Peri-implantitis is a progressive disease that threatens the long-term success of dental implants. The condition is defined by an inflammatory response in the tissues surrounding a functional dental implant, characterized by both soft tissue inflammation and the progressive loss of supporting bone. This advanced stage is distinct from peri-implant mucositis, which is an earlier, reversible stage involving inflammation of the soft tissue only, without measurable bone loss. Peri-implantitis results from a combination of factors, ranging from microbial infection to mechanical stresses.
The Primary Role of Bacterial Biofilm
The most common cause of peri-implantitis is the accumulation of a bacterial biofilm on the implant surface, a process that mirrors the development of periodontitis around natural teeth. Plaque, an organized community of microorganisms, forms on the implant and the abutment, eventually colonizing the sub-gingival space. The host’s immune system reacts to this bacterial challenge, initiating an inflammatory response in the surrounding soft tissues.
If this inflammation is not controlled, the condition progresses from reversible peri-implant mucositis to peri-implantitis. The bacteria involved are often the same aggressive, anaerobic species associated with severe gum disease, such as Porphyromonas gingivalis and Prevotella intermedia. These microorganisms produce toxins and enzymes that provoke the immune system to destroy the bone supporting the implant.
Poor daily plaque control is the main driver behind this infectious origin, allowing the biofilm to mature and shift toward a more pathogenic composition. Once the bacteria and their byproducts reach the bone level, the inflammatory cycle accelerates, leading to the irreversible bone loss that defines peri-implantitis.
Systemic Health and Individual Risk Factors
A patient’s overall health and lifestyle modulate their body’s ability to resist the bacterial challenge, contributing to the development and severity of peri-implantitis. Smoking is a risk factor, as the chemicals in tobacco reduce blood flow in the gums and impair the local immune response. This compromised circulation and suppressed healing capacity make the tissues around the implant more vulnerable to infection and subsequent bone breakdown.
Uncontrolled diabetes, specifically marked by high blood sugar levels (hyperglycemia), increases susceptibility to the disease. Elevated glucose levels compromise the function of immune cells and promote a hyper-inflammatory state, affecting bone metabolism and accelerating tissue destruction. Individuals with poorly controlled diabetes have a higher risk of developing peri-implantitis.
A prior history of periodontitis is a major predictor of peri-implantitis. Patients who lost teeth due to gum disease already harbor the specific pathogenic bacteria that cause the condition, making their implants susceptible to colonization. The presence of these existing pathogens increases the likelihood of an inflammatory response and subsequent bone loss around the dental implant.
Mechanical and Procedural Contributions
Factors related to the implant’s placement, design, and restoration can create environments that facilitate bacterial accumulation or place undue stress on the supporting bone. One common iatrogenic factor is the retention of excess cement used to secure a crown to the implant abutment. Residual cement pushed below the gum line acts as a foreign body, creating a rough, inaccessible niche where bacteria can thrive and trigger a persistent inflammatory reaction.
Occlusal overload, caused by excessive or misdirected biting forces on the implant, contributes to bone loss. Because implants lack the natural shock-absorbing ligament found around a natural tooth root, they are less tolerant of non-axial forces, such as those caused by nighttime teeth grinding or clenching. This mechanical stress can accelerate bone loss when combined with an existing bacterial infection, stressing the bone-to-implant connection.
Suboptimal surgical placement or prosthetic design can compromise the patient’s ability to clean the area, leading to bacterial retention. If an implant is placed too deep, too close to an adjacent tooth, or if the final crown shape is bulky, proper flossing and brushing become impossible. This difficulty in plaque removal allows the biofilm to mature undisturbed, establishing the conditions for peri-implant mucositis to progress into peri-implantitis.