Peri-Implant Disease: Diagnosis, Treatment, and Prevention Protocol

Peri-implant mucositis is an inflammatory process that is confined to the soft tissues surrounding the implant, whereas peri-implantitis involves the expansion of this process to the alveolar bone, causing bone destruction. Other terms given to peri-implant diseases include ailing (mucositis), failing (peri-implantitis), and failed (clinically mobile). Another term that has been recently recognized, apical or retrograde peri-implantitis, is detected radiographically as a peri-apical lesion that develops shortly after implant placement.

Although there are no standardized diagnostic criteria for implant diseases, assessment is universal. It includes taking radiographs and checking periodontal probing depths, bleeding on probing (BOP), exudate, mobility, and occlusion. Other supplemental parameters, including inflammatory markers, genetic markers, and bacterial profiles, may confirm disease progression; however, these are not commonly included in diagnostic classifications.

According to Zitzmann and Berglundh,¹ peri-implant mucositis is defined as inflamed mucosa surrounding the implant with a bleeding index ≥2 and/or suppuration with no radiographic evidence of bone loss. Peri-implantitis is defined by inflamed mucosa, BOP, probing depths ≥5 mm, cumulative bone loss ≥2 mm, and/or ≥ 3 threads of implant exposure.¹ Another term recently recognized by Quirynen,² apical or retrograde peri-implantitis, is detected radiographically as a peri-apical lesion developing shortly after implant placement. Establishing baseline records is critical to be able to distinguish a normal, healthy status from a changing peri-implant environment. For example, 2 mm of bone loss during the first year with no more than 0.2 mm of bone loss each year thereafter is considered normal,3 and 5-mm probing depths could be tolerated in cases with apically positioned implants respective to adjacent bone peaks. However, when disease is present and degeneration continues, implant loss may be inevitable if it is not identified and triaged properly. Implant failures are clinically diagnosed by mobility and are categorized as early or late. An early failure refers to an implant that is unable to establish osseointegration prior to loading, whereas a late failure refers to an implant that does not maintain osseointegration after functional load. Early failures occur as a result of complicated wound healing, surgical trauma, or premature loading, whereas late failures are attributed to biomechanical overload and infection.⁴

Due to the lack of standardized criteria for diagnosing and reporting peri-implant diseases, the prevalence is given over a wide range of 6.47% to 56%.⁵ A recent meta-analysis of 504 studies found the frequency of peri-implant mucositis and peri-implantitis to be 30.7% and 9.6%, respectively.⁶ On a patient level, this represented 63.4% of patients having mucositis and 18.8% having peri-implantitis.⁶

Because peri-implant disease has a relatively high prevalence, it is paramount to assess the risk profile and communicate this risk to the patient and the implant team. According to the 2013 Academy of Periodontology Consensus Report,⁷ risk factors for peri-implant disease supported by the greatest level of evidence include a history of periodontitis,⁸ smoking,⁹ poor plaque control,¹⁰ residual cement,¹¹ and occlusal disharmony. A low to moderate level of evidence supports a link between diabetes and cardiovascular disease, among other systemic factors.^12,13 These risk factors are not contraindications to implant therapy; however, they may contribute to implant failure. Although not all of these risk factors are modifiable, poor oral hygiene, active periodontal disease, occlusion, and excess crown cement should be corrected or eliminated to increase the implant’s chances of survival and success.

As with periodontitis, the primary etiologic factor for peri-implant disease is bacterial insult. As witnessed with the change in flora from health to gingivitis around natural teeth, there is an increase in cocci, spirochetes, and motile bacilli with the onset of mucositis around implants. Once this infection invades the connective tissue and there is evidence of bone loss with the onset of peri-implantitis, there is an increase in gram-negative, anaerobic, and motile flora analogous to periodontitis.¹⁴ Although the microflora of peri-implant disease is similar to periodontitis, implants are more vulnerable to bacterial insult because of the lack of a true connective tissue attachment and reduced blood supply.¹⁵ Understandably so, the host immune response to a similar bacterial challenge is also more robust around an implant than it is around a natural tooth.¹⁶

During the progression of gingivitis to periodontitis, the bacterial insult to the connective tissue causes an up-regulation of inflammatory mediators interleukin, matrix metalloproteinase, and tumor necrosis factor-alpha, among others, leading to bone destruction after a cascade of cell signaling. In vitro and animal studies confirm this process during peri-implantitis initiation;¹⁷ however, these studies have found that the process is not “self-limiting,” meaning the lesion is spontaneous and may continue even when bacterial contamination is removed.¹⁸ Implant detoxification is challenging to achieve without altering the surface topography because the rough surface favors biofilm formation and retention,¹⁹ and access for adequate instrumentation is often not attainable. Nonetheless, therapy aims to decontaminate the implant surface and create an environment amenable to re-osseointegration of bone lost around implant threads.

The management of peri-implant diseases is undoubtedly a challenge. Despite the demonstrated success of implant therapy, complications do arise and can be distressing given the significant time and financial investments. Like gingivitis, mucositis has been shown to be reversible if it is detected early, diagnosed correctly, and treated with proper nonsurgical techniques.²⁰ Peri-implantitis, on the other hand, requires surgical therapy while minimizing contributing risk factors to prevent disease progression, much like periodontitis. The most effective and predictable surgical technique has not been identified because there is insufficient evidence to support a specific treatment protocol.²¹ Long-term prospective studies are needed to validate one technique over others. To date, various methods have been researched with varying levels of success. Both nonsurgical and surgical techniques center around implant surface decontamination with the hopes of re-osseointegration in cases of peri-implantitis, along with the identification and
management of risk factors.

Regarding mucositis therapy, there are many studied methods of implant decontamination including traditional subgingival instrumentation alone or in combination with laser therapy, photodynamic therapy, air-abrasive techniques, and chemotherapy using tetracycline, citric acid, chlorhexidine, and/or saline irrigation.^22-24

In cases of peri-implantitis, the goal of surgical therapy is to achieve access given the limitations of a closed nonsurgical approach. Surgical options include open flap debridement with or without reconstructive therapy (bone graft and membrane), resective surgery (osseous defect removal), implantoplasty (removal of implant threads), or explantation (implant removal). As with periodontal disease, local and systemic antibiotics can be used with other nonsurgical and surgical techniques; however, as monotherapy they are ineffective and should only be used as adjunctive therapy.

To reiterate, the ultimate treatment goal is re-osseointegration; however, there is no substantial evidence to support predictable regeneration techniques.²⁵ A recent meta-analysis on reconstructive procedures found that mean radiographic bone fill was 2 mm, probing depth reduction was 3 mm, and BOP reduction was roughly 50% after reconstruction. The variability noted from the 12 studies was attributed to patient risk profile, defect shape, and reconstructive materials used. The authors, therefore, concluded there was insufficient evidence to support this therapy over others.²⁶

As with periodontal health, peri-implant health requires close supervision. It is recommended that implant patients undergo a strict oral hygiene and maintenance regimen, including biannual examination, instrumentation, diagnosis, and referral if warranted. Examination involves assessment of probing depths, BOP, exudate, mobility, keratinized mucosa, occlusion, and radiographic bone loss. For supramucosal instrumentation, air-abrasive devices and rubber cups aid in plaque removal. Although it has been controversial in the past, submucosal implant instrumentation is safe and encouraged with proper technique. Modern surface topographies are generally tolerable to minor surface changes caused by common instrumentation methods.²⁷ The preventive benefits of biofilm removal outweigh the slight surface character alterations inflicted by proper technique. Hand or ultrasonic instrumentation should be oriented parallel to the implant surface and achieved with plastic, metal, graphite, or gold tips. Extreme caution is advocated for metal tips because they are more damaging if an improper technique is employed. During maintenance visits, implants require thorough evaluation, as do their natural-tooth counterparts. If any signs of peri-implant disease are detected, the dentist should partner with the periodontist or oral surgeon to relay such findings.

Typically, peri-implantitis cases share similar characteristics that are easily identifiable during clinical examination. These include marginal erythema, BOP, exudate, and saucer-shaped bone loss seen radiographically with or without implant thread exposure. Implant crowns present a unique challenge for accurate probing because of the crown contours. To minimize errors, the probe should be oriented as parallel as possible to the implant body at all six probing sites.

Radiographs to evaluate the crestal bone levels and the presence of any residual cement, if applicable, are required at implant placement, crown installation, and annually thereafter. Residual cement acts as a vehicle for biofilm retention and is a preface to peri-implant infection. The abutment-to-crown connection, therefore, should be as coronal as possible to allow for cement removal, and this junction should be kept the farthest away from the alveolar crest as possible. Moreover, screw-retained restorations should be pursued whenever possible to avoid the effect of luting agents.

Regarding occlusal relationships, restoring implant-protective occlusion is desirable, with light centric contacts and no contacts in lateral excursions.²⁸ Occlusal forces should be axial, with no lateral torque because off-axial loading can correlate with radiographic bone loss and reduced success rates. For this reason, severely angled abutments and cantilevers are discouraged. As with natural-tooth–supported bridges, shorter occlusal spans are suggested for implant bridges to prevent failures from overload. In the same vein, occlusal guards should be fabricated for patients with parafunctional habits or those with multiple implants to reduce occlusion-related complications.

Standardizing diagnostic criteria and establishing predictable therapeutic techniques are critical next steps in peri-implantitis research. While researchers aim to unify criteria and determine clinical protocol, private practitioners should focus on prevention. Because peri-implantitis may take years to manifest, ongoing clinical and radiographic monitoring are essential to identify disease, triage appropriately, and increase survival rates.

Lauren E. Anderson, DDS, MS
Private Practice
Bloomfield Hills, Michigan