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\\n
Seeing 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\\n
Over 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\\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\n
Thank you all for being part of the journey. 5,000 times thank you!
\\n\\n
Now with 5,000 titles available Open Access, which one will you read next?
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\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\n
Seeing 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\n
Over 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\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\n\n
Thank you all for being part of the journey. 5,000 times thank you!
\n\n
Now with 5,000 titles available Open Access, which one will you read next?
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She has also written popular science books for the public.\n Orcid: https://orcid.org/0000-0002-2009-4898. \nWebsite https://www.nottingham.ac.uk/vet/people/catrin.rutland",institutionString:"University of Nottingham",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"8",totalChapterViews:"0",totalEditedBooks:"2",institution:{name:"University of Nottingham",institutionURL:null,country:{name:"United Kingdom"}}}],coeditorOne:{id:"309529",title:"Dr.",name:"Albert",middleName:null,surname:"Rizvanov",slug:"albert-rizvanov",fullName:"Albert Rizvanov",profilePictureURL:"https://mts.intechopen.com/storage/users/309529/images/9189_n.jpg",biography:'Albert A. Rizvanov is a Professor and Director of the Center for Precision and Regenerative Medicine at the Institute of Fundamental Medicine and Biology, Kazan Federal University (KFU), Russia. He is the Head of the Center of Excellence “Regenerative Medicine” and Vice-Director of Strategic Academic Unit \\"Translational 7P Medicine\\". Albert completed his Ph.D. at the University of Nevada, Reno, USA and Dr.Sci. at KFU. He is a corresponding member of the Tatarstan Academy of Sciences, Russian Federation. Albert is an author of more than 300 peer-reviewed journal articles and 22 patents. He has supervised 11 Ph.D. and 2 Dr.Sci. dissertations. 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1. Introduction
Recently, the food industry and the consumer sector have shown a growing interest in the research, development and commercialization of beverages with high nutritional content and particular properties relevant to human health. In this context, green tea infusions (Camellia sinensis) are rich in bioactive compounds, particularly in phenolic compounds with antioxidant activity. It is therefore not surprising that green tea has attracted significant attention for its positive effects on health-related issues of oxidative stress such as cancer, cardiovascular and neurodegenerative diseases [1, 2].
The tea manufacturing process is designed to either preclude or permit tea polyphenolic compounds to be oxidized by naturally occurring polyphenol oxidase in the tea leaves during fermentation (white and green tea are unfermented; oolong tea is semi-fermented; and black tea is fully fermented). Green tea is produced by inactivating the heat-labile enzyme polyphenol oxidase in fresh leaves by either applying heat or steam, which prevents the enzymatic oxidation of polyphenolic compounds. Although the components of green tea include proteins, carbohydrates, lipids, alkaloids, vitamins and minerals, its health-beneficial properties are attributed mainly to its high content of catechins (flavan-3-ols, or flavanols), such as (−)-epicatechin (EC), (−)-epigallocatechin (EGC) and their gallate forms (+)gallocatechin (GC), (−)epicatechin-3-gallate (ECG) and (−)epigallocatechin-3-gallate (EGCG). Recent studies have also identified biological functionality of other phenolic compounds found at lower concentrations, particularly flavonols and phenolic acids [1, 3, 4, 5].
A cup of green tea contains approximately 300 mg of catechins. It is considered that EGCG intake in the form of green tea infusions should be safe up to a maximum consumption of 734 mg EGCG/person/day and even a regular or high dose of green tea (8–16 cups a day) has positive effects in general health [4, 5, 6, 7]. The catechin content of green tea also depends on a number of factors including the growing conditions of the plant, age of leaves harvested and the method used to prepare the infusion [4, 8].
In the last part of the twentieth century, interest in food polyphenols has increased due to activities such as free radical scavenging, modulation of signal transduction and metal chelation, as well as anti-inflammatory, anti-microbial and anti-proliferation activities [9, 10, 11]. In addition, polyphenols may exert an indirect antioxidant effect by protecting endogenous antioxidant enzymes in the human body [12]. Thus, substances with antioxidant properties such as polyphenols emerge as putative preventives and coadjuvants in the treatment of chronic degenerative diseases related to oxidative stress and DNA damage [13].
2. Oxidative stress, antioxidants and green tea flavonoids
“Oxidative stress” is a term used mainly in the fields of biology and medicine since 1985. Initially, it was defined as the lack of balance between the formation of reactive oxygen species (ROS) and molecules capable of counteracting their action (antioxidant defense system). Naturally, as our understanding has increased over the past years, this concept has been accordingly redefined and more elements like the interruption of signaling and redox control have been added [14]. Nevertheless, oxidative stress has always had a negative connotation because it has been linked to various potentially severe human diseases, including neurological diseases such as Alzheimer’s and Parkinson’s, and metabolic diseases, like diabetes and atherosclerosis, in addition to being involved in the development of some types of cancers, inflammatory processes and cardiomyopathies, among others [15].
The terms “ROS” and “free radicals” are often used interchangeably. However, it is important to note that even though both terms might fulfill operational and practical purposes in some contexts, they are not always fully interchangeable. The term “free radicals” refers to a reactive chemical species that has an unpaired electron in its last orbital, identified in the nomenclature as a dot “•,” which makes them highly reactive species. However, ROS includes oxygenated free radicals, such as the superoxide radical (•O2−) and the hydroxyl radical (•OH), as well as the oxygenated molecule precursors of free radicals, such as hydrogen peroxide (H2O2) and singlet oxygen (1O2) [15, 16]. In short, all oxygenated free radicals are ROS, but not all ROS are free radicals.
The generation and elimination of ROS are closely related processes. Living organisms possess regulatory systems to maintain ROS at safe levels, that is, their production and elimination are well balanced. However, under certain circumstances this balance can be disturbed. These include (i) increased level of endogenous and exogenous compounds entering autoxidation coupled with ROS production; (ii) depletion of reserves of low molecular mass antioxidants; (iii) inactivation of antioxidant enzymes; (iv) decrease in the production of antioxidant enzymes and low molecular mass antioxidants; and, finally, (v) certain combinations of two or more of the listed above factors [16]. When ROS levels increase, aerobic organisms employ defense mechanisms such as “antioxidants” which remove reactive species or transform them into stable molecules. The maintenance of tissue redox homeostasis is only possible through a balance between the generation and elimination of ROS. Therefore, an antioxidant can be defined as a molecule capable of delaying or preventing the oxidation of the substrate when it is at a lower concentration than the oxidizable substrate. In biological terms, a good antioxidant should be characterized by high effectiveness, versatility and operational variability to prevent formation, inhibit propagation and enhance the elimination of ROS and stimulate cell repair processes. In addition, they may act as chelating agents, inhibitors of oxidizing enzymes or cofactors of antioxidant enzymes [17].
Antioxidants can be classified as enzymatic or non-enzymatic based on their reactivity to ROS. Enzymatic antioxidants metabolize and stabilize ROS, while non-enzymatic antioxidants sequester metals that participate in the formation of ROS [17]. Therefore, the “first line of defense” is identified as the enzymatic antioxidant system, whose main function is to reduce the production of ROS by preventing interaction between reactive species or with transition metals that could give rise to species of greater reactivity. Since an imbalance or interference in the equilibrium of these enzymes could favor the increase of ROS and therefore cause cellular damage, the cellular maintenance of this system is essential for homeostasis.
The enzymatic antioxidant system is based on the joint action of three systems: (i) superoxide dismutase (SOD) catalyzes a dismutation reaction where one molecule of •O2− is oxidized to O2, while the other is reduced to H2O2; (ii) catalase (CAT) catalyzes the reduction of H2O2 into H2O and O2 and (iii) glutathione peroxidases (GPx) catalyze the reduction of a large variety of peroxides (including H2O2) with the aid of a hydrogen acceptor substrate, in this case glutathione (GSH), which is oxidized (GSSG) and then returned to its original state by the enzyme glutathione reductase [17, 18]. In addition to the endogenous enzymatic system, the intervention of other non-enzymatic compounds, the “second line of defense,” is essential to ensure redox cell homeostasis. Reduced thiols and low molecular weight antioxidants like coenzyme Q, urate, lopoic acid and GSH are some examples of these non-enzymatic antioxidant compounds.
On the other hand, some exogenous dietary antioxidants can interfere with oxidative cycles to inhibit or retard oxidative damage to biomolecules. The major classes of compounds with antioxidant activity are ascorbate (AscH−), tocopherol, carotenoids and polyphenols. These compounds show significant antioxidant power in the organism and can reach up specific sites of the cell with oxidative damage. Furthermore, it has been shown that these compounds also contribute to the endogenous antioxidant defense. It is suggested that the total amount and position of OH groups in the structure of these compounds may play a role in their anti-ROS activity (12, 17). Figure 1 shows the main dietary sources of these compounds.
Figure 1.
Main sources of diet with high in the antioxidant compounds ascorbate, tocopherol, carotenoids and polyphenols.
AscH− is the water-soluble bioactive form of vitamin C and is present in all body fluids. At physiological pH, 99% of vitamin C is present as AscH−, 0.05% in the form AscH2 and 0.004% as dianion ascorbate (Asc2−). AscH− is the chemical form that confers its main antioxidant effects. The antioxidant activity of vitamin C is either direct, through the purification of ROS, or indirect, through the regeneration of other antioxidant systems. Its antioxidant effects have been observed both in vitro and in vivo [19, 20].
Tocopherols and tocotrienols make up vitamin E. In humans, α-tocopherol is particularly important because it is found in cell membranes and plasma lipoproteins. The reactivity of tocopherols with the organic peroxyl radicals is associated with the redox properties of the chroman ring, which is responsible for its antioxidant capacity. Peroxyl radicals formed during lipoperoxidation have a higher affinity for α-tocopherol OH, which makes it a less active radical and unable to react with other fatty acids, thus stopping the chain of lipoperoxidation reactions. At this point AscH− plays an important role as it regenerates the antioxidant form of vitamin E [21].
Carotenoids are lipid-soluble antioxidants and can react with ROS by three possible mechanisms: electron transfer, hydrogen abstraction and radical addition. The antioxidant activity of carotenoids is mainly due to their double-bond conjugate structure that can delocalize unpaired electrons, hence the excellent ability of carotene to neutralize 1O2, •O2−, •OH and peroxyl radicals (ROO•). Nevertheless, it has to be highlighted that although carotenoids are considered antioxidants, there is not enough evidence yet to support the notion that carotenoids actually function as antioxidants in vivo, except for their well-documented role as photoprotectors in the inhibition of 1O2 generated by UV light in the skin and in the eyes [17, 22].
Polyphenols are compounds with variable phenolic structures that are generally classified as flavonoids, phenolic acids, stilbenes and lignans (Figure 2I). The flavonoid compounds have a central structure containing a diphenylpropane skeleton. The primary flavonoids found in fresh green tea leaves are flavanols, flavonols and theaflavins (Figure 2II). It has been observed that polyphenols act as inhibitors of lipoperoxidation and are capable of interacting directly with ROS, as well as acting as chelating agents, and they have indirect effects through their ability to modulate the levels of transcription factors and enzymes [23]. Furthermore, in the context of prophylaxis and cancer therapy polyphenols have manifested beneficial effects through the cytoprotective antioxidant response and proapoptotic action [24]. It has been observed that the anticarcinogenic activity of polyphenols is attributed to their pro-oxidant properties, which occur under certain conditions (i.e., low or very high concentration and presence of metal ions) increasing oxidant DNA damage [25, 26].
Figure 2.
(I) The classification of the phenolic structures of polyphenols. (II) Structure of flavonoids; the core structure contains a diphenylpropane skeleton. The main flavonoids found in fresh green tealeaves are: (a) flavanols, (b) flavonols and (c) theaflavins.
The flavonoids are the most powerful and effective antioxidants among the known plant phenols. For instance, EGCG is 20 times more active than vitamin C and 30 times more active than vitamin E. Just like other molecules, the chemical structures of catechins contribute to their antioxidant properties. Some catechins, including EGCG, possess an esterified gallate moiety at the third position of the C ring, the catechol group on the B ring and the OH groups at the fifth and seventh positions on the A ring (Figure 2II). The potential free radical scavenging activity of EGCG has been attributed to the presence of the gallate group [10, 27].
3. Genotoxic roles of chromium and oxidative stress
The initial stages of the biological processes of mutagenesis, carcinogenesis and aging show permanent alterations of the genetic material. In fact, it has been well documented that in various cancer tissues, free radical-mediated DNA damage has occurred. Of all the ROS (half-life <1 ns), •OH is the most reactive and interacts with all components of the DNA molecule, inducing single- or double- stranded DNA breaks, DNA cross-links and purine, pyrimidine or deoxyribose modifications [22, 28, 29]. Most of the hydroxyl radicals (•OH) generated in vivo are derived from the metal-catalyzed breakdown of hydrogen peroxide (H2O2) via the Fenton and Haber-Weiss reactions [30, 31]:
Exposure to transition metal ions(n+) such as chromium (Cr) represent a real in vivo production of ROS and free radicals due to intra-cellular reduction, since it has been established that redox-active metals participate closely in the generation of different free radicals [32]. The main genotoxic mechanism of Cr(VI) compounds has been linked to the intracellular reduction and generation of •OH [33, 34]. Furthermore, the way Cr(VI) produces ROS is a sophisticated step-wise process that starts by entering the cells through the mechanism of pinocytosis and endocytosis using channels for the transfer of isoelectric and isostructural anions, such as those for SO42− and HPO42− [35]. Inside the cell, Cr(VI) immediately binds with GSH-forming complexes, which causes it to reduce to Cr(V) and Cr(IV) intermediates (Figure 3 R-I). Alternatively, nicotinamide adenine dinucleotide phosphate (NAD(P)H) can reduce Cr(VI) to Cr(V), mediated by AscH− (Figure 3 R-II). The generated Cr(V) and Cr(IV) intermediates can react with H2O2 forming •OH and 1O2 [33, 36] via the Fenton reaction (Figure 3 R-III).
Figure 3.
Routes of Cr(VI) and polyphenols in the induction, protection and modulation of DNA oxidative stress damage.
Nevertheless, the genotoxic mechanism of Cr(VI) can be neutralized or altered. Antioxidants such as AscH- could react with •OH, quenching and converting it into a poorly reactive semi-hydroascorbate radical, which is harmless to the DNA molecule. The C8-OH-adduct radical of deoxyguanosine is formed during catalysis of •OH in the reaction of 2-deoxyguanosine with molecular oxygen, (Figure 3 R-IV); since it induces DNA strand breaks, it is considered a form of oxidative DNA damage [37, 38]. Therefore, by activating repair mechanisms, this adduct can be removed through 8-hydroxydeoxyguanosine (8-OHdG, 7,8-dihydro-8-oxodeoxyguanosine), which is a marker repairer of oxidative stress in biological systems that can be measured in fluids such as blood, urine and saliva (Figure 3 R-VII). 8-OHdG undergoes keto-enol tautomerism, which favors the oxidized 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxo-dG) product. In the scientific literature both 8-OHdG and 8-oxo-dG are equivalent and refer to the same compound. The formation of the 8-OHdG adduct is of particular importance as it indicates the interaction between •OH and guanine [22, 39].
Although the direct relationship between DNA damage and •OH is not completely clear, it has been suggested that the ROS have a role in Cr(VI)-induced genotoxicity and cytotoxicity by showing Cr(VI)-induced genomic DNA damage through the formation of 8-OHdG [40]. Furthermore, it has also been observed that Cr(VI) produces oxidative stress by inducing time- and concentration-dependent cytotoxicity through suppression of antioxidant systems and by activation of p53-dependent apoptosis [41]. Other studies have called into question the genotoxic/mutagenic effect of •OH by Cr exposure, suggesting that reduction of Cr(VI) by physiological concentrations of AscH− generates ascorbate-Cr(III)-DNA cross-links and binary Cr(III)-DNA adducts. Therefore, Cr-DNA adducts are responsible for both the mutagenicity and genotoxicity of Cr(VI) [42].
Compounds of Cr are major inorganic environmental pollutants. Its valence states range from −2 to +6 and mainly exists in two different redox forms: (i) Cr(III), an essential micronutrient that plays an important role in protein, sugar and fat metabolism and (ii) Cr(VI), known to be highly toxic, with well-documented carcinogenesis in lung, nasal and sinus tissues in toxicological and epidemiological studies. The increase of Cr(VI) compounds in the environment is caused by anthropogenic sources such as metallurgy, electroplating, inorganic chemical production, pigment and fungicide manufacturing, wood preservation, leather tanning and refractory industry. The high mobility, solubility and bioavailability of Cr(VI) compounds increase risk in human populations [36, 43, 44, 45, 46]. There are three ways in which Cr(VI) could induce effects on human health: first, by the generation of •OH (oxidative stress); second, by the modification of antioxidant enzymes like SOD, CAT and peroxidase (POX) [10, 36, 46]; and finally, by the intervention of non-oxidative mechanisms of Cr(VI) [47].
It has been demonstrated that Cr(VI) compounds induce DNA damage, gene mutation, sister chromatid exchange, chromosomal aberrations, micronuclei and cell transformation. Dominant lethal mutations have also been observed in a variety of test systems in cultured human and animal cells and in experimental animals. These effects are related to multiple mechanisms of DNA damages including DNA adducts, DNA modification caused by the covalent attachment of a chemical, cross-links such as DNA protein cross-links and DNA–DNA cross-links, abasic sites and oxidized DNA bases. Cr(VI) also plays a critical role in altering gene expression [10, 36].
4. Protection against chromium(VI)-induced DNA damage by green tea polyphenols
Green tea and its polyphenols have shown the ability to quench free radicals generated by oxidative environmental toxicants and, consequently, to reduce genotoxic damage and cancer [48]. Particularly, it has been observed that the administration of green tea to mice CD-1 protects against genotoxic damage induced by metal compounds with carcinogenic potential such as Cr(VI), suggesting that its antioxidant compounds such as polyphenols have an antigenotoxic effect on the oxidative stress generated during reduction of Cr(VI) to Cr(III) [49]. However, the protection is only partial, and this may be related to different factors such as the origin of the tea, because the amount of polyphenols in plants is influenced by environmental factors (i.e., weather, light, nutrients, preparation process, storage, horticulture leaf age, etc.) [50]. In order to eliminate this source of variation, the effects of polyphenols (polyphenon60®, extracted from green tea) have been evaluated directly. The results showed that these polyphenolic extracts reduce almost 100% of the genotoxic damage induced by Cr(VI) compounds [13].
In other studies in which specific polyphenols of green tea have been tested individually, it has been observed that protection from the genotoxic damage induced by Cr(VI) compounds has the following order: rutin (82%) > EGCG (71%) > quercetin (64%) > quercetin-rutin (59%) (Figure 4) [10, 25]. Due to their phenolic structure, it is possible that these polyphenols may act as hydrogen donors to suppress the formation of lipid radicals and free radicals, including the •O2− and •OH generated during reduction of Cr(VI) to Cr(III), in addition to being able to chelate metals [51, 52]. The decrease in genotoxic damage by these extracted polyphenols was greater than those observed when administering green tea or red wine (Figure 4) [49, 53].
Figure 4.
Levels of protection of different compounds from DNA damage caused by CrO3.
Apparently, the sugar of rutin makes it more efficient by protecting against the genotoxic damage induced by Cr(VI) by increasing its bioavailability and absorption. Rutin is hydrolyzed to its aglycone forms (quercetin) by β-glycosidase and is thus metabolized more slowly, which leads to increased activity [54]. The route of administration of polyphenols plays an important role in how efficiently they protect against genotoxic damage. For example, EGCG protected cells against Cr(VI)-induced genetic damage more effectively when administered orally than when administration following the ip route was done [10, 25]. While the ip route is more sensitive and direct [55] and therefore useful for detecting inducibility of micronuclei in polychromatic erythrocytes in short-term protocols (peripheral blood); when testing compounds with potential clastogenic properties, it is an artificial exposure route, and the route for human exposure to EGCG is oral. This is important because it has been observed that polyphenols might be biotransformed into more bioavailable forms in the gut [56] sometimes by intestinal bacteria [57]. Therefore, it is considered that the effects of polyphenols may be affected by (i) the kinetics of their absorption and elimination, (ii) the nature and the extent of their metabolism (e.g., conjugation and methylation) and (iii) the activity of each circulating compound [25].
There are two ways in which polyphenols can protect from DNA oxidative damage induced by Cr(VI) compounds. First, polyphenols can react with •OH, generating an unreactive radical and therefore preventing damage to DNA (Figure 3 R-V). Second, polyphenols can activate repair mechanisms to remove adducts through 8-OHdG (Figure 3 R-VI) which is subsequently eliminated (Figure 3 R-VII). If the oxidative damage to DNA is not repaired, breaks can lead to formation of micronuclei [13]. The administration of green tea polyphenol extracts and EGCG led to an increase in the average number of apoptotic cells. Even when green tea polyphenol extracts and EGCG was administered prior to Cr(VI), the frequency of apoptotic cells was higher than with Cr(VI) treatment alone. The enhanced induction of apoptosis following polyphenols and Cr(VI) treatments suggests that this process may contribute to elimination of the cells with Cr(VI)-induced DNA damage (micronuclei) [10, 13]. Also, it has been observed that in vivo dietary polyphenols in combination with other antioxidants such as ascorbic acid enhance inhibition of micronuclei formation induced by endogenous nitrosation in mice [58]. This proposal is consistent with the observed protection against genetic damage by antioxidants, since the frequencies of apoptotic cells increase with the administration of antioxidants. Hence, it is suggested that the combined treatments of antioxidants contribute positively to the elimination of cells with DNA damage through apoptosis [10, 59].
Apoptosis plays a crucial role in a number of physiological and pathological processes and is accompanied by characteristic morphological changes that include cytoplasmic shrinkage, plasma membrane blebbing, condensation or fragmentation of nuclei and extensive degradation of chromosomal DNA. Polyphenols are capable of regulating cell signaling pathways related to proliferation and apoptosis [60, 61]. It has been observed that polyphenols such as EGCG not only protect normal cells against genotoxic alterations induced by N-methyl-N´-nitro-N-nitrosoguanidine but that they are able to remove cancer cells by apoptosis in vitro [62]. In addition to other mechanisms, at a human achievable dose, EGCG is known to activate cell death signals and to induce apoptosis in precancerous or cancer cells, resulting in inhibition of tumor development and/or progression [63]. Therefore, it is plausible that substances able to induce apoptosis in cancer cells could be used as new anticancer agents. In fact, these findings suggest and strongly encourage more investigation into the potential of polyphenols in the treatment of cancer. Currently, few clinical trials are being carried out, and further studies are urgently needed to assess the anticancer activity of polyphenols in vivo.
Figure 5 summarizes the proposed interaction between polyphenols and Cr(VI) compounds; polyphenols can: (i) scavenge ROS such as •OH generated by Cr(VI) during its reduction to Cr(III), inhibiting their genotoxic effects; (ii) reactivate the repair mechanisms inactivated by Cr(VI), contributing to the elimination of 8-OHdG; (iii) regulate cell signaling pathways to eliminate the cells with DNA damage (micronuclei) via apoptosis.
Figure 5.
Summary of the interaction between polyphenols and heavy metals.
5. Conclusions
The relationship between diet and health has aroused great scientific interest. The consumption of antioxidants naturally present in the diet is of particular interest due to their action against the harmful effects of oxidative stress. The World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations (FAO) recommend the intake of a minimum of 400 g of fruit and vegetables a day (excluding potatoes and other starchy tubers) to prevent chronic diseases such as cancer, especially in less developed countries, on the basis that at least one-third of all cancers can be prevented [1].
A healthy diet with a sufficient daily intake of fruits and vegetables with a high content of antioxidants can contribute to the prevention of diseases caused by exposure to pollutants with carcinogenic potential, such as heavy metals associated with oxidative stress. Antioxidants found in fresh fruits and vegetables can be easily absorbed and distributed at a physiologically relevant level in tissues and biofluids where they can play an essential role in capturing ROS, chelating redox metals and regenerating other antioxidants within the “antioxidant network.” Dietary antioxidants such as polyphenols are able to protect against genotoxic damage caused by Cr(VI) metal compounds, which could be related to the prevention of carcinogenic processes associated with these metals. Although the main mechanism described for antioxidants is the clearance of ROS, DNA repair and apoptosis are possible additional pathways involved in the protection and modulation of damage to genetic material.
Although compelling new evidence shows promising protective effects of the polyphenols in green tea against genotoxic damage induced by Cr(VI) compounds, there is a lack of clinical evidence that needs to be addressed in future studies. `Some suggestions include the development of predictive biomarkers for green tea polyphenols consumption in the human population. These markers will greatly improve our current understanding of the relationship between polyphenols and the endogenous and exogenous factors that affect its bioavailability, which will in turn help establish safe and effective doses for human consumption.
Acknowledgments
The authors wish to thank for his excellent technical assistance Lourdes Hernández-Cortés. Financial support was obtained from DGAPA-UNAM, PAPIIT-IN219216.
Conflict of interest
The authors declare that they do not have any competing interests.
\n',keywords:"green tea polyphenols, genotoxic damage, hexavalent chromium, antioxidants, oxidative stress",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/60775.pdf",chapterXML:"https://mts.intechopen.com/source/xml/60775.xml",downloadPdfUrl:"/chapter/pdf-download/60775",previewPdfUrl:"/chapter/pdf-preview/60775",totalDownloads:525,totalViews:386,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,dateSubmitted:"November 21st 2017",dateReviewed:"March 20th 2018",datePrePublished:null,datePublished:"July 18th 2018",dateFinished:null,readingETA:"0",abstract:"In this chapter, the proposal that green tea polyphenols can be used effectively to protect against genotoxic effects associated with hexavalent chromium (Cr(VI)) exposure is analyzed. After explaining the chemical mechanisms involved in oxidative stress associated with the reduction of Cr(VI) compounds, the relationship between green tea polyphenols and oxidative stress is analyzed. Particular emphasis is given in elucidating how these proposals fit with our own experimental results with green tea polyphenols and Cr(VI) compounds, which show an increase of apoptotic cells and a decrease in micronucleus frequency. Finally, the gaps in our understanding of the role of green tea and its polyphenols, as well as their key importance to human health, are highlighted.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/60775",risUrl:"/chapter/ris/60775",book:{slug:"polyphenols"},signatures:"María del Carmen García-Rodríguez, Mario Altamirano-Lozano and\nAlejandro Gordillo-García",authors:[{id:"202429",title:"Dr.",name:"Carmen",middleName:null,surname:"García-Rodríguez",fullName:"Carmen García-Rodríguez",slug:"carmen-garcia-rodriguez",email:"carmen.garcia@unam.mx",position:null,institution:{name:"National Autonomous University of Mexico",institutionURL:null,country:{name:"Mexico"}}},{id:"202432",title:"MSc.",name:"Alejandro",middleName:null,surname:"Gordillo-García",fullName:"Alejandro Gordillo-García",slug:"alejandro-gordillo-garcia",email:"gordillo.alejan@gmail.com",position:null,institution:null},{id:"202433",title:"Dr.",name:"Mario",middleName:null,surname:"Altamirano-Lozano",fullName:"Mario Altamirano-Lozano",slug:"mario-altamirano-lozano",email:"maal@unam.mx",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Oxidative stress, antioxidants and green tea flavonoids",level:"1"},{id:"sec_3",title:"3. Genotoxic roles of chromium and oxidative stress",level:"1"},{id:"sec_4",title:"4. Protection against chromium(VI)-induced DNA damage by green tea polyphenols",level:"1"},{id:"sec_5",title:"5. Conclusions",level:"1"},{id:"sec_6",title:"Acknowledgments",level:"1"},{id:"sec_9",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'Lorenzo JM, Munekata PES. Phenolic compounds of green tea: Health benefits and technological application in food. Asian Pacific Journal of Tropical Biomedicine. 2016;6:709-719'},{id:"B2",body:'Gramza-Michałowska A, Kobus-Cisowska J, Kmiecik D, et al. Antioxidative potential, nutritional value and sensory profiles of confectionery fortified with green and yellow tea leaves (Camellia sinensis). Food Chemistry. 2016;211:448-454'},{id:"B3",body:'Bhagwat S, Haytowitz DB, Holden JM. 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Seminars in Cancer Biology. Epub ahead of print. 2017. DOI: 10.1016/j.semcancer.2017.08.005'},{id:"B62",body:'Roy M, Chakrabarty S, Sinha D, et al. Anticlastogenic, antigenotoxic and apoptotic activity of epigallocatechin gallate: A green tea polyphenol. Mutation Research, Fundamental and Molecular Mechanisms of Mutagenesis. 2003;523-524:33-41'},{id:"B63",body:'Singh BN, Shankar S, Srivastava RK. Green tea catechin, epigallocatechin-3-gallate (EGCG): Mechanisms, perspectives and clinical applications. Biochemical Pharmacology. 2011;82:1807-1821'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"María del Carmen García-Rodríguez",address:"carmen.garcia@unam.mx",affiliation:'
Research Unit in Genetics and Environmental Toxicology, “Facultad de Estudios Superiores-Zaragoza, UNAM”, Mexico City, Mexico
Research Unit in Genetics and Environmental Toxicology, “Facultad de Estudios Superiores-Zaragoza, UNAM”, Mexico City, Mexico
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Haq",slug:"iahtisham-haq"}]},{id:"60775",title:"The Role of Green Tea Polyphenols in the Protection from Hexavalent Chromium-Induced Genotoxic Damage",slug:"the-role-of-green-tea-polyphenols-in-the-protection-from-hexavalent-chromium-induced-genotoxic-damag",totalDownloads:525,totalCrossrefCites:1,signatures:"María del Carmen García-Rodríguez, Mario Altamirano-Lozano and\nAlejandro Gordillo-García",authors:[{id:"202429",title:"Dr.",name:"Carmen",middleName:null,surname:"García-Rodríguez",fullName:"Carmen García-Rodríguez",slug:"carmen-garcia-rodriguez"},{id:"202432",title:"MSc.",name:"Alejandro",middleName:null,surname:"Gordillo-García",fullName:"Alejandro Gordillo-García",slug:"alejandro-gordillo-garcia"},{id:"202433",title:"Dr.",name:"Mario",middleName:null,surname:"Altamirano-Lozano",fullName:"Mario Altamirano-Lozano",slug:"mario-altamirano-lozano"}]},{id:"60359",title:"Potentials of Polyphenols in Bone-Implant 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\n
1. Introduction
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Obstructive sleep apnea (OSA) is a common disease of the head and neck respiratory tract with severe systemic ramifications [1, 2]. It is characterized by multiple episodes of apnea or hypopnea during sleep resulting from partial and/or complete collapse of the upper airway. [3]
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OSA affects 10% or more of the population with males at increasingly greater risk than females. [4] It contributes to chronic conditions such as obesity, diabetes, myocardial infarction, and daytime drowsiness that leads to frequent motor vehicle accidents. [3] Many surgical and non-surgical treatment modalities exist, including continuous positive air pressure (CPAP) devices that keep the patency of the airway via exerting a baseline artificial inspiratory pressure. When patients are unable or unwilling to tolerate these bulky fixtures, they often require surgery to mechanically increase their airway volume. [5]
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Studies have described factors associated with the presentation and severity of OSA. Conditions that narrow the upper airway are particularly injurious to the at-risk patient. Physiologic features such as obesity (which increases the mass of the soft tissues around the neck), decreases in muscle or neural tone (which frequently results from sedation or old age), congenital gnathic hypoplasias (which may exist without other notable medical findings), and craniofacial syndromes (which could contribute to abnormal hypoplasia of multiple craniofacial features) have been implicated. [6]
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\n
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2. History
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Ancient Greeks first noted OSA or OSA-like snoring conditions in their 4th century BC accounts of Dionysius, the tyrant of Heraclea who was said to be “obese beyond measure.” The first modern medical description is attributed to James Russell and his peers as a syndrome of obesity and daytime drowsiness. OSA was poetically if not erroneously named the “Pickwickian syndrome” after the snoring “fat boy Joe” in Charles Dickens’s novel “The Posthumous Papers of the Pickwick Club.” [7] Dickens’s tale would depict the life of an obese servant boy whose daytime activities were marred by debilitating drowsiness as often noted in modern OSA patients.
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While clinicians and writers alike noted the distinct obesity of most OSA patients, obstruction was deemed inevitable until the development of the CPAP device in 1981 by Colin Sullivan and colleagues at the University of Sydney. [8] CPAP first saw use as a bulky nasal device that soon became the gold standard in OSA care.
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\n
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3. Causes
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OSA frequently co-presents with chronic conditions, the most prevalent of which is obesity. Obesity increases the mass and volume of parapharyngeal tissues, which can fall back in a supine position to cause respiratory obstruction during sleep. In fact, supine sleepers and patients with adeno-tonsillar enlargements experience OSA more frequently [9]. Metabolic conditions like hyperlipidemia and diabetes that may result from one or both of OSA and obesity. [10]
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Similarly, other pathoses leading to airway narrowing also predispose patients to OSA. Central and peripheral neural injuries that decrease the airway muscle tone have been shown to contribute to OSA in patients suffering from trauma. [11] Craniofacial syndromes like Down Syndrome that cause retrolingual hyperplasia and/or mandibular hypoplasia have been implicated in higher instances of OSA. [6] As such, OSA may also entail a genetic component with shared genes involving the formation of the nose, mouth, and throat likely predisposing certain families to higher rates of disease.
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4. Signs and symptoms
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As noted above, OSA has historically been defined by daytime drowsiness, loud snoring, and nighttime choking. This frequently leads to a higher incidence of automotive accidents and narcolepsy-like episodes [4]. Furthermore, implications in neurocognitive pathoses including impairments to attention, executive functioning, and long-term memory have been documented. [12]
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More recent studies indicate that OSA may also be an etiological factor behind diabetes, hypertension, coronary artery disease, and stroke. Appropriate treatment of OSA may reduce the risk of developing these conditions. [10] Obesity may also play a role as both a risk factor and a complication of OSA. Studies stipulate that alterations of molecular signaling pathways via repeated hypoxic episodes contribute to autonomic dysregulation, systemic inflammation, cardiopulmonary irregularities, and organic oxidation which predispose patients to metabolic diseases. [13] In fact, OSA has been linked to an increased risk of early death in patients under the age of 70. [2]
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Studies of OSA in children are less common and may be confounded by the effects of puberty. They nonetheless indicate that while children with sleep-disordered breathing are at risk of attention and executive deficits like their adult counterparts, they show additional deficits in empathy, social behaviors, and phonological processing. [12] Children with OSA may also be predisposed to pulmonary hypertension and nocturnal enuresis. [14]
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5. Diagnosis
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Today, polysomnography plays a central role in the diagnosis of both central and obstructive sleep apnea. A patient’s apnea-hypopnea index (AHI) is taken along with the patient’s brain (electroencephalography or EEG), eye (electrooculography or EOG), muscle (electromyography or EMG), and/or heart (electrocardiography or ECG) activities which enumerates the average number of apneic or hypopneic events per hour of physiologic sleep. An apneic event is defined as a 90% or more reduction of airflow lasting at least 10 seconds. An hypopneic event is defined as a 30–90% reduction of airflow lasting at least 10 seconds accompanied by a 3% or greater decrease in pulse oxygenation. [15] A diagnosis of mild OSA is made with an AHI of 5 to 15, moderate OSA with AHI of 15 to 30, and severe OSA with AHI of 30 or more events per hour (Table 1). Significant ECG abnormalities may also be present, which could indicate an increased severity of disease. [13] This scale is adjusted for the categorization of OSA in children. Pediatric OSA is classified as mild if AHI is between 1 to 5, moderate if between 5 to 10, and severe if greater than 10 events per hour.
Though less common, some literature instead utilize the respiratory disturbance index (RDI) to diagnose or monitor the progress of OSA. The RDI is determined as a sum of AHI and respiratory-effort related arousals (RERAs), which are characterized by increasing respiratory effort for 10 seconds or more leading to an arousal from sleep. Similarly to the AHI scale, the American Academy of Sleep Medicine regards RDI of 5 to 15 as mild, 15 to 30 as moderate, and more than 30 as severe. [16]
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Drug-induced sleep endoscopy (DISE) is another diagnostic modality for the detection of upper airway collapse during sleep. A sedative agent such as propofol, midazolam, or dexmedetomidine is administered to create a somewhat artificial state of sleep, during which a flexible endoscope is utilized to view the nasopharyngeal and oropharyngeal airways to monitor areas of collapse. While DISE can be a useful modality in detecting the degree and pattern of obstruction, its use may be limited as a result of 1) unnatural sleep patterns as a result of drug-induced nature of the slumber, 2) difficulty of maintaining the appropriate degree of sedation without causing undue cessation of respiration, and 3) uncertain reproducibility when scoring the degree of obstruction across different observers [17]. The use of propofol and/or dexmedetomidine purportedly re-creates a more natural pattern of sleep when compared to other medications like benzodiazepines.
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The clinical manifestation of daytime sleepiness can be monitored via several patient surveys such as the Berlin and Epworth Sleepiness questionnaires (Tables 2 and 3). Recent studies suggest that the STOP-BANG questionnaire (Table 4) as devised by researchers at the University of Toronto is particularly effective not only as a screening tool but also as an adjunct to clinical follow up after operative interventions. [21, 22]
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How likely are you to doze off or fall asleep in the following scenarios?
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0 = Never
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1 = Slight chance of dozing off
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2 = Moderate chance of dozing off
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3 = High chance of dozing off
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Total Score – A score of greater than 10 denotes a higher risk of OSA
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0 – 5: Lower normal daytime sleepiness
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6 – 10: Higher normal daytime sleepiness
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11 – 12: Mild excessive daytime sleepiness
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13 – 15: Moderate excessive daytime sleepiness
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16 – 24: Severe excessive daytime sleepiness
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\nScenarioScore
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Sitting and reading________
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Watching TV________
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Sitting inactive in a public place (i.e. theater)________
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As a passenger in a car for an hour________
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Lying down to rest in the afternoon________
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Sitting and talking to someone________
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Sitting quietly after lunch without alcohol________
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While stopped in traffic for a few minutes________
In general, patients with a score of 2 or below are considered low risk, 3 to 4 intermediate risk, and 5 or greater high risk.
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6. Management
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Treatment of OSA may frequently reverse its systemic consequences, though permanent brain alterations may occur that prevent complete recovery of deficits in psychomotor functioning. [12] However, most studies concur that metabolic consequences (including those associated with diabetes and obesity) improve after resolution or improvement of OSA. [4, 6, 12]
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An effective management of OSA can be categorized as either a “success” or a “cure.” In general, a successful treatment denotes a 50% or greater reduction in AHI such that it decreases to an AHI of 20 events per hour or less. The definition of a curative treatment is more stringent and requires the reduction of AHI to 5 events s per hour or less. [13] Interventional success may also be defined as a 50% or greater reduction in RDI with a post-procedural RDI of 15 or less. [23]
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7. Conservative management
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Conservative therapy remains the mainstay of OSA treatment because of their low risk and reversibility of treatment. Furthermore, pharmacologic and/or surgical interventions may require a stricter set of inclusion criteria and may not be appropriate for every patient. [24]
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Conservative therapy can be as non-invasive as a simple avoidance of certain substances or dietary patterns. As described previously, avoidance of obesity via healthy diet and possibly even exercise alone may improve symptoms of OSA. [25] Abstinence from sedating compounds and airway muscle relaxants – such as alcohol - is also beneficial. [26] Patients should cease exposure to airway irritants like tobacco smoke and partake in activities that encourage patency of the airway like sleeping in inclined or lateral positions and playing wind instruments. [26, 27, 28, 29]
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CPAP devices are considered the gold standard of OSA therapy. They function by creating consistent air pressures in airways to keep them patent during sleep. CPAP has a long history of demonstrated efficacy, and its use has also been associated with decreases in a number of associated conditions including cognitive impairment, daytime drowsiness, and cardiovascular disease. [30, 31, 32] CPAP machines are nonetheless bulky and uncomfortable to wear, leading to a high rate of noncompliance. [33] Modified equipment such as bilevel positive airway pressure (BiPAP) or automatically-titrated (APAP) devices, which monitors breathing to exert a higher pressure during inhalation and a lower pressure during exhalation, can reduce discomfort associated with their use. [34]
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Oral appliance therapy is also considered an acceptable, reversible therapy for OSA especially in cases of mild or moderate sleep apnea. [35] The devices typically function by inducing an anterior posture of the mandible that, in theory, helps increase the antero-posterior diameter of the retrolingual airway. While oral appliances are much more compact and often better tolerated, its efficacy remains controversial and long term use may be associated with dry mouth, dental trauma, and jaw pain. [26, 36]
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8. Pharmacologic interventions
\n
In general, the evidence supporting pharmacotherapy remains insufficient. [24, 37] Antidepressants and serotonin-promoting compounds were studied because activation of serotonin 5-HT2 receptors in the brainstem was shown to induce excitatory input to the hypoglossal neurons, which in turn incites an anterior advancement of the tongue. [38] Mirtazapine in particular was shown to reduce AHI in the short term, but its long-term administration is associated with sedation and weight gain, which are known adverse risk factors of worsening OSA. [39] Paroxetine was also studied but its effects were found not to be significant, [40] possibly because non-discriminatory activation of both peripheral 5-HT3 and 5-HT2 and receptors has been associated with REM-associated apnea. [41]
\n
Parasympathomimetics like donepezil may modulate airway and/or tongue muscle contraction via cholinergic pathways. Its use was associated with a reduction in AHI by approximately 20%, [42] which would not meet the clinical definition of successful or curative treatment in all but mild cases. Respiratory smooth-muscle relaxants like theophylline were found to be either ineffective or to trigger counter-productive deteriorations in sleep quality because of their stimulatory properties. [43]
\n
Dronabinol and a combination of ondansetron and fluoxetine demonstrated some promise in controlling the rate of AHI in sleep apneic patients. While ondansetron or fluoxetine alone were ineffective, their combination showed more than a 40% reduction in AHI. Investigators stipulate that fluoxetine may stimulate central 5-HT2 receptors while ondansetron suppresses the activation of their peripheral 5-HT3 counterparts. [44] Dronabinol also incurred dose-dependent 40–50% reductions in AHI over a 6-week period of use. Cannabinoids like dronabinol activates cannabinoid type 1 (CB1) receptors, which in turn also antagonizes the actions of 5-HT3 receptors. [45] However, neither the ondansetron-fluoxetine combination nor dronabinol showed clear clinical improvements in daytime drowsiness.
\n
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9. Sleep surgery
\n
While conservative therapy is considered the first line intervention for OSA, surgery may be indicated in patients who are unable or unwilling to tolerate lifelong conservative therapy. [5] A 2004 study of military veterans suggested that even singular surgical therapy may provide more than a 30% increase in overall survival benefit. [46] In fact, a combination of multiple surgical modalities may achieve a 60% reduction in AHI, which is comparable to that of CPAP which demonstrates between a 60 to 70% reduction. [47, 48]
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10. Tonsillectomy
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Surgical intervention may encompass the soft and/or the hard tissues of the upper airway. Tonsillectomy is a soft tissue-oriented procedure that may be of benefit especially in children since their apneic episodes are predominantly caused by enlarged lymphoid tissues of the upper airway. [3] The long-term efficacy, however, is not yet well established. [49] In tonsillectomy, the lymphoid tissues and its capsular container are dissected wholly from its surrounding tissues. Sharp dissection with scalpel and electro- or diathermic-cautery may be used, followed by blunt dissection. [50] Notable vessels in the area are ligated using sutures which may be assisted by using topical thrombin. Post-operative bleeding may be significant which manifests in approximately 2% of patients and typically occurs approximately 1 to 2 weeks post-operatively. [51]
\n
\n
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11. Septoplasty with or without turbinate reduction
\n
Septoplasty may also be conducted to address obstructions of the nasal passageway, which could worsen OSA symptoms. It is frequently conducted in patients with or without OSA to help relieve internal nasal valve obstruction. While nasal surgery alone may not significantly reduce AHI, it may be a viable adjunct therapy when utilized with another intervention. [52] Septoplasty with turbinate reduction has been associated with better tolerance of CPAP therapy. [53]
\n
To conduct septoplasty, an intranasal vertical incision is made through the septal mucosa and the perichondrium on the side of the obstruction. (Figure 1) The approach is then taken posteriorly in a sub-perichondral fashion using a blunt instrument. The overlying soft tissues are carefully dissected from the obstructing spur or deviation to avoid tears. Vertical chondrotomies are made anterior and posterior to the obstruction so that the mucosa may be detached from the contralateral septal surface. A horziontal chodrontomy is made connecting the superior edges of the vertical chondrotomies. The horizontal chondrotomy is made at least 1 cm from the superior margin of the septum to preserve the structural integrity of the septum and prevent a saddle defect. The portion of cartilage containing the spur or deviation is then freed from the nasal spine and removed.
\n
Figure 1.
The cartilaginous septum.
\n
Adjunctive turbinate reduction may be accomplished via another vertical, full-thickness incision anterior to the inferior turbinate (or concha) at the attachment point to the lateral nasal wall. (Figure 2) A subperiosteal plane is raised to expose the osseous turbinate. Forceps may then be introduced through the incision to remove the turbinate in small pieces. The overlying mucosa should also be reduced using a microdebrider without perforating through the soft tissue. Any remaining osseous portions may then be outfractured with a blunt instrument by applying lateral pressure.
\n
Figure 2.
Inferior turbinate position in the nasal cavity.
\n
The septal and/or turbinate mucosal incisions are sutured closed using a resorbable suture. Doyle splints or multiple interrupted transseptal sutures may be placed for five days to prevent the formation of a septal hematoma.
\n
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12. Uvulopalatopharyngoplasty
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Uvulopalatopharyngoplasty (UPPP) is perhaps the most performed sleep surgery. While the large variety of OSA-associated factors make it difficult to gauge the exact success rate of UPPP, it appears to be more efficacious in patients without excessive neck size or BMI. UPPP is also notably less effective in those with multilevel obstructions beyond those of the retropalatal and retrolingual tissues. [54]
\n
In UPPP, the uvula, tonsils, and sometimes adenoids are first removed to remove the protrusive bulks of oropharyngeal tissue with particular attention towards preserving the posterior tonsillar pillars. (Figure 3) The uvula may be excised with a wedge incision through its base to aid in closure.
\n
Figure 3.
An anatomic depiction of the uvula, tonsils, and their surrounding pillars.
\n
The operator could then elect to further widen the lateral soft tissues of the oropharynx via lateral expansion pharyngoplasty. The bilateral palatopharyngeus muscles are located through the tonsillectomy incisions, dissected from the pharyngeal walls, then transected at a point approximately 2/3rds of the way from the palate to the tonsillar pillar base. The freed muscles may then be folded antero-superiorly through a tunnel deep to the palatal mucosa or through an incision placed through the palatal soft tissues. The previously transected edge of the palatopharyngeus is then sutured to the fixed aponeurotic tissues around the hamulis such that the action of the palatopharyngeus triggers a lateral expansion of the airway at the soft palate.
\n
The posterior palatal pillars may then be suspended anteriorly via suturing the pillars to the pterygomandibular raphe. The incision sites for the uvula, tonsils, adenoids, and/or palatopharyngeus are sutured closed to create a smooth mucosal surface.
\n
\n
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13. Hyoid suspension
\n
Hyoid suspension (HS) is a relatively noninvasive surgical procedure that is commonly performed in conjunction with UPPP or genioglossus advancement. Like UPPP, HS is indicated for milder cases of OSA with retrolingual and hypopharyngeal (not retropalatal) obstructions. [55] HS alone may not provide significant improvements to the AHI and is typically conducted as a component of comprehensive therapy. [23] In a study of female OSA patients, isolated HS consistently failed to achieve surgical success but obtained near-curative results when hyoid-mandibular suspension was conducted alongside UPPP. [55]
\n
HS functions via an artificial anteropositioning of the hyoid and thus increased anteroposterior dimensions of the airway. [23] The hyoid bone would traditionally be suspended to the lingual surface of the mandible, (Figure 4) though the need for an additional incision at the submental region as well as extensive dissection through the submental tissues have led to modified procedures that suspend the hyoid bone to the thyroid cartilage instead. [55]
\n
Figure 4.
Position of the hyoid bone.
\n
In both surgical variants, the hyoid bone is first approached via a direct incision. The infra-hyoid muscles are dissected from the bony surface and the stylohyoid ligaments are sectioned from the lesser cornu. (Figure 5) In cases of hyoid suspension to the mandible, the submental region is then approached via sharp and/or blunt dissection to the lingual surface of the mandible. The digastric and mylohyoid muscles are separated laterally to avoid complete dissection from the mandible.
\n
Figure 5.
The muscular and ligamentous attachment sites of the hyoid bone.
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Two or more bony anchors are placed near the attachment site of the genioglossus. (Figure 6) Non-resorbable sutures or wires may be wrapped around the body of the hyoid then passed through the bony anchors (in the case of hyo-mandibular suspension) or the thyroid cartilage (in the case of hyo-thyroid suspension) to advance the hyoid bone approximately 3 cm, inducing tension in its muscular attachments. [23, 55] A drain may left in place for 2 to 3 days to help reduce the risk of seroma or hematoma.
\n
Figure 6.
Depiction of the genioglossus and its attachment site.
\n
\n
\n
14. Genioglossus advancement
\n
Genioglossus advancement (GA) is another surgical procedure commonly conducted in combination with HS or maxillomandibular advancement. The genioglossus muscle - and therefore, the base of the tongue – is advanced anteriorly to increase the anteroposterior diameter of the retrolingual airway. [56] While its rate of success as a standalone treatment remains at approximately 50%, this rate may increase greatly when conducted in conjunction with maxillomandibular advancement. [57] As expected, GA is not effective in treating obstructions at the palate.
\n
GA may be performed as an anterior mandibular osteotomy to advance the genioglossus muscle without altering the external appearance of the chin. A pre-operative CT scan is utilized to locate the anterior attachment site of the genioglossus at the mental spine of the mandible. (Figure 7) An osteotomy guide – frequently made as an occlusal-based appliance to fit over the mandibular dentition - is then created to separate this site from the rest of the mandible via a rectangular bicortical osteotomy approached from the buccal side of the mandible. [56]
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Figure 7.
Mental spine and the attachment sites of the genioglossus muscle.
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An intraoral incision is made through the anterior mandibular buccal vestibule to reach the osteotomy site at the symphysis. The subperiosteal dissection should be extended down to the inferior border of the mandible and laterally to the regions of the bilateral canines. Once the osteotomy is conducted, the freed segment of mandibular bone is typically advanced such that the lingual cortex of the freed segment is at or anterior to the buccal cortex of the surrounding mandible. The buccal cortex and the cancellous portions of the freed segment may be trimmed away to minimize bony protrustion at the chin. The freed segment is fixated in place using titanium plates, which may be custom-made for convenience.
\n
GA may also be performed as a part of cosmetically driven genioplasty in individuals with retrognathia. A large portion of the mental protuberance is advanced in addition to the segment of bone attached to the genioglossus muscle, which increases chin volume and esthetic outcome. [57] Instead of osteotomizing just the attachment site of the genioglossus, the operators would utilize an osteotomy guide that also encompasses a bulk of the mental protuberance. (Figure 8).
\n
Figure 8.
Mental protuberance at the inferior aspect of the mandibular symphysis.
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\n
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15. Maxillomandibular advancement
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Maxillomandibular advancement (MMA) is considered an effective surgical modality for patients affected by nasopharyngeal, retropalatal and/or retrolingual obstructions. [5, 58, 59] A recent meta-analysis suggests that MMA has greater than a 98% rate of clinical improvement, 85% rate of treatment success, and approximately 40% rate of a complete cure. [59] A potential downside of MMA treatment includes its invasiveness and applicability only in individuals who are esthetically amenable to an increasing prominence of the bimaxillary complex. Conversely, an MMA may be especially well suited for patients with hypoplastic dentofacial deformities who require such bony changes. [60]
\n
Like GA, MMA requires pre-operative planning frequently aided by CT scans. The radiographs may then be supplemented by stone models or optical scans of the patient’s dentition to increase the accuracy in virtual surgical planning (VSP). Occlusal dental splints are produced which help execute the planned bony movements. MMA also frequently requires that approximately 1 year of pre-operative orthodontics be conducted to create a stable occlusion that is not only esthetic but is amenable to intermaxillary fixation (IMF).
\n
To conduct MMA, a LeFort 1 osteotomy and a bilateral sagittal splint osteotomy (BSSO) are conducted to advance the palatal-alveolar complex and the body of the mandible, respectively. (Figure 9) These horizontal advancements may be conducted in conjunction with a counterclockwise rotation of the maxillomandibular complex (when viewed in a right lateral position) to accomplish a total advancement of the mandibular symphysis by at least 10 mm from its native position. [57, 60]
\n
Figure 9.
The palatal-alveolar complex of the maxilla.
\n
Typically, the LeFort 1 osteotomy is conducted first to establish a stable upper dental position. The anterior and lateral walls of the maxilla are exposed via an incision through the maxillary buccal vestibule. A subperiosteal dissection is conducted, after which a saw osteotomy is made through the anterior and anterolateral walls of the maxillary sinuses. (Figure 10) The osteotomies are continued posteriorly through the medial and lateral walls of the sinuses using osteotomes. The lateral pterygoid plates are also detached from the maxilla proper using a curved osteotome. The operator may elect to make a lateral approach to the pterygoid plates by gently “walking” the osteotome posteriorly along the lateral and posterior walls of the maxillary sinuses until the tip of the osteotome makes contact with a slight concavity at the pterygomaxillary junction. Gentle mallet impacts are then utilized to accomplish the detachment.
\n
Figure 10.
The anterior, medial, lateral, and posterior walls of the maxillary sinus and their relationships to the lateral pterygoid plate.
\n
The nasal mucosae are also bluntly dissected from its attachments to the inferior and lateral walls of the nasal cavity. At this point, the posterior walls of the maxillary sinuses are the only osseous connections between the palatal-alveolar and the midface segments of the maxilla. (Figure 11) A gentle downward pressure is applied at the anterior maxillary dentition to cause a controlled, horizontal fracture across the posterior walls of the maxillary sinuses. The soft tissue attachments to the palatal-alveolar segment are then stretched in preparation for its anterior movement.
\n
Figure 11.
A coronal section demonstrating the darkened, intact posterior walls of the maxillary sinuses.
\n
The freed palatal-alveolar segment is then advanced approximately 10 mm via the use of preformed “intermediate” dental occlusal splints, which engages the mandibular dentition to hold the maxillary teeth approximately 10 mm anteriorly from their original positions. IMF is conducted with the splint in place (either with arch bars, pre-existing orthodontia, or intermaxillary screws) to stabilize the palatal-alveolar segment to the mandible. This allows the surgeons to trim and apply plate fixation to the palatal-alveolar segment in its new position relative to the rest of the maxilla.
\n
The BSSO is performed next, although some providers may elect to perform the BSSO first followed by the LeFort 1 osteotomy. IMF is released and incisions are made through the bilateral buccal vestibules of the mandible to reveal the lateral cortex of the mandibular body as well as the antero-medial surfaces of the ramus. A monocortical saw osteotomy is then started from a point just superior to the lingula and continued downwards along the superolateral cortex of the mandibular body until it reaches the cortex just lateral to the first molar. (Figure 12) The positioning of this osteotomy reduces the risk of injury to the inferior alveolar neurovascular bundle at its entrance and through its canal. Gentle osteotome pressure is applied through the osteotomies to propagate controlled fractures at the posterior wall of each ramus and the inferior wall of each mandibular body.
\n
Figure 12.
The maxillomandibular complex. BSSO are conducted through the superolateral cortex of the mandibular body just medial to the ramus and just lateral to the posterior dention.
\n
Once the body of the mandible is freed from its bilateral ramus-condyle segments, preformed “final’ dental occlusal splint may be used to advance the mandibular body segment. The splint engages the now-stable maxillary dentition to hold the mandibular teeth approximately 10 mm anteriorly from their original positions. IMF is again conducted with the new splint in place. The mandibular segment may be fixated in its new position (using orthopedic plates) relative to the bilateral ramus-condyle segments. After releasing the IMF and confirming correct occlusion, the patient should be re-placed in IMF for approximately two weeks followed by four additional weeks of non-chew diet.
\n
The BSSO should be conducted first in cases where the pre-operative CT scans were taken without the condylar heads seated in the temporal fossa. The condyles may be seated after a proper mandibular advancement, and the new mandibular dental occlusion may then be used as the reference against which the palatal-alveolar segment is advanced.
\n
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16. Hypoglossal nerve stimulator
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The hypoglossal nerve stimulator (HGNS) is a newly developed device that activates the hypoglossal nerve upon detection of an apneic episode. It includes a sensing and a stimulating electrode, which detects then mitigates apnea, respectively. HGNS is particularly effective in individuals with non-concentric, antero-posterior collapse of the retrolingual airway on DISE. It demonstrated a median AHI improvement of 68% in individuals with BMIs under 32 kg/m^2. [61] After implantation, the HGNS impulses may be adjusted according to the patient’s post-operative AHI and/or RDI values. Higher impulse charges may be avoided in sensitive individuals who are awakened by a sudden activation of the hypoglossal nerve.
\n
To place the HGNS, a submandibular incision is first made approximately 2 cm below the inferior border of the mandible to avoid the marginal mandibular branch of the facial nerve. The site is dissected until the hyoid bone is appreciated, followed by a slight lateral extension to identify the posterior and anterior bellies of the digastric muscle. (Figure 13) The digastric tendon is identified and isolated from the surrounding soft tissues using retractors. The hypoglossal nerve is found in the space medial to the digastric muscle just lateral to the hyoid bone. It is close to the Ranine vein which lies immediately posterior.
\n
Figure 13.
Main anatomic landmarks for HGNS surgery including the hyoid bone and the digastric muscles.
\n
The Ranine vein may be ligated and the hypoglossal nerve further dissected anteriorly from the surrounding tissues to locate its “inclusion” and “exclusion” branches. The inclusion branches are those that protrude the tongue and the exclusion branches are those that retrude it. The two branches may be distinguished with a stimulator, and the HGNS stimulating electrode is cuffed to the primary inclusion branch. The electrode itself should be secured to the digastric tendon using nonresorbable sutures to prevent dislocation from the nerve.
\n
The upper chest incision is then made approximately 4 cm below the mid- clavicle down to the pectoralis fascia, which is left intact. A supra-fascial dissection is made to create a small cavity for the pulse generator. A lateral chest incision is also needed about 2 cm below and 5 cm laterally from the nipple for the implantation of the sensing lead. The approach is continued through the serratus anterior and external intercostal muscles to secure the sensing electrode in a plane between the external and internal intercostal muscles. (Figure 14) The internal intercostal muscles must be left intact to avoid pneumothorax.
\n
Figure 14.
The external and internal intercostal muscles.
\n
The sensing electrode wires are tunneled subcutaneously from the lateral chest site to the pulse generator at the upper chest site. Similarly, the stimulating electrode wires are also tunneled in a sub-platysmal plate from the neck site to the pulse generator. The pulse generator is sutured in place at the upper chest pocket and connected to the respective electrode wires. The generator’s power supply should be replaced approximately every ten years.
\n
\n
16.1 Tracheostomy
\n
Tracheostomy is perhaps the oldest and the most definitive intervention for OSA. An incision is made through the anterior neck to insert a semi-permanent airway, bypassing both the naso- and oropharynx. Though it is typically performed to establish an emergency airway and/or to create a long-term ventilation port, it may be performed in cases of severe obstructive sleep apnea that is otherwise refractory to other treatment modalities. Tracheostomy is considered a treatment of last resort owing to its invasive nature and a relatively high rate of complications such as hemorrhage, tracheal stenosis, tracheoesophageal or tracheocutaneous fistula, and bronchospasm regardless of the approach taken. [62, 63] A recent systematic review indicated that percutaneous dilatational tracheostomy carries an overall mortality rate of approximately 1 in 600. [64] It also requires dedicated maintenance including frequent suctioning and regular replacement of its parts.
\n
Elective tracheostomy for OSA should be conducted in a sterile fashion in the operating room. A horizontal incision is made approximately 2 cm superior to the suprasternal notch then dissected through the subcutaneous and platysmal layers. The subsequent fascia and strap muscles are divided along a vertical line until the thyroid gland or the pretracheal fascia are encountered. Any thyroid tissues encountered may be retracted superiorly, and the pretracheal fascia bluntedly dissected away from the airway.
\n
At this point, the patient’s FiO2 should be lowered and the endotracheal tube advanced further to avoid the risk of fire and cuff puncture, respectively. A horizontal incision is first made between the tracheal rings. (Figure 15) This is connected to a vertical, downward incision through the tracheal ring just below from each end of the horizontal incision to raise a Bjork flap. Resorbable sutures are passed under the cartilagenous ring to fixate the flap to the overlying skin. An appropriately sized tracheostomy tube is inserted atraumatically then stabilized to the neck using a trap. The endotracheal tube may be removed, and the tracheostomy tube cuff inflated.
\n
Figure 15.
The anatomy of the thyroid, cricoid, and tracheal cartilages.
\n
\n
\n
\n
17. Pediatric OSA
\n
In general, both the prevalence and treatment threshold for OSA in children is lower. [65] Children with AHI greater than 5 should undergo treatment to help normalize breathing. For patients with AHI ranging from 1 to 5, treatment should be considered if OSA-related comorbidities such as obesity, hyperactive behaviors, lymphoid hyperplasia, enuresis, and/or increased inflammatory markers are present. [65, 66] Non-invasive measures like weight loss and avoidance of irritants like tobacco smoking are universally helpful. [65]
\n
Most literature indicate an OSA incidence of 1 to 4%. [67] This occurrence peaks between the ages of 2 to 8, which roughly coincides with the peak instances of lymphoid hyperplasia. Traditional treatment therefore consists of tonsillectomy with or without adenoidectomy. However, the success rate may range as low as 27% even though delaying correction of disordered breathing can lead to gnathic or craniofacial anomalies. [66] While removal of tonsillar or adenoidal tissues can be conducted at any age, other surgical interventions may incur a greater rate of complications (in non-syndromic patients) if conducted prior to age 3 or in individuals weighing less than 15 kg. [65, 68]
\n
Alternative surgical modalities include septoplasty and UPPP. Osseous surgeries should be reserved for those with craniofacial deficits as extensive osteotomies frequently disrupt the rate and pattern of skeletal growth. Maxillary and/or mandibular distraction may be employed early to utilize the rapid healing potential in children with severe micrognathia. [65]
\n
Unlike in adults, CPAP should be reserved for moderate or severe cases of pediatric OSA that cannot be treated surgically. [69] CPAP compliance rate is even lower in children, and a lack of appropriate pediatric CPAP appliances as well as long sleeping hours exacerbate this issue. [70] CPAP can also trigger nasal symptoms such as congestion, epistaxis, and midface retrusion. [65] Patients who cannot tolerate or are refractory to surgery and CPAP should undergo treatment via tracheostomy. [69]
\n
\n
\n
18. Surveillance
\n
Post-intervention polysomnography or DISE may be conducted at least 3 months after therapy to reduce confounding effects of post-operative edema. STOP-BANG, Epworth, and/or Berlin questionnaires should also be utilized to ensure improvements in the patient’s quality of life.
\n
The Stanford Protocol is a predictable and effective protocol outlining the proper elevation of care in cases of OSA relapse. [71] Surgical management of OSA should begin with the phase 1 treatments consisting of septoplasty, UPPP, then GA. Phase 2 treatment is MMA and may be conducted in case of relapse after phase 1. While phase 2 treatment appears sufficient for most patients, a recent update to the Protocol showed that HGNS could be conducted in cases of phase 2 treatment failure. [72] MMA may prevent lateral pharyngeal wall components of airway collapse, thereby increasing the efficacy of HGNS which best addresses antero-posterior obstructions.
\n
\n
\n
19. Conclusions
\n
Obstructive sleep apnea is a complex disease of numerous significant ramifications which require careful diagnosis and management. As with many chronic conditions, OSA should be first approached via conservative treatment which often remains equally or more effective as their invasive counterparts. Once the reversible conservative modalities are exhausted, the more invasive therapies should be approached with caution. Modern interventional protocols like the Stanford Protocol may provide guidance based on the successes of large volume surgical cohorts.
\n
\n
Acknowledgments
\n
The anatomic figures in this chapter (Figures 1 through 13) have been obtained from the work of Drs. Henry Gray and Henry Vandyke Carter within the public domain of the United States of America.
\n
Conflict of interest
The authors declare no conflicts of interest.
\n',keywords:"polysomnography, apnea, hypopnea, obstructive sleep apnea, obesity, continuous positive airway pressure, septoplasty, uvulopalatopharyngoplasty, hyoid suspension, genioglossus advancement, maxillomandibular advancement, hypoglossal nerve stimulation",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/74581.pdf",chapterXML:"https://mts.intechopen.com/source/xml/74581.xml",downloadPdfUrl:"/chapter/pdf-download/74581",previewPdfUrl:"/chapter/pdf-preview/74581",totalDownloads:60,totalViews:0,totalCrossrefCites:0,dateSubmitted:"June 26th 2020",dateReviewed:"November 19th 2020",datePrePublished:"December 25th 2020",datePublished:null,dateFinished:"December 25th 2020",readingETA:"0",abstract:"Obstructive sleep apnea (OSA) represents a major public health issue affecting over 10% of the general adult, more than 80% of the geriatric, and up to 11% of the pediatric populations. Numerous studies have demonstrated distinct associations between OSA and diabetes, daytime drowsiness, and cardiopulmonary compromise including myocardial infarction. Considering the estimated rate of underdiagnosis, OSA is expected to exert a significant unrealized toll on the global healthcare infrastructure with the number of diagnoses increasing each year. The diagnosis of OSA entails subjective and objective evaluations including sleep surveys and polysomnography. Accordingly, treatment of OSA also encompasses a large variety of conservative, pharmacologic, and surgical interventions. Treatment selection remains a difficult but critical part of intervention especially when multiple modalities are required. This chapter aims to describe not only the presentation of this head and neck airway pathology but the interprofessional management strategies employed.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/74581",risUrl:"/chapter/ris/74581",signatures:"Ho-Hyun (Brian) Sun and Sally Sun",book:{id:"9790",title:"Surgical Management of Head and Neck Pathologies",subtitle:null,fullTitle:"Surgical Management of Head and Neck Pathologies",slug:null,publishedDate:null,bookSignature:"Dr. Ho-Hyun (Brian) Sun",coverURL:"https://cdn.intechopen.com/books/images_new/9790.jpg",licenceType:"CC BY 3.0",editedByType:null,editors:[{id:"184302",title:"Dr.",name:"Ho-Hyun (Brian)",middleName:null,surname:"Sun",slug:"ho-hyun-(brian)-sun",fullName:"Ho-Hyun (Brian) Sun"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. History",level:"1"},{id:"sec_3",title:"3. Causes",level:"1"},{id:"sec_4",title:"4. Signs and symptoms",level:"1"},{id:"sec_5",title:"5. Diagnosis",level:"1"},{id:"sec_6",title:"6. Management",level:"1"},{id:"sec_7",title:"7. Conservative management",level:"1"},{id:"sec_8",title:"8. Pharmacologic interventions",level:"1"},{id:"sec_9",title:"9. Sleep surgery",level:"1"},{id:"sec_10",title:"10. Tonsillectomy",level:"1"},{id:"sec_11",title:"11. Septoplasty with or without turbinate reduction",level:"1"},{id:"sec_12",title:"12. Uvulopalatopharyngoplasty",level:"1"},{id:"sec_13",title:"13. Hyoid suspension",level:"1"},{id:"sec_14",title:"14. Genioglossus advancement",level:"1"},{id:"sec_15",title:"15. Maxillomandibular advancement",level:"1"},{id:"sec_16",title:"16. Hypoglossal nerve stimulator",level:"1"},{id:"sec_16_2",title:"16.1 Tracheostomy",level:"2"},{id:"sec_18",title:"17. Pediatric OSA",level:"1"},{id:"sec_19",title:"18. Surveillance",level:"1"},{id:"sec_20",title:"19. Conclusions",level:"1"},{id:"sec_21",title:"Acknowledgments",level:"1"},{id:"sec_24",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'\nSenaratna C V, Perret JL, Lodge CJ, Lowe AJ, Campbell BE, Matheson MC, et al. Prevalence of obstructive sleep apnea in the general population : A systematic review. Sleep Medicine Reviews. 2020;34(2017):70-81.\n'},{id:"B2",body:'\nFranklin KA, Lindberg E. Obstructive sleep apnea is a common disorder in the population-A review on the epidemiology of sleep apnea. Vol. 7, Journal of Thoracic Disease. 2015. p. 1311-22.\n'},{id:"B3",body:'\nSchwab RJ, Kim C, Bagchi S, Keenan BT, Comyn FL, Wang S, et al. Understanding the anatomic basis for obstructive sleep apnea syndrome in adolescents. American Journal of Respiratory and Critical Care Medicine. 2015;191(11):1295-309.\n'},{id:"B4",body:'\nCaporale M, Palmeri R, Corallo F, Muscarà N, Romeo L, Bramanti A, et al. Cognitive impairment in obstructive sleep apnea syndrome: a descriptive review. Sleep and Breathing. 2020;\n'},{id:"B5",body:'\nPirklbauer K, Russmueller G, Stiebellehner L, Nell C, Sinko K, Millesi G, et al. Maxillomandibular advancement for treatment of obstructive sleep apnea syndrome: A systematic review. Journal of Oral and Maxillofacial Surgery. 2011;69(6):e165-76.\n'},{id:"B6",body:'\nDe Miguel-Díez J, Villa-Asensi JR, Álvarez-Sala JL. Prevalence of sleep-disordered breathing in children with down syndrome: Polygraphic findings in 108 children. Sleep. 2003;26(8):1006-9.\n'},{id:"B7",body:'\nBray GA. What’s in a Name? Mr. Dickens’ “Pickwickian” Fat Boy Syndrome. Obesity Research. 1994;2(4):380-3.\n'},{id:"B8",body:'\nSullivan C, Berthon-Jones M, Issa F, Eves L. Reversal of Obstructive Sleep Apnoea by Continuous Positive Airway Pressure Applied Through the Nares. The Lancet. 1981;317(8225):862-5.\n'},{id:"B9",body:'\nGoyal A, Pakhare AP, Bhatt GC, Choudhary B, Patil R. Association of pediatric obstructive sleep apnea with poor academic performance: A school-based study from India. Lung India : official organ of Indian Chest Society. 2018;35(2):132-6.\n'},{id:"B10",body:'\nMcNicholas WT. Diagnosis of obstructive sleep apnea in adults. Proceedings of the American Thoracic Society. 2008 Feb;5(2):154-60.\n'},{id:"B11",body:'\nSaboisky JP, Butler JE, Gandevia SC, Eckert DJ. Functional role of neural injury in obstructive sleep apnea. Frontiers in Neurology. 2012;JUN(June):1-12.\n'},{id:"B12",body:'\nKrysta K, Bratek A, Zawada K, Stepańczak R. Cognitive deficits in adults with obstructive sleep apnea compared to children and adolescents. Journal of Neural Transmission. 2017;124:187-201.\n'},{id:"B13",body:'\nFoldvary-Schaefer NR, Waters TE. Sleep-Disordered Breathing. CONTINUUM: Lifelong Learning in Neurology. 2017;23(4).\n'},{id:"B14",body:'\nDehlink E, Tan H-L. Update on paediatric obstructive sleep apnoea. Journal of thoracic disease. 2016 Feb;8(2):224-35.\n'},{id:"B15",body:'\nSleep-Related Breathing Disorders in Adults: Recommendations for Syndrome Definition and Measurement Techniques in Clinical Research. Sleep. 1999 Aug 1;22(5):667-89.\n'},{id:"B16",body:'\nKapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R, Ramar K, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea. Journal of Clinical Sleep Medicine. 2017;1313(3):479-504.\n'},{id:"B17",body:'\nKotecha B, De Vito A. Drug induced sleep endoscopy: Its role in evaluation of the upper airway obstruction and patient selection for surgical and nonsurgical treatment. Journal of Thoracic Disease. 2018;10(1):S40-7.\n'},{id:"B18",body:'\nJohns MW. A new method for measuring daytime sleepiness: The Epworth sleepiness scale. Sleep. 1991;14(6):540-5.\n'},{id:"B19",body:'\nNetzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire To Identify Patients at Risk for the Sleep Apnea Syndrome. Annals of Internal Medicine. 1999 Oct 5;131(7):485-91.\n'},{id:"B20",body:'\nVasu TS, Doghramji K, Cavallazzi R, Grewal R, Hirani A, Leiby B, et al. Obstructive Sleep Apnea Syndrome and Postoperative Complications: Clinical Use of the STOP-BANG Questionnaire. Archives of Otolaryngology–Head & Neck Surgery. 2010 Oct 18;136(10):1020-4.\n'},{id:"B21",body:'\nChiu HY, Chen PY, Chuang LP, Chen NH, Tu YK, Hsieh YJ, et al. Diagnostic accuracy of the Berlin questionnaire, STOP-BANG, STOP, and Epworth sleepiness scale in detecting obstructive sleep apnea: A bivariate meta-analysis. Sleep Medicine Reviews. 2017;36(2017):57-70.\n'},{id:"B22",body:'\nAmra B, Javani M, Soltaninejad F, Penzel T, Fietze I, Schoebel C, et al. Comparison of Berlin Questionnaire, STOP-Bang, and Epworth Sleepiness Scale for Diagnosing Obstructive Sleep Apnea in Persian Patients. International journal of preventive medicine. 2018 Mar 9;9:28.\n'},{id:"B23",body:'\nStuck BA, Neff W, Hörmann K, Verse T, Bran G, Baisch A, et al. Anatomic changes after hyoid suspension for obstructive sleep apnea: An MRI study. Otolaryngology - Head and Neck Surgery. 2005;133(3):397-402.\n'},{id:"B24",body:'\nQaseem A, Holty J-EC, Owens DK, Dallas P, Starkey M, Shekelle P. Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians. Annals of Internal Medicine. 2013 Oct 1;159(7):471-83.\n'},{id:"B25",body:'\nIftikhar IH, Kline CE, Youngstedt SD. Effects of exercise training on sleep apnea: A meta-analysis. Lung. 2014;192(1):175-84.\n'},{id:"B26",body:'\nAzagra-Calero E, Espinar-Escalona E, Barrera-Mora JM, Llamas-Carreras JM, Solano-Reina E. Obstructive sleep apnea syndrome (OSAS). Review of the literature. Medicina Oral, Patologia Oral y Cirugia Bucal. 2012;17(6).\n'},{id:"B27",body:'\nNeill AMK, Angus SM, Sajkov D, McEvoy RD. Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. American Journal of Respiratory and Critical Care Medicine. 1997;155(1):199-204.\n'},{id:"B28",body:'\nNakano H, Ikeda T, Hayashi M, Ohshima E, Onizuka A. Effects of body position on snoring in apneic and nonapneic snorers. Sleep. 2003;26(2):169-72.\n'},{id:"B29",body:'\nWard CP, York KM, McCoy JG. Risk of obstructive sleep apnea lower in double reed wind musicians. Journal of Clinical Sleep Medicine. 2012;8(3):251-5.\n'},{id:"B30",body:'\nBUCKS RS, OLAITHE M, EASTWOOD P. Neurocognitive function in obstructive sleep apnoea: A meta-review. Respirology. 2013 Jan 1;18(1):61-70.\n'},{id:"B31",body:'\nJackson ML, McEvoy RD, Banks S, Barnes M. Neurobehavioral impairment and CPAP treatment response in mild-moderate obstructive sleep apnea. Journal of Clinical Sleep Medicine. 2018;14(1):47-56.\n'},{id:"B32",body:'\nDrager LF, Togeiro SM, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: A cardiometabolic risk in obesity and the metabolic syndrome. Journal of the American College of Cardiology. 2013;62(7):569-76.\n'},{id:"B33",body:'\nZozula R, Rosen R. Compliance with continuous positive airway pressure therapy: assessing and improving treatment outcomes. Current opinion in pulmonary medicine. 2001 Nov;7(6):391-8.\n'},{id:"B34",body:'\nMorgenthaler TI, Aurora RN, Brown T, Zak R, Alessi C, Boehlecke B, et al. Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: An update for 2007 - An American Academy of Sleep Medicine Report. Sleep. 2008;31(1):141-7.\n'},{id:"B35",body:'\nRamar K, Dort LC, Katz SG, Lettieri CJ, Harrod CG, Thomas SM, et al. Clinical Practice Guideline for the Treatment of Obstructive Sleep Apnea and Snoring with Oral Appliance Therapy: An Update for 2015. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2015 Jul 15;11(7):773-827.\n'},{id:"B36",body:'\nPantin CC, Hillman DR, Tennant M. Dental side effects of an oral device to treat snoring and obstructive sleep apnea. Sleep. 1999;22(2):237-40.\n'},{id:"B37",body:'\nGaisl T, Haile SR, Thiel S, Osswald M, Kohler M. Efficacy of pharmacotherapy for OSA in adults: A systematic review and network meta-analysis. Sleep Medicine Reviews. 2019;46(2019):74-86.\n'},{id:"B38",body:'\nFenik P, Veasey SC. Pharmacological characterization of serotonergic receptor activity in the hypoglossal nucleus. American journal of respiratory and critical care medicine. 2003;167(4):563-9.\n'},{id:"B39",body:'\nCarley DW, Olopade C, Ruigt GS, Radulovacki M. Efficacy of mirtazapine in obstructive sleep apnea syndrome. Sleep. 2007;30(1):35-41.\n'},{id:"B40",body:'\nKraiczi H, Hedner J, Dahlöf P, Ejnell H, Carlson J. Effect of serotonin uptake inhibition on breathing during sleep and daytime symptoms in obstructive sleep apnea. Sleep. 1999;22(1):61-7.\n'},{id:"B41",body:'\nCarley DW, Radulovacki M. Role of Peripheral Serotonin in the Regulation of Central Sleep Apneas in Rats. Chest. 1999;115(5):1397-401.\n'},{id:"B42",body:'\nSukys-Claudino L, Moraes W, Guilleminault C, Tufik S, Poyares D. Beneficial effect of donepezil on obstructive sleep apnea: A double-blind, placebo-controlled clinical trial. Sleep Medicine. 2012;13(3):290-6.\n'},{id:"B43",body:'\nHein H, Behnke G, Jörres RA, Magnussen H. The therapeutic effect of theophylline in mild obstructive sleep Apnea/Hypopnea syndrome: results of repeated measurements with portable recording devices at home. European journal of medical research. 2000 Sep;5(9):391-9.\n'},{id:"B44",body:'\nPrasad B, Radulovacki M, Olopade C, Herdegen JJ, Logan T, Carley DW. Prospective trial of efficacy and safety of ondansetron and fluoxetine in patients with obstructive sleep apnea syndrome. Sleep. 2010;33(7):982-9.\n'},{id:"B45",body:'\nCarley DW, Prasad B, Reid KJ, Malkani R, Attarian H, Abbott SM, et al. Pharmacotherapy of apnea by cannabimimetic enhancement, the PACE clinical trial: Effects of dronabinol in obstructive sleep apnea. Sleep. 2018;41(1).\n'},{id:"B46",body:'\nWeaver EM, Maynard C, Yueh B. Survival of Veterans With Sleep Apnea: Continuous Positive Airway Pressure Versus Surgery. Otolaryngology–Head and Neck Surgery. 2004 Jun 1;130(6):659-65.\n'},{id:"B47",body:'\nLin H-C, Friedman M, Chang H-W, Gurpinar B. The Efficacy of Multilevel Surgery of the Upper Airway in Adults With Obstructive Sleep Apnea/Hypopnea Syndrome. The Laryngoscope. 2008 May 1;118(5):902-8.\n'},{id:"B48",body:'\nStuck BA, Leitzbach S, Maurer JT. Effects of continuous positive airway pressure on apnea–hypopnea index in obstructive sleep apnea based on long-term compliance. Sleep and Breathing. 2012;16(2):467-71.\n'},{id:"B49",body:'\nVenekamp RP, Hearne BJ, Chandrasekharan D, Blackshaw H, Lim J, Schilder AG. Tonsillectomy or adenotonsillectomy versus non-surgical management for obstructive sleep-disordered breathing in children ( Review ) SUMMARY OF FINDINGS FOR THE MAIN COMPARISON. The Cochrane Library. 2015;(10):CD011165.\n'},{id:"B50",body:'\nPinder DK, Wilson H, Hilton MP. Dissection versus diathermy for tonsillectomy. Cochrane Database of Systematic Reviews. 2011;\n'},{id:"B51",body:'\nWindfuhr JP, Chen YS, Remmert S. Hemorrhage following tonsillectomy and adenoidectomy in 15,218 patients. Otolaryngology–Head and Neck Surgery. 2005 Feb 1;132(2):281-6.\n'},{id:"B52",body:'\nLi H-Y, Wang P-C, Chen Y-P, Lee L-A, Fang T-J, Lin H-C. Critical Appraisal and Meta-Analysis of Nasal Surgery for Obstructive Sleep Apnea. American Journal of Rhinology & Allergy. 2011 Jan 1;25(1):45-9.\n'},{id:"B53",body:'\nMickelson SA. Nasal Surgery for Obstructive Sleep Apnea Syndrome. Otolaryngologic Clinics of North America. 2016;49(6):1373-81.\n'},{id:"B54",body:'\nYousuf A, Beigh Z, Khursheed RS, Jallu AS, Pampoori RA. Clinical predictors for successful uvulopalatopharyngoplasty in the management of obstructive sleep apnea. International journal of otolaryngology. 2013/09/19. 2013;2013:290265.\n'},{id:"B55",body:'\nMickelson SA. Hyoid advancement to the mandible (hyo-mandibular advancement). Operative Techniques in Otolaryngology - Head and Neck Surgery. 2012;23(1):56-9.\n'},{id:"B56",body:'\nCheng A. Genioglossus and Genioplasty Advancement. Atlas of the Oral and Maxillofacial Surgery Clinics of North America. 2019;27(1):23-8.\n'},{id:"B57",body:'\nLiao YF, Chiu YT, Lin CH, Chen YA, Chen NH, Chen YR. Modified maxillomandibular advancement for obstructive sleep apnoea: Towards a better outcome for Asians. International Journal of Oral and Maxillofacial Surgery. 2015;44(2):189-94.\n'},{id:"B58",body:'\nPRINSELL JR. Maxillomandibular advancement surgery for obstructive sleep apnea syndrome. The Journal of the American Dental Association. 2002 Nov 1;133(11):1489-97.\n'},{id:"B59",body:'\nZaghi S, Holty JEC, Certal V, Abdullatif J, Guilleminault C, Powell NB, et al. Maxillomandibular advancement for treatment of obstructive sleep apnea ameta-analysis. JAMA Otolaryngology - Head and Neck Surgery. 2016;142(1):58-66.\n'},{id:"B60",body:'\nLiu SYC, Awad M, Riley RW. Maxillomandibular Advancement: Contemporary Approach at Stanford. Atlas of the Oral and Maxillofacial Surgery Clinics of North America. 2019;27(1):29-36.\n'},{id:"B61",body:'\nStrollo PJ, Soose RJ, Maurer JT, De Vries N, Cornelius J, Froymovich O, et al. Upper-airway stimulation for obstructive sleep apnea. New England Journal of Medicine. 2014;370(2):139-49.\n'},{id:"B62",body:'\nFerlito A, Rinaldo A, Shaha AR, Bradley PJ. Percutaneous Tracheotomy. Acta Oto-Laryngologica. 2003 Sep 1;123(9):1008-12.\n'},{id:"B63",body:'\nKlemm E, Nowak AK. Tracheotomy-related deaths-a systematic review. Deutsches Arzteblatt International. 2017;114(16).\n'},{id:"B64",body:'\nSimon M, Metschke M, Braune SA, Püschel K, Kluge S. Death after percutaneous dilatational tracheostomy: A systematic review and analysis of risk factors. Critical Care. 2013;17(5).\n'},{id:"B65",body:'\nAhn YM. Treatment of obstructive sleep apnea in children. Korean Journal of Pediatrics. 2010;53(10):872-9.\n'},{id:"B66",body:'\nGuilleminault C, Lee JH, Chan A. Pediatric Obstructive Sleep Apnea Syndrome. Archives of Pediatrics & Adolescent Medicine. 2005 Aug 1;159(8):775-85.\n'},{id:"B67",body:'\nMarcus CL, Chapman D, Ward SD, McColley SA, Herrerias CT, Stillwell PC, et al. Clinical practice guideline: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704-12.\n'},{id:"B68",body:'\nKatz ES, D’Ambrosio CM. Pathophysiology of pediatric obstructive sleep apnea. Proceedings of the American Thoracic Society. 2008;5(2):253-62.\n'},{id:"B69",body:'\nPowell S, Kubba H, O’Brien C, Tremlett M. Paediatric obstructive sleep apnoea. BMJ (Online). 2010;340(7754):1018-23.\n'},{id:"B70",body:'\nMarcus CL, Rosen G, Davidson Ward SL, Halbower AC, Sterni L, Lutz J, et al. Adherence to and effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics. 2006;117(3).\n'},{id:"B71",body:'\nHolty JEC, Guilleminault C. Maxillomandibular advancement for the treatment of obstructive sleep apnea: A systematic review and meta-analysis. Sleep Medicine Reviews. 2010;14(5):287-97.\n'},{id:"B72",body:'\nLiu SY, Riley RW. Continuing the Original Stanford Sleep Surgery Protocol From Upper Airway Reconstruction to Upper Airway Stimulation: Our First Successful Case. Journal of Oral and Maxillofacial Surgery. 2017;75(7):1514-8.\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Ho-Hyun (Brian) Sun",address:"hsun@westernu.edu",affiliation:'
University of California, San Francisco – Highland Hospital, Kaiser Permanente Oakland Medical Center, Western University of Health Sciences, College of Dental Medicine, USA
University of the Pacific, Thomas J. Long School of Pharmacy, Kaiser Permanente Dublin Medical Offices and Cancer Center, USA
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Integrity - We are consistent and dependable, always striving for precision and accuracy in the true spirit of science.
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Openness - We communicate honestly and transparently. We are open to constructive criticism and committed to learning from it.
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Disruptiveness - We are eager for discovery, for new ideas and for progression. We approach our work with creativity and determination, with a clear vision that drives us forward. We look beyond today and strive for a better tomorrow.
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What makes IntechOpen a great place to work?
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IntechOpen is a dynamic, vibrant company, where exceptional people are achieving great things. We offer a creative, dedicated, committed, and passionate environment but never lose sight of the fact that science and discovery is exciting and rewarding. We constantly strive to ensure that members of our community can work, travel, meet world-renowned researchers and grow their own career and develop their own experiences.
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If this sounds like a place that you would like to work, whether you are at the beginning of your career or are an experienced professional, we invite you to drop us a line and tell us why you could be the right person for IntechOpen.
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