EFFECT OF EXTRACORPOREAL SHOCK WAVE THERAPY ON DIABETIC CHRONIC WOUND HEALING AND ITS HISTOLOGICAL FEATURES_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

YAN Xiaoyu , YANG Guang , CHENG Liang , CHEN Ming , CHENG Xiangguo , CHAI Yimin , LUO Congfeng , ZENG Bingfang.

Corresponding author: ZENG Bingfang, E-mail: bingfangz@yahoo.com.cn;

Corresponding author：

Keywords：

Extracorporeal shock wave; Diabetic chronic wound; Angiogenesis; Wound healing; Rat

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Objective Extracorporeal shock wave (ESW) can promote angiogenesis and tissue repair. To investigate the influence of ESW therapy on the histological features of diabetic chronic wounds and wound healing. Methods Ninety-six male Sprague Dawley rats with weight (220 ± 20) g were divided into 3 groups (n=32): diabetic control group, ESW treatment group, and normal control group. The diabetic rats were prepared in diabetic control group and ESW treatment group by intraperitoneal injection of Streptozotocin (60 mg/kg). Then a circular full-thickness skin wound of 1.8 cm in diameter was made at the back of diabetic rats to establish the diabetic chronic wound model, and the same wound was made in normal control group. In ESW treatment group, ESW (0.11 mJ/mm2, 1.5 Hz energy, and 500 pulses) was applied to treat the wound at 1 day after wounding; in two control groups, no ESW treatment was given. The wound healing and histological changes were observed by HE and Masson staining at 3, 7, and 14 days after treatment; and the cell proliferation, angiogenesis, and collagen deposition were observed by CD31 and proliferating cell nuclear antigen (PCNA) immunohistochemical staining. Results The wound closure rate in diabetic control group was lower, and the healing time was significantly longer than those in normal control group (P lt; 0.05); at 3, 7, and 14 days after treatment, the inflammatory cell infiltration in wound tissue was obvious, and the relative area density of collagen fibers, wound microvessel density (MVD), and the relative density of PCNA-positive cells were significantly lower than those in normal control group (P lt; 0.05). The wound healing time was significantly shorter and the wound closure rate was significantly higher in ESW treatment group than those in the diabetic control group (P lt; 0.05). At different time points in ESW treatment group, the inflammatory cells signficantly reduced, while the relative area density of collagen fibers, MVD, and relative density of PCNA-positive cells significantly increased when compared with those in diabetic control group (P lt; 0.05). No significant difference in MVD and relative density of PCNA-positive cells was found between ESW treatment group and normal control group (P gt; 0.05). Conclusion Low-energy ESW treatment can inhibit the local inflammatory response, promote cell proliferation, increase angiogenesis and collagen deposition, and enhance granulation tissue formation, and so it can promote chronic wound healing in diabetic rats.

Citation： YAN Xiaoyu,YANG Guang,CHENG Liang,CHEN Ming,CHENG Xiangguo,CHAI Yimin,LUO Congfeng,ZENG Bingfang.. EFFECT OF EXTRACORPOREAL SHOCK WAVE THERAPY ON DIABETIC CHRONIC WOUND HEALING AND ITS HISTOLOGICAL FEATURES. Chinese Journal of Reparative and Reconstructive Surgery, 2012, 26(8): 961-967. doi: Copy

1.	Fard AS, Esmaelzadeh M, Larijani B. Assessment and treatment of diabetic foot ulcer. Int J Clin Pract, 2007, 61(11): 1931-1938.
2.	Chao YH, Tsuang YH, Sun JS, et al. Effects of shock waves on tenocyte proliferation and extracellular matrix metabolism. Ultrasound Med Biol, 2008, 34(5): 841-852.
3.	Speed CA. Extracorporeal shock-wave therapy in the management of chronic soft-tissue conditions. J Bone Joint Surg (Br), 2004, 86(2): 165-171.
4.	燕晓宇, 曾炳芳, 柴益民, 等. 低能量体外震波扩大随意皮瓣成活面积的实验研究. 中华显微外科杂志, 2008, 31(1): 43-46.
5.	Kuo YR, Wang CT, Wang FS, et al. Extracorporeal shock-wave therapy enhanced wound healing via increasing topical blood perfusion and tissue regeneration in a rat model of STZ-induced diabetes. Wound Repair Regen, 2009, 17(4): 522-530.
6.	Qureshi AA, Ross KM, Ogawa R, et al. Shock wave therapy in wound healing. Plast Reconstr Surg, 2011, 128(6): 721e-727e.
7.	Wang CJ, Kuo YR, Wu RW, et al. Extracorporeal shockwave treatment for chronic diabetic foot ulcers. J Surg Res, 2009, 152(1): 96-103.
8.	Wang CJ, Wu RW, Yang YJ. Treatment of diabetic foot ulcers: a comparative study of extracorporeal shockwave therapy and hyperbaric oxygen therapy. Diabetes Res Clin Pract, 2011, 92(2): 187-193.
9.	Moretti B, Notarnicola A, Maggio G, et al. The management of neuropathic ulcers of the foot in diabetes by shock wave therapy. BMC Musculoskelet Disord, 2009, 10: 54.
10.	Saggini R, Figus A, Troccola A, et al. Extracorporeal shock wave therapy for management of chronic ulcers in the lower extremities. Ultrasound Med Biol, 2008, 34(8): 1261-1271.
11.	Zins SR, Amare MF, Tadaki DK, et al. Comparative analysis of angiogenic gene expression in normal and impaired wound healing in diabetic mice: effects of extracorporeal shock wave therapy. Angiogenesis, 2010, 13(4): 293-304.
12.	Yang G, Luo C, Yan X, et al. Extracorporeal shock wave treatment improves incisional wound healing in diabetic rats. Tohoku J Exp Med, 2011, 225(4): 285-292.
13.	Junod A, Lambert AE, Stauffacher W, et al. Diabetogenic action of streptozotocin: relationship of dose to metabolic response. J Clin Invest, 1969, 48(11): 2129-2139.
14.	Chao CY, Cheing GL. Microvascular dysfunction in diabetic foot disease and ulceration. Diabetes Metab Res Rev, 2009, 25(7): 604-614.
15.	Laing T, Hanson R, Chan F, et al. The role of endothelial dysfunction in the pathogenesis of impaired diabetic wound healing: a novel therapeutic target? Med Hypotheses, 2007, 69(5): 1029-1031.
16.	Yavuz D, Tu?tepe H, Cetinel S, et al. Collagen ultrastructure and TGF-beta1 expression preserved with aminoguanidine during wound healing in diabetic rats. Endocrine research, 2005, 31(3): 229-243.
17.	Black E, Vibe-Petersen J, Jorgensen LN, et al. Decrease of collagen deposition in wound repair in type 1 diabetes independent of glycemic control. Arch Surg, 2003, 138(1): 34-40.
18.	Bermudez DM, Herdrich BJ, Xu J, et al. Impaired biomechanical properties of diabetic skin implications in pathogenesis of diabetic wound complications. Am J Pathol, 2011, 178(5): 2215-2223.
19.	Li J, Chen J, Kirsner R. Pathophysiology of acute wound healing. Clin Dermatol, 2007, 25(1): 9-18.
20.	Brem H, Tomic-Canic M. Cellular and molecular basis of wound healing in diabetes. J Clin Invest, 2007, 117(5): 1219-1222.
21.	Stadelmann WK, Digenis AG, Tobin GR. Physiology and healing dynamics of chronic cutaneous wounds. Am J Surg, 1998, 176(2A Suppl): 26S-38S.
22.	Velnar T, Bailey T, Smrkolj V. The wound healing process: an overview of the cellular and molecular mechanisms. J Int Med Res, 2009, 37(5): 1528-1542.
23.	Kalra B, Kalra S, Chatley G, et al. Rat bite as a cause of diabetic foot ulcer—a series of eight cases. Diabetologia, 2006, 49(6): 1452-1453.
24.	田晓红, 柏树令, 田伟, 等. 表皮干细胞在糖尿病创面愈合过程中的动态变化. 中国修复重建外科杂志, 2007, 21(7): 693-697.
25.	Martin A, Komada MR, Sane DC. Abnormal angiogenesis in diabetes mellitus. Med Res Rev, 2003, 23(2): 117-145.
26.	Roy H, Bhardwaj S, Yla-Herttuala S. Biology of vascular endothelial growth factors. FEBS Lett, 2006, 580(12): 2879-2887.
27.	Vetrano M, d’Alessandro F, Torrisi MR, et al. Extracorporeal shock wave therapy promotes cell proliferation and collagen synthesis of primary cultured human tenocytes. Knee Surg Sports Traumatol Arthrosc, 2011, 19(12): 2159-2168.
28.	Wang FS, Wang CJ, Sheen-Chen SM, et al. Superoxide mediates shock wave induction of ERK-dependent osteogenic transcription factor (CBFA1) and mesenchymal cell differentiation toward osteoprogenitors. J Biol Chem, 2002, 277(13): 10931-10937.
29.	Nurzynska D, Di Meglio F, Castaldo C, et al. Shock waves activate in vitro cultured progenitors and precursors of cardiac cell lineages from the human heart. Ultrasound Med Biol, 2008, 34(2): 334-342.
30.	Yu TC, Liu Y, Tan Y, et al. Shock waves increase T-cell proliferation or IL-2 expression by activating p38 MAP kinase. Acta Biochim Biophys Sin, 2004, 36(11): 741-748.

1. Fard AS, Esmaelzadeh M, Larijani B. Assessment and treatment of diabetic foot ulcer. Int J Clin Pract, 2007, 61(11): 1931-1938.
2. Chao YH, Tsuang YH, Sun JS, et al. Effects of shock waves on tenocyte proliferation and extracellular matrix metabolism. Ultrasound Med Biol, 2008, 34(5): 841-852.
3. Speed CA. Extracorporeal shock-wave therapy in the management of chronic soft-tissue conditions. J Bone Joint Surg (Br), 2004, 86(2): 165-171.
4. 燕晓宇, 曾炳芳, 柴益民, 等. 低能量体外震波扩大随意皮瓣成活面积的实验研究. 中华显微外科杂志, 2008, 31(1): 43-46.
5. Kuo YR, Wang CT, Wang FS, et al. Extracorporeal shock-wave therapy enhanced wound healing via increasing topical blood perfusion and tissue regeneration in a rat model of STZ-induced diabetes. Wound Repair Regen, 2009, 17(4): 522-530.
6. Qureshi AA, Ross KM, Ogawa R, et al. Shock wave therapy in wound healing. Plast Reconstr Surg, 2011, 128(6): 721e-727e.
7. Wang CJ, Kuo YR, Wu RW, et al. Extracorporeal shockwave treatment for chronic diabetic foot ulcers. J Surg Res, 2009, 152(1): 96-103.
8. Wang CJ, Wu RW, Yang YJ. Treatment of diabetic foot ulcers: a comparative study of extracorporeal shockwave therapy and hyperbaric oxygen therapy. Diabetes Res Clin Pract, 2011, 92(2): 187-193.
9. Moretti B, Notarnicola A, Maggio G, et al. The management of neuropathic ulcers of the foot in diabetes by shock wave therapy. BMC Musculoskelet Disord, 2009, 10: 54.
10. Saggini R, Figus A, Troccola A, et al. Extracorporeal shock wave therapy for management of chronic ulcers in the lower extremities. Ultrasound Med Biol, 2008, 34(8): 1261-1271.
11. Zins SR, Amare MF, Tadaki DK, et al. Comparative analysis of angiogenic gene expression in normal and impaired wound healing in diabetic mice: effects of extracorporeal shock wave therapy. Angiogenesis, 2010, 13(4): 293-304.
12. Yang G, Luo C, Yan X, et al. Extracorporeal shock wave treatment improves incisional wound healing in diabetic rats. Tohoku J Exp Med, 2011, 225(4): 285-292.
13. Junod A, Lambert AE, Stauffacher W, et al. Diabetogenic action of streptozotocin: relationship of dose to metabolic response. J Clin Invest, 1969, 48(11): 2129-2139.
14. Chao CY, Cheing GL. Microvascular dysfunction in diabetic foot disease and ulceration. Diabetes Metab Res Rev, 2009, 25(7): 604-614.
15. Laing T, Hanson R, Chan F, et al. The role of endothelial dysfunction in the pathogenesis of impaired diabetic wound healing: a novel therapeutic target? Med Hypotheses, 2007, 69(5): 1029-1031.
16. Yavuz D, Tu?tepe H, Cetinel S, et al. Collagen ultrastructure and TGF-beta1 expression preserved with aminoguanidine during wound healing in diabetic rats. Endocrine research, 2005, 31(3): 229-243.
17. Black E, Vibe-Petersen J, Jorgensen LN, et al. Decrease of collagen deposition in wound repair in type 1 diabetes independent of glycemic control. Arch Surg, 2003, 138(1): 34-40.
18. Bermudez DM, Herdrich BJ, Xu J, et al. Impaired biomechanical properties of diabetic skin implications in pathogenesis of diabetic wound complications. Am J Pathol, 2011, 178(5): 2215-2223.
19. Li J, Chen J, Kirsner R. Pathophysiology of acute wound healing. Clin Dermatol, 2007, 25(1): 9-18.
20. Brem H, Tomic-Canic M. Cellular and molecular basis of wound healing in diabetes. J Clin Invest, 2007, 117(5): 1219-1222.
21. Stadelmann WK, Digenis AG, Tobin GR. Physiology and healing dynamics of chronic cutaneous wounds. Am J Surg, 1998, 176(2A Suppl): 26S-38S.
22. Velnar T, Bailey T, Smrkolj V. The wound healing process: an overview of the cellular and molecular mechanisms. J Int Med Res, 2009, 37(5): 1528-1542.
23. Kalra B, Kalra S, Chatley G, et al. Rat bite as a cause of diabetic foot ulcer—a series of eight cases. Diabetologia, 2006, 49(6): 1452-1453.
24. 田晓红, 柏树令, 田伟, 等. 表皮干细胞在糖尿病创面愈合过程中的动态变化. 中国修复重建外科杂志, 2007, 21(7): 693-697.
25. Martin A, Komada MR, Sane DC. Abnormal angiogenesis in diabetes mellitus. Med Res Rev, 2003, 23(2): 117-145.
26. Roy H, Bhardwaj S, Yla-Herttuala S. Biology of vascular endothelial growth factors. FEBS Lett, 2006, 580(12): 2879-2887.
27. Vetrano M, d’Alessandro F, Torrisi MR, et al. Extracorporeal shock wave therapy promotes cell proliferation and collagen synthesis of primary cultured human tenocytes. Knee Surg Sports Traumatol Arthrosc, 2011, 19(12): 2159-2168.
28. Wang FS, Wang CJ, Sheen-Chen SM, et al. Superoxide mediates shock wave induction of ERK-dependent osteogenic transcription factor (CBFA1) and mesenchymal cell differentiation toward osteoprogenitors. J Biol Chem, 2002, 277(13): 10931-10937.
29. Nurzynska D, Di Meglio F, Castaldo C, et al. Shock waves activate in vitro cultured progenitors and precursors of cardiac cell lineages from the human heart. Ultrasound Med Biol, 2008, 34(2): 334-342.
30. Yu TC, Liu Y, Tan Y, et al. Shock waves increase T-cell proliferation or IL-2 expression by activating p38 MAP kinase. Acta Biochim Biophys Sin, 2004, 36(11): 741-748.

Chinese Journal of Reparative and Reconstructive Surgery

EFFECT OF EXTRACORPOREAL SHOCK WAVE THERAPY ON DIABETIC CHRONIC WOUND HEALING AND ITS HISTOLOGICAL FEATURES

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