Peri-Implantitis Associated With a Pre-Existing Pathology

Peri-implantitis is defined as an inflammatory lesion in the mucosa around the implant, which affects the supporting bone.¹  In peri-implantitis, osseointegration is eventually lost due to the ongoing infection of bone tissue.²  Thus, peri-implantitis has been suggested to be a major reason for late implant failure along with occlusal overload.³ 

The signs and symptoms of peri-implantitis include the presence of redness and swelling of the mucosa, bleeding or suppuration on probing, deepening of the pockets around the implant, and loss of the implant-supporting bone.⁴  However, different thresholds for probing depths and crestal bone loss have been applied to define peri-implantitis in the literature.⁵ 

Crestal bone remodeling begins immediately after preparation of the implant site and continues during the healing process. This bone remodeling often results in early crestal bone loss.⁶  Possible contributing factors for early crestal bone loss are reformation of biological width, microgap, implant crest modules, and occlusal overload.⁷  The classic criteria of implant success allowed for 1–1.5 mm of bone loss during the first year after loading and less than 0.2 mm annually thereafter.⁸ 

More crestal bone loss during the submerged healing period was reported in a grafted bone site than in a natural bone site.⁹  Therefore, early crestal bone loss could be more than 2 mm from the implant placement. If the clinician deems the implants to be stable despite excessive crestal bone loss, implant-retained prostheses might be delivered. Consequently, some implants have exhibited excessive crestal bone loss from the healing abutment connection or the delivery of definitive prostheses. It is difficult to make the final diagnosis of peri-implantitis in those cases. Clinical evaluation for those implants may also vary based on the condition of the mucosa, the zone of keratinized tissue, the design of prostheses, and probing pressure.¹⁰  It is also challenging to maintain the implant with excessive crestal bone loss and treat peri-implantitis developed afterward.

While peri-implantitis is generally based on the assumption that pathogenic biofilms on the implant surface result in bone loss and treatment focuses on removal of the biofilm from the implant surface,¹¹  this case report presents a treatment of peri-implantitis associated with a pre-existing pathology.

A 60-year-old female presented to the clinic at University of Maryland School of Dentistry in 2013, reporting that her implant-retained crown was displaced (Figure 1a). The patient reported no discomfort. Upon probing, however, pus discharged from the pocket around implant #19 (Figure 1b). The probing depths ranged from 5–6 mm with no mobility. Crestal bone loss around the implant #19 was evident on the radiograph (Figure 1c). The initial diagnosis was moderate peri-implantitis.¹² 

Since other providers had performed the previous treatments regarding #19 implant, the dental history was reviewed before formulating a treatment plan. A radiolucent lesion at the extraction site of #19 was present on the initial cone beam computerized tomograph (CBCT) taken in 2008 (Figure 2a). The series of radiographs exposed during the implant placement in 2009 also showed the radiolucent lesion with a focal calcification area (Figure 2b and c). According to treatment notes, no bone graft procedure was performed at implant placement. The follow-up radiograph prior to implant restoration exhibited early crestal bone loss with reduced size of radiolucency (Figure 2d). The implant crown was delivered in 2012 and no abnormality was noted. No probing depths were available.

Since the implant was deemed stable, guided bone regeneration (GBR) was recommended. A full thickness flap was retracted after the administration of local infiltration anesthesia. The soft tissue around the implant was removed with one piece (7W × 3H × 2D mm) using a titanium curette.¹³  The soft tissue taken from the site was fixed in 10% formalin solution (Fisher Scientific, Pittsburgh, Pa). It was then prepared for histopathologic evaluation.

An 8-mm infrabony circumferential defect was present around the buccal and distal aspects of the implant (Figure 3a). One capsule of 250 mg tetracycline HCl diluted with saline was applied repeatedly to the implant surface using cotton pellets for 5 minutes to disinfect the implant surface, followed by copious saline irrigation.¹⁴  Demineralized ground cortical bone grafts (LifeNet, Virginia Beach, Va) were gently packed into the defect (Figure 3b), and a collagen resorbable membrane (Cytoplast, RTM collagen, Osteogenics Biomedical, Lubbock, Tex) was placed to cover the bone graft material (Figure 3c). The flap was repositioned and secured with 5-0 monofilament (Ethilon^, Ethicon, Somerville, NY). A one-week course of clindamycin 300 mg, 4 times a day plus 3 weeks of Peridex (3M, St Paul, Minn) were prescribed since the patient was allergic to penicillin. The suture was removed 1 week later. No membrane exposure was observed.

Histopathologic evaluation of the soft tissue removed from the defect showed a cystic lesion lined with stratified squamous epithelium (Figure 4). Heavy infiltration of chronic inflammatory cells was observed in the epithelial lining and the connective tissue stroma. Therefore, a peri-implant cyst was diagnosed.

Clinical evaluation 3 months after the surgery exhibited a good tissue healing (Figure 5). The postsurgical CBCT (Kodak 9000C 3D) was taken to evaluate the healing of defect 8 months after the surgery. The maturing bone graft was noted around the implant #19 (Figure 6). A screw-retained metal ceramic crown was delivered 12 months after the surgery. The reduced size of the previous defect around the implant was evident on the radiograph exposed 14 months after the surgery (Figure 7). The pocket depths were 3–4 mm with no bleeding on probing at 14 months follow-up.

Many lesions occurring in the mandible have a radiolucent appearance, including radicular cysts, residual cysts, osteomyelitis, and unhealed extraction sockets. However, these lesions are often difficult to differentiate based on their radiographic features alone.¹⁵ 

In this study, the histopathologic evaluation of soft tissue taken from the defect confirmed a cyst (Figure 4). This may imply that the previous lesion was a residual cyst. The radiopaque lesion could be either a root tip or bone sequestra.¹⁶  The presence of cyst and a possible root tip at the time of implant placement may have prevented the bone from osseointegration to the implant surface, causing the subsequent defect.

However, after the removal of soft tissue around the implant, a root tip was not detected at the defect site. Since the defect was already extensive, additional bone removal to retrieve the possible root tip was not attempted. Although the final diagnosis was a peri-implant cyst, conditioning of the implant surface was performed with tetracycline HCl followed by copious saline irrigation because there were clear signs of infection.

Improvements in clinical parameters and a reduced size of the defect around implant #19 were observed after GBR (Figure 7). The studies investigating the efficacy of GBR to treat peri-implantitis have reported favorable outcomes.¹⁷  However, there is limited data available regarding re-osseointegration on implant surfaces previously exposed to inflammation in humans. Using a radiographic method to assess regenerative therapy has its limitations since a radiographic evaluation cannot distinguish between actual osseointegration and a defect fill.¹⁸ 

The postsurgical CBCT taken 8 months later confirmed maturing of bone graft and no radiolucent lesion around the implant #19, even though the radiopaque lesion still existed (Figure 6). Therefore, regular follow-up is recommended.

Abbreviations

CBCT

cone beam computerized tomograph

GBR

guided bone regeneration

The author reports no conflicts of interest.