Volume 133, Number 1 • Letters REFERENCES 1. Tanaka SA, Mahabir RC, Jupiter DC, Menezes JM. Updating the epidemiology of isolated cleft palate. Plast Reconstr Surg. 2013;131:650e–652e. 2. Tanaka SA, Mahabir RC, Jupiter DC, Menezes JM. Updating the epidemiology of cleft lip with or without cleft palate. Plast Reconstr Surg. 2012;129:511e–518e.
The Effect of Platelet-Rich Plasma on Flap Survival in Random Extension of an Axial Pattern Flap in Rabbits Sir: read with great interest the article by Kim et al. This article was published in July of 2013 and concerns the effect of platelet-rich plasma on flap survival.1 The authors nicely showed that platelet-rich plasma can improve flap survival area. I would like to complete the discussion of Kim and colleagues by introducing a major complementary route through which platelet-rich plasma could reduce flap necrosis. There is a growing body of evidence that a significant portion of flap necrosis is triggered by a sequence of events associated with reperfusion of ischemic tissues, termed “reperfusion injury.”2 The major explanation for reperfusion phenomena is up-regulation of surface adhesion molecules on the vascular endothelium with subsequent adherence and accumulation of polymorphonuclear leukocytes within the vessel lumen. Adherence of polymorphonuclear leukocytes is mediated predominantly by beta-2 integrins (CD11/CD18) on their surface through activation of the NF-kappaB/RANKL pathway.3 Osteoprotegerin, which is a decoy receptor of RANKL, can block the NF-kappaB/RANKL pathway.4 Platelet-rich plasma, which is also called platelet gel, effectively stimulates osteoprotegerin production, leading to significant block of the beta-2 integrin/ NFkappaB/RANKL pathway, which subsequently leads to decreased polymorphonuclear leukocyte aggregation and reperfusion injury.5 Therefore, this important mechanism should be borne in mind as the major complementary mechanism for platelet-rich plasma– reduced flap necrosis.
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DOI: 10.1097/01.prs.0000436527.70708.07
Hamid Namazi, M.D.
Department of Orthopedic Surgery Shiraz University of Medical Sciences Shiraz, Islamic Republic of Iran [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication. REFERENCES 1. Kim HY, Park JH, Han YS, Kim H. The effect of platelet-rich plasma on flap survival in random extension of an axial pattern flap in rabbits. Plast Reconstr Surg. 2013;132:85–92.
2. Freitas FA, Piccinato CE, Cherri J, Marchesan WG. Effects of pentoxyfilline and heparin on reperfusion injury island skin flaps in rats exposed to tobacco. J Surg Res. 2010;164:139–145. 3. Kim CH, Lee KH, Lee CT, et al. Aggregation of beta2 integrins activates human neutrophils through the IkappaB/NFkappaB pathway. J Leukoc Biol. 2004;75:286–292. 4. Nelson CA, Warren JT, Wang MW, Teitelbaum SL, Fremont DH. RANKL employs distinct binding modes to engage RANK and the osteoprotegerin decoy receptor. Structure 2012;20:1971–1982. 5. Ogino Y, Ayukawa Y, Kukita T, Atsuta I, Koyano K. Platelet-rich plasma suppresses osteoclastogenesis by promoting the secretion of osteoprotegerin. J Periodontal Res. 2009;44:217–224.
Reply: The Effect of Platelet-Rich Plasma on Flap Survival in Random Extension of an Axial Pattern Flap in Rabbits Sir:
We appreciate Dr. Namazi for his interest in our recently published article. Ischemia-reperfusion injury can be the basis of many clinical disorders, including myocardial infarction and stroke. In the field of plastic surgery, it is the major cause of complications that cause cellular and tissue organ injuries during flap surgery. Reperfusion injury has been known to be caused by the accumulation of neutrophils, and some studies have shown that tissue necrosis of the pedicle flap is reduced by blocking the aggregation of neutrophils.1 Other than our research, studies that applied platelet-rich plasma to a flap have recently been reported and explain the mechanism as angiogenesis.2 When we proposed the hypothesis, we assumed that arteriogenesis and angiogenesis, which dilate the choke vessel, were the major mechanisms, but we did not hypothesize that platelet-rich plasma could reduce the reperfusion injury. We thank Dr. Namazi, who proposed another important mechanism that enabled platelet-rich plasma to reduce flap necrosis. Platelet-rich plasma’s reduction of reperfusion injury had already been experimentally proven through the reduction of the size of myocardial infarction in rabbits.3 Although it had not been proven that platelet-rich plasma reduces reperfusion injury in flap surgery, we believe that the topic is significant enough to be the subject of experiments. DOI: 10.1097/01.prs.0000436819.41956.18
Hyo Young Kim, M.D. Jin Hyung Park, M.D., Ph.D. Yea Sik Han, M.D., Ph.D. Department of Plastic and Reconstructive Surgery Kosin University College of Medicine Busan, Republic of Korea Correspondence to Dr. Han Department of Plastic and Reconstructive Surgery Kosin University College of Medicine 34 Amnam-dong Seo-gu, Busan 602-702, Republic of Korea [email protected]
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The Effect of Platelet-Rich Plasma on Flap Survival in Random Extension of an Axial Pattern Flap in Rabbits Sir: read with great interest the article by Kim et al. This article was published in July of 2013 and concerns the effect of platelet-rich plasma on flap survival.1 The authors nicely showed that platelet-rich plasma can improve flap survival area. I would like to complete the discussion of Kim and colleagues by introducing a major complementary route through which platelet-rich plasma could reduce flap necrosis. There is a growing body of evidence that a significant portion of flap necrosis is triggered by a sequence of events associated with reperfusion of ischemic tissues, termed “reperfusion injury.”2 The major explanation for reperfusion phenomena is up-regulation of surface adhesion molecules on the vascular endothelium with subsequent adherence and accumulation of polymorphonuclear leukocytes within the vessel lumen. Adherence of polymorphonuclear leukocytes is mediated predominantly by beta-2 integrins (CD11/CD18) on their surface through activation of the NF-kappaB/RANKL pathway.3 Osteoprotegerin, which is a decoy receptor of RANKL, can block the NF-kappaB/RANKL pathway.4 Platelet-rich plasma, which is also called platelet gel, effectively stimulates osteoprotegerin production, leading to significant block of the beta-2 integrin/ NFkappaB/RANKL pathway, which subsequently leads to decreased polymorphonuclear leukocyte aggregation and reperfusion injury.5 Therefore, this important mechanism should be borne in mind as the major complementary mechanism for platelet-rich plasma– reduced flap necrosis.
I
DOI: 10.1097/01.prs.0000436527.70708.07
Hamid Namazi, M.D.
Department of Orthopedic Surgery Shiraz University of Medical Sciences Shiraz, Islamic Republic of Iran [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication. REFERENCES 1. Kim HY, Park JH, Han YS, Kim H. The effect of platelet-rich plasma on flap survival in random extension of an axial pattern flap in rabbits. Plast Reconstr Surg. 2013;132:85–92.
2. Freitas FA, Piccinato CE, Cherri J, Marchesan WG. Effects of pentoxyfilline and heparin on reperfusion injury island skin flaps in rats exposed to tobacco. J Surg Res. 2010;164:139–145. 3. Kim CH, Lee KH, Lee CT, et al. Aggregation of beta2 integrins activates human neutrophils through the IkappaB/NFkappaB pathway. J Leukoc Biol. 2004;75:286–292. 4. Nelson CA, Warren JT, Wang MW, Teitelbaum SL, Fremont DH. RANKL employs distinct binding modes to engage RANK and the osteoprotegerin decoy receptor. Structure 2012;20:1971–1982. 5. Ogino Y, Ayukawa Y, Kukita T, Atsuta I, Koyano K. Platelet-rich plasma suppresses osteoclastogenesis by promoting the secretion of osteoprotegerin. J Periodontal Res. 2009;44:217–224.
Reply: The Effect of Platelet-Rich Plasma on Flap Survival in Random Extension of an Axial Pattern Flap in Rabbits Sir:
We appreciate Dr. Namazi for his interest in our recently published article. Ischemia-reperfusion injury can be the basis of many clinical disorders, including myocardial infarction and stroke. In the field of plastic surgery, it is the major cause of complications that cause cellular and tissue organ injuries during flap surgery. Reperfusion injury has been known to be caused by the accumulation of neutrophils, and some studies have shown that tissue necrosis of the pedicle flap is reduced by blocking the aggregation of neutrophils.1 Other than our research, studies that applied platelet-rich plasma to a flap have recently been reported and explain the mechanism as angiogenesis.2 When we proposed the hypothesis, we assumed that arteriogenesis and angiogenesis, which dilate the choke vessel, were the major mechanisms, but we did not hypothesize that platelet-rich plasma could reduce the reperfusion injury. We thank Dr. Namazi, who proposed another important mechanism that enabled platelet-rich plasma to reduce flap necrosis. Platelet-rich plasma’s reduction of reperfusion injury had already been experimentally proven through the reduction of the size of myocardial infarction in rabbits.3 Although it had not been proven that platelet-rich plasma reduces reperfusion injury in flap surgery, we believe that the topic is significant enough to be the subject of experiments. DOI: 10.1097/01.prs.0000436819.41956.18
Hyo Young Kim, M.D. Jin Hyung Park, M.D., Ph.D. Yea Sik Han, M.D., Ph.D. Department of Plastic and Reconstructive Surgery Kosin University College of Medicine Busan, Republic of Korea Correspondence to Dr. Han Department of Plastic and Reconstructive Surgery Kosin University College of Medicine 34 Amnam-dong Seo-gu, Busan 602-702, Republic of Korea [email protected]
69e
