Williams, R. J., III, Attia, E., Wickiewicz, T. L., & Hannafin, J. A. (2000). The effect of ciprofloxacin on tendon, paratenon, and capsular fibroblast metabolism. Am J Sports Med, 28(3), 364-369.

BACKGROUND

For some time there has been evidence that a particular family of antibiotics known as fluoroquinolones may produce chronic tendon degeneration and tendon ruptures. However, the mechanism by which this occurs is not well understood. This study was an effort to determine the mechanism underlying the fluoroquinolone-induced tendinopathy. The particular fluoroquinolone used in this study was ciprofloxacin, one of the most commonly used in this family of antibiotics. Ciprofloxacin has the highest number of reported cases involving tendon pathology of any of the fluoroquinolone family of antibiotics. There are other fluoroquinolones that have also been associated with tendon pathology, including ofloxacin and norfloxacin.

These antibiotics are most commonly used to treat upper respiratory, urinary tract, and intestinal infections. They are a highly effective medication for that purpose. Shortly after their introduction there were reports surfacing of people having unexplained tendon pathologies, such as tendinitis and tendon ruptures, without engaging in any increased levels of activity or repetitive overuse. The most commonly affected tendon sites are the Achilles, rotator cuff, long head of the biceps brachii, and patellar tendons. A similar feature of all these tendons is that they all have high tensile loads placed on them.

Tendons from individuals who have experienced tendon pathology from fluoroquinolones have been examined and they reveal irregular collagen alignment. This suggests that ciprofloxacin may adversely affect fibroblast function in the tendon. In this study tendon tissue was placed in a solution that contained ciprofloxacin and the effect of the solution on the tendon fibers was recorded.

RESULTS AND DISCUSSION

After exposing tendon tissue to ciprofloxacin, the authors found that this antibiotic has a direct effect on fibroblast metabolism in the tendon tissue. They found increased matrix-degrading activity, decreased matrix synthesis, and decreased cell proliferation within the tendon tissue.

Varying levels of ciprofloxacin concentration were used to determine if these effects only occurred at very high dosage levels. The most profound effects were observed at high concentration levels, but most of the detrimental effects were observed at all drug concentrations. This means that even small amounts of the fluoroquinolone family of antibiotics could cause tendon pathology.

Most tendon pathologies are ascribed to repetitive overuse. However the problem with this particular family of antibiotics indicates that there may be an underlying pathological process that is not related to overuse at all. It is unclear whether the common methods of treating tendon pathology, such as deep transverse friction massage, would have any beneficial effect on tendon degeneration that is induced by antibiotics. That would be a valuable topic for future study. Yet, what is apparent from this report is that a more detailed questioning of our client’s history should look for involvement of fluoroquinolones when there is tendon pathology, especially if that tendon pathology does not appear to be associated with any repetitive overuse or significant change in activity levels.

It was assumed that the manner in which the tendon tissue was put in contact with the fluoroquinolone antibiotic medication in the laboratory would simulate the tendon’s exposure to the antibiotic in the body. However, this is an assumption, and we can’t be sure that this simulated laboratory environment duplicates exactly what happens in the body. Further investigation will be necessary to determine if tendon fibroblast function in the body is impaired the same way as in this laboratory experiment.

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