An inflammatory process

02 October 2012
Volume 28 · Issue 9

Michael Norton discusses his approach to decontamination and treatment.

Peri-implant mucositis is defined as inflammation of the mucosal cuff around the neck of a dental implant and is associated with oedema, rubor and bleeding on probing. Peri-implantitis is typically considered to be a more advanced disease, associated with purulence and marginal bone loss around the implant. The prevalence of peri-implantitis varies according to the source of the study and this is due in no small part to the variation in definition and the methodology of how the disease is measured. As such data varies from as little as 10 per cent to over 40 per cent in some studies. It has been proposed as being 29 per cent in patients whose implants are placed within a partial dentition, and who may have a prior history of periodontal disease. Bacteria found in peri-implant defects are similar to those found in deeper periodontal pockets; the implication being that cross infection is a risk. However, even implants placed into edentate jaws have revealed a significant colonisation of periodontal pathogens, if somewhat less than in the partially dentate dentition.

Treatment of these conditions is still anecdotal and there is little evidence for one technique over another, but broadly treatment falls into three categories:

  • Non-invasive antimicrobial therapy
  • Mechanical debridement with non-invasive antimicrobial therapy
  • Open surgical debridement and decontamination

The choice of treatment will very much depend on the degree/extent of the disease with the following parameters to be assessed:

  • Pocket depth greater than 5mm
  • Bleeding on probing
  • Presence of suppuration
  • Crestal bone loss/cratering

As stated above the decision as to whether disease exists and whether it is categorised as mucositis or peri-implantitis will depend on the presence or absence of a given pocket depth, light or profuse bleeding on probing and so on. Depending on whether the pocket depth should be 4mm, 5mm or greater than 5mm will influence the prevalence and herein lies the problem, as all studies use different parameters.

At the Centre for the Treatment of Peri-Implant Disease (CTPID) we do not consider pockets less than 5mm or light bleeding on probing as an indicator of mucositis. In our experience a majority of sites where implants have been placed in association with thicker mucosa will present with a deeper pocket and low grade bleeding on probing. The pocket is a pseudo pocket and the bleeding is more likely due to mechanical rupture of the connective tissue cuff below the apical extent of the junctional epithelium. This is a vastly different clinical picture to sites where profuse bleeding can be obtained by simple manual pressure on the mucosa to the side of the implant or light probing.

Again in many studies the presence of suppuration is an indicator of more advanced disease, in other words peri-implantitis, but such infection may or may not be associated with bone loss and bone loss has been cited as a major indicator for advanced disease. As with mucositis this is not always so simple because we have found difficulty in interpreting peri-implant sulcular exudate, which we feel can be categorised into passive exudate that exists within a deeper pocket but is not necessarily part of a bone degrading infection, and active suppuration which is clearly associated with bone loss/cratering. Clearly all of these various clinical pictures represent a scale of disease on a curve of severity and as such we have found they respond variously to the different treatment regimens described above.

Professor Tomas Albrektsson currently lectures on the true nature of this disease and poses the question as to whether bone loss precedes the onset of this disease process, such that peri-implantitis is a secondary opportunistic infection of the exposed surface or whether bone loss is the result of a primary infection which erodes the bone. I believe we have seen both these conditions, both primary and secondary infection and their treatment and response to treatment varies.

In the first case example (figs 1-8) we have seen a protracted and progressive bone loss from six months after loading and have monitored this loss of bone over many years.

At no time was there ever any clinical evidence for the cause of this bone loss, with an absence of any purulence, and culturing using sterile paper points placed within the peri-implant sulci proving negative for periodontopathogens. There was a clinical picture of mild mucositis as seen below, with exposure of the most coronal margin of the implants, but nothing that related to the devastating bone loss. The occlusion was variously checked and re-checked and ultimately the crowns were taken out of occlusion but the bone loss continued unabated. Eventually one implant fractured at its apex and a surgical exposure revealed a thick cortical bone surrounding the implant without evidence of granulation. It is difficult to know how such a case fits into the very rigid classification of the disease as has been variously described.

By contrast other cases reveal a more typical picture such as in the single tooth implant shown (figs 9-11) which presented with spontaneous bleeding and suppuration from the sulcus on digital pressure adjacent to the neck of the implant and radiographic evidence of bone loss. The observant will note the porcelain fracture and as such one must again question whether bone loss from occlusal overload preceded the onset of infection. In any case the porcelain was adjusted and the case was treated with mechanical instrumentation within the sulcus and three treatments with topical sub-mucosal antimicrobial therapy according to an established protocol used within the centre.

It is important that the three treatments take place within a two week period in order to be effective, but as this case demonstrates the results can be dramatic without recourse to bone grafting and also proves that this de novo bone recovery is possible and sustainable.

Other more advanced or protracted cases require full surgical intervention such as in the case shown in figures 12-19, which the patient's infection had been neglected for over 10 years with the patient being advised that it was only the result of inadequate home hygiene. The bridge was very tight fitting to the mucosa and there was little possibility for any effective cleaning.

Interestingly the patient had been told "implants cannot become infected because they are metal" but contrary to this view these implants had become badly infected being an earlier variety of titanium plasma spray coated implant. This coating was known to be like a sponge for bacteria once exposed to the supra-crestal environment and in this case the bone loss was very advanced and their removal was the only option. The most difficult aspect of this treatment is managing the patient's disappointment and occasionally their anger at the failure, even if years after the original treatment as in this case. But in particular because the patient felt the providing dentist had tried to always blame her and never offered any interventional or even non-interventional therapy other than flossing under the bridge.

On removing the implants it was apparent that there was a breach of the cortical floor of the nose, but fortunately both sites revealed an intact nasal mucosa. Cross-linked collagen membranes (Osseoguard, Biomet 3i) were fixed into position on both the labial and palatal cortices using titanium tacks and the defect filled with a bovine derived bone mineral (BioOss, Geistlich).

Membranes were folded over the graft to create a lid and further fixed for stabilisation. The mucosa periosteum was released to allow tension free flap closure and suturing with a 6/0 monofilament. As a temporary measure the bridge was re-inserted deriving support from the two compromised natural abutments. This graft will be left for at least a year before re-entry and further reconstruction can be considered.

These cases highlight the diverse nature and ramifications of these disease processes. Much information remains obscure and much knowledge still needs to be gleaned to fully understand the cause and the best approach to treatment. In the meantime it is our hope that as we accept more such cases at The Centre for the Treatment of Peri Implant Disease we will begin to get a better feel for the categorisation of disease severity and the appropriate treatment regimen indicated.

Figures available on request.