The provision of dental implant-supported restorations has increased exponentially during the last twenty years and in particular the last ten years.
 During this time we have also seen the increasing prevalence of problems associated with the use of implants, one of the most common being a condition called peri-implantitis.
Before I discuss this in detail, it is important to appreciate that we are still learning about this condition and the presenting factors, together with the diagnosis and recommended treatment regimes.

Furthermore, there can be some confusion over the relevant definitions and terminology that are applied when discussing the condition among both colleagues and patients. The Academy of Osseointegration in the United States is planning a consensus conference next year – which I shall attend and where hopefully some clarification can be given – and which I hope will result in some kind of algorithm that will give guidance to the implant clinician as to how to manage a given situation.
It is pertinent to add that it was not even ten years ago that I heard experienced clinicians and academics claiming at major meetings that the condition was either extremely rare or did not even exist!

I had the honor of chairing a one-day focus meeting on peri-implantitis last year in London, where four clinicians – Tord Berghlund, Stefan Renvert, Andrea Mombelli and Niklaus Lang, all leading researchers in this field – presented to over 400 dentists and hygienists, shedding much light on this condition.
It is also important to note that there is no implant type or brand that is immune from peri-implant disease and anyone who has placed and/or restored a significant number of implants will be familiar with the occasional presentation of inflammation and bleeding around an implant or even a discharge of fluid when palpating the peri-implant tissues over a restoration. So, for the purposes of this article, we shall refer to two main conditions, peri-implant mucositis and peri-implantitis.
The conditions:
Peri-implant mucositis can be defined as inflammation around the marginal tissue at the neck of an implant-supported restoration and is associated with edema, redness, and bleeding on probing.
Peri-implantitis is considered as a more advanced form of the disease and presents with a purulent discharge associated with marginal bone loss around the implant itself.
The prevalence of peri-implantitis has been shown to be as much as 29 percent in partially dentate patients and among these, up to 56 percent of patients had more than one implant affected. Berghlund et al showed greater than 3mm bone loss around implants at ten years in 28 percent of patients. This, therefore, is a common disease in the implant patient.
There appears to be a link with periodontal disease in that the bacteria found in peri-implant defects are similar to those found in deeper periodontal pockets and that the risk factors are similar in that it is more common in genetically susceptible patients, with secondary factors being smoking and poor oral hygiene.
For several years, I have had much success with the following protocols for managing the disease in both a non-surgical and surgical manner for peri-implant mucositis and peri-implantitis respectively.
Peri-implant mucositis:
One of the reasons that the condition has only been widely documented over the last ten years or so appears to be because of the trend to have the textured surface roughened up to the top of the implant, as opposed to a machined surface or a hybrid design.
As stated earlier, it is characterized by edema and profuse bleeding on gentle probing and has been shown to be related to inflammatory markers identifiable within peri-implant sulcular fluid. There may also be some horizontal bone loss and gingival recession.
In these cases, a non-surgical approach can be applied with a combination of mechanical debridement, sub-mucosal decontamination, and antimicrobial therapy. The treatment should be repeated three times within a ten to 14 day period.

Peri-implantitis:
Peri-implantitis tends not to be associated with the recession, but with a deep peri-implant pocket that becomes colonized by anaerobic periodontal pathogens. It presents with a purulent milky exudate on palpation or probing, together with vertical and crater shaped bone defects.
Like mucositis, it is an inflammatory mediated condition as evidenced by the presence of inflammatory markers within the sulcular fluid.
The condition is site-specific rather than pathogen-specific as it does not necessarily affect neighboring implants in a similar manner. Figure two is a periapical radiograph of two implants at 11 and 21 placed four years ago into the good bone and with uneventful healing. Tooth 11 shows a crater-like vertical defect, whereas 21 has optimal proximal bone levels. It is relevant to note that clinically, 11 has a milky crevicular exudate on palpation, as compared with healthy marginal tissues at 21.
Historically, the macro-rough surfaces such as titanium plasma spray, hydroxyapatite, and porous coatings have been implicated in a severely aggressive form of peri-implantitis which led to implant failure. In contrast, the newer micro roughened implant surface texture, popular in many current brands, shows excellent long-term data; however, it is unquestionable that the very common placement of implants in the partially dentate patient is leading to higher incidences of cross-infection into the peri-implant tissues.
Many treatment modalities have been advocated but most lack predictability, such as the polishing of the roughened implant surface, removing the implant threads, the use of CO2 lasers and the application of various acids.
The suggested protocol in this article, and one with which I have achieved much success over the years, focuses on mechanical direct debridement coupled with systemic and local anti-microbial therapy, and I am grateful to Michael Norton who originally gave me these protocols. Tetracyclines are recommended because they chelate to hydroxyapatite within bone from where they can mediate their effect. High doses of antibiotics are recommended as the pathogens in the peri-implant biofilm form a ’protected niche’, and low doses will contribute to hosting resistance.
It is usual, even sometimes desirable, to expect some recession of the hard and soft tissues which exposes the implant surface, and in the same way, as gingival recession following treatment of periodontitis will eliminate pockets thus aiding ongoing mechanical cleansing, this occurrence can improve the medium to long-term prognosis of the implant(s). It does, however, place the implants at future risk of peri-implant mucositis and as such, regular follow-up with the occasional decontamination for mucositis is to be recommended.
Further, I advise the following points should be considered:
  • Always probe implants in order to determine their health
  • Taking peri-apical radiographs will indicate the status of the proximal bone levels, but do not show the facial, palatal or lingual bone – these being the sites commonly affected by peri-implantitis. Figure three illustrates this point, as this is the case highlighted in the clinical images in this article
  • CBCT imaging can also be unreliable due to the scatter usually seen around the metal implant, not to mention IRMER and justification issues
  • Always treat peri-implant mucositis to prevent it from developing into peri-implantitis, which is more difficult to treat.
The progression of implant design, from machined surfaces through to the micro-textured biologically active surfaces, has seen the survival rates of dental implants soar to levels in excess of 96 percent, even in risk groups such as smokers. But this has to be tempered by the fact that this progress has also seen the increased prevalence of the peri-implant disease.
The possibility of future remedial care of their implants must be discussed with patients prior to commencing treatment, especially those with known risk factors such as genetic susceptibility and smoking, and all this assumes that good oral hygiene is a given.
Torsten Jemt, a member of the original Branemark Clinic team and a clinician with over 35 years of documented data, suggested somewhat controversially, at the recent ADI Congress, that if we wanted long term predictability for an implant in a young patient with a long life expectancy, free from peri-implant disease, maybe we should consider a machined surface implant! These implants are not even available for purchase nowadays!
In conclusion, in my practice, we have seen increasing numbers of cases presenting, ranging from implants that I have placed some time before, to those referred from worried colleagues. While I have traditionally treated them cautiously and conservatively, I am now intervening in a more aggressive manner because there is now undisputable evidence that peri-implant mucositis, if left untreated, will develop into peri-implantitis. Without a doubt, we are going to be treating this condition with increasing regularity for the foreseeable future.

PROTOCOL FOR TREATING PERI-IMPLANT MUCOSITIS

1. Mechanical scaling of the implant surface with plastic, titanium or carbon fiber instruments. The implant insert for the Cavitron is also useful.
2. Applying to any exposed implant surface, gauze strips soaked with chlorhexidine (0.2 percent).
3. Sub-mucosal circumferential irrigation of the implant pocket with 5ml chlorhexidine (0.2 percent).
4. Application of 2 percent minocycline gel (Dentomycin, Blackwell supplies Ltd).

PROTOCOL FOR TREATING PERI-IMPLANTITIS

1. Systemic antibiotics for three days pre-operatively and five days post-operatively. Advise a combination of Amoxycillin (500mg tds) and metronidazole (200mg tds).
2. Pre-operative two-minute mouthwash with chlorhexidine (0.2 percent).
3. Full-thickness mucoperiosteal flap extending beyond the infected site to healthy tissues.
4. Thorough debridement and curettage down to the healthy bone, combined with mechanical cleaning of the implant surface with titanium or plastic-tipped instruments.
5. Pack gauze strips soaked in chlorhexidine (0.2 percent) around the implant, into a defect, and under the flap. Leave in situ for five minutes.
6. Remove the gauze and irrigate thoroughly with tetracycline solution (1g in 20ml of sterile saline).
7. If possible, graft defect with hydroxyapatite bone mineral of either allogenic or xenogenic origin, rehydrated in tetracycline solution.
8. Once again, if possible, apply a resorbable collagen barrier membrane.
9. Closure of flap and regular reviews.

Peri-implantitis is an inflammatory process affecting the soft and hard tissues surrounding an implant. This disease is associated with loss of supporting bone, bleeding on probing, and occasionally suppuration. The etiopathogenesis of peri-implantitis is complex and related to a variety of factors that affect the peri-implant environment. Peri-implantitis can be influenced by three factors:
  1. Patient-related factors including systemic diseases (e.g, diabetes, osteoporosis) and prior dental history (periodontitis)
  2. Social factors such as inadequate oral hygiene, smoking, and drug abuse
  3. Parafunctional habits (bruxism and malocclusion).
In addition to the above, iatrogenic factors such as faulty restorations, cement left following restoration delivery, and/or loose components can also play a significant role in the development of peri-implantitis.
Although restorations of endosseous implants have demonstrated a very high survival rate1, one study suggested that over a five-year period, 0 to 14.4% of dental implants demonstrated peri-implant inflammatory reactions associated with crestal bone loss.2
Many methods of treating peri-implantitis have been documented in the literature and most focus on the removal of the contaminating agent from the implant surface. These treatments include:
  1. Administration of systemic antibiotics alone
  2. Mechanical debridement with or without systemic antibiotic treatment
  3. Mechanical debridement with or without localized drug delivery and chlorhexidine oral rinses
  4. Mechanical debridement combined with LASER decontamination
  5. Surgical debridement, and more recently ...
  6. Surgical debridement with guided bone regeneration (GBR) for reparation of bony and soft-tissue defects.
To date, GBR using a bone graft and membrane has had the best success as in demonstrating bone fill of the defects associated with peri-implantitis as described in the literature.
Because there are biologic differences between teeth and implants, the progression of infection around implants is different than natural teeth. The inflammatory cell infiltrates around implants was reported to be larger and extend more apically when compared to a corresponding lesion in the gingival tissue around natural teeth. In addition, the tissues around implants are more susceptible to plaque-associated infections that spread into the alveolar bone.
Implant surface bacterial decontamination is essential in treating peri-implantitis infections. Systemic administration of antibiotics has been used in the treatment of peri-implantitis, resulting in a reduction of inflammation. However, the efficacy of antibiotic therapy as a sole therapy has limited efficacy due to bacterial recolonization of the implant surface.
Because nonsurgical treatment approaches failed to promote the reosseointegration of the exposed implant sites, additional surgical interventions have been used in order to minimize the risk for reinfection of the peri-implant pocket. Some of the treatment modalities suggested for peri-implantitis are:
  1. Mechanical/ultrasonic debridement with localized drug delivery; i.e., antimicrobial minocycline spheres (Arestin®)
  2. Laser treatment with and without flap access
  3. Open flap debridement
  4. Open flap debridement with guided bone regeneration
Renvert et al. (2006) compared the combination of mechanical debridement and topical application of minocycline microspheres to the combination of mechanical debridement and 1% chlorhexidine gel application in peri-implant lesions. The results obtained after a follow-up period of 12 months showed that with the chlorhexidine group, only a limited reduction in bleeding on probing was achieved and the mean peri-implant probing depth (PD) remained unchanged (3.9 mm). On the other hand, in the minocycline group, the reduction of bleeding on probing was greater and an improvement in mean peri-implant PD (from 3.9 mm to 3.6 mm) was seen. These results suggest that the topical application of chlorhexidine provides limited or no adjunctive clinical improvement when treating shallow peri-implant lesions as compared with using mechanical debridement alone.
Schwarz et al. (2005, 2006a) compared the efficacy of the Er:YAG laser with that of the combination of mechanical debridement (using plastic curettes) and antiseptic (0.2% chlorhexidine digluconate) administration for the treatment of peri-implantitis. In both studies, the results obtained six months after therapy suggested that the treatment modalities were equally effective in improving peri-implant probing pocket depth (PPD) and clinical attachment level (CAL). However, at 12 months, the mean values for both groups of peri-implant PPD and CAL were not statistically significantly different from the corresponding values at baseline. Therefore, the results of the Er:YAG laser seem to be limited to a six-month period, particularly for advanced peri-implantitis lesions.
Leonhardt et al. evaluated the five-year outcome of a combined surgical (open flap) and antimicrobial treatment of peri-implantitis in humans. Leonhardt studied the effect of systemic antimicrobial therapy (amoxicillin and metronidazole) together with an open flap procedure and in conjunction with mechanical debridement of the implant surface for decontamination. The treatment was successful in 58% of the implants treated during follow-up for five years. Smoking was found to be a negative risk factor for treatment success.
Schwarz et al. (2006b) evaluated and compared the efficacy of two bone regenerative procedures for the treatment of moderate intrabony peri-implantitis lesions that included a greater than 6 mm probing depth and an intrabony component of 3 mm as detected on radiographs. The defects were randomly treated either with surgical debridement and filled with nanocrystalline hydroxyapatite, or surgical debridement and filled with bovine-derived xenograft (Bio-Oss®, Geistlich, Wolhusen, Switzerland) combined with a bioresorbable porcine-derived collagen membrane (Bio-Gide®, Geistlich, Wolhusen, Switzerland). After two years, the study showed that the combination of bovine bone mineral and the collagen membrane seemed to yield greater improvements in clinical parameters, showing 0.9 ± 0.2 mm more in PD reduction and 1.0 ± 0.3 more clinical attachment gain.

 Conclusion:
The ideal management of peri-implant infections should focus both on infection control of the lesion, detoxification of the implant surface, and regeneration of lost support. Treatment options can be surgical or nonsurgical. To date, studies suggest that nonsurgical treatment of peri-implantitis is unpredictable, and the use of chemical agents such as chlorhexidine has only limited effects on clinical and microbiological parameters. Adjunctive local or systemic antibiotics have shown to reduce bleeding on probing and probing depths in combination with mechanical debridement. The beneficial effects of laser therapy on peri-implantitis have been shown, but this approach needs to be further evaluated. Implant surface bacterial decontamination is essential in treating peri-implantitis infections. Most studies suggest that establishing an adequate healthy peri-implant tissue environment proves to be difficult since inflammation is still present in a significant number of patients. New treatment modalities need to be evaluated using long-term randomized-controlled studies to identify the predictable and successful treatment of peri-implantitis
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