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Are We ‘Cleaning’ Dental Implants Correctly?

If the foreign body hypothesis is correct, how can the resulting effects be minimized?

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For years, most dental scientists and clinicians agreed that the etiology of the inflammatory lesions found around dental implants were caused by an infection engendered by bacterial biofilm. It was therefore assumed that the pathophysiology of these lesions was similar to that seen around teeth. As a result, it was suggested that therapy for peri-implant mucositis and peri-implantitis mimic that used for patients with gingivitis and periodontitis. The logic was that if the etiology and pathology are similar, then similar therapies are appropriate. This meant that one of the goals of therapy was to completely remove biofilm. This led therapists to use a multitude of mechanical approaches for cleaning the implant surface. These included but were not limited to curettes, burrs, ultrasonic devices, acids, and air-powder abrasives. Unfortunately, all of these approaches result in the distribution of dental cements and metallic particles and ions into the surrounding tissues. We now understand that these foreign bodies can engender inflammatory responses that can endanger the health and longevity of implants.

The role of dental cement in implant loss has been explored since the later part of the last century. Originally, questions arose about why cements initiated an inflammatory response around implants but not around teeth since the luting agents are the same. Later studies demonstrated that when the cement comes in contact with titanium it alters its chemical structure, which is then seen as a foreign body.

More recently, small particles and ions of titanium and zirconium have been implicated in some inflammatory lesions seen around implants. These particles have negative effects on epithelial cells, fibroblasts, and osteo­blasts. Smaller particles are phagocytized by macrophages and bacteria and can lead to an inflammatory cascade resulting in bone loss. This process is termed metallosis. Particles and ions can also be released by bacterial acid and implant micromovement or a combination, a process termed tribo­corrosion. Metallosis can also be caused by any attempt to clean or “sterilize” the surface of the implant. This routinely occurs during active and maintenance therapy.

If the foreign body hypothesis is correct, how can the resulting effects be minimized? A screw-retained prostheses or careful removal of excess, using minimal surface contact, will reduce the cement problem. Unfortunately, preventing metallosis is more complex. Emerging data show that the use of sterile saline on cotton pellets or water sprays can adequately remove biofilm with minimal distribution of metallic particles. This has been shown to allow reosseointegration in animals. This concept argues against both routine scaling at maintenance visits as well as closed approaches to treating peri-implantitis and removing cement. In these cases, where appropriate, surgical procedures that allow visualization of the implant surface seem warranted. If one accepts this hypothesis, it calls for a reexamination of current approaches to “cleaning“ implants.

Thomas G. Wilson Jr., DDS
Editor in Chief
twilson@belmontbusinessmedia.com

From Decisions in Dentistry. April/May 2024; 10(3):6

 

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