Peri-Implantitis, Biofilm Contamination and Peri-Implant Bone Loss

Dental implants have been successfully used to treat all types of edentulism for many decades. With survival rates over 98% at 10 years and very low complications, dental implant treatments have proven to be safe and predictable, provided the surgical technique is accurate and the prosthetic work has a good passive fit and a proper occlusal load.

However, even though the survival rates of dental implants are very high, literature data shows there is also a very high prevalence of peri-implant disease – peri-implantitis, which was reported by some authors [1] to be as high as 47%.

While in the first stages it only manifests as a peri-implant soft tissue inflammation, with bleeding on probing and secretion, in the later stages the peri-implant disease is always associated with marginal bone loss, which can be observed on radiologic images and can be evidentiated by probing depth.

Many studies have focused on the bacterial species associated with peri-implantitis. There seems to be a general agreement that the surface of the implant is contaminated with bacteria, and the bacterial species involved are organized as biofilm on the outer surface of the implant. Some studies [4] have found a predominance of Aggregatibacter actinomycetemcomitans and Prevotella intermedia around diseased implants, while other studies [3] have reported Porphyomonas, Fusobacterium, Treponema, Tannerella to be abundant in peri-implantitis sites.

But all this data needs to be put into context. The oral cavity has a very complex microbiome. At all times, on different surfaces in the oral cavity (teeth, fillings, exposed roots, orthodontic appliances, prosthetic crowns, etc.) there is always a biofilm present. The composition of this biofilm varies from individual to individual, and can also vary in the same person. So, all surgical procedures performed inside the oral cavity are considered to be septic procedures. This also applies to the placement of dental implants, which is performed through a small surgical procedure consisting of an incision of the alveolar process mucosa, a reflection of a mucoperiosteal flap to expose the underlying bone. Using a dedicated surgical kit of burrs, the operator performs a calibrated osteotomy in the alveolar process, with a depth corresponding to the length of the implant, and then the dental implant is screwed inside the bone.

By comparison to a similar medial specialty, orthopaedics, dental implants are very similar to the titanium screws used for the internal or external fixation of bone fragments. However, there is a a major difference in the surgical techniques of the two medical specialties, because in orthopaedics the placement of the screws must be done in perfectly sterile conditions, while in the oral cavity this is impossible to obtain. So more than 98% of the implants survive anyway, and are still there in function more than 10 years later. So one may ask not why there is a prevalence of up to 47% of peri-implantitis, but why this prevalence is not 100%? Why there are still implants with zero bone loss and healthy peri-implant soft tissue?

One possibility is that even though all studies indicate that in peri-implantitis, the surface of the implant is contaminated with different bacterial species, there is no universal agreement on the exact ethiology of the peri-implant disease. In other words, we don’t know if the bone loss is actually caused by the bacterial biofilm, or the bone loss is produced by other mechanisms, and there is a subsequent contamination of the implant surface from the oral microbiome. Another possibility is a combination of mechanisms – a host-mediated inflammation [2], an initiation of cervical bone loss, which leaves room for an initial formation of biofilm, which then continues the bone loss process.

Also, the initial bone loss around the cervical part of the dental implant can be related to surgical or prosthetic factors. Inadequate placement of the implant in a narrow bone ridge can lead to a resorbtion of the cortical plate. Initially this can’t be observed on a control radiograph due to the bi-dimensional nature of this radiologic exam. But in time, the exposed surface of the implant will get contaminated, especially if the surrounding peri-implant soft tissue has a poor quality (lack of keratinized gingiva and a low thickness), and this will eventually lead to an exacerbation of peri-implant bone loss and the installation of peri-implantitis. Of course, in a case like this one will most likely find different bacterial species, which are usually associated with periodontal disease and peri-implantitis. But the fact that there are pathogenic bacteria present doesn’t automatically mean that bacteria is responsible for the installation of peri-implantitis.

The studies of Linkevicius et al demonstrate that if a series of anatomic, surgical and prosthetic requirements are met, the implants will exhibit zero bone loss in time.

So, at least for now, we can’t affirm with 100% certainty that peri-implantitis has a bacterial etiology. Of course, bacteria plays an important role on the progression of the disease and the response to treatments, so the management of the infection is crucial in order to be able to achieve a remission of the affection.