Microbiota Around Root-Form Endosseous Implants: A Review of the Literature
Kees Heydenrijk, DDS, PhD, Henny J. A. Meijer, DDS, PhD, Wil A. van der Reijden, PhD, Gerry M. Raghoebar, MD, DDS, PhD, Arjan Vissink, MD, DDS, PhD, Boudewijn Stegenga, DDS, PhD
Although high success rates for root-form endosseous implants have been reported, failures occasionally occur, and these implants must be removed. At least 10% of the failures have been suggested to be the result of peri-implantitis. There is some evidence that periodontal pathogens, mainly those belonging to the group of Gram-negative anaerobic rods, play a role in the etiology of peri-implantitis. This article provides an overview of the literature associated with common peri-implant microbiology and an assessment as to whether bacteria associated with periodontitis exert a possible risk for periimplant tissue breakdown. The peri-implant area is colonized by a large variety of oral microbial complexes. The microflora of the oral cavity prior to implant placement determines the composition of the microflora in the peri-implant area. Implants involved in peri-implantitis are colonized with large amounts of Gram-negative anaerobic bacteria, including Fusobacteria, spirochetes, Bacteroides forsythus, and “black-pigmented bacteria” such as Prevotella intermedia, Prevotella nigrescens, and Porphyromonas gingivalis. Also, Actinobacillus actinomycetemcomitans can be isolated from these lesions. Thus, the microflora of peri-implantitis lesions resembles that of adult or refractory periodontitis. However, the presence of periodontal pathogens does not always lead to a destructive process. Therefore, the etiologic role of specific microorganisms in implant failure related to infection is still not resolved. Controversy remains as to whether organisms recovered from the original microflora cause the failure (and if so to what extent) or merely result from the infection. Nevertheless, there is accumulating evidence that bacteria cause the disease, while the individual’s genetic makeup and environmental influences determine the severity of the disease.