Anatomic reconstruction of neglected Achilles tendon rupture with autogenous peroneal longus tendon by EndoButton fixation.

BACKGROUND: Neglected or chronic rupture of the Achilles tendon usually needs a reconstruction procedure. Many graft sources have been reported for this procedure, such as a proximal V-Y gastrocnemius tendon flap, flexor hallucis longus tendon, fascia lata, plantaris tendon, synthetic materials, and peroneus brevis. However, how to fix the graft at the calcaneal site remains controversial. METHODS: An alternative technique to anatomically reconstruct the Achilles tendon using an autogenous peroneal longus tendon with EndoButton-CL fixation at the calcaneal site for treatment of a patient who had a chronic neglected rupture of the Achilles tendon is described. RESULTS: The patient was allowed to begin gentle exercise, such as swimming and cycling 12 weeks after surgery, and encouraged to augment rehabilitation of hindfoot eversion and ankle plantar flexion. The ankle plantar flexion and hindfoot eversion strength was not reduced after active rehabilitation in 2.5 years of follow-up. CONCLUSIONS: Our technique reuses two small central incisions, thus, preserving skin integrity as much as possible to reduce wound breakdown or infection. The management of chronic or neglected Achilles tendon rupture by autogenous peroneal longus tendon with EndoButton-CL fixation at the calcaneal site is an anatomic and safe, but technically demanding technique.

Restoration of skin pigmentation after deep partial or full-thickness burn injury.

Significant skin pigmentation changes occur when patients suffer deep burn injuries. These pigmentation disorders may cause not only cosmetic and psychological issues, but more importantly it increases the risk of skin cancer or photoaging. Severe burns significantly effect on the process of repigmentation as the pigmentation is tightly regulated by cell proliferation and differentiation of melanocytes and melanocyte stem cells which are housing in the epidermis and hair follicles of the skin. In the present review, we discuss the possible mechanisms to replenish the melanocytes from the healthy epidermis and hair follicles surrounding burn wounds. The molecular mechanisms of skin repigmentation following healing of burn injuries includes the differentiation of melanoblasts into melanocytes, the distribution and responses of melanocytes and melanocyte stem cells after burn injury, and the regulation of melanin production. We also reviewed advanced therapeutic strategies to treat pigmentation disorders, such as convectional surgery, laser, UV treatment and emerging concepts in skin tissue-engineering.

Probing the Effects and Mechanisms of Electroacupuncture at Ipsilateral or Contralateral ST36-ST37 Acupoints on CFA-induced Inflammatory Pain.

Transient receptor potential vanilloid 1 (TRPV1) and associated signaling pathways have been reported to be increased in inflammatory pain signaling. There are accumulating evidences surrounding the therapeutic effect of electroacupuncture (EA). EA can reliably attenuate the increase of TRPV1 in mouse inflammatory pain models with unclear signaling mechanisms. Moreover, the difference in the clinical therapeutic effects between using the contralateral and ipsilateral acupoints has been rarely studied. We found that inflammatory pain, which was induced by injecting the complete Freund's adjuvant (CFA), (2.14 ± 0.1, p < 0.05, n = 8) can be alleviated after EA treatment at either ipsilateral (3.91 ± 0.21, p < 0.05, n = 8) or contralateral acupoints (3.79 ± 0.25, p < 0.05, n = 8). EA may also reduce nociceptive Nav sodium currents in dorsal root ganglion (DRG) neurons. The expression of TRPV1 and associated signaling pathways notably increased after the CFA injection; this expression can be further attenuated significantly in EA treatment. TRPV1 and associated signaling pathways can be prevented in TRPV1 knockout mice, suggesting that TRPV1 knockout mice are resistant to inflammatory pain. Through this study, we have increased the understanding of the mechanism that both ipsilateral and contralateral EA might alter TRPV1 and associated signaling pathways to reduce inflammatory pain.