We report our experience with the Ilizarov apparatus in performing ankle arthrodesis in 6 patients. The average age of the patients was 52 (42-60) years. 3 patients had posttraumatic arthrosis and active infection of the ankle or distal tibia and the other 3 had posttraumatic arthrosis of the ankle without infection. Solid and painless arthrodesis was achieved in all patients in 7-15 weeks, including those with an active infection or failed multiple previous operations. While the method is useful for primary treatment of ankle arthrosis, we think it is better for treatment of certain complicated cases. n Painful ankle arthrosis that is refractory to medical treatment is the commonest indication for arthrodesis of the ankle joint. Ilizarov and Okulov (1976) originally proposed a method for performing ankle arthrodesis which, however, did not gain much popularity and only a few reports on it have been published. Hawkins et al. (1994) performed ankle arthrodesis with the Ilizarov apparatus in 21 patients having complex distal tibial pathology or previous failed ankle arthrodesis. They obtained good results in 16 of their patients. Johnson et al. (1992) treated another 6 patients. Tibiotalar fusion occurred at an average of 7 months in 3 of 4 infected patients with previous failed ankle arthrodesis, while the 2 primary ankle fusions healed at an average of 3.5 monthsWe have prospectively analyzed the results of the Ilizarov method for ankle arthrodesis in our institution. Patients and methodsAll 6 patients (4 men) who underwent tibiotalar arthrodesis by the Ilizarov method in our department during 1994-1998 were included in this study. They were under the care of MY who operated on them all. The average age was 52 (42-60) years. The average hospital stay was 10 (6-20) days, and they were followed in the outpatient clinic for an average of 36 (3-48) months (Table).3 patients had posttraumatic arthrosis of the ankle, following bimalleolar, trimalleolar or pilon fractures on average 12 (1-30) years before the arthrodesis. 2 of them had previously undergone surgery (internal fixation of the fracture, and the hardware had been removed in both) and 1 had been treated with a plaster cast. 1 patient had undergone open reduction and internal fixation of a distal tibial fracture and hardware removal 10 years earlier. This patient had chronic osteomyelitis of the distal tibia and severe arthrosis of the ankle, and had undergone several operations with debridement and drainage ( Figure). 2 patients had undergone open reduction and internal fixation of open trimalleolar fractures of the ankle 2 months earlier, and the hardware had been removed. Both had active wound and joint infections. Operative techniqueArthrotomy was performed through a lateral incision and an oblique distal fibulotomy. Debridement of devitalized tissue and irrigation were performed when there was an infection. Articular cartilage was removed with an osteotome, with preservation of as much bone as possible. The

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Parathyroid hormone-related (PTHrP), the major mediator of humoral hypercalcemia of malignancy, may also regulate placental calcium flux, uterine contraction and fetal tissue development. In the present study, we demonstrated that the mean immunoreactive PTHrP concentrations in amniotic fluid at mid-gestation (21.2 +/- 3.7 pmol/l) and at term (19.0 +/- 2.7 pmol/l) were 13-16-fold higher than levels measured in either fetal (1.6 +/- 0.1 pmol/l) or maternal plasma (1.4 +/- 0.3 pmol/l) at term and equal to levels found in plasma of patients with humoral hypercalcemia of malignancy. In vitro studies pointed to three possible sources of PTHrP in amniotic fluid: cultured amniotic fluid cells, cells derived from the amniotic membrane overlying the placenta and placental villous core mesenchymal cells. Treatment of cultured amniotic fluid cells with human prolactin, human placental lactogen (hPL) or human growth hormone (100 micrograms/l) increased PTHrP secretion after 24 h by 43%, 109% and 90%, respectively. Insulin-like growth factors I and II (100 micrograms/l), insulin (100 micrograms/l) and epidermal growth factor (EGF) (10 micrograms/l) increased PTHrP secretion by 53%, 46%, 68% and 118%, respectively. The stimulation of PTHrP secretion by EGF or by hPL was both time- and dose-dependent. In contrast, calcitriol and dexamethasone (10 nmol/l) decreased PTHrP secretion by 32% and 75%, respectively. Estradiol, progesterone, dihydrotestosterone and human chorionic gonadotropin had no effect on PTHrP secretion. These findings support the notion that PTHrP may play a physiological role in the uteroplacental unit and demonstrate that human amniotic fluid cells could be a useful model for studying the regulation of PTHrP production and secretion by hormones and growth factors.

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