Missing teeth and supporting structures lost to dental diseases and trauma have been replaced in myriad ways through fixed and/or removable dental prostheses. In 1977, Dr. P.I. Brånemark demonstrated that bone will integrate into the surface of endosseous titanium dental implants,29 and the modern era of root form endosseous dental implantology arose. It is estimated that up to 5 million dental implants are placed in the United States each year.30 While longitudinal survival rates of osseointegrated dental implants range between 90-95%,8,31 these numbers represent implants that are present and in function, but may not fully capture rates of peri-implant disease and or health. It is estimated that rates of peri-implantitis range from 10-47%32-34 and rates of peri-implant mucositis have been observed in up to 65% of subjects with dental implants.33 Futhermore, it has also been demonstrated that these peri-implant diseases are increased in patients who smoke and have a history of periodontal disease, which may increase the difficulty in treating these implants.35
Given the high prevalence of peri-implant diseases, surveillance, early identification of disease, and intervention is critical. A key factor in long-term success of implants is proper maintenance of their surrounding soft and hard tissues. It has been shown that bacterial accumulation induces inflammatory changes in the tissues surrounding implants.38 Furthermore, it has been estimated that a monitoring program including regular examination and supportive implant therapy to identify and intercept peri-implant mucositis is highly cost-effective and the economic advantage is increased in high risk patients.39 In order to determine proper treatment steps to intervene for an implant with signs of peri-implant disease, it is essential to distinguish between “ailing” and “failing”/”failed” implants and progression of disease.
The primary etiology for both peri-implant and periodontal diseases is virulent bacterial plaque.38,40 While the inflammatory process that occurs around implants is similar to that around natural teeth, progression of disease is quicker in the peri-implant environment and the histologic peri-implant inflammatory lesions are larger and may prove more difficult to resolve at implant sites.41 This may relate to the peri-implant attachment apparatus and lack of a periodontal ligament as well as the unique implant-soft tissue interface.41 Multiple systematic reviews and randomized controlled trials have evaluated the efficacy of various treatment strategies for peri-implant diseases and identification of one ideal treatment strategy has proven elusive.42-44 Ideal therapy of peri-implantitis would result in active disease resolution (no suppuration, bleeding on probing, no further bone loss) and the establishment and maintenance of healthy hard and soft peri-implant tissues in a patient and clinical environment where plaque removal was feasible over time.42 Studies have shown that many therapies may be used to achieve these goals including non-surgical and surgical interventions, alone or combined, including mechanical debridement, pharmaceutical therapy, laser therapy, and open flap debridement with either resective or regenerative procedures.42 This discussion will focus on laser interventions as an adjunct to improve overall implant health.