The Possible Protective Role of Magnesium on Ciprofloxacin Induced Chondrotoxicity on the Epiphyseal Plate Growth of Juvenile Albino Rat: A Histological and Morphometric Study

Abstract

Background: Ciprofloxacin is one of the most effective antibiotics used in the treatment of many infectious diseases in adults, but it has undesirable toxic effects on the growing cartilage. The present study was designed to detect the toxic effect of ciprofloxacin on growing cartilage in the immature albino rats and the possible protective role of magnesium in prevention of such toxicity. Methods: Seventy rats were used in the current study. They were divided into five groups Group I: control group, group II: ciprofloxacin treated group, group III: magnesium given before ciprofloxacin, group IV: ciprofloxacin with magnesium and group V: magnesium given after ciprofloxacin). The region of the knee joint was prepared and stained with hematoxylin and eosin stain for light microscopic examination. Morphometric studies were also done using the image analyzer. Results: ciprofloxacin treated group revealed different changes in the tibial epiphyseal growth plate of juvenile rats in the form of decreased thickness, loss of chondrocytes, karryorrhexis, pyknotic nuclei, interlacunar hemorrhage, irregularity in the columns and myxomatous degeneration. Partial improvement was observed in the group treated with magnesium before ciprofloxacin and in the group treated with magnesium concurrently with ciprofloxacin, meanwhile no improvement was detected in the group treated with magnesium given after ciprofloxacin. Conclusion: The present study concluded that the use of ciprofloxacin in juvenile rats caused epiphyseal plate growth retardation; accordingly the use of this drug in pediatrics should be restricted to carefully selected indications. Owing to its protective role in reducing such chondrotoxic effects, the use of magnesium before (in chronic cases like cystic fibrosis of the lung) and concomitantly with ciprofloxacin is highly recommended.