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Professor Andrea Mombelli
Differential microbial diagnosis and appropriate antimicrobial therapies for peri-implant infections

Report by Simon Wright and David Speechley

The Audience
Aetiology and Clinical Features

Peri-implantitis is an inflammatory process affecting the tissues around an osseointegrated implant in function, resulting in the loss of supporting bone. The clinical features of this process may involve clinical signs of inflammation, but is always associated with circumferential bone loss.

Radiological evaluation is a useful tool in the assessment of peri-implantitis, but due to projection artefacts often under-estimates the size of the defect. It is therefore recommended that peri-implant probing is essential in the diagnosis of this condition. A probing force of 0.4N is recommended, allowing the estimation of pocket probing depth to within 1 mm of the alveolar bone. Probing around an implant allows the early detection of peri-implantitis which is vital in both its treatment and mitigating further disease progression, it is however a technique sensitive investigation and care must be taken not to probe the implant shoulder when investigating bone level implants. A key diagnostic feature of inflammation is bleeding on light probing

Implant mobility is a terminal stage of peri-implantitis, and careful diagnosis is required as other causes of apparent implant mobility are more common, in particular mobility or fracture of the superstructure. Pain is not normally a feature and frequently the patient is unaware of any problems.

Peri-implantitis is an infectious disease and therefore it is important in the differential diagnosis to exclude other causes of inflammation, the most common being retained cement. It is also imperative not to confuse the normal physiological remodelling of bone due to surgical trauma which can occur for up to 1 year post placement, with this disease process.

There is considerable evidence that the aetiology is of a bacterial nature. These include:

Experimental studies; where a mucocitis resulted from biofilm and plaque accumulation, which then resolved when the biofilm was disrupted and the plaque removed.

Associated studies; these demonstrated that the pus collected contained gram –ve bacteria and rods in the patients that had clinical symptoms and these were absent in those that were ‘healthy’. The conclusions were that peri-implantitis is regarded as site specific and has characteristics that are similar to chronic periodontitis. This would suggest that a history or periodontitis is a significant risk factor.

Therapy Studies; suggest that if the cause is of a bacterial nature then antimicrobials should be included in the treatment regime.

All the above study types suggest that teeth and implants share risk factors, the most important being poor oral hygiene and smoking.

The bacteria typically have a low pathogenicity without invasive properties, they are not aggressive and produce low chain polymer substances that contribute to the biofilm. The infections tend to chronic, evade the hosts defence mechanisms and tend to be localised to a specific site not becoming systemic.

A dental implant is type 3 medical device, as it crosses the epithelial barrier into a non-sterile environment. Exposure to micro-organisms is therefore inevitable, and colonisation of the sterile implants surface will occur. ‘Normal implant flora’ is compatible with health, however ecological factors that promote an unwanted shift in resident flora are to be avoided.

Periodontitis and Peri-Implantitis – One cause for two diseases?

The arguments for this concept include the common microbial and clinical features, along with common risk factors (smoking, genetic factors and poor oral hygiene), and the higher incidence of peri-implantitis in patients with a history of periodontal disease. The counter argument is that peri-implantitis is also seen in patients with no history of periodontal disease, and the disease is defined by the site rather than the pathogen.

Diagnosis

It is suggested that the following scheme is adopted, it must be noted however, that the most important clinical feature in the diagnosis of peri-implantitis is the peri-implant probing depths.

  1. Is there suppuration?
  2. Are there clinical signs of inflammation?
  3. Are there pocket depths >3mm?

    If the answers to the above are all no, this indicates health. If any are yes then proceed to question 4.

  4. Does the pocket extend more than 3mm beyond the implant shoulder?
  5. Is there bone loss?
  6. Is there a plausible cause other than peri-implantitis?
  7. Is the pocket deeper than 5mm?

Treatment

The most important aspect of the treatment is to clean the implant surface. The ability to be able to do this depends on the implant type. Rough surface implants cannot be cleaned effectively with mechanical methods alone. It is important to realise that this is not a ‘disease of the bone’. The process starts in the connective tissue, on the smooth surface with a biofilm, subsequently the rough surface is affected. The associated bone loss is a result of this process.

A pocket depth of 5mm or over is very difficult to treat non-surgical, as it challenging to clean the implant surface effectively. Studies suggest that Actisite (tetracycline) local antimicrobial, in combination with mechanical cleaning, is more effective in treating peri-implantitis than in controls. This product however is no longer available. The limitations of locally delivered medicaments is that they are difficult to get to the base of the pocket.

A key element in the treatment is ensuring that site is not going to be re-infected, therefore oral hygiene instruction and plaque control measures are fundamental.

The treatment regime for all peri-implant infections is that they should be treated with 500mg Amoxicillin and 375 mg Metronidazole TDS for 7 days. This should be combined with mechanical cleaning, surgical reduction of pockets, and grafting crater defects with Bio-Oss and Bio-gide.

Summary

  1. Implant failure, fracture, primary complications (within 6 months of placement)
    Explanation or 2
  2. Cementitis , infection from a foreign body
    Debridement and disinfection
  3. Moderate peri-implantitis, probing depth <4mm bone loss <2mm.
    Debridement and disinfection and systemic antibiotics
  4. Advanced peri-implantitis, probing depths >5mm bone loss >2mm.
    Surgical access. Debridement and disinfection and systemic antibiotics

Questions

As it is easier to clean a smooth surface implant, in patients with a high risk of developing peri-implantitis should we be using turned implants?
It is better to have a smooth surface in the oral environment, and epithelial cells prefer smooth surface. However bone cells prefer the roughened surface, so it is a compromise.

Do we need keratinised mucosa around our implants to prevent peri-implantitis?
Presence of lack of keratinised mucosa is not a major factor in the presence or absence of peri-implantitis. What is important is that we have mechanically stable peri-implant tissues that are compatible with health.

To what extent do occlusal forces affect the progression of peri-implantitis?
Again, this is not a major factor. The passive fit of the superstructure is much more important. It is this small continuous force that is more important than the occasional high load. It was suggested that the superstructures are to be as small as possible, single units, and to avoid splitting implants together or to teeth whenever possible.

Does it make a difference if the crown is screw-retained or cement retained?
Bacteria do colonise the microgap, but there is no major microbial difference between them. You obviously need to ensure that all the cement residues are removed with cement retained restorations.

Can you treat Mucocitosis with local measures?
Yes, it is very important to treat mucocitosis as early and as quickly as possible. It is very easy to stop this developing into a peri-implantitis which is much more difficult to treat. You can treat it with Tetracycline, Chlorohexidine and mechanical cleaning.

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