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Histopathologic Observations on Late Oral Implant Failures

Identifieur interne : 008F18 ( Main/Exploration ); précédent : 008F17; suivant : 008F19

Histopathologic Observations on Late Oral Implant Failures

Auteurs : Marco Esposito [Suède] ; Peter Thomsen [Suède] ; Lars E. Ericson [Suède] ; Lars Sennerby [Suède] ; Ulf Lekholm [Suède]

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RBID : ISTEX:8A3C1DC6F7B6BD4B434A05C127CFDD53EE83A2C9

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Abstract

Background: Despite good success rates of osseointegrated oral implants, failures do occur. To minimize losses, failure mechanisms should be elucidated. Purpose: This study sought to describe the morphology of tissues surrounding late failed Brånemark implants in relation to their clinical and radiographic findings to acquire a better understanding of the etiologic factors. Material and Methods: Ten failed implants and their surrounding tissues were consecutively retrieved from nine patients after prosthesis placement (late losses). On radiographs, a radiolucent line was visible around nine clinically mobile implants. Tightening of the abutment screw evoked pain at seven mobile implants. Clinically, no other visual inflammatory sign or symptom was manifest. A fistula originated from one stable implant, surrounded on radiographs by a diffuse bone rarefaction. Retrieved implants were electrochemically dissolved. Intact tissue‐implant thin (1 μm) and ultrathin (70–80 nm) sections were analyzed with light and transmission electron microscopy. Results: Peri‐implant marginal tissues displayed moderate inflammatory infiltrates located adjacent to and beneath the junctional epithelium. One patient affected by oral lichen planus displayed an intense lymphocyte/plasma cell‐dominated immune reaction. Deep peri‐implant tissues surrounding mobile implants consisted of a dense, fibrous tissue capsule with minimal inflammation. Epithelial downgrowth was observed around four implants. Small areas of nonmineralized bone in contact with the implant were noticed in the apical portion of two implants. One implant was almost entirely colonized by bacterial plaque with the exception of its apical portion, where bone‐implant contact was observed. The stable implant was characterized by bone‐implant contact. Conclusion: Altogether clinical, radiographic, and histologic findings indicated that two major etiologic factors might have been implicated in the failure process of the investigated implants: excessive occlusal load in relation to the bone‐supporting capacity and, in two cases, infection.

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DOI: 10.1111/j.1708-8208.2000.tb00103.x


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<term>Oral maxillofac implants</term>
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<term>Fistula</term>
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<term>Goteborg university</term>
<term>Ground sections</term>
<term>Hirsch lekholm</term>
<term>Histological evaluation</term>
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<term>Histopathologic observations</term>
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<term>Implant failures</term>
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<term>Inflammation</term>
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<term>Interface</term>
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<div type="abstract" xml:lang="en">Background: Despite good success rates of osseointegrated oral implants, failures do occur. To minimize losses, failure mechanisms should be elucidated. Purpose: This study sought to describe the morphology of tissues surrounding late failed Brånemark implants in relation to their clinical and radiographic findings to acquire a better understanding of the etiologic factors. Material and Methods: Ten failed implants and their surrounding tissues were consecutively retrieved from nine patients after prosthesis placement (late losses). On radiographs, a radiolucent line was visible around nine clinically mobile implants. Tightening of the abutment screw evoked pain at seven mobile implants. Clinically, no other visual inflammatory sign or symptom was manifest. A fistula originated from one stable implant, surrounded on radiographs by a diffuse bone rarefaction. Retrieved implants were electrochemically dissolved. Intact tissue‐implant thin (1 μm) and ultrathin (70–80 nm) sections were analyzed with light and transmission electron microscopy. Results: Peri‐implant marginal tissues displayed moderate inflammatory infiltrates located adjacent to and beneath the junctional epithelium. One patient affected by oral lichen planus displayed an intense lymphocyte/plasma cell‐dominated immune reaction. Deep peri‐implant tissues surrounding mobile implants consisted of a dense, fibrous tissue capsule with minimal inflammation. Epithelial downgrowth was observed around four implants. Small areas of nonmineralized bone in contact with the implant were noticed in the apical portion of two implants. One implant was almost entirely colonized by bacterial plaque with the exception of its apical portion, where bone‐implant contact was observed. The stable implant was characterized by bone‐implant contact. Conclusion: Altogether clinical, radiographic, and histologic findings indicated that two major etiologic factors might have been implicated in the failure process of the investigated implants: excessive occlusal load in relation to the bone‐supporting capacity and, in two cases, infection.</div>
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