Evaluating and Managing Peri-Implantitis: Part 1
In this article, you will read:
- Key Points
- What's the problem?
- Risk Factors
- Prevention and Management
This content is based on the article "Peri-implantitis Evaluation and Management" published in Dental Clinics of North America (April 2020)
- 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.
What's the problem?
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. Osseointegration is the direct structural and functional connection between host bone and the implant surface with no intervening tissue between the bone and the integrated surfaces of an endosseous
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 due to the different orientation of collagen fibers from 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 because of the absence of a periodontal ligament and surgical manipulation during implant placement.
The integrity of the mucosal barrier heavily depends on the appropriate implant placement in a suitable environment, 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 between the patient and the clinician-administered modalities.
Periimplantitis involves hard tissue loss, most importantly, the supporting bone around the implant beyond biological bone remodeling. 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.
According to the literature, RPI can be divided into 2 groups:
- 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.
- 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.
The likelihood of developing peri-implantitis may be increased in patients with unfavorable medical and/or social histories; hence, the importance of a thorough medical history and physical examination before any surgical procedure.
It is essential to explore the methods used to achieve control of blood glucose and assess their success. 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. Similar effects may be anticipated at the implant-soft tissue interface.
Studies have demonstrated greater marginal bone loss around the implants of smokers. 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.
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
Inadequate attached gingiva, occlusal overload, residual cement from crown restoration, and poor oral hygiene.