Possible molecular mechanism of promotion of repair of acute Achilles tendon rupture by low intensity-pulsed ultrasound treatment in a rat model.

Author: Kosaka T, Masaoka T, Yamamoto K.
Affiliation:
Department of Orthopaedic Surgery, Tokyo Medical University, Tokyo, Japan. tikosaka@h6.dion.ne.jp
Conference/Journal: West Indian Med J.
Date published: 2011 Jun
Other: Volume ID: 60 , Issue ID: 3 , Pages: 263-8 , Word Count: 238


OBJECTIVE:
This study investigated the effect of Low Intensity-pulsed Ultrasound (LIPUS) on the repair process of ruptured Achilles tendon using a rat model and also examined the regulation of a biological molecule that may contribute to this in vivo and in vitro.
METHODS:
To investigate the effect of LIPUS and its biological mechanism of promoting Achilles tendon repair after acute injury, ninety-eight male Sprague-Dawley (SD) rats (mean body weight, 258 +/- 9.8 g) aged 12 weeks were used in this study. To create the model, the Achilles tendon attachment site and musculotendinous junction were ruptured under direct vision. The leg on one side was exposed to LIPUS (frequency at 1.5 MHz, the repetition cycle at 1.0 kHz, the burst width at 200 msec and the power output at 45 mW/cm2), for 20 minutes daily with a 0.7 mm diameter probe.
RESULTS:
Low Intensity-pulsed Ultrasound treatment accelerated the repair of the Achilles tendon compared to the untreated group, judged by electron microscopy. Both cyclo-oxygenase (COX)-2* and EP4* expressions were over-expressed in the LIPUS treated group in the inflammatory period, and TGFbeta1* expression was markedly induced in LIPUS treated groups followed by collagen I* and II* expression in the repair and reconstitution process.
CONCLUSION:
These findings suggest that LIPUS is potentially able to accelerate the repair of acute ruptured Achilles tendon in several ways: by exaggerating inflammation by inducing COX-2 and EP4 and reconstituting tissue by inducing TGFbeta1 followed by collagen I and III. (*: p < 0.05, **: 0.001).
PMID: 22224336

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