PERI-EDU University Education
Peri-implantitis is not defined by a single deep probing measurement or by bleeding alone. It is a biofilm-associated pathological condition in which inflammation of the peri-implant mucosa is accompanied by progressive loss of supporting bone. Understanding how the disease is defined, measured and followed over time is essential for interpreting research and for recognising meaningful change in an individual patient.
Educational focus: peri-implant health and disease, prevalence and incidence, case definitions, disease progression, risk indicators, clinical significance and surveillance.
Why epidemiology matters
Epidemiology describes how frequently disease occurs, how it develops over time and which characteristics are associated with increased or reduced risk. These findings help universities, healthcare systems and clinical teams plan prevention and follow-up. They do not, however, diagnose an individual implant.
A pooled estimate reflects the populations, case definitions and study methods from which it was derived. If one study defines peri-implantitis using a small amount of radiographic bone loss and another requires deeper pockets plus more extensive loss, their estimates cannot be compared as if they measured the same outcome.
Three peri-implant conditions
| Condition | Clinical findings | Bone-level interpretation | Key distinction |
|---|---|---|---|
| Peri-implant health | No clinical signs of inflammation and no bleeding or suppuration on gentle probing. | No additional loss beyond initial remodelling. Health can exist around implants with reduced support. | There is no universal probing-depth range that defines health around every implant. |
| Peri-implant mucositis | Bleeding on gentle probing is the principal sign. Erythema, swelling or suppuration may also occur. | No continuing marginal bone loss after initial healing. | The lesion is confined to the soft tissues and is potentially reversible. |
| Peri-implantitis | Inflammation with bleeding and/or suppuration, often with increasing probing depth or recession. | Progressive supporting bone loss beyond initial remodelling. | Structural support is being lost, increasing treatment complexity. |
Case definitions shape measured frequency
A case definition specifies the combination of clinical and radiographic findings required to count a case. Small changes in the required probing depth, bleeding threshold or amount of bone loss can produce large changes in prevalence. The definition must therefore be read before a percentage is interpreted.
When baseline records are available, the strongest evidence of peri-implantitis is clinical inflammation accompanied by increasing probing depth or recession and progressive bone loss after initial healing. When previous data are unavailable, the 2018 World Workshop proposed a pragmatic definition: bleeding and/or suppuration on gentle probing, a probing depth of at least 6 mm and a bone level at least 3 mm apical to the most coronal intra-osseous part of the implant. These thresholds support classification in the absence of baseline data; they do not mean that every shallower inflamed site is healthy.
Prevalence and incidence answer different questions
Prevalence
Prevalence describes how common disease is in a population at a defined time. It includes both newer and long-standing cases. It is useful for estimating current burden, but it does not show when disease began or how quickly it progressed.
Incidence
Incidence describes how many disease-free people or implants develop disease during a period of follow-up. It requires longitudinal observation and a clearly documented disease-free baseline. Loss to follow-up can bias the result if non-attenders differ systematically from participants who remain in a study.
Patient level and implant level
A patient-level estimate counts a person as affected when at least one implant meets the case definition. An implant-level estimate counts the proportion of implants affected. These denominators are not interchangeable. A person with one affected implant and a person with several affected implants each contribute one patient-level case, while implant-level analysis must also account for the clustering of implants within the same person.
What current pooled evidence suggests
A 2025 AO/AAP systematic review and meta-analysis included 102 studies. It estimated patient-level prevalence at 46% for peri-implant mucositis and 21% for peri-implantitis. Weighted mean patient-level incidence within up to 20 years of function was 53% and 22%, respectively. These figures indicate substantial disease burden, but they should not be interpreted as universal probabilities for every clinic, implant system or patient population.
Frequency estimates vary because of differences in case definitions, sampling, duration of implant function, maintenance exposure, restorative design, patient characteristics and management of missing data. Excluding failed implants or non-attenders may also underestimate the true burden.
Disease may begin early and progress non-linearly
Peri-implantitis can begin relatively early after restoration. Its progression may be non-linear and accelerating rather than slow and constant. A stable observation at one visit therefore does not guarantee lifelong stability, while a single cross-sectional radiograph cannot reveal the previous speed of change.
This makes the post-restorative reference examination particularly valuable. Baseline probing depths, bleeding, suppuration, mucosal margin position and a reproducible radiograph allow future findings to be interpreted as change rather than isolated numbers. The most informative comparison is often the implant with itself over time.
Interpreting risk evidence
| Evidence category | Examples | Clinical meaning |
|---|---|---|
| Established signals | History of periodontitis, inadequate plaque control and absence of regular supportive care. | Increase preventive intensity and ensure periodontal stability and effective maintenance. |
| Supported patient-level association | Diabetes or hyperglycaemia, especially when glycaemic control is poor. | Coordinate medical care and improve modifiable control; do not infer peri-implantitis from diagnosis alone. |
| Contextual local contributors | Implant position, excessive prosthetic contour, poor cleansability, residual cement and restricted access for examination. | Assess whether design or position sustains plaque retention or makes prevention and treatment more difficult. |
| Heterogeneous or uncertain indicators | Smoking and several systemic, behavioural or implant-related variables for which estimates differ across studies. | Use calibrated language and avoid treating association as proof of causation. |
A risk factor should precede the disease and have credible longitudinal support. Cross-sectional studies more often identify risk indicators: characteristics associated with disease at one point in time. The distinction matters because an association may reflect confounding, reverse causation or selection effects.
Why peri-implantitis is clinically significant
The consequences extend beyond implant survival. Progressive bone loss alters the supporting envelope, while recession and defect formation can make daily cleaning and professional decontamination more difficult. Treatment may require surgical access, prosthetic modification or implant removal. In multi-unit restorations, disease affecting one implant can influence the prognosis and design of the entire rehabilitation.
Peri-implant tissues also differ anatomically from periodontal tissues. There is no cementum or periodontal ligament, connective-tissue fibres do not insert into titanium as they do into a natural tooth, and the vascular arrangement close to the crestal barrier is different. Peri-implantitis lesions may be large and rich in plasma cells, lymphocytes, neutrophils and macrophages. These features do not independently cause disease, but they shape the response to persistent biofilm.
From evidence to surveillance
- Establish a reference. Record clinical measurements and obtain a post-restorative radiograph that can be repeated.
- Assess context. Review periodontitis history, plaque control, supportive-care attendance, glycaemic control and prosthetic cleansability.
- Detect inflammation. Use gentle probing at reproducible sites and record bleeding, suppuration and changes in the mucosal margin.
- Verify progression. Compare measurements and radiographs using stable implant landmarks and similar image geometry.
- Act and reassess. Control biofilm and modifiable local factors; escalate the diagnostic and treatment pathway when bone loss or persistent inflammation is present.
Common interpretation errors
- Comparing prevalence estimates without checking whether patients or implants form the denominator.
- Treating a cross-sectional association as proof that an exposure caused disease.
- Diagnosing peri-implantitis from one deep probing depth without evaluating inflammation and bone-level change.
- Assuming that absence of pain or implant mobility indicates health.
- Failing to distinguish initial bone remodelling from progressive loss after the restorative baseline.
- Applying the same recall interval to every patient regardless of risk and current findings.
Key learning points
- Peri-implantitis combines clinical inflammation with progressive supporting bone loss.
- Prevalence, incidence, patient-level estimates and implant-level estimates describe different quantities.
- Case definitions, implant function time and follow-up quality strongly influence measured disease burden.
- Progression may begin early and follow a non-linear, accelerating pattern.
- History of periodontitis, plaque control and supportive care have the most consistent clinical relevance.
- Baseline documentation and risk-based surveillance translate epidemiological evidence into prevention.
Download the full educational material
The extended PDF explains case definitions, prevalence and incidence, disease trajectory, risk interpretation, clinical significance and the practical use of baseline documentation.
Download the full educational material (PDF)
Selected references
- Berglundh T, Armitage G, Araujo MG, et al. Peri-implant diseases and conditions: consensus report of workgroup 4 of the 2017 World Workshop. Journal of Clinical Periodontology. 2018;45(Suppl 20):S286-S291. doi:10.1111/jcpe.12957.
- Renvert S, Persson GR, Pirih FQ, Camargo PM. Peri-implant health, peri-implant mucositis, and peri-implantitis: case definitions and diagnostic considerations. Journal of Clinical Periodontology. 2018;45(Suppl 20):S278-S285. doi:10.1111/jcpe.12956.
- Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. Journal of Clinical Periodontology. 2018;45(Suppl 20):S246-S266. doi:10.1111/jcpe.12954.
- Herrera D, Berglundh T, Schwarz F, et al. Prevention and treatment of peri-implant diseases: the EFP S3 level clinical practice guideline. Journal of Clinical Periodontology. 2023;50(Suppl 26):4-76. doi:10.1111/jcpe.13823.
- Galarraga-Vinueza ME, et al. Prevalence, incidence, systemic, behavioral, and patient-related risk and protective factors for peri-implant diseases: an AO/AAP systematic review and meta-analysis. Journal of Periodontology. 2025. doi:10.1002/JPER.24-0154.
- Wang HL, et al. AO/AAP consensus on prevention and management of peri-implant diseases and conditions: summary report. Journal of Periodontology. 2025. doi:10.1002/JPER.25-0270.
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This educational material does not replace individual clinical assessment or specialist consultation.
This work was co-funded by the European Union under grant agreement No. 2024-1-PL01-KA220-HED-000251208. Views and opinions expressed are those of the author(s) only and do not necessarily reflect those of the European Union or the Foundation for the Development of the Education System (FRSE). Neither the European Union nor FRSE can be held responsible for them.