Microbial differences in 2 clinically distinct types of failures of osseointegrated implants
Identifieur interne : 00B622 ( Main/Exploration ); précédent : 00B621; suivant : 00B623Microbial differences in 2 clinically distinct types of failures of osseointegrated implants
Auteurs : E. S. Rosenberg ; J. P. Torosian [États-Unis] ; J. SlotsSource :
- Clinical Oral Implants Research [ 0905-7161 ] ; 1991-07.
Abstract
The microflora associated with osseointegrated implants suspected of failing from infection or trauma were evaluated. Of 75 patients examined, 11 demonstrated failing fixtures. 22 of 48 fixtures failed in 6 fully edentulous patients and 10 of 34 failed in 5 partially edentulous patients. The etiology of failure was attributed to infection if there was bleeding, suppuration, pain, high plaque and gingival indices and granulomatous tissue upon surgical removal. Traumatic etiology was suspected in the absence of these signs. Direct phase‐contrast microscopy and culture analysis were performed on samples from the implant sulcus, the implant itself and the extraction socket. The 2 failure types exhibited distinct bacteriologic profiles. For implants failing with infection, spirochetes and motile rods averaged 42% of total morphotypes. Many suspected periodontopathic organisms including Peptostreptococcus micros, Fusobacterium species, enteric gram‐negative rods and yeasts, constituted high proportions of the cultivable microflora. In contrast, implants failing from suspected traumatic etiology demonstrated a morphotype profile consistent with periodontal health and cultivable microflora predominated by streptococci. When evaluating the time of failure after initial insertion, it was found that fixture loss resulting from infection occurred most often between initial placement and second‐stage surgery, whereas failure in the absence of infection occurred primarily after insertion of the final prosthesis. The terms infectious and traumatic failure have been introduced to describe these 2 clinically and microbiologically distinct phenomena.
Url:
DOI: 10.1034/j.1600-0501.1991.020306.x
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Slots</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:FF415F7ECFACF39E0D12BF528D450ACCDF0F6A52</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1034/j.1600-0501.1991.020306.x</idno><idno type="url">https://api.istex.fr/document/FF415F7ECFACF39E0D12BF528D450ACCDF0F6A52/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">007E22</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">007E22</idno><idno type="wicri:Area/Istex/Curation">007E22</idno><idno type="wicri:Area/Istex/Checkpoint">005562</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">005562</idno><idno type="wicri:doubleKey">0905-7161:1991:Rosenberg E:microbial:differences:in</idno><idno type="wicri:Area/Main/Merge">00BD31</idno><idno type="wicri:Area/Main/Curation">00B622</idno><idno type="wicri:Area/Main/Exploration">00B622</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Microbial differences in 2 clinically distinct types of failures of osseointegrated implants</title><author><name sortKey="Rosenberg, E S" sort="Rosenberg, E S" uniqKey="Rosenberg E" first="E. S." last="Rosenberg">E. S. Rosenberg</name><affiliation><wicri:noCountry code="subField">Medicine;</wicri:noCountry></affiliation></author><author><name sortKey="Torosian, J P" sort="Torosian, J P" uniqKey="Torosian J" first="J. P." last="Torosian">J. P. Torosian</name><affiliation></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Thomas Jefferson University, Philadelphia, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Slots, J" sort="Slots, J" uniqKey="Slots J" first="J." last="Slots">J. Slots</name><affiliation><wicri:noCountry code="subField">Medicine;</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Clinical Oral Implants Research</title><title level="j" type="alt">CLINICAL ORAL IMPLANTS RESEARCH</title><idno type="ISSN">0905-7161</idno><idno type="eISSN">1600-0501</idno><imprint><biblScope unit="vol">2</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="144">144</biblScope><publisher>Munksgaard International Publishers</publisher><pubPlace>Copenhagen</pubPlace><date type="published" when="1991-07">1991-07</date></imprint><idno type="ISSN">0905-7161</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0905-7161</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The microflora associated with osseointegrated implants suspected of failing from infection or trauma were evaluated. Of 75 patients examined, 11 demonstrated failing fixtures. 22 of 48 fixtures failed in 6 fully edentulous patients and 10 of 34 failed in 5 partially edentulous patients. The etiology of failure was attributed to infection if there was bleeding, suppuration, pain, high plaque and gingival indices and granulomatous tissue upon surgical removal. Traumatic etiology was suspected in the absence of these signs. Direct phase‐contrast microscopy and culture analysis were performed on samples from the implant sulcus, the implant itself and the extraction socket. The 2 failure types exhibited distinct bacteriologic profiles. For implants failing with infection, spirochetes and motile rods averaged 42% of total morphotypes. Many suspected periodontopathic organisms including Peptostreptococcus micros, Fusobacterium species, enteric gram‐negative rods and yeasts, constituted high proportions of the cultivable microflora. In contrast, implants failing from suspected traumatic etiology demonstrated a morphotype profile consistent with periodontal health and cultivable microflora predominated by streptococci. When evaluating the time of failure after initial insertion, it was found that fixture loss resulting from infection occurred most often between initial placement and second‐stage surgery, whereas failure in the absence of infection occurred primarily after insertion of the final prosthesis. The terms infectious and traumatic failure have been introduced to describe these 2 clinically and microbiologically distinct phenomena.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region></list><tree><noCountry><name sortKey="Rosenberg, E S" sort="Rosenberg, E S" uniqKey="Rosenberg E" first="E. S." last="Rosenberg">E. S. Rosenberg</name><name sortKey="Slots, J" sort="Slots, J" uniqKey="Slots J" first="J." last="Slots">J. Slots</name></noCountry><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Torosian, J P" sort="Torosian, J P" uniqKey="Torosian J" first="J. P." last="Torosian">J. P. Torosian</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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