Peri implant mucositis, Peri implantitis, Definition, classification, treatment modality, Comprehensive implant supportive therapy protocol

1. IMPLANT RELATED PERIODONTAL
DISEASE
PRESENTED BY:
PRABLEEN ARORA
MDS STUDENT

2. IMPLANT LOSS / FAILURE
• Considered relative to the time of placement or
restoration.
Early implant failures
• Occur before implant restoration
• It probably did not achieve
osseointegration, or the integration
was weak or jeopardized.
• Improper preparation of the recipient
site which results in undue hard tissue
damage such as necrosis of the bone.
• Bacterial contamination and extensive
inflammation of the wound that may
delay healing of the soft and hard
tissues
• Improper mechanical stability of the
implant following its insertion
• Premature loading of the implant.
Late implant failures
• Occur after the implant has been
restored.
• Late implant failures occur after
prosthesis installation.
• Infection
• Implant overload
• Flemmig & Renvert (1999)

3. EXCESSIVE LOAD
• “Excessive load" may be difficult to define and may vary
from one subject and site to the next, factors such as
occlusal force (trauma from occlusion) in relation to :
1) size of implant,
2) surface features of implant,
3) Quality of the host bone, must obviously be
considered.
• Clinical studies have indicated that peri-implant bone
loss may be associated with load.
(Lindquist et al. 1988, Sanz et al. 1991, Quirynen et al. 1992, Rangert et al. 1995)

4. INFECTION
• The host response to biofilm formation on the
implant includes a series of inflammatory reactions
which initially occur in the soft tissue but which
may subsequently progress and lead to loss of
supporting bone.
• The tissue destruction in the bone compartment
starts in the "marginal", i.e. neck region, of the
implant and crater-like bone defects develop and
become visible in the radiograph.

5. • Peri-implant mucositis: Reversible inflammations of
the soft tissues surrounding implants in function.
• Peri-implantitis is defined as an inflammatory
process affecting the tissues around an
osseointegrated implant in function, resulting in
loss of supporting bone.
(Albrektsson & Isidor 1994)

7. Peri-implant mucositis
• Clinical features of peri-implant mucositis :similar to
those of in gingivitis at teeth and include classical
symptoms of inflammation, such as swelling and
redness.
• Assessment of peri-implant mucositis must
therefore always include assessment of bleeding
following probing

8. HISTOPATHOLOGY
• Zitzmann et al. (2001) studied the response to plaque formation in the soft
tissues at implant and tooth sites in humans.
• Twelve subjects with healthy periodontal and peri-implant conditions were
asked to refrain from tooth/implant cleaning for a period of 3 weeks.
• Clinical examinations were performed and soft tissue biopsies were
harvested prior to and at the end of the plaque accumulation period.
• The tissues were examined using histologic techniques. It was
demonstrated that plaque buildup was associated with clinical signs of soft
tissue inflammation.
• Furthermore, the initially minute lesions in the gingiva and in the peri-
implant mucosa markedly increased in size after 3 weeks of plaque build-
up: from 0.03 mm at baseline to 0.3 mm (gingiva) and 0.2 mm2 (peri-
implant mucosa).
• In addition, the proportion of B cells and neutrophils increased more in the
lesion in the gingiva than in its counterpart in the peri-implant mucosa.

9. • Berglundh et al. (1992) compared the reaction of the gingiva and
the peri-implant mucosa to 3 weeks of de novo plaque formation.
• Observed that similar amounts of plaque formed on the tooth and
implant segments of the dentition.
• The composition of the two developing plaques was also similar. It
was therefore concluded that early microbial colonization on
titanium implants followed the same pattern as that on teeth
(Leonhardt et al. 1992).
• Both the gingiva and the peri-implant mucosa responded to this
microbial colonization with the establishment of overt
inflammatory lesions, i.e. infiltrates of leukocytes in the connective
tissue.
• The lesions in the gingiva and in the peri-implant mucosa were
matched both with respect to size and location.
• Hence, both lesions were consistently found in the marginal
portion of the soft tissues and between the keratinized oral
epithelium and the junctional or barrier epithelium

10. Peri-implantitis
Clinical features
1. An inflammatory lesion in the
peri-implant mucosa .
2. Loss of periimplant bone.
3. Swelling and redness as well as
bleeding on gentle probing.
4. Suppuration is also a frequent finding
Diagnosis
• Bleeding on probing (BoP)
• Bone loss in radiographs.
• Peri-implantitis initially affects the marginal part of the peri-implant tissues and the
implant may remain stable and in function for varying periods of time.
• Implant mobility is therefore not an essential symptom for peri-implantitis but may
occur in a final stage of disease progression and indicates complete loss of
integration.

11. SIGNS AND SYMPTOMS
• There is radiological evidence for vertical destruction of the crestal bone.
• The defect usually assumes the shape of a saucer around the implant ,
while the bottom part of the implant retains perfect osseointegration.
• In some instances wedge-shaped defects develop along the implant.
• Vertical bone destruction is associated with the formation of a peri-implant
pocket.
• There is bleeding after gentle probing with a blunt instrument and there
may be suppuration from the pocket.
• Tissues may or may not be swollen. Hyperplasia is frequently seen if
implants are located in an area with nonkeratinized mucosa or if the
suprastructure is an overdenture .
• Pain is not a typical feature of peri-implantitis.

12. • Crater-formed defects around implants are
frequently found in radiographs obtained from sites
with peri-implantitis

13. • Estimation of the frequency of peri-implantitis is
difficult and depends on the criteria used to separate
health from disease.
• A mean crestal bone loss of 0.9-1.6 mm during the first
postsurgery year and bone loss in the range of 0.02 mm
to 0.15 mm in the following years have been reported
in numerous studies on two-stage implants with
submerged initial healing phase and are considered
normal for these systems.
Adell R et al 1986.
• A mean loss of 0.09 mm for mandibular implants and
0.01 mm for maxillary implants has been reported for
one-stage nonsubmerged implants in the second year
of service.
Weber HP et al 1992.

14. Prevalence
• Fransson et al. (2005) suggest that the
prevalence of subjects with peri-implantitis
within this implant population was about 28%.
• Roos-Jansåker et al. (2006 b) examined 216
implant treated patients (Brånemark System®)
after 9–14 years of function and reported that
16% of the subjects and 6.6% of the implants
had peri-implantitis.

15. HISTOPATHOLOGY
• Sanz et al. (1991) analyzed soft tissue biopsies from six patients with peri-implantitis and
reported that 65% of the connective tissue portion was occupied by an inflammatory lesion.
• Piattelli et al. (1998) described some pathological features of tissues harvested from 230
retrieved implants. It was reported that at sites where implants were removed due to peri-
implantitis, “an inflammatory infiltrate, composed of macrophages, lymphocytes and plasma
cells, was found in the connective tissue around the implants”.
• Berglundh et al. (2004) found that the mucosa contained very large lesions in which
numerous plasma cells, lymphocytes, and macrophages were present.
• It was furthermore observed that the inflammatory cell infiltrate consistently extended to
an area apical to the pocket epithelium and that the apical part of the soft tissue lesion
frequently reached the bone tissue.
• Berglundh et al. (2004) also reported that numerous neutrophil granulocytes (PMN cells)
were present in the lesions.
• Gualini and Berglundh (2003) included six subjects in a study and used
immunohistochemical techniques to analyze the composition of peri-implantitis. PMN cells
were found in large numbers in the central portions of the infiltrate.

16. CLASSIFICATIONS

17. • Schwarz et al. (2007) classified peri implant defect
depending on the configuration of the bony defect
as:
Class I defect – Intraosseous
Class II defect – Supra-alveolar in the
crestal implant insertion area.
Limitations:
• This Classification informs about only two classes.
• No clinical and radiological interpretation is evident.

18. Peri-implantitis is classified into
Early Peri-implantitis PD4mm, Bleeding and/or suppuration on probing, Bone loss
<25% of the implant length.
Moderate Peri-implantitis PD6mm, Bleeding and/or suppuration on probing, Bone loss
ranging from 25% to 50% of the implant length.
Advanced Peri-implantitis PD8mm, Bleeding and/or suppuration on probing, Bone loss
>50% of the implant length.
LIMITATIONS:
This classification provides a standarised method about clinical and
radiographic status of implant but it does not share any information of
information related to management of periimplantitis and prognosis.
Atleast two aspect of implant with evidence of Bleeding and/or
suppuration.
 Bone loss was measured on most recently radiograph taken and
compare with radiograph taken at the time of prothetic loading

19. Lang NP et al (2004) classification included treatment
part in its classification.
LIMITATIONS:
This is a good classification which provides clinical radiological
information and therapeutic part but still insufficient detail about
type of bony defect and prognosis.

20. Zhang L et al (2014) demostrated classification of peri-implant bone
defects (PIBDs) on the basis of their Panoramic radiographic shapes
in patients with lower implant-supported overdentures.
They are broadly classifieds into decreasing order of occurrence.
1. Saucer-shaped defects
2. Wedge-shaped defects
3. Flat defects
4. Undercut defects
5. Slit-like defects
LIMITATIONS
 This classification is given for lower implant-supported
overdentures cases only and focus on different shapes and
patterens of bony defects exclusively.
 Lacks clinical and detailed radiographic interpretations.

22. Retrograde implantitis
• Bone loss was measured on apico-coronal direction from
apex of the implant to the most coronal point of extension of
bone loss in millimeters.
• Coronal portion of the implant sustains a normal bone to the
implant interface.
• Class I (Mild lesion) – Radiographic bone loss that extends <
25% of the implant length from implant apex.
• Class II (Moderate lesion) – Extends 25–50% of the implant
length fron implant apex.
• Class III (Severe) – >50% of the implant length fron implant
apex.
It is a good classification of retrograde implantitis. None of the
classifications described have mentioned any point about this.

24. RISK INDICATORS
• A recent review by Lindhe and Meyle from the
Consensus Report of the Sixth European Workshop on
Periodontology concluded that risk indicators for peri-
implantitis included:
(1) Poor oral hygiene
(2) History of periodontitis
(3) Diabetes
(4) Cigarette smoking
(5) Alcohol consumption
(6) Implant surface
J Clin Periodontol 2008.

25. Dental plaque and poor oral hygiene
• In a study by Ferreira et al. 2006 higher total plaque scores were statistically
associated with peri-implant disease and a very poor oral hygiene status, as
described by median scores of full-mouth plaque >2, was highly associated
with peri-implantitis.
• In another study, most patients had relatively good plaque control in their
residual teeth but not at implant sites, and inadequate plaque control was
detected in around 74% of the implants. Implant sites less accessible by oral
hygiene measures showed more peri-implant infectious lesions (48%) than
other favorable sites (4%). Strom C et al 2009.
• This observation suggested that local factors such as poor oral hygiene and
the presence of dental plaque play an important role in the development of
peri-implantitis. Thus, the control of oral hygiene and periodontal status
should be monitored before and after the implant insertion to prevent or at
least to minimize the risk of developing peri-implantitis.
• Furthermore, plaque retention is also influenced by the form of implant-
supported prostheses, which must be determined before establishing a
treatment plan as well as choosing the number and type of implants.

26. History of periodontitis
• The frequency of implant failure in a partial loss of teeth was
significantly higher than in a total loss.
• However, study by Renvert et al. 2007 indicates that while peri-
implantitis is not dependent on the partial or total loss of teeth, a
history of periodontitis was a crucial risk for periimplant
mucosititis and peri-implantitis.
• Patients with a history of chronic periodontitis have a higher
prevalence of peri-implantitis (28.6%) than healthy patients
(5.8%). Lang NP et al 2003.
• A recent study by Koldsland et al. 2011 also indicates that
individuals with a history of periodontitis are prone to peri-
implantitis if they had peri-implant bone loss >2 mm.
• Likewise, a systematic review by Renvert et al. concluded that
patients with treated periodontitis may be at greater risk for peri-
implant infections than those without. Because the pathogenic
flora in peri-implantitis are similar to that found in periodontitis,
periodontal pockets are probably a reservoir of microorganisms
colonizing implant surfaces.

27. Diabetes
• A study by Ferreira et al. 2006 showed that patients
with diabetes (diagnosed by fasting blood sugar >126
mg/dL or taking anti-diabetic medicine over the
previous 2 weeks) were more prone than those
without diabetes to develop peri-implantitis.
• Furthermore, the presence of diabetes was statistically
associated with an increased risk of peri-implantitis. It
seems that poor metabolic control in diabetics made
patients more susceptible to infection and implant loss.
The clinician should inform diabetic patients of their
possible increased risk for periimplantitis.

28. Smoking
• Smoke was identified as a major risk factor of both periodontitis and peri-
implantitis.
• A recent study by Rodriguez-Argueta et al. 2011 showed that smokers had
an increased risk of infection, implant loss, mucositis and peri-implantitis
than non-smoking patients.
• The pathogenic mechanisms of smoking may be explained by the toxic
effects of the more than 4000 toxins present in cigarettes.
• Nicotine is a potent vasoconstrictor that reduces blood flow and nutrient
delivery to healing sites.
• Some compounds of tobacco also act as chemotactic substances that
enhance tissue destruction by enzymes released by neutrophils and
macrophages.
• Peri-implantitis was more frequent in smokers (9.2%) than non-smokers
(5.3%).30 Smokers had more severe inflammatory signs, deeper peri-
implant pockets and larger peri-implant bone loss than non-smokers.
• The influence of smoking on peri-implant tissue was greater in the maxilla
than the mandible. Several retrospective studies over 8 years have also
shown that smokers had a high risk of developing peri-implantitis and bone
loss.

29. Alcohol consumption
• Individuals who use alcohol may have a vitamin K
deficit disrupting the production of prothrombin, thus
affecting coagulation mechanisms.
• Alcohol consumption is associated with deficiencies of
the complement system, alteration of the neutrophil
function and modulating T lymphocyte activity.
• Moreover, some substances contained in alcoholic
drinks such as fusel oil, nitrosamines and ethanol, can
cause bone destruction and block the stimulation of
bone neoformation.
• Only one study by Galindo-Moreno et al. concluded
that peri-implant marginal bone loss was statistically
linked to alcohol consumption >10 g per day and that
alcohol induced more serious peri-implantitis than
cigrarettes.

30. Implant surface characteristics
• Most recent titanium implants with a rough surface showed more favorable
osseointegration than those with smooth surfaces.
• However, a rough surface also favored the formation and retention of
dental plaque.
• Roughness increased both the adhesive surface of bacteria and the
difficulty in cleaning the implant.
Quirynen M et al 2006.
• In a study by Astrand et al. in 2004, ITI Dental Implant System implants
(Straumann AG, Waldenburg, Switzerland) with a plasma-sprayed surface
had a statistically higher incidence of peri-implantitis than Branemark
System implants (Nobel Biocare AB, Gothenburg, Sweden) with a smooth
surface.
• Conversely, a systematic review by Esposito et al. showed that there was no
statistically significant difference in the incidence of peri-implantitis
between smooth and rough implant surfaces.
• Likewise, in a recent review by Renvert et al., there was no evidence that
implant surface characteristics can have a significant effect on the initiation
of peri-implantitis.

31. Genetic traits
• A study by Cornelini et al. showed a significant increase in the
density of blood microvessels in peri-implantitis sites, but the
expression of vascular endothelial growth factor (VEGF) was
statistically low.
• Thus, VEGF could play a protective role in peri-implantitis.
• There was an correlation between the polymorphisms of the
interleukin (IL)-1-specific gene and peri-implant bone loss in
smokers.
• Jansson et al. showed that the IL-1 genotype was a risk indicator of
peri-implantitis and there was a synergistic effect between the IL-1
genotype and smoke.
• However, two other studies failed to find an association between
the IL-1 genotype and peri-implantitis or of implant failure or bone
loss. Therefore, future prospective studies with large numbers of
patients are necessary to confirm this association.

32. Lacking keratinized mucosa
• A study by Block et al. suggested that the presence
of keratinized gingiva around implants was
correlated with the health of both soft and hard
tissue as well as implant survival.
• However, an analysis of multiple potential factors of
peri-implant mucositis and peri-implantitis was
performed, but no association between the
absence of keratinized gingiva and peri-implant
infection was found.
• Therefore, lacking keratinized mucosa has not
currently been confirmed as risk factor of peri-
implantitis.

33. Other non-confirmed risks
• Xerostomia could be a risk factor for peri-
implantitis.
• In fact, a decrease of salivary flow was often
accompanied by a change in its composition and
reducing bacterial clearance in the oral cavity.
• More viscous saliva with a reduction of
antibacterial activity promoted the formation of
dental plaque and bacterial growth

34. Evidence based risk factors
Substantial evidence
•Poor oral Hygiene
•History of periodontitis
•Smoking
Limited evidence
•Diabetes
•Alcohol consumption (> 19g / day)
Controversial and limited evidence
•IL-1 Polymorphism
•Absence of Keratinized mucosa
•Microtopography of implant surface
Lindhe J, Meyle J. J Clin Periodontol 2008;35:282-285

35. DIAGNOSIS
• Peri-implant diagnostic procedures can serve
several functions:
(i) Screening for peri-implant disease or for factors
increasing the risk to develop an undesirable
condition.
(ii) Differential diagnosis of peri-implantitis and peri-
implant mucositis.
(iii) Treatment planning.
(iv) Evaluation of therapy and monitoring.

36. Clinical diagnosis
• A periodontal probe is an essential tool for the clinical
diagnosis of peri-implantitis. Probing with a light force
of 0.25 N does not cause peri-implant tissue damage
and it is recommended for evaluating peri-implant
disease.
• Clinical signs of peri-implantitis are bleeding on probing
in conjunction with peri-implant pockets >5 mm with or
without suppuration.
• In fact, bleeding on probing and suppuration indicate
the presence of inflammation and infection. Because
healthy implants generally have probing depths that
are less than 4 mm, peri-implant pockets of 5 mm or
more should be regarded as an indicator of bone loss
and hence, a radiographic evaluation is required.

37. • A peri-implant pseudopocket could be present as soft
tissues that are positioned above the implant shoulder
intentionally for esthetic reasons.
• Also, peri-implant hyperplasia is often found in an area
of absence of keratinized gingiva or the overflow of
supra-implant structures.
• Contrariwise, platform-switched or abutment designs
could also provoke difficult probing and the probing
depth may hence underestimate the extent of the
lesion
• Implant mobility is not used to diagnose peri-
implantitis because it indicates the complete loss of
osseointegration and the failure of the implant.
• Moreover, pain is not a typical sign of peri-implantitis

38. Radiographic assessment
• In the First EWOP (1994) it was proposed that marginal bone loss of less than 1.5 mm
during the first year in function and less than 0.2 mm per year thereafter to be one of the
major criteria for success.
• Baseline radiographs should be taken to determine alveolar bone levels after physiological
remodeling and when clinical signs suggest peri-implantitis, a radiograph of the site is
required to confirm the diagnosis.
• In two recent studies by Koldsland et al (2010) it was proposed that a radiographic peri-
implant bone loss >2 mm was a possible risk indicator of peri-implantitis.
• In terms of dental radiographic techniques, panoramic radiography gives a complete
visualization of anatomical structures around implants but its use is limited because of its
low resolution and image distortion.
• Periapical radiography is often used to verify marginal bone level or interproximal bone loss
in peri-implantitis. However, our inability to assess facial and lingual or palate bone tables
and the underestimation of intraosseous lesions are still limiting conventional radiography.
• For minimizing the eventual error of a radiographic assessment of bone loss, the utilization
of individual or fixed angulators could be useful to prevent image deformation.
• Currently, multi-slice computer tomography and cone beam volume imaging offer implant
dentistry certain advantages, such as representing infrabony lesions in three planes, true to
scale and without any overlay or distortion.
• Furthermore, computer-assisted image analysis, such as subtraction radiography, permits
the detection of small changes in bone density.

39. Microbiological test
• A microbiological test of subgingival microflora
using a bacteria culture, checkerboard DNA–DNA
hybridization, polymerase chain reaction (PCR),
monoclonal antibody and enzyme assays have been
proposed to determine an elevated risk for
periodontal disease or peri-implantitis.
• High levels of Porphyromonas gingivalis, P
intermedia and Actinobacillus
actinomycetemcomitans increased the risk for
further attachment loss in maintenance patients

40. Differential Diagnosis
Peri-implant mucositis
• Peri-implant mucositis may be identified clinically by redness, swelling of the soft
tissue without loss of supporting bone (probing depth <5 mm) and bleeding on
probing are currently considered to be important indicators.
• The treatment of peri-implant mucositis includes the removal of dental plaque and
calculus by using appropriate instruments and oral hygiene instruction without
antiseptic or combined with antiseptic.
• Likewise, the literature review of Renvert et al (2008) confirmed that mechanical
non-surgical therapy could be effective in the treatment of periimplant mucositis
and the adjunctive use of antimicrobial mouth rinses enhanced the outcome of
such therapy.
• However, two later studies indicated that an adjunctive application of chlorhexidine
did not enhance results in comparison with mechanical cleansing alone.
• Furthermore, the treatment of peri-implant mucositis is useful for the prevention
of peri-implantitis because mucositis represents an obvious precursor of peri-
implantitis.

41. Occlusal overload
• Occlusal overload together with peri-implantitis are the major causes of implant
loss.
• Factors associated with occlusal overload or occlusal trauma probably consist of an
 excessive expansion of a prosthesis in the posterior region,
 implant alignments,
 a significant deviation of the implant axis from the function axis,
 an important ratio of crown height/implant length,
 a discrepancy in dimensions between the implant head and occlusal table.
• An occlusal overload can cause the complete bone loss of an osteointegrated
implant.
• Bone destruction is accelerated if occlusal trauma is combined with peri-implant
infection.
• In fact, the marginal bone loss due to overload is often accompanied by attachment
loss and deepening of the pockets.
• After some time the newly created anaerobic environment will inevitably harbor
periopathogenic flora.
• Therefore, the presence of pathogenic subgingival flora after occlusal overload may
reflect a secondary infection of a favorable environment which can contribute to
further loss of marginal bone.

42. • Occlusal correction is necessary to stop the
progress of bone destruction. Control of occlusion
by progressive loading depending on bone density
can reduce peri-implant bone loss in a healing
phase.
• A case report of occulsal overload associated with
peri-implantitis used combined treatment methods
including occlusal adjustment, the surgical removal
of contaminated tissue and an autogenous bone
graft. After 12 months, a radiograph revealed
marginal bone regeneration and a normal clinical
aspect was observed.
Uribe R et al 2004.

43. Retrograde peri-implantitis
• Retrograde peri-implantitis is defined as a clinically
symptomatic periapical lesion (diagnosed as a
radiolucency) that develops shortly after implant
insertion while the coronal portion of the implant
becomes a healthy bone at the implant interface.
Quirynen M et al 2005
• Clinical symptoms include:
• pain,
• Tenderness
• swelling or presence of a fistulous tract.

44. • The etiology of retrograde peri-implantitis may be bacterial contamination
during the implant insertion or pre-existing bone inflammation (such as
bacteria, a cyst or granuloma after tooth extraction).
• Compared with successful implants, these periapical lesions appear on
extracted tooth sites that have a history of endodontic pathology.
• The lesion forms at the apex of the implant but it does not extend to the
coronal, proximal or facial area.
• Quirynen et al. (2005) suggested the treatment method of retrograde
lesions, includes :
 the complete removal of granulation tissue,
 curettage of bony cavity walls
 Filling substitutive bone (Bio-Oss).
• The surgery was performed under the antibiotic coverage of forms of b-
lactamase-resistant penicillin.
• Once diagnosed, the lesion should be treated surgically rather than by
observation and conservative management

45. Non-surgical treatment of peri-implantitis
• Mechanical therapy alone
• The formation of dental plaque was crucial to the development of the peri-
implant infections (such as periimplant mucositis and peri-implantitis) that
altered the biocompatibility of the implant surface.
• Treatment of infected implant surface and the reduction of pathogenic
bacterial flora around the implant are the main goals of peri-implantitis
treatment.
• The specific morphology of implant thread combined with a modified
surface facilitated bacterial colonization but limited the efficiency of
conventional cleaning instruments.
• In addition, debridement using metal instruments harder than titanium
could alter the implant surface, therefore curettes or inserts in plastic or
carbon fiber were recommended.
• A study by Karring et al. showed that non-surgical mechanical treatment
alone was insufficient to eliminate peri-implant lesions. Although bleeding
on probing had improved after 6 months, the peri-implant pocket depth
was unchanged.

46. • A microbiological test of subgingival microflora using a bacteria culture,
checkerboard DNA–DNA hybridization, polymerase chain reaction (PCR),
monoclonal antibody and enzyme assays could suggest antibiotic therapy
• In fact, peri-implantitis is associated in most cases with a mixed anaerobic
flora, including Fusobacterium spp. And P. intermedia in high numbers.
Antimicrobial agents such as metronidazole and ornidazole, which act
specifically against strict anaerobes, seem to be an excellent choice for this
type of infection.
• However, a limited number of patients may have peri-implantitis lesions
that are dominated by Staphylococcus spp. or metronidazole-resistant
Aggregatibacter actinomycetemcomitans or enteric bacteria and yeasts.
• Moreover, certain cases of peri-implantitis are characterized by periods of
rapid and marked destruction compared with periodontitis.
• This progression may be explained by the host response to specific
infectious agents.

47. Mechanical therapy with an adjunct of
an antiseptic agent
• The mechanical non-surgical debridement alone was not effective in
reducing bacterial flora around infected
implants.
• The addition of antimicrobial treatment therefore seems necessary to
improve clinical results.
• The antimicrobial treatment using a topical application of chlorhexidine was
proposed to complete the mechanical treatment.70,71
• However, a local irrigation of 0.12% chlorhexidine combined with a local
application of 0.12% chlorhexidine gel and a mouthwash containing 0.12%
chlorhexidine for 10 days gave a no better result.
• Peri-implantitis was treated using a plastic curette associated with an
antiseptic (chlorhexidine 0.2%) and improved clinical parameters such as
the reduction of bleeding on probing and of the pocket depth after 6
months, but residual defects still persisted.
• These results suggested that chlorhexidine has a limited antimicrobial
effect in infectious peri-implant lesions.

48. Mechanical therapy with an adjunct of
antibiotic therapy
• Mombelli and Lang 1992 conducted a study for the treatment of peri-implant infections by
combining mechanical debridement with systemic antimicrobial therapy.
• The bleeding on probing index immediately decreased after systemic antibiotic therapy and
there were also quantitative and qualitative changes of pathogenic flora.
• However, these parameters were reversible after the treatment period.
• A local application releasing a high dose of antibiotic in infected sites for several days
effectively cleared bacteria that were not eliminated by mechanical treatments.
• In fact, debridement followed by an insertion of non-resorbable fibers containing
tetracycline (Actisite) in peri-implant pockets for 10 days showed a significant reduction of
pocket depth after 12 months.
• Buchter et al. 2004 compared the efficiency of mechanical treatment alone using a plastic
curette with mechanical treatment combined with a local application of bioresorbable
polymer-releasing doxycycline (Atridox). The results after 4 months showed that patients
treated with Atridox had a higher clinical attachment gain than those treated by
debridement alone. The reduction of bleeding on probing and peri-implant pockets was
statistically significant only among patients in the Atridox treatment group.
• A recent study combining mechanical treatment with a repeated local application of
minocycline microspheres (Arestin) after 30 and 90 days showed benefits in the therapy of
peri-implantitis. This study also indicated that mechanical treatment combined with the
local application of an antibiotic achieved a better result

49. Surgical treatment of peri-implantitis
• The major objective for such an approach is to provide
access for removal of the biofilm and calcified deposits
from the implant surface in order to allow healing and
reduce the risk for further disease progression.
• If non-surgical treatment fails, surgical intervention
with open debridement and resective or regenerative
therapy is recommended.
• The basic principles include the elimination of the
periimplant osseous defect using ostectomy and
osteoplasty as well as bacterial decontamination.
• Additionally, smoothening and polishing of the
supracrestal implant surface (implantoplasty) may be
applied.

50. • When surgical intervention is necessary, an
inverse bevel incision is recommended to
facilitate flap elevation and preserve soft
tissue.
• Following removal of the soft-tissue collar from
the infected tissue around the implant,
mechanical decontamination to remove plaque
and mineralized deposits from the implant
surface should be performed and, for this task,
instruments made of pure titanium are
recommended .
• The use of a titanium rotary brush makes this
procedure easier than use of conventional
curettes .

51. • In the presence of a crater-like fourwall bony
defect or a three-wall defect, regenerative
techniques are recommended and the use of
autogenous bone or bone substitutes can be
used to obtain bone fill.

53. • Airborne-particle abrasion devices have also been
recommended for the decontamination of implant
surfaces during surgery but because of the risk of
developing subcutaneous emphysema, care must be
taken during their use.
• A number of other methods for decontamination, such
as the use of lasers or abrasive devices, and
implantoplasty of the exposed part of the implant, have
been suggested as adjuncts to surgical resective or
regenerative surgery.
• Implantoplasty is an alternative option to improve the
implant surface topography to reduce microbial
adhesion and colonisation thus preventing re-infection
of the site.This involves mechanically adjusting the
exposed implant threads with rotary instruments to
reduce the roughness of the surface and therefore
minimise future plaque retention.

54. • Serino et al. (2011) showed that in patients with
active periimplant disease surgical pocket
elimination and bone recontouring in combination
with plaque control before and after surgery
represents an effective treatment. Two years after
open reduction of inflammated peri-implant soft
tissue and osseous surgery 48% of the patients had
no signs of peri-implantitis and 77% of the patients
had no implants with pocket depths ≥ 6 mm with
bleeding and/or suppuration.

55. • In a radiographic study with 3 years follow-up, Romeo et al. (2007)showed that the
marginal bone loss after resective surgery with implantoplasty was significantly
lower than after resective therapy only

56. • Resective surgical therapy for peri-implantitis is a
recommendable therapy option.
• Ostectomy and osteoplasty combined with
implantoplasty represent an effective therapy to
reduce or even stop peri-implantitis progression.
• Nevertheless, due to the increased postoperative
recessions, this procedure is not suitable for every
situation, especially in highly esthetic sensitive
areas.

57. Regeneration
• Resective surgical therapy may result in re-
osseointegration in only minor superficial defects.
• From functional, esthetic and long-time-survival
point of views, full regeneration and re-
osseointegration is aspired.

59. A study of autogenous
bone graft on 17 patients
with 25 treated implants
showed a reduction of the
peri-implant pocket from
6.9 to 0.7 mm (P = 0.001),
corresponding to
90% bone reconstruction
and improvement of
marginal bone level from
6.2 to 2.3 mm after 2–3
years. Vertical
bone resorption under 4.5
mm was completely
regenerated.
Behneke A et al (2000

61. MAINTENANCE FOR DENTAL
IMPLANT PATIENTS
• Patients with periodontitis-associated tooth loss are at significantly increased risk
of developing periimplantitis.
• The overall periodontal condition in partially edentulous implant patients can
influence the clinical condition around implants.
• The microflora of implants in partially edentulous patients differs from that in
edentulous patients.
• The implant microflora is similar to tooth microflora in the partially edentulous
mouth.
• Periodontal and implant maintenance are linked because maintenance of a tooth
microflora consistent with periodontal health is necessary to maintain implant
microflora consistent with periimplant health.
• Because periimplantitis is difficult to treat,it is extremely important to treat
periodontal disease before implant placement and to provide good supportive
therapy with implant patients.

62. • In general, procedures for maintenance of patients with implants
are similar to those for patients with natural teeth, with the
following three differences:
1. Special instrumentation that will not scratch the implants are
used for calculus removal on the implants.
• Metal hand instruments and ultrasonic and sonic tips should be
avoided because they can alter the titanium surface.
• Only plastic instruments or specially designed gold plated curettes
should be used for calculus removal because the implant surfaces
can be easily scratched.
• The rubber cup with flour of pumice, tin oxide, or special implant-
polishing pastes should be used on abutment surfaces with light,
intermittent pressure
2. Acidic fluoride prophylactic agents are avoided because they
cause surface damage to titanium abutments
3. Nonabrasive prophy pastes are used.

63. • Known as the cumulative interceptive supportive
therapy (CIST).
• Depending on the clinical and eventually the
radiographic diagnosis, protocols for preventive and
therapeutic measures designed to intercept the
development of peri-implant lesions.
• This system of supportive therapy is cumulative in
nature and includes four steps.
• The 4 steps are Mechanical debridement, CIST
• protocol A
• 1. Antiseptic therapy, CIST protocol A and B
• 2. Antibiotic therapy, CIST protocol A + B
• 3. Antibiotic therapy, CIST protocol A + B + C
• 4. Regenerative or resective therapy, CIST protocol
• A+B+C+D

65. Conclusion
• Successful management of peri implantitis
requires a thorough understanding of the
underlying medical and dental factors involved
in the overall complex of the disease. The
continuous development of new diagnostic
and therapeutic methods has made it possible
to prevent progression of the disease in most
cases and to give these patients a long-term
perspective for retention of their implant
bone restoratio