Peri-implantitis at a mandibular molar implant in an erratic attender

Diagnosis: peri-implantitis. The 2018 case definition requires bleeding and/or suppuration on gentle probing, increased probing depth compared with previous examinations, and radiographic evidence of progressive bone loss. All three are present: bleeding and suppuration, 7–8 mm depths, and 3.5 mm of bone loss compared with a documented baseline. When baseline data are unavailable, the working threshold is bone loss ≥3 mm together with probing depth ≥6 mm plus bleeding or suppuration - the same conclusion is reached either way.

Why not peri-implant mucositis: mucositis is reversible inflammation with bleeding/suppuration but no progressive bone loss. The documented 3.5 mm change excludes it.

Before treating, exclude:

• Retained cement or restoration-related factors - although the crown is screw-retained at this site, check the contralateral cemented crown and any subgingival margins; excess cement is a common, correctable cause.
• Occlusal overload - assess fremitus, parafunction, and implant-level contacts; overload alone rarely causes crater defects but can contribute.
• Retrograde peri-implantitis / endodontic origin - relevant if a tooth was extracted for endodontic reasons; check for a periapical radiolucency at the apex.
• Implant fracture or component loosening - check mobility of the crown, torque, and radiograph for component fit.
• Poorly positioned implant or thin phenotype with 1 mm keratinised mucosa, which compromises plaque control and surgical outcomes.
• Systemic modifiers - smoking and the history of periodontitis are established risk factors; HbA1c 6.8% is reasonably controlled but still relevant.

Documenting the baseline-to-now bone change is the decisive step; without it, the diagnosis would rest on the ≥3 mm surrogate threshold.

Phase 1 - cause-related, non-surgical (mandatory but usually insufficient alone).

• Re-instruct oral hygiene; the 45% plaque score must improve before any surgery, or the surgical outcome is compromised.
• Subgingival debridement around the implant with titanium or carbon-fibre instruments; avoid steel curettes that roughen the surface. Remove the restoration only if needed to access a cement or contour problem.
• Check and adjust occlusion; consider an occlusal splint if parafunction is evident.
• Adjuncts such as chlorhexidine or local antimicrobials can reduce inflammation in mucositis; evidence that they resolve peri-implantitis is weak.
• Smoking cessation referral; confirm diabetes control with the physician.
• Re-evaluate at 6–8 weeks: the criterion for success is reduced bleeding/suppuration and reduced depth, not necessarily radiographic change so early.

Phase 2 - surgical, if bleeding plus ≥6 mm depth persist.

• Raise a flap for debridement, decontamination (chemical or mechanical), and where possible implantoplasty of exposed rough suprastructure, aiming to re-establish a clean, smooth, cleansable transmucosal contour.
• Consider soft-tissue augmentation for the 1 mm band of keratinised mucosa, ideally at the same time or as a separate procedure once inflammation is controlled.
• Regenerative approaches are unpredictable in crateriform peri-implant defects and should not be promised as routine.

Explantation is considered when there is uncontrolled infection, severe bone loss with a defect not amenable to decontamination, implant mobility, or a restoratively hopeless position. The judgement point is that non-surgical therapy alone will not resolve peri-implantitis; it is preparation for surgery and a test of the patient's compliance.

Prognosis should be framed as conditional rather than fixed. This implant has several negative modifiers: a history of treated periodontitis, current smoking, erratic attendance, high plaque and bleeding scores, a 1 mm keratinised mucosal band, and a crateriform defect. Each of these is a modifiable or partly modifiable risk factor, so the honest answer is that the implant can be maintained only if the patient commits to a defined programme - and that without compliance, further bone loss and eventual loss of the implant are likely.

I would explain that published survival figures for implants in maintenance are high at the patient level, but that peri-implantitis is a leading cause of late failure, and that treated peri-implantitis has a meaningful recurrence rate. I would avoid quoting a single number as a promise, and instead state functional goals: no bleeding or suppuration, probing depths ≤5 mm, stable bone on annual radiographs, and a plaque score low enough to sustain health.

Maintenance schedule: 3-monthly for the first year after active treatment, because the re-infection and re-inflammation risk is highest in that window and because the interval is short enough to detect relapse early; then extend to 3–6 monthly only if all parameters are stable. Each visit: peri-implant probing with light force, bleeding and suppuration recording, plaque score, occlusion check, and radiograph annually or if there is a change in depth. Re-enter active therapy if bleeding plus increasing depth recurs. The critical judgement is that the maintenance interval is a therapeutic decision based on risk, not a default six-month booking.