1) Peri-implant infections include peri-implant mucositis, characterized by inflammation without bone loss, and peri-implantitis, with accompanying bone loss. Risk factors include implant surface characteristics, the local oral environment and biofilm, and reconstruction design impacting oral hygiene. 2) Implant surfaces that are rough or titanium plasma sprayed are more likely to develop peri-implantitis due to enhanced biofilm formation. The local oral environment, including the resident microbiota from remaining teeth, also impacts risk. 3) Treatment aims to disrupt biofilms and establish a healthy local environment. Non-surgical approaches show limited effectiveness while surgical approaches combined with antimicrobials provide modest success rates

1. PERI-IMPLANT
INFECTIONS
Clinical periodontology and implant dentistry, 6th edition, Chapter 11
Presented by:
Mostafa Montazeri - Resident of Periodontics, IAU Tehran

2. Introduction
 Peri-implant infections:
1. Peri-implant mucositis  Clinical signs of inflammation (BOP)
without bone loss
2. Peri-implantitis 
Concomitant loss of supporting bone
– Pocket depths ≥ 5mm
– Suppuration

3. Introduction
 Risk factors for peri-implant infections:
1. Material surface characteristics
2. Local environment (Resident oral microbiota)
3. Reconstruction design (and its accessibility for oral hygiene)

4. Peri-implant biofilm formation
 Endosseous part of implant:
1. Should ideally be surrounded by bone
2. Usually not exposed to biofilm
 Transmucosal part of implant:
1. Exposed to oral cavity
2. Rapidly colonized by microorganisms  They attach to
salivary proteins and peptides  Form Pellicle (Contains
receptors for adhesins on the cell surface of bacteria

5. Peri-implant biofilm formation
 Titanium pellicles:
 High molecular weight mucins, α-amylase, secretory IgA,
proline-rich proteins
 Enamel pellicles:
 Cystatins, low molecular weight mucins
The differences between pellicles formed on titanium
surface or tooth enamel DO NOT influence the
bacterial composition of the biofilm

6. Peri-implant biofilm formation
 Due to common ecologic environment  Similar principles and
sequence of biofilm formation
 Formation of biofilm:
1. Adhesion of early colonizers; S.sanguinis, A.naeslundii to
salivary pellicle
2. Early colonizers grow, modify the environment and promote
the adhesion of secondary colonizers via co-aggregation
3. The biofilm becomes Stable  Forms a protective environment

8. 1- Surface characteristics of the implant
 Chemical composition, Surface free energy (SFE; wettability),
Surface roughness (Ra)
 Surface roughness  Greater bacterial adhesion and biofilm
accumulation
 Ra≥ 0.2µm, SFE  Facilitated biofilm formation
 Teflon-coated abutments 
1. Less mature biofilm
2. Higher cocci
3. Lower motile organisms & spirochetes(low SFE)

9. 1- Surface characteristics of the implant
 When all surface characteristics interact with each other,
surface roughness found to be predominant
 The impact of surface roughness on biofilm formation:
1. The protection from shear forces
2. Increased area for adhesion
3. Difficulty in cleaning
 Rapid regrowth of the biofilm (In supramucosal areas)

10. 1- Surface characteristics of the implant
 FrÖjd et al. 2011; The effect of surface characteristics on
biofilm formation
o After 2 hours  Surfaces with increased surface roughness 
Higher bacterial adhesion
o After 14 hours  Similar volume of biofilm on all surfaces

11. 1- Surface characteristics of the implant
 Various restorative materials for implant components 
Titanium, gold, ceramics, zirconium
 Zirconia exhibit low biofilm accumulation (Bremer et al. 2011)
 Zirconia vs. Titanium abutments (Salihoglu et al. 2011)
1. Lower SFE
2. No difference in the adhesion of A.a & P.gingivalis 5 weeks
after abutment connection

12. 1- Surface characteristics of the implant
 Based on the surface roughness value Sa (average 3D height
deviation):
1. Smooth Sa≤0.5µm
2. Minimally rough Sa:0.5-1.0µm
3. Moderately rough Sa:1.1-2.0µm
4. Rough Sa>2.0µm
 Commercially available titanium implants: Moderately rough or
Rough  If exposed, enhanced biofilm formation

13. 1- Surface characteristics of the implant
If exposed to oral cavity, rough surface implants
(Titanium plasma sprayed TPS) are more likely develop
peri-implantitis than minimally rough implant surfaces

14. 2- Local oral environment
 Biofilm formation (oral hygiene) & peri-implant mucositis 
Cause and effect relationship
 Deeper pockets  Greater number of pathogens
 Sumida et al. 2002; isolate of P.gingivalis & P.intermedia
were identical at implant and teeth areas
 Takanashi et al. 2004; 75% of all P.gingivalis and 100% of
all P.intermedia isolates in samples from one subject were
identical  Primary source of bacteria is from remaining
dentition

15. 2- Local oral environment
 Edentulous patients (with the history of periodontitis) 
1. Distinct patterns of microbial colonization on soft tissues and
saliva;
2. A.a and P.gingivalis detected in edentulous patients;
Previously thought that these microorganisms would no be
present following removal of all teeth
 Lang & Berglundh 2011; Pathogenic conditions in the oral
environment  Ecosystem alteration  Colonization of
pathogenic microorganisms at implant sites

16. 2- Local oral environment
1. Treatment of periodontal diseases prior to implant placement
2. Supportive periodontal/peri-implant maintenance care
 Reduce the risk of peri-implant infections

17. 3- Oral hygiene and accessibility
 Poor oral hygiene  Greater incidence of
peri-implant infections
 Good compliance following treatment is
important:
1. Prophylaxis/supportive periodontal
therapy (SPT)
2. Maintaining full-mouth plaque score <20%

18. 3- Oral hygiene and accessibility
 No access for oral hygiene  Higher risk for
peri-implantitis
 Good access for oral hygiene  Rarely
associated with peri-implantitis
 Wilson 2009; Cemented prosthesis should be
designed with accessible cement margins
 Excess luting in the sulcus  Foreign body
 Removal of excess cement  74%
reduction in clinical signs of infection

19. Microbiota associated with peri-implant
mucosal health
 Peri-implant biofilm forms
within minutes of exposure to
oral cavity (similar to teeth)
 It may take longer for a
mature biofilm to develop
at implant sites.
 Complex community of
multispecies develops within
weeks

20. Microbiota associated with peri-implant
mucosal health
 De Boever 2006;
 Increase in detection
frequency of
P.gingivalis &
T.forsythia over time
after implant
placement in subjects
with the history of
aggressive
periodontitis

21. Microbiota associated with peri-implant
mucosal health
 Mombelli et al. 1987 1988 1990; The microbiota associated
with peri-implant health (similar to healthy periodontal subjects)
1. Predominantly G+ facultative cocci
2. High levels of Actinomyces & Veillonella
3. Low anaerobic counts
4. Low levels of G- anaerobic rods
5. Low proportions of F.nucleatum, Spirochetes, Fusiforms,
Motile curved rods

22. Microbiota associated with peri-implant
mucosal health
 Low levels of Periodontal pathogens; A.a, T.forsythia,
P.gingivalis, T.denticola, P.micra, S.intermedius detected in
healthy peri-implant sulci in fully edentulous subjects
 Patients with good oral hygiene and stable periodontal
condition  Successful implants despite the presence of
periodontal pathogens

23. Microbiota associated with peri-implant
infections
 Similar to that in chronic periodontitis; mixed anaerobic
infection dominated by G- bacteria
 Some studies also found:
1. Enteric rods
2. Yeasts
3. Staphylococci (S.aureus and S.epidermidis)
4. Peptostreptococci

24. Microbiota associated with peri-implant
infections

25. Microbiota associated with peri-implant
infections
 Peri-implant mucositis microbiota
≈ Peri-implantitis microbiota
 Maximo et al. 2009; In peri-
implantitis compared to
mucositis:
1. Higher levels of T.forsythia
2. Lower levels of A.gerencseriae
and C.ochracea

26. Microbiota associated with peri-implant
infections
 Deeper peri-implant pockets  Higher numbers of P.gingivalis
 CMV and EBV  Possible etiologic role in peri-implantitis 
immune suppression  overgrowth of periodontal pathogens
 In peri-implantitis sites; Jankovic et al. 2011
 CMV 65%
 EBV 45%
 CMV with EBV 33%

27. Microbiota associated with peri-implant
infections
 16S rRNA sequencing  Identification and discovery of
previously unrecognized microorganisms in the oral cavity
 Chloroflexi, Tenericutis, Synergistes
 P.micra, P.stomatis, P.alactolyticus, S.moorei
 Archaea (Methanobrevibacter oralis); Single-cell
microorganisms that:
1. Produce methane
2. Associate with periodontal disease severity
Also found at peri-implantitis sites with higher rates than healthy
sites

28. Patients at risk for peri-implant infections
1. History of treated periodontitis
 In patients with advanced periodontitis  Persistence of
pathogens following full-mouth extraction and implant
placement
 Extraction of periodontally involved teeth  Significant
reduction in periodontal pathogens (Not eliminated)
 The pathogens could colonize the peri-implant sites

29. Patients at risk for peri-implant infections
2. Residual probing depths
 ≥ 6mm; Increased risk
 ≥ 5mm with BOP
3. Specific bacteria; Few studies available
 Luterbacher et al. 2000; Positive DNA test of A.a, P.gingivalis,
P.intermedia, T.denticola  Enhanced the diagnostic power of
the presence of bleeding on gentle probing to predict
progression of peri-implant disease

30. Anti-infective treatment and microbiologic
effects
 Most studies have reported a reduction in the total bacterial
counts and pathogens in the first 3 months following treatment
 Longer follow-up periods  Gradual return to baseline
microbiota
 Treatment strategies:
1. Non-surgical mechanical therapy
2. Non-surgical mechanical therapy and adjunctive microbial
agents
3. Surgical access and implant surface decontamination

31. Non-surgical mechanical therapy
 In Peri-implant mucositis  Effective alone
 In Peri-implantitis  Limited and unpredictable results due to
difficulty in gaining access to the biofilm
 Transient changes in few microbial species
 Return to baseline levels 6 months afterwards with no clinical
improvement
 Limited improvement even with Er:YAG or air-abrasive polish

32. Non-surgical mechanical therapy and
adjunctive microbial agents
 Mechanical debridement + Irrigation with 0.5% chlorhexidine
+ systemic administration of ornidazole 100mg/day for 10
days; at
 10 days:
 Dramatic reduction in total anaerobic microbiota
 Mainly G+ facultative bacteria(95%)
 Pathogens could not be recovered
 After 12 months
 Detection of F.nucleatum, A.odontolyticus significantly lower
 Reduction in BOP and mean pocket depths

33. Non-surgical mechanical therapy and
adjunctive microbial agents
 Local delivery of antimicrobials:
 Non-resorbable tetracycline fibers and minocycline
hydrochloride microspheres
 Microbiologic improvements up to 12 months
 Gradual recolonization

34. Surgical access and implant surface
decontamination
 Flap therapy + Decontamination
 Chemicals; Citric acid, Hydrogen peroxide, saline,
chlorhexidine
 Lasers; Nd:YAG, Er:YAG
 Photodynamic therapy; reduction in periodontal pathogens
 Mechanical approaches; Curettes, ultrasonic, air-abrasion

35. Surgical access and implant surface
decontamination
 Charalampakis et al. 2012;
 Treating peri-implantitis most with surgical access and various
antimicrobial agents (most amoxicillin+ metronidazole)
 45% success

36. Conclusion
 Treatment of peri-implantitis is challenging, but anti-infective
approach is indicated
 Goals: biofilm control, establishment of healthy local
environment
 Prevention of peri-implantitis
1. Identification of high-risk patients
2. Treatment of periodontitis prior to implant placement
3. Access for good oral hygiene
4. Avoidance of iatrogenic problems
5. Supportive care

37. THE END