Diagnosis and Treatment of Peri-Implant Disease

DIAGNOSIS AND TREATMENT PLAN OF PERI-
IMPLANT DISEASE
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

INTRODUCTION
Artificial replacements for missing teeth during the early 15-
16th century. A fine dark stone shaped tooth was found in a
Mayan skull 600A.D. Later on the development of stainless steel,
vitallium titanium implants brought oral implantology to the
forefront. All play essential roles in the placement and
maintenance of oral implants ,However the principles of
periodontal therapy play an important role in influencing the
final success of treatment.

Pathologic alterations in the tissues that contact a dental
implant fall under the definition of peri implant pathology.
The development of inflammatory process that is limited to
the peri-implant soft tissue can be defined as peri-implant
mucositis. The progressive peri-implant bone loss occupied
by inflammatory pathology in the soft tissue is refered to as
peri-implantitis.

Peri-implant tissue breakdown can be the result of microbial
action as well as of biomechanical and occlusal overload.
The long-term goal of the treatment of per-implant
breakdown is to arrest the progression of the disease and to
achieve a maintainable site for the patient. Peri-implant bony
defects around functioning implants can be treated with
either non-surgical or surgical.

NORMAL PERI-IMPLANT MUCOSA
The mucosal tissues around intraosseous implants form a
tightly adherent band consisting of a dense collagenous lamina
propria covered by stratified squamous keratinizing epithelium. The
implant-epithelium junction is analogous to the junctional epithelium
around natural teeth, in that the epithelial cells attach to the titanium
implant by means of hemidesmosomes and a basal lamina.

The Histologic examination of the sections revealed that the two soft
tissues units, the gingiva and the peri-implant mucosa, have several
features in common. The oral epithelium of the gingiva is well keratinized
and is continuous with a smooth junctional epithelium that faces the
crown of the tooth and ends at the cemento-enamel junction(arrow). The
supra-alveolar connective tissue is about 1mm(arrow) high and the
periodontal ligament about 0.2-0.3mm wide. The principal fibers extend
from the root cementum in a fan-shaped pattern into the soft and hard
tissues of the marginal periodontium.

The outer surface of the peri-implant mucosa is also covered by a well –
keratinized oral epithelium, which in the marginal border (arrow) connects
with a barrier epithelium is facing the abutment part of the implant. The
barrier epithelium is only a few cell layers thick and terminates about 2 mm
apical of the soft tissue margin. In a zone that is about 1-1.5mm high, between
the apical level of the barrier epithelium and the alveolar bone crest, the
connective tissue appears to be in direct contact with the TiO2 layer of the
implant. The collagen fibres originates from the periosteum of the bone crest
and extend towards the margin of the soft tissue in directions parallel to the
surface of the abutment.
Microphotograph of a
Peri –Implant mucosa

Collagen fibres are nonattached and run parallel to the implant
surface, woing to the lack of cementum. This is an important
difference between periimplant and periodontal tissues.
However some reports have suggested that microscope
irregularities and porosities like those found on plasma
sprayed titanium surfaces may favor the appearance of fibres
oriented perpendicularly to the implant surface.

Peri-implant mucositis is a term used to describe
reversible inflammatory reactions in the mucosa adjacent to
an implant. In the lesion within the peri-implant mucosa, the
tissue breakdown that occurred during the 3 months of plaque
exposure was not fully recovered by reparative events. The
small number of fibroblasts 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.

Peri-implantitis defined as an inflammatory process that affects the
tissues around an osseointegrated implant in function, and tissue in loss
of supporting bone. Berglundh et al (2003) found that mucosa contained
large lesions with numerous plasma cells, lymphocytes and
macrophages. It was further demonstrated that the inflammatory cell
infiltrate consistently extended to an area apical of the pocket epithelium
and that the apical part of the soft lesion frequently reached the bone
tissue. He also observed that numerous PMN cells were present in the
human peri-implantitis lesion.

PERIODONTAL TISSUES VERSUS PERI-IMPLANT TISSUES
The soft and hard tissues surrounding an
osseointegrated implant show some similarities with the
periodontium in the natural dentition .
The absence of a periodontal ligament in the peri-
implant region.
The orientation of the collagen fibres of the soft tissues
around the implants, which are non-attached and
parallel to the implant surface, while the gingival fibres
around teeth are perpendicular and attached to the root
cementum.

The response to a pathological insult. the coronal portion of the
implant and/or abutment is surrounded by a thin layer of
collagen fibres arranged circumferentially and with minimal
vascular structures. This low vascularity soft tissue band may
affect the defense mechanisms around an implant as compared
to those seen in tissues around teeth with a periodontal
ligament. If plaque accumulates on the implant surface, the
subepithial connective tissue is infiltrated by large numbers of
inflammatory cells and the layer of epithelial cells appears
ulcerated and loosely adherent..

A recent report comparing plaque-associated lesions around
teeth and around implants showed that lesions became more
pronounced and occupied a larger volume of the connective
tissue around implants. If the plaque front continued to
migrate apically, the clinical and radiographic signs of tissue
destruction were seen around both implants and teeth
however, the size of the soft tissue inflammatory lesion was
larger around implants.

Smith and Zarb proposed the following criteria for implant
success.
1.The individual unattached implant is immobile when
tested clinically.
2. No evidence of peri-implant radiolucency is represent as
assessed on an undistorted radiograph.
3. Mean vertical bone loss is less than 0.2mm annually after
the first year of function or service.

4. Three is no persistence pain, discomfort or infection
attributable to the implant.
5. Implant design does not preclude placement of a crown
or prosthesis with an appearance that is satisfactory to
the patient and dentist.
6. There is an 85% success rate at the end of a 5 year post
restorative period, with an 80% success rate at the end of
10 years postrestorative or function.

MICROBIOLOGIC FINDINGS IN PERIIMPLANTITIS:-
Bacterial flora is associated with periodontitis and
periimplantitis. It has shown that pathogens associated with
periodontal disease are a gram – negative, black – pigmented
anaerobic flora. Failing implants were clinically characterized
by increased mobility and periimplant radiolucency and
probing depths greater than 6mm where as associated with
periodontal pathogenesis, including Actinobacillus
actinomycetemcomitans, prevotella intermedia.

Becker et al has been demonstrated that the bacteria found in
the implant crevice in the successful implant case are basically
the same flora as found in the natural tooth crevice/sulcus in a
state of health.
Implants in partially edentulous cases / patients appear to
be at greater risk for periimplantitis than implants in
completely or fully edentulous cases/ patients. There are few
qualitative differences in the microflora surrounding implants
and teeth in partially edentulous patients.

However, there are marked quantitative decreases in the
number of periodontal pathogens around implants in
completely edentulous patients. It is possible that the
natural teeth may serve as a reservoir for periodontal
pathogens from which they may colonize implants in the
same mouth.

Rosenberg et al. demonstrated that, in failing implants
with a primarily infectious etiology, 42% of the sub
gingival flora consists of Peptostreptococcus spp.,
Fusobacterium spp., and enteric gram – negative rods.
Failing implants with a traumatic etiology have a
microflora more consistent with gingival health and
composed primarily of streptococci.

Periodontitis is the same as periimplanttitis is the study by
Dharmer et al that shows that
1.There is higher enzymatic activity in teeth/implants with 3
to 4mm pocket depth than in those with 1 to 2mm pocket
depth.
2. There are more motile rods in implants/teeth with 3 to
4mm pockets compared with those with 1 to 2mm
pockets.
3.There are no spirochets around implants in the totally
edentulous patients as compared with partially
edentulous patients.

4. The enzymatic tests revealed that the microflora around
BRanemark implants is similar to that around natural
teeth.
5. Cervicular fluid from partially edentulous cases in both
healthy and inflamed sites, found no differences in
periimplant crevicular fluid (PICF) and gingival crevicular
fluid (GCF) in healthy Vs. inflamed sites, and they
concluded that the inflammatory and immune responses
were similar around tooth and implant.

RETROGRADE PERIIMPLANTITIS:-
A condition known as retrograde periimplantitis may also
be associated with implant failure. Retrograde implant failure
may be due to bone micro fractures caused by premature
implant loading or overloading, other trauma, or occlusal
factors. Implant failures from retrograde periimplantitis are
characterized by periapical radiographic bone loss without, at
least initially, gingival inflammation. The distinction between
implant failure caused by infection with periodontal pathogens
(infective failure) and implant failure associated with
retrograde periimplantitis (traumatic failure) is also reflected
in the microflora.

ETIOLOGIC FACTORS
Two primary etiologic factors are acknowledged today as
causative in peri-implant marginal bone loss:
Bacterial infection
Biomechanical overload

Biomechanical Overload
Bone loss at the coronal aspect of implants can result form
biomechanical overloading and the resultant microfractures at
the coronal aspect of the implant-bone interface. The loss of
osseointegration in this region results in apical down growth of
epithelium and connective tissue. The speed and degree of loss
of implant-bone contact depends upon the frequency and
magnitude of the occlusal loading as well as superimposed
bactrerial invasion.

While it should be obvious that occlusal loading alone cannot
cause progressive bone resorption, in the presence of
marginal infection is certainly an important etiologic factor,
similar to the situation with natural teeth. The role of over
loading is likely to increase in four clinical situations:
1.The implant is placed in poor quality bone.
2.The implant’s position or the total amount of implants placed
does not favor ideal load transmisson over the implant surface.

3.The patient has a pattern of heavy occlusal function
associated with parafunction.
4.The prosthetic superstructure does not fit the implants
precisely.
other etiologic factors such as traumatic surgical
techniques, smoking, inadequate amount of host bone
resulting in an exposed implant surface at the time of
placement and a compromised host response can act as co-
factors in the development of periimplant disease.

BACTERIAL INFECTIONS
Most authors have assumed that peri-implant diseases
(mucositis, peri-implantitis) are comparable to periodontal
diseases in that they are primarily plaque-induced. If plaque
accumulates on the implant surface, the subepithelial
connective tissue becomes infiltrated by large number
inflammatory cells and the epithelium appears ulcerated and
loosely adherent. When the plaque front continues to migrated
apically, the clinical and radiographic signs of tissue
destruction are seen around both implants and teeth. However
the size of the soft tissue inflammatory lesion and the bone
loss is larger around Implants.

In addition, the implant lesions extend into the
supracrestal connective tissue and approximate/populate the
bone marrow. While the lesions associated with teeth do not.
These studies suggest that plaque-associated soft tissue
inflammation around implants may have more serious
implications than marginal inflammation around an implant
might be the low-vascularity soft tissue band and the
difference in collagen/fibroblast ratio of gingival tissue, which
affects the defense mechanisms around teeth with a
periodontal ligament.

In addition, different implant surface characteristics
influence the amount of periimplant tissue breakdown and
inflammation; specially, HA-coated implants seem to have
increased bone loss when compared with titanium implants.
Bacterial plaque removed from implant surfaces is very
similar to
that removed from natural teeth in both healthy and diseased
states.
Peri-implant inflammation can be successfully treated by
plaque
control and effective oral hygiene.www.indiandentalacademy.com

Additional Possible Etiologic and Modifying Factors
In addition to bacterial infection and excessive
biomechanical loading, other etiologic and modifying cofactors
have been considered as potential initiators of peri-implant
disease.
Implant Shape and Implant Surface
Peri-implant soft tissue attachment

IMPLANT SHAPE AND IMPLANT SURFACE
Over the long term, users of the branemark system have
generally observed peri-implant bone loss of approximately
1.5mm during the first year implant insertion and 0.1 mm per
year in subsequent years. Bone resorption was reported to be
exclusively horizontal in nature: vertical defects were not
observed. (Adell et al. 1986, Alberktson et al. 1988).

with other systems (eg : IMZ, care vent) higher bone
resorption rates and occasionally vertical defect have been
reported very little information is available regarding whether
the implant design (cylindrical ,screw type) implant surface
morphology (e.g. highly polished cervical region) the
technique of surgical placement, or other factors may be
responsible for the various peri-implant reactions.

Peri-implant soft tissue attachment
Several authors have proposed that the maintenance of
healthy peri-implant conditions requires a collar of attached
gingival around the implant neck. Furthermore, clinical and
animal experimental research has demonstrated that if oral
hygiene is sufficient, healthy peri-implant conditions can be
maintained even if mobile oral mucosa surrounds the implants.
(Krekeler et al. 1985, Adell et al. 1986, van Steenberghe 1988,
Strub et al. 1991). Zone of attached gingiva as a means to
prevent peri-implant disease (mucositis, peri-implantitis) is not
necessary; this is comparable to the situation with natural teeth
(Wennstrom et al. 1981). www.indiandentalacademy.com

Nevertheless, if recurrent inflammation persists around
implant surrounded by mobile mucosa, it may be prudent to
surgically create a peri-implant zone of attached gingiva, which
will also simplify implant hygiene. In the visible, anterior
segments of the mouth, the presence of keratinized gingival
may be necessary for esthetic reasons (Langer et all 1980).

CLASSIFICATION
Classification – Peri-implantitis
Peri-implantitis - Class 1

Peri-implantitis - Class 1
Slight horizontal bone loss with minimal peri-implant
defects

Peri-implantitis class 2
Moderate horizontal bone loss with isolated vertical defects.

Moderate to advanced horizontal bone loss with broad, circular
bony defects.

Advanced horizontal bone loss with broad, circumferential
vertical defects, as well as loss of the oral and/or vestibular
bony wall.

DIAGNOSIS OF IMPLANT TISSUE BREAKDOWN:-
To diagnose a compromised implant site, soft tissue
measurements using manual or automated probes have been
suggested. A probe with a tip diameter of 0.5mm was inserted
into the buccal “pocket” using a standardized force of 0.5 N.
Probing depth was markedly deeper than at the tooth site,
namely 2.0mm. The tip of the probe was consistetly positioned
deep in the connective tissue/abutment interface and apical of
the barrier epithelium. The distance between the probe tip and
the bone crest at the tooth sites was about 1.2mm. The
corresponding distance at the implant site was 0.2mm

This means that at the implant sites, the probe almost made contact with
the bone crest. From these observations, it may be concluded that the
attachment between the implant surface and the mucosa was weaker than
the corresponding attachment between the tooth and gingiva, and care
must be exercised when data from probing depth measurements from
tooth and implant sites are compared.
if a light probing pressure is applied during probing, the epithelial
attachment of the transmucosal tissue seal will be disrupted but will heal
within 5-7days. (Etter et al 2002) This means that – as is the case in
probing around teeth probing the peri-implant tissue can be performed
without causing permanent damage to the integrity of the transmucosal
attachment.

Although some reports say that probing is contraindicated, careful
monitoring of probing depth and clinical attachment level over time
seems useful in detecting changes of the peri -implant bone level have
been shown to be useful. Standardized radiography, both with and
without computerized analysis, has been documented in a number of
studies.
suppuration Besides pocket formation and radiographic bone
destruction,, swelling, color changes, and bleeding upon gentle probing
have been documented as signs of peri-implant disease.
Microbial monitoring is useful in evaluating the peri implant health
condition and the microbial composition of a peri–implantitis site. This
information can then potentially be used to determine the etiology of the
breakdown and to select a specific antiobiotic regimen.

MANAGEMENT
Depending on the etiology of the problem, specific treatment is
selected. When biomechanical forces are considered the main
etiologic factors for peri – implant bone loss, treatment is
undertaken into two phases.
The first phase involves an analysis of the fit of the
prothesis, the number and position of the implants, and an
occlusal evaluation. Prosthesis design changes, improvement
of implant number and position, can arrest the progression of
peri – implant tissue breakdown.
To eliminate deep peri – implant soft tissue pockets or to
regenerate bone around the implant, surgical techniques can be
employed in a second phase of treatment. awww.indiandentalacademy.com

Peri- implant disease caused by bacterial infection is also
treated in phases. The first phase controls the acute
bacterial infection and reduces the inflammation present
in the tissues.
The treatment involves mechanical debridement, localized
and/ or systemic antimicrobial therapy and improved oral
hygiene until a healthy peri –implant site is established.
The second phase will involve the surgical procedure.

INITIAL PHASE OF PERIIMPLANTITIS TREATMENT
Occlusal therapy
When excessive forces are considered the main etiologic factor
for periimplant bone loss, treatment involves analysis of the fit
of the prosthesis, the number and position of the implants, and
an occlusal evaluation. Prostheses design changes,
improvement of implant number and position, and occlusal
equilibration can contribute to arrest the progression of
periimplant tissue breakdown

ANTI-INFECTIVE THERAPY
The non surgical treatment of periimplant bacterial
infection involves the local removal of plaque deposits with
plastic instruments and polishing of all accessible surfaces
with pumice; subgingival irrigation of all peri-implant pockets
with 0.12% chlorhexidine; systemic antimicrobial therapy for 10
consecutive days; and improved patient compliance with oral
hygiene until a healthy periimplant site is established

The implant surface is contaminated with soft tissue
cells, bacteria, and bacterial by-products. Bacterial
adherence is enhanced by the micro-irregularities of implant
surfaces, and as long as the contamination is present, wound
healing is compromised. Therefore if regeneration of new
bone and reosseointegration is to occur, the defect must first
be debrided and the contaminated implant surface prepared.
Reosseointegration can be defined as the growth of new
bone in direct contact to the previously contaminated implant
surface without an intervening band of organized connective
tissue.

Acess may be gained via full thickness or split-thickness
periodontal flap reflection. The peri-implant pocket epithelium
and any granulation tissue are removed using conventional
curettes. Care must be taken to avoid damaging or
contaminating implant surface. Subsequently plastic curettes
are used to remove plaque and calculus as thoroughly as
possible from the surface of the implant.
PLASTIC CURETTE

Prophy-Jet Device (30-60 seconds application) are used to clean the
implant surface. The Prophy-Jet Device using sodium hydrocarbonate
with sterile water are indicated (Bass et al. 1992). The high pressure air
powder abrasive, suggest that this instrument removes microbial
deposits completely from titanium implant surfaces. In addition, in vitro
morphologic and statistical comparisons of gingival fibroblast
interactions with titanium surfaces treated with air-powder abrasives
showed these surfaces have no adverse effect on cell adhesion.
Prophy - Jet Device

Consideration should be given to the potential for air-
emphysema when using high-pressure air spray
instrumentation in the surgical site. Therefore, the spray should
never be directed parallel to the implant surface into the
surface, but rather at an angle of atleast 450
.(Brown et al 1992)
PROPHY-JET

The final Step in cleaning the surface of the implant consists of
detoxification using citric acid (pH 1-3) 30 – 60 seconds on a
soaked gauze strip around the implant surface. It has been
shown that the use of citric acid provides the greatest potential
to remove bacteria and endo toxins from the implant surface,
in comparison with other chemical agents. (Zablowsky et al.
1992). Before closing the flap, the entire area is rinsed again
using sterile saline solution.
De-toxification with
Citric Acid

SURGICAL TECHNIQUES FOR TREATMENT OF
PERIIMPlANTITIS
The surgical techniques presently advocated to control
periimplant lesions are modified from techniques used to treat
bone defects around teeth. The type and size of bone defect
has to be identified before deciding on the appropriate
treatment modality. Therefore prob-ing and sounding of the
defects is done using local anes-thesia, and radiographs are
evaluated so that the surgical treatment plan is finalized
immediately prior to begin-ning the procedure. This forms the
basis to determine whether the implant will be removed or a
resective type of surgery or a regenerative procedure will be
used.

The resective therapy is used to reduce pockets, correct
nega-tive osseous architect ure and rough implant surfaces,
and increase the area of keratinized gingiva if needed. The
regenerative therapy is also used to reduce pockets but with
the ultimate goal of regeneration of lost bone tissue. As in the
treatment of certain types of periodontitis, systemic antibiotics
have been advocated as a supportive regimen during the
treatment phase of periimplant dis-ease. This may be
especially important due to the close proximity of the
inflammatory lesion to the im-plant and the bone marrow
.Antibiotics frequently used without sensitivity testing are
doxycycline and metronidazole.

PERI –IMPLANT RESECTIVE THERAPY
The type of osseous defect should be identified before deciding
on the treatment modality. Apically positioned flap techniques
and osseous resective therapy are used to correct horizontal
bone loss and moderate vertical bone defects and reduce
overall pocket depth. Full-thickness or split-thickness flap
management are used to access the surgical area.

With the flap raised, de-granulation of the osseous
defect is performed. Care should be taken to avoid contact
between the implant and metal instruments. An implant
surface can now be prepared with chemicals and air
abrasives. Implant surface preparation is performed by
applying the air spray of the air-powder abrasive for a
maximum of 60 seconds on the implant surface, followed by
copious irrigation with saline solution. Then the application
of supersaturated citric acid is applied for 30 seconds,
followed again by irrigation with saline solution.

IMPLANTOPLASTY
Many times the effort to level the bone and apically position
the soft tissues during surgical treatment for peri-implantitis
leads to exposure of the rough surface of the implant. Such
rough surface tend to accumulate plaque, So they should be
smoothed and polished. Diamond stones with copious cooling
can be used to grind away plasma-spray coatings or threads
on the implant surface, with final polishing accomplished
using rubber disks (Jovanovic 1990).
Implantoplasty

This type of “implantoplasty” remains the single effective
method for reducing plaque accumulation; it also makes plaque
control considerably easier for the patient (Lazada et. Al 1990). If
this type of implant surface treatment is necessary, it should be
performed immediately after flap reflection and before any
contouring of the bone. Metal particles always result from this
procedure and must be removed by copious rinsing.

PERI – IMPLANT REGENERATIVE THERAPY:
An increasing number of reports have shown successful
treatment of periimplant bone defects around functioning dental
implants. To accomplish regeneration of lost bone tissue and
reosseointegration, guided bone regeneration (GBR) and bone
graft techniques have been suggested. In several experimental
and clinical studies, the GBR principle using a nonresorbable
expanded poly-tetra-fluoroethylene membrane has been used
for healing of bone defects seen at the time of implant
placement and around failing implants

Regeneration of bone seems to be enhanced if the area
is isolated from the oral environment. Therefore it is
recommended to remove the implant prosthesis 4 to 8 weeks
prior to the regenerative surgical procedure to allow optimal
compliance with oral hygiene procedures and the soft tissue
to collapse and heal over the implant site with a newly
attached cover screw in place. Thus at the time of
regenerative surgery, a more intact soft tissue flap can be
helpful to seal off the peri-implant tissues during the healig
period. A crestal incision is then used for the flap design.

The surgical therapy includes implant surface preparation
by air-powder abrasive for 30 to 60 seconds and the
application of an oversaturated citric acid solution for 30 to 60
seconds. Consecutively, an elaborate rinse of the surgical
area is performed with saline solution. A membrane is then
trimmed to extend 3 to 4 mm beyond the margins of the bone
defect a hole (3mm) where punched in the rigid centre of the
membrane, which permitted from attachment to the fixtures.
The osseous defects were completely covered by the
membrane. A space was left beneath the membrane ,If the
defect is large graft material (demineralized freeze – dried
bone and HA )was placed to support the membrane.

The surgical phase was then sutured closely to the implant
neck. The surgical phase was supported by the systemic
administration of 250 mg tetracycline HCL every 6 hours for 1
week. After 5 to 8 weeks, the membrane were removed and
the patients placed on a strict maintenance program.
The membrane was surgically removed 6 weeks later. The
previous osseous defect had completely filled with
regenerating tissue.

As the membrane is being removed and during repositioning
and suturing of the flaps, care must be taken not to disturb the
newly formed osteoid tissue.

ROLES IN IMPLANT MAINTENANCE
PATIENT ROLE
1. Plaque control of 85%.
2. Use of interdental (ID) brushes,hand and
motorized.(Proxa-Brush,Oral-B Brush,Rota-Dent,Sonic).
3. Dip bruses in chlorhexidine,0.12% (Peridex,Periogard).
4. Use of flosses,,tapes,dipped in chlorhexidine (Super-
Floss,Perio-Floss,G-Floss)
5. If patient has tooth-colored materials,composites,sand so
on, use a cotton swab dipped in chlorhexidine.

HYGIENIST ROLE
1. Check plaque control effectiveness (85%).
2. Check for inflammatory changes
3. IF pathology is present,probe gently with plastic probe
(sensor).
4. Scale supragingivally only (or slightly subgingivally).
5. Check for problems such as loose suprastructure.
6. No need to probe if no pathology is present.

CLINICAL ROLE
1.Check every 3 or 4 months
2.Check for 85% plaque control effectiveness.
3. Expose radiographs every 12 to 18 months if no pathology is
present and as needed pathology is present.
4. Is suprastructure is retrievable, remove and clean the
ultrasonic every 10 to 24 months.
5. If implant needs it repair, degranulate, detoxify and graft with
guided bone regeneration (GBR) if necessary.

REVIEW OF LITERATURE
Mc Kinney, Atelic, koth D L (1984) defined the terms
permucosal, perimucosal and transmucosal can all be used
correctly to describe the unique and interesting biologic seal
that occurs around a dental implant. Per means ‘through’ and
peri means ‘around’. The term per-perimucosal seal is used to
describe most accurately the biologic function of the division
between the internal and external environments of dental
implants. Permucosal designates the vertical orientation of
the implant penetration though the oral mucosa and
perimucosal designates the horizontal or circumferential seal
of the mucosa to the biomaterial.

D. Van Steenberghe (1988) drew parallels between tissue
attachment on teeth and permucosal implants for both
epithelial and connective tissue parts. Plaque accumulates
more rapidly on titanium abutments than on natural teeth.
Presence of deep pockets with probing depths of 7mm have
been found to occur around osseointegrated implants. It is due
to the thickness of the mucoperiostium through which the
abutment is installed.

Block M, Kent J 1990 found on follow up examinations or
a non scheduled visit, recognized soft and hard tissue
compromise i.e. bleeding on probing, pain, purulent drainage,
discharge or progressive bone loss. Patient prosthesis were
removed and cleaned of plaque. It may be modified to provide
the patient easier access for maintenance. The patient was
instructed regarding implant hygiene. Chlorhexidene is
recommended for use on the floss, proxy brush or electric
tooth brush as well as with demineralised bone graft is placed
over the implant. The flap in then closed primarily. At least 4
months is allowed for consolidation of the graft where upon
the implants are the re-exposed the abutment heads replaced
and the restoration replaced or remade.

Buser Daniel, Weber H.P et al 1992 examined the soft
tissue reactions to non-submerged unloaded titanium implants.
A complication free tissue integration with a dense connective
tissue indirect contact to the implant surface in the
supracrestal area of epithelial structures similar to those
around teeth.

Heretel R.C. et al 1993 discussed that the influence of the
dimensions of implant superstructures on peri-implant bone
loss is the implant position and consequently the design and
dimensions of the superstructure influence the way in which
occlusal forces are transmitted to the implant and surrounding
bone. In certain areas these forces may reach greater level-
arm action. This leads to high-stress zones and potential bone
resorption. As with the natural dentition, long span fixed
partial dentures should not be splinted by only a few implants.

Jovanovic sascha. A 1993 suggested that experimental peri-
implant bone loss can be induced by plaque accumulation.
Moderate tissue destruction can be arrested with careful
surgical techniques. Bony defects treated with resective or
regenerative surgical therapy. Detoxification of
contaminated implant surface based on biological principle
of GTR, a concept of bone regeneration around failing
implants has been developed. Histological data shows
evidence of new bone formation and ‘reosseointegration’. a

Touhlar Richards 1998 discussed the primary difference
between dentogingival and implantogingival soft tissues is the
structure and arrangement of the collagen fibres. Decreased
vascular supply may account for functional differences in
inflammatory responses.

Weber Hans Peter and Cochran David 1998 reviewed the
morphologic and clinical features of peri-implant soft tissues
around titanium abutments or non-submerged one-stage
implants. The major connective tissues fibres run parallel to the
long axis of the implant. The connective tissue forms a
nonvascularized circular scar type structure surrounded by a
less dense vascularized connective tissue. Thus the epithelial
components around implants appear to be consistent with the
epithelial components around teeth.

Carmagnda et al 1999 examined bone tissue alterations that
occurred around implants at which the marginal level of bone
support at fixture installation was different at buccal and lingual
surfaces. Findings demonstrated that osseointegration
occurred at implants placed in a chronic defect with large
discrepancies and function, marked modeling and remodeling
of bone tissue took place. Buccal surface bone regrowth and
osseointegration occurred while at lingual wall substantial
resorption of marginal bone and an enhanced number of bone
multicellular units.

REFERENCES
Glickman Irvin : Clinical periodontology 3rd ed.
Lindhe jan : Clinical periodontology and implant diseases
3rd ed 1997.
Schlunger saul et al : Periodontal diseases 2nd 1990
Abrahamsson I et al : Peri-implant tissues at submerged
and non-submerged titanium implants J. clin periodontal
1999, 26:600-607
Haas Robert et al : The relationship of smoking on peri-
implant tissue – A retrospective study JPD 1996, 76, 6:
592-6.

James Robert A: Periodontal considerations in implant
dentistry JPD Aug 1973, vol 30, no. 2, 202-209.
Jovanovic Sacha A: The management of peri-implant
breakdown around functioning osseointegrated dental
implants J. periodontology 1993; 64: 1176-1183.
Truhlar Richard – Peri-implantitis cause and treatment.
Journal of OMFS clinics of North America May 1998, Vol 10,
No.2, 299- 306.
Weber Hans Peter and Cochran David K: The soft tissue
response to osseointegrated dental implants JPD 1998, 79,
79- 89.

Diagnosis and Treatment of Peri-Implant Disease

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