An XPS and SEM evaluation of six chemical and physical techniques for cleaning of contaminated titanium implants

The purpose of the present study was to analyse clinically failed and retrieved implants prior to and after cleaning by means of scanning electron microscopy (SEM) and X-ray induced photoelectron spectroscopy (XPS) as compared to unused controls. Six different chemical and physical techniques for cleaning of contaminated titanium implants were evaluated: 1) rinsing in absolute ethanol for 10 min, 2) cleaning in ultrasonic baths containing trichloroethylene (TRI) and absolute ethanol, 10 min in each solution, 3) abrasive cleaning for 30 s, 4) cleaning in supersaturated citric acid for 30 s, 5) cleaning with continuous CO2-laser in dry conditions at 5 W for 10 s, 6) cleaning with continuous CO2-laser in wet conditions (saline) at 5 W for 10 s. SEM of failed implants showed the presence of contaminants of varying sizes and XPS showed almost no titanium but high carbon signals. XPS of unused titanium implants showed lower levels of titanium as previously reported, probably due to contamination of carbon which increased with time in room air. Cleaning of used implants in citric acid followed by rinsing with deionized water for 5 min followed by cleaning in ultrasonic baths with TRI and absolute ethanol gave the best results with regard to macroscopical appearance and surface composition. However, as compared to the unused implants the results from an element composition point of view were still unsatisfactory. It is concluded that further development and testing of techniques for cleaning of organically contaminated titanium is needed.     

Systemic and peritoneal host defense in peritonitis

Most of the work of host defense has been carried out in mixed patient populations. It is now clear that elective preoperative surgical patients have totally different host defense capabilities as compared to posttrauma patients or those suffering from peritonitis. Specific cell-mediated immune studies need to be repeated in these 2 patient groups as well. What will contribute clinical relevance to these studies will be the means to correct the defects. If these defects or—more correctly termed—abnormalities of host defense are, indeed, important and contribute to an increased sepsis rate and mortality from sepsis in affected patients, then correcting them should reduce these complications. This hypothesis can only be tested when such means become available. The issues of most interest in the next few years will be the significance of serum albumin in host outcome, the role of immunomodulators, the involvement of cytokines in the overall process of host defense, and the use of specific nutritional support regimens targeted to the immune system.

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Resumen La mayor parte del trabajo sobre los mecanismos de defensa del huésped ha sido realizada en poblaciones mixtas de pacientes. Actualmente aparece claro que los pacientes preoperatorios electivos poseen una capacidad de defensa de huésped totalmente diferente que la de los pacientes en estado posttrauma o de aquellos con peritonitis. Aparece necesario realizar estudios específicos de inmunidad celular en estos 2 grupos de pacientes; aquello que aporte pertinencia clínica en tales estudios habrá de representar medios para corregir estos defectos. Si tales defectos, mejor denominados anormalidades en las defensas del huésped, son de verdad importantes y contribuyen a mayores tasas de infección y de mortalidad por sepsis en los pacientes afectados, su corrección debe resultar en reducción de estas complicaciones. Esta hipótesis sólo puede ser puesta a prueba cuando tales medios se hallen disponibles. Los aspectos de mayor interés en los próximos años serán el significado de la albúmina sérica en la evolución final del huésped, el papel de los inmunomoduladores, la participación de las citocinas en el proceso general de defensa del huésped, y el uso de regimenes especificos de soporte nutricional dirigidos hacia el sistema inmune.

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Résumé La plupart des travaux sur les mécanismes de défense ont été faits sur les populations mixtes. Il est à présent certain que les patients opérés électivement ont des mécanismes de défense préopératoire totalement différents de ceux des traumatisés ou des patients ayant une infection péritonéale. Les études immunologiques sur la médiation cellulaire spécifique méritent d'être refaites chez ces deux populations. Ce qui ressortira de ces études donnera les moyens de corriger les défauts ou plutôt les anomalies des mécanismes de défense qui contribuent à augmenter septicité et mortalité en rapport avec l'état septique. Cette hypothèse ne peut être vérifiée qu'avec ces moyens. Les questions les plus intéressantes dans les années à venir sera peut-être de connaître l'influence de l'albumine sérique sur l'évolution, le rôle des immunomodulaterus, celui des cytokinines dans le procédé global des mécanismes de défense, et celui de l'utilisation de l'alimentation spécifique pour améliorer le système immune.

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Supported in part by grants from the Medical Research Council of Canada and the Fonds de recherche de Santé.     

Das Jo-1-Syndrom und seine klinischen Manifestationen

Namensgebend für das Jo-1-Syndrom sind Autoantikörper gegen das Jo-1-Antigen, die bei diesem Krankheitsbild im Serum der betroffenen Patienten nachgewiesen werden. Der Name Jo-1 leitet sich von dem ersten Patienten (John P.) ab, bei dem diese Antikörper gefunden wurden. Dieser Patient litt an einer Polymyositis und fibrosierenden Alveolitis. Das Jo-1-Antigen ist identisch mit der Histidyl-Transfer-RNA-Synthetase im Zytosol. Das Jo-1-Syndrom gehört zu einer Familie von Autoimmunerkrankungen, die als Anti-Synthetase- Syndrome bezeichnet werden. Diese Syndrome haben gemeinsam, dass jeweils Autoantikörper gegen unterschiedliche Aminosäure-Transfer-RNASynthetasen nachweisbar sind. Klinisch handelt es sich beim Jo-1-Syndrom um eine Sonderform der Poly- bzw. Dermatomyositis von bisher ungeklärter Ätiologie. Neben einer Muskelbeteiligung kommt es charakteristischerweise zu einer interstitiellen Lungenbeteiligung, die auch prognostisch das Krankheitsbild bestimmt. Zusätzlich können klinisch eine Polyarthritis und weitere Symptome bestehen, die dem klinischen Bild anderer Kollagenosen ähneln. Ebenso wie die Polymyositis und Dermatomyositis kann sich das Jo-1-Syndrom in sog. Myositis-Overlap-Syndromen präsentieren. Zu dieser Diagnose führt ein Symptomenkomplex, der die klare Zuordnung zu einer einzelnen Erkrankung nicht möglich macht. Häufig werden in solchen Fällen U1-RNP-Antikörper nachgewiesen. Therapeutisch spricht das Jo-1-Syndrom auf die Gabe von Kortikosteroiden und—falls notwendig—Azathioprin, Methotrexat und Cyclophosphamid an. Eine Kurzbeschreibung von zwei klinischen Fällen stellt das Krankheitsbild anschaulich dar.     

Immunology

A selection of interesting papers that were published in the two months before our press date in major journals most likely to report significant results in immunology.     

Successful Treatment of Kasabach-Merritt Syndrome with Prednisone and Epsilon-Aminocaproic Acid

The Kasabach-Merritt syndrome is characterized by thrombocytopenia and localized coagulopathy associated with a hemangioma. Most techniques applied to eradicate the tumor or accelerate its involution (surgery, radiation therapy, embolization) are invasive and require transfusion of large amounts of blood products. In some cases, medical treatment is the only alternative. Efficacy of steroids and antifibronolytic agents has already been described, but even this approach is associated with the administration of blood products. We report two cases of infants with Kasabach-Merritt syndrome associated with cardiac and hepatic hemangiomas. At admission, both had signs of cardiac failure. They were successfully treated with prednisone and epsilon-aminocaproic acid (EACA). Blood products were not required once the diagnosis was made. These observations have important implications for the management of patients with Kasabach-Merritt syndrome because they show that even in severe cases blood transfusions can be avoided by the use of prednisone and EACA.