Periimplant diagnosis/cosmetic dentistry courses

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 mucosites. 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.www.indiandentalacademy.com

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.. www.indiandentalacademy.com

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.www.indiandentalacademy.com

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.

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).

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 0.2mmwww.indiandentalacademy.com

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.

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.www.indiandentalacademy.com

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. www.indiandentalacademy.com

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.www.indiandentalacademy.com

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. www.indiandentalacademy.com

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. www.indiandentalacademy.com

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’.

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.

Periimplant diagnosis/cosmetic dentistry courses

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Periimplant diagnosis/cosmetic dentistry courses

Similar to Periimplant diagnosis/cosmetic dentistry courses (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Periimplant diagnosis/cosmetic dentistry courses