Peri-Implant Disease Management

§6.1.1 — Overview

Diagnosis precedes treatment

Peri-implant disease is the leading cause of late implant failure — failure to maintain an osseointegration that was once achieved — and yet its management is, more than almost any other implant problem, a discipline of diagnosis before intervention. The single decision that determines the entire treatment pathway is not which laser to buy or which graft to pack, but whether the lesion in front of you is reversible soft-tissue inflammation or progressive, bone-destructive disease. Get that wrong and every downstream step is mis-aimed: a mucositis treated as peri-implantitis is over-surgicalized, while a peri-implantitis treated as mucositis is allowed to consume the supporting bone unchecked.¹

This chapter codifies that discipline. It opens with the 2017 World Workshop case definitions — health, mucositis, and peri-implantitis — including the much-tested rule for diagnosing peri-implantitis when no baseline radiograph exists. It then ports the management algorithm onto the 2023 EFP S3 clinical practice guideline, whose central idea is cumulative, stepwise care: cause-related therapy first, then non-surgical instrumentation, then surgical access and decontamination, then reconstruction where geometry allows, and supportive peri-implant care for the rest of the implant's life. Finally it addresses the hardest conversation in implant maintenance — when to stop salvaging and explant — anchoring it to the two findings that override all others: mobility and bone loss exceeding half the implant length.³

Two principles recur. First, reversibility is the organizing axis: mucositis is the implant analogue of gingivitis and resolves with non-surgical control, whereas peri-implantitis, like periodontitis, is managed but rarely "cured." Second, re-evaluation gates escalation: each phase is reassessed — conventionally at six to eight weeks — before the next is invoked, so that no patient is escalated to surgery for a lesion that simpler care would have settled.

The diagnosis you make at the chairside, not the instrument you reach for, decides whether this implant is over-treated, under-treated, or treated.

◆ Key concept · The three case definitions

Peri-implant health: no bleeding on probing or suppuration, no probing-depth increase, and no bone loss beyond initial physiologic remodeling. Peri-implant mucositis: bleeding and/or suppuration on probing with no progressive bone loss — an inflammatory lesion of the soft tissue that is reversible. Peri-implantitis: bleeding/suppuration plus progressive bone loss beyond remodeling. Where no baseline radiograph exists, peri-implantitis may be inferred from the combination of probing depth ≥ 6 mm and bone level ≥ 3 mm apical to the implant shoulder, together with bleeding on probing.¹²

§6.1.2 — Case definitions

Health, mucositis, and peri-implantitis

The 2017 World Workshop, reported by Berglundh and colleagues for Workgroup 4 and elaborated by Renvert and colleagues, replaced a scatter of competing thresholds with a single coherent framework built on three clinical observations: bleeding on probing (the marker of inflammation), probing depth change (the marker of attachment/soft-tissue change), and radiographic bone level change (the marker of disease progression).¹² Probing of implants is legitimate and necessary; a gentle force (~0.25 N) does not damage the mucosal seal, and serial probing — referenced to the bone level recorded at prosthesis delivery — is the backbone of surveillance.

The framework's elegance is that each diagnosis maps to a category of action. Health is maintained; mucositis is reversed non-surgically; peri-implantitis is managed by the staged pathway. The diagnostic difficulty in practice is almost always the same: a patient inherited from another practice, with no baseline radiograph against which to judge "progressive" loss. For exactly this situation the Workshop supplied a fallback case definition — described below and tested relentlessly on board examinations.

Table 1 · 2017 World Workshop case definitions for peri-implant conditions
Condition	Bleeding / suppuration	Probing depth	Radiographic bone level	Reversibility & action
Peri-implant health	Absent	No increase vs. baseline	No loss beyond initial remodeling	Stable — routine supportive care
Peri-implant mucositis	Present (BOP and/or suppuration)	May increase from swelling/edema	No progressive loss beyond remodeling	Reversible — non-surgical control
Peri-implantitis (baseline available)	Present	Increased vs. baseline	Progressive loss beyond remodeling	Managed — staged intervention
Peri-implantitis (no baseline)	Present	≥ 6 mm	Bone level ≥ 3 mm apical to shoulder	Managed — staged intervention

✦ Clinical pearl · Capture the baseline you wish you had

The diagnostic agony of the no-baseline patient is entirely preventable for your own cases. Record a periapical radiograph and a full set of probing depths at the time the prosthesis is delivered — this, not surgery day, is the reference point against which all later "progressive" loss is measured. The fallback ≥ 6 mm / ≥ 3 mm rule is deliberately specific but has limited sensitivity for early disease; it will miss incipient lesions a documented baseline would have caught.²

§6.1.3 — The S3 stepwise pathway

Cumulative, re-evaluated, escalating care

The 2023 EFP S3 clinical practice guideline, developed by Herrera and colleagues from the 2022 Perio Workshop, frames treatment as a cumulative protocol that mirrors the established staged approach to periodontitis.³ Each step is a prerequisite for — not an alternative to — the next, and a formal re-evaluation gates escalation. The figure below renders the pathway from the diagnostic fork through the four therapeutic phases to lifelong supportive care; the prose that follows expands each phase.

Figure 1. The cumulative, re-evaluated peri-implant disease pathway. Diagnosis forks to reversible mucositis (non-surgical control then maintenance) or peri-implantitis (cause-related → non-surgical → surgical access ± reconstruction → SPIC). Re-evaluation at 6–8 weeks gates each escalation; explantation is an exit available when removal criteria are met. Synthesized from the 2017 World Workshop case definitions and the 2023 EFP S3 guideline.¹³

Phase 1 — Cause-related (pre-therapeutic) therapy

No instrumentation succeeds against an uncontrolled cause. This phase reinforces patient-performed plaque control, corrects plaque-retentive prosthetic factors (overcontoured or over-cemented restorations, emergence profiles that defeat hygiene access), and removes residual subgingival cement — a common and reversible driver. It also treats concurrent periodontitis and addresses systemic and behavioral modifiers, chiefly smoking and glycemic control. Where access for cleaning or instrumentation is inadequate, the restoration is removed or modified.³

Phase 2 — Non-surgical mechanical debridement

Submucosal instrumentation is performed with implant-appropriate instruments — titanium or PEEK curettes, air-polishing with low-abrasive glycine or erythritol powder, and ultrasonics with soft tips — to disrupt the biofilm without scoring the surface. Adjuncts (local antiseptics, systemic antibiotics, lasers) show limited additive benefit and are not recommended routinely. Non-surgical therapy alone reliably resolves mucositis and may settle early, accessible peri-implantitis; the site is re-evaluated at 6–8 weeks before any decision to escalate.³

Phase 3 — Surgical access & decontamination

For peri-implantitis that persists after the non-surgical phase, open-flap surgery provides direct access for thorough implant-surface decontamination. Defect morphology dictates the approach: predominantly supracrestal or horizontal defects are managed resectively, with an apically positioned flap and, where indicated, implantoplasty to smooth exposed threads; contained intrabony components are candidates for reconstruction.³

Phase 4 — Reconstructive therapy

Reconstruction is reserved for contained intrabony defects (broadly, three- or four-wall geometries), where a bone substitute, with or without a barrier membrane, can produce radiographic defect fill. Predictability depends on defect geometry and on the quality of decontamination — a graft placed onto a contaminated surface fails. Circumferential, non-contained defects are poor reconstructive candidates and are typically managed resectively or, if severe, drive the explant decision.³

Phase 5 — Supportive peri-implant care (SPIC)

Whatever the route to resolution, the implant enters lifelong supportive care at risk-based intervals of 3–6 months: probing, bleeding-on-probing assessment, radiographic monitoring, and professional debridement. Adherence to SPIC is the single strongest predictor of long-term stability after treatment — the phase most often neglected and most decisive for the result.³

Interactive treatment selector

Select the scenario that matches your patient to reveal the recommended pathway. Treat reversible disease first and re-evaluate before escalating.

Tap a scenario. Re-evaluate 6–8 weeks after each phase before escalating.

▲ Common pitfalls

Jumping to surgery (or to systemic antibiotics) before the cause-related and non-surgical phases — escalating a lesion that hygiene and prosthetic correction would have controlled.
Leaving residual subgingival cement unaddressed and then "treating" the resulting peri-implantitis indefinitely with debridement.
Grafting a non-contained or circumferential defect, or grafting onto an inadequately decontaminated surface — predictable failure dressed up as reconstruction.
Discharging the patient after resolution instead of enrolling in SPIC — forfeiting the strongest predictor of long-term success.

§6.1.4 — Explant vs. salvage

Knowing when to stop salvaging

No single criterion mandates removal in isolation, but two findings dominate the decision. Clinical mobility signifies loss of osseointegration — the implant is, by definition, failed, not failing, and is removed. Bone loss exceeding roughly half the implant length (or loss approaching the apex) leaves too little anchorage for predictable salvage and tilts the balance decisively toward explantation.³⁴ Around these two anchors sit the modifiers — defect containment, prosthetic value and restorability, the trajectory of response to staged care, and the burden of recurrent infection or symptoms. The presence of any "removal-favored" finding shifts the weighing strongly, and the combination of mobility or > 50% loss with progression despite treatment effectively settles it.

Table 2 · Salvage versus removal — weighing the full picture
Finding	Salvage favored	Removal favored	Evidence
Implant mobility	Stable clinically immobile	Mobile = osseointegration lost	Consensus
Bone loss	< 50% of implant length	> 50% or approaching apex	Consensus
Defect morphology	Contained, accessible (intrabony)	Circumferential, non-contained	Syst. review
Position / restorability	Prosthetically valuable, correctable	Malpositioned, unrestorable	Consensus
Response to therapy	Improving after staged care	Progressive loss despite treatment	Syst. review
Symptoms / infection	Controlled	Recurrent suppuration, pain, fistula	Consensus

✦ Clinical pearl · Atraumatic removal protects the next implant

When removal is indicated, favor reverse-torque / counter-torque devices over the trephine where the implant geometry permits; they sacrifice far less peri-implant bone and preserve the site for simultaneous or staged grafting and re-implantation. Decide grafting timing on the residual defect at removal, plan the reconstruction interval, and — critically — address the original cause (hygiene access, cement, occlusal load, systemic risk) before placing a replacement into the same unfavorable environment.⁴

§6.1.5 — Glossary

Key terms

Peri-implant health: Absence of bleeding/suppuration on probing, no probing-depth increase, and no bone loss beyond initial physiologic remodeling.
Peri-implant mucositis: Reversible inflammatory lesion of the peri-implant soft tissue with bleeding/suppuration on probing but no progressive bone loss.
Peri-implantitis: Plaque-associated pathological condition with peri-implant mucosal inflammation and progressive supporting-bone loss.
No-baseline case definition: In the absence of baseline records, peri-implantitis may be inferred from bleeding on probing plus probing depth ≥ 6 mm and bone level ≥ 3 mm apical to the implant shoulder.
Cause-related therapy: Pre-therapeutic phase correcting plaque control, prosthetic/cement factors, and systemic/behavioral risk before instrumentation.
SPIC: Supportive peri-implant care — lifelong, risk-based recall (3–6 months) of probing, BOP, radiographs, and professional debridement.
Implantoplasty: Mechanical smoothing/removal of exposed implant threads during resective surgery to reduce biofilm-retentive surface.
Reconstructive therapy: Grafting (bone substitute ± membrane) of contained intrabony peri-implant defects to achieve radiographic defect fill.
Reverse-torque removal: Atraumatic explantation using a counter-torque device that unscrews the implant, sparing peri-implant bone relative to trephination.

§6.1.S — Self-test

Board & oral-defense preparation

1. The single clinical finding that distinguishes peri-implant mucositis from peri-implantitis is:

C is correct. Both conditions share inflammation (BOP/suppuration). Peri-implantitis is defined by the additional feature of progressive supporting-bone loss; mucositis has none beyond physiologic remodeling.

2. In a patient with no baseline radiograph, the 2017 World Workshop fallback case definition of peri-implantitis requires bleeding on probing plus:

B is correct. The secondary (no-baseline) definition is BOP/suppuration with probing depth ≥ 6 mm and bone level ≥ 3 mm apical to the most coronal portion of the intraosseous implant. Its sensitivity for early disease is limited.

3. Peri-implant mucositis is best characterized as:

B is correct. Mucositis is the implant analogue of gingivitis — reversible with professional and patient-performed plaque control, without surgery.

4. According to the EFP S3 guideline, the correct sequence of peri-implantitis therapy is:

B is correct. The S3 protocol is cumulative: cause-related (pre-therapeutic), then non-surgical debridement, then surgical access/decontamination with reconstruction in selected defects, then lifelong supportive care.

5. The finding most specific for loss of osseointegration — and an absolute indication for removal — is:

C is correct. A mobile implant has lost osseointegration; it is failed rather than failing and should be explanted. BOP and modest probing depth do not establish loss of integration.

6. Approximately what degree of bone loss tips the balance strongly toward explantation rather than salvage?

C is correct. Loss exceeding roughly half the implant length leaves insufficient anchorage for predictable salvage and, combined with other adverse findings, favors removal.

7. The cause-related (pre-therapeutic) phase includes all of the following EXCEPT:

D is correct. Surface decontamination under a flap is the surgical phase. Cause-related therapy is non-surgical: hygiene, prosthetic/cement correction, and systemic/behavioral risk modification.

8. Which instrument/adjunct is appropriate for non-surgical submucosal debridement of an implant?

B is correct. Implant-appropriate, low-abrasive instrumentation (titanium/PEEK curettes, glycine/erythritol air-polishing, soft-tip ultrasonics) disrupts biofilm without scoring the surface. Steel instruments and burs damage it; antibiotics do not replace mechanical therapy.

9. After a phase of therapy, the conventional re-evaluation interval before deciding to escalate is:

C is correct. Re-evaluation at 6–8 weeks allows resolution of inflammation to be judged before escalating to the next, more invasive phase.

10. Reconstructive (grafting) therapy is most predictable in which defect type?

C is correct. Contained, multi-wall intrabony defects retain graft material and support defect fill. Horizontal/supracrestal defects are managed resectively; non-contained defects are poor graft candidates.

11. Implantoplasty is most appropriately used for:

B is correct. Implantoplasty smooths supracrestally exposed threads during resective surgery, reducing the biofilm-retentive surface. It is not a reconstructive or first-line measure.

12. The single strongest predictor of long-term stability after peri-implantitis treatment is:

C is correct. Enrollment in and adherence to risk-based supportive peri-implant care is the strongest predictor of maintained stability after treatment.

13. A common, reversible, and frequently overlooked local driver of peri-implantitis is:

B is correct. Residual subgingival cement is a well-documented, reversible plaque-retentive factor; removing it is part of cause-related therapy and may itself resolve the lesion.

14. Probing of dental implants for surveillance is:

B is correct. Gentle probing does not harm the seal and is essential; serial probing depth and BOP, referenced to a delivery baseline, underpin diagnosis and monitoring.

15. The recommended reference time point for the baseline radiograph and probing depths is:

B is correct. Bone level and probing depths recorded at prosthesis delivery form the baseline against which later "progressive" loss is judged, accounting for initial physiologic remodeling.

16. Routine adjunctive use of systemic antibiotics in non-surgical peri-implantitis therapy is best described as:

B is correct. The S3 guideline finds limited additive benefit for routine systemic antibiotics and other adjuncts; mechanical biofilm disruption remains the core intervention.

17. A patient presents with progressive bone loss despite completed staged therapy, recurrent suppuration, and a non-contained circumferential defect, but the implant is immobile. The most appropriate decision is:

C is correct. Although immobility alone favors salvage, progression despite treatment, recurrent infection, and an ungraftable non-contained defect together shift the weighing strongly toward removal.

18. The preferred technique for removing a salvage-failed implant when geometry permits is:

B is correct. Reverse-torque/counter-torque removal sacrifices the least bone and best preserves the site for grafting and re-implantation, compared with trephination.

19. Peri-implant health, by the 2017 case definition, is characterized by:

B is correct. Health requires absence of inflammatory signs (BOP/suppuration), no increase in probing depth, and no progressive bone loss — not merely the absence of mobility.

20. The fundamental reason early failure (failure to achieve integration) and peri-implantitis (failure to maintain it) must not be conflated is that:

B is correct. Early failure reflects a cascade that never completed (micromotion, thermal/compressive trauma, stalled host response); peri-implantitis is biofilm-driven loss of established integration. Their causes, timing, and management differ entirely.

1. Define peri-implant health, mucositis, and peri-implantitis, and explain how you would distinguish them at the chairside.

Model answer. Health is the absence of bleeding or suppuration on probing, no increase in probing depth, and no bone loss beyond initial physiologic remodeling. Mucositis adds bleeding and/or suppuration — an inflammatory soft-tissue lesion — but with no progressive bone loss; it is reversible. Peri-implantitis is inflammation plus progressive supporting-bone loss beyond remodeling. At the chairside I integrate three signals: BOP/suppuration (inflammation), probing depth referenced to the delivery baseline (soft-tissue change), and serial radiographs (bone change). The decisive discriminator between mucositis and peri-implantitis is progressive bone loss.

Examiner follow-ups:

What probing force do you use, and is probing safe?
Why is the prosthesis-delivery time point the correct baseline?

2. A patient transfers in with no baseline radiograph. Walk me through how you diagnose peri-implantitis and the limitations of that approach.

Model answer. Without a baseline I apply the 2017 Workshop fallback definition: bleeding/suppuration on probing together with a probing depth of at least 6 mm and bone level at least 3 mm apical to the implant shoulder on a periapical radiograph. I would also look for any prior imaging from referring providers to reconstruct a trajectory. The key limitation is sensitivity: this threshold is specific but misses early or incipient disease that a true baseline would have caught, so a negative result does not exclude active disease. I therefore establish my own baseline at that visit and monitor closely, and I counsel the patient that early documentation is what makes future diagnosis reliable.

Examiner follow-ups:

Why is the fallback definition's sensitivity low?
What records would you create at this first visit?

3. Take me through the EFP S3 stepwise management of peri-implantitis and the logic of its cumulative structure.

Model answer. The protocol is cumulative — each step is a prerequisite for the next, not an alternative. First, cause-related (pre-therapeutic) therapy: reinforce hygiene, correct plaque-retentive prosthetic factors, remove residual cement, and address smoking and glycemic control. Second, non-surgical mechanical debridement with implant-appropriate instruments and air-polishing, then re-evaluate at 6–8 weeks. Third, if disease persists and the implant is stable and restorable, surgical access with thorough surface decontamination — resective with implantoplasty for horizontal/supracrestal defects. Fourth, reconstruction for contained intrabony defects with graft ± membrane. Fifth, lifelong supportive peri-implant care. The logic is that you never escalate to a more invasive, less predictable step before confirming the simpler one has failed at re-evaluation — and you never operate on an uncontrolled cause.

Examiner follow-ups:

Which defects do you graft, and which do you treat resectively?
What role do adjunctive antibiotics and lasers play?

4. How do you decide between salvaging and explanting an implant with peri-implantitis? Anchor your reasoning to specific thresholds.

Model answer. I weigh the whole picture but around two dominant anchors. Clinical mobility means osseointegration is lost — that implant is failed, not failing, and comes out. Bone loss exceeding roughly half the implant length, or approaching the apex, leaves too little anchorage for predictable salvage and strongly favors removal. Around those I weigh modifiers: defect containment (a contained intrabony defect is salvageable and graftable; a circumferential non-contained one is not), prosthetic value and restorability, the trajectory of response to staged care, and the burden of recurrent suppuration, pain, or fistula. Any single removal-favored finding shifts the balance; mobility or > 50% loss combined with progression despite treatment effectively settles it. When I remove, I prefer reverse-torque devices to spare bone, plan grafting timing on the residual defect, and correct the original cause before re-implanting.

Examiner follow-ups:

Why is mobility an absolute rather than relative indication?
How does removal technique affect the next implant?

5. Why is supportive peri-implant care so heavily emphasized, and how would you structure it for a treated peri-implantitis patient?

Model answer. SPIC is emphasized because adherence to it is the single strongest predictor of long-term stability after treatment — peri-implantitis, like periodontitis, is managed rather than cured, so without structured maintenance the same biofilm-driven process recurs. I structure it as lifelong, risk-based recall, typically every 3–6 months depending on the patient's risk profile (history of periodontitis, smoking, glycemic control, plaque control, residual deep sites). Each visit I record probing depths and BOP, take radiographs at appropriate intervals, perform professional debridement with implant-safe instruments, and re-reinforce home care and any prosthetic access issues. Crucially, SPIC is also surveillance: it is where I catch recurrence early enough to intervene non-surgically rather than discovering it as advanced bone loss.

Examiner follow-ups:

What factors lengthen or shorten the recall interval?
What findings at a recall would trigger re-treatment?

§6.1 — References

References

Berglundh T, Armitage G, Araujo MG, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S313–S318. doi:10.1002/JPER.17-0739 PMID: 29926955
Renvert S, Persson GR, Pirih FQ, Camargo PM. Peri-implant health, peri-implant mucositis, and peri-implantitis: Case definitions and diagnostic considerations. J Periodontol. 2018;89(Suppl 1):S304–S312. doi:10.1002/JPER.17-0588 PMID: 29926953
Herrera D, Berglundh T, Schwarz F, et al. Prevention and treatment of peri-implant diseases — The EFP S3 level clinical practice guideline. J Clin Periodontol. 2023;50(Suppl 26):4–76. doi:10.1111/jcpe.13823 PMID: 37271498
Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. J Periodontol. 2018;89(Suppl 1):S267–S290. doi:10.1002/JPER.16-0350 PMID: 29926957

Evidence grades: Systematic review Consensus Preclinical.

Peri-Implant Disease Management

Diagnosis precedes treatment

Health, mucositis, and peri-implantitis

Cumulative, re-evaluated, escalating care

Phase 1 — Cause-related (pre-therapeutic) therapy

Phase 2 — Non-surgical mechanical debridement

Phase 3 — Surgical access & decontamination

Phase 4 — Reconstructive therapy

Phase 5 — Supportive peri-implant care (SPIC)

Interactive treatment selector

Knowing when to stop salvaging

Key terms

Board & oral-defense preparation

Related modules

References

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