M. Shakibaei et al., Ultrastructure of Achilles tendons of rats treated with ofloxacin and fed a normal or magnesium-deficient diet, ANTIM AG CH, 44(2), 2000, pp. 261-266
Fluoroquinolones can cause tendinitis and tendon rupture. However, toxicolo
gical as well as clinical information on quinolone-induced tendopathy is sc
arce. We performed extensive electron microscopic studies with Achilles ten
don specimens from ofloxacin-treated rats. The drug was given at a dose of
1,200 mg/kg (body weight) orally. Juvenile Wistar rats received one or thre
e oral doses each of 1,200 mg of ofloxacin/kg (body weight)/day, Three days
after treatment, the tenocytes of their Achilles tendons showed degenerati
ve alterations, such as multiple vacuoles and vesicles in the cytoplasm tha
t had developed due to swellings and dilatations of cell organelles. Other
indications of cell degradation were the occurrence of cell debris and cell
detachment from the extracellular matrix accompanied by a loss of cell-mat
rix interaction. The tenocytes of juvenile Wistar rats that had been treate
d at day 36 with a single oral dose of 1,200 mg of ofloxacin/kg (body weigh
t) and sacrificed either 3 or 6 months later exhibited similar degenerative
alterations. The number of degenerative alterations of tenocytes after ofl
oxacin treatment was considerably higher in rats that had received a magnes
ium-deficient diet than in rats with normal magnesium status. Of the adult
rats that had been treated once, 5 times, and 10 times with ofloxacin and k
illed 1 day Later, only those with the 10-times treatment showed a signific
antly increased number of degeneratively altered tenocytes. In summary, eff
ects observed in tendons show similar pathological features as described ea
rlier in cartilage, indicating that quinolone-induced arthropathy and quino
lone-induced tendopathy probably are different clinical manifestations of t
he same toxic effect on cellular components of connective tissue structures
.