PERIIMPLANTITIS

Shilpa ShivanandIII MDS

CONTENTS• Introduction • Epidemiology• Classification of Periimplant Diseases• Etiology• Possible Pathogenic Mechanisms • Genetic polymorphism & periimplantitis • Periodontitis & Periimplantitis• Diagnosis of Periimplantitis • Treatment of periimplantitis• Conclusion • References

• Use of implants has developed significantly during the past two decades

• Widely accepted treatment modality of high success and predictability

• Despite the high success and survival rates of oral implants, failures do occur and implant-supported prosthesis may require a substantial periodontal

and prosthodontic maintenance over time

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

Two common forms : Peri-implant mucositis and Peri-implantitis

: Inconsistencies in defining and reporting Chen S, Darby I 2003Peri-implant mucositis : An inflammatory response limited to the

soft tissues surrounding a functioning oral implant

Peri-implantitis : An inflammatory response that involves loss of marginal bone around a functioning oral implant

Failed to set rigid clinical parameters

Albrektsson T, Isidor F Proceedings of the 1st European Workshop on Periodontology 1994

3rd International Team for Implantology (ITI) Consensus Conference

Similar definitions, and additional diagnostic parameters for periimplantitis

Peri-implant sulcular fluid analysis was also included as a diagnostic aid for peri-implantitis

PlaqueSuppuration

Bleeding on probing (BOP)Probing depth (PD) > 5 mm

Pathologic changes of the peri-implant tissues

An inflammatory condition confined to the soft tissue surrounding an implant.

Progressive peri-implant bone loss in conjunction with a soft tissue inflammatory lesion

PERI-IMPLANT DISEASE

PERI-IMPLANT MUCOSITIS

PERI-IMPLANTITIS

Definition:

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

The term peri-implantitis was introduced in the 1987 (Mombelli A,1987)

PERI- IMPLANTITIS

1st European workshop on periodontology, Ittingen, Switzerland, 1993

Peri-implantitis begins at the coronal portion of the implant

while the apical portion of the implant maintains an

osseointegrated status, resulting with a nonmobile implant

until bone loss progresses to involve the complete implant

surface.

• McAllister et al. in 1992 : Reported an entity separate from peri-implantitis as retrograde peri-implantitis (RPI).

“Clinically symptomatic peri-apical lesion that develops within the first few months after implant insertion while the

coronal portion of the implant sustains a normal bone to implant interface.’’

EPIDEMIOLOGY

• Prevalence (5–10 year period) : 9.6%of implants : 18.8 % of patients

• Retrograde periimplantitis: <1% to 9.9%.

• Affected by smoking, poor oral hygiene, and a history of

periodontitis

• Wide range of reported prevalence values Differences in the definition of peri-implantitis.

CLASSIFICATION

I. Jovanovic & Klinge 1990, Spiekermann 1991 :

On the basis of:

• Clinical status of peri-implant bone.

• Required therapy

A new approach for treating periimplantitis: reversibility of osseointegration

CLASS ISlight horizontal bone loss with minimal peri-implant defect

CLASS IIModerate horizontal bone loss with isolated vertical defect

CLASS IIIModerate to advanced horizontal bone loss with broad, circular bony defect

CLASS IVAdvanced horizontal bone loss with broad, circumferential vertical defects as well as loss of the oral or vestibular bony wall.

II. Forum & Rosen 2012IJPRD

Based on severity of the d/s BOP, suppuration, PPD, radiographic extent of BL

A proposed classification for periimplantitis

Periimplant

mucositis

periimplantitis

Renvert & Claffey

III.

GRADE 0,I,II,III

Treatment of periimplant diseases: a review of literature & protocol proposal, Dent Update J, 2013

According to causative factor & degree of soft & hard tissue loss

Dr H Ryan Kazemi 2012Periimplantitis class I

• Similar to mucositis

Periimplantitis class II

• Similar to implantitis

IV.

The painful dental implant

V. Carl E Misch & Jon B Suzuki 2014J Korean Assoc Oral Maxillofac Surg

GROUP MANAGEMENT CLINICAL CONDITIONI. SUCCESS(Optimum group health)

• Normal • No pain, No mobility, No exudate• <2mm BL• <5mm PD

II. SURVIVAL (Satisfactory health) • Reduction of stress• More maintenance• Yearly RGs• OH Reinforcement

• No pain, No mobility, No exudate• 2-4mm BL• 5-7 mm PD (stable)

III. SURVIVAL (Compromised health)

• Reduction of stress• Drug therapy• Surgical reentery• Change in prosthesis/implants

• No pain, No mobility• Possible exudate• >4mm BL• >7 mm PD

IV. FAILURE (Clinical/absolute failure)

• Removal • Pain• Mobility• Uncontrolled exudate• >50% BL

Comparison of the reproducibility of results of a new periimplant assessment system (implant success index) with Misch classification

AAP 2013

Periimplant mucositisPeriimplantitis

VI.

VII.

Ata Ali et alA classification proposed for periimplant mucositis &

periimplantitis: a critical update, The Open Dentistry J, 2015

VIII. Newman 1992:

• Subclassification of non-successful implants • Based on severity of peri-implantitis

Compromised successful implant : Inflammation, hyperplasia, and fistula formation occur near an otherwise fully osseointegrated implant.

Failing implant : The implant is characterized by progressive bone resorption, but remains functional.

Failed implant : Infection persist around an implant whose function is compromise

RETROGRADE PERIIMPLANTITIS

IX. Reiser & Nevins (1995)• Inactive lesions• Infected lesions (active)

X. Sussman HI (1998)• Type 1: Implant to tooth• Type 2 :Tooth to implant

32

occurs during osteotomy preparation either by direct trauma or through indirect damage, which causes the adjacent pulp to undergo devitalization

occurs shortly after the placement of the implant when an adjacent tooth develops a periapical pathology, either by operative damage to the pulp or through reactivation of a

prior apical lesion

Radiographic Classification of RPI

Mild lesion (class I) is characterized by radiographicbone loss that extends to <25% of the implant lengthfrom the implant apex

Moderate lesion (class II) is characterized by radiographic bone loss between 25 and 50% of the implant length as measured from the implant apex

Advanced lesion (class III) is characterized byradiographic bone loss extending to > 50% of theimplant length from the implant apex

Raison Thomas. A Radiographic Classification for Retrograde Periimplantitis. J Contemp Dent Pract 2016

ETIOLOGY

I. Bacterial infection ( “plaque theory”)

II. Biomechanical overload ( “loading theory”)

Newman et al 1988,1992 & Quirynen et al 1992

SUBGINGIVAL MICROBIOLOGY AND DENTAL IMPLANTS

In good oral health, teeth and implants have similar microflora with streptococci and nonmobile rods predominating

Apse et al 1989, Lekholm et al 1986, Mombelli et al 1987, Mombelli and Mericske –Stern, 1990, Newman and Flemming

1985, Palmisano et al 1991, Quirynen and Listgarten 1990

The same groups of recognized periodontopathogens are involved in periodontal diseases and in periimplantitis or infectous failure of implants

Apse et al 1989, Becker et al 1990, Mombelli et al 1987, Nakou et al 1987, Newman and Flemming 1988, Rosenberg et al 1991

Commonly found microflora:A. actinomycetemcomitansP. gingivalisT. forsythiaP. intermediaC. rectus

Other: P. aerugenosaEnterobacteriaceaeC. albicansStaphylococci sp

Peri-implant microflora is established shortly after implant placement.

Successful implants experience no shifts in microbial composition over time.

(Bower et al 1989; Mombelli et al 1990)

Induction of peri-implantitis by placement of plaque retentive ligatures in animals

(Lindhe et al 1992; Lang et al 1993)

Therapy aimed at a reduction of the peri-implant microflora improves clinical conditions

(Ericsson et al 1996; Mombelli et al 1992)

EVIDENCE FOR A BACTERIAL CAUSE OF PERIIMPLANTITIS

II. BIOMECHANICAL OVERLOAD:

Excessive biomechanical forces may lead to high stress or microfractures in the coronal bone-to-implant contact and thus lead to loss of osseointegration around the neck of the implant.

Likely to increase in four clinical situations.

1. Poor quality bone.

2. Incorrect implant’s position or number

3. Patient with heavy occlusal function

(Parafunction)

4. Prosthetic superstructure does not fit the implants

precisely.

Consensus statement: Occlusal overloadThird EAO Consensus Conference 2012

• Overload > 3000 micro strain

• Response depend on peri-implant tissue health

• Healthy peri-implant tissues : No loss /gain of bone mass

• Inflamed : Increased marginal bone resorption occurs

• Non-physiological loading : Bone/implant loss.

OTHER ETIOLOGIC FACTORS

1. Patient related factors

• Systemic diseases • Social factors• Para functional habits • Inadequate amount of host bone resulting in an exposed implant

surface at the time of placement

Quirynen M et al 1993

2. Iatrogenic factors

e.g. Traumatic surgical techniques

Lack of primary stability

Premature loading during the healing period

Quirynen M et al 1993

45

• Unclear (paucity of information)• May be attribute to:

Implant surface contamination

Residual bacteria in the implant site

Presence of adjacent endodontic lesions

Residual root particles or foreign bodies

Etiology: Retrograde periimplantitis

• Violation of minimal distance from adjacent teeth

• Surgical drilling beyond the length of the implant

• Fenestration of vestibular bone

• Development of osteomyelitis

46

Genetic polymorphism & periimplantitis

• Association was checked to dental implant loss/ peri-

implantitis/peri-implant marginal bone loss

• IL-2, IL-6, TNF-ά, TGF-b1 genotype polymorphism: NO

association

• IL-1 A & IL-1B gene polymorphisms : SHOWN

ASSOCIATION.

• OPG, RANKL, IL-17 gene polymorphism: Shown

association in Iranian population

• No obvious association in terms of biological complicationsSystemetic review : Dereka X et al 2011

POSSIBLE PATHOGENIC MECHANISMS IN IMPLANT FAILURE

• Most important factor : Microbial plaque accumulation

• Disruption of the perimucosal and loss of peri-implant

bone, analogous to the destruction of soft and hard tissue

seen in periodontitis.

Decreased resistance to mechanical probing

Ericsson & Lindhe (1993),

2mm 0.7mm

Defense mechanism of the gingiva is more effective around teeth than peri-implant mucosa in preventing further apical propagation of the pocket microbiota.

Periimplantitis:

• Apical extension of the inflammatory cell infiltrate (ICT) was

more pronounced

• ICT located apical of the pocket epithelium

• Increased Neutrophil granulocytes and Macrophages

Plasma cells and lymphocytes: Same in both

Experimental studies: After ligature removal

PERIODONTITIS: SELF LIMITING

PERIIMPLANTITIS: EXTENDED TO BONE CREST

Are peri-implantitis lesionsdifferent from periodontitislesions?

Berglundh T et al 2011

PERIODONTITIS

AND

PERIIMPLANTITIS

PERIIMPLANTITIS & UNTREATED PERIODONTITIS

Surviving status

HEALTHY MODERATE SEVERE

Early Failure

2.1% 1.3% 2%

Late failure

0.9% 2% 3.2%

• Until 50 months: No significant effect;• After 50 months : 8 times greater risk in severe chronic periodontal patients.

Continuous and cumulative nature of periodontal disease

Levin L et al 2011

PERIIMPLANTITIS & TREATED PERIODONTITIS

Lisa J. A. Heitz-Mayfield 20093.1 to 4.7 higher riskSurvival rates > 90%

Cho-Yan Lee J et al 2012• Better outcome in non periodontitis patient.• Prevalence of implant with PPD ≥ 5mm+BOP (27% vs 13%)• Higher implant PPD : Residual pockets present (3.18 mm vs 2.81 mm)

Karoussis I K et al 2007

• Chronic periodontitis• No significant difference : Implant survival• Long-term: Greater incidence, PPD, crestal bone loss • Aggressive Periodontitis:

Short-term prognosis : Acceptable Long-term prognosis: Open to question

Pjetursson B E et al 2012Higher risk if:• Residual pockets > 5 mm• Reinfections occur during SPT

SUGGESTED RISK-ASSESSMENT PARAMETERS

• Responded favorably to periodontal therapy• optimal oral hygiene• Non-smoker• Systemically healthy• Low risk for periodontal disease

• Limited number of residual sites with PPD ≥ 5mm + BOP• Oral hygiene : Not constantly optimal.• Attempt for further pocket reduction should be considered• Options other than dental implants

• Significant number of residual sites with with PPD ≥ 5mm + BOP

• Oral hygiene is suboptimal • heavy smoker/uncontrolled type 2 diabetes. • implant placement should be delayed

Donos N et al 2012

DIAGNOSIS

Indices (similar to periodontal)

Peri-implant probing

Peri-implant probing depth (3-4mm normal)

Bleeding after gentle probing

Exudation & suppuration

Mobility: Late (Insensitive)

Pain

Peri-implant sulcular fluid analysis

Blunt, straight plastic periodontal probe (Automated probe or TPS probe)

Microbial monitoring: to determine the microbial composition of a peri-implantitis site

Peri-implant radiography: Standardized IOPA radiographs or OPG.• Vertical bone loss• Saucer shaped defect.• Progressive bone loss : Definite indicator

IMPLANT SUCCESS CRITERIA ALBREKTSSON 1986

Treatment: Focus: Removal of the contaminating agent

1. Systemic antibiotics

2. Mechanical debridement

• With/without systemic antibiotic treatment

• With/without LDD & Chlorhexidine oral rinse.

• Combined with LASER decontamination

3. Surgical debridement

• With/without guided bone regeneration (GBR)

INITIAL PHASE

I. OCCLUSAL THERAPY

When excessive forces are main etiologic factor Includes:

• Prosthesis design changes• Improvement in implant number and position• Occlusal adjustment

II. ANTI-INFECTIVE THERAPY

Microbial etiology Local removal of plaque deposits (plastic instruments) Polishing of accessible surfaces with pumice. Subgingival irrigation of all peri-implant pockets

(0.2 % chlorhexidine) Systemic antimicrobial therapy for 10 consecutive days.

NONSURGICAL THERAPY

Indications Mucosal inflammation detected by clinical signs

Radiographic bone level stable

Phase I therapy before surgery.

Debridement / detoxification

Plastic curettes Carbon fibre curettes (Calculus) Rubber points Abrasive paste Abrasive air US+ Teflon Titanium brush

Antiseptics Citric acid (40%) Tetracycline 5%

Antibiotics Metronidazole If GBR: Doxycycline + Ornidazole.

Disadvantage : Failed to promote the re-osseointegration of the exposed implant sites

Schwarz F et al 2006

Other treatment modalities

• Mechanical/ultrasonic debridement with LDD• Laser treatment with and without flap access• Open flap debridement• Open flap debridement with guided bone regeneration

Peri-implantitis lesions are usually well demarcated

Controlled delivery devices

Release sustained high dose of antimicrobial agents

Antimicrobial minocycline spheres (Arestin®)Tetracycline fibres

LOCAL DRUG DELIVERY

More improvements in probing depths compare to CHX gel sustained for 6 months

Renvert S et al 2008

IRRADIATION WITH A SOFT LASER

Er:YAG and CO2 :

CO2 Laser: Deppe et al 2007, Romanos & Nentwig 2008, Romanos et al 2009

Er:YAG Laser: Schwarz et al 2011, Renvert et al 2011, Persson et al 2011

• With and without flap access• Destruction of bacterial cells• Plaque control measures should be adhered to reduce the effect of

plaque and associated inflammation on healing.

• Positive treatment outcomes after 6 months • Improvements relapse after 6 months.

Nicholas Peters 2012

COMPARISON OF ADJUNCTIVE USE OF

LDD & LASER

• Equally effective

• Complete resolution of inflammation not achieved

with either of two

Schar D et al 2013

Reduction of clinical signs of peri-implant mucosal inflammation:

Long-term RCT are needed

To assess the efficacy of non-surgical therapy on

• Progressing bone loss

• Implant survival rates

• Measures of oral health-related quality of lifeMuthukuru M et al 2012

Submucosal debridement + Adjunctive local delivery of antibiotics + Submucosal glycine powder air polishing or Er:YAG laser treatment

Submucosal debridement using curettes +Adjunctive irrigation with chlorhexidine.

More effective

TREATMENT OF CHOICE:

• Smooth implant surfaces: Non-metal instruments + rubber cups.

• Rough implant surfaces: Non-metal instruments + air abrasives

• If smoothening of the surface roughness required : Metal

instruments and burs

The clinical impact of these findings requires clarification.

Systematic review: Louropoulou A et al 2011

• Peri-implant mucositis : Treated successfully.

• Peri-implantitis : Limited efficacy.

• Clinical recommendations

Patients should be monitored regularly for

Plaque control

Signs of peri-implant inflammation

A regular maintenance program for the long-term

management of peri-implantitis lesions

Highvigilance monitoring

Consensus statement: Non-surgical interventionThird EAO Consensus Conference 2012

SURGICAL TREATMENT OF PERI-IMPLANTITIS

PERI-IMPLANT RESECTIVE THERAPY Identify the type of osseous defect before deciding on the

treatment modality Apically displaced flap techniques and osseous resective

therapy are used to correct • Moderate to severe Horizontal bone loss• Moderate (<3 mm) vertical bone defects

(1and 2 wall bone defects)• Reduce overall pocket depth.• Implant position in unesthetic area.

SURFACE POLISHING / IMPLANTOPLASTY (Before resection)

Objective:• To arrest the progression of the disease.• To achieve a maintainable site by the patient.

Implant topography should be altered with high-speed diamond

burs and polishers to produce smooth continuous surfaces.

Performed before any osseous resective therapy is initiated and

with profuse irrigation.

PERI-IMPLANT REGENERATIVE THERAPY

• Accomplish regeneration of lost bone tissue and re-

osseointegration

• Guided bone regeneration (GBR) and bone graft techniques

have been suggested.

Guided Bone Regeration (GBR) principle using a nonresorbable

expanded polytetrafluoroethylene membrane has been used for

healing of bone defects seen at the time of implant placement

and around failing implants.

Indications: • Implant allows complete closure with flap • Moderate to advanced circumferential vertical defects• 2/3 wall bone defects • Detoxification of implant surface possible

SUBMERGED REGENERATIVE THERAPY

Consensus statement: Surgical interventionThird EAO Consensus Conference 2012

• Superior to non-surgical therapy: For periimplantitis

• Should include:

Removal of the granulation tissue.

Thorough cleaning of the contaminated surface

• Adjunctive measures : Better but variable outcomes influenced

by factors not yet fully understood.

• Regenerative or resective surgical approach: Adjunct to

mechanical instrumentation

• Regenerative : Use of a membrane does not seem to improve

the healing results

EXPLANTATIONOr

IMPLANT EXTRACTION

INDICATION

1. Suppurative exudate

2. Overt BOP

3. Severely increased peri-implant probing depth

(≥ 8mm)

5. Radiographically: Peri-implant radiolucency may be

extending far along the outline of the implant. (>half

length)

6. Mobile

7. Non surgical & surgical therapy ineffective

• Many treatment modalities available• Implant extraction• Peri-apical surgery (With/Without implant apex resection)• Debridement • Regenerative• Local decontamination (antimicrobials/lasers)• Antibiotics

• No conclusive evidence to advocate any specific treatment approach

Treatment : Retrograde Periimplantitis

Nevins M et al 1996

Decision tree for management of periimplantitis

Kozue Okayasu & Hom-Lay Wang 2011

MAINTENANCE

After surgical intervention, all patients are placed on a close

recall schedule; maintenance visits every 3 months are

advised as a minimum. This allows for monitoring of

plaque, levels, soft tissue inflammation, and changes in the

level of the bone

• Train patient for self-performed plaque control with individually

designed professional supportive care program

• Professional plaque-control measures (every 3–6 month)

• Clinical examinations every 3, 6 or 12 months depending on severity

• Radiographic documentation

(Implant placement, post prosthetic, every 1 year)

• High BOP scores PPD > 5 mm : Radiographic examination

No evidence available to suggest the frequency of recall intervals or to propose specific hygiene regimes

SUPPORTIVE PERIODONTAL THERAPY RECOMMENDATION

Donos N et al 2012

CIST PROTOCOL

• Protocol of therapeutic measures

• Depend on the clinical and the radiographic diagnosis

• Diagnosis : Key characteristic

• Cumulative in nature

Not a single procedures, rather a sequence of therapeutic

procedures with increasing antibacterial potential,

depending on the severity and extent of the lesion.

• Four steps

Lang et al 2004

CLINICAL PARAMETERS USED

• Dental plaque : ±

• Bleeding on gentle probing : ±

• Suppuration : ±

• Periimplant probing depth

• Radiographic evidence of bone loss.

CLINICALLY STABLE

(Not currently at risk for peri-implant disease)

• No evidence of plaque or calculus adjacent to healthy

peri-implant tissues

• Absence of BOP

• Absence of suppuration

• Probing depth < 3–4 mm

Revaluate Annually

Decision tree for CIST

Lang & Lindhe 2008

MECHANICAL DEBRIDEMENT (Supportive therapy protocol A)

Instruments:

• Plaque : Polishing ( rubber cups and polishing paste)

• Calculus : Carbon-fiber curettes

• Conventional steel curettes or ultrasonic instruments with metal tips : Avoided

• Leave marked damage on the implant surface conducive to future plaque accumulation

Chlorhexidine digluconate:

• Daily rinse of 0.1%, 0.12%, or 0.2%

• Gel applied to the site of desired action.

• 3–4 weeks of regular use necessary

ANTISEPTIC TREATMENT (Supportive therapy protocol B)

ANTIBIOTIC TREATMENT (Supportive therapy protocol C)

• To eliminate or reduce the pathogens

• Done in last 10 days of the antiseptic treatment

(Metronidazole 350 mg TID or Ornidazole 500 mg BD)

• Prophylactic procedures instituted to prevent reinfection

• Local antibiotics application:

1. Tetracycline periodontal fibers

2. Microspheres containing minocycline hyclate

REGENERATIVE OR RESECTIVE THERAPY (Supportive Therapy protocol D)

Done to accomplish regeneration of lost bone tissue and re-

osseointegration

REOSSEOINTEGRATION : Growth of new bone in direct

contact to the previously contaminated implant surface without

an intervening band of organized connective tissue.

CONCLUSION:

• Patient should be informed in detail about the possibility of

developing inflammation and infection around implants.

• Informed consent should include need of maintenance

therapy

• Oral hygiene practices should be given along with an

organized maintenance recall care system on a regular basis

(at least once a year).

• Prophylactic measures should be intervened if mucositis

(bleeding) is noted around the implant.

• View a pocket with a probing depth of 6 mm as an

ecologic niche harboring anaerobic bacteria and should be

treated.

• CIST protocol should be followed.

• Optimal oral hygiene standards should be maintained for

peri-implantitis therapy.

REFERENCES

• Clinical Periodontology – Carranzas 10th ed• Clinical Periodontology & Implant Dentistry, Jan Lindhe

4th ed• Contemporary Implant Dentistry, Carl Misch• Antibiotics in treatment of periimplantitis, Quintescence

Int 2012• A proposed classification for periimplantitis, IJPRD 2012• Perio 2000, vol 53, 2010• Therapy of periimplantitis: a systematic review, Int J Oral

Maxillofac Implants 2014

• Ata-Ali et al, A Classification Proposal for Peri-Implant Mucositis and Peri-Implantitis: A Critical Update, The Open Dentistry Journal, 2015, 9, 393-395.

• Eduardo Anitua , A New Approach for Treating Peri-Implantitis: Reversibility of Osseointegration.

• Raison Thomas, A Radiographic Classification for Retrograde Peri-implantitis, J Contemp Dent Pract 2016;17(4):313-321.