Soft Tissues Around Dental Implants

7/13/2019 Soft Tissues Around Dental Implants

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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

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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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Soft Tissues Around Dental Implants

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