\\n\\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\nThank you all for being part of the journey. 5,000 times thank you!
\\n\\nNow with 5,000 titles available Open Access, which one will you read next?
\\n\\nRead, share and download for free: https://www.intechopen.com/books
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\nDr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\n\nThank you all for being part of the journey. 5,000 times thank you!
\n\nNow with 5,000 titles available Open Access, which one will you read next?
\n\nRead, share and download for free: https://www.intechopen.com/books
\n\n\n\n
\n'}],latestNews:[{slug:"intechopen-signs-new-contract-with-cepiec-china-for-distribution-of-open-access-books-20210319",title:"IntechOpen Signs New Contract with CEPIEC, China for Distribution of Open Access Books"},{slug:"150-million-downloads-and-counting-20210316",title:"150 Million Downloads and Counting"},{slug:"intechopen-secures-indefinite-content-preservation-with-clockss-20210309",title:"IntechOpen Secures Indefinite Content Preservation with CLOCKSS"},{slug:"intechopen-expands-to-all-global-amazon-channels-with-full-catalog-of-books-20210308",title:"IntechOpen Expands to All Global Amazon Channels with Full Catalog of Books"},{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"}]},book:{item:{type:"book",id:"3042",leadTitle:null,fullTitle:"Wireless Sensor Networks - Technology and Applications",title:"Wireless Sensor Networks",subtitle:"Technology and Applications",reviewType:"peer-reviewed",abstract:"The aim of this book is to present few important issues of WSNs, from the application, design and technology points of view. The book highlights power efficient design issues related to wireless sensor networks, the existing WSN applications, and discusses the research efforts being undertaken in this field which put the reader in good pace to be able to understand more advanced research and make a contribution in this field for themselves. It is believed that this book serves as a comprehensive reference for graduate and undergraduate senior students who seek to learn latest development in wireless sensor networks.",isbn:null,printIsbn:"978-953-51-0676-0",pdfIsbn:"978-953-51-5573-7",doi:"10.5772/1100",price:139,priceEur:155,priceUsd:179,slug:"wireless-sensor-networks-technology-and-applications",numberOfPages:388,isOpenForSubmission:!1,isInWos:1,hash:"1ce60819c311c1a7c028042585dd601e",bookSignature:"Mohammad Matin",publishedDate:"July 18th 2012",coverURL:"https://cdn.intechopen.com/books/images_new/3042.jpg",numberOfDownloads:41523,numberOfWosCitations:20,numberOfCrossrefCitations:19,numberOfDimensionsCitations:35,hasAltmetrics:1,numberOfTotalCitations:74,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 6th 2011",dateEndSecondStepPublish:"January 10th 2012",dateEndThirdStepPublish:"April 15th 2012",dateEndFourthStepPublish:"July 14th 2012",dateEndFifthStepPublish:"August 13th 2012",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7",editedByType:"Edited by",kuFlag:!1,editors:[{id:"12623",title:"Prof.",name:"Mohammad Abdul",middleName:"A",surname:"Matin",slug:"mohammad-abdul-matin",fullName:"Mohammad Abdul Matin",profilePictureURL:"https://mts.intechopen.com/storage/users/12623/images/1967_n.jpg",biography:"Dr. Mohammad A Matin is a Professor of the Department of Electrical and Computer Engineering at North South University (NSU), where he has been since 2008. He was first appointed as Assistant Professor and then promoted to Associate Professor at North South University in 2011 and later on Professor. While in that post he was also the coordinator of EEE program. During 2012-2017, he was an Associate Professor at Universiti Teknologi Brunei (UTB), Brunei Darussalam (QS World University ranking 379). He received his B.Sc. degree in Electrical and Electronic Engineering from BUET (Bangladesh), his M.Sc. degree in Digital Communication from Loughborough University, UK and PhD in Wireless Communication from Newcastle University, UK. He has taught several courses in communications, electronics and signal processing at KUET, Khulna University, BRAC University, and UKM (Malaysia) during his career. He has published over 90 peer-reviewed journals and conference papers, and is the author/editor of 16 (sixteen) academic books such as Towards Cognitive IoT Networks (Springer, 2020), Communication Systems for Electrical Engineers (Springer, 2018), Spectrum Access and Management for Cognitive Radio Networks (Springer, 2016), Coding for MIMO-OFDM in Future Wireless Systems (Springer, 2015), Advances in Sensor Networks Research (Nova publisher, USA, 2014) and 10 (ten) book chapters. He has presented invited talks in Bangladesh and Malaysia and has served as a member of the program committee for more than 50 international conferences. He is on the editorial board of several international journals such as IEEE Communications Magazine, IEEE, USA, IET Wireless Sensor Systems (IET-WSS), and so on. Dr. Matin is a member of the IEEE, IEEE Communications Society (IEEE ComSoc), and several other international organizations. He served as a counselor of IEEE North South University (2008–2011), and secretary of the IEEE Communication Society, Bangladesh Chapter (2010–2011). He has received a number of prizes and scholarships including the Best student prize (Loughborough University), Commonwealth Scholarship, and Overseas Research Scholarship (ORS) conferred by the Committee of Vice Chancellors and Principals (CVCP) in the UK. He has been fortunate enough to work in WFS Project with Wireless Fibre Sytems Ltd, UK as an expert. His current research interests include UWB communication, wireless sensor networks, cognitive radio, EM modeling, and antenna engineering.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"4",totalChapterViews:"0",totalEditedBooks:"7",institution:{name:"North South University",institutionURL:null,country:{name:"Bangladesh"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"530",title:"Computer Network",slug:"communications-and-security-computer-network"}],chapters:[{id:"37866",title:"Efficient Node Placement for Congestion Control in Wireless Sensor Networks",doi:"10.5772/48201",slug:"efficient-node-placement-for-congestion-control-in-wireless-sensor-networks",totalDownloads:3097,totalCrossrefCites:2,totalDimensionsCites:3,signatures:"Charalambos Sergiou and Vasos Vassiliou",downloadPdfUrl:"/chapter/pdf-download/37866",previewPdfUrl:"/chapter/pdf-preview/37866",authors:[{id:"140399",title:"Dr.",name:"Charalambos",surname:"Sergiou",slug:"charalambos-sergiou",fullName:"Charalambos Sergiou"},{id:"140463",title:"Dr.",name:"Vasos",surname:"Vassiliou",slug:"vasos-vassiliou",fullName:"Vasos Vassiliou"}],corrections:null},{id:"37846",title:"Power Optimization for Wireless Sensor Networks",doi:"10.5772/50603",slug:"power-optimization-for-wireless-sensor-networks",totalDownloads:3502,totalCrossrefCites:3,totalDimensionsCites:4,signatures:"A.R. 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Malignant mesothelioma (MM) is a rare, aggressive cancer that originates from mesothelial tissue in the pleura, peritoneum, and pericardium; MM has been associated with asbestos exposure, especially in occupational settings [1]. In some countries, such as Turkey and Japan, MM is also due to environmental asbestos exposure, which affects people who live in the vicinity of natural asbestos mines or factories that use asbestos [2, 3, 4]. Mesothelioma is highly resistant to conventional cancer therapies. MM patients usually have a poor prognosis, with a median survival of 12–18 months, due to the lack of effective treatments and difficulty in diagnosing this disease at the early stage [5, 6, 7]. In general, there are three main histological subtypes of mesothelioma. The epithelioid and sarcomatoid subtypes are characterized by cuboid and fibroblastoid cells, respectively. The biphasic subtype contains a mixture of both cell types and confers the worst prognosis. The most widely used treatments for MM are surgery with or without adjuvant chemotherapy and/or radiotherapy [8]. The first-line treatment option for unresectable MM is chemotherapy with cisplatin plus pemetrexed [9, 10]. Nevertheless, MM may be resistant to these conventional therapeutic approaches, and palliative care strategies are controversial. Although crocidolite and/or chrysotile have not been used for more than 10 years in many developed and developing countries, high mortality rates associated with mesothelioma persist since the clinical manifestations of MM are insidious and nonspecific. It is worth noting that MM has a long latency period (mean, 30–40 years) from the time of asbestos exposure to tumorigenesis [4, 11]. Thus, valuable biomarkers for the prediction or diagnosis of MM at early stages, prognostic markers, and novel therapeutic strategies are urgently needed.
Matrix metalloproteinases (MMPs, also known as matrixins) are a family of zinc-dependent endopeptidases that degrade all components of the extracellular matrix (ECM); thus, MMPs are involved in ECM remodeling. In addition to functioning as the main ECM regulators, MMPs also modulate intra- and extracellular signaling pathways and networks through the proteolytic processing of various biomolecules. The first MMP was reported by Gross and Lapiere as a collagenase engaged in tail resorption during tadpole metamorphosis [12]. To date, 24 MMP genes, including a gene duplication, that encode 23 unique MMP proteins have been identified in humans [13, 14]. According to substrate specificity, sequence similarity, and specific role, MMPs can be divided into eight main groups: (1) collagenases (MMP-1, MMP-8, and MMP-13), (2) matrilysins (MMP-7 and MMP-26), (3) metalloelastase (MMP-12), (4) stromelysins (MMP-3, MMP-10, and MMP-11), (5) gelatinases (MMP-2 and MMP-9); (6) enamelysin (MMP-20); (7) membrane-type MMPs (MMP-14, MMP-15, MMP-16, MMP-17, MMP-24, and MMP-25), and (8) others (MMP-19, MMP-21, MMP-23, MMP-27, and MMP-28) [13, 15]. Interestingly, the proteolytic activities of MMPs are precisely controlled by activation of their precursors and inhibition by endogenous inhibitors, α-macroglobulins, and tissue inhibitors of metalloproteinases [13]. Except for six membrane-associated MMPs, the other 17 MMPs are soluble secreted enzymes [16]. In addition, growth factors, chemokines, and cytokines modulate the expression of MMPs through various pathways to affect ECM degradation and, in turn, influence growth factors, which ultimately affect cancer cell migration and invasion [17, 18].
Of note, MMPs are expressed in various cancer tissues, and their expression levels are closely associated with the properties of invasive growth and metastasis [15]. Accumulating evidence suggests that ECM degradation by MMPs at the cell surface enhances tumor growth, invasion, and metastasis through the proteolytic degradation of ECM, altered cell-cell, and cell-ECM interactions and effects on cell migration and angiogenesis [17, 19]. More recently, the roles of different MMPs have become increasingly studied in the field of MM research. Experimental evidence indicates that MMP-1, MMP-2, and MMP-9 are involved in mesothelial carcinogenesis. Several MMPs, such as MMP-7, MMP-14, and MMP-9, are potential biomarkers for MM. In the following sections, we will describe the roles of MMPs in carcinogenic mechanisms based on in vivo and in vitro experimental evidence, outline the clinical findings, and highlight the possible roles of MMPs in MM, as well as future prospects.
Some MMPs are upregulated and considered mesenchymal markers of epithelial-to-mesenchymal transition (EMT), such as MMP-1, MMP-2, and MMP-9 [20]. EMT not only is associated with many physiological processes, such as embryonic development, but also plays a vital role in pathological processes, including cancer cell invasion and migration [21, 22, 23]. During EMT, epithelial cells lose their phenotype and acquire a mesenchymal phenotype, including the loss of cell polarity and cell adhesion in cell-cell and cell-basement membrane interactions and the acquisition of ECM degradation ability, which is directly related to MMPs. Currently, published studies implicate MMPs as inducers of EMT during MM progression. In addition, MMPs play a mediator role in cellular signaling pathways controlled by growth factors and cytokines [17, 24]. Here, we describe these two main roles of MMPs in MM carcinogenesis. Moreover, we propose possible mechanisms involving MMPs, as shown in Figure 1.
Schematic representation of MMP-involved mechanisms in MM carcinogenesis. See detail in text. MM, malignant mesothelioma; EMT, epithelial-to-mesenchymal transition; ECM, extracellular matrix.
MMP-1 is an interstitial collagenase that specifically targets the degradation of collagen types I–III [25]. Schelch et al. reported that in malignant pleural mesothelioma (MPM) cells in vitro, fibroblast growth factor 2(FGF2) and epidermal growth factor (EGF) may induce EMT via mitogen-activated protein kinase kinase (MEK)/MMP-1 signaling [26]. The experimental results indicated that MMP-1 inhibition by the pan-MMP inhibitor GM6001 or transfection with siRNAs targeting MMP-1 could prevent FGF2-induced cell scattering and invasion in the M38K cell line (a biphasic MPM cell line) [26]. In MPM tissue specimens, higher MMP-1 expression was observed in the sarcomatoid compartment than in the epithelioid compartment. Normal pleura were weakly positive for MMP-1 [26]. These results suggest that MMP-1 causally contributes to sarcomatoid morphology and increases cell invasiveness during EMT.
MMP-2, also named gelatinase A, is expressed by almost all cell types, and its classical substrates are denatured collagen (gelatin) and basement membrane [25, 27]. Indeed, MMP-2 acts as a cancer-associated EMT inducer or modulator in a number of tumors, such as breast cancer [16, 28], hepatocellular carcinoma [29], prostate cancer [30], ovarian cancer [31], oral squamous cell carcinoma [32], and MM [33]. Regarding MM, MMP-2 secretion from human normal mesothelial MeT-5A cells increased upon treatment with chrysotile or transforming growth factor-β (TGF-β) [33], and EMT was induced. This in vitro experimental result of increased MMP-2 secretion by cells exposed to chrysotile asbestos suggests changes in the surrounding microenvironment that render the ECM more amenable to degradation and invasion [33, 34]. Of course, the underlying mechanism of MMP-2-induced EMT in MM development requires further study.
MMP-9 is a type IV collagenase also known as gelatinase B [35] that has a similar ability to cleave gelatin as MMP-2. MMP-9 has been recognized as an EMT mediator in cancer progression and appears to be a potential therapeutic target [35, 36, 37]. Elevated MMP-9 levels were observed in a 3D microtumor model of patient-derived mesothelioma cells, consistent with the elevated MMP-9 levels in patient breast tumors compared to healthy mammary glands [38]. Moreover, MMP-9 secreted into conditioned media by large microtumors induced a migratory phenotype in nonmigratory small microtumors, and blocking MMP-9 with GM6001 effectively abolished the collective migration of mesothelioma microtumors [38]. These findings imply that a self-regulated positive feedback loop involving MMP-9 is established during tumor progression and migration [38]. Additionally, the invasion of H2052 (mesothelioma cell line) and JP5 cells (primary mesothelioma cell line) into a 3D collagen matrix induced by gremlin-1 (a protein antagonist of bone morphogenetic proteins) was significantly alleviated by GM6001 and BB2516 (broad-spectrum MMP inhibitors) [39]. Interestingly, in our previous study, we found that serum MMP-2 and MMP-9 levels were correlated with each other in both healthy control and MM groups in a Han cohort from Eastern China [40]. Nevertheless, there were no significant differences in MMP-2/MMP-9 levels between the healthy control and MM groups.
Various growth factors, cytokines, and miRNAs engage specific cellular signaling pathways, such as the MEK and extracellular signal-regulated kinase (ERK) signaling pathways, to regulate MMP expression levels to degrade the ECM, and MMPs then contribute to the release of tumor-related factors, such as vascular endothelial growth factor and TGF-β, from the ECM [17, 24].
MMP-1 expression showed an increasing trend in MM cell lines from no treatment to treatment with FGF2 and EGF and a pronounced decrease upon treatment with selumetinib (MEK inhibitor), suggesting that the growth factors FGF2 and EGF regulate MMP-1 expression via the MEK signaling pathway in MM [26]. TGF-β, another important growth factor that regulates cell growth and differentiation, affects MMP-2 expression in MeT-5A [33] and JL-1 cells [39]. Moreover, growth hormone-releasing hormone (GHRH) antagonists (MIA-602 and MIA-690) equally blunted MMP-2 and MMP-9 mRNA levels in both REN and MSTO-211H cells (MM cell lines), indirectly indicating that MMP-2/MMP-9 expression is induced by GHRH [41], as well as by adenosine diphosphate in ZL55 cells (an epithelioid MM cell line), via the nuclear factor kappa-B, protein kinase B, and ERK1/2 signaling pathways [42]. Interestingly, microtumor treated with GM6001 showed reduced pERK/ERK ratios and ERK activation [38]. Notably, miR-591 targets MMP-2 expression, and overexpression of miR-591 inhibited MMP-2 levels in MPM cells [43]. These experimental results show that MMP expression is regulated by various factors via multiple signaling pathways and that MMPs interact with such inducers and signaling pathways in MM carcinogenesis.
To date, MM is still difficult to diagnose in early stages due to our limited knowledge of its molecular pathogenesis. Indeed, pathological examination techniques to diagnose MM and distinguish MM from other diseases must be improved [44]. However, more molecular markers are required to distinguish benign from malignant mesothelial disease or other tumors. In addition, effective pathologic predictors of prognosis and therapeutic response are urgently needed. Since MMPs are involved in tumor pathogenesis, some MMPs may be potential pathological markers.
In general, MMP expression and activation are very low and tightly regulated during normal tissue homeostasis. MMP production and activation are rapidly induced during active tissue remodeling and in pathological conditions such as cancer [37]. MMP-7 and MMP-14 are potential diagnostic and prognostic biomarkers of mesothelioma, respectively. MMP-7 is a highly specific negative biomarker to distinguish MM from other high-grade serous carcinomas with 100% specificity and moderate sensitivity, but it cannot distinguish mesothelial cells from reactive mesothelial cells in serous effusion due to uniformly negative expression of MMP-7 in reactive mesothelial cells [45]. It is intriguing that MMP-14 is a potential biomarker for the differential diagnosis of MPM and reactive mesothelial hyperplasia (MH). A group from Italy found that MMP-14 expression is markedly increased in MPM patient specimens compared with MH specimens based on polymerase chain reaction array and immunohistochemistry analyses [46]. MMP-14 levels have been reported to be elevated in all tissue samples from MM patients compared to those from normal individuals, but more evidence is needed to substantiate MMP-14 as a diagnostic biomarker for MM [47]. MMP-14 expression has prognostic value for MM. Clinically high MMP-14 expression in MM patients is significantly correlated with poor prognosis [47].
Although most mesotheliomas are attributable to asbestos exposure, genetic factors are also important causes of carcinogenesis. Gene mutations influence the prognosis of MM. For example, heritable mutations in BRCA1-associated protein-1 (BAP1), a tumor suppressor gene, may predispose individuals to asbestos-related MM [48, 49]. Moreover, Baumann et al. reported that mesothelioma patients with germline BAP1 mutations have a seven-fold improvement in long-term survival [50].
More recently, some MMP single-nucleotide polymorphisms (SNPs) have been found to have potential as genetic biomarkers for MM. For instance, Štrbac et al. reported that patients carrying a polymorphic MMP-9 rs2250889 allele had a negative outcome, with a shorter time to progression (TTP) (6.07 vs. 10.03 months, HR = 2.45, 95% CI = 1.45–4.14, p = 0.001) and worse overall survival (OS) (9.23 vs. 19.2 months, HR = 2.39, 95% CI = 1.37–4.18, p = 0.002) than those with the reference allele [51]. However, patients harboring at least one polymorphic MMP-9 rs20544 allele had a positive outcome, with a longer TTP (10.93 vs. 9.40 months, HR = 0.57, 95% CI = 0.38–0.86, p = 0.007) and improved OS (20.67 vs. 13.50 months, HR = 0.56, 95% CI = 0.37–0.85, p = 0.007) [51]. These researchers also found that the MMP-2 rs243865 polymorphism plays a protective role in MM; carriers of this polymorphism have a decreased risk for MM (OR = 0.66, 95% CI = 0.44–1.00, p = 0.050) [52]. Interestingly, the decreased risk for MM is more pronounced in people exposed to asbestos [52]. These findings provide insight into some MMP SNPs that are considered genetic biomarkers, indicate the prognosis of MM patients, and predict susceptibility to MM. In the future, appropriate genetic counseling and clinical management should be considered for MM patients who are carriers of MMP-2/MMP-9 susceptibility SNPs.
In this chapter, we provide an overview of recent findings on MMP function in MM and the mechanisms by which MMPs may induce both phenotypic and genotypic alterations that facilitate MM progression and invasion. Accumulating evidence indicates that tumor-associated MMPs can stimulate processes associated with EMT, a developmental event that is activated in MM cells during invasion and metastasis. Meanwhile, future investigations on extracellular targets and intracellular signaling pathways through which MMPs can induce EMT of MM cells will provide insight into novel therapeutic targets. We also describe possible roles of MMPs as pathological markers or genetic biomarkers in MM. Certainly, the underlying mechanisms of secreted MMPs, including their function and circulation, are complex in MM and remain to be elucidated in the future.
This study was supported by the National Natural Science Foundation of China (81502794, 81973011), the Qianjiang Talents Project of Zhejiang Province (QJD1602027), the Science and Technology Department of Zhejiang Province (1925D), the Zhejiang Provincial Natural Science Foundation of China (LY16H240001), the Health Commission of Zhejiang Province (2017PY015, 2018KY038), and the Science and Technology Project of Cixi City (CN2018023). The research assistance of Dr. Xing Zhang and Dr. Jianlin Lou is gratefully acknowledged.
The authors declare no conflicts of interest.
Cerebrospinal fluid (CSF) is produced by the choroid plexus in the lateral ventricles, third, and fourth ventricles at a rate of 0.35 mL/min (20 mL/hour or 350–500 mL/day) in the normal physiologic states and is reabsorbed into the dural venous sinuses through the arachnoid villi. The total volume of circulating CSF is 90–150 mL. The entire volume of CSF turns over three to five times per day. Typical intracranial pressure is 5–15 cm H2O and is considered elevated when it is greater than 15 cm H2O. The three layers of the meninges are the dura mater, arachnoid, and pia mater. The dura mater is separated into the superficial layer and the meningeal layers. Common causes of CSF leaks can be divided into trauma, both surgical and nonsurgical, neoplasm, congenital, and spontaneous [1].
An encephalocele is herniation of neural tissue through a defect in the skull base and is defined by the type of tissue that herniates through the defect. A meningocele contains herniated meninges, a meningoencephalocele contains herniated brain matter and meninges, and a meningoencephalocystocele is made up of herniated brain matter and meninges that communicate with a cerebral ventricle.
The most common cause is nonsurgical (70–80%). 1–3% of acute head injuries result in a CSF leak. Conservative management is often the first step in managing CSF leaks resulting from acute trauma. Seventy percent of leaks close spontaneously with observation and conservative management which may include bed rest, head of bed elevation, and lumbar drainage. Overall, there is a 30–40% risk of meningitis with conservative treatment [2].
Surgical causes (planned and unplanned) make up a large portion of leaks requiring intervention. Functional endoscopic sinus surgery (FESS) carries <1% incidence of CSF leak. The most common site of skull base injury is the lateral lamella of the cribriform plate. The posterior ethmoid skull base is at greater risk when the maxillary sinus is highly pneumatized in the superior–inferior dimension, which creates a relatively decreased posterior ethmoid height. Neurologic Surgery caries an increased risk albeit typically include planned CSF leak with expected violation of the meninges. Transsphenoidal approach for sellar and suprasellar lesions carry a reported 0.5–15% incidence of CSF leak [3].
Neoplasms can result in CSF leak via direct tumor invasion and/or mass effect leading to intracranial hypertension. Congenital causes result from failure of closure of developmental spaces with resultant herniation of intracranial contents. Foramen cecum is the most common location. Spontaneous leaks are often the result of idiopathic intracranial hypertension (IIH) resulting from decreased CSF reabsorption. Patient characteristics and symptoms often include middle-age, obesity, female, pressure-type headaches, pulsatile tinnitus, and balance dysfunction.
Empty sella syndrome is a radiographic appearance of CSF-filled sella due to flattening of the pituitary gland which is an endocrine gland that resides in the sella turcica and functions to control other endocrine glands by secretion of controlling hormones. Empty sella syndrome can be seen in IIH, which typically affects obese women. Patients typically will present with headaches, pulsatile tinnitus, and diplopia. A hallmark physical exam finding is bilateral optic disc edema secondary to increased intracranial pressure (ICP). Treatment is focused on decreasing ICP with pharmacologic therapy consisting of acetazolamide and furosemide to lower ICP, and headache management, which may include amitriptyline and propranolol. In severe cases with vision problems, surgical intervention may be required, including optic nerve decompression or CSF shunting. Empty sella syndrome can be seen in conjunction with spontaneous CSF leaks.
Encephaloceles can occur in both the skull and spinal column. Twenty percent occur within the cranium and 15% of these are associated with the nasal cavity. Nasal encephaloceles are divided into two types: sincipital and basal. Sincipital (anterior and superior) encephaloceles make up approximately 60% of nasal encephaloceles and typically present as a soft compressible mass over the glabella. Basal encephaloceles occur through the skull base more posteriorly and make up approximately 40% of nasal encephaloceles. They may remain hidden for many years because they are located more posteriorly than the sincipital type.
Clear rhinorrhea that is unilateral, watery, and salty to taste is the most common complaint in CSF leaks. It may run out of the nose in more anterior leaks, or down the back of the throat in more posterior leaks. The drainage can be exacerbated by the Dandy maneuver, which entails tilting the head forward into a chin-tuck position and straining.
Patients with an encephalocele will often present with rhinorrhea or recurrent meningitis and may have a broad nasal dorsum or hypertelorism. Encephaloceles may characteristically transilluminate, expand with the Valsalva maneuver, and demonstrate a positive Furstenberg sign (enlargement with compression of internal jugular veins). Radiologic imaging including computed tomography (CT) and magnetic resonance imaging (MRI) may be used to evaluate the size and location of encephaloceles.
The most sensitive and specific test is qualitative β2-transferrin evaluation of the nasal drainage. β2-transferrin is detected in few fluids in the body including CSF, perilymph, and aqueous humor. Only 0.2 mL is needed for an adequate specimen. β2-transferrin has a sensitivity of 97% and specificity of 93%. False positive results can occur with abnormal transferrin metabolism from chronic liver disease, glycogen metabolic disease, and carcinomas; therefore, results should be verified with a negative serum β2-transferrin. β-trace protein is a newer laboratory test with higher sensitivity and specificity which offers faster results than β2-transferrin.
The radiologic evaluation of a CSF leak can be extensive and often begins with a fine cut maxillofacial CT scan to demonstrate bony abnormalities such as defects and fractures. CT is the mainstay for radiologic workup of CSF rhinorrhea with a sensitivity of 92% and a specificity of 92–96%. If the initial imaging does not show an obvious abnormality but suspicion is still high, a CT cisternogram may be useful. This study entails injection of radiopaque material through a lumbar drain into the intrathecal space to help delineate the CSF leak. Presence of contrast within the nasal space or paranasal sinuses indicates a CSF leak. CT cisternography has a sensitivity of 92% with an active leak to 40% with an intermittent leak. MRI cisternography (T2 weighted fast-spin protocol) can be helpful in cases of neoplasm, meningoencephalocele, encephalocele, and in patients with an iodine allergy.
In patients who have a traumatic leak and normal CSF pressure, conservative treatment consists of bed rest with head of bed elevation and lumbar drainage of CSF for 5–10 days. With conservative management, there is a reported risk ranging from 7 to 30% of ascending meningitis. The incidence of spontaneous resolution with conservative management is reported to be 70%.
The general consensus among practicing otolaryngologist is that antibiotics should not be used for conservative management unless there is a very large defect with comminuted bone of the skull base as a simple CSF leak carries a 7% infection rate (meningitis, intracranial abscess, cellulitis abscess, and osteomyelitis) and prophylactic antibiotics have not been shown to decrease the risk of infection. After endoscopic repair, antibiotics are generally recommended for 24–48 hours including Cefazolin (1 gm q8), Vancomycin (1 gm q12), or Clindamycin (600 mg q8). This is done to cover possible contamination at the time of surgery in a non-sterile field with concomitant sealing of the sterile to non-sterile flushing of an active leak [4, 5].
Endoscopic repair of CSF leaks is effective and offers decreased morbidity compared to open approaches. Meticulous technique is key to success in repair of skull base defects. Materials used and procedures employed are less important than the quality of the repair [6].
Advancements in the endoscopic surgical repair of CSF leaks and encephaloceles have resulted from improvements in instrumentation, visualization, access, and technique. Improved diagnostic imaging and surgical navigation have also improved management. Advancements in endoscopic reconstructive techniques of the skull base including utilization of local vascularized flaps have improved success rates with endoscopic approaches [7].
Compared to open surgery, the endoscopic approach allows for more direct visualization with less manipulation of the surrounding soft tissues. This may allow for a more precise reconstruction of the skull base due to better visualization, and minimal manipulation of nearby neurovascular structures. Compared to the traditional microscopic view, endoscopes give a dynamic operative view with the added ability to see around corners using angled endoscopes. ESBS can avoid scars, decrease hospital stays, and cause less postoperative pain [8].
Not all areas of the skull base can be visualized and safely instrumented via a transnasal endoscopic route. As a general rule, the endoscopic approach should not compromise the ability to achieve the appropriate reconstruction, and crossing major neurovascular structures is not suggested [9].
Common complications from skull base surgery include anosmia and associated taste dysfunction, epistaxis and neurologic complications such as cranial nerve injury. Major skull base surgery complications include CSF rhinorrhea, meningitis, intracranial hemorrhage, orbital complications such as diplopia or vision loss, vascular injury, stroke, and death [8, 9, 10, 11].
Intrathecal fluorescein is often used in the surgical repair of CSF leaks. Its advantages include the ability to stain defects that may be more difficult to identify clinically, through the visible dye of CSF to a light green color. The surgeon can also use it to confirm a water-tight repair. It carries a 0% false positive rate. Its disadvantages include a moderate false negative result. It requires a lumbar puncture, and the use of fluorescein intrathecally is not FDA-approved. Rare complications including seizures (0.3%) and death have been reported; however, these have more commonly been associated with administration through a suboccipital puncture. If used to help localize a CSF leak it should be used with caution and should be dosed as 0.05–0.1 mL per 10 kg body weight up to maximum 0.1 mL 10% fluorescein. This is mixed in 10 mL of preservative-free normal saline or CSF. The surgeon should inject slowly (over 5–10 min) without paralytics in the anesthetic regimen to assess for seizure activity. Fluorescein should be avoided in patients with abnormal renal function [12].
The primary goal in endoscopic repair of CSF leaks and skull base reconstruction is to definitively identify all leaks in order to completely reconstruct all defects. After identifying the leak or leaks, the goals of reconstruction are creation of a safe barrier with separation of intracranial and sinonasal spaces and elimination of any dead space. As with any surgical intervention, meticulous surgical technique is paramount for success.
A reconstructive ladder should be used to help determine the type of repair performed. For simple, small (less than 1 cm) defects, a fat plug harvested from the earlobe or abdomen can be used to plug the defect. The next option includes a simple overlay graft harvested from the nasal floor mucosa, turbinate mucosa, or nasal septum. If a more complex, larger reconstruction is in order, a composite (underlay and overlay) graft can be used consisting of an intracranial underlay of bone or cartilage from nasal septum, auricular cartilage or turbinate bone, and an overlay graft of mucosa (free or pedicled) as above. Local pedicled flaps should include the nasoseptal flap, which is supplied by the posterior nasal septal artery, a terminal branch of the sphenopalatine artery. Additional grafts that can be useful in larger defects include temporal fascia or tensor fascia lata grafts. These grafts are often bolstered in the sinonasal cavity with abdominal fat, a nasoseptal flap or both. In complex situations of extensive defects or poor local tissue, such as in chemoradiated patients, a craniotomy with pericranial flap or free flap reconstruction of the skull base may be necessary.
Lumbar drains are often used to decrease intracranial pressure and thereby reduce the pressure applied to the skull base reconstruction; however, they may be associated with significant morbidity and potential for complications. The use of lumbar drain primarily following a repair varies from different surgeons, and should not be universally utilized in a routine fashion. When used, the duration of drainage is also up to surgeon discretion.
Most reconstructive methods appear to have similar efficacy, and therefore there is no universal “best type of reconstruction.” In general, small defects (<1 cm) can be closed in a single layer, and multilayer repair is preferred for larger defects. Some surgeons prefer to use a rigid layer of bone or cartilage to reconstruct the skull base, although this is not required [13]. Vascularized mucosal tissue (e.g., nasoseptal flap) has been demonstrated to improve repair results for larger defects; however, single layer nonvascularized tissue can also be successful in this setting.
Postoperative antibiotics are an important consideration for skull base surgery because of the temporary connection between the intracranial space and external world. Rates of postoperative wound infection following ESBS are approximately 2%, and appear to be higher in open skull base surgery. Broad coverage with IV cephalosporins with or without vancomycin (or oral amoxicillin/clavulanate) is most often recommended. Studies are lacking to support the use of prolonged postoperative antibiotics, although most surgeons prefer to use systemic or topical antibiotics in some form after surgery.
A multitude of studies over the past 25 years have shown high success rates of primary repair around 90%, and secondary repair around 97%. These success rates compare favorably to traditional craniotomy approaches with reported success rates between 70 and 80% that carry a higher morbidity profile. Symptoms of failure in reconstruction include clear rhinorrhea and constant postnasal drip. Other signs may include meningitis, severe headaches, seizures, and worsening pneumocephalus.
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