lindhe 2015, chapter 11, peri-implant infections

PERI-IMPLANT INFECTIONS

Clinical periodontology and implant dentistry, 6th edition, Chapter 11

Presented by:

Mostafa Montazeri - Resident of Periodontics, IAU Tehran

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

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)

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


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


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

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)


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)


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


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


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


If exposed to oral cavity, rough surface implants

(Titanium plasma sprayed TPS) are more likely develop

peri-implantitis than minimally rough implant surfaces

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


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


1. Treatment of periodontal diseases prior to implant placement

2. Supportive periodontal/peri-implant maintenance care

Reduce the risk of peri-implant infections

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%

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

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

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

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

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

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

Microbiota associated with peri-implant infections

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

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%

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

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

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

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

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

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

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

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

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

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

THE END

lindhe 2015, chapter 11, peri-implant infections

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