October 1, 2007
by Oral Health
Appearance of localized pathology around the apex of implants has been documented in the literature1-4 and attributed to various etiologies. They range from contamination of the implant surface at the time of placement to periapical infection from adjacent teeth. Implant design has been rarely mentioned as possible causative and perhaps primary factor. This case report will illustrate the proposed notion that implant design may be one of the major causes of Implant Periapical Lesions (IPL).
A 36-year-old female patient, with non-contributory medical history, returned to the Implant Prosthodontic Unit (IPU) at the Faculty of Dentistry of the University of Toronto. Seven and a half years after crown delivery a 37-year-old patient presented with an asymptomatic recurring swelling in the buccal vestibule corresponding to the apex of an otherwise well functioning and asymptomatic, load bearing implant-supported single crown (ISC) replacing tooth 2.1 (Fig.1)
The left central maxillary incisor (2.1) had sustained an impact accident and subsequently both 2.1 and 2.2 received root canal obturations. In time, the left upper central incisor was noted to be in a “submerged” position relative to the adjacent teeth, consistent with a diagnosis of ankylosis. The adjacent lateral incisor (2.2) remained asymptomatic without showing signs of ankylosis (Fig. 2, Fig. 3 & Fig. 4). Ten years after the original trauma, 2.1 was extracted. The patient then attended the IPU to replace the missing 2.1 with an ISC. The implant surgery was performed observing standard operating room protocol. The surgery, post-surgical recovery, abutment placement, and crown delivery were all uneventful.
Radiographic views using parallax established that the observed radiolucent area was related to the implant apex, and the patient was referred to the periodontist who was the original staff-supervising surgeon. His primary diagnosis was an IPL originating from the implant vent. The differential diagnosis included IPL secondary to periapical periodontitis at the adjacent left maxillary lateral incisor (2.2).
An exploratory surgery was planned and discussed with the patient prior to proceeding. Alternatives, possible outcomes and likely post-surgical events were reviewed and informed consent was obtained. The patient accepted that, based on the intra-surgical findings, several outcomes may occur: partial or total removal of the 2.1 implant and/or periapical surgery for 2.2. Since the surgical plan included combined endodontic/periodontal procedures, both of these specialist-training programs were involved from the planning stages. The surgery was completed in an operating room setting by graduate students in periodontics and endodontics, supervised by their respective University of Toronto teaching staff.
After local anesthetic infiltration, a flap was raised to gain access to a large intra-bony lesion found about the implant apex. This “periapical” cross-vented portion of the implant had to be amputated with an air-rotor to allow access for complete removal of granulation tissue. After thorough irrigation the extent of the bony defect was inspected and, under operating microscope, the defect wall facing the periapical region of tooth 2.2 was found to be intact. The decision was made not to perform apicoectomy for the adjacent 2.2. Instead, the bony lesion was meticulously cleaned and repeatedly irrigated. Anorganic bovine matrix containing carbonate apatite material (BioOss, Osteohealth, New York, USA) was tightly packed and a resorbable collagen membrane (Bioguide, sManufacterer) was laid over the defect. Then, the surgical wound was closed (Figs. 5-15).
Post-surgical events were unremarkable, and after the third day the patient was asymptomatic. On follow-up appointments, up to 11 months thereafter, the patient was asymptomatic and the surgical area showed no clinical signs of a recurrence. The radiographic appearance was consistent with bony healing.
Many implant designs incorporate bone chambers of various shapes and sizes. The rationale behind their design can only be guessed because there is no clear published explanation. Bone chambers were presumed to collect “bone chips” that result in the preparation of the implant recipient sites or form “shavings” during the insertion of the implants into the bone. Instead of being compressed into the adjacent bone the “chips and shavings” were captured by these chambers. The vents, in addition, would provide macro-mechanical stabilization of the implants provided a “bone-bridge” formed through the vents. It is our hypothesis, based on observation of several of our cases, and analyzing the reports of IPL in literature, that these chambers can harbour necrotic bone debris that can become infected. The likely sources of infection are readily identifiable, such as blood borne transient bacteria, adjacent boney/soft tissue pathology, or residual tooth-related infected materials. Based on careful review of 10 cases of retrograde periodontitis out of 539 successful Brnemark implants, Quiriyanen et al6 suspected that residual infected material from endodontic pathology of either adjacent or associated to teeth that had pathology prior to extraction were the most likely cause of the lesions. Although they found a difference in incidence of IPL between the two types of implant surfaces, the authors did not implicate implant design (i.e. the configuration of the apical portion of the implants) as a predisposing etiologic factor.
Implant surface contamination can seed the bacteria into the recipient site and the retentive apexes would likely enhance this occurrence. Contamination could also occur during insertion of the implant via irrigation that “washed” bacteria from adjacent tooth surfaces. Communications created with the oral cavity due to perforations of the bony plates and soft tissues during the preparation of the implant recipient sites are sources related to surgical technique but mediated by implant design. This article does not prove our hypothesis, but suggests a strong possibility. The fact that the overwhelming majority of current implant designs have little or no sizable bone chambers or vents adds further circumstantial evidence to support our hypothesis.
Implant design may be one of the primary causes of IPL. We document a clinical case to illustrate our hypothesis. The fact that most current implant designs have no vents and few have bone chambers may diminish the value of the information presented here. However, understanding the history of implant design could help us identify and avoid the repetition of past mistakes.
Dr. Birek is an Associate Professor at the Faculty of Dentistry of the University of Toronto, and maintains a practice of Periodontics and Implant Surgery in Toronto. He has served as a surgeon in the Implant Prosthodontic Unit since 1986.
Dr. DaCosta is a clinical demonstrator at the Faculty of Dentistry of the University of Toronto and practices endodontics in Toronto.
Dr. Mindy Pho is a senior resident in Periodontics at the Faculty of Dentistry of the University of Toronto.
Aaron Fenton is Professor of Dentistry and IPU Director, Faculty of Dentistry of the University of Toronto.
Oral Health welcomes this original article.
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