Peri-implantitis: Diagnosis, Staging and Evidence-Based Treatments According to 2023 EFP Guidelines
Peri-implantitis is today the main threat to medium- and long-term implant longevity. Its prevalence has turned out higher than initially expected: Derks and Tomasi's systematic review (J Clin Periodontol, 2015) reported implant-level prevalence of 18.5% and patient-level prevalence of 22% in European observational studies over 9-year follow-up periods. More recent data, using the stricter diagnostic criteria of the EFP/AAP 2017 classification, confirm a cumulative peri-implantitis prevalence of 14-31% at 5 years, with wide variability tied to implant system, patient characteristics, and the diagnostic definition adopted. Early recognition and prompt treatment are decisive for prognosis: peri-implant lesions progress faster than periodontal disease for intrinsic biological reasons (absence of supracrestal connective attachment, lower peri-implant vascularization, cone-morse connection morphology affecting micro-gap dispersion).
The EFP/AAP 2017 classification distinguishes peri-implant mucositis (inflammation confined to peri-implant soft tissue, reversible with non-surgical therapy, without progressive bone loss) from peri-implantitis (inflammation associated with progressive bone loss and pocket formation). Diagnostic criteria for peri-implantitis require the simultaneous presence of: bleeding on probing (BOP) and/or suppuration, probing depth ≥6 mm or an increase ≥2 mm compared to post-loading values, and radiographic bone loss ≥3 mm compared to post-loading baseline (in cases without baseline radiography, the expected physiological bone level corresponds to 1-1.5 mm subcrestal at 1 year post-loading). Severity staging (mild: bone loss <25% of implant length; moderate: 25-50%; severe: >50% or exposure of the implant apex) guides treatment choice.
Non-surgical treatment of peri-implantitis is based on mechanical decontamination of the exposed implant surface, elimination of local, modifiable etiological factors, and reassessment at 8-12 weeks. Decontamination with titanium, carbon or PEEK instruments (to avoid altering implant surface topography), combined with 0.2% chlorhexidine irrigation or erythritol powder (Air-Flow, EMS), has shown statistically significant clinical improvements but with limited predictability of complete resolution: Khoshkam et al.'s meta-analysis (J Periodontol, 2016) reported an average probing depth reduction of 1.07 mm and a 30% BOP reduction after non-surgical decontamination. The intrinsic difficulty lies in the mechanical inaccessibility of the micro-irregularities of the SLA/SLActive surface that harbor subgingival biofilm.
The surgical approach to peri-implantitis — indicated in moderate and severe forms not responding to non-surgical treatment — involves three main strategies: resective therapy (surgical removal of granulation tissue, osteoplasty to reduce infrabony depths and apical repositioning of the mucosal margin to improve maintenance accessibility), regenerative therapy (use of bone graft materials and membranes in confined infrabony defects, aiming for bone level gain), and combining the two based on the bone defect's morphology. Selection criteria for defect type suited to the regenerative approach follow CIVD morphology (circular, intrabony, vertical, with favorable residual bone walls): defects with 3-4 bone walls show superior regenerative outcomes compared to open supracrestal defects. Decontaminating the implant surface during the surgical flap can use an Er:YAG laser (2,940 nm wavelength, highly absorbed by water, with selective biofilm ablation effect without surface overheating) or chemical solutions (40% citric acid, EDTA, imidacloprid — protocols with still-limited evidence).
Adjunctive systemic antibiotic management has a rationale in decontaminating implant surfaces inaccessible to mechanical therapy. The Heitz-Mayfield protocol — metronidazole 500 mg + amoxicillin 500 mg 3 times/day for 7 days combined with surgical debridement — is the most documented, with prospective cohort studies at 5 years (Heitz-Mayfield et al., J Clin Periodontol, 2018) showing implant survival rates of 86% in moderate-severe forms. Antibiotic prescribing should follow antimicrobial stewardship principles: surgically justified indication, minimum effective duration, monitoring of local resistance patterns. Current evidence doesn't support using slow-release local antibiotics (minocycline microspheres, doxycycline gel) as substitutes for mechanical decontamination.
Preventing peri-implantitis through a personalized implant support program (SIM/SPT, Supportive Implant/Periodontal Therapy) is the strategy with the best documented cost-benefit ratio. The standard program includes visits at 3, 6 and 12 months after prosthetic loading and subsequently every 6-12 months based on individual risk profile (history of periodontitis, smoking, plaque control, diabetes, residual peri-implant probing depth). Essential elements of every SIM visit include: removal of the implant prosthesis (or at least circumferential peri-implant assessment), probing with a calibrated probe (force 0.2-0.25 N), recording BOP, probing depth and radiographic bone level (intraoral X-ray with a positioner for longitudinal comparability), and professional supra- and subgingival hygiene of implant surfaces.