2. PERI-IMPLANTITIS
Guided by:
Dr. Monica Mahajani
Dr. Chandrahas Goud
Dr. Anup Shelke
Dr. Subodh Gaikwad
Dr. Anup Gore
Dr. Kuldeep Patil
Dr. Amrita Das
Presented by:
Dr. Chavan Sneha S.
(3rd Year PG)
4. INTRODUCTION:
• The term peri-implantitis was introduced in 1987.
(Mombelli A.1987)
Defination:
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Destructive inflammatory process affecting the soft and hard tissues
around osseointegrated implants, leading to the formation of a peri-
implant pocket and loss of supporting bone.
(Albrektsson et al. 1994)
5. • Two common forms : Peri-implant mucositis and Peri-
implantitis : Inconsistencies in defining and reporting
Chen S, Darby I 2003
Peri-implant mucositis
Peri-implantitis
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6. • PERI-IMPLANT DISEASES: It is a descriptive term used to describe a site-
specific inflammatory process affecting the tissues surrounding an implant,
yielding many features in common with chronic periodontitis (Emrani et al. 2009).
• PERI-IMPLANT MUCOSITIS: It is the reversible inflammatory process of the
soft tissues surrounding a functioning implant with no loss of supporting bone.
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Albrektsson T, Isidor F Proceedings of the 1st European Workshop on Periodonto
7. Implant failure: Traditionally described as early or late:
Early failures: Prior to implant loading : Surgical, implant or host-related factors
Late failures: After prosthodontic rehabilitation
Peri-implant disease or biomechanical overload
Bone loss around the implant
Loss of osseointegration
Esposito M et al 1998
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8. 3rd International Team for Implantology (ITI)
Consensus Conference
Similar definitions, and additional diagnostic parameters
for periimplantitis
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Peri-implant sulcular fluid analysis was also included
as a diagnostic aid for peri-implantitis
Plaque
Suppuration
Bleeding on probing (BOP)
Probing depth (PD) > 5 mm
9. • According to Frank Schwarz 2017,
Peri-implantitis is a pathological condition occurring in tissues
around dental implants, characterized by inflammation in the peri-
implant mucosa and progressive loss of supporting bone.
Peri-implantitis is an implant related disease condition which
contributes to significant proposition of implant failure.
This condition was first described Levignac in 1965.
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11. Froum and Rosen, 2012
• Based on distinct clinical stages as follows:
• Early PD ≥ 4 mm (bleeding and/or suppuration on probing) Bone loss
< 25% of the implant length
• Moderate PD ≥ 6 mm (bleeding and/or suppuration on probing) Bone
loss 25% to 50% of the implant length
• Advanced PD ≥ 8 mm (bleeding and/or suppuration on probing) Bone
loss > 50% of the implant length
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12. Bogaerde et al 2014
• Proposed classification of bone defects adjacent to dental implants
highlighting the defect anatomy in the progression of the
regenerative process.
• Closed defects- It is characterized by the maintenance of intact
surrounding bone walls
• Open defects- It is the one which lack one or more bone walls.
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13. Ata-Ali et al (2015)
• classified peri-implantitis based on the clinical status:
• Stage I BoP and/or SUP and bone loss ≤ 3 mm beyond biological bone
remodeling
• Stage II BoP and/or SUP and bone loss > 3 mm and < 5 mm beyond
biological bone remodeling
• Stage III BoP and/or SUP and bone loss ≥5 mm beyond biological bone
remodeling
• Stage IV BoP and/or SUP and bone loss ≥50% of the implant length beyond
biological bone remodeling
• BoP- Bleeding on Probing; SUP- Suppuration
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14. Sarmiento et al (2016)
• classified peri-implantitis based on etiology
Origin Example
• Peri-implantitis induced by pathogenic bacteria/biofilm- Plaque, calculus, biofilm,
previous host susceptibility to periodontitis (previous/active)
• Peri-implantitis induced by exogenous irritants- Residual cement, smoking,
impacted food debris
• Peri-implantitis induced by iatrogenic factors- Buccal implant placement,
inadequate inter-implant distance, overheating during surgical placement, poorly
fitting restorations
• Peri-implantitis induced by extrinsic pathology- Proximal periapical pathology,
proximal carcinoma, latent endodontic lesion post extraction
• Peri-implantitis induced by absence of keratinized tissue (AKT)- Absence of
attached gingival, lack of keratinized tissue with or without muscle attachment
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15. Passi D et al (2016)
• classified peri-implantitis based on bleeding on probing, probing
depth, percentage of bone loss and mobility.
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16. According to Rucha Shah et al (2016),
• Retrograde Peri-implantitis is classified as
• Class I (Mild) Extends < 25% of the implant length from implant apex.
• Class II (Moderate) Extends 25–50% of the implant length from
implant apex.
• Class III (Advanced) >50% of the implant length from implant apex.
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The Journal of Contemporary Dental Practice, April 2016;17(4):313-321
17. 13-01-2023 17
Figs 2A to C: Figure demonstrating the various proposed classes for retrograde peri-
implantitis (RPI):
(A) Class I mild RPI (bone loss 50% of implant length from implant apex)
(B) Class II moderate RPI (bone loss 25–50% of implant length from implant apex),
and
(C) Class III advanced RPI (bone loss>50% of implant length from implant apex)
18. According to Sarmast et al 2017,
• Retrograde periimplantitis is classified as
• Class 1 Implant placement resulting in devitalization of adjacent
previously vital tooth
• Class 2 Implant apex infected by persistent periapical lesion on
adjacent tooth/implant
• Class 3 Implant apex placed/angulated labially or lingually outside
envelope of bone
• Class 4 Implant apex lesion developed due to residual infection at
placement site
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19. Classification based on defect morphology
1. Nishimura et al, 1997 gave another system of classification exists
amount of bone loss with shaped of defect associated
• Class 1: Slight horizontal bone loss with minimal peri-implant defects
• Class 2: Moderate horizontal bone loss with isolated vertical defects
• Class 3: Moderate to advanced horizontal bone loss with broad,
circular bony defects.
• Class 4: Advanced horizontal bone loss with broad, circumferential
vertical defects, as well as loss of the oral and/or vestibular bony wall
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20. 2. Schwarz et al 2019
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.
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21. • Spiekermann 1984 characterized peri-implant defect into the type of
bone resorption pattern into 5 category.
Class I – Horizontal,
Class II – Hey-shaped
Class III a – Funnel shaped
Class III b – Gap-like
Class IV – Horizontal-circular form
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22. Etiology of peri –implantitis
• Though peri-implantitis, like periodontitis is considered a
multifactorial disease, two major etiological factors are:
• Microbial colonisation (Bacterial infection).
• Biomechanical factors associated with overloaded implant i.e.
Excessive mechanical stress (Quirynen et al. 1992, Rangert et al.
1995).
Others:
• Traumatic surgical techniques
• Compromised host response
• Inadequate amount of host bone
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25. • 4. Implant related factors :
• Implant design and surface characteristics TPS & HA - high incidence
• Deep implant placement Excess cement remaining in submucosal
region following cementation of a superstructure may contribute to
periimplant infection.
• Surface characteristic of an implant: Hydroxy apatite coated implant
have clinical & histological evidence that resorption of the surface is
by inflammatory phagocytosis under the influence of bacterial
inflammation.
• Treated & detoxified HA surface show continued phagocytosis .
• Titanium implant shows little or no resorption of surfaces if the
inflammatory lesions can be arrested.
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26. Bacterial infection- Role of plaque microbiota
• The microbiota at peri-implantitis sites presented much higher
level of motile rods, spirochetes and fusiforms while coccoid cells
accounted for only 50% of the microbiota (George et al. 1994).
• The microflora in the peri-implant sulcus is established as early as
30 minutes to 2 weeks following implant placement and is nearly
identical to that found at adjacent teeth.
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27. • The microorganisms most commonly related to the failure of an
implant are rods and motile forms of gram negative anaerobes and
spirochetes. These includes:
1. Prevotella intermedia,
2. Porphyromonas gingivalis(PG),
3. Aggregatibacter actinomycetemcomitans(AA),
4. Bacteroides forsythus,
5. Treponema denticola(TD),
6. Prevotella nigrescens, Peptostreptococcus micros and
7. Fusobacterium nucleatum,
8. S.aureus
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28. • Samples from partial edentulous patients have greater gram-negative
aerobic species when compared to completely edentulous cases.
• Periodontal pathogens Aggregatibacter actinomycetemcomitans (AA),
Porphyromonas gingivalis (PG) and Treponema denticola (TD) where
more commonly reported in partially edentulous cases than
completely edentulous cases.
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29. • Plaque Biofilm Development and Colonization:
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From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.
30. Excessive mechanical stress
• It has been postulated that Occlusal overload is influenced by
prosthetic design. Implants subjected to occlusal overload results in
micro motion at the implant abutment interface and compromises
the osseointegration during early healing.
• The location of implant, the dimension of the implant, proportion of
the prosthesis are some of the factors leading to occlusal overload.
The occlusal overload also depends on the magnitude, duration,
transmitted as lateral or axial stress on to the bone.
• This creates micro fractures of the bone around the implant and
initiate peri-implant crestal bone loss which will further propagate in
the presence of microbial plaque.
.
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31. • The excess occlusal can be a consequence of placement of implant in
poor quality bone, Placement of an implant is an unfavorable position
that does not favor ideal load transmission over implant surface, The
patient has a pattern of heavy occlusal function associated with para
functional habits, Improper prosthetic superstructure that does not
fit the implant precisely.
• In specific occlusal overload conditions like bruxism, the habit often
results in fracture of the suprastructure, but never affects the
marginal bone around implants.
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Soldatos N, Romanos GE, Michaiel M, Sajadi A, Angelov N, Weltman R, et al. Management of retrograde peri-implantitis using an airabrasive device, Er,Cr:YSGG laser, and guided
bone regeneration. Case Rep Dent. 2018.
32. Clinical Features
• 1. Increased redness & swelling.
• 2. Bleeding on probing
• 3. Suppuration
• 4. Formation of peri-implant pocket (>4mm).
• 5. Pain on mastication
• 6. Supra occlusion at implant site
• 7. Mobility – final stage of peri-implantitis (Mombelli & Lang, 1998)
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33. • 8 th European workshop of periodontology in 2012 reported that
> 2mm bone loss from the expected marginal level is considered
as case definition.
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34. Radiological Features:
• Usually assumes the shape of saucer around the implant and is well
demarcated (vertical bone destruction with periimplant pocket).
Because the bottom part of implant retains the perfect
osseointegration bone destruction may proceed without notable
signs of implant mobility until osseointegration is completely lost.
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35. • Peri-implantitis can occur in the type of etiology:
• Patho-physiology:-
Traditional pathway
Retrograde pathway
And also through implant contamination
• Traditional Pathway: Accumulation of microbes at the peri- implant
or mucosal margin leading to local inflammatory response,
subsequently decreased collagen content. Large inflammatory cells
infiltrate into the apical portion of pocket epithelium leading to
pocket formation, bone loss and De-osseointegration (Mombelli,
2002).
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36. • Retrograde Pathway
Occlusal trauma or defective restorations (Steenberghe et al. 1999)
Microfractures of bone implant surface
Bone loss and loosening of implant
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37. • Zitzmann et al. quantified the incidence of the development of peri-
implantitis in patients with a history of periodontitis almost six times
higher than in patients with no history of periodontal inflammation.
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Zitzmann NU, Walter C, Berglundh T: Ätiologie, Diagnostik und Therapie der Periimplantitis –
eine Übersicht. Deutsche Zahnärztliche Zeitschrift 2006, 61:642–649.
38. • Berglundh et al investigated the effects of plaque formation on teeth
and implants in Beagle dogs. The study demonstrated that both peri-
implant and periodontal tissues reacted similarly. An inflammatory
response was provoked, characterized by an increase of leukocyte
transmigration and the establishment of a connective tissue lesion.
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Berglundh T, Lindhe J, Marinello C, Ericsson I, Liljenberg B. Soft tissue reaction to de novo plaque
formation on implants and teeth. An experimental study in the dog. Clin Oral Implants Res 1992;3(1):1–
39. • De Bruyn et al have shown that 19 to 43% of implants with signs of
progressive bone loss did not present PD > 6 mm or pus on probing.
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De Bruyn H, Christiaens V, Doornewaard R, et al. Implant surface roughness and patient factors on
long-term peri-implant bone loss. Periodontol 2000 2017;73(1):218–227
40. • In another experiment in Labrador dogs, by Ericsson et al, implants
exposed to daily plaque control displayed healthy surrounding
tissues. In contrast, this procedure’s termination resulted in creating
an inflammatory cell infiltrate in the marginal portion of peri-implant
mucosa.
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Ericsson I, Persson LG, Berglundh T, Marinello CP, Lindhe J, Klinge B. Different types of inflammatory
reactions in peri-implant soft tissues. J Clin Periodontol 1995;22(3):255–261
41. • In particular, Staphylococcus aureus appears to play a predominant
role for the development of a peri-implantitis. This bacterium shows
an high affinity to titanium and has according to the results of Salvi et
al. a high positive (80%) and negative (90%) predictive value.
• As another beneficial cause, smooth implant surfaces in comparison
to rough surfaces can accelerate the peri-implant inflammation
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Salvi GE, Fürst MM, Lang NP, Persson GR: One-year bacterial colonization patterns of Staphylococcus aureus and other bacteria at implants and adjacent
teeth. Clin Oral Implants Res 2008, 19:242–248.
44. 1. Peri-Implant Radiography
• Vertical bone loss of less than 0.2 mm annually following the
implant’s first year of service has been proposed as one of the major
criteria for success.
• The mean annual bone height changes in the range of 0.1mm are only
mathematically derived and cannot be detected by comparison of
two radiographs from a single implant. Because of concerns about
undue exposure of subjects to radiation, radiographs cannot be taken
at every recall visit.
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45. • IOPA should be obtained because OPG have lower discrimination
power. Direct digital imaging may replace conventional radiography.
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46. 2. Peri-implant probing
• Manual, automated or plastic pressure controlled probes are used.
• Pocket depth of 3-4 mm is commonly seen even in a healthy implant.
• Increased probing depth is due to the absence of a connective tissue
attachment zone, which is present approximately 1 mm coronal to
the crestal bone (Mombelli & Lang 1998).
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47. • Probing with a conventional probe with a light pressure of 0.25 N
does not cause any damage to peri-implant tissue.
• Advantages -Simplicity of method
Immediate availability of results
• Ability to demonstrate topographic disease patterns
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48. • PROBING - an indispensable part of implant maintenance assessment.
• Probing depths are influenced by thickness and type of mucosal
epithelium surrounding the implant.
• Use of a fixed reference point on an implant abutment or prosthesis
for a reliable measurement of attachment levels is recommended.
• The peri-implant probing attachment level correlates closely with
radiographically measurable peri-implant bone changes.
• Probing be a part of each maintenance recall appointment.
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49. • Implant probing:
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(A) A titanium or plastic periodontal probe to be used to evaluate pocket depth. (B) Because
of nontypical prosthetics, in some cases it may be dificult to probe along the long axis of the
implant because of access. (C) Impossible to probe.
50. 3. Bleeding on Probing
• Bleeding on probing represents a clinical parameter defined as the
reaction of soft tissue seal following the penetration of a periodontal
probe into the peri-implant pocket by using a gentle force.
• BOP indicates inflammation of soft tissue whether around natural
teeth or implants.
• A positive correlation was found between BOP & histologic signs of
inflammation at peri-implant sites.
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51. • 4. Suppuration: High numbers of leukocyte have been shown at
implant site that have increased gingival inflammation - Suppuration
is associated with disease activity and indicates a need for anti-
infective therapy
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52. 5. Mobility:
• Even if disease conditions in the peri-implant tissues have
progressed, implants may still appear immobile due to remaining
direct bone to implant contact. Mobility is thus insensitive in
detecting early stages of periimplant disease.
• This parameter serves to diagnose the final stage of osseointegration
and my help to decide that an implant has to be removed.
• Implant Stability Non-invasive techniques developed are
1. Mirror handles
2. Perio-test.
3. Resonance Frequency Analysis
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53. • Mirror handles
Clinical Implant Mobility Scale:
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From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby; data from Misch CE: Implant quality scale: a
clinical assessment of the health-disease continuum, Oral Health 88:15–25, 1998.
54. • Perio-Test: A non-invasive, electronic device that provides an
objective measurement of the reaction of periodontium to a defined
impact load applied to the tooth crown.
• Originally developed for detecting damping characteristics of the
periodontium.
• A score of greater than 5 indicates severe mobility (Mombelli & Lang,
1998).
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56. • Resonance Frequency Analysis (RFA) This method uses a transducer
that is attached to the implant or abutment. The RFA value is a
function of the stiffness of implant in the surrounding tissues.
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57. • Osstell (Ostell) :
A second device exists to evaluate the implant bone interface that is
nondestructive and noninvasive.
The Osstell is based on resonance frequency analysis (RFA) and was
developed by Huang.
Osstell Values vs. Clinical Interpretation:
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58. 13-01-2023 58
FIG: Implant Stability Quotient (ISQ) is a scale from 1 to 100 that measures the stability of an
implant. The ISQ scale has a nonlinear correlation to micro mobility. (A) Osstell Smart Peg that is
implant specific. (B) Hand driver that is used to place Smart Peg into implant.
59. 13-01-2023 59
(C) Smart Peg hand-torqued into implant. (D) Handle removed, Osstell reader is placed in
approximation (without touching the Peg).
61. • 6. Clinical Indices Swelling and redness of marginal tissues have been
reported from peri-implant infections.
• It is reasonable to define peri-implant parameters based on
periodontal indices such as Sulcus Bleeding Index and Gingival
bleeding Index .
• The bleeding tendency of the marginal peri-implant tissues can be
assessed by Modified Sulcus Bleeding Index. Amount of plaque on
implants may be assessed by Modified plaque index.
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62. 7. Microbiology Test
I. Bacterial culture
II. DNA probes
III. PCR
IV. Monoclonal antibody
V. ELISA
Monitoring the subgingival microflora has been proposed to determine an
elevated risk for periodontal disease or peri-implantitis. It is biologically
sound and good medical practice to base systemic antimicrobial therapy
based on microbiological data (Mombelli, 2002).
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63. • 8. Peri-Implant Crevicular Fluid:
MMP-7 & MMP-8 are significantly elevated in diseased peri-implant
sulcular fluid as compared with healthy controls. Elevated levels of
laminin -5 and Gelatinase B at diseased sites.
Biomarkers may be predictive of peri-implant tissue changes and
ultimately implant failure.
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64. Diagnosis of Peri-Implant Disease
• Baseline probing depth relative to reference point should be recorded
• Baseline radiograph to establish margin bone level should be taken
• Regular systematic monitoring of peri-implant tissues is required for
assessment of presence of peri-implant health or disease and its
severity.
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66. Management
• Lang et al (2004) reported that the system of supportive therapy is
cumulative and consists of few steps. The major clinical parameters
used are Presence of biofilm, Presence or absence of bleeding on
probing (BOP), Presence or absence of suppuration, increased peri-
implant Probing depth and evidence and extent of radiographic
alveolar bone loss.
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67. Cummulative Interceptive Supportive Therapy
• Involves a series of treatment modalities used in cummulative
manner according to disease severity
• Method for implant maintenance and therapy of peri-implantitis
• To detect peri-implant infections as early as possible and to intercept
the problems with appropriate therapy
• CIST (Cumulative Interceptive Supportive Therapy) Protocol by
Mombelli and Lang(1998).
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69. • Lang et al (2004) modified the CIST protocol and termed it as AKUT
concept which is as follows:
Table: AKUT protocol
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70. Aids for implant maintenance
Regular recall visit
OHI reinforcement
At home implant care
• Brushing
• Soft manual tooth brush
• Motorized tooth brush
• End tufted brush
Professional hygiene care
• Scaling and curettage
• Plastic instruments
• Plastic instruments reinforced with graphites
• Gold-plated curette
• Ultrasonic or sonic scalers covered with plastic sleeve
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71. Interproximal cleaning/circumferential cleaning
• Floss, foam tips, Disposable wooden picks, Interproximal cleaners
Polishing
• Rubber cup with non-abrasive polishing paste E.g.: aluminum oxide, low abrasive dentifrice
Locally applied therapeutics
• Chlorhexidine digluconate
• Arestin, Periochip, Atridox
Water irrigation
• Hydro floss
Subgingival irrigation
• Antiseptic agents such as peroxide, chlorhexidine using a plastic irrigation tip.
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72. Treatment of Peri-Implant Disease
• Peri-implant mucosistis
Removal of plaque and calculus deposits using carbon fibre or titanium coated curettes
OHI with or without incorporation of CHX
• Treatment strategies for peri-implantitis
Non-surgical therapy
Surgical management
• Non-surgical therapy indications
Mucosal inflammation detected by clinical signs
Stable-radiographic bone level
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73. • When periimplant infection has been diagnosed, there are many
therapeutic approaches to save the implant (RoosJansaker et al. 2003).
• Treatment procedure generally follows in FOUR stages (Lang et al.
1997).
1st stage: scaling / root planning or mechanical debridement to remove
the biofilm from the implant in the periimplant pocket.
2nd stage: antiseptic treatment to decontaminate the implant surface.
3rd stage: antibiotic treatment to eliminate infectious bacteria in the
surrounding periimplant tissue.
4th stage: regenerative or resective surgeries to establish the bone-
implant interface (osseoreintegration).
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74. Management Based on Etiology :
• Bacterial infection –
• Detoxification of implant surface
• Surface conditioning
• Surface decontamination of implant surface
• Mechanical Debridement –
• Plastic scalers
• Carbon fibre curette
• Ultrasonic scalers with plastic or carbon tip
• Polishing of all accessible implant surface
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75. • Antiseptic therapy –
• 0.2%CHX subgingival irrigation of peri-implant pockets
• 0.2%CHX mouth rinse twice daily
• CHX gel application
• Local drug delivery –
• Polymeric Tetracycline HCL containing fibers (Actisite)
• Doxycycline ( slow release)
• 2% Minocycline gel
• Minocycline microspheres
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77. • Conditioning of implant surface
Super saturated solution of citric acid - 30-60 secs highest potential for
removal of endotoxins
High air powder abrasive system NaHCO3+sterile water- removes
microbial deposits completely and does not effect cell adhesion
adversely
Laser therapy CO2 laser & Er:YAG laser
Ozone therapy
Photodynamic therapy: bacteria could be killed on titanium surfaces
with photosensitising substance (toluidine blue, azulene)
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78. • Biomechanical Factors
• Leads to high stress or microfractures in coronal bone-implant contact
– loss of osseointegration
• Occlusal therapy – arrest of peri-implant tissue breakdown and
progression
• Improvement of implant number and position Prosthesis design
changes
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79. Limitations of Non-Surgical Therapy
1. The microbiological parameters tended to shift back towards pre-
treatment value (microbiological recurrence)
2. Difficult to advance local drug delivery to bottom of narrow & deep
defect
3. Unfavourable peri-implant tissue morphology after therapy
4. Gaining access for adequate implant surface decontamination
5. To improve or re-establish osseointegration
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80. Surgical Techniques:
• Used to treat bone defects around the teeth. Type and size of bone
defect has to be identified before deciding on appropriate treatment
modality.
• Group-I Moderate horizontal bone loss with minimal intra-bony
component, the implants is usually covered by a thin buccal and
lingual / palatal bone crest at time of implant placement. Early stage
of peri- implant breakdown.
• Group II Presents moderate to severe horizontal bone loss with a
minimal intrabony component. Advanced condition of the implants in
group I.
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81. • Group III Minimal to moderate horizontal bone loss with an advanced
circumferential intra bony lesion. The pattern of bone loss frequently
has a symmetrical feature with a circular trough of uniform width and
depth occurring around the circumference of the implant.
• Group IV Presents more complicated implant defects with moderate
horizontal bone loss with an advanced circumferential intrabony
lesion; additionally, the buccal and / or lingual plate has been lost.
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82. Peri Implant Resective Therapy Indications:
• Moderate to severe horizontal bone loss.
• One & two-walled bone defects.
• Implant position in unaesthetic area.
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83. Peri-Implant Regenerative Therapy
• GBR techniques & bone graft techniques. The GBR principle using a
non-resorbable expanded polytetrafluroethylene membrane has been
used for healing of bony defects seen at the time of implant placement
and peri-implantitis.
A. Submerged Regenerative Therapy Indication:
• Implants allowing complete closure with flap.
• Moderate to severe circumferential intrabony defects.
• Two & three-walled bone defects.
• Detoxification of implant surface possible. - Deeper and narrower
vertical defects have better prognosis
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84. B. Per-Gingival Regenerative Therapy Indication:
• One stage Implant or non retrievable prosthesis
• Moderate to severe circumferential intra-bony defects.
• Three-walled bone defects.
• Detoxification of implant surface possible.
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85. Surgical Management of Peri-Implantitis:
• There are various surgical techniques to treat peri-implantitis,
depending on the final objective:
• Access flap: for cleaning and decontamination of implants with pus,
heavy bleeding, or with evidence of probing or craterlike radiographic
bone loss.
• Regenerative procedures: provides access for cleaning, plus
regeneration procedures for deep crater defects past the first thread of
nonmobile implants.
• Apically positioned flap: provides access for cleaning and
decontamination, and is used for implants showing generalized
horizontal bone loss past first thread.
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86. Access Flap:
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(A) Crestal incision with full thickness reflection. (B) Buccal and lingual lap to obtain full exposure.
87. • Implants are detoxified with citric acid, cleaned with curettes and
titanium brush if needed.
• Flaps are readapted over osseous structure and should be in relatively
similar position.
• Horizontal mattress sutures or interrupted sutures can be used being
careful to not exert too much tension that causes bunching of tissues.
Tissue does not have to be completely approximated; new tissue will
form and granulate in the wound site.
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88. • Degranulation can be completed with curettes, specialized titanium
brushes with an implant handpiece, and/or a glycine polishing
handpiece. Along with mechanical decontamination, a chemical
decontamination process should be followed, using compounds such
as doxycycline or citric acid. The flaps are then reapproximated in
their original position using a horizontal mattress suture,
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89. • Heitz-Mayield et al published a 12-month prospective study with
antiinfective surgical therapy outcomes. Thirty-six patients with
moderate to advanced peri-implantitis had access flap disinfection
followed with a combination of systemic antibiotics (amoxicillin and
metronidazole).
• They found at 1 year the patients were 92% with stable crestal bone
height, and all had a marked reduction of probing depth; 47% had
complete resolution of bleeding on probing.
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Heitz-Mayeld LJA, Salvi GE, Mombelli A, et al: Anti-infective surgical therapy of peri-implantitis. A 12-month prospective clinical
study. Clin Oral Impl Res 23:205–210, 2012.
90. • Schwarz et al concluded that simultaneous tissue grafting with
debridement had a significant reduction of bleeding on probing,
pocket depth, and clinical attachment loss at a 6-month postoperative
evaluation.
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Schwarz F, Sahm N, Becker J: Combined surgical therapy of advanced peri-implantitis lesions with concomitant
soft tissue volume augmentation. A case series. Clin Oral Implants Res 25(1):132–136, 2014.
91. Regenerative procedures:
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(A) Radiograph depicting significant bone loss surrounding implant in the irst molar position.
(B) Full-thickness reflection showing extent of defect with retained cement.
92. 13-01-2023 92
(C) Detoxiication with tetracycline hydrochloride, after removal of cement. (D) Augmentation with allograft.
(E) Postoperative radiograph two years postoperative. (Courtesy of Dr. Nolen Levine.)
93. • A resorbable membrane (extended resorbable collagen membrane:
4–6 months) is then draped over bone graft being careful to cover 3
mm past all edges of bone graft.
• Tissue tension is reduced via tissue-stretching techniques. Flap is
resutured (i.e., high-tensile strength suture material: vicryl) being
careful to provide tensionfree closure to produce maximal contact
between tissue edges (primary closure).
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94. • In addition to the steps listed above, Froum and Rosen proposed the
use of enamel matrix derivative, platelet-derived growth factor, and
human allograft or bovine xenograft in conjunction with a collagen
membrane or subepithelial tissue graft. The study followed 51
consecutive patients treated with up to 7.5-year follow-up, and the
result is encouraging.
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Froum SJ, Froum SH, Rosen P: Successful management of peri-implantitis with a regenerative approach: a consecutive
case series of 51 treated implants with 3- to 7.5-year follow-up. Int J Periodontics Restorative Dent 32:11–20, 2012.
95. Apically Positioned Flap:
• This surgical technique is used for implants that have generalized
horizontal bone loss past the first thread when regeneration is not
considered feasible.
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FIG : Apical-positioned lap.
(A) Apical repositioning of the tissue
to decrease pocket depth.
(B) Closure showing stabilized
apically repositioned lap.
96. Surface Characteristics of Implant & Re-
Osseointegration
• Contaminated implant surface has a decreased surface energy.
• Do not allow tissue integration and may elicit a foreign body
reaction.
• Rough surface (SLA) acts as a better surface for re-
osseointegration because of better blood clot stability in the bone
crater.
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97. Re-Osseointegration
• Growth of new bone in direct contact to the previously contaminated
implant surface without an intervening band of organised connective
tissues.
Goals of Re-Osseointegration
• Ensure that substantial regeneration of bone from the walls of the
defect can occur.
• Re-juvenate the contaminated (exposed) implant surface.
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98. 13-01-2023 98
Comparison of Tooth and Implant Support Structures
From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.
99. Guidelines for diagnosing peri-implantitis
• BOP-Bleeding on Probing; PD- Probing Depth; SUPPSuppuration; ABL- Amount of bone loss; PBL- Pathological bone loss; RBL- Rate of bone loss
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100. CONCLUSION
• Successful implant therapy implies healthy and stable peri-implant
conditions.
• Early detection of signs of inflammation and appropriate CIST is
essential to prevent peri-implantitis.
• The importance of maintenance procedures should never be
underestimated.
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It represents serious diseases after dental implant treatment, which affects both surrounding hard and soft tissues.
Mucositis describes a bacteria-induced, reversible inflammatory process of the peri-implant soft tissue with reddening, swelling and bleeding on periodontal probing
Numerous classification systems have been proposed in literature for peri-implantitis. However there is no universally accepted classification so far. The following are the classification systems for peri-implantitis:
PD-Probing Depth classified peri-implantitis
Retrograde peri-implantitis (RPI) is an inflammatory disease that affects the apical part of an osseointegrated implant, while the coronal portion of the implant sustains a normal bone-to-implant interface.
Titanium plasma sprayed and hydroxyapetitie
In edentulous patients colonisation of peri-implant sulcus originates from the microflora found in saliva. Gupta Renu, Debnath Nitai, Hota Sadanan, Rawat Pratibha, Kumar Sandeep , Sahoo pradyumna kumar, Das Abhaya Chandra. Peri-implantitis and its management – a review. Medical Science, 2014, 11(43), 61-69
Fürst MM, Salvi GE, Lang NP, Persson GR. Bacterial colonization immediately after installation on oral titanium implants. Clin Oral Implants Res. 2007;18:501–8.
Mombelli A, Lang NP. Microbial aspects of implant dentistry 2000. Periodontology. 1994;4:74–80.
Peri-implantitis present with the mixed and variable microbial pattern, although predominated by gramnegative bacteria.
Microbiota associated with failing dental implants is similar to flora commonly associated with periodontally involved teeth.
Mombelli A, Lang NP. Microbial aspects of implant dentistry 2000. Periodontology. 1994;4:74–80.
Kocar M, Seme K, Hren NI. Characterization of the normal bacterial flora in peri-implant sulci of partially and completely edentulous patients. Int J Oral Maxillofac Implants. 2010;25(4):690–8.
Karbach J, Callaway A, Kwon YD, Hoedt B, Al-Nawas B. Comparison of five parameters as risk factors for peri-mucositis. Int J Oral Maxillofac Implants. 2009;24(3):491–7.
mechanical overloading a contributing factor for peri-implant bone loss and late implant failure.
Mombelli A, Lang NP. Microbial aspects of implant dentistry 2000. Periodontology. 1994;4:74–80.
Lindhe J, Meyle J. Peri-implant diseases: Consensus report of the Sixth European Workshop on Periodontology. J Clin Periodontol. 2008;35(8):282–7
:Early signs of peri-implantitis include increase in GCF production and bleeding on probing.
Two important features that differentiates peri-implantitis from peri-implant mucositis are the presence of peri-implant pocket and attachment loss.
The preservation of marginal bone height is considered crucial for implant maintenance and is often used as primary success criteria for implant systems. . For the accurate assessment of bone level changes, longitudinal series of standardized radiographs are required.
Recommended to take radiograph 1 year after implant installation, but additional radiographs are taken to determine the extent of marginal bone loss if clinical parameters indicate sign of peri-implant infection.
Peri-implant probing should be avoided during the first 3 months after abutment connection to avoid disturbance of healing and establishment of soft tissue seal.
It is an indication for lack of osseointegration. Bone destruction may proceed without any notable signs of implant mobility until osseointegration is completely lost.
Oral implants without plaque and calculus with healthy peri-implant tissue there may be absence of BOP, suppuration, Probing depth should not exceed greater than 3mm to be considered as clinically stable and these sites should not be exposed to therapeutic measures.
1. Sulcular incision around desired dentition being careful to extend at least one tooth mesial and one tooth distal in anticipation to the area of treatment 2. Full thickness lap relection is complete past the mucogingival junction on both buccal and palatal/lingual if necessary
This surgical technique is used to maintain the soft tissues around the implant with the goal of decontamination (Fig. 18.38). A sulcular incision is made around the implant and extends at least one tooth mesial and one tooth distal on both the buccal and palatal/lingual side. This allows the clinician to have proper visualization and access for the next step. A full-thickness lap relection is performed to gain access to the implant and bone surface. Although it is desirable to minimize the incision on healthy tissue, if access is inadequate, a vertical incision may be included to gain further access.
1. Sulcular incision around area of interest with one tooth mesial and one tooth distal 2. Full-thickness lap is relected past mucogingival junction being careful to ensure enough tension release from lap tissue. It is essential to produce adequate release so there is minimal tension when closing lap. Inadequate relection will result in incision line opening, which will increase morbidity of the graft.
. 3. The bone surface is curetted to clean and remove all soft tissue remnants. Bone surface is curetted being careful to remove all remnants of soft tissue. Detoxiication: a. Citric acid is applied to exposed surface for 30 to 60 seconds. b. Rinse with sterile saline for 30 seconds
. Sulcular incision around desired dentition being careful to extend at least one tooth mesial and one tooth distal in anticipation to the area of treatment 2. Full-thickness lap relection is complete past the mucogingival junction on both buccal and palatal/ lingual if necessary. 3. Osseous recontouring is complete at this time to create a positive architecture. 4. Implants are detoxiied with citric acid, cleaned with curettes and titanium brush if needed. 5. Flaps are readapted over remaining osseous structure and should be apical in comparison to original lap position. 6. Horizontal mattress sutures or interrupted sutures can be used being careful to not exert too much tension that causes bunching of tissues. Tissue does not have to be completely approximated; new tissue will form and granulate in the wound site..
