Jan Lindhe. Clinical Periodontology

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IMPLANTS USED FOR ANCHORAGE IN ORTHODONTIC THERAPY • 1007

bone labeling fluorochromes documented that bone

apposition took place in the orthodontic loading pe-

riod, as bone markers were administered exclusively

in that period. These results suggest that long-term

orthodontic loading may induce endosseous and even

marginal hard tissue apposition. The latter was also

observed by Majzoub et al. (1999) at the pressure

surfaces of orthodontically loaded osseointegrated

short implants in a short-term trial (8 weeks of con-

tinuous horizontal loading with around 1.5 N). So far,

no negative effects of orthodontic loading on the peri-

implant bone of osseointegrated prosthetic implants

are known.

Indications for orthodontic-prosthetic

implant anchorage

Orthodontic-prosthetic implant anchorage may be in-

dicated in the partially edentulous patient with, for

example:

• malpositioned anterior teeth and either unilateral

or bilateral free-end situations, or

• malpositioned anterior or posterior teeth in associa-

tion with edentulous spaces (gaps of two or more

missing teeth), most frequently in the posterior

mandible or maxilla.

Fig. 43-2 gives an example of how prosthetic implants

may be used for orthodontic anchorage purposes be-

fore serving as abutments for a fixed oral rehabilita-

tion.

Age and orthodontic-prosthetic implant anchorage

Implants should not be inserted into the alveolar bone

before the completion of growth, because they impair

the development of the surrounding bone and even

that of adjacent teeth (Odman et al. 1991, Thilander et

al. 1994). In clinical terms, early implant placement

will lead to infraocclusion of the implant and adjacent

teeth with development of an open bite.

ORTHODONTIC IMPLANT

ANCHORAGE

(OIA)

With respect to the insertion site, implant dimension,

biomechanical type of implant anchorage and dura-

tion of use, there are fundamental differences between

OPIA and exclusively OIA.

Insertion sites

Since regular orthodontic patients have a full denti-

tion or extraction sites to be closed, no edentulous

alveolar bone section is available for insertion of a

prosthetic implant. Therefore, orthodontic implant

anchors have to be inserted into other topographical

regions.

The following insertion sites have been described:

• the interradicular septum (e.g. Bousquet et al.

1996, Kanomi 1997)

• the supra-apical and infra-zygomatical area (e.g.

Kanomi 1997, Costa et al. 1998)

• the retromolar area in the mandible (Roberts et al.

1990b, Higuchi & Slack 1991)

• the median or paramedian anterior palate (Triaca et

al. 1992, Block & Hoffman 1995, Hoffman 1995,

Glatzmaier et al. 1996, Wehrbein et al. 1996, 1999b)

Fig. 43-3 presents some insertion sites of orthodontic

implant anchors in patients and a histologic section of

the median and paramedian region of the anterior part

of the palate.

Implant designs and dimensions

As the insertion sites listed above have significantly

less vertical or horizontal supporting bone than the

alveolar bone, orthodontic implant anchors differ

from prosthetic implants in their design and dimen-

sion. Depending on the insertion site, length-reduced

and/or diameter-reduced implants (e.g. length < 6

mm; diameter < 2 mm) are essential if adjacent ana-

tomical structures are not to be violated.

As diameter-reduced orthodontic implant anchors,

titanium pins (Bousquet et al. 1996) and titanium

mini-screws (Kanomi 1997, Costa et al. 1998) have

been described. Various types of length-reduced or-

thodontic implant anchors have been used:

• titanium flat screw (Triaca et al. 1992)

• resorbable orthodontic implant anchor (Glatzmaier

et al. 1996)

• T-shaped orthodontic implant (Wehrbein et al.

1996, 1999b).

The onplant described by Block and Hoffman (1995)

and by Hoffman (1995) has a special status. In view of

its design principle, this fixture is not an endosseous

implant but a subperiosteal orthodontic anchorage

element.

Aspects relating to the use of orthodontic

implant anchors

In addition to their diameter-reduced and length-re-

duced characteristics, orthodontic anchorage im-

plants should still fulfill the following requirements:

positional stability despite their small dimensions,

minimum strain on the patient, reliable fixation of

orthodontic wires, and anchorage facilities for many

types of tooth movement with one implant.

Ioo8 •

CHAPTER 43

Fig. 43-3. Potential insertion sites for orthodontic /orthopedic implant anchorage. (a) Transseptal (alveolar bone)

area to reinforce the premolars for molar uprighting. (b) Intrazygomatical area to protract the maxilla (radiograph). (

c) Retromolar area to distalize molars (radiograph). (d) Palate to retract and intrude incisors and canines (radio-

graph). (e) Transversal histologic section of the median palate from a 40-year-old male. At the center of the figure,

the suture is seen to be penetrating through the bone from the nasal to the oral surface. In the broad median suture

zone, the bone is relatively dense as compared to the more paramedian regions. Therefore, this is the area of choice

for palatal orthodontic implant placement in adults. Staining: toluidine blue, bar 1000

µ.

Positional stability/small dimension

Despite their small dimensions, orthodontic implant

anchors must maintain positional stability under or-

thodontic loading. As connective tissue encapsulation

would initiate implant dislocation, osseointegration is

vital. Histologic examination of explanted human or-

thodontic implant bone specimens with Orthosystem'

implants (length 4 or 6 mm) inserted palatally, in the

retromolar area of the mandible or the infrazygomatic

region, revealed that osseointegration was maintained

during long-term orthodontic and orthopedic loading

under clinical conditions. The percent-

IMPLANTS USED FOR ANCHORAGE IN ORTHODONTIC THERAPY • 1009

age of implant-to-bone contact at the removed im-

plants in patients was between 34% and 93% with an

average of 75% (Wehrbein et al. 1998, 1999b).

Minimizing strain on patients

Strain on patients

can be

minimized

during

implantation

and/or explantation

by applying an atraumatic surgical

technique (Fig. 43-4). Using a mucosal punch during

insertion or a standardized system-compatible tre-

phine during explantation permits surgical interven-

tions involving both hard and soft tissues to be mini-

mized (Feifel et al. 1998, Bernhard et al. 2000) (Fig.

43-4c). As no findings on "sleeping orthodontic im-

plants" have been published to date, orthodontic an-

chorage implants should be retrieved after use. In a

prospective clinical-radiological study, palatal im-

plant anchorage reinforcement was investigated in

nine adult patients (Wehrbein et al. 1999a), with the

surgeon applying the atraumatic implantation and

explantation procedure specified above. Following

insertion, five of the nine patients reported no postop-

erative pain, while four required 1-2 paracetamol tab-

lets to achieve total postoperative painlessness. All

implants were successfully osseointegrated and had

to be retrieved after orthodontic treatment. Primary

wound healing after retrieval was observed in eight

patients. No postoperative bleeding or other compli-

cations were recorded in these patients. In one of the

nine patients secondary wound healing was ob-

served. Two weeks after local treatment the bone de-

fect had healed.

Attachment of orthodontic wires

Reliable three-dimensional attachment of orthodontic

wires at the orthodontic implant is of major clinical

relevance when the indirect implant anchorage sys-

tem is to be applied (e.g. Wehrbein et al. 1996a,

Wehrbein & Merz 1998a). The underlying principle is

that the orthodontic force systems are applied at an-

chorage teeth which are not to be moved and which

are kept in position through a rigid connection with

the implant (e.g. transpalatal arch or lingual arch).

Three-dimensional attachment of the orthodontic

wires to the implant may be guaranteed by using a

clamping cap or a welding and soldering cap (Figs.

43-4d,g).

In the case of indirect implant anchorage, the con-

necting element between implant and anchorage teeth

is of crucial significance. Besides offering reliable fix-

ing of the connecting element to the implant abut-

ment, the connecting element itself must be suffi-

ciently rigid to prevent deflection. With .032 x .032"

stainless steel TPAs, a mean anchorage loss of about 1

mm was registered in the retraction or in the torquing

of incisors to the buccal teeth (Wehrbein et al. 1999).

Although this anchorage loss was clinically irrelevant,

the use of thicker wires (.051 x .051" = 1.2 x 1.2 mm;

Figs. 43-4d,g) is recommended. Other TPA configura-

tions may further reduce the deformation of the con-

necting element.

DIRECT AND INDIRECT

ORTHODONTIC IMPLANT

ANCHORAGE

Comprehensive anchorage facilities using one single

orthodontic implant anchor for many different types

and directions of active orthodontic tooth movement

during the same treatment can be achieved only by the

indirect implant anchorage method. This is due to the

anchorage teeth being supported by the implant, so

that conventional intra-arch appliance designs allow-

ing many different types and directions of orthodontic

tooth movement may be used. However, a connecting

element (e.g. transpalatal arch) is mandatory if any

benefit is to be derived from these practical advan-

tages.

As the force systems act between the teeth to be

moved and the implant(s) in direct orthodontic im-

plant anchorage, the types and directions of active

tooth movement are somewhat limited with one im-

plant. As the implant position determines the direc-

tion of potential tooth movements, the implants have

sometimes to be positioned in topographical areas

such as the infrazygomatic or infranasal bone (e.g.

Costa et al. 1998). In this context the risk of discomfort

and infection in relation to different topographical

areas and their specific soft tissue covering conditions

have to be considered. Furthermore, the orthodontic

force systems (e.g. coil springs) may run unfavorably

and cause some discomfort. The restricted facilities of

direct implant anchorage may, however, be extended

by using lever arms.

Treatment schedule and anchorage facilities

with palatal orthodontic implant anchors

Interdisciplinary treatment with palatal implant an-

chors using the indirect implant anchorage method

most frequently runs as follows: evaluation of the

vertical bone quantity in the lateral cephalogram

(

Wehrbein et al. 1999a), atraumatic implant insertion,

2-3 months of unloaded implant healing, impression

taking for transpalatal arch construction, integration

of the transpalatal arch, and start of orthodontic treat

ment. Depending on the treatment goal and schedule,

different transpalatal arches may be necessary during

one course of treatment in one and the same patient.

Implant removal may be carried out during the ortho-

dontic retention period. An overview of the possibili-

ties of preoperative diagnosis and surgical procedures

with three different implant systems used in the palate

was presented by Bernard et al. (2000).

The treatment facilities involved in one single pala-

tal implant anchor using the indirect anchorage

method are relatively comprehensive: preparation of

stationary posterior anchorage unit to retract canines

and incisors or to torque incisors. Using this method,

1010 • CHAPTER 43

Fig. 43-4. Young woman with "impaired smile" and too much tooth display. Clinical findings: Class II of

/4 premo-

lar width on the right side, nearly Class I on the left side; deep bite, retroinclined upper and lower incisors with up-

per and lower crowding and midline deviation (a). Treatment goal: extraction of tooth 15, midline correction in the

maxilla (to the right), leveling, space closure and deep bite correction through pure incisor intrusion. Situation di-

rectly after atraumatic implant insertion using a punch for soft tissue removal (b,c). Three-month implant healing

period, insertion of a unilateral palatal bar, and at start of orthodontic treatment (d). The TPA is three-dimension-

ally fixed with a clamping cap to the implant abutment; reduced orthodontic appliance in this treatment phase due

to a stable osseous-periodontal anchorage unit (implant supported 16). Conventional orthodontics would require

bonding of a large part of the dentition for anchorage purposes and wearing of Class II elastics or headgear to pre-

vent mesial migration of 16. Cephalogram (e) after midline correction, deep bite treatment and superimposed trac-

ings (f) from before orthodontic treatment, and after midline correction as well as deep bite treatment: significant in-

cisor root torque and intrusion without extrusion of posterior teeth, normal overbite. Modified TPA now for prepa-

ration of an anterior implant-supported anchorage unit for residual space closure from distal (g). The TPA is

welded to the abutment cap and bonded at the premolars. Occlusal view (h) and cephalogram (i) three months af-

ter implant removal: healed palatal mucosa in former insertion area; radiologically, the former osseous explanta-

tion cavity seems to be filled with bone (i). Frontal view after implant anchored orthodontic treatment (j): compare to

initial finding (a). Differential (alternated) anchorage support of different teeth or tooth groups during different

treatment phases by only one implant through TPA modification offers maximum treatment control and predict-

ability without compliance.

IMPLANTS USED FOR ANCHORAGE IN ORTHODONTIC THERAPY • 1011

Fig. 43-4f-j.

deep bite can be corrected with incisor intrusion alone,

with no posterior tooth extrusion. Furthermore,

preparation of a stationary anterior anchorage unit

can be used to mesialize, distalize or intrude posterior

teeth (Fig. 43-4).

Periodontal considerations for orthodontic implant

anchorage

It is clear that implant supported teeth receive con-

tinuous osseous reinforcement, with unfavorable jig-

gling forces on anchor teeth — as might be found with

headgear or temporarily worn Class II elastics — being

reduced or even avoided. This may play a more deci-

sive role in cases where the periodontal anchorage

potential is compromised (e.g. reduced attachment

level due to periodontitis or other problems impairing

the anchorage capacity of the remaining teeth). When

direct orthodontic implant anchorage is used, no teeth

are integrated into the anchorage unit.

Palatal implants in adolescents

The use of palatal implants in adult patients has been

reported by various authors (e.g. Triaca et al. 1992,

Wehrbein et al. 1996, 1999b, Bernard et al. 2000). When

this technology is to be applied in adolescents, inter-

actions with residual growth changes have to be re-

duced to a clinically irrelevant level. That may well be

the case when the fully erupted teeth include the

second molars. Furthermore, the implant should not

be placed in the median but in the paramedian (

parasutural) area of the anterior palate to prevent

interactions with potential residual intermaxillary su-

ture growth changes (transversal plane).

The most important maxillary growth changes,

however, occur in the vertical plane through displace-

ment and cortical drift. In specific areas, different

mean amounts of growth from the age of four to

adulthood were measured (Bjork 1977): sutural low-

ering of the maxilla (displacement) by 11.2 mm, appo-

1012 • CHAPTER 43

sition at the orbit floor (drift) 6.4 mm, apposition at the

infrazygomatic crest (displacement) 2.5 mm, resorp-

tive lowering of the nasal floor (drift) 4.6 mm, and

appositional increase of alveolar bone height 14.6 mm.

If it is speculated that one third of these growth

changes has still to be realized from the age of 12 to

adulthood, then that implies a residual vertical

growth of about 1.5 mm in the palate and of about 5

mm in the alveolar bone (both by drift). As an osseoin

tegrated implant is not involved in the growth of its

site because it behaves like an ankylosed tooth, a

palatal implant would remain 1.5 mm behind its sur

rounding bone whereas an alveolar bone implant

would produce an infraocclusion of 5 mm in the same

time unit. Furthermore the time factor has to be con

sidered. In comparison with an alveolar bone pros-

thetic implant, a palatal orthodontic implant remains

in situ

for only 1-2 years. Thus, potential growth im-

pairment is likely to be limited to values of less than 1

mm.

First experiences with palatal implants in growing

individuals aged 12 years or more, using the parame

dian orthodontic implant placement technique, pro-

duced the following clinical and radiologic observa-

tions: implant stability, no clinically detectable growth

impairment in the implant-surrounding bone of the

palate and no tendency to implant submersion, but

migration of the palatal complex with its implant to a

more forward and downward position, probably due

to the growth of more cranially located bony struc-

tures leading to displacement and drift.

At present, however, the use of palatal orthodontic

implants in clinical practice should be confined to

patients whose growth is completed or approaching

completion, since no long-term results are available,

e.g. effects on residual growth after implant removal.

Advantages

In addition to dispensing with compliance dependent

intraoral and extraoral anchorage aids, some other

advantages have to be discussed. If an anchorage unit

is stable, its behavior can be controlled by the clinician

and is no longer left to chance, so that the orthodontic

treatment outcome is more predictable. Furthermore,

positionally stable anchorage unit allows en masse

retraction to be performed without the risk of clini-

cally significant anchorage loss. This may reduce the

treatment time as compared with fractional retraction

of canines and incisors. In some situations the ortho-

dontic appliances can be reduced temporarily or for

the whole treatment, enhancing the comfort of the

orthodontic appliance as well as its esthetic appear-

ance. Finally, a combination of palatal implant and

lingual appliance conceals both the anchorage and the

appliance.

Disadvantages

If they are to benefit from the above advantages, pa-

tients have to undergo two minor surgical procedures.

The main risks of any orthodontic implant anchorage

treatment are loss of the implant and peri-implant

infection. The success rate of palatal orthodontic an-

chorage implants was investigated in a clinical-radio-

logical study (Wehrbein et al. 2001). Each of the 22

adult patients enrolled in the study received one Or-

thosystem

implant (length 4 or 6 mm) in the median

palate. Insertion was done by two experienced sur-

geons. In all patients primary stability was recorded.

In 2 of the 22 patients mobility and subdued percus-

sion sound were found at the 1-month control session.

In the remaining 20 patients the fixtures underwent

osseointegration and were used as orthodontic an-

chors. In the orthodontic loading period no loosening

or positional changes of the implants were recorded.

The success rate after the first insertion was thus 91%.

In the two patients with implant loss, reinsertion was

performed after a 2-month healing period, after which

the implants osseointegrated and were positionally

stable during the orthodontic treatment period.

Conclusions

Osseointegrated implants are a tool providing abso-

lutely stable osseous orthodontic anchorage and are

thus superior to any kind of tooth-borne anchorage

facilities. Indications for orthodontic-prosthetic or

purely orthodontic implant anchorage include: inade-

quate periodontal anchorage facilities, non-accep-

tance of extraoral anchorage aids, prevention of po-

tential side effects of conventional intraoral anchorage

aids, and esthetic aspects. Preconditions for a high

acceptance of this promising, relatively new technol-

ogy are: simplicity in use, minimum strain on patients,

high success rate and reliability of the respective

method under clinical conditions. This may be real-

ized by a close interdisciplinary co-operation, and

profound know-how in the fields of both implantol-

ogy and orthodontics.

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CHAPTER 44

Mucositis and Peri-implantitis

TORD BERGLUNDH, JAN LINDHE, NIKLAUS P. LANG AND LISA MAYFIELD

Treatment of peri-implant tissue

inflammation

Resolution of the inflammatory lesion

Re-osseointegration

Microbial aspects associated with implants

in humans

Microbial colonization

Excessive load

Infection

Peri-implant mucositis

Peri-implantitis

Failure sometimes happens in implant therapy. Such

failures occur due to complications that take place

either early following the installation of the implant

device or later when the implant supported recon-

struction has been in function for various periods of

time.

Early implant failures

are the result of events that

may jeopardize or prevent osseointegration from oc-

curring and include among others:

Improper preparation of the recipient site which

results in undue hard tissue damage such as ne-

crosis of the bone

Bacterial contamination and extensive inflamma-

tion of the wound that may delay healing of the soft

and hard tissues

Improper mechanical stability of the implant fol-

lowing its insertion

Premature loading of the implant.

Late failures

occur in situations during which osseoin

tegration of a previously stable and properly function-

ing implant is lost. It was suggested (Proceedings of

the 3rd European Workshop on Periodontology; Flem

mig & Renvert (1999)) that such late failures are often

the result of excessive load and/or infection.

EXCESSIVE LOAD

Forces applied to the restoration placed on implants

are, at least in part, transferred to the bone (Skalak

1985). It is realized that although "excessive load" may

be difficult to define and may vary from one subject

and site to the next, factors such as occlusal force

(

trauma from occlusion) in relation to (1) size of im-

plant, (2) surface features of implant, and (3) quality

of the host bone, must obviously be considered. Clini-

cal studies have indicated that peri-implant bone loss

may be associated with load (e.g. Lindquist et al. 1988,

Sanz et al. 1991, Quirynen et al. 1992, Rangert et al.

1995). A few experimental studies have indicated that

relationship may exist between load and bone loss

(e.

g. Hoshaw et al. 1994, Isidor 1997, Miyata et al.

2000)

. But other investigators have been unable to

confirm

this association (e.g. Asikainen et al. 1997, Wehrbein

et al. 1997, Hiirzeler at al. 1998, Gotfredsen

et al. 2001,

2002).

The peri-implant tissue response to excessive load

released during function is thus not fully understood

but may involve the bone tissue around the entire

implant. The tissue in the zone of osseointegration is,

due to the load, broken down and

implant mobility

becomes the cardinal feature.

INFECTION

The host response to biofilm formation on the implant

includes a series of inflammatory reactions which

initially occur in the soft tissue but which may sub-

sequently progress and lead to loss of supporting

bone. The tissue destruction in the bone compartment

starts in the "marginal", i.e. neck region, of the implant

and crater-like bone defects develop and become vis-

ible in the radiograph. Implant stability may be main-

tained for long periods of time.

Peri-implant mucositis

is a term used to describe

MUCOSITIS AND PERI-IMPLANTITIS • 1015

Fig. 44-1. A clinical view illustrating 3 weeks (3 W) and 3 months (3 M) of undisturbed plaque formation on the im-

plants and the teeth of a beagle dog.

reversible inflammatory reactions in the mucosa adja

cent to an implant.

Peri-implantitis is

defined as an

inflammatory process that (1) affects the tissues

around an osseointegrated implant in function, and (

2) results in loss of supporting bone (Albrektsson &

Isidor 1994).

The prevalence of

peri-implantitis

in man is difficult

to estimate but may vary between 2% and 10% of all

implants inserted (Esposito et al. 1998, Mombelli &

Lang 1998). Clinical studies have documented that

peri-implantitis

may lead to implant failure and loss.

Thus findings from, for example, a multicenter study

by van Steenberge et al. (1993) including 159 patients

and 558 implants (Branemark system revealed that

during the second and third year (1) as many as 2% of

the remaining implants failed, and (2) failure occurred

more frequently in subjects with a high degree of

plaque accumulation. Weyant & Burt (1993) and Wey

ant (1994) reported data from 598 subjects and 2098

implants that were monitored during a 5-year period.

The authors found that close to 4% of the implants

failed and that risk factors for implant loss included

plaque, smoking and local factors. Bragger et al. (2001)

described biological and technical complications that

may occur with fixed partial dentures placed on tooth

abutments or implant abutments or on a combination

of teeth and implants. This study included 85 patients

and measurements were made on 142 teeth and 103

implants that supported a total of 116 fixed partial

dentures. During the course of a follow-up period of

about 5 years, ten (about 9%) implant sites (peri-im-

plantitis) and six (about 4%) tooth sites (periodontitis)

exhibited signs of advanced inflammation and tissue

breakdown, i.e. bleeding on probing, suppuration and

increased probing depth. Findings made in a 5-year

retrospective study (Hardt et al. 2002) further demon

strated that implants placed in "periodontitis-suscep-

tible" patients exhibited a higher failure rate (8%) than

similar type implants that were placed in periodon-

tally healthy subjects (3.3%). In this study it was also

pointed out that the amount of bone loss that occurred

around implants during the 5 years correlated well

with the amount of bone loss that had occurred at the

remaining teeth at the time of implant installation. The

observations by Hardt et al. (2002) are important be-

cause they do indicate that similar mechanisms may

be involved in periodontal and peri-implant tissue

breakdown.

PERI-IMPLANT MUCOSITIS

The response of the gingiva and the peri-implant mu-

cosa to early and more long-standing periods of

plaque formation was analyzed both in experiments

in animals and in studies in man.

In experiments in the dog, Berglundh et al. (1992)

and Ericsson et al. (1992) compared the reaction of the

gingiva and the peri-implant mucosa to 3 weeks and

3 months of

de novo

plaque formation. The mandibular

premolars in one side of the mandible were extracted,

leaving the premolars on the contralateral side as

controls. After 3 months of healing, fixtures (Brane-

mark® system) were inserted and, another 3 months

later, abutment connection was performed in a sec-

ond-stage procedure. The animals were placed in a

careful plaque control program to allow for ideal heal

ing of the mucosa at the implants and to prevent

gingivitis from occurring in the tooth segments of the

dentition. Four months after abutment connection, the

dogs were examined clinically and samples from the

minute plaques that were present on the marginal

portion of the implant and tooth surfaces were har-

vested. The plaque control program was terminated

and the animals given a soft diet, which allowed gross

plaque formation. Re-examinations, including clinical

assessment (Fig. 44-1) and sampling of plaque bacteria

from teeth and implants as well as biopsy, were per-

formed after 3 weeks and 3 months.

During the course of the study, it was observed that

similar amounts of plaque formed on the tooth and

implant segments of the dog dentition. The composi-

tion of the two developing plaques was also similar. It

was therefore concluded that early microbial coloni-

1o16

•

CHAPTER 44

Fig. 44-2. Microphotographs illus

trating the establishment of in-

flammatory cell infiltrates (ICT) in

the peri-implant mucosa (a) and

the gingiva (b) (3W = 3 weeks; 3M

= 3 months). Note, in the micro-

photographs representing 3

months, the infiltrate in the peri-

implant mucosa extends much

deeper into the tissue than is the

case in the gingiva.

zation on titanium implants followed the same pat-

terns as that on teeth (Leonhardt et al. 1992).

Both the gingiva and the peri-implant mucosa re-

sponded to this microbial colonization with the estab-

lishment of overt inflammatory lesions, i.e. infiltrates

of leukocytes in the connective tissue. The lesions in

the gingiva and in the peri-implant mucosa were in

this early phase (up to 3 weeks) matched both with

respect to size and location. Hence, both lesions were

consistently found in the "knee" between the kerati-

nized oral epithelium and the junctional or barrier

epithelium (Fig. 44-2a,b).

Similar observations were made by Pontoriero et al.

(1994) in a clinical study in human volunteers. Twenty

partially edentulous subjects who had been restored

with implants in one or several segments of the den-

tition were asked to participate. After a baseline ex-

amination they refrained from all oral hygiene meas-

ures for 3 weeks. It was observed that plaque forma-

tion (amount and composition) and the soft tissue

response to plaque, i.e. inflammation, developed in a

similar manner in the tooth and implant segments.

Zitzmann et al. (2001) examined the tissue reaction

de novo

plaque formation at implants and teeth in

humans using immunohistochemical techniques.

Twelve subjects with healthy periodontal and peri-im-

plant conditions were asked to refrain from tooth/im-

plant cleaning for a period of 3 weeks. Soft tissue

biopsies were sampled at baseline and on day 21. It

was demonstrated that plaque formation was associ-

ated with clinical signs of soft tissue inflammation.

The lesions in the gingival and in the peri-implant

mucosa increased in size in a similar manner during

the 3 weeks of experiment.

In other words, in a given

individual, the early soft tissue response to plaque seems to

be similar in the mucosa at implants and in the gingiva of

the teeth.

With increasing duration of plaque build-up (3

months) in the dog model, the lesions in the peri-im-

plant mucosa expanded more and progressed further

"apically" than was the case in the gingiva (Fig. 44-

2a,b). The

composition

of the lesions in the two tissues,

the gingiva and the peri-implant mucosa, differed

mainly with respect to their content of fibroblasts.

Thus, the lesion in the peri-implant mucosa was found

to have a much smaller number of fibroblasts than the

corresponding compartment in the gingiva.

It may be anticipated that in an inflammatory tissue

lesion of long standing, periods of breakdown and

periods of repair interchange. The gingival lesion in

the dog model retained its size unchanged between 3

weeks and 3 months of plaque exposure. It is sug-

gested, therefore, that in the gingival lesion, the

amount of tissue destruction that occurred during a

breakdown phase was more or less fully compensated

by tissue build-up occurring during a subsequent

phase of repair. In the lesion within the peri-implant

mucosa, the tissue breakdown that occurred during

the 3 months of plaque exposure was not fully recov

ered by reparative events. The small number of fi-

broblasts present in this particular lesion may simply

have been unable to produce enough collagen and

matrix during the reparative phase. This reduced

build-up resulted in an additional propagation and

spread of the inflammatory cell infiltrate in the peri-

implant mucosa.

Conclusion

The peri-implant mucosa seems less effective than the

gingiva in encapsulating plaque-associated lesions.

PERI-IMPLANTITIS

In order to study the ability of the peri-implant mu-

cosa to respond to more longstanding plaque expo-

sure and to manage the associated inflammatory le-

sions, an experimental periodontitis/peri-implantitis

model was developed in the dog (Lindhe et al. 1992)