOLOGY OF PERI-
IMPLANT AREA
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INITIAL COLONIZATION
The microflora associated with stable osseointegrated implantsserving successfully as abutments for overdentures wasinvestigated in 18 edentulous patients.
50% FACULTATI VELY ANAEROBIC COCCI
17% FACULTATI VELY ANAEROBIC RODS7% GRAM NEGATIVE ANAEROBIC RODS
9% F.nucleatum, P.intermedia
Porphyromonas gingivalis and Spir ochetes not found
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PARTIALLY EDENTULOUS RIDGES
Higher percentages of black pigmenting Gram negativeanaerobes and wet spreaders (Capnocytophaga)
MICROBIAL STATUS OF THE REMAINING TEETH
INFLUENCES THE FATE OF NEWLY INCORPORATED
IMPLANTS
Thus the teeth microbiota are the primary source of putative
pathogens.
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MICROBIOLOGY OF DISEASED IMPLANTS
Microbiologyplays important role in etiology of peri-
implantitis
The main cause of peri- implantitis is dental plaque(MeffertR.M.)
Aggretebacter actinomycetemcomitans
Porphyromonas gingivalisBacteroides forsythus
Fusobacterium nucleatum
Campylobacter
Peptostreptococcus micros
Prevotella intermedia
( Tanner A et al , 1997)
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From an experimental study it was reported that: For teeth, 3 weeks to 3 months of
undisturbed plaque accumulation resulted in no further extension of the
inflammatory lesion. However, for implants, under identical experimental
conditions, a further spread in apical direction of the inflammatory cell infiltratewas consistently observed.
This implies that the defense mechanism of the gingiva may be more effective
than that of the peri-implant mucosa in preventing further apical propagation
of the pocket microbiota.
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