With a very large number of endosseous dental implants placed by generalists and specialists, complications are to be expected. Among them are problems with the soft tissue interface and the hard tissue attachment. Peri-implant mucositis and peri-implantitis are not uncommon, but their prevalence and impact may be reduced with diagnosis and appropriate management, as can the likelihood of progression from mucositis to peri-implantitis. Successful implant dentistry does not end with integration and restoration, and both patient and professionally administered modalities are important for long-term implant maintenance.
Because of their prevalence and potential impact on outcome, peri-implant mucositis and peri-implantitis are important complications of implant placement.
Clinicians placing and/or restoring implants must be familiar with the diagnostic features of these conditions and monitor their patients carefully.
Management strategies should take into account local and systemic factors and should be as evidence-based as allowed by available data.
As do our natural teeth, endosseous implants emerge from the bone through oral soft tissues into a cavity that harbors a vast array of microorganisms. The mucosal barrier is heavily colonized and also subjected to repeated trauma from normal functions. , Placement of implants requires not only adequate bony anatomy, but a favorable soft tissue covering and a healthy oral environment. Maintenance is critical to the long-term success of implant-borne restorations just as it is to natural teeth and conventional prosthetic devices. Having a clear understanding of the techniques used for maintenance is essential to implant health as is patient selection.
Foundational to understanding, preventing, and managing diseases affecting implant attachment is a review of the ways that hard and soft tissues interface with implants and how those differ from teeth. Clinicians are quite familiar with the concept of osseointegration, the direct structural and functional connection between host bone and the implant surface. This resembles ankylosis, as there is no intervening tissue between the bone and the integrated surfaces of an endosseous fixture. Many technical aspects of implant placement contribute to successful osseointegration, from site selection to surgical technique to the need for undisturbed healing. The long-term success of implant-borne restorations depends not only on osseointegration, but on the soft tissue interface that exists where the implant and associated hardware emerge into the oral cavity. Teeth and implants share the same basic structures at the mucosal barrier: a sulcus, junctional epithelium, and a connective interface. However, implants have a weaker implant connective interface as the orientation of collagen fibers is different than for teeth with Sharpey’s fibers providing a tight seal between the bone and cementum. In addition, blood supply to peri-implant soft tissues may not be as robust as in the natural periodontium due to the absence of a periodontal ligament and surgical manipulation during implant placement. The integrity of the mucosal barrier is established by appropriate implant placement in an environment that is suitable, or in a site that has been developed for that purpose, allowing for well-designed prosthetic connections that support the soft tissue interface. Maintenance of this important barrier over time is a shared responsibility involving the patient as well as clinician-administered modalities.
Peri-implant complications may be limited to soft tissue inflammation or can lead to bone loss. Similar to gingivitis, peri-implant mucositis ( Fig. 1 ) is the term applied to soft tissue inflammation alone. This inflammatory response is strictly limited to the soft tissue, with no evidence of progressive bone loss subsequent to the initial remodeling after implant placement, and is known to be reversible. Peri-implantitis, such as periodontitis, involves hard tissue loss, most importantly, the supporting bone around the implant beyond biological bone remodeling ( Fig. 2 ). , In retrograde peri-implantitis (RPI), a symptomatic periapical lesion is associated with a coronally osseointegrated fixture. RPI is thought to be caused by bacteria that are retained in the extraction socket and may remain in that site for up to a year after the tooth is removed. Some authors divide cases of RPI into 2 groups: (1) those that occur at the time of implant placement, including contaminated surgical sites, excessive heat or compression at the time of implant placement, large osteotomies, presence of a foreign body, and premature loading causing microfractures of the bone, and (2) those associated with preexisting diseases, including a pulpoperiapical pathological condition in the extraction site, retained root tips, underlying bone disease, periapical radiolucencies in adjacent teeth, and remnant cells from cysts or granulomas. Symptoms of pain and swelling can manifest as early as 1 week after implant placement and have been reported to occur as late as 4 years after the procedure. Because RPI is related to microorganisms similar to those found in chronic periodontitis, its treatment is the same as other forms of peri-implantitis, which include the removal of the biofilm and bacteria that are the source of the infection.
Data on the prevalence of peri-implant disease are inconsistent and vary greatly among published studies. Lee and colleagues conducted a systematic review and meta-analysis published in 2017 that estimated the mean prevalence of implant-based and subject-based peri-implantitis. They found it to be 9.25% and 19.83%, respectively, and the estimated implant-based and subject-based peri-implant mucositis prevalence was 29.48% and 46.83%, respectively. In an earlier meta-analysis published in 2013, Atieh and colleagues found the estimated prevalence of implant-based and subject-based peri-implantitis to be 9.6% and 18.8%, respectively. The estimated prevalence of implant-based and subject-based peri-implant mucositis in this review was 30.7% and 63.4%, respectively. Although not perfectly aligned, the results of these 2 analyses demonstrate that the process of providing patients with implants does not end with successful integration and restoration. It seems that about half of our patients, perhaps more, will develop peri-implant mucosal inflammation and a smaller, but significant number will lose bone.
Prevalence data may be affected by many factors, including the duration of follow-up after implant placement—the longer the follow-up period the higher the prevalence of peri-implantitis and the number of fixtures placed per patient—higher numbers are associated with an increased risk of peri-implantitis. Other associations with an increased risk of peri-implant disease are: poor oral hygiene, dental cement from the implant restoration, history of periodontal disease, certain systemic diseases, and cigarette smoking. Among these, a history of periodontal disease is most compelling, as that is often the reason for tooth loss and the need for implants. However, patients who have a history of periodontal disease may have a 5-fold increase of the risk of peri-implantitis. All of factors listed above may contribute to individual risk for developing peri-implant disease and point to the need for careful patient selection, a strong emphasis on patient education and a commitment to professionally guided and monitored long-term maintenance. Critical risk factors are discussed later.
The likelihood of developing peri-implantitis may be increased in patients with unfavorable medical and/or social histories. Before undertaking any surgical procedure, a thorough medical history and physical examination must be done. For diabetics, it is essential to explore the methods used to achieve control of blood glucose and to assess the success of these methods. Hemoglobin A1c provides information about blood glucose levels over the preceding 3 months and is a valuable tool in determining how well controlled a particular patient is over time. The established associations between diabetes and periodontal disease should increase concerns about peri-implant disease in this population because bacteria responsible for periodontal disease are the same as those found in peri-implantitis. , Patients with poor control of blood glucose have periods of sustained hyperglycemia, decreased white blood cell chemotaxis, a negative impact on wound healing, and a potentially adverse effect on the implant-bone attachment ( Fig. 3 ). Similar effects may be anticipated at the implant-soft tissue interface. Smokers should be urged to discontinue the habit as studies have demonstrated greater marginal bone loss around the implants of smokers. The negative effects of smoking are well documented and the oral cavity is not spared. Smoking impairs wound healing, including bone consolidation by reducing the inflammatory chemotactic response, migration, and bacteriocidal mechanisms. These and other smoking-related defects may contribute to peri- implantitis and eventual implant failure. Another concern is a history of periodontal disease before implant placement. Alterations in the normal oral flora associated with periodontal disease include an increase in the total bacterial load as well as selective increases in potentially pathogenic organisms that may then impact on the integrity of the peri-implant soft tissue interface and ultimately on the bony attachment. Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis , which are normally present in small quantities in healthy implant biofilms, may become the predominant pathogens responsible for peri-implant mucositis and progression to peri-implantitis. Other risk factors include inadequate attached gingiva, occlusal overload, residual cement from crown restoration, and poor hygiene. Compliance with supportive therapy in patients has been shown to significantly decrease the likelihood of progression to peri-implantitis. ,