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The influence of fluoride in poly(d,l-lactide)/apatite composites on ectopic bone formation was evaluated in sheep. Nano-apatite powders with different replacement levels of OH groups by fluoride (F) (0% (F0), 50% (F50), 100% (F100), and excessive (F200)) were co-extruded with poly (d,l-lactide) at a weight ratio of 1:1. Fluoride release from the composites (CF0, CF50, CF100, and CF200) was evaluated in vitro and bone formation was assessed after intramuscular implantation in sheep. After 24 weeks in simulated physiological solution, CF0 and CF50 showed negligible fluoride release, whereas it was considerable from the CF100 and CF200 composites. Histology showed that the incidence of de novo bone formation decreased in implants with increasing fluoride content indicating a negative influence of fluoride on ectopic bone formation. Furthermore, a significant decrease in resorption of the high fluoride-content composites and a reduction in the number of multinucleated giant cells were seen. These results show that instead of promoting, the presence of fluoride in poly(d,l-lactide)/apatite composites seemed to suppresses their resorption and osteoinductive potential in non-osseous sites.

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In the treatment of orbital floor fractures, bone is ideally regenerated. The materials currently used for orbital floor reconstruction do not lead to the regeneration of bone. Our objective was to render polymeric materials based on poly(trimethylene carbonate) (PTMC) osteoinductive, and to evaluate their suitability for use in orbital floor reconstruction. For this purpose, osteoinductive biphasic calcium phosphate (BCP) particles were introduced into a polymeric PTMC matrix. Composite sheets containing 50 wt% BCP particles were prepared. Also laminates with poly(D,L-lactide) (PDLLA) were prepared by compression moulding PDLLA films onto the composite sheets. After sterilisation by gamma irradiation, the sheets were used to reconstruct surgically-created orbital floor defects in sheep. The bone inducing potential of the different implants was assessed upon intramuscular implantation. The performance of the implants in orbital floor reconstruction was assessed by cone beam computed tomography (CBCT). Histological evaluation revealed that in the orbital and intramuscular implantations of BCP containing specimens, bone formation could be seen after 3 and 9 months. Analysis of the CBCT scans showed that the composite PTMC sheets and the laminated composite sheets performed well in orbital floor reconstruction. It is concluded that PTMC/BCP composites and PTMC/BCP composites laminated with PDLLA have osteoinductive properties and seem suitable for use in orbital floor reconstruction.

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To examine the effect of inhaled platelet-activating factor (PAF) on airway sensitivity and on maximal airway narrowing, we measured airway response to doubling concentrations of methacholine (MCh) 48 h before and 48 h after inhalation of 10, 50 and 100 micrograms of PAF in six nonatopic, nonasthmatic subjects. The forced expiratory volume in one second (FEV1) and airflow at 30 percent of vital capacity (V30) from partial forced expiration were used to assess changes in airway calibre. Inhalation of PAF caused only minor changes in FEV1. In contrast, inhalation of 100 micrograms of PAF caused a significant fall in V30 from 2.64 +/- 0.35 to 1.35 +/- 0.43 l.min-1 (p < 0.05). Two days after PAF inhalation a leftward shift of the concentration-response curve to MCh was observed. The MCh concentration causing a 20% fall in FEV1 (PC20FEV1) was 11.25 +/- 1.78 and 2.38 +/- 1.29 mg.ml-1 (geometric mean +/- GSEM; p < 0.05) before and after PAF inhalation, respectively. PAF did not affect the maximal airway response to MCh. The maximum percentage fall in FEV1 was 36.2 +/- 1.9% at baseline and 37.6 +/- 1.8% after PAF inhalation. Likewise, maximum percentage change in V30 was 72.8 +/- 3.7% at baseline and 73.6 +/- 3.4% after PAF inhalation. The results of this study show that PAF inhalation increases airway sensitivity without altering the maximal bronchoconstrictive response to MCh in normal subjects.

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Chronic endoscopic esophageal sclerotherapy represents a primary technique for the prevention of recurrent bleeding in cirrhotic patients who have already experienced one variceal bleeding episode. 131 patients with portal hypertension and a history of esophageal variceal bleeding underwent endoscopic sclerotherapy. 74 of these patients constituted a subgroup which was singled out for special analysis. In these patients, treatment had been started after conservative management of an acute bleeding episode had stopped the bleeding and follow-up data for at least 6 months were available. 90.5% of these patients had nonalcoholic etiology for their portal hypertension. 60.8% of patients developed recurrent varices and 11.1% had recurrent bleeding from esophageal varices. The bleeding risk index, calculated as the number of hemorrhages/patient/months of follow-up, correlated strongly with the number of previous hemorrhages and inversely with hepatic reserve (Child's class). The bleeding risk index decreased tenfold after sclerotherapeutic obliteration of varices. These data suggest that chronic elective endoscopic sclerotherapy may play a primary role in the management of patients who have bled from esophageal varices.

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Between June, 1984 and December, 1985, a total of 41 patients were enrolled in a prospective controlled randomized trial comparing prophylactic sclerotherapy and medical treatment for the prevention of the first esophageal variceal bleeding. All patients had nonalcoholic liver cirrhosis, fourth degree varices, and no past history of gastrointestinal bleeding. The patients were randomly assigned to the control group (20 patients) or to the sclerotherapy group (21 patients); most of the patients belonged to Child's classes A and B. After a mean follow-up of 16.8 months, there were 3 variceal bleeding episodes and a 10% mortality rate in the control group whereas neither hemorrhage nor death was observed in the sclerotherapy group. In the latter group, severe complications occurred in 9.5% of the patients; the rate of recurrence after eradication of esophageal varices was 40%. Although there were no statistically significant results, the favorable trend toward a lower bleeding risk and better survival observed in the treated patients suggests that a longer trial in a larger population of cirrhotic patients with a longer follow-up should be considered.

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We report the complications of perendoscopic sclerotherapy observed during treatment of oesophageal varices in 104 patients and 409 sclerotherapy sessions. Complications were related to each individual session and to the aim of the treatment (therapeutic or prophylactic). Major complications occurred in 17.3% of the patients treated: 13 cases of severe bleeding and 5 of oesophageal stricture. Conservative therapy stopped haemorrhage in all but 4 patients, who died of uncontrolled bleeding (3.8%). Three oesophageal strictures recovered spontaneously, while the remaining two required endoscopic dilations. Minor complications occurred after 102/409 sessions (24.9%). Epigastric and/or retrosternal pain developed after 17.6% of the sessions, oesophageal ulcerations after 12.5%, fever after 11.7% and transient dysphagia after 3.7%. Bleeding was observed only in Child's category C patients who underwent therapeutic treatment. The risk of bleeding remained unchanged until complete eradication of varices was achieved. The incidence of minor complications did not correlate with the progression or the aim of the treatment.

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