Peri implantitis/ oral surgery courses /prosthodontic courses

Periimplantitis
and other
complications
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

• Introduction
• Terminologies
• Minimum criteria for success of implants
• Failures (causes)
• Trans mucosal attachment
• Peri mucositis
• Peri implantitis
• Clinical examination
• Decision making
• Treatment of peri implantits

• Bio mechanical overload
• Pre operative errors contributing to implant
failure
• Patient related factors
• Conclusion
• Bibliography

Introduction
• Dental implants provide a unique treatment
modality for the replacement of the lost
dentition
• This is accomplished by the insertion of a
relatively inert material (bio materials) into
the soft and hard tissue of the jaw, thereby
providing support and retention to the
dental prosthesis

• Over the last 20 years the survival of osseo
integrated implants has been successfully
established
• But for the long term prognosis of an
implant it is essential to identify the various
factors that can lead to implant related
complications and eliminate them

Terminologies
• Osseointegration is defined as a relationship where
bone is in direct contact with the implant,without
any intermediate connective tissue. (Branemark
1952)
• Peri-implant disease: a general category of
pathologic changes of the peri implant tissues
• Peri implant mucositis: inflammatory changes
confined to the soft tissue surrounding an implant

• Peri- implantitis: radiographically detectable peri-
implant bone loss combined with a soft tissue
inflammatory lesion that demonstrates suppuration
and probing depths ≥ 6 mm.
• The Ailing implant :an implant that may demonstrate
bone loss with deeper clinical probing depths but
appears to be stable when evaluated at 3- to 4- month
intervals
• The Failing implant : An implant that may
demonstrate bone loss, increasing clinical probing
depths, bleeding on probing and suppuration. The
bone loss may be progressive.

• The Failed implant : An implant that demonstrates
clinical mobility , a peri-implant radioluscency, a
dull sound when percussed. A failed implant is non-
functional and must be removed
• Early failures :failures that occur a weeks to few
months after placement.
• Late failures : failures that arise from pathologic
process that involve a previously osseo integrated
implant

MINIMUM CRITERIA FOR
SUCCESS OF DENTAL
IMPLANTS (Albrektsson et al 1986)
1. An individual, unattached implant is
immobile when tested clinically.
2. Radiographic examination does not reveal
any peri-implant radiolucency.
3. After the first year in function, radiographic
vertical bone loss is less than 0.2 mm per
annum.

4. The individual implant performance is
characterized by an absence of signs and
symptoms such as pain, infections, neuropathies,
paraesthesia or violation of the inferior dental
canal.
5. As a minimum, the implant should fulfill the
above criteria with a success rate of 85% at the
end of a year observation period and 80% at the
end of a 10 year period.

Failures
• Failures happen in implant therapy, such
failures either occur early due to
complications following installation of the
implant device or late when the implant
supported reconstructions have been in
function for a period of time.

Early Implant failures :
• Improper preparation of the recipient site
• Bacterial contamination and extensive
inflammation of the wound that may delay
the healing of soft and hard tissue
• Pre mature loading of the implant

Late failures:
The pathological process leading to late
failures may be
• Marginal infection (peri implantitis).
• Bio mechanical over load
• Combination of the two ( Tonetti and
Schmid 1994 )

Trans mucosal attachment

• The two soft tissue units the gingiva and the
peri implant mucosa have many things in
common
• The outer epithelium of the gingiva is well
keratinized and is continuous with the
smooth Junctional epithelium (J.E)
• The supra alveolar connective tissue is 1
mm high. The periodontal ligament fibers
extend in a fan shaped pattern from the crest
of the alveolar bone.

• The outer surface of the peri implant mucosa is also
well keratinized , which in the marginal border is
continuous with barrier epithelium that is facing the
abutment part.
• The barrier epithelium has several features in
common with the J.E. The barrier epithelium is a
few cells thick and terminates about 2 mm apical to
the soft tissue margin.
• In a zone about 1- 1.5 mm high the C.T, between
the apical margin of the barrier epithelium and the
bone crest . the C.T seems to be in direct contact
with the titanium di oxide layer of the implant.

• Both the epithelia are attached via hemi-
desmosomes to the tooth /implant surface
(Gould et al 1984)
• The collagen fibers seem to originate from
the crest of the bone and extend towards
the soft tissue

• In dog experiments (Abrahmsson 1996 , 2001)
noted identical transmucosal attachments when
different types of implant systems were used .

Connective tissue :
• At the implant site the collagen fiber bundle are
oriented completely different , The fibers invest in
the periostium at the bone crest and either project
in a direction parallel with the implant surface or
aligned in course more or less perpendicular to the
implant surface.
• These horizontal fibers appear to bend in a
“vertical direction” ie, become parallel with the
implant surface in compartment close to the
implant (Buser et al 1992)

• Immunohistochemical analysis by Romanos et al of
human keratinized gingiva around ITI implants and
healthy teeth (1995) showed
• similar distributions of types I,III ,IV and VII collagen.
• There were differences in distribution of type V and
VI, with more of type V collagen seen around the
implants
• The C.T at the attachment site contain more collagen
and fewer fibroblast and vascular structures than
tissues at the corresponding location at the teeth.www.indiandentalacademy.com

• In a detailed analysis done by Moon et al
(1999) in a dog experiment they reported
that the border tissue can be divided into 2
zones

Zone A – 40 μm wide , there
are no blood vessels , but a
large number of fibroblast are
present with their long axis
parallel to the implant surface
(collagen 67 %, vascular
structures 0.3% and fibroblast
32%)
Zone B – that is in a lateral
direction , 160 μm wide .
There are fewer fibroblasts and
more collagen fibers and more
vascular structures ( collagen
85 %, vascular structures 3%,
fibroblast 11%)

Vascular supply
:

• The vascular supply to the gingiva comes from 2
sources.
• Large supra periosteal blood vessels
• Vascular plexus from the periodontal ligament.
Berglundh (1994) observed that the vascular supply to the
peri implant mucosa of dogs originated solely from the
large supra periosteal blood vessels on the out side of
the ridge.
This vessel
• Gives a branch to form plexuses located immediately
adjascent/ lateral to the barrier epithelium
• Gives branches and forms capillaries beneath the oral
epithelium
As a result the C.T part contains a few blood vessels, all
terminal branches of the supra periosteal vesselswww.indiandentalacademy.com

Seal formation :

• The epithelium around the base of the sulcus
produce a series of biological attatchment
structures
• of a basal lamina collagenous structure
composed of type IV collagen
• hemidesmosomes and laminin are present to
hold the epithelial cells to the basal lamina
The basal lamina consists of
• lamina lucida, lamina densa, sub lamina lucida
and a glycos aminoglycan structure on the
implant surface called the leniar body

• the high content of glycosaminoglycans in
the linear body that coats the implant has
sufficient glue like properties to form a
biologically active and trauma resistant
attachment
• This biological seal is a definitive entity and
must be present to prevent the external
toxins and agents entering the peri implant
region.

Perimucositis

• Peri implant mucositis: inflammatory
changes confined to the soft tissue
surrounding an implant
• The peri implant mucosa is less effective
than the gingiva in encapsulating plaque
associated lesions

In experiments in dog , Berglundh et al (1992) and
Ericsen et al (1992) compared the reaction of the
gingiva and peri implant mucosa to 3 weeks and 3
months of de novo plaque formation
• After 4 months : clinical examination and the
minute plaque samples were collected . the plaque
control program was now terminated
• Re examination of clinical parameters , sampling
of the plaque bacteria and biopsy was done at 3
weeks and 3 months

• Based on the observation of the plaque
samples collected it was concluded that
early microbial colonization on titanium
implants followed the same pattern as on
teeth.

End of 3 weeks

• The inflammatory lesions observed at the
end of 3 weeks both in the gingiva and the
peri implant mucosa were matched both in
respect to size and location.
Similar observations have been observed
since then by Ponterio et al ( 1994) and in
another study by Zitzmann et al (2001) in
human volunteers

3 months

• With increased duration of plaque build up (3
months) in the dog model the lesion of the peri
implant mucosa expanded more and progressed
further ‘apically’ than the case with the gingiva.
• It was seen that the lesion in the peri implant
mucosa had very few fibroblasts , than the
corresponding compartment of the gingiva
• It was suggested that in the gingival lesion the
amount of tissue break down that occurred during
the break down phase was more or less
compensated by the reparative phase .

• In the peri implant mucosa the tissue break
down that occurred was not fully recovered by
the reparative events
• . The smaller number of fibroblasts present in
the particular lesion may simply have been
unable to produce enough collagen and matrix
during the reparative phase.
• This reduced build up resulted in the additional
propagation and spread of inflammatory cell
infiltrate in the peri implant mucosa.

Peri implantitis

• Peri- implantitis: Radiographically
detectable peri-implant bone loss combined
with a soft tissue inflammatory lesion that
demonstrates suppuration and probing
depths ≥ 6 mm.

• The histo pathologic samples from the dog
study ( Lindhe 1992 ) showed that the lesions in
the periodontal sites were consistently
separated from the alveolar bone by a zone ,
about 1 mm high of non inflamed C.T.
• the lesions of the peri implant tissue in most
situations extended into and involved the
marrow spaces of the alveolar bone.

It was suggested that the peri implant tissues were in variance with
the periodontal tissues poorly organized to resolve progressive
plaque associated lesion .www.indiandentalacademy.com

• In a histo pathologic study of human peri
implantitis site , Berglundh et al (2003)
found that the mucosa contained large
lesions with numerous plasma cells ,
lymphocytes and macrophages and it was
seen that the apical part of the soft tissue
lesions frequently reached the bone tissue.

• In another study by Berglundh et al (2003) also
noted that in the apical part of the lesion the
inflamed C.T was in direct contact with the bio
film on the implant surface.
• In another immunohistochemical study by Gialini
and Berglundh (2003) found a large number of
PMN activity in the central portion of the
infiltrate in lesions with peri implantitis.

Prevalence
• The prevalence of peri implantitis in man is
difficult to establish but may vary between
2-10 % of all implants inserted ( Esposito
1998, Mombelli and Lang 1998 )

Microorganisms
• The first evidence of a specific role of
bacteria in peri implant infection originated
from the microscopic examination done by
Rams et al (1990, 1984) where implants
with advanced pockets showed high levels
of spirochetes, whereas implants with
stabilized pockets not exceeding 5 mm
yielded sparse, predominantly coccoid
microbiota

Mombelli et al (1987) found in peri implant
pockets deeper than 5mm with radiographic
evidence of bone loss
• -abundance of motile rods, fusiform
bacteria and spirochetes
• -41% of failing implants showed increased
numbers of Fusobacterium sp., Prevotella
intermedia
• Becker (1990) found increased number of P.
gingivalis on one and P. intermedia on two
other patients with failing blade implantswww.indiandentalacademy.com

George et al (1994) using latex agglutination test found
Actinobacillus actinomycetem comitans in
• 12 % of edentulous patients
• 17 % partially edentulous patients
P. intermedia amd P. gingivalis were found in
• - 39 % partially edentulous mouths
• - 19 % fully edentulous mouths
implants harboring the above organisms had a
significantly higher PD, higher bleeding score.

• It was observed in dog models that the
plaque build up that had formed in the deep
pockets was similar at the tooth and
implant sites and was dominated by Gr –ve
and anaerobic species.
( Leonhardt et al 1992 )

Microbiota around implants of partially
edentulous and fully edentulous subjects
• Spirochetes are not detected
microscopically in fully edentulous implant
wearers , but found in partially edentulous
mouths
• Black pigmented Gram –ve anaerobes were
found more in samples from partially
edentulous mouths.

• P. gingivalis, P. intermedia, F nucleatum
were found within 14-28 days to colonize
implant surface exposure to oral
environment in partially edentulous mouths
(Koka et al 1993)

• In a longitudinal study for 6 months in patients
with a history of periodontal disease , showed
that 3-6 months after exposure of the implants to
the oral cavity the detection of bacterial species
on the implant and teeth were the same.
(Mombelli et al 1995)
• In a 5 year retrospective study ( Hardt et al 2002)
demonstrated that implants placed in
periodontitis susceptible patients exhibited a
higher failure rate (8 %) than similar implants
placed in periodontally healthy subjects (3.3%)

• These findings suggest that the microflora
present in the oral cavity before
implantation determines the composition of
the newly established microflora of the
implant.

Surface characteristics of the
implant and peri implantitis
Esposito (1997)evaluated prevalence of losses
attributed to peri implantitis before 1997 and did
found that implants with a rough surface did fail
more often due to peri implantitis
Buser in a prospective study involving 2359
implants having titanium plasma sprayed surfaces
over a period of 5 years showed only 5 implants
had to be surgically removed due to peri
implantitis (1997)

• Implants do not have a rough surface
everywhere , the parts exposed to the oral
cavity have a smooth design , if the implants
are positioned correctly , contamination of the
implant surface will not occur unless a peri
implant pocket forms
• Therefore bacterial colonization of the rough
surface is a consequence and not the cause of
initial bone loss.

• Implants with a smooth coronal titanium
neck and non splinted maxillary implants
have shown increased risk of peri implant
bone loss during the functional phases.
• The bone loss is attributable to the non
functional; characteristic of smooth and
polished titanium, which do not maintain
bone integration during loading.

Clinical examination :
• Serve several functions
– Screening for periimplant diseases or factors
that may lead to implant breakdown
– Differential diagnosis between periimplantitis
and periimplant mucositis.
– Treatment planning
– Evaluation of therapy and monitoring.

Soft tissue examination :
• Redness, swelling and alteration in colour,
contour and consistency are signs of peri
implant disease
• A positive correlation has been found with BOP
and histological signs of inflammation at the
peri implant site (Lang 1986)
• BOP is a suggested parameter for evaluation of
status of implants during maintenance.

Probing peri implant mucosa :

• Erricsson and Lindhe (1993) examined the
outcome of probing in a Beagle dog model,
a probe tip of diameter 0.5mm was used.,
with a standardized force of 0.5 N, the
probe was anchored and biopsy was taken.

• - At the dentogongival interface the probe tip
was located coronal to the apical cells of the
Jn. Epithelium.
• At the implant site , probing caused the
compression and lateral dislocation of the
peri implant muosa,
• The average histological depth was also
deeper than the tooth site by 2 mm
• The distance between the probe tip and bone
crest was 0.2 mm at the implant site, the
probe tip almost made contact with the bone

• Lang in 1994 found similar results again,
with probing forces of only 0.2 N
• Scou et al (2002) found using a electronic
probe (probing force 0.3 – 0.4 N) that at site
with peri implantitis and mucositis the
probe tip was consistently at a more apical
position than at sites on teeth with gingivitis
and periodontitis

• When probing the force should be light (0.2 – 0.3
N)
• In the presence of inflammation the probe tip
penetrates to a more apical position
• Peri implant probing to be avoided during the first
3 months of abutment connection to avoid
disturbing the healing and establishment of a soft
tissue seal. (Baumann 1992)

• Generally non metallic instruments such as
the Meritt B probe, Audio probe or the
HAWE probe are used.

Radiographic examination :
• Most valuable since due to presence of prosthesis ,
probing may not be possible.
• Failing implants show a radiolucent space around
the implant and large saucer like defects may be
present at the alveolar crest
• A stable land mark should be identified for each
fixture, implant shoulder for single stage implants
or the apical termination of the cylinder portion for
a two stage implant. (Salvi 2004)

• Can be used to compare osseous changes
over time
• OPG should be used only for screening
purposes , Peri apical radiograpghs using
Long cone paralleling technique are
recommended (Friedland 1987)

• One post operative radiograph is taken
immediately after placement of implant, future
imaging should be based on the clinical situation
of the particular patient , one interval
recommended (Wennstrom 1999, 3 rd European
workshop) is 1, 3 and 5 years
• Anticipated bone loss in 1 year is approx 1mm,
with average 0.1 mm subsequent bone loss/ year
• Adell 1981- found greater bone loss in the maxilla
, this finding though is not universal

Implant mobility
• May be done digitally or using periotest.
• Mobility is an indicator of loss of
osseointegration.
• Does not present until the final stages of
periimplantitis.
• Remove implant.

Decision making

Implant mobile
Clean implant.
Correct soft.t morpho
PD no more than 3 mm
beyond the shoulder
Probing depth
less than 3 mm, no inflammation Reduce recall freq.
Clean implants
Improve O Hyg
Correct soft tissue
morphology
No loss of peri
Implant bone
no
no
no
Take
radiograph
yes
yes
yes
yes
Reason

Bone loss other than
Peri implantitis
Take a microbial
sample
Peri implant pockets are
not deeper than 5 mm
Mechanical debridement
Systemic antibiotics
Surgical intervention to correct resid
pockets
Local delivery device
Surgical intervention to
eliminate residual pocket
Clean implants
Improve O hyg
Correct soft and Hard tissue defects
It is a local problem
Clean and improve O hyg
Topical anti microbials
Correct soft and Hard tissue defects
no
no
no
yes
yes
yes

Treatment of peri implantitis
• The removal of bacterial plaque from within the
peri implant pocket
• Decontamination and conditioning of the
implant surface
• The reduction or elimination of the areas that
cannot be maintained plaque free
• Establishment of a efficient plaque control
program
• Regeneration of bone

Surface decontamination and
conditioning
• The contamination of the titanium dioxide surface of
implants by sterile and bacterial contaminants
reduces the free energy of the surface and may
provoke a foreign body reaction
• The currently available clinical procedures of
implant placement do not allow for the implant to be
completely isolated from sources of contamination,
• Further more agents used to kill bacteria or
detergents used to remove the contaminants are
deposited themselves on the treated surfaces

Air powder abrasive unit removed more LPS other
than other treatment modalities on titanium surfaces,
On Hydroxyapatite surfaces citric acid was superior in
the removal of LPS
• (Invitro study , Zablotsky M et al 1991)

Another study using radioactive endotoxins
of P. gingivalis found that burnishing with
cotton pellet soaked in water , citric acid
solution , 0.12 % CHX or treated with a air
powder abrasive .
• The machined implants it was seen were
decontaminated by all the above procedures
• (Dennison DK, 1994)

Anti microbial therapy
• Mechanical
instrumentation on
implants will damage
the surface if
performed with
standard periodontal
curettes (Matarasso
1996)

In a in vivo study , surface texture of titanium
implants were evaluated after exposure to
• Plastic scalers
• Air powder abrasives
• Polishing with rubber cups and pumice
None of the above methods roughened the surface ,
but rubber cup with pumice provided the
smoothest surface ( Mc Collum , 1992)

A photosensitizing substance (toluidiene
blue ) was used and then irradiated with a
soft laser.
• In the in vitro study ( Huus 1997) it killed
all the bacteria
• In the in vivo study (Dortbudok 2001) it was
found to reduce the bacterial count by 2 log
steps , but could not eliminate the bacteria
from the surfaces completely

• Almost all implants now have a roughened
surface in the area where osseo integration
is supposed to occur
• Mechanical debridement of such surfaces
has limited effect and cannot remove all the
bacteria, therefore adjunctive chemical
agents have been recommended.

• Systemic Amoxicillin and Metronidazole
and local debridement on ligature induced
peri implantitis was evaluated in 5 dogs
(Ericsson et al 1996)
• Resulted in the resolution of the peri
implantitis lesion, with significant recession
of marginal mucosa, and a marginal apical
shift of the base of the bone defect. There
was no improvement in the untreated site.

Systemic Ornidazole, 100 mg for 10 consecutive
days was tested in a study involving 9 patients
with pocket depths of greater or equal to 5 mm
around implants ( Mombelli 1992)
• Treatment given - mechanical debridement
• irrigation with 0.5 % chlorhexidene
• systemic antimicrobial therapy
• gradual reduction on PD was seen in 1 year
period, only one case showed no difference.

Local drug delivery
25 partially edentulous patients with radiographic
evidence of circumferential bone loss were treated with
polymeric Tetracycline HCl containing fibers
( Actisite) clinical ad baseline recordings were taken at
1,3,6 and 12 months after treatment.
• Mean reduction in PD was seen from 6mm to 4.1 mm
(1 month) which was maintained over 12 months
• The reduction in PD was attributed to increase in tissue
tonus, increasing the resistance to probe penetration .
and not primarily by shrinkage of the tissues.

• From aesthetic point of view this is
important because surgical revision of peri
implantitis leads to tissue recession and
possible exposure of the metal and implant
surface

Limitations of Non surgical therapy :
• microbial parameters tend to shift to pre
treatment values, particularly in deep peri
implantitis lesions
• unfavorable peri implant morphology might
be present which cannot be kept plaque free
by the patient with conventional means of
oral hygiene

SURGICAL MANAGEMENT :

Morphology of osseous defects:
Group 1: moderate horizontal
bone loss,
Minimal intra bony component

• Group 2: moderate to
severe horizontal bone
loss with a minimal
intra bony component
• Advanced condition of
group 1

• Group 3 : minimal to
moderate horizontal
bone loss with an
advanced
circumferential intra
boney lesion. The
pattern of bone loss is
usually symmetrical,
with a circular trough
with uniform width
and depth.

• Group 4: complicated
implant defect with
moderate horizontal
bone loss with
advanced
circumferential intra
bony lesion,
additionally the buccal
and lingual boney
plates are lost

PERI IMPLANT RESECTIVE
THERAPY
• Indications
– Moderate to severe horizontal bone loss
– One/two wall bone defects
– Implant in unaesthetic area.

• The type of defect should be identified before
deciding the treatment modality
• Horizontal bone loss and moderate vertical defects
(≤ 3mm)
Apically positioned flap and osseous resective
therapy is used
• Implant surface can be prepared by applying air
powder abrasive for 60 sec followed by copious
irrigation with saline, application of
supersaturated citric acid, irrigation with salinewww.indiandentalacademy.com

Surface polishing/ implantoplasty
Implant surfaces coronal to the bone level
should be smooth and clean.
• Surfaces with threads, roughened
topography (HA) are indicated for alteration
with high speed diamond burs and polishers
• copious irrigation for cooling is used
• only done during resective procedures and
not regenerative procedures
• 6 months after regenerative therapy, if
moderate defect exists, or rough implant
surface is seen, implantoplasty can be done

PERI IMPLANT REGENRATIVE
THERAPY
• To regain lost tissues and to obtain re
osseointegration – GBR and use of bone
grafts has been suggested

• In 8 case reports identified till 2003 for treatment of
peri implantitis using bone grafts ( literature review,
2003)
• - most treated lesions were in the mandible
• - involved the use of Autogenous bone,
demineralized freeze dried allogenic bone, and
hydroxyapatite
• - the use of all the above graft materials led to
improved fill of defects and improved the soft tissue
condition www.indiandentalacademy.com

Regeneration was enhanced if the area was isolated
from the oral environment
• remove implant prosthesis 4-8 weeks prior to
regenerative surgical procedure, to allow soft tissue
to collapse and heal over the implant with a new
cover screw in place
• crestal incision is now given
• if prosthesis not removed , a sulcular incision is
given to raise a full thickness flap

Implant surface is prepared by air powder abrasive
for 30-60 sec
• the bone surface is prepared by roughening with a
round burr and penetration with small round burrs
• membrane is then trimmed to extend 3-4 mm
beyond the margin of the defect and secured
• during suturing care is taken not to have tension
on the flap

• sutures removed after 14 days
• membrane is left submerged for 4-6 months

if one stage implants are used ,
• the membrane is perforated with a 3 mm hole
and slid over the implant, the flap is then sutured
• with the per gingival healing environment the
membrane has to be removed in 6-8 weeks due
to plaque accumulation and the potential of
causing peri implant infection

• In the various reports it is seen that e PTFE
membranes were used in a majority, other
membranes used polylactic acid membrane,
lamellar bone sheet, calcium sulfate
membrane

• Mellonig et al (1993 ) treated 12 lesions
with Demineralized freeze dried allogenic
bone graft and e PTFE membrane and
• reported complete success in coverage of all
threads in 10 lesions and partial success – a
maximum of 2 threads or 2mm left
uncovered in the remaining 2 lesions.

• Haas et al (2000) treated 24 lesions with
autogenous bone grafts and e PTFE
membrane and reported average
radiographic bone fill of 2 mm, only 2
lesions showed a bone loss of 0.5 mm

• From the various reports it may be stated
that the treatment of peri implantitis lesion
with a combination of grafts and a e-PTFE
membrane may lead to bone fill and
improvement of soft tissue conditions.

• STRATEGY FOR THE TREATMENT
OF PERI IMPLANT MUCOSOTIS AND
PERI IMPLANTITIS

Lang et al (1997)Peri implant mucosotis/ Peri
implantitis
• PD <4mm : oral hygiene +debridement (soft
scalers +rubber cup+paste) (step A)
• PD 4-5 mm : step A +antiseptic therapy (CHX
rinse or topical CHX gel daily) (Step A+ B)
• PD ≥6mm : step A+B+ tetracycline fibers for 10
days+ systemic antibiotics for 10 days (Ornidazole or
metronidazole or combination amoxicillin and
metronidazole) ( step A+B+C)

• Surgery only after successful elimination of
infection
• Regenerative approach or resective
approach depending on the esthetic
requirements and morphological
characteristics of the defect
• No specific method recommended for
implant smoothening and detoxification

Bio mechanical equilibrium
• Radiographically it is seen that the alveolar bone
around implants undergo continuous remodeling
• Wolfs law states that the course and balance of
remodeling can be affected by mechanical
function
• Radiographically thus it is seen that there is
increase in radio opacity and rearrangement of
bony trabaculae around loaded implants

• An equilibrium is thus formed that allows
the dispersion of loading forces from the
bone implant interface along the trabacular
bone.
• Important factors here are
– Magnitude of force
– Number of load cycles
– Repair capacity of the bone

• Implants are subjected to load cycles
during mastication and swallowing—
2500-800 cycles/day
• Due to lack of proprioception , the forces
are more for implants than natural teeth
131 N and 5.8 N resp.
• These forces are nonetheless very small to
cause acute bio mechanical failure

• But repeated loading of any bio material
including bone leads to the development
fatigue following the application of forces
considerably smaller than the static strength
of the material itself
• In bone this leads to development of micro
cracks during the loading cycles,---constant
bone remodeling repairs this micro fracture
and prevents the excess loss of strength and
mechanical properties.

• By analogy : repeated application of masticatory
and swallowing forces (parfunctional habits
included) might cause the development of micro
cracks within the alveolar bone.
• This has not been demonstrated mechanically but ,
microfractures have been observed at the bone
implant inter face from retrieved oseointegrated
implants (Sennerby 1991)
• Also it has been observed histologically that direct
bone to implant is not achieved along the whole
interface, there fore the percentage of
osseointegration may represent a relevant factor
in determining the magnitude of loading cycles a
fixture may withstand

• When biomechanical demands exceed the
capacity of the bone/ bone implant interface
• Bone remodeling is triggered by the
accumulation of micro cracks
• Results in initial bone resorption ( further
compromising the mechanical strength)
• Continued application of stress cycles leads
to accumulation of microdamage
• Which may lead to micro motion at the
interface or at the sites of micro fractures
within the tissues

• When micro motion occurs, a critical point
in bio mechanical loosening is reached
• In such situations bone implant interface is
replaced by a soft tissue layer (Schroeder
1981)
• The presence of a soft tissue layer is a
common finding of both aseptically
loosened orthopedic prosthesis and mobile
dental implants

• In 1997 , Isidor subjecting implants to
biomechanical loads showed that 75 % of
the implants displayed clinical mobility
with a sharp decrease in direct bone to
implant contact.
• Histologicaly a complete replacement of the
bone to implant contact with a non
mineralized soft tissue
• There fore it was seen that it was possible to
loose osseointegration without loosing
clinical attachment.

• Piatteli and co workers (1998) reported
histopathological observations and time
explanation of a series of 230 implants
that had failed and had to be retrieved
– Early failure associated with infection
– Late failure associated with infection
– Late failure associated with loss of
osseointegration in the absence of infection
– Late failure due to the fracture of the implant
device

• In the implants retrieved due to mobility
they were surrounded by a dense capsule
consisting of CT fibers running parallel to
the implant surface
• A bone to implant gap of 150-400 μm was
seen
• These histopathological study beyond doubt
show that both bacterial and bio mechanical
factors lead to osseo disintegration

Occlusal evaluation
• Must be evaluated on a routine basis
• It is not determined if non axial loading is
detrimental to osseointegration, but it is
established that abnormal loading will
negatively effect the various parts of
implant supported prosthesis (Cochran
1996)
• Pre mature contacts or interferences should
be identified and corrected to prevent
occlusal overload

• Implant prosthesis should be examined
when bruxism or other parafunctional habits
are present Miyatta and coworkers (1998)
found rapid substantial peri implant bone
loss with excessive concentrated forces

Removal of a failed Implant
• Indications
– Severe periimplant bone loss [>50% of implant
length]
– Bone loss involving implant vents or holes
– Advanced one wall defect
– Rapid severe bone destruction [within 1 year of
loading]
– Non surgical/ surgical therapy is ineffective.

Pre operative errors contributing to
implant failures

Failure to anticipate anatomic variations/
abnormalities
• Bone immediately surrounding the nasal cavity
and the maxillary sinus is thin, these areas may be
penetrated accidentally– but the perforation of
these 2 cavities does not necessarily cause failure
• Lingual aspect of the mandible is often concave
and supports a ledge– perforation of the lingual
plate can occur if the prominence and the
concavity are not anticipated or placed too
lingually to avoid the inferior alveolar nerve.

MANDIBULAR NERVE INJURY
The nerve can be injured by stretching, compression,
partial resection or total resection.
Conventional OPG is the most effective means to
locate and position the neurovascular bundle
But this method causes a inherent magnification or
distortion of 20-25% and should be considered

Errors due to implant contamination
• Surgical gloves should be free of any
powder– surface contamination can
interfere with the implants ability to
integrate with bone
• Regardless of system implant should be
carried directly to the osteotomy site
• Implant should not come in contact with
any stainless steel surfaces

Errors in surgical technique
• Implant must be surrounded by adequate
keratinized tissue
• When there is minimal keratinized tissue the
incision should be placed labial to the crest into
the alveolar mucosa
• The flap should not closed with tension and the
surface epithelium should not come in contact
with the periostium as this would delay the
healing
• There should be no gap in the suture line–
additional sutures should be placed if gaps are
present. www.indiandentalacademy.com

• Heat injury during drilling should be
avoided
– Threshold temperature for heat induced injury
was 47 deg applied for 1 min (Eriksson and
Alberktsson 1983)
– Temperature above this leads to bone
resorption and fat cell death
– Also heat injured bone is replaced by less
differentiated bone which is incapable of
normal adaptive remodelling
– Heat also affects the ability to regenrate which
is critical for osseintegration

• Generation of excess heat can be avoided
by
– Using sharp drills
– Gradually increasing the drill diameter

For secure anchoring of endosteal implants one
requires not only bone quantity, but also
density and therefore the bone quality is of
importance.
Low bone density at the site implant placement
(Type IV bone) has been associated with
increased risk of implant failure.(Lang et al
1990, Jaffin et al 1991).
QUANTITIY AND QUALITY
OF
BONE

Patient factors

CIGARETTE SMOKING
AND DENTAL IMPLANTS
• Studies have suggested that smoking may
be associated with
– impaired wound healing at the implant site,
– sub optimal peri implant health
– Increased peri implant bone loss

• Bain and Moy et al 1993 observed that
a significantly greater percentage of implant
failures occurred in smokers than in non-smokers.
• In fact, smokers had an overall implant
failure rate of 11.3% whereas only 4.8% of the
implants were placed in non-smokers failed.

• Recent research conducted at the university
of Toronto indicates that cigarette smoking
has a negative role on implant survival even
after accounting for the various
confounding variables (Habasha 2000)

• INADEQUATE ORAL HYGEINE
• An increased incidence of implant
failure and an increased prevalence of soft
tissue problems have been reported in
subjects with sub-optimal levels of oral
hygiene.(Steenberghe et al 1993, Weyant et
al 1994)

Systemic factors

AGE
• Implants should not be used in
young patients before the end of their
growth which is approximately 16 yrs in
females and 17-18 yrs in males.
• On the other hand, there is no
upper age limit.

• DIABETES MELLITUS.
• Uncontrolled diabetes has been shown to
be risk factor for periodontal disease.(Nelson et al
1990).
• Shernoff et al reported that the failure rate
of implants in NIDDM is 7.3%.
• This seems to indicate that osseo
integration can be obtained in diabetic patients but
the medium to long term prognosis is currently
guarded.

• Zeilter and Fredrich (1996) reported that the tissue
perfusion and microvascular disease have a
important role in wound healing ,
• They report diseases like DM,
• Collagen diseases like scleroderma, Systemic
lupus erythematosus, rheumatoid artheritis and
Sjogrens syndrome have microvascular changes
that can cause decreased oxygenation and have
poor wound healing potential.

Osteoporosis
• The implant surgeon should be concerned with the
amount of bone mass and density present in the
jaws of osteoporosis patient
• Dao et al (1993), Freiedberg (1994), Fujimato et al
(1996) have found no data to contraindicate the
use of osseointegrated implants in these patients
• But , Blomqvist (1996) found evidence in a
retrospective analysis of 49 patients , to conclude
that osteoporosis may contribute to excessive
implant loss

Conclusion

Bibliography
• Clinical Periodontology and Implant Dentistry
• Jan Lindhe 4th
edition.
• Newman, Takei, Carranza. Clinical Periodontology, 9th
edition
• Implant therapy-Clinical approaches and Evidence of
success Vol II
–Nevins and Mellonig
• Contemporary Implant Dentistry
Carl Misch 3rd
edition.

• Egelberg et al. Treatment of periimplantitis:
a literature review. J Clin Periodontol 2003.
• Mombelli et al. The diagnosis and treatment
of periimplantitis. Periodontol 2000, 1998;
vol 17.
• Linkow-Implant Dentistry Today.
• Microbiology and antimicrobial therapy of
peri implantitis, Mombelli A. Perio 2000;
vol 28, 2002,177-189.

• Ageing, Osteoporosis and Dental Implants
Lekholm & Zarb
• Dental Implants DCNA: (50);2006
• Implant failures, Oral and maxillofacial surgery
clinics of North America, 1998
• Pathogenesis of implant failure , Tonneti et al,
vol 4, perio 2000
• Dental implants in peridontal therapy, position
paper; J Periodontol 2000;71:1934-1942

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