Proposed etiologic factors include bone overheating, microbial involvement of adjacent teeth, pre-existing bone infection, and overload. However, the mandible and maxilla seem to have different predispositions in response to these causative agents. Treatment protocols for peri-implant infection have included minimally invasive approaches such as granulation tissue removal and detoxification of the implant surface, as well as more aggressive measures.
According to Behnam aghabeigi Birmingham the achievement of osseous healing and reosseointegration in a patient who presented with presented apical bone loss and signs of infection around a mandibular implant. Reosseointegration was achieved following an intraoral apicoectomy-like approach, i. e, removal of the infected nonintegrated portion of the implant, and meticulous debridement of the granulation tissue. A literature review of 13 relevant published studies was conducted. The current understandings regarding the etiology and treatment strategies for management of apical bone loss around dental implants are summarized and presented.
In general, bone loss around an implant has been recognized as a complication that can follow implant treatment.1,2 While the first case in the literature demonstrating isolated apical bone loss was described by McAllister and colleagues3 in 1992, it was Reiser and Nevins in 1995 who first defined bone loss limited to the apical segment of an otherwise osseointegrated implant as an “implant periapical lesion” and further described the rationale for such an occurrence and possible treatment options. Sussman further described periapical implant pathology and proposed 2 patterns of bone loss apical to implants. However, this report was limited to implants placed in partially edentulous jaws adjacent to natural teeth with a history of periapical dental pathology.
While the term “implant periapical lesion” appears often in the literature,6–10 other terms for the same phenomenon such as “apical peri-implantitis,”11 “retrograde peri-implantitis”12–14 “abscess around the apex of an implant”15,16 and “implant demonstrating periapical radiolucencies” have also been identified in Medline searches of the English-language literature.
Reiser and Nevins reported on 10 implant periapical lesions (9 infected and 1 asymptomatic) in a study sample of approximately 3,800 placed implants, suggesting a prevalence of 0.26%. This is the only value for prevalence of implant periapical lesions reported in the literature. Although the incidence of implants with apical bone loss is still unknown, the authors’ literature search found 23 case reports in 13 studies. This suggests that they occur more frequently than initially thought.
Many etiologic factors have been suggested in previous studies. However, the exact mechanism of bone loss in the apical area of an implant is still not well understood. It has not been possible to determine whether related lesions are composed of healthy tissue or created by the destruction of new tissue. It is also possible that such lesions may result from activation of a pre-existing condition. The etiology is likely to be multifactorial.
While observation and monitoring appears to be the preferred management option for small inactive lesions, various treatment modalities have been suggested for infected lesions of larger diameter. Detoxification of the implant surface3,12,13 and/or surgical treatment (an implant apicoectomy-type procedure following an extraoral15 or an intraoral approach and placement of either a bone substitute with membrane coverage 4,9 or autogenous bone chips18 in the bone defect) have been described.
The clinical management of apical bone loss around a mandibular implant using an intraoral apicoectomy-like surgical approach alone is presented. The results of a critical review of the literature on suggested etiologic factors and management options are also presented.
A 56-year-old male patient under went stage-1 implant surgery at the Eastman Dental Hospital (London, UK) for the placement of implants to support an overdenture. Most mandibular teeth had been lost secondary to periodontal disease. The only remaining mandibular teeth were the left second premolar and first molar, which were to be extracted at implant placement. A panoramic radiograph showed no preexisting bone pathology. Two 3.75 18-mm Brånemark Mk III implants (Nobel Biocare, Göteborg, Sweden) were placed in the anterior interforaminal region of the mandible. A nonsubmerged protocol was followed, and two 3-mm healing abutments were connected to the implants before suturing. The patient was advised to keep his mandibular denture out for 2 weeks. The early postoperative period was uneventful.
Standard transmucosal abutments were attached at stage-2 surgery after 4 months. Following a standard prosthetic protocol, a mandibular denture supported by a gold bar with a small distal cantilever was inserted 9 months after implant placement. The unusual delay was caused by the patient’s inability to attend the prosthetic appointments scheduled.
Six months after seating of the mandibular denture, the patient attended an emergency clinic complaining of discomfort around the right implant. He reported the initiation of pain 1 month after placement of the definitive prosthesis. On examination following removal of the gold bar, the right implant was found to be immobile. However, the soft tissues in the apical area appeared erythematous and slightly tender to palpation. The mucosa around the implant neck appeared healthy, and the probing depth was normal. A periapical radiograph showed a small radiolucent area around the apical third of the right implant (Fig 1). Marginal bone loss was stable at the first thread, which is consistent with previous studies on Brånemark System dental implants. Metronidazole was prescribed, and it was decided to explore the periapical lesion with resection of the apical portion of the implant.
The procedure was carried out under local anesthesia. A buccal incision exposed the area in the right mandible. No bone fenestration was found. A bony window was created over the apical area of the implant until the titanium implant could be seen. There was granulation tissue around the apical 4 mm of the implant, which was debrided. Under profuse sterile saline irrigation, the nonintegrated portion of the implant (4 mm) was trimmed using a tungsten carbide fissure bur. Hemostasis was achieved, and the wound was sutured to obtain primary closure. The patient was advised to avoid denture wear for 1 week and was prescribed metronidazole (400 mg 3 times a day for 7 days) and a chlorhexidine gluconate 0.12% mouthwash. No complaints were reported when the patient was examined 1 week later, and the tissues were found to be healing satisfactorily.
The patient was followed for 2 years during which time the implant and the surrounding tissue remained asymptomatic. There were no signs of adverse tissue reaction. There was no tenderness on palpation in the area, and the prosthesis has been stable and has functioned satisfactorily in the postoperative period.
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