Peri-Implants

PERI-IMPLANTITIS
Presented by: Kriti Dalmia.

Moderated by: Dr. Shobha R.

CONTENT:
• Introduction • Diagnosis of peri-implantitis

• Peri-implant diseases • Treatment of peri-implantitis

• Epidemiology • Prognosis of peri-implantitis

• Classification • Prevention of peri-implantitis

• Etiology • Conclusion

• Risk factors • References

• Possible pathogenic mechanism

• Periodontitis and peri-implantitis

INTRODUCTION:

The introduction of dental implants has created a paradigm shift in the oro-dental rehabilitation
of patients.

Despite the high success and survival rates, failures do occur and implant-supported prosthesis
may require a substantial periodontal and prosthodontic maintenance over time.

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Peri-implant diseases may develop if bacterial biofilms are allowed to accumulate.

This is corroborated by the fact that peri-implant diseases are initiated by the presence of similar
etiological factors as those involved in the development of periodontal diseases (Heitz-Mayfield
and Lang 2010).

PERI IMPLANT DISEASES:

• Peri‐implant disease is a collective term used to describe inflammatory processes in
tissues that surround implant(s) that is peri‐implant mucositis and peri‐implantitis
(Albrektsson & Isidor 1994).

• Peri-implant diseases were first defined and described at the First European Workshop on
Periodontology in Ittingen,1993.

2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases:

Peri-implant health was characterized by the absence of erythema, bleeding on probing,

swelling and suppuration (Araujo and Lindhe 2018, Berglundh et al. 2018).

Peri-implant mucositis was defined as an inflammatory lesion of the soft tissues surrounding an
endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss
(Berglundh et al. 2018, Heitz Mayfield and Salvi 2018)

Peri-implantitis was defined as a plaque-associated pathological condition occurring in tissues

around dental implants, characterized by inflammation in the peri-implant mucosa (i.e. bleeding
on probing and/or suppuration) and subsequent progressive loss of supporting bone
(Berglundh et al. 2018, Schwarz et al. 2018).

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EPIDEMIOLOGY:
• Systematic review with meta-analysis (Derks and Tomasi 2015) prevalence for peri-
implant mucositis was 43% (19-65%) and peri-implantitis was 22% (1-47%)

• Outcomes from cross-sectional studies reported comparable prevalence for peri-

implantitis with a range from 12.9 to 26%.

• The prevalence of peri-implant mucositis and peri-implantitis was reported as 54.7% and
22.1% respectively in a case series study with a 21–26 year-follow-up (Renvert et al.
2018).

• A cross-sectional multicenter study on Japanese patients showed prevalence of patient-

based peri-implant mucositis as 33.3% and peri-implantitis as 9.7%

CLASSIFICATION
• Jovanovic & Klinge 1990, Spiekermann 1991

• Newman 1992

• Froum & Rosen 2012

• Ata Ali et al, 2015

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• Carl E Misch & Jon B Suzuki 2014

• Retrograde peri-implantitis 2016

• Classification of periodontal and peri-implant diseases and conditions 2017

• Spiekermann 1991 and Jovanovic & Klinge 1990:

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• Newman 1992:

• Froum & Rosen 2012

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• Ata Ali et al 2015

• Carl E Misch & Jon B Suzuki 2014

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Retrograde implantitis: A clinically symptomatic periapical lesion that develops with in the
first few after implant insertion

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ETIOLOGY:
• Subgingival microbiology and dental implants

Human experiments reveal plaque deposition on implants that can induce peri-implant mucositis.

Distinct quantitative and qualitative differences are demonstrated in the microflora associated
with successful and failing implants

Shift in the composition of the microflora and peri-implantitis due to placement of plaque
retentive ligatures in animals

Clinical status of peri-implantitis patients improved by antimicrobial therapy

Evidence indicates that oral hygiene level has an impact on the long-term success of implant
therapy.

Bacterial flora, which are associated with periodontitis and peri-implantitis, are found to be
similar.

The microorganisms most commonly related to the failure of an implant are the Gram-negative
anaerobes, like 

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⮚ Prevotella intermedia,

⮚ Porphyromonas gingivalis,

⮚ Aggregatibacter actinomycetemcomitans,

⮚ Bacteroides forsythus,

⮚ Treponema denticola,

⮚ Prevotella nigrescens,

⮚ Peptostreptococcus micros

⮚  Fusobacterium nucleatum

• Biomechanical overload:

Excessive biomechanical forces or overloading may lead to high stress or microfractures at

the coronal aspect of implant bone interface, thereby causing bone loss.

The apical downgrowth of epithelium and connective tissue result in loss of osseointegration
around the implant region.

The degree of loss of implant bone contact depends on the frequency and magnitude of the
occlusal loading as well as superimposed bacterial invasion.

Naert et al (1991), reported greater bone loss around the implant with respect to the
magnitude of implant loading.

• Other etiologic factors:

Patient related factors Iatrogenic factors

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• Systemic diseases • Traumatic surgical techniques

• Smoking • Lack of primary stability

• Poor plaque control/irregular • Premature loading during the healing

maintenance therapy period

• Para functional habits

• Inadequate amount of bone resulting

in an exposed implant surface at the
time of placement

RISK FACTORS:

Poor plaque control/lack of regular maintenance therapy

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• Patients who, during a 10‐year period, failed to adhere to the recommended maintenance
therapy required substantially more treatment for peri‐implantitis (41%) than those
attending the follow‐up visits (27%) (Roccuzzo et al.)

• According to cross‐sectional studies, patients complying to maintenance therapy

following implant therapy during a mean observation time of 3.8 years were less likely to
be diagnosed with peri‐implantitis than non‐compliers

• Serino and Ström evaluated the accessibility of implant‐supported restorations for oral
hygiene measures in patients diagnosed with peri‐implantitis.The authors noted that only
few sites with access for oral hygiene were affected (18%), while 65% of the non‐
cleansable sites showed peri‐implantitis.

There is evidence that poor plaque control and lack of regular maintenance therapy
constitute risk factors/indicators for peri‐implantitis

History of periodontitis:
• The 10‐year incidence of peri‐implantitis in the non‐periodontitis group was 6% (implant
level) compared to 29% in subjects with a history of periodontitis. Karoussis et al.

• Roccuzzo et al. reported that both the frequency of implant

sites demonstrating PD ≥6 mm and bone loss ≥3 mm differed
significantly between groups. The results also showed that
treatment of peri‐implantitis was more time consuming in
patients with a history of periodontitis.

• Roos‐Jansåker et al. and Koldsland et al. reported that implants placed in patients with a
history of periodontitis had significantly higher odds for peri‐implantitis when compared
to implants in patients without.

• Daubert et al. found that severe periodontitis at follow‐up was the strongest indicator for
peri‐implantitis of all variables examined.

There is strong evidence from longitudinal and cross‐sectional studies that a history of
periodontitis constitutes a risk factor/indicator for peri‐implantitis. Thus, patients with
a history of periodontitis were found to be at higher risk for peri‐implantitis

Smoking

• Lindquist et al. reported that smokers presented with substantially more crestal bone loss
than non‐smokers.

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• In a 10‐year cohort study, Karoussis et al. found that 18% of all implants in smokers
developed peri‐implantitis, while only 6% of implants in non‐smokers were affected.

• Aguirre‐Zorzano et al. after a mean follow‐up time of about 5 years and found an overall
prevalence of peri‐implantitis of 15%.Smokers were not at higher risk.

• The reasons for the conflicting findings and the apparent weak association between
smoking and peri‐implantitis may be related to differences in categorization of smokers
and non‐smokers. Thus, criteria for the factor “smoking" varied considerably from study
to study

There is currently no conclusive evidence that smoking constitutes a risk

factor/indicator for peri‐implantitis.

Diabetes:

• Ferreira et al. recorded peri‐implantitis in 24% of individuals

who either medicated for glycaemic control or presented with
fasting blood sugar ≥126 mg/dL at the final examination. In
contrast, only 7% of non‐diabetic patients were diagnosed
accordingly

• Patients with elevated HbA1c levels (7% to 9%), six out of 141 implants developed peri‐
implantitis. Tawil et al

• In the retrospective study by Costa et al., patients with diabetes diagnosed with mucositis
were not at higher risk to develop peri‐implantitis when compared to non‐diabetics.

Available evidence is inconclusive as to whether diabetes is a risk factor/indicator for

peri‐implantitis.

Iatrogenic factors:

• The Consensus report of the 7th European Workshop on Periodontology recognized that
the onset and progression of peri‐ implantitis may be influenced by iatrogenic factors
such as inadequate restoration‐abutment seating, over contouring of restorations or
implant‐malpositioning

• Canullo et al. reported 18% of the diseased implants had received a bone grafting
procedure at installation while the percentage of healthy implants sites with a history of
bone augmentation was significantly smaller (7%).

• Schwarz et al observed that implants with residual defects of >1 mm were at a higher
risk of developing peri‐implant disease.

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It can be reasonably suggested that implant position and design of the suprastructure
may influence the access for home care‐ and professionally administered plaque
removal

Keratinized mucosa

• Systematic reviews have indicated that a KM of <2 mm was

associated with more plaque accumulation and peri‐implant soft
tissue inflammation when compared with implants that were
surrounded by a KM of ≥2 mm.

• Implant sites lacking KM were associated with significantly higher plaque scores,
marginal bleeding and BOP scores than sites with KM. However, no significant
differences were noted with regard to PD and radiographic bone levels (Ladwein et al)

While studies suggest that the absence or a reduced width of KM may negatively affect
self‐performed oral hygiene measures, there is limited evidence that this factor
constitutes a risk for peri‐implantitis.

Excess cement:

• It was suggested that the presence of excess cement was closely linked to the occurrence
of either peri‐implant mucositis or peri‐implantitis.

• Cement‐retained restorations were not found to be at higher risk for peri‐implantitis when
compared to screw‐retained reconstructions.

• Nevertheless, a systematic review emphasized that the rough surface structure of cement
remnants may facilitate retention and biofilm formation.

It is suggested that excess cement is a potential risk factor/indicator for peri‐implantitis.

Genetic factors:

• Gruica et al. reported an association between a positive IL‐1 composite gene

polymorphism and the occurrence of biological complications

• Laine et al., Hamdy and Ebrahem identified a significantly higher prevalence of IL‐1
receptor antagonist (IL‐1RA) polymorphisms in patients that were diagnosed with peri‐
implantitis

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• Observational studies have also pointed to a potential association with gene

polymorphisms of osteoprotegerin, IL‐6, CD14 and TNFα

While prospective clinical studies and studies with sufficient sample size are still
lacking, the available evidence points to a potential influence of various gene
polymorphisms in the patho‐ genesis of peri‐implantitis.

PATHOGENESIS OF PERI-IMPLANTITIS

• The pathogenesis of peri-implantitis is similar to that of periodontitis.

• Microbes in plaque stagnated on implant surface(s) release chemotactic peptides that

attract neutrophils toward the peri-implant pocket(s).

• Cytokines are released into the peri-implant crevicular fluid as a result of microbial
damage to epithelial cells, which attract more leukocytes (predominantly neutrophils)
toward the affected site.

• If neutrophils become overloaded with microbes, they degranulate and the toxic enzymes
released from neutrophils cause tissue damage and gingival inflammation.

• If the inflammation persists, it may progress to marginal gingiva and ultimately cause
bone loss, a classical feature of peri-implantitis.

Stromal cells (such as granulation tissue fibroblasts) also may participate in the pathogenesis
of peri-implantitis by upregulating vascularity and matrix breakdown, thereby promoting
migration/maintenance of infiltrates (proinflammatory cytokines) into the inflamed site.

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When compared with human periodontitis lesions, peri-implantitis lesions were shown to:

(a) Be larger in size

(b) Contain higher numbers and densities of plasma cells, macrophages and neutrophils

(C) Extend apically of the pocket epithelium

(d) Not be encapsulated by healthy connective tissue (Carcuac and Berglundh 2014).

Retrograde Peri-implantitis (RPI)

• A symptomatic periapical lesion is associated with a coronally osseointegrated fixture.

• RPI is thought to be caused by bacteria that are retained in the extraction socket and may
remain in that site for up to a year after the tooth is removed.

Occur at the time of implant placement: Associated with pre-existing diseases

• Contaminated surgical sites • Pulpo-periapical pathological

condition in the extraction site
• Excessive heat or compression at the
time of implant placement • Retained root tips

• Large osteotomies • Underlying bone disease

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• Presence of a foreign body • Periapical radiolucencies in adjacent

teeth
• Premature loading causing
microfractures of the bone • Remnant cells from cysts or
granulomas.

PERIODONTITIS AND PERI-IMPLANTITIS

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DIAGNOSIS OF PERI-IMPLANTITIS:
The diagnosis of peri-implantitis needs careful differentiation from peri-implant mucositis,
primary failures to achieve tissue integration, and problems lacking an inflammatory
component.

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Microbial monitoring- Bacterial culture, DNA probes, monoclonal antibody, enzyme assays
and polymerase chain reaction.

Sulcular fluid analysis- In 1991, Tetsch proposed a classification of these periotron values:

• >10- no inflammation

• 10 – 40 - mild inflammation,

• >40 – acute peri implant infections.

Osstell- Developed by Huang to evaluate the implant bone interface which is non-destructive
and non-invasive. It is based on resonance frequency analysis

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TREATMENT OF PERI-IMPLANTITIS
• The treatment of peri-implant infections comprises conservative (non-surgical) and
surgical approaches.

• Depending on the severity of the peri-implant disease (mucositis, moderate or severe

peri-implantitis) a nonsurgical therapy alone might be sufficient or a step-wise approach
with a non-surgical therapy followed by a surgical treatment may be necessary.

• One of the main aims of peri-implant therapy is to detoxify the contaminated implant
surface

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Treatment of peri-implant mucositis:

Non-surgical therapy aims at infection control through debridement of the implant surface
and thereby minimizing the bacterial load below the threshold level for causing disease

Occlusal therapy

Debridement: Curettes

Ultrasonic devices

Air abrasive systems

Adjunctive antimicrobial products and antiseptics

Citric acid

Locally or systemically delivered antimicrobials

Laser decontamination and photodynamic therapy

Adjunctive therapy for mucositis

• Some antimicrobials, mainly including chlorhexidine based, have been tested to prevent
bacterial recolonization after mechanical instrumentation (Thöne-Mühling et  al. 2010)
and/or to improve patients’ oral-hygiene procedures with controversial results on their
efficacy (Salvi and Ramseier 2015).

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• Clinical improvements observed at 6 months should have be attributed to improvements

in oral hygiene and not to the adjunctive administration of antibiotics (Hallström et al.
2012)

• Administration of oral probiotics (Hallström et  al. 2016) and sodium hypochlorite locally
delivered (Iorio Siciliano et  al. 2019 under review) have investigated: none of them
provided better clinical results when compared to the mechanical debridement only

Adjunctive therapy for peri-implantitis:

• Topical application of chlorhexidine in gel (Renvert et  al. 2006) or in chip (Machtei et al.
2012) as well as the use of local (Salvi et al. 2007) and systemic antibiotics (Mombelli
and Lang 1992) have been given promising results in term of mean PD reduction in the
short term, but not lead to disease resolution.

• Beneficial effect of photodynamic (Bassetti et al. 2014, Romanos et al. 2006) and laser
therapy (Bach et al. 2000, Sculean et al. 2005, Schwarz et al. 2006), has been proposed
and investigated both in pre-clinical and clinical studies, with promising results. In
particular,

• Positive results in terms of mean PPD, BOP and PUS reduction, have been assessed in a
2-year follow-up study where implant sites were treated with carbon fiber and metal
curettes followed by repeated application of a diode laser (Mettraux et al. 2016).

Guidelines for the Non-Surgical Treatment of Peri-Implant Mucositis and Peri-

Implantitis

1) Evaluation of smoking habits and advice for cessation

2) Instruction and motivation for adequate self-performed oral hygiene procedures

3) Correction of the prosthetic reconstruction in order to facilitate proper plaque control

4) Professional mechanical debridement with hand- or power-driven instruments in

conjunction with nonsurgical periodontal therapy, if needed

5) Adjunctive use of antiseptics (i.e. chlorhexidine mouth rinse or local application), locally
delivered antimicrobials, laser therapy or antimicrobial photodynamic therapy (aPDT)

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Surgical therapy in peri implantitis

Aim is to facilitate the removal of all granulation tissue and also to allow a thorough
debridement and decontamination of the exposed implant surface (Lindhe and Meyle 2008).

Rationale: to provide implant surface cleanability, thereby changing the anatomy of soft and
hard peri-implant tissues in order to acquire re-osseointegration. (Figuero et al. 2014)

Practically when there is an evident bone loss and pocket formation over 5 mm a surgical
approach is necessary (Renvert et al. 2018, Roccuzzo et al. 2016)

Resective therapy:

The objective of the resective therapy is bone remodeling in order to eliminate the infra-bony
component of the peri-implant defect together with the cleaning and decontamination of the
implant surface with or without apically repositioned of the flap.

Access Flap

• This technique allows to keep intact all the soft tissue around the implant which
consecutively will be repositioned at the previous presurgical level.

• The advantage of this procedure is the direct access to the affected implant surface to
eliminate the inflammatory changes responsible for the disease process (Figuero 2014)

Implantoplasty

• aimed to smooth the exposed implant surface in order to limit bacterial plaque retention.

• It may be indicated for suprabony or one wall defect.

• To smooth the implant surface the use of rotary diamond burs in decreasing roughness,
followed by an Arkansas stone appears to be an optimal treatment option (Ramel et al.
2016).

Apically Positioned Flap

• The flap design depend on the probing pocket depth and the amount of keratinized tissue

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• The soft tissue is sutured apically with a tight adaptation to the new bone anatomy
leaving the previously contaminated surface exposed to the oral cavity

Regenerative Therapy

• The main objective of the regenerative surgical technique is to regenerate peri-implant

bone defects, stabilize the soft tissues during the healing phase and lessen the risk of
mucosal recession.

• This surgical regenerative procedure is indicated in circumferential and infra-bony

defects (Figuero et  al. 2014, Roccuzzo 2011, Schwarz et al. 2011)

Combined Therapy

• Regenerative and resective therapy has been proposed (Schwartz 2011) to treat peri-
implant lesions.

• This surgical procedure is based on the morphology of the bony defects around implants.
In the suprabony component an extensive implantoplasty is performed, conversely for the
infrabony component a regenerative approach is used. Full thickness flaps are raised
buccally and orally/lingually by means of intra sulcular incisions.

The long-term outcome seems not to be influenced by the method of decontamination. The
morphology of the defect and the physico-chemical properties of the bone graft has a major
impact on the outcome than the method of decontamination.

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PROGNOSIS OF PERI-IMPLANTITIS:
• It might be hypothesized that those patients who are at high risk for development of peri-
implantitis, also run a higher risk for failure of peri-implantitis treatment once the disease
has been diagnosed.

• Establishing such risk profiles for peri-implantitis treatment could expedite improvement
of treatment protocols, assist in selection of the most effective individual treatment and
could allow for optimal information and motivation of patients.

• Furthermore, it could be helpful in clinical decision making and would enable clinicians
to estimate the chances on a successful treatment.

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PREVENTION OF PERI-IMPLANTITIS:
Routine monitoring of dental implants as a part of a comprehensive periodontal evaluation
and maintenance is essential. it is suggested to:

• Identify risk factors associated with developing peri-implant diseases

• Establish radiographic baseline at the time of implant placement

• Establish clinical and radiographic baseline at final prosthesis insertion

• Employ methods that monitor implant health and determine inflammatory complications
as part of an ongoing periodontal maintenance program

• Establish an early diagnosis and intervention, which will contribute to more effective
management of peri-implant diseases

• Patient education.

• Maintain a strict hygiene program at home

• Consistent follow-up appointments with the dentist and/or hygienist should include
clinical examination with recording of probing depths and radiographs

• Professionally administered plaque removal modalities have also been shown to reduce
inflammation

• Adjunctive techniques, including antiseptics, local and systemic antibiotics and abrasive
devices did not impact on reduction of inflammation.

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CONCLUSION:
• Oral implants are anchored in the jawbone and yet penetrate the mucosa, reaching the
highly contaminated environment of the oral cavity. 

• If plaque is allowed to accumulate over prolonged periods of time, peri-implant mucositis

may develop into lesions extending further apically, with associated loss of alveolar bone,
defined as peri-implantitis

• Owing to the infectious nature of peri-implant mucositis and peri-implantitis, preventive

procedures have to be rendered in a well-organized recall program to assure adequate
supportive therapy for a lifetime.

REFERENCE:
• Carranza’s clinical periodontology 11th edition, vol. 2

• Smeets R, Henningsen A, Jung O, Heiland M, Hammächer C, Stein JM. Definition,

etiology, prevention and treatment of peri-implantitis–a review. Head & face medicine.
2014 Dec 1;10(1):34.

• Ephros H, Kim S, DeFalco R. Peri-implantitis: Evaluation and Management. Dental

Clinics. 2020 Apr 1;64(2):305-13.

• Regi BM, Savita S, Kaimal G. Peri implantitis: An overview.

• Ogata Y. Risk Factors for Peri-implant Diseases. Springer Nature; 2020.

• Aroca S, Salvi GE, Roccuzzo A, Renert U, Sculean A, Artzi Z. Prevention and

Management of Peri‐Implant Diseases. Bone Augmentation by Anatomical Region:
Techniques and Decision‐Making. 2020 May 15:505-22.

• Ravidà A, Galli M, Siqueira R, Saleh MH, Galindo Moreno P, Wang HL. Diagnosis of
peri‐implant status after peri‐implantitis treatment: Proposal of a new classification.
Journal of Periodontology. 2020 May 25.

• Ravidà A, Galli M, Siqueira R, Saleh MH, Galindo Moreno P, Wang HL. Diagnosis of
peri‐implant status after peri‐implantitis treatment: Proposal of a new classification.
Journal of Periodontology. 2020 May 25.

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