Effect of hydrogen intervention on refractory wounds after radiotherapy:A case report

BACKGROUND Patients with keloids who receive radiotherapy(RT)after surgery can develop refractory wounds that cannot be healed by the patient's own repair system.Such chronic wounds are uneven and complex due to persistent abscess and ulceration.Without external intervention,they can easily result in local tissue necrosis or,in severe cases,large area tissue resection,amputation,and even death.CASE SUMMARY This article describes the use of hydrogen to treat a 42-year-old female patient with a chronic wound on her left shoulder.The patient had a skin graft that involved implanting a dilator under the skin of her left shoulder,and then transferring excess skin from her shoulder onto scar tissue on her chest.The skin grafting was followed by two rounds of RT,after which the shoulder wound had difficulty healing.For six months,the patient was treated with 2 h of hydrogen inhalation(HI)therapy per day,in addition to application of sterile gauze on the wound and periodic debridement.We also performed one deep,large,sharp debridement to enlarge the wound area.The wound healed completely within 6 mo of beginning the HI treatment.CONCLUSION After HI therapy,the patient showed superior progress in reepithelialization and wound repair,with eventual wound closure in 6 mo,in comparison with the previous failures of hyperbaric oxygen and recombinant bovine basic fibroblast growth factor therapies.Our work showed that HI therapy could be a new strategy for wound healing that is cleaner,more convenient,and less expensive than other therapies,as well as easily accessible for further application in clinical wound care.

Wound Closure on the Neonatal Rat Skin II. The Potential Ability of Epidermis to Close Small-Sized Wounds Independently of the Underlying Dermis

Reepithelialization of skin which comprises epidermis and dermis has not been fully elucidated due to the complexity of the participants as well as the interactions therein. In this study, the intrinsic roles and behaviors of epidermis itself during wound closure on neonatal rat skin were explored by developing and utilizing a novel in vivo wound model, termed “shallow incisional wound” in which the injury of dermis was minimized. The shallow wounds were closed by 12 h postwounding (PW) by the migration of the wound-marginal epidermal sheets in which activated myosin light chain (p-MLC) was predominantly detected at the lateral plasma membrane of individual cells. By local administration of Rho-associated protein kinase (ROCK) inhibitor Y27632, p-MLC disappeared at the wound margin and wounds were not closed by 12 h PW. Inhibition of Rac 1 by NSC23766 also resulted in hold of wound closure by 12 h PW, though NSC23766 somewhat slowly acted on p-MLC expression. These results suggest that, without joining of dermis, epidermal cells have a potential ability of closing wounds by active epithelial sheet movement integrated by Rho family small GTPases-dependent extension and contraction of the individual cell bodies.

Wound Closure on the Neonatal Rat Skin I. The Modulation of the Thickness of Epidermis at the Closing Incisional Wounds

Full-thickness incisional wounds were made on the dorsal skin of 1-day-old rats to elucidate the mechanism of the fluctuation of the epidermal thickness after the wound closure. The thickness of the epidermis covering the wound reached a peak around 96 h post-wounding (PW), and became thinner thereafter. The analyses of the cell proliferation and apoptosis at the epidermal wound regions revealed that the rate of TUNEL-positive cells that displays the cells undergoing apoptosis increased as the epidermis became thinner around 120 h PW. Next, immunohistochemical analyses using antibodies against keratinocyte differentiation marker proteins indicated that the delay or interruption of the spinous to granular transition from 96 to 120 h PW might result in the epidermal thickening in the wound region. Third, the region undyed with anti-caspase-14 antibody extended downward in the thickened epidermis by 96 h PW, and in turn, it became intensely and widely stained with this antibody in the thinning epidermis by 120 h PW. Taken together, it is likely that the delay and acceleration of the terminal differentiation, including cornification of the epidermal keratinocytes may coordinately cause the fluctuation of the thickness of the epidermis at the wound site in rat neonates.