For many years, peri-implantitis has been described primarily as a consequence of bacterial biofilm and the local inflammatory response around the implant. This model remains fundamental to understanding the disease, but it is becoming increasingly clear that it does not fully explain the complexity of the problem. Bone loss around an implant may result from the interaction of multiple factors: microbial, immunological, systemic, biomechanical, and material-related. This broader perspective is at the core of the PERI-EDU project, which aims to better understand the mechanisms of peri-implantitis and translate this knowledge into education, diagnostics, and clinical practice.
In everyday implant dentistry, peri-implantitis remains one of the most challenging complications of implant treatment. For clinicians, it means not only inflammation around the implant, but also the risk of progressive bone loss, impaired treatment prognosis, and ultimately implant failure. For patients, who often perceive an implant as a durable and predictable solution, the diagnosis of peri-implantitis may come as a difficult and unexpected moment — especially when the disease develops after an initially successful course of treatment.
The simplest explanation of this process refers to biofilm. Bacteria colonizing the implant surface and peri-implant tissues initiate a local inflammatory response. In peri-implant mucositis, inflammation remains limited to the soft tissues, while in peri-implantitis it is accompanied by the loss of bone supporting the implant. This model is clinically important because it emphasizes the role of oral hygiene, plaque control, and regular supportive care.
However, clinical practice shows that not all patients respond in the same way. In some individuals, inflammation around an implant develops slowly, remains controlled, and responds well to treatment. In others, the disease progresses more rapidly, leads to extensive tissue destruction, and proves difficult to stop. A similar level of hygiene, comparable prosthetic conditions, or even a similar local clinical picture does not always translate into a similar prognosis. This clinical variability raises a broader question: is biofilm the only factor we should be considering?
Increasing attention is now being paid to the role of the host response. Peri-implantitis is not merely the presence of bacteria around an implant, but the result of an interaction between biofilm and the patient’s immune system. It is the immune system that determines how strong the inflammatory response will be, how long it will persist, and whether it will activate mechanisms leading to bone destruction. Pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, play an important role in this process, as they may enhance osteoclast activity and promote bone resorption.
In this sense, peri-implantitis is increasingly viewed not only as a bacterial disease, but also as a disruption of the balance between microbial challenge and the patient’s biological response. If the inflammatory reaction is excessive, chronic, or insufficiently resolved, even a local stimulus may lead to disproportionate tissue destruction. This is particularly relevant around implants, where the anatomical conditions, tissue structure, and regenerative capacity differ from those observed around natural teeth.
Another important element of this broader model is the patient’s systemic health and metabolic status. Diabetes, obesity, metabolic syndrome, cardiovascular disease, osteoporosis, and autoimmune disorders do not necessarily act as single, direct causes of peri-implantitis. They may, however, create a biological environment in which the inflammatory response is more pronounced, healing is less effective, and bone metabolism is disturbed. From this perspective, an implant patient is not merely a “local” case assessed only through the implant and the surrounding bone, but a person with a specific systemic profile.
This approach has important practical implications. Risk assessment in peri-implantitis should not be limited to checking hygiene and prosthetic design. It also becomes important to consider chronic diseases, glycemic control, periodontal history, smoking, medication use, body weight, metabolic parameters, and the patient’s overall inflammatory susceptibility. This does not mean that every patient with a systemic disease will develop implant-related complications. It does mean, however, that in some patients this broader context may significantly influence the course of the disease and require more individualized monitoring.
Another area of interest is the possibility of making the inflammatory response more objectively measurable. If peri-implantitis may also have a systemic dimension, it is reasonable to ask whether routine or specialized laboratory tests could support patient assessment. Classical inflammatory markers, such as CRP, leukocyte count, or pro-inflammatory cytokines, provide information about inflammatory activity, but they have limited specificity. They may increase in many different situations: infection, trauma, chronic disease, inflammatory stress, or other processes not directly related to the implant.
For this reason, the PERI-EDU project also analyzes aggregated inflammatory indices derived from blood count parameters, such as NLR, PLR, MLR, SII, SIRI, and AISI/PIV. Their potential value lies in the fact that they do not describe a single element of inflammation, but attempt to capture relationships between different components of the immune response. In simplified terms, they represent an attempt to assess the balance between inflammatory activation and immune regulation.
However, these indices are not ready-made, definitive diagnostic tests for peri-implantitis. Their interpretation requires caution, clinical context, and further validation. This is why it is so important to combine laboratory data with clinical, radiological, and medical assessment. A single number cannot replace probing, assessment of bleeding on probing, evaluation of bone loss, examination of soft tissues, or analysis of prosthetic factors. In the future, however, it may become an additional piece of the puzzle, helping clinicians better understand disease risk and progression.
The broader model of peri-implantitis also includes local and material-related factors. Implant surface characteristics, microgeometry, biofilm retention, biomechanical overload, cement remnants, hygiene limitations, and prosthetic misfit may all influence the peri-implant environment. The possible relevance of titanium particles, metal ions, surface microdamage, and corrosion processes as factors that may modulate the local inflammatory response is also increasingly discussed. This is not about making a simple claim that implant material is the cause of the disease, but rather about better understanding the environment in which an implant functions for many years.
In this context, peri-implantitis can be described as a disease at the intersection of microbiology, immunology, biomechanics, material science, and general medicine. This approach is more demanding than the classical plaque-centered model, but it better reflects clinical reality. It also helps explain why standard treatment may be effective in some patients, while in others the disease recurs or progresses despite therapy.
This is where the PERI-EDU project becomes particularly relevant. Its aim is not to replace existing knowledge about peri-implantitis, but to organize and expand it. The project combines clinical, radiological, biological, and material-based assessment in order to better understand the mechanisms leading to peri-implant tissue destruction. At the same time, it has a strong educational dimension: research findings are intended to be translated into teaching materials that will help students, academic teachers, and dental professionals understand peri-implantitis as a multifactorial disease, rather than only as a local bacterial complication.
For clinical practice, this direction of thinking may be especially important. Implant dentistry is becoming increasingly predictable from a technological perspective, but its long-term success still depends on the patient’s biology. A better understanding of the inflammatory response, the role of systemic conditions, and potential risk markers may support earlier identification of patients who require closer monitoring. It may also help clinicians plan treatment more responsibly, communicate risk more clearly to patients, and make more informed therapeutic decisions.
Peri-implantitis, therefore, does not end with biofilm. Biofilm remains the starting point, but the further course of the disease depends on many more variables. A contemporary approach to peri-implantitis requires us to look at the implant, the surrounding tissues, the patient, and the immune response as one interconnected system. This is the system that PERI-EDU seeks to describe more precisely — with the aim of helping scientific knowledge translate more effectively into education, diagnostics, and everyday implant dentistry.