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.
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]
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Plastic and Reconstructive Surgery • January 2014 ACKNOWLEDGMENT This study was supported by a grant from Kosin University College of Medicine. DISCLOSURE The authors have no commercial associations that might pose or create a conflict of interest with information presented in this communication. REFERENCES 1. Vedder NB, Winn RK, Rice CL, et al. A monoclonal antibody to the adherence-promoting leukocyte glycoprotein, CD18, reduces organ injury and improves survival from hemorrhagic shock and resuscitation in rabbits. J Clin Invest. 1988;81:939–944. 2. Li W, Enomoto M, Ukegawa M, et al. Subcutaneous injections of platelet-rich plasma into skin flaps modulate proangiogenic gene expression and improve survival rates. Plast Reconstr Surg. 2012;129:858–866. 3. Hargrave B, Li F. Nanosecond pulse electric field activation of platelet-rich plasma reduces myocardial infarct size and improves left ventricular mechanical function in the rabbit heart. J Extra Corpor Technol. 2012;44:198–204.
Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos Sir:
W
e read with interest the article entitled “Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos” by Rozen and Lehrman.1 Although the methods were sound and the article was well written, the authors failed to mention that this surgical technique has been previously published. Tower and Dailey described almost the same technique in 2004.2 In their original description, they placed the gold weight in a postseptal location, sutured it to the levator aponeurosis, and closed the septum and skin. The current article differs only in the intraoperative adjustment of the weight and the closure of the orbicularis layer. Although this article provides a valuable contribution to the literature, it is incumbent on the authors to cite and credit the work of previous surgeons. DOI: 10.1097/01.prs.0000436807.42917.99
Brett W. Davies, M.D., M.S. Eric M. Hink, M.D. Vikram D. Durairaj, M.D. Oculofacial Plastic and Reconstructive Surgery University of Colorado Hospital Aurora, Colo. Correspondence to Dr. Davies Department of Oculofacial Plastic and Reconstrucive Surgery University of Colorado Hospital 1675 Aurora Court Aurora, Colo. 80045 [email protected]
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DISCLOSURE The authors have no financial interest to declare in relation to the content of this communication. REFERENCES 1. Rozen S, Lehrman C. Upper eyelid postseptal weight placement for treatment of paralytic lagophthalmos. Plast Reconstr Surg. 2013;131:1253–1265. 2. Tower RN, Dailey RA. Gold weight implantation: A better way? Ophthal Plast Reconstr Surg. 2004;20:202–206.
Reply: Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos Sir:
I would like to thank Drs. Davies, Hink, and Durairaj for their gracious comment. I read with great interest the article by Tower and Dailey.1 Indeed, this is technically a similar technique and we are certainly happy to acknowledge this article, which we did not previously encounter. After reading this article, I would like to point out a few subtle differences. The first is the choice of weight. Having a facial palsy practice teaches you that in cases of incomplete palsy, there is often a timedependent dynamic in terms of ability to close the eye— often improving although not normalizing. Therefore, we perform surgery with the patient under intravenous sedation, enabling us to insert the smallest possible weight that will provide protection when changing from previously placed weights. Second, the article details some additional considerations in secondary surgery, including position change from the pretarsal position to the postseptal position, including concomitant repair of entropion commonly encountered. Third, as the authors noted, we also emphasized using the postseptal fat as an additional layer of coverage when available and orbicularis muscle closure, and I am sure this was performed by Dr. Tower and Dailey in their original operation but not mentioned. Fourth, we suggested a general rule of increasing the measured weight in the office by 0.2 g because of its more posterior position, based on our experience, again enabling use of the smallest effective weight for closure yet minimizing the chance for ptosis. With this said, once more, I would like to thank Drs. Davies, Hink, and Durairaj for their comment, and humbly admit that no progress in surgery can be achieved without the experiences of our predecessors. DOI: 10.1097/01.prs.0000438064.31043.b7
Shai Rozen, M.D.
Department of Plastic Surgery University of Texas Southwestern Medical Center 1801 Inwood Road Dallas, Texas 75390-9132 [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication.
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
Plastic and Reconstructive Surgery • January 2014 ACKNOWLEDGMENT This study was supported by a grant from Kosin University College of Medicine. DISCLOSURE The authors have no commercial associations that might pose or create a conflict of interest with information presented in this communication. REFERENCES 1. Vedder NB, Winn RK, Rice CL, et al. A monoclonal antibody to the adherence-promoting leukocyte glycoprotein, CD18, reduces organ injury and improves survival from hemorrhagic shock and resuscitation in rabbits. J Clin Invest. 1988;81:939–944. 2. Li W, Enomoto M, Ukegawa M, et al. Subcutaneous injections of platelet-rich plasma into skin flaps modulate proangiogenic gene expression and improve survival rates. Plast Reconstr Surg. 2012;129:858–866. 3. Hargrave B, Li F. Nanosecond pulse electric field activation of platelet-rich plasma reduces myocardial infarct size and improves left ventricular mechanical function in the rabbit heart. J Extra Corpor Technol. 2012;44:198–204.
Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos Sir:
W
e read with interest the article entitled “Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos” by Rozen and Lehrman.1 Although the methods were sound and the article was well written, the authors failed to mention that this surgical technique has been previously published. Tower and Dailey described almost the same technique in 2004.2 In their original description, they placed the gold weight in a postseptal location, sutured it to the levator aponeurosis, and closed the septum and skin. The current article differs only in the intraoperative adjustment of the weight and the closure of the orbicularis layer. Although this article provides a valuable contribution to the literature, it is incumbent on the authors to cite and credit the work of previous surgeons. DOI: 10.1097/01.prs.0000436807.42917.99
Brett W. Davies, M.D., M.S. Eric M. Hink, M.D. Vikram D. Durairaj, M.D. Oculofacial Plastic and Reconstructive Surgery University of Colorado Hospital Aurora, Colo. Correspondence to Dr. Davies Department of Oculofacial Plastic and Reconstrucive Surgery University of Colorado Hospital 1675 Aurora Court Aurora, Colo. 80045 [email protected]
70e
DISCLOSURE The authors have no financial interest to declare in relation to the content of this communication. REFERENCES 1. Rozen S, Lehrman C. Upper eyelid postseptal weight placement for treatment of paralytic lagophthalmos. Plast Reconstr Surg. 2013;131:1253–1265. 2. Tower RN, Dailey RA. Gold weight implantation: A better way? Ophthal Plast Reconstr Surg. 2004;20:202–206.
Reply: Upper Eyelid Postseptal Weight Placement for Treatment of Paralytic Lagophthalmos Sir:
I would like to thank Drs. Davies, Hink, and Durairaj for their gracious comment. I read with great interest the article by Tower and Dailey.1 Indeed, this is technically a similar technique and we are certainly happy to acknowledge this article, which we did not previously encounter. After reading this article, I would like to point out a few subtle differences. The first is the choice of weight. Having a facial palsy practice teaches you that in cases of incomplete palsy, there is often a timedependent dynamic in terms of ability to close the eye— often improving although not normalizing. Therefore, we perform surgery with the patient under intravenous sedation, enabling us to insert the smallest possible weight that will provide protection when changing from previously placed weights. Second, the article details some additional considerations in secondary surgery, including position change from the pretarsal position to the postseptal position, including concomitant repair of entropion commonly encountered. Third, as the authors noted, we also emphasized using the postseptal fat as an additional layer of coverage when available and orbicularis muscle closure, and I am sure this was performed by Dr. Tower and Dailey in their original operation but not mentioned. Fourth, we suggested a general rule of increasing the measured weight in the office by 0.2 g because of its more posterior position, based on our experience, again enabling use of the smallest effective weight for closure yet minimizing the chance for ptosis. With this said, once more, I would like to thank Drs. Davies, Hink, and Durairaj for their comment, and humbly admit that no progress in surgery can be achieved without the experiences of our predecessors. DOI: 10.1097/01.prs.0000438064.31043.b7
Shai Rozen, M.D.
Department of Plastic Surgery University of Texas Southwestern Medical Center 1801 Inwood Road Dallas, Texas 75390-9132 [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication.
