Peri-implantitis: Is it a crisis?|
In the US over 500,000 implants are placed each year, while in the UK that figure was around 140,000 for 2010
Peri-implantitis: Is it a crisis?
Post a comment by Dr Michael R. Norton, UK
In the US over 500,000 implants are placed each year, while in the UK that figure was around 140,000 for 2010. The prevalence of peri-implantitis has been reported to be up to 29%, most notably in patients whose implants are placed within a partial dentition. This yields a potentially vast number of implants, possibly as many as 185,000 in the US and UK alone, that might succumb to some form of peri-implant disease on an annual basis.
The bacteria found in peri-implant lesions are similar to those found in deeper periodontal pockets,[2, 3] and cross-infection by periodontopathogens as a primary aetiology has been implicated as a possible pathway. However, the wide variety of implant designs, surfaces, etc. makes the treatment of peri-implantitis much less predictable and subject to much greater variability than with periodontal disease, where natural teeth present a known anatomy and well-defined surface structure.
In 2008, a systematic review of the literature regarding peri-implantitis using PubMed and the Cochrane Library found little consensus on the treatment of this troublesome condition. One study reported on the efficacy of submucosal debridement using ultrasonics or carbon-fibre curettes, while two others compared the effect of an Er:YAG laser against that of mechanical debridement and 2% chlorhexidine as a combined therapy.[6, 7] The first found similar results between laser and combined therapies, while the second concluded that the laser effect was limited to a six-month period. A further study compared combinations of oral hygiene instruction, mechanical debridement and topical minocycline with a similar regime that substituted 1% chlorhexidine as the antimicrobial. The former seemed to confer some benefit, while the latter showed limited or no clinical improvements. Finally, a study comparing two bone regeneration procedures reported clinically significant improvements mediated by both.
Nonetheless, a multitude of studies have also been published reporting on the efficacy of tetracycline, carbon dioxide laser, and photocatalytic decontamination, among others, in the treatment of peri-implantitis. Such a plethora of therapies makes it difficult for the clinician to choose a regimen that is within the reach of the average clinician and has some documented reliability.
There have been a number of risk factors cited for peri-implantitis. Recently, in a study published in the Journal of Clinical Periodontology, a clear association was demonstrated through multilevel statistical analysis between the risk of peri-implantitis and location, specifically the maxillae, while overt peri-implantitis was shown to be highly correlated to patients with a predisposing history of periodontitis, and being male. Surprisingly, in this particular study, no correlation with smoking was demonstrated, yet this has been a consistently cited risk factor in many other studies. Indeed, in a study published in the Swedish Dental Journal in 2010, the percentage of implants with peri-implantitis was significantly increased for smokers compared with non-smokers (p = 0.04).
Other factors that have been implicated include excess cement, poor oral hygiene, and prosthesis design. These are, of course, interrelated with some prostheses making effective oral hygiene untenable, while others present deep margins that make removal of excess cement almost impossible.
Peri-implantitis rarely presents unannounced, unless, of course, the patient is not placed on a regular recall programme or fails to attend for regular review. Early signs are often apparent in the form of peri-implant mucositis. This condition is characterised by mucosal oedema, rubor and bleeding on probing. By definition, it is not associated with purulence or bone loss. However, this condition is often asymptomatic to the patient and as such is typically only diagnosed at routine recall. Hence, there is a need to recognise that the patient should remain on annual reviews for at least the first five years after implant treatment has been completed, and thereafter once every two years.
On presentation with mucositis, a combination of mechanical debridement, submucosal decontamination and antimicrobial therapy is indicated. The treatment should be repeated three times within a two-week period; hence, it is called triple therapy. The protocol is as follows:
- Mechanical scaling of the implant surface with titanium or carbon-fibre curettes
- Submucosal irrigation with 5–10 ml chlorhexidine (0.2%) per site, at the deepest level of the pocket on all sides of the implant
- Application of a 2% minocycline gel (Dentomycin, Henry Schein) at the deepest level of the pocket on all sides of the implant.
However, once peri-implant mucositis has taken hold, it is unfortunate that it is often exacerbated by the design of implants today. The presence of a rough surface, taken to the top of an implant, and the application of micro-threads or grooves have been proposed as potential confounding factors for the advance of the lesion owing to biofilm formation and bacterial contamination of the surface, which leads to bone loss and further surface exposure. With advancing bone loss, there is often colonisation of the deeper pockets with well-known periodontopathogens and infection ensues. This then is peri-implantitis.
Peri-implantitis is characterised by the presence of vertical or crater-like bone defects and spontaneous purulence and bleeding on palpation. It is typically associated with deep peri-implant pocketing (> 5 mm). This condition is undoubtedly of increasing concern owing to some principal factors, such as the almost exclusive use of roughened implant surfaces, the treatment of partially dentate patients with a history of periodontal disease, the placement of implants with inadequate bone volume, resulting in facial dehiscences, as well as the use of cement-retained prostheses.Implants with a micro-roughened surface texture have presented excellent long-term data, and until recently there has been very little published in the literature demonstrating a susceptibility of these surfaces to this condition. However, recent work by Albouy et al.[15, 16] has received widespread attention with concern regarding the evidence that suggests some modern micro-textured surfaces may be completely resistant to decontamination.
Ultimately, if left unchecked and untreated, it may become impossible to arrest the condition, leading to wholesale failure of the case. Such failures impose a tremendous strain and burden on the clinician (let alone the patient), destroy the confidence of a patient who has endured significant expense and trauma, and occasionally results in a breakdown of communication between both parties that all too often sadly results in a legal claim of negligence. Such claims can be difficult to defend in cases in which no warnings or supportive periodontal or peri-implant therapy has been undertaken.
Treatment typically requires surgical access to excise any fibrous capsule and for direct access to the implant for surface decontamination. The author’s preference until now has been to use chlorhexidine and tetracycline solution for this purpose, while others have reported the use of citric acid and hydrogen peroxide among others. The use of lasers has also been extensively reported.[6, 7, 18–20] However, in a recent systematic review, a meta-analysis could only be done for the Er:YAG laser, as the literature on all other laser types was weak or heterogenous.
The author has recently completed the acquisition and treatment of 20 patients in an efficacy study using an Er:YAG water laser (AdvErl Evo, Morita), and it is hoped that publication of the results will be forthcoming. Indeed, promising data has already been published to date using this same machine.[22, 23]
Nonetheless, this methodology remains outside the reach of most general practitioners and has yet to be proven predictably effective. As such, most attention therefore remains focused on physical debridement via surgical intervention and topical antimicrobial therapies. Open-flap debridement, defect decontamination and repair, as well as pocket elimination, have all become the mainstay of those treating this condition.
So is there a crisis? The problem is that there is no clear consensus on the prevalence of the disease, since this will vary according to the cut-off values for the clinical parameters measured and to date there appears to have been little consensus on these cut-off values. As such, estimates of incidence of the disease appear to vary from 28% to 56% of subjects and 12% to 43% of implant sites.
Furthermore, there is an ongoing controversy about the initiating process of peri-implant disease, since it is potentially considered a primary infection of periodontopathic origin by some, while others hold that it is a secondary opportunistic infection subsequent to bone loss caused by other aetiological factors, such as a provoked foreign body reaction or iatrogenic dehiscence of the bone, exogenous irritants such as dental cement, bone loss through occlusal overload, etc. If the latter is true, then controlling the disease is theoretically made more simple by controlling the conditions for the implant, such as ensuring adequate buccal bone thickness, avoiding or controlling more carefully the use of dental cement, and paying closer attention to the occlusion.
In an effort to gauge the rate of mucositis and peri-implantitis requiring surgical intervention, the author audited his patient pool in 2014. Out of a total of 191 patient reviews, constituting 795 implants, only 15 patients (7.9%) required triple therapy at 20 implants (2.5%) for mucositis, while 10 patients (5.2%) required surgical decontamination at 10 implants (1.3%). As can be seen, this is well below the figures proposed by Zitzmann and Berglundh. This may, of course, reflect a more liberal approach to cut-off values for parameters such as pocket depth and bleeding on probing as proposed by Klinge.
Nonetheless, after over 20 years of running a practice dedicated to implant dentistry, the author’s own audited failure rates indicate that less than 1% of implants present as late failures due to peri-implantitis or fixture fracture as a result of bone loss. This would corroborate the findings by Jemt et al., in which a cohort of patients already diagnosed with peri-implant bone loss showed a slow rate of additional progressive bone loss over a nine-year follow-up with an implant failure rate of 3%.
It is the author’s view that, in all likelihood, peri-implantitis is only a crisis if we allow poor implant dentistry, where there is a lack of control of the initiating factors as described above, to persist and that it is more rather than less likely that it is the result of a secondary opportunistic infection rather than a direct susceptibility to primary infection of periodontopathic origin. However, there will clearly be some patients with a high genetic susceptibility with other predisposing factors, such as the presence of untreated periodontal disease, smoking and diabetes, who may well succumb as a result of primary infection.
Furthermore, there remains a clear need to better define the different types of peri-implant disease and to establish a consensus as to the cut-off values for the different parameters used to evaluate the disease, so that future figures for incidence and prevalence are comparable.