Residency · Residency · Oral Maxillofacial Surgery
Peri-Implantitis: Diagnosis and Management
Overview
Peri-implant diseases encompass peri-implant mucositis and peri-implantitis. Peri-implant mucositis is a reversible inflammatory condition of the soft tissue surrounding an implant without bone loss. Peri-implantitis is an irreversible inflammatory condition with progressive loss of supporting bone beyond initial remodeling. Peri-implant mucositis affects approximately 43% of implant sites, while peri-implantitis affects approximately 22%. Peri-implantitis is a significant cause of late implant failure.
Definitions (2017 World Workshop on Classification)
| Condition | BOP | Bone Loss | Reversibility | Prevalence |
|---|---|---|---|---|
| Peri-implant health | Absent | None beyond initial remodeling | N/A | — |
| Peri-implant mucositis | Present | None beyond initial remodeling | Reversible | ~43% of sites |
| Peri-implantitis | Present | Progressive beyond initial remodeling | Irreversible without treatment | ~22% of sites |
Peri-Implant Health
Peri-implant health is characterized by the absence of clinical signs of inflammation (no erythema, swelling, or suppuration), no bleeding on probing, and no bone loss beyond initial remodeling with radiographic stability.
Peri-Implant Mucositis
Peri-implant mucositis presents with bleeding on probing and/or suppuration, potentially with erythema and swelling of peri-implant soft tissue, but without bone loss beyond initial physiologic remodeling. It is reversible with appropriate treatment, analogous to gingivitis around natural teeth.
Peri-Implantitis
Peri-implantitis presents with bleeding on probing and/or suppuration, increasing probing depths over time, and progressive radiographic bone loss beyond initial remodeling. When baseline radiographs are unavailable, bone loss of 3 mm or more and/or probing depths of 6 mm or more with bleeding on probing are diagnostic. Without treatment, it is irreversible and typically progressive.
Etiology and Risk Factors
Microbiology
Peri-implantitis is a biofilm-mediated disease similar to periodontitis but with some differences. The microbiome shifts from health-associated organisms (Gram-positive cocci) to disease-associated organisms (Gram-negative anaerobes). Key pathogens include Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, and Staphylococcus aureus. The biofilm composition on implant surfaces may differ from that on natural teeth, with a broader diversity of pathogens.
Risk Factors
A history of periodontitis is the strongest risk factor, with affected patients having a 2-5 times higher risk. Poor oral hygiene with inadequate plaque control around implants is another major factor. Smoking increases risk in a dose-dependent fashion. Poorly controlled diabetes (HbA1c above 7%) elevates risk. Lack of keratinized tissue is controversial but may increase plaque accumulation and difficulty with hygiene. Excess cement from subgingival residual cement is a well-documented local risk factor. Over-contoured prosthetic designs that impede hygiene access contribute to disease. Rough implant surfaces (SLA, TiUnite) may harbor more bacteria once exposed. A history of peri-implantitis at other implant sites also increases risk.
Diagnosis
Clinical Examination
Probing should be performed with a plastic or titanium probe at gentle force (0.25 N), recording probing depths at 4-6 points per implant. Bleeding on probing indicates inflammation. Suppuration, either on probing or spontaneous, is a significant finding. Mucosal assessment evaluates erythema, swelling, and fistula formation. Implant mobility indicates complete loss of osseointegration and requires removal. The prosthesis should be evaluated for cement remnants, overcontoured margins, and hygiene access.
Radiographic Assessment
A baseline radiograph taken at the time of prosthetic loading is essential, as it records the initial bone level after physiologic remodeling. Standardized periapical radiographs with a holder are compared to baseline for bone loss assessment. The bone loss pattern is typically circumferential or crater-shaped around the implant. Progressive bone loss is documented through sequential radiographs showing increasing bone loss over time. CBCT is useful for assessing the 3D extent of bone loss, particularly buccal and lingual defects not visible on periapical radiographs.
<image>Periapical radiograph series comparing a healthy implant at baseline (time of loading) with progressive peri-implantitis at 1, 3, and 5 years, demonstrating circumferential bone loss pattern with annotations of probing depths and bone levels</image>
Classification of Bone Defects
Schwarz et al. Classification
Class 1 defects are intrabony or infrabony. Class 1a is a buccal dehiscence. Class 1b is a buccal dehiscence with semicircular bone resorption. Class 1c is a buccal dehiscence with circular bone resorption. Class 1d is circular bone resorption forming a circumferential crater. Class 1e is circumferential bone loss with an intact buccal wall. Class 2 defects involve suprabony or horizontal bone loss without an intrabony component and are less amenable to regenerative treatment.
Management
Prevention (Most Important)
Patient education on implant hygiene (interdental brushes, floss or tape around implants, water flosser) is the foundation. Regular maintenance visits every 3-6 months with probing and radiographic monitoring are essential. Cement-free (screw-retained) restorations are preferred when possible. If cemented, minimal cement and radiopaque cement should be used, with the implant platform placed at or above tissue level. Prosthetic design must allow hygiene access.
Treatment of Peri-Implant Mucositis
Non-surgical mechanical debridement with plastic curettes, titanium curettes, rubber cups, or air-polishing (glycine or erythritol powder) is the primary treatment. Adjunctive antiseptics such as chlorhexidine 0.12% rinse or gel are used short-term (2-4 weeks). Oral hygiene is reinforced, and the prosthesis is modified if needed. Bleeding on probing resolves in 70-80% of treated sites. Early intervention is key, as it prevents progression to peri-implantitis.
Non-Surgical Treatment of Peri-Implantitis
Mechanical debridement with titanium or plastic instruments forms the basis of treatment. Adjunctive therapies include chlorhexidine irrigation, local antibiotic delivery (minocycline microspheres, doxycycline gel), systemic antibiotics (amoxicillin plus metronidazole for 7-10 days, though this is controversial), air-polishing with glycine or erythritol powder, and laser therapy (Er:YAG, photodynamic therapy) with some evidence for adjunctive benefit. Non-surgical treatment alone has limited predictability for advanced peri-implantitis and is only effective for early or mild disease.
Surgical Treatment of Peri-Implantitis
Access Flap with Surface Decontamination (Resective Approach)
A full-thickness flap is elevated to access the defect. Granulation tissue is removed with curettes, and the implant surface is decontaminated. Osseous recontouring eliminates pockets, and the flap is positioned apically. This approach is indicated for Class 2 (horizontal/suprabony) defects and is effective at reducing probing depths and bleeding on probing.
Regenerative Approach
After flap elevation and thorough debridement and decontamination, bone graft (xenograft or allograft) is placed in the intrabony defect and covered with a resorbable membrane. This is indicated for Class 1 (intrabony/circumferential) defects. Results are variable, with some studies showing radiographic bone fill, though long-term stability is debated. The best results occur in well-contained circumferential defects (Class 1d, 1e).
Combined Approach
A combined approach uses resective surgery on the buccal surface (accessible for hygiene) and regenerative surgery on the lingual, palatal, or interproximal surfaces (contained defects).
Implant Surface Decontamination Methods
Mechanical methods include titanium curettes, plastic curettes, air-polishing, and titanium brushes. Chemical methods include chlorhexidine (0.12-0.2%), hydrogen peroxide (3%), citric acid, EDTA, tetracycline paste, and sodium hypochlorite. Laser options include Er:YAG (which does not damage the surface), CO2 (used with caution), and photodynamic therapy (antimicrobial dye plus low-level laser). Electrolytic cleaning (GalvoSurge) is an emerging approach with developing evidence. No single decontamination method has been shown to be clearly superior, and no gold standard exists. A combination of mechanical and chemical decontamination is most commonly recommended.
<image>Intraoperative photograph sequence showing surgical treatment of peri-implantitis: (A) full-thickness flap elevation revealing circumferential bone loss around the implant, (B) granulation tissue removal and implant surface decontamination, (C) bone graft placement in the intrabony defect, and (D) membrane coverage and flap closure</image>
Explantation (Implant Removal)
Explantation is indicated when the implant is mobile (complete loss of osseointegration), when advanced bone loss compromises adjacent teeth or implants, when peri-implantitis is refractory despite repeated treatment, or when the implant is in a non-restorable prosthetic position. Techniques include reverse torque (counterclockwise rotation), trephine bur around the implant, and piezosurgery. Site debridement and consideration of re-grafting for future implant placement follow removal.
Outcomes of Peri-Implantitis Treatment
Non-surgical treatment has limited long-term success for established peri-implantitis but is useful for early disease. Surgical resective treatment effectively reduces probing depths but has a moderate recurrence rate. Surgical regenerative treatment can achieve bone fill in contained defects with variable long-term stability. Recurrence rates range from 10-50% at 3-5 years after surgical treatment, making ongoing maintenance essential. Smoking cessation and optimal oral hygiene significantly improve treatment outcomes.
Clinical Pearls
Prevention is far more effective than treatment, so a rigorous maintenance protocol should be established from the time of implant loading. A baseline radiograph at the time of prosthetic loading is indispensable, as diagnosing progressive bone loss is impossible without a baseline. Excess cement is a preventable and treatable cause of peri-implantitis, and cement removal should always be verified radiographically after cementation. When choosing between resective and regenerative approaches, defect morphology should guide the decision: contained defects regenerate better, while horizontal loss is managed resectively. Probing should be avoided in the first 3 months after placement or loading to allow osseointegration and soft tissue maturation. Peri-implant probing is safe and necessary for monitoring, as the myth that probing damages the peri-implant seal has been debunked. Increasing probing depths and bleeding on probing at an implant demand early action, since peri-implantitis is progressive and will not resolve spontaneously.
References
- Berglundh T, et al. Peri-implant diseases and conditions: Consensus report. J Clin Periodontol. 2018.
- Schwarz F, et al. Peri-implantitis. J Clin Periodontol. 2018.
- Renvert S, et al. Non-surgical treatment of peri-implant mucositis and peri-implantitis. J Clin Periodontol. 2019.
- Ramanauskaite A, et al. Surgical treatment of peri-implantitis: meta-analysis. J Oral Maxillofac Res. 2021.
- Derks J, Tomasi C. Peri-implant health and disease. A systematic review of current epidemiology. J Clin Periodontol. 2015.
- Heitz-Mayfield LJ, Mombelli A. The therapy of peri-implantitis: a systematic review. Int J Oral Maxillofac Implants. 2014.
