There is a sequence of events that leads to the chain reaction of peri-implant inflammations. The first step is contamination. Bacteria of the mouth will populate the exposed implant surfaces almost within minutes after implant placement. Infection, the second stage, is defined as the active multiplication of bacteria on a tissue or surface. And the bacteria will start to multiply on the exposed implant components within the first few hours. If bacteria are left to multiply uninterrupted, they will create a biofilm, which will soon increase in complexity and thickness. If the biofilm matures, then the tissues will respond with inflammation, which we will diagnose clinically as peri-implant mucositis. The role of the biofilm in the development of peri-implant mucositis is documented in numerous studies, including a couple of studies of experimental mucositis in humans. In these studies, it took three weeks of complete absence of oral hygiene for peri-implant mucositis to develop in patients. If the biofilm is removed at this stage, the peri-implant tissues can return to health. If the biofilm persists however, transition to the peri-implantitis, the final stage of inflammation, is very likely. Peri-implantitis, the condition where implants are losing supporting bone due to inflammation is today a major therapeutical challenge. As a new disease entity, the prevalence of peri-implantitis is not easy to define and estimations vary depending on the sensitivity of the diagnostic indicators used. Although some authors have estimated peri-implantitis to affect as many as 40% of the patients after 10 years with implants, the majority of studies place peri-implantitis between 5-20% of patients for the same period. It is also clear that the occurrence of plaque-induced inflammation greatly depends on the oral hygiene and the maintenance of the patients, and consequently, the prevalence will be very low in well-maintained patient populations. The diagnosis of peri-implantitis is mainly clinical. First, as we discussed previously, start by continuously assessing the risk of your patients. Patients with compromised oral hygiene, smokers, patients with diabetes mellitus, or history of periodontitis, are also in higher risk to develop peri-implantitis. Second, probe around the dental implants at every maintenance appointment. Bleeding on probing with light force is an indication of inflammation. Unlike teeth however, there is no definitive pathological probing depth around implants. As we often place implants rather deep in the tissues, especially in the aesthetic zone, probing depths of 4 or 5 mm are not uncommon around healthy implants. Therefore, compare the probing depths at follow up with that at baseline, when the implant was first restored. Any increase in probing depth might indicate initiated peri-implantitis. Finally a periapical radiograph with parallel cone can confirm the clinical diagnosis if we can see evidence of marginal bone loss. Bone loss around implants in peri-implantitis follows typically a uniform circumferential pattern that often resembles a crater. The treatment of peri-implantitis is depending on our ability to remove the aetiological factor and maintain thereafter healthy conditions for the peri-implant tissues. Consequently, plaque control is the first essential step. Two important parameters here: First, ensure that the patient can practice an optimal level of oral hygiene, and second, ensure that the design of the prosthesis allows for good cleaning. In a study by Serino et al, peri-implantitis was diagnosed almost 10 times more frequently when the implant prosthesis would not allow full access to oral hygiene. Very often, your very first step to solve the puzzle of peri-implantitis is to modify the prosthesis. In a case like this, inability to clean under the implant bridge has caused a rampant inflammation of the peri-implant tissues. In such a case we have to send the prosthesis back to the lab to trim the emergence profile of the pontics and open the interdental spaces, so that the patient can use interdental brushes and super floss. This step alone will not halt peri-implantitis, but it can significantly reduce the inflammation burden and the swelling and allow to proceed further with the next step. The second step is to remove plaque and calculus or deposits from the implant and the prosthesis surfaces. This is commonly an adequate treatment for peri-implant mucositis and it will be initially done with a combination of closed debridement and antiseptics. Common devices for debridement can be rubber-coated ultrasonic tips or specially-made hand curettes, while common antiseptics include chlorhexidine mouthrinse and gel. Finally, in the case of peri-implantitis, surgical treatment will be required in most cases in order to access and decontaminate the exposed implant surfaces. This is usually done with an access flap, where the implant surface can be disinfected with mechanical or chemical agents. In certain cases where the local anatomy allows, regenerative or resective surgery can be applied. In the case of resective surgery, after the removal of the granulation tissue and disinfection of the implant surface, the bone is flattened in order to allow the exposed implant surface to be accessible by oral hygiene. In the case of regenerative approach, when the defect morphology allows, after cleaning the defects are filled with a bone substitute, and then covered with a membrane as directed by the guided bone regeneration techniques we discussed in Module 4. Peri-implantitis is, today, a significant therapeutical challenge and the major threat to the long term success of dental implants. Even with the best of our treatments, complete resolution of the inflammation is often not possible. The most effective point to break the vicious circle of inflammation is exactly where it starts, at the biofilm. Keep the level of oral hygiene high, and your patients under a strict maintenance program and you will see little of the problem.
