Feature Article

Peri-implantitis is a treatment-related complication with a biofilm-mediated pathogenesis. Several studies have demonstrated that the progression from peri-implant mucositis to peri-implantitis can be effectively managed by supportive implant therapy. However, the impact of implant prostheses on the evaluation of peri-implant tissues, the control of biofilm by oral hygiene and professional prophylaxis as well as the impact of cement or other prosthetic materials on peri-implant inflammation receive little attention. This report will consider prosthesis factors, abutment factors, and cement factors in the evaluation, management and prevention of peri-implantitis. The existing literature clearly indicates that mechanical disruption of dysbiotic biofilm is central to the prevention and management of peri-implantitis. Thus, prosthetic factors that enable or enhance biofilm formation or preclude its mechanical disruption may contribute to the progression of peri-implant mucositis to peri-implantitis. Unfortunately, many of the prosthetic factors that negatively impact peri-implant tissue health are the result of improper implant placement decisions. Both the surgical planning and prosthetic execution of therapy must be addressed in efforts to reduce the risk of peri-implantitis.


As the practice of dental implant therapy has evolved, the importance of implant and prosthesis longevity has come into prominent focus. Two forces have directed our attention to the longevity of dental implant therapy. One is the acknowledgement that tissues surrounding dental implants are not resistant to inflammatory disease and that peri-implantitis is common in the population of treated patients. The second is the growing acknowledgement that implant prostheses and components are subject to wear, complications and failure. The intent of this report is to adjust our clinical perspectives of care from planning and executing therapies based on short-term objectives to considering our planning and execution of dental implant therapy in terms of increasing therapeutic longevity. Central to this goal is to appreciate the connection between prosthesis design, execution and maintenance and the potential associated, increased risks for peri-implantitis.

Peri-implantitis is a pathologic condition affecting the tissues surrounding dental implants. It is an inflammatory condition that is preceded by mucositis and is dependent on biofilm accumulation on prostheses, abutments or implant surfaces adjacent to the affected tissue (Schwarz et al. 2018). The pathogenesis is described as relatively aggressive when compared to periodontitis and it affects the implant circumferentially. Peri-implantitis is common. The reported prevalence of peri-implantitis at longer evaluation times may approach 50% (Roos-Jansåker et al. 2006). Systematic review and meta analyses indicate peri-implantitis affects approximately 10% of implants and 20% of subjects in reported studies (Lee et al. 2017; Derks et al. 2015). The reported prevalence is influenced by the definition used and the time period of implant use investigated.

Other hypotheses concerning the etiology of peri-implantitis have been proposed. Regarding the role of hyper-occlusion, earlier studies in primates failed to demonstrate that hyper-occlusion led to implant loss (Naert et al. 2012). Several animal studies have examined the impact of hyper-occlusion on peri-implant tissue destruction in the presence of induced peri-implant mucosal inflammation (Chambrone 2010). While these studies demonstrated increased bone loss in the combined presence of peri-implant mucosal inflammation and hyper-occlusion, hyper-occlusion alone failed to cause similar peri-implant tissue loss akin to peri-implantitis. More recent systematic reviews have implicated bruxism as an important risk factor for implant loss, but not directly related to peri-implantitis. It may be concluded that excessive force alone does not cause peri-implantitis. Others have promoted altered immunity and a foreign body response as the basis for peri-implant bone loss as observed in peri-implantitis (Trindade et al. 2016). While there is evidence that micron-scale particulate materials can induce soft tissue inflammation, there is no compelling clinical or experimental data to demonstrate that the lesion defined as biofilm-mediated peri-implantitis is the result of a foreign body reaction. However, particulate debris associated with a biofilm-mediated inflammation may contribute to tissue destruction. To this end, it is critical to reduce and eliminate procedure-generated particulate materials from the peri-implant tissues exposed during surgical and prosthetic manipulations.

Management of peri-implant health or treatment of peri-implantitis by supportive implant therapy or peri-implant maintenance therapy has demonstrable effectiveness (Gay et al. 2016) and again infers the biofilm-based pathology of this disease. The management of peri-implant mucositis has been promoted as a front-line measure for control of further disease. However, beyond biofilm as a primary etiologic agent, local and systemic patient factors, as well as prosthetic factors may influence the onset and prevention of peri-implant mucositis and ensuing peri-implantitis (Heitz-Mayfield 2008). Studies that have assessed risk factors influencing the incidence of peri-implantitis have often considered systemic diseases (e.g. diabetes), smoking, periodontitis, and local factors (e.g. presence of keratinized tissues), the impact of prostheses and implant components on the onset, progression, treatment and overall prevalence of peri-implantitis has received less attention. This is striking because the lack of efficacy of adjunctive measures (e.g. antiseptics, local antibiotics) in reducing peri-implant inflammation indicates that the mechanical disruption of the dysbiotic biofilm is a requirement for resolution of peri-implant inflammation. How prostheses and implant components may impede investigation of peri-implant tissues, evaluation of the presence of biofilm and the mechanical disruption of biofilm should be considered in the planning, execution and management of implants and the related prostheses.

Prostheses can impede oral hygiene at implant sites. This is borne out in several studies and was exemplified by the evaluation of 23 subjects with peri-implantitis in which 48% of implants presenting with peri-implantitis allowed no access for oral hygiene compared with 4% of implants with access for oral hygiene (Serino et al. 2009). The impact of the implant prostheses on peri-implant mucosal health is significant. In a most recent summary statement regarding local risk factors influencing peri-implantitis, the impact of prostheses was considered in some depth (Giovannoli et al. 2019). Included in the discussion of potential prosthetic factors affecting peri-implantitis were 1) the nature of the prosthetic superstructure, 2) residual cement, 3) prosthetic margin location, and 4) the morphology or shape of the prosthesis. In a recent consensus report, several steps were proposed for the management of peri-implantitis and included: 1) thorough assessment and diagnosis, 2) control of modifiable local and systemic risk factors for peri‐implantitis, 3) nonsurgical debridement, 4) early reassessment of peri‐implant health, 5) surgery including implant decontamination and tissue debridement followed by optional regeneration, if resolution has not been achieved, and 6) prescription of supportive care tailored to the patient risk profile, most likely 3–6 monthly (Heitz-Mayfield et al. 2018). Item 2 of this list infers but does not explicitly state that modification of the prosthesis may be required in the reduction of risk for peri-implantitis or to enable oral hygiene and supportive care. When considering a removable solution for implant prostheses, a 10-year follow-up study reported an incidence of peri-implantitis of 16.9% and 29.7% at 5 and 10 years, respectively (Meijer et al. 2014). The nature of the prostheses may profoundly influence the patient’s and professional’s ability to control the formation of a dysbiotic biofilm and its therapeutic removal. In the following sections, prosthesis factors, abutment factors, and residual cement will be discussed in the context of contributing to peri-implantitis and its management.