Replacement of missing teeth using dental implants has revolutionized dentistry. High survival rates of both implants (95.4 per cent) and the reconstructions they support (95 per cent) have been documented following five years in function.1 In clinical practice it is not only the survival, but more importantly, the success of the implant and the reconstruction which is critical. Complications, of either a technical or biologic nature, are common and have been reported in 38.7 per cent of implant supported reconstructions after five years in function.2
The objective of this review is to outline important clinical considerations for diagnosis and management of biologic complications defined as peri-implant diseases. Left undiagnosed and untreated, peri-implant disease may lead to implant loss.
Healthy soft tissue implant interface
The peri-implant mucosal seal is important for the maintenance of health and aesthetics. Peri-implant mucosa is comprised of a connective tissue component and an epithelial component. The composition and dimensions of the peri-implant soft tissue complex have been studied in animal models. A recent experimental study3 showed that the peri-implant mucosal unit takes at least six weeks to form in a dog model. Therefore, in a clinical situation, it should be recognized that the formation of a healthy peri-implant mucosal seal takes time. While peri-implant mucosa differs from gingiva in its vascularity, collagen content and connective tissue fibre arrangement, the inflammatory response to plaque is similar.4
Periodontal probing — is it safe?
Periodontal probing using light pressure (0.25 Ncm) does not damage the mucosal seal,5 and is considered an important and reliable tool for diagnosing and monitoring the presence of peri-implant health or disease.6,7 Clinical signs of peri-implant health include absence of bleeding and suppuration on probing, and stable peri-implant probing depths relative to a fixed reference point (e.g., the crown margin). The clinician should record baseline probing depth measurements relative to a fixed reference point once the implant restoration is completed. The clinician should then monitor the peri-implant soft tissues using a periodontal probe at four or more sites per implant on a regular basis.8 Radiographs are also required to establish baseline marginal bone levels. However, the periodontal probe is an invaluable tool for diagnosis of peri-implant health and disease.
Peri-implant diseases are oral diseases caused by a biofilm infection in a susceptible individual. At the First European Workshop on Periodontology in 1994, the following definitions were presented:9 (1) peri-implant mucositis: defined as a reversible inflammation of the soft tissues surrounding an implant in function with no loss of supporting bone (Fig 1). Clinical signs are bleeding and/or suppuration on probing and increased probing depths (4–5 mm); (2) peri-implantitis: defined as an inflammatory process affecting the tissues around an osseointegrated implant in function resulting in loss of supporting bone (Fig 2). Clinical signs are deep probing depths (> 5 mm), bleeding and/or suppuration on probing. Loss of supporting bone resulting from peri-implantitis usually forms a circumferential crater defect (Fig 4).
Reports of biologic complications in the literature do not consistently use these definitions. Other terms reported include “soft tissue complications”, “excessive hyperplasia” and “fistula”.
Incidence of peri-implant mucositis and peri-implantitis
The occurrence of peri-implantitis has been inconsistently reported and the assessment methods and definitions for peri-implantitis vary considerably between publications. Therefore, the incidence and prevalence of peri-implantitis are difficult to determine. However, a recent systematic review, comparing the survival and complication rates of tooth-supported fixed dental prostheses (FDPs) and implant-supported FDPs and single crowns, reported a biologic complication rate of 8.6 per cent at five years for implant supported reconstructions.2
The frequency of implant loss10 and presence of peri-implant lesions11 were evaluated in a cross-sectional study of a group of patients who had received Brånemark implants 9–14 years previously. Peri-implant disease was a common clinical entity after 9–14 years. Forty-eight per cent of the implants had peri-implant mucositis. The authors reported that peri-implantitis (defined as bone loss ≥ 1.8 mm compared with 1-year data, combined with bleeding on probing and/or pus), was diagnosed among 16 per cent of the patients and 6.6 per cent of the implants. It is of note that the patients in this study were not enrolled in a structured maintenance care programme.
In another retrospective study from Sweden, radiographic bone levels were evaluated at Brånemark implants which had been placed by experienced clinicians and followed for up to 13 years. Progressive bone loss was found in 28 per cent of patients and 14 per cent of implants.12
These findings highlight not only the common occurrence of peri-implant disease, but the importance of evaluating the data on a patient level as well as an implant level. When evaluation is only performed on an implant level the incidence of disease is diluted.
Aetiology of peri-implant disease
Clinical studies have documented the similarities between the microflora associated with peri-implant diseases and periodontitis. High levels and proportions of periodontal pathogens, mainly gram negative anaerobic bacteria including Porphyromonas gingivalis Tanerella forsythia and Treponema denticola, have been identified.13,14 Interestingly, some studies have identified organisms associated with peri-implantitis which are not commonly found in the oral cavity, including S. aureus and enteric rods.15,16 The identification of organisms present may have implications for treatment strategies.
Recent evidence regarding the dynamics of colonization around implants has highlighted the importance of infection control prior to implant placement in the partially dentate patient. The microflora in the peri-implant sulcus is established as early as 30 minutes to two weeks following implant placement and is nearly identical to that found at the adjacent teeth.17,18 Thus in partially dentate patients, deep pockets harbouring high numbers and large proportions of periodontal pathogens act as a reservoir for recolonization and establishment of a microflora which is not conducive to health.
There are a number of factors which may contribute to the development of and the progression of peri-implantitis. These include patient factors and implant related factors.
A number of longitudinal and cross-sectional studies indicate that periodontally susceptible individuals (those who have been treated for periodontitis) have an increased risk for peri-implantitis.19–26
Recent systematic reviews also provide evidence for the increased susceptibility to peri-implantitis in patients treated for periodontitis27 or patients who had tooth loss due to periodontitis.28 Smokers24 and patients with the IL-1 positive genotype29 have also been reported to have a greater risk for marginal bone loss and peri-implantitis.
It is therefore important to inform susceptible patients that they are at risk for peri-implantitis and offer them a structured maintenance care programme. However, there is limited evidence evaluating the long-term effect of maintenance on implant patients. A recent systematic review found that of the nine studies included, only two documented the use of an individualized maintenance protocol providing recall at 3–6 monthly intervals.30
Implant related factors
Implant design and surface characteristics may also be contributing factors for the progression of peri-implantitis. Studies have indicated that implants with very rough surfaces, such as the titanium plasma sprayed surface (TPS) and hydroxyapatite surface (HA), have a high incidence of peri-implantitis.31–33
Deep implant placement may result in excess cement remaining in the submucosal region following cementation of a reconstruction. Failure to remove excess cement may contribute to peri-implant infection.
It is important to recognize that some technical complications, e.g., a fractured abutment screw, may present with a soft tissue complication such as a draining sinus (Fig 3). The correct diagnosis is therefore important for appropriate management.
Diagnosis of peri-implant health and disease
Following successful implant therapy patients should be offered an individually tailored maintenance care programme. Baseline probing depths relative to a reference point such as the crown margin should be recorded. Baseline radiographs to establish marginal bone levels should be taken. Following this, regular systematic monitoring of the peri-implant tissues is required for assessment of the presence of peri-implant tissue health, or disease and its severity. The following diagnostic parameters have been recommended:1 (1) presence of plaque and calculus; (2) probing depth measurements using a light probing force (0.25 Ncm); (3) presence or absence of bleeding on probing/suppuration using a light probing force (0.25 Ncm); (4) radiographic assessment if indicated.
Treatment of peri-implant diseases
The main goal of treatment of peri-implant disease is to control the infection and to prevent disease progression.
Treatment of peri-implant mucositis requires removal of plaque and calculus deposits using appropriate instruments (carbon fibre curettes, titanium coated curettes). In addition, oral hygiene instruction should be provided, with or without the incorporation of antiseptics (such as chlorhexidine). A number of studies have documented the successful treatment of peri-implant mucositis using this approach.34
A variety of antimicrobial treatment regimens in combination with non-surgical or surgical debridement, with and without regenerative therapy have been proposed for peri-implantitis treatment. The cumulative interceptive supportive therapy (CIST) protocol has been documented as a guide to treatment of peri-implantitis. This protocol involves a series of treatment modalities which are used in a cumulative manner according to disease severity.1
Use of systemic or local antibiotics in conjunction with non-surgical mechanical debridement has been shown to be effective in resolution of the peri-implant infection in the majority of patients and implants treated in moderate peri-implantitis.34 Nevertheless, in these studies some implants in some patients had persistent peri-implantitis and required surgical intervention.
One of the difficulties in treating peri-implantitis is obtaining access for adequate implant surface decontamination. Recent prospective cohort studies have documented a surgical approach in combination with systemic antibiotics for peri-implantitis treatment35,36 and reported a five-year success rate of 58 per cent.
Decontamination procedures including the use of sterile saline, chlorhexidine, citric acid, hydrogen peroxide and CO2 laser have been evaluated in animal studies. No significant differences in the amount of bone regeneration, or the percentage of reosseointegration differences were observed when comparing different decontamination agents.37
Regenerative surgery has also been evaluated in experimental animal studies. Barrier membranes with or without the use of autogenous bone grafts or bone substitutes were used to treat implants with experimentally induced peri-implantitis. Varying degrees of bone regeneration and reosseointegration were observed at these implants which had a moderately rough sandblasted acid etched surface.37 These encouraging results following regenerative treatment have not been documented for implants with other surfaces. Furthermore, whilst regenerative treatment is possible, there is limited evidence for the success of this treatment approach in human studies.38,39
One important clinical consideration is that mucosal recession following surgical treatment of peri-implantitis will occur. Whilst the implant may remain in function, the aesthetic outcome may be compromised.
Mobility of an implant indicates complete loss of osseointegration and implant failure. Progressive peri-implantitis may lead to loss of the implant.