\r\n\tAbout 25 percent of all foods produced globally are lost due to microbial growth. L. monocytogenes is a microorganism ubiquitously present in the environment and affects animals and humans. L. monocytogenes can enter a factory and is able to survive in biofilms in the food processing environment. The use of adequate sanitation procedures is a prerequisite in risk prevention. Moreover, effective control measures for L. monocytogenes are very important to food operators.
\r\n\r\n\tThe safety and shelf life maximizing of food products to meet the demand of retailers and consumers is a challenge and a concern of food operators.
\r\n\r\n\tTo obtain food systems more sustainable, several developments are ongoing to ensure safe food products with an extended shelf life and a reduction of food loss and waste. The problem of antimicrobial resistance is also a great issue that must be taken into consideration.
\r\n\r\n\tThe implementation of natural antimicrobials, using food cultures, ferments, or bacteriophages, is one approach to control L. monocytogenes in food products that meet the consumer preference for clean label solutions.
\r\n\tThis book intends to provide the reader with a comprehensive overview of the current state-of-the-art about Listeria monocytogenes in terms of occurrence in humans, animals, and food-producing plants. Its control by more natural agents allows for more sustainable food systems and points future directions to transform challenges into opportunities.
Periodontitis is a chronic disease, determined by the dysbiotic biofilm that does not merely affect the oral cavity, but also impacts the systemic health by triggering a persistent low-grade, systemic inflammation and recurrent bacteriemia. Its clinical consequences, especially in extended and severe forms, impair the overall quality of life of the individuals.
Significant progress has been made in determining the relationship between periodontitis and various systemic diseases. Some researchers consider periodontitis as an independent risk factor that mediates the development and even progression of certain systemic disease. Conversely, specific systemic diseases and conditions have a negative impact on the periodontium and can even interfere with periodontitis’ progression. Valuable information are available with respect to several mechanisms underlying the correlation between periodontitis and systemic conditions. However, there are still plenty of issues, for which the scientific literature cannot currently provide specific answers, emphasizing their complexity and the need for further research in this area of interest.
We conducted a search on the electronic database MEDLINE (PubMed) using MeSH terms and key words to identify relevant studies published between January 2011 and November 2020. One search strategy included the following subject terms combination: ([“periodontitis”] OR [“periodontal disease”]) AND ([“pregnancy outcome”) OR [“preterm delivery”] OR [“birth weight”] OR [“pre-eclampsia”]). We searched another set of keywords as follows: ([“periodontitis”]) OR [“periodontal disease”]) AND ([“microbiota”] OR [“porphyromonas gingivalis”]) AND ([“squamous cell carcinoma of head and neck”] OR [“head and neck neoplasms”] OR [“oropharyngeal neoplasms”] OR [“oral squamous cell carcinoma”] OR [“mouth neoplasms”]). Filters used were: Humans and English. A hand-search was also conducted to identify any additional related articles in Journal of Periodontology, Journal of Clinical Periodontology, and on the EFP Official Website/Gum disease & General Health Resources. Further articles of interest were searched based on reference lists of the publications where papers were available online. The presence of duplicates was assessed through Zotero version 5.0.93 software.
Periodontitis is a highly prevalent, chronic multifactorial infectious disease, induced by the subgingival dysbiotic biofilm that produces a local immune-inflammatory response leading to the destruction of periodontal tissues. Its clinical manifestation, especially in extended and severe forms, impairs the overall quality of life, by affecting the psychosomatic, social and functional aspects of the individuals. Periodontitis also impacts the systemic health by triggering a persistent low-grade, systemic inflammation and recurrent bacteremia [1, 2, 3, 4].
The concept of periodontal medicine was first introduced by Offenbacher [5]. Periodontal medicine is a broad term that describes an emerging branch of periodontology exploring the two way relationship between periodontal and systemic status, as well as new diagnostic tools and advanced treatment approaches that take into consideration the link between periodontitis and various systemic diseases [5]. Current evidence suggests that periodontitis acts as a biologically plausible risk factor for the development and progression of other chronic, inflammatory diseases [4].
Some associations between periodontitis and certain systemic conditions, such as diabetes mellitus, cardiovascular disease, and adverse pregnancy outcomes have been reported [6, 7]. However, there is still inconsistent information on the association between periodontitis and other systemic pathologies such as cancers, chronic renal disease, chronic obstructive pulmonary disease, minor cognitive impairment, rheumatoid arthritis, metabolic syndrome, and obesity [7, 8]. Contrarily, certain systemic diseases and conditions directly affect or worsen the periodontal status [9].
Establishing the potential causal relationship between periodontitis and chronic inflammatory systemic diseases and conditions is a difficult task, because complex pathologic conditions are the consequence of multiple exposures and broad interactions of external and host-derived factors that modulate disease initiation and development [1].
Noncommunicable diseases account for seven of ten worldwide deaths. In 2016, approximately 71% of the 56.9 million worldwide deaths were due to noncommunicable diseases and around 80% were due to cancers, cardiovascular diseases, chronic respiratory diseases and diabetes [10]. Since periodontitis is a potential, independent risk factor for many of these diseases, further investigations might bring additional benefits in improving the overall health status of the population and downsizing the socioeconomic burden at the same time.
Today there is increasing recognition that inflammation is a common molecular pathway that underlies the pathogenesis of diverse human diseases, ranging from infection to immune-mediated disorders, cardiovascular pathology, diabetes, metabolic syndrome, neurodegeneration, and cancer. Two pathogenic mechanisms might be involved in the activation of the pathways driving to development of pathologies at distant sites [11, 12].
The direct mechanism relies on the translocation of periodontal pathogens via systemic blood circulation, causing colonization and inflammation at a distance from the diseased periodontium. This mechanism corresponds to the concept of the “mobile oral microbiome” [13]. Moderate and severe periodontitis are characterized by deep periodontal pockets, with an ulcerated internal gingival epithelium, providing direct access for periodontal pathogens and their toxic by-products into the blood flow [12, 14]. Periodontal treatment, as well as daily tooth brushing cause episodic injuries to the periodontal tissues, which further leads to recurrent, transient bacteremia and endotoxinemia [11, 14]. On the other hand, bacterial and endotoxin dissemination may be enabled by macrophages and dendritic cells, serving as carriers for the pathogens [13, 15].
The indirect mechanism is defined by the systemic inflammatory response towards periodontal pathogens or as a result of metastatic periodontal inflammation [12, 13]. Systemic dissemination of periodontal pathogens triggers the activation of acute phase proteins in the liver, which amplify the systemic inflammatory response in order to provide protection against the bacterial threat. Acute phase protein production and the following events, as a response to periodontal infection, may affect the physiological functionality of other organs and systems. Moreover, cytokines play critical roles in orchestrating the effective immune response of leukocytes and parenchymal cells towards systemic bacteremia. Leukocytes are the major source of innate cytokine responses. A healthy immune system has the capacity to effectively eliminate pathogens and restore homeostasis. However, a dysfunctional immune response and an ineffective clearance will eventually lead to the initiation and progression of inflammatory diseases [11, 13, 14].
Pregnancy is characterized by significant fluctuations in the levels of progesterone and estrogen hormones reaching up to 30 times higher plasma levels, by the end of the third trimester. Various types of periodontal cells display receptors for these hormones [16, 17], which could explain the functional changes in the periodontal cells consecutive to fluctuating hormone levels during gestation, as well as microcirculatory system alterations [18]. These modifications are triggering an increased periodontal inflammatory manifestation, even in the presence of low levels of dental plaque, especially in the second and third trimesters of pregnancy. A gradual decrease of inflammatory manifestations after parturition has been reported [16, 17, 18].
Major alterations in the maternal immune system occur during pregnancy, which could favor periodontal infection and consecutive inflammation. Pregnant women have a reduction in phagocytosis and bactericidal activities of peripheral neutrophils and changes in the monocytes stimulated secretion of proinflammatory mediators after the contact with bacterial endotoxines [16].
Pregnancy not only impacts periodontal inflammation and host immune response, but also induces an increase in the oral microbial load and modifications in the oral microbiological profiles, as a consequence of elevated levels of steroid hormones [16, 18]. Significant changes in the subgingival microbiota with increases in the proportion of some periodontal pathogens such as
Pregnancy increases the risk of new-onset periodontal disease, but it can also activate preexisting periodontitis leading to an infectious and inflammatory load similar to new-onset periodontitis. Maternal periodontitis may reflect an intrinsic inflammatory or innate immunity trait that places the woman at risk for severe forms of periodontal disease, as well as for the common terminal biochemical inflammatory cascade associated with adverse pregnancy outcomes [19].
Many studies have associated adverse pregnancy outcomes, such as low birth weight, preterm birth and preeclampsia, with maternal periodontitis. The first case–control study referring to the relationship between periodontitis and preterm-birth reported a 7.5 higher risk ratio for preterm births for the group of women with periodontitis as compared to the periodontal healthy control group [19]. Other studies have indicated oral maternal infections, including chronic periodontitis, as potential independent risk factors for various complications throughout the pregnancy. A systematic review including case–control, cohort case-control and controlled trials, confirmed the positive association between periodontitis and adverse pregnancy outcomes [20]. A meta-analysis reported a significant association between periodontitis and preterm birth, with an odds ratio of 1.38 [21]. A more recent meta-analyses including 10.215 women, indicates that periodontitis doubles the risk for preterm delivery, the calculated odds ratio being of 2.01 (95% CI 1.71–2.36) [22]. However, the level of association is mostly modest, mainly due to the high degree of heterogeneity between the studies, particularly with respect to the diversity of periodontitis disease case definitions [23].
The relationship between periodontitis and adverse pregnancy outcomes was investigated also by means of surrogate markers defining both conditions. Many studies indicate a positive association between gingival crevicular fluid, inflammatory mediators and adverse pregnancy outcomes [23, 24].
An umbrella review which analyzed systematic reviews and meta-analysis showed that non-surgical periodontal therapy with or without antibiotic therapy has low to moderate positive effects on reducing the frequency of the common pregnancy complications related to periodontitis [25]. The large heterogeneity of the outcomes of the interventional studies is due to variations in periodontitis case definition, sample particularities, follow-up period, control of confounding factors, as well as the therapy moment throughout the pregnancy [14, 25]. The nonsurgical periodontal therapy may be ineffective in reducing inflammatory cascade once activated and thus eventually lead to preterm birth [14].
Preterm birth is defined as the birth prior to 37 weeks of gestation [26]. Complications of preterm birth are a leading cause of infant deaths worldwide raising the neonatal mortality risk rate up to 11.4 [27, 28]. The prevalence of preterm birth ranges from 5 to 7% in high-income countries, and is generally higher in low-income ones [29]. In 2014, the estimated global preterm birth rate was 10.6%, the equivalent of about 14.84 million preterm births from a total number of 139.95 million livebirths [30]. Therefore, prematurity is considered a major public health issue and the identification of any potential risk factor is of tremendous importance [27, 28, 30].
Low birth weight is defined as a birth weight below 2500 g regardless of gestational age of live infants [31, 32]. Various maternal factors such as extremes of maternal age, multiple pregnancies, obstetric complications, chronic maternal conditions like hypertensive disorders, and nutritional status or environmental exposures such as tobacco and drug use, can contribute to the low birth weight of the neonate. The estimates rate of global low birth weight for 2015 was 14.6% [31].
Maternal mortality is another important adverse outcome during pregnancy and is considered the death of a woman during pregnancy, within 42 days post-partum or during an abortion, as a consequence of any pregnancy associated pathological condition or complication [33]. The yearly number of global maternal deaths decreased from 532.000 in 1990, to 303.000 in 2015 [34]. Between 1990 and 2015, 10.7 million women worldwide died from various causes related to the evolution of pregnancy. Among the main risk factors of maternal mortality, pre-eclampsia and eclampsia are still in leading positions. Strategies aiming to reduce the number of deaths related to eclampsia showed a relatively low efficacy, which indicates the need to turn the attention to other potential risk factors in order to significantly lower mortality rates associated to eclampsia [33].
Hematogenous dissemination of periodontal bacteria is suspected to cause adverse pregnancy outcomes, by genitourinary tract and fetal–maternal unit colonization [16, 35]. Recent research indicates the presence of bacteria derived from supra- and subgingival biofilms in the placental microbiome. Moreover, some studies suggest that placental microbial profiles are closer to the oral microbial profiles than to the gut microbiome [36, 37, 38]. However, there is no general agreement on the bacterial translocation concept. The presence of oral bacteria in the placenta could be the consequence of an external contamination [39].
Although maternal infection is considered a major contributor of adverse pregnancy outcomes, a critical factor which can trigger the preterm birth might be rather the persistent inflammation generated by chronic periodontal infections. Inflammatory mediators that are abundantly produced at the affected sites determine periodontal tissue breakdown [14]. From a clinical point of view, deep periodontal pockets indicate the magnitude of the periodontal inflammation [39]. Chronic, long-term periodontal inflammation will eventually lead to a continuous passage of cytokines, chemokines, and gingival-derived C-reactive protein from the affected periodontal tissues into the bloodstream inducing a systemic acute-phase reaction and also maintaining a chronic, systemic inflammatory status [11, 12, 14]. High levels of C reactive protein over longer periods of time increases the risk for premature birth, but also of diabetes, and cardiovascular disease [13, 40].
Local and systemic accumulations of pro-inflammatory mediators, such as prostaglandins E2, interleukins, tumor necrosis factor α (TNF- α) and metalloproteinase (MMP) can stimulate the labor [41]. It is likely that spontaneous preterm parturition is induced by a high level of inflammation in the early stage of pregnancy [39]. However, the exact role of periodontal inflammation and the potential biological mechanisms that link periodontal disease with adverse pregnancy outcomes is not fully understood.
European Federation of Periodontology guidelines for oral-health professionals provides the following recommendations [42]:
During the examination of the oral status, dental professionals should always ask any female patient of childbearing age whether she is pregnant and should always consider pregnancy status before recommending any oral-health intervention.
Inform women who are not pregnant of the importance of oral and periodontal health during pregnancy and of the treatment of existing periodontal diseases before becoming pregnant.
For any pregnant women, perform a comprehensive clinical periodontal examination and formulate a diagnosis of “healthy”, “gingivitis”, or “periodontitis”.
Pregnant women with a healthy periodontium should be provided with oral-health education and preventive personal plaque control measures that should became healthy habits throughout life. Also, provide information on the inflammatory periodontal events that could occur during pregnancy (increased gingival bleeding and gingival enlargement).
Pregnant woman with gingivitis should be provided with the same oral-health education and personal plaque control measures, as well as professional mechanical instrumentation for removing plaque and calculus deposits from the tooth surfaces. The reevaluation of the periodontal status, in terms of efficacy of the professional and personal interventions and periodontal monitoring throughout pregnancy are mandatory.
Pregnant women with periodontitis should also have the same oral-health educational measures, as well as additional professional intervention by means of standard non-surgical periodontal therapy (scaling and root planing).
Non-surgical periodontal therapy, dental treatments and extractions are safe during pregnancy, mainly during the second trimester of gestation.
Local anesthesia, common painkillers and systemic antibiotics are generally safe without additional risk to the foetus or the pregnant woman.
Tetracyclines should be strictly avoided. Other medication should be prescribed to the pregnant woman after communication with her obstetrician.
Although EFP recommends dental x-rays and chemical plaque-control agents during pregnancy, the authors of the present chapter are not keen to recommending them.
Cancer is one of the leading causes of worldwide mortality. In 2016, 1.1 million new cases were reported, and the prevalence was of 4.1 million cases. Head and neck squamous cell carcinomas (HNSCCs) constituted 5.7% of global cancer-related mortality, the equivalent of 512.770 deaths. Also the global mortality burden is expected to increase; by 2030 an estimated 705.902 people worldwide will be expected to die due to HNSCC [43]. This great burden of cancer worldwide strongly indicates the need for implementing rigorous screening and control programs in order to facilitate the identification of all potential HNSCC related risk factors, including periodontitis, and the early detection of HNSCC.
Squamous cell carcinoma is the most common histological subtype of oral and oropharyngeal malignant tumors, accounting for about 90% of the cases. The incidence of HNSCCs are reported to be on the rise, with a global estimated incidence of over 300.000 new cases registered each year [44, 45].
Emerging evidence indicates periodontitis as a potential independent risk factor for the development of premalignant lesions and HNSCC [46, 47]. Current evidence regarding a positive association between periodontitis and oral and oropharyngeal cancers are currently controversial [48]. Some studies suggest an increased susceptibility to HNSCC in periodontitis patients [49]. Extended and severe forms of periodontitis have been frequently identified among patients with HNSCC [48].
A meta-analysis reported a 2.66-fold higher risk for oral cancer in patients with periodontal disease as compared to periodontal healthy controls [50]. A hospital-based case-cohort study, after controlling for important confounders, found that individuals with periodontitis were 3.7 times more likely to have oral squamous cell carcinoma as compared to individuals without periodontitis [51].
Positive associations between periodontitis and other cancers such as digestive tract cancer, pancreatic cancer, prostate cancer, breast cancer, corpus uteri cancer, lung cancer, hematological cancer, and Non-Hodgkin lymphoma have been reported [46].
The relationship between periodontitis and HNSCC has been reported based on the specific periodontal parameters or surrogate markers of periodontal disease. An increased risk of HNSCC development, with respect to the number of missing teeth has been observed. A 2.7-fold increased risk of oral cancer in patients having 11 to 16 missing teeth as compared to dentate subjects has been reported [52]. A 5.23-fold increase in the risk of tongue cancer and a 4-fold increased risk of head and neck squamous cell carcinoma for each millimeter of alveolar bone loss, after the adjustment for important confounders has been reported [53, 54]. This data suggest that the severity and extension of periodontitis might be a risk indicator for HNSCC [55].
The investigation of the causal role of periodontitis in the cancer development is challenging due to the major independent and shared risk factors of these conditions. Periodontitis may have a direct effect on the rise of cancer risk or may impact through shared genetic and environmental factors [56]. Smoking is one of the main independent risk factors for periodontitis and HNSCC, while smoking and alcohol consumptions account for up to 85% of all oral cancers. The synergic effect of alcohol and tobacco consumption increases the risk for of oral cancer by 15 times [57, 58] However, about 15% to 20% of the HNSCCs occur independently to any of these risk factors, and the clinical features and evolution of the cancer in this group is often particularly aggressive [57, 58, 59, 60].
Some molecular pathogenic mechanism could associate periodontitis to oral cancers and are briefly detailed below.
Chronic periodontal inflammation might be an extrinsic pathway in cancer development [46, 47, 61, 62]. The damage of the junctional epithelium mediated by periodontal pathogens alters its protective function promoting the absorption of toxic compounds from alcohol and tobacco, which in turn create a chronic inflammatory environment [61, 63]. The inflammatory process and the presence of cell-stimulating signals may create an optimal environment for the atypical cell proliferation and differentiation, which may eventually lead to cancer development [46, 61, 63].
In periodontitis, the complex inflammatory response developed to eliminate periodontal pathogens leads to the accumulation of excessive levels of endogenous compounds such as cytokines, chemokines, prostaglandins, reactive oxygen and nitrogen species, matrix metalloproteinases, and endothelial and epidermal growth factors. The anarchic and excessive release of these molecules is responsible for the indirect destruction of periodontal tissues [64]. In the meantime, these proinflammatory molecules may irreversibly damage the cellular DNA, deregulate the mechanisms of DNA repair and subvert the cell cycle regulatory mechanisms [65, 66]. Thus, cumulative, permanent genetic alterations lead to oncogenes activation or tumor suppressor genes inactivation [67].
Epigenetic changes occur more frequently than gene mutations and may persist for the entire cell life and even for multiple generations. Extensive exposure of oral mucosa to bacteria and chemokines may contribute to carcinogenesis by causing epigenetic alterations. The epigenetic changes, which refer to any heritable modifications in gene expression without alterations of the DNA sequence, also promote genomic instability. Epigenetic mechanisms include DNA methylation, posttranslational modifications of histone proteins and post-transcriptional gene down-regulation by microRNAs. Any of these three distinct epigenetic mechanisms leads to inappropriate gene expression and cancer development [61, 67, 68]. A relatively stable epigenetic change may induce the increase of carcinogenesis mechanisms such as faster cellular proliferation, stimulation of an increased angiogenesis, and inhibition of apoptosis [61].
The methylation of DNA refers to the covalent addition of a methyl group to the 5-carbon position of cytosine base from a CpG dinucleotide. Hypermetilation of CpG islands of growth-regulatory genes promoter regions causes the transcriptional “silencing” of tumor suppressor genes and promotes tumor progression [68]. Although some aberrant methylation patterns have been already identified, the complex underlying molecular mechanisms that address the association of chronic periodontal inflammation and oral cancers are still not fully understood [61].
Histones, proteins binding to the DNA in the nucleus and condensing it into chromatin, can undergo multiple aberrant post-translational modifications, which induce structural and functional modification in the chromatin and thus alterations of the pattern of gene expression directly contributing to the initiation of neoplasia and its subsequent course [68].
The increased release of inflammatory mediators in periodontitis, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor–α (TNF–α) [61], may trigger epithelial-mesenchymal transition and activation of inflammatory cells which facilitate cancer invasion [61, 69].
IL-8 is primarily produced by periodontal cells in response to periodontal bacteria, like
More recent studies investigated the topic of inflammasome-mediated inflammation in cancer. The inflammasome is a part of the innate immune system and it responds to microbial challenge through regulation of caspase-1 activation and induction of inflammation. The most studied and best characterized inflammasome, Nucleotide-Binding Domain, Leucine-Rich–Containing Family, Pyrin Domain–Containing-3 (NLRP3), is an emerging, key player in the development and progression of cancer. Activation of NLRP3 may promote inflammation induced tumor growth and metastasis in HNSCC [71]. Certain periodontal pathogens, such as
Inflammatory mediators, microbes, as well as environmental factors (tobacco and alcohol consumption) could activate some transcription factors, such as the nuclear signal transducers and activators of transcription-3 (STAT-3), the activator protein-1 (AP-1) and the nuclear factor-kB (NF-kB). These transcription factors activate oncogenes that regulate apoptosis, cell proliferation and angiogenesis as well as genes regulating the production of pro-inflammatory molecules. These oncogenic changes drive a tumor-promoting inflammatory milieu through the intrinsic pathway that favors the development of already established tumors. Moreover, the inflammatory microenvironment favors the tumor to escape from immune surveillance and alters the response to chemotherapy [65, 66, 74].
Oxidative stress occurs as a state of disturbance between free radical production and the capability of antioxidant system to counteract the free radicals. The activity of periodontal bacteria induces oxidative stress through free radical release, and decreased plasma antioxidant capacity. On the other hand, oxidative stress causes inflammation, which can increase the production of free radicals. Patients with chronic periodontitis showed low serum and salivary antioxidants levels and elevated oxidative stress biomarkers such as 8-isoprostane and malondialdehyde. Moreover, assessment of blood and gingival tissues of chronic periodontitis patients also revealed mitochondrial DNA deletion mediated by lipid peroxidation [73].
Oxidative stress is also correlated to oral cancer. Increased lipid peroxidation and reduced antioxidants was reported in patients with oral cancer. Lipid peroxidation and irreversible protein modifications are essential molecular mechanisms involved in the oxidative damage of cell structures eventually leading to programmed cell death [73, 75]. Elevated levels of malondialdehyde and low levels of glutathione were observed in the saliva and serum of HNSCC patients [73, 76].
Chronic periodontal inflammation induces a prolonged exposure of oral cells to free radicals that can lead to genomic alterations through DNA damage, lipid and protein peroxidation and activation of signal transduction by post translational modification [66]. Therefore, the accumulation of oxidative stress products in periodontal tissues may significantly contribute to the development of oral cancer.
Oncogene and tumor suppressor pathways are proven intracellular targets for therapies, but recent scientific data are pointing out to new potential,
The heat shock protein GroEL is another virulence factor of
Currently, among the known virulence molecules of
Understanding the dynamics and common, underlying pathophysiological mechanisms that link periodontitis to systemic diseases is essential to the development of coherent, patient centered diagnostic and therapeutic strategies.
An increased risk for preterm birth and low birth weight of newborns in mothers with periodontitis has been reported. Pregnant women should be provided with oral-health education and preventive personal plaque control measures that should become healthy habits throughout life. Non-surgical periodontal therapy is safe during pregnancy, and especially during the second trimester of gestation.
The epigenetic alterations in periodontal disease such as histone acetylation and DNA methylation, and the subsequently altered gene expression might partially explain the role of periodontal inflammation in cancer development and tumor growth.
The authors declare no conflict of interest.
Stress can be defined as any external and internal constraints that limit the photosynthetic rate and reduces the energy conversion ability of a plant to biomass [1]. Respond of a plant to stress is in different ways, some of which include variation in gene expression, cellular metabolism, growth rates, crop yields, and so on. Plant stress as a result of its response to varying environmental conditions. However, exposure to a particular stress by stress-tolerant plant species leads to the development of resistance with time to a particular stress [2]. The main types of stress that plants face are biotic and abiotic stresses. Abiotic stress is an environmental factor that is placed on plants, as a result of variation of physical or chemical stress [3], whereas biotic stress is a biological unit such as illnesses, insects, and other pests that are exposed to crop plants [4]. Some stresses cause injury in plants. These plants have a number of metabolic issues [5].
Plants can recover from injuries if the stress is light or only lasts a short time, as the effect is just transient; however, extreme stress results in death. However, many plants like xerophytic plants (Ephemerals) can escape the stress altogether. Biotic stress in plants is induced by living organisms, such as viruses, bacteria, fungus, nematodes, insects, arachnids, and weeds [2]. The agents that cause biotic stress deplete their hosts of nutrients, which can lead to plant mortality. Because of pre- and postharvest losses, biotic stress might become severe. Despite the absence of an adaptive immune system, plants have evolved sophisticated methods to deal with biotic stresses [6]. These stresses are controlled by the plant’s genetic codes. Hence, there is a need to combat resistant varieties of crops so as to ensure food security and safety in subsequent growing seasons. Seed priming with growth and rooting hormones should also be considered.
Plants are subjected to a variety of abiotic stresses, all of which have an impact on crop yield around the world. The major biotic and abiotic stresses in plants are described in Figure 1. These include drought, salt, cold, heat, and toxins.
An overview of major abiotic and biotic stresses [
Water scarcity is a significant environmental limitation on plant productivity. Drought-induced crop output losses are likely to outnumber losses from all other sources because both the severity and duration of the stress are crucial [8]. The severity of the drought depends on the occurrence and distribution of rainfall, evaporative demands, and moisture storing capacity of soils, all of which are unpredictable [9]. Nowadays, climate has changed all around the globe by continuously increasing in temperatures and atmospheric CO2 levels. The distribution of rainfall is unequal as a result of climate change, which functions as a major stress in the form of drought. Due to extreme drought conditions, the amount of soil water available to plants is steadily decreasing, causing plants to die prematurely. After drought is imposed on crop plants, growth will be arrested. Drought circumstances cause plants to lower their shoot growth, as well as their metabolic demands [7].
One of the most important limiting factors for crop growth and productivity is salt stress. Soil salinity is a global danger to world agriculture because it reduces crop yields and, as a result, crop productivity in salt-affected areas. Salinity is caused by the accumulation of salts in the soil or groundwater over a lengthy period of time as a result of natural processes or through human activities, for example, wethering of rocks or as a result of irrigation schemes using salt-rich irrigation water or having insufficient drainage [10]. There are several ways by which salt stress reduces the growth and yield of crops. Salt stress has two main effects on crop plants: osmotic stress and ion toxicity. These primary effects of salinity stress cause some secondary effects such as assimilate production, reduced cell expansion, and membrane function as well as decreased cytosolic metabolism [2].
Cold stress, as an abiotic stress, has been shown to be one of the most important abiotic stresses that reduce agricultural crop output by altering crop quality and post-harvest life. Many crop plant species have been found to be substantially hampered in their reproductive growth by chilling such as rice displaying sterility when exposed to chilling temperatures during anthesis [11]. Plants are sessile in nature; therefore, they have evolved unique ways to cope with temperature variations in their habitat [12]. In temperate conditions, plants are encountered by chilling and freezing conditions that are very harmful to plants as stress.
In order to adapt themselves, plants acquire chilling and freezing tolerance against such lethal cold stresses by a process called acclimation [13]. However, many important crops are still incompetent to the process of cold acclimation.
The temperature rises around the world have become a major problem, affecting not only plant development but also plant productivity, particularly in agricultural products. Heat stress has become the most important limiting factor to crop productivity and ultimately the food security [14]. When plants are subjected to heat stress, their seed germination rate, photosynthetic efficiency, and yield all suffer. Under heat stress, during the reproductive growth period, the function of a petal cell is lost, and the anther is dysplastic. For example, maize yields decrease sharply when the plants are exposed to temperatures greater than approximately 29–30°C [15].
Toxic metals have been added to agriculture soils as a result of increased reliance on chemical fertilizers and sewage wastewater irrigation, as well as increasing industrialization, having detrimental consequences on the soil–plant environment system [16]. These metals bioaccumulate and slowly enter plants through air, water, and progression of the food chain over a certain period of time [17].
Plants are subjected to a variety of biotic stress caused by various living organisms such as fungi, viruses, bacteria, nematodes, and insects [2]. These biotic stress agents induce a variety of diseases, infections, and damage to crop plants, lowering agricultural yields. However, different strategies for overcoming biotic stressors have been created through research methodologies. The biotic stresses in plants can be overcome by studying the genetic mechanism of the agents causing these stresses [18]. Genetically modified plants have proven to be a great effort against biotic stresses in plants by developing resistant varieties of crop plants.
Plant-parasitic nematodes feed on the contents of plant cells and can feed on all sections of the plant, but they predominantly cause soil-borne illnesses and affect the root system. They cause wilting and stunting, which are signs of nutritional inadequacy. Viruses cause not only local but also systemic damage to plants, causing stunting, chlorosis, and deformities in many areas of the plant, despite the fact that they rarely kill their hosts [19]. Plants are harmed when insects feed or lay eggs on them. Viruses can be transmitted to plants by piercing-sucking insects
Plants use five general botanical defenses against abiotic stresses. These include cuticle, unsaturated fatty acids, reactive species scavengers, molecular chaperones, and compatible solute, which are also an economic important trait [21].
This is the exterior translucent lipid structure in land plants, which seals the aerial surface of their organs. It is coated by cuticular waxes and is described as a hydrophobic layer. As the primary interface between plant and environment, the cuticle plays critical role in restricting liquid and gas fluxes, defending pathogen and insect attacks, and resisting various abiotic stresses. It is an elegant innovation of land plants to deploy an outermost shield derived from simple molecules, which is fundamental to their success in terrestrial colonization [22]. Wax accumulation in the cuticle is closely associated with multiple stress tolerance [23].
Unsaturated fatty acids containing 16 or 18 carbon atoms are the key ingredients of the membrane and the prime stocks for the cuticle. The unsaturated nature of fatty acids is a major determinant of membrane fluidity [21]. Dysfunction of biomembrane due to protein deactivation and ion leakage are caused by cold-driven rigidification and heat-driven fluidization, which makes membrane fluidity susceptible to various abiotic stresses, especially at high temperatures [24]. An increase in the level of normal alkanes with a decrease in the level of primary alcohols can lead to cold susceptibility, which can cause growth retardation, while an increase in the levels of both n-alkanes and primary alcohols resulted in better viability, where drought and freezing will have no effect on plant growth [25]. When polyunsaturated fatty acids are liberated by lipase form glycerolipids, they serve as raw materials for the synthesis of oxylipins, a bioactive molecule that is involved in the diverse physiological processes of stress resistance [26].
The reactive species scavengers include reactive carbonyl species (ROS) and reactive oxygen species (RCS). The ROS and RCS are interwoven, due to the fact that RCS can arise from ROS-induced lipid peroxidation, while ROS can be raised by RCS activities the other way round. Abiotic stresses can trigger a burst in both ROS and RCS thereby turning the two scavengers into a general defenses. Plants utilize both enzymatic and non-enzymatic means to developed sophisticated ROS scavenging system [21]. The application of excessive nitrogen fertilization in crop cultivation depresses the ROS scavenging system causing the increase in stress susceptibility [27].
Molecular chaperones are induced to facilitate protein folding, assembly, transport, and degradation. Heat shock protein (HSP), which are good examples of molecular chaperon, is employed by all living organisms to counteract all detrimental conditions that can induce protein damage, wherein they function to prevent aggregation of denatured proteins, assist in their refolding, or present them to lysosomes or proteasomes for proteolysis, thereby restoring cellular homeostasis [28].
They are electrical neutral small organic compounds with high solubility and low toxicity. The molecules include sugar, amino acids, and their derivatives [21]. In an abiotic stress, these metabolites may accrue to act as osmoprotectants against dehydration, scavengers of RS, and/or stabilizers of proteins and membranes [29].
Plants are sessile organisms that are susceptible to environmental damages. In a broad sense, both biotic (viruses, bacteria, insects) and abiotic (heat, drought, salt, etc.) are adversaries facing world food production. Plants affected by these biotic and abiotic stress factors surfers physiological and metabolism changes. Hormonal and genetic defense mechanisms of the plant are also affected. Here, there is a need for phytologist and plant Breeders to develop tolerant varieties so as to combat these stresses to ensure good security. Plants will continue to be subjected to biotic and abiotic stresses until responsive mechanisms are created, and this will pose a significant threat to global agriculture. In plant cells, glycolysis operates as the principal source of this cytotoxin, due to the non-enzymatic dephosphorylation of two intermediates, glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. Once over accumulated, methylglyoxal can also damage various biomolecules, especially with its aldehyde group.
Authors are listed below with their open access chapters linked via author name:
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\\n\\n\\n\\n\\n\\n\\n\\n\\n\\nJocelyn Chanussot (chapter to be published soon...)
\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\nYuekun Lai
\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\n\\nPrevious years (alphabetically by surname)
\\n\\nAbdul Latif Ahmad 2016-18
\\n\\nKhalil Amine 2017, 2018
\\n\\nEwan Birney 2015-18
\\n\\nFrede Blaabjerg 2015-18
\\n\\nGang Chen 2016-18
\\n\\nJunhong Chen 2017, 2018
\\n\\nZhigang Chen 2016, 2018
\\n\\nMyung-Haing Cho 2016, 2018
\\n\\nMark Connors 2015-18
\\n\\nCyrus Cooper 2017, 2018
\\n\\nLiming Dai 2015-18
\\n\\nWeihua Deng 2017, 2018
\\n\\nVincenzo Fogliano 2017, 2018
\\n\\nRon de Graaf 2014-18
\\n\\nHarald Haas 2017, 2018
\\n\\nFrancisco Herrera 2017, 2018
\\n\\nJaakko Kangasjärvi 2015-18
\\n\\nHamid Reza Karimi 2016-18
\\n\\nJunji Kido 2014-18
\\n\\nJose Luiszamorano 2015-18
\\n\\nYiqi Luo 2016-18
\\n\\nJoachim Maier 2014-18
\\n\\nAndrea Natale 2017, 2018
\\n\\nAlberto Mantovani 2014-18
\\n\\nMarjan Mernik 2017, 2018
\\n\\nSandra Orchard 2014, 2016-18
\\n\\nMohamed Oukka 2016-18
\\n\\nBiswajeet Pradhan 2016-18
\\n\\nDirk Raes 2017, 2018
\\n\\nUlrike Ravens-Sieberer 2016-18
\\n\\nYexiang Tong 2017, 2018
\\n\\nJim Van Os 2015-18
\\n\\nLong Wang 2017, 2018
\\n\\nFei Wei 2016-18
\\n\\nIoannis Xenarios 2017, 2018
\\n\\nQi Xie 2016-18
\\n\\nXin-She Yang 2017, 2018
\\n\\nYulong Yin 2015, 2017, 2018
\\n"}]'},components:[{type:"htmlEditorComponent",content:'New for 2018 (alphabetically by surname).
\n\n\n\n\n\n\n\n\n\nJocelyn Chanussot (chapter to be published soon...)
\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\nYuekun Lai
\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\nPrevious years (alphabetically by surname)
\n\nAbdul Latif Ahmad 2016-18
\n\nKhalil Amine 2017, 2018
\n\nEwan Birney 2015-18
\n\nFrede Blaabjerg 2015-18
\n\nGang Chen 2016-18
\n\nJunhong Chen 2017, 2018
\n\nZhigang Chen 2016, 2018
\n\nMyung-Haing Cho 2016, 2018
\n\nMark Connors 2015-18
\n\nCyrus Cooper 2017, 2018
\n\nLiming Dai 2015-18
\n\nWeihua Deng 2017, 2018
\n\nVincenzo Fogliano 2017, 2018
\n\nRon de Graaf 2014-18
\n\nHarald Haas 2017, 2018
\n\nFrancisco Herrera 2017, 2018
\n\nJaakko Kangasjärvi 2015-18
\n\nHamid Reza Karimi 2016-18
\n\nJunji Kido 2014-18
\n\nJose Luiszamorano 2015-18
\n\nYiqi Luo 2016-18
\n\nJoachim Maier 2014-18
\n\nAndrea Natale 2017, 2018
\n\nAlberto Mantovani 2014-18
\n\nMarjan Mernik 2017, 2018
\n\nSandra Orchard 2014, 2016-18
\n\nMohamed Oukka 2016-18
\n\nBiswajeet Pradhan 2016-18
\n\nDirk Raes 2017, 2018
\n\nUlrike Ravens-Sieberer 2016-18
\n\nYexiang Tong 2017, 2018
\n\nJim Van Os 2015-18
\n\nLong Wang 2017, 2018
\n\nFei Wei 2016-18
\n\nIoannis Xenarios 2017, 2018
\n\nQi Xie 2016-18
\n\nXin-She Yang 2017, 2018
\n\nYulong Yin 2015, 2017, 2018
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In cases, the ultrasound appearance is a cystic image with different content and the differential diagnosis is often difficult. Body—research methods: the organs affected by abdominal congenital anomalies involve the gastrointestinal tract (stomach, duodenum, small bowel or colon, and gall bladder), the kidney and urinary tract, the peritoneal cavity (ascites), suprarenal glands, and tumors of the reproductive system (especially the ovaries). In order to identify the affected structures, it is mandatory to know the normal aspect of the abdominal content at different gestational ages. The diagnosis may be very difficult, but its accuracy is important, considering the need of further counseling the couple. In minor conditions, without chromosomal anomalies or associations, the outcome is usually good, and there are even possibilities of in utero treatment. In severe conditions, with poor outcome, the couple can choose to terminate the pregnancy, after counseling is provided. Conclusion: abdominal congenital anomalies are common findings in ultrasound screenings for anomalies in all the trimesters of pregnancy and their recognition is important for subsequent management.",book:{id:"6307",slug:"congenital-anomalies-from-the-embryo-to-the-neonate",title:"Congenital Anomalies",fullTitle:"Congenital Anomalies - From the Embryo to the Neonate"},signatures:"Ples Liana and Anca Lesnic",authors:[{id:"212333",title:"Associate Prof.",name:"Liana",middleName:null,surname:"Ples",slug:"liana-ples",fullName:"Liana Ples"}]},{id:"64417",title:"Introductory Chapter: A Comprehensive Approach to the Process of Breastfeeding",slug:"introductory-chapter-a-comprehensive-approach-to-the-process-of-breastfeeding",totalDownloads:1267,totalCrossrefCites:0,totalDimensionsCites:0,abstract:null,book:{id:"6191",slug:"selected-topics-in-breastfeeding",title:"Selected Topics in Breastfeeding",fullTitle:"Selected Topics in Breastfeeding"},signatures:"René Mauricio Barría P",authors:[{id:"88861",title:"Dr.",name:"R. Mauricio",middleName:null,surname:"Barría",slug:"r.-mauricio-barria",fullName:"R. Mauricio Barría"}]},{id:"62854",title:"The Surgical Technique of Caesarean Section: What is Evidence Based?",slug:"the-surgical-technique-of-caesarean-section-what-is-evidence-based-",totalDownloads:2448,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Caesarean section is the most frequent obstetric operation which is associated with increased maternal morbidity and mortality. Although these risks are low, affected women may suffer from severe consequences and this may affect subsequent pregnancies and deliveries. A variety of surgical approaches have been described, however, on low evidence level. The objective of this chapter is therefore to systematically search the literature and analyse the available evidence including preoperative workup, prophylactic antibiotics, skin disinfection, preoperative bladder catheterization as well as details of the individual steps of the actual operation itself such as skin incision types, preparation of soft tissue and womb, removal of the placenta, cervical dilatation and stitching of the womb, peritoneum, rectus muscle, fascia, subcutaneous fat, and skin. We systematically searched for meta-analysis, systematic reviews, and big studies and evaluated the evidence for each individual step.",book:{id:"6707",slug:"caesarean-section",title:"Caesarean Section",fullTitle:"Caesarean Section"},signatures:"Jan-Simon Lanowski and Constantin S. von Kaisenberg",authors:[{id:"100660",title:"Prof.",name:"Constantin",middleName:"Sylvius",surname:"Von Kaisenberg",slug:"constantin-von-kaisenberg",fullName:"Constantin Von Kaisenberg"},{id:"240353",title:"Dr.",name:"Jan-Simon",middleName:null,surname:"Lanowski",slug:"jan-simon-lanowski",fullName:"Jan-Simon Lanowski"}]},{id:"18348",title:"Anaesthetic Considerations during Laparoscopic Surgery",slug:"anaesthetic-considerations-during-laparoscopic-surgery",totalDownloads:28882,totalCrossrefCites:1,totalDimensionsCites:5,abstract:null,book:{id:"916",slug:"advanced-gynecologic-endoscopy",title:"Advanced Gynecologic Endoscopy",fullTitle:"Advanced Gynecologic Endoscopy"},signatures:"Maria F. Martín-Cancho, Diego Celdrán, Juan R. Lima, Maria S. Carrasco-Jimenez, Francisco M. Sánchez-Margallo and Jesús Usón-Gargallo",authors:[{id:"14715",title:"Prof.",name:"Francisco M.",middleName:null,surname:"Sánchez-Margallo",slug:"francisco-m.-sanchez-margallo",fullName:"Francisco M. Sánchez-Margallo"},{id:"29449",title:"Dr.",name:"Maria Fernanda",middleName:null,surname:"Martín-Cancho",slug:"maria-fernanda-martin-cancho",fullName:"Maria Fernanda Martín-Cancho"},{id:"39772",title:"Dr.",name:"Juan R.",middleName:null,surname:"Lima",slug:"juan-r.-lima",fullName:"Juan R. Lima"},{id:"39773",title:"Mr.",name:"Diego",middleName:null,surname:"Celdran",slug:"diego-celdran",fullName:"Diego Celdran"},{id:"39774",title:"Prof.",name:"Jesus",middleName:null,surname:"Usón-Gargallo",slug:"jesus-uson-gargallo",fullName:"Jesus Usón-Gargallo"},{id:"62320",title:"Prof.",name:"Maria Sol",middleName:null,surname:"Carrasco-Jiménez",slug:"maria-sol-carrasco-jimenez",fullName:"Maria Sol Carrasco-Jiménez"}]},{id:"41721",title:"Artificial Insemination in Poultry",slug:"artificial-insemination-in-poultry",totalDownloads:9531,totalCrossrefCites:5,totalDimensionsCites:14,abstract:null,book:{id:"3206",slug:"success-in-artificial-insemination-quality-of-semen-and-diagnostics-employed",title:"Success in Artificial Insemination",fullTitle:"Success in Artificial Insemination - Quality of Semen and Diagnostics Employed"},signatures:"M.R. Bakst and J.S. Dymond",authors:[{id:"155683",title:"Dr.",name:"Murray R.",middleName:null,surname:"Bakst",slug:"murray-r.-bakst",fullName:"Murray R. Bakst"},{id:"167852",title:"Dr.",name:"Jessica",middleName:null,surname:"Dymond",slug:"jessica-dymond",fullName:"Jessica Dymond"}]}],onlineFirstChaptersFilter:{topicId:"189",limit:6,offset:0},onlineFirstChaptersCollection:[{id:"80860",title:"From Open to Minimally Invasive: The Sacrocolpopexy",slug:"from-open-to-minimally-invasive-the-sacrocolpopexy",totalDownloads:35,totalDimensionsCites:0,doi:"10.5772/intechopen.101308",abstract:"With an increased demand for pelvic organ prolapse surgeries as the population ages, mesh-related osteomyelitis will become more prevalent. This case series enriches the paucity of data on management options for delayed osteomyelitis related to pelvic organ prolapse mesh. A literature review revealed no case reports of delayed onset osteomyelitis presenting up to a decade after colpopexy mesh placement. We present three cases of delayed osteomyelitis, their presentation, diagnosis and management at a tertiary academic referral center. Patients presented between 1 and 10 years after mesh colpopexy. Three different mesh materials were utilized during the initial procedures: Restorelle Y, Gynamesh and Gore-Tex mesh. The first case demonstrates failed expectant management with eventual surgical intervention on a medically compromised patient. The two subsequent cases describe elective complete mesh resection after several prior failed mesh revision attempts. This short case series and literature review illustrates that mesh-related osteomyelitis after a remote sacrocolpopexy carries significant morbidity. Mesh removal by means of minimally invasive surgery in the hands of an experienced surgical team utilizing DaVinci Robotic System is a good option and may lead to best patient outcomes.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Adriana Fulginiti, Frank Borao, Martin Michalewski and Robert A. Graebe"},{id:"80782",title:"Cases of Postpartum Hemorrhage and Hysterectomy in Thailand’s Northern and Northeastern Provincial Hospitals",slug:"cases-of-postpartum-hemorrhage-and-hysterectomy-in-thailand-s-northern-and-northeastern-provincial-h",totalDownloads:30,totalDimensionsCites:0,doi:"10.5772/intechopen.102948",abstract:"PPH is a major cause of maternal death. Hysterectomy is safe to treat uncontrollable PPH. However, it may not be the best option for women who want to have children. The risk score tool to detect PPH earlier is needed in low-resource cities such as Chiang Rai and Sakon Nakhon province. This study aims to perform a risk score tool to prevent PPH in the northern and northeastern hospitals in Thailand; using mixed methods, identify risk factors for PPH from 20 articles globally and in Thailand using Med Calc, and develop the tool for prediction of PPH; and tool testing and a one-year follow-up on PPH-related hysterectomy cases. Results showed that this risk score tool can detect PPH earlier, reducing the number of PPH and hysterectomy cases. This risk score tool needs to be implemented in the same situations as hospitals to save pregnant women’s lives.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Thawalsak Ratanasiri, Natakorn I. Tuporn, Somnuk Apiwantanagul, Thitima Nutrawong, Thawalrat Ratanasiri and Amornrat Ratanasiri"},{id:"80633",title:"Hysterectomy: Past, Present and Future",slug:"hysterectomy-past-present-and-future",totalDownloads:27,totalDimensionsCites:0,doi:"10.5772/intechopen.103086",abstract:"Hysterectomy is a major operation and is as old as time. This chapter touches briefly on the history of this procedure, its present aspects and general advice for these women who may need a hysterectomy, and finally the direction of new developments about it.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Zouhair Odeh Amarin"},{id:"80589",title:"Total Vaginal Hysterectomy for Unprolapsed Uterus",slug:"total-vaginal-hysterectomy-for-unprolapsed-uterus",totalDownloads:54,totalDimensionsCites:0,doi:"10.5772/intechopen.101383",abstract:"Vaginal hysterectomy was the first method to extract the uterus. Vaginal hysterectomy goes back a long way into the history of medicine. Although the first hysterectomy was carried out by Themison of Athens in the year 20 B.C., the idea of extracting the uterus through the vagina was first mentioned in 120 B.C. by Soranus of Ephesos, a distinguished obstetrician. The first elective vaginal hysterectomy was performed by J. Conrad Langenbeck in 1813. The patient was a 50-year-old multipara, who suffered from chronic pelvic pain attributed to a prolapsed uterus with a hard, bleeding tumor. The operation was carried out in challenging conditions, without anesthesia, proper instruments, or surgical assistants. Until the early 1950s, vaginal hysterectomy was the method of choice for removing the uterus. With the widespread introduction of general anesthesia and antibiotic therapy, the site of vaginal hysterectomy was taken over by abdominal hysterectomy. With the introduction of minimally invasive surgery in gynecology, vaginal hysterectomy has regained its place. Harry Reich performed the first total laparoscopic hysterectomy in 1989, being one of the most renowned vaginal surgeons, and he still claims at the beginning of the 21st century that … when the first choice of approach for hysterectomy is possible, is the vaginal route. This chapter presents the relevant anatomy from the point of view of the vaginal surgeon and the standard technique used by the author in over 5,000 vaginal hysterectomies. All intraoperative drawings and photographs are original.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Petre Bratila"},{id:"80400",title:"Laparoscopic Hysterectomy in Morbidly Obese Patients",slug:"laparoscopic-hysterectomy-in-morbidly-obese-patients",totalDownloads:33,totalDimensionsCites:0,doi:"10.5772/intechopen.101307",abstract:"The following chapter will focus on laparoscopic hysterectomy in morbidly obese patients. The discussion reviews the physiological changes associated with morbid obesity and the potential implications on pneumoperitoneum during laparoscopic surgery. Important considerations such as perioperative care and operating room setup are discussed. Additionally, obtaining abdominal access, reviewing the surgical approach, and post-operative considerations are all highlighted within this chapter.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Merima Ruhotina, Annemieke Wilcox, Shabnam Kashani and Masoud Azodi"},{id:"80238",title:"Surgical Site Infection after Hysterectomy",slug:"surgical-site-infection-after-hysterectomy",totalDownloads:59,totalDimensionsCites:0,doi:"10.5772/intechopen.101492",abstract:"Surgical site infections (SSIs) are associated with increased morbidity, mortality, and healthcare costs. SSIs are defined as an infection that occurs after surgery in the part of the body where the surgery took place. Approximately 1–4% of hysterectomies are complicated by SSIs, with higher rates reported for abdominal hysterectomy. Over the past decade, there has been an increasing number of minimally invasive hysterectomies, in conjunction with a decrease in abdominal hysterectomies. The reasons behind this trend are multifactorial but are mainly rooted in the well-documented advantages of minimally invasive surgery. Multiple studies have demonstrated a marked decrease in morbidity and mortality with minimally invasive surgeries. Specifically, evidence supports lower rates of SSIs after laparoscopic hysterectomy when compared to abdominal hysterectomy. In fact, the American College of Obstetricians and Gynecologist recommends minimally invasive approaches to hysterectomy whenever feasible. This chapter will review the current literature on surgical site infection (SSI) after hysterectomy for benign indications.",book:{id:"11040",title:"Hysterectomy - Past, Present and Future",coverURL:"https://cdn.intechopen.com/books/images_new/11040.jpg"},signatures:"Catherine W. Chan and Michael L. 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The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}},{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}}]},series:{item:{id:"10",title:"Physiology",doi:"10.5772/intechopen.72796",issn:"2631-8261",scope:"Modern physiology requires a comprehensive understanding of the integration of tissues and organs throughout the mammalian body, including the cooperation between structure and function at the cellular and molecular levels governed by gene and protein expression. While a daunting task, learning is facilitated by identifying common and effective signaling pathways mediated by a variety of factors employed by nature to preserve and sustain homeostatic life. \r\nAs a leading example, the cellular interaction between intracellular concentration of Ca+2 increases, and changes in plasma membrane potential is integral for coordinating blood flow, governing the exocytosis of neurotransmitters, and modulating gene expression and cell effector secretory functions. Furthermore, in this manner, understanding the systemic interaction between the cardiovascular and nervous systems has become more important than ever as human populations' life prolongation, aging and mechanisms of cellular oxidative signaling are utilised for sustaining life. \r\nAltogether, physiological research enables our identification of distinct and precise points of transition from health to the development of multimorbidity throughout the inevitable aging disorders (e.g., diabetes, hypertension, chronic kidney disease, heart failure, peptic ulcer, inflammatory bowel disease, age-related macular degeneration, cancer). With consideration of all organ systems (e.g., brain, heart, lung, gut, skeletal and smooth muscle, liver, pancreas, kidney, eye) and the interactions thereof, this Physiology Series will address the goals of resolving (1) Aging physiology and chronic disease progression (2) Examination of key cellular pathways as they relate to calcium, oxidative stress, and electrical signaling, and (3) how changes in plasma membrane produced by lipid peroxidation products can affect aging physiology, covering new research in the area of cell, human, plant and animal physiology.",coverUrl:"https://cdn.intechopen.com/series/covers/10.jpg",latestPublicationDate:"May 14th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:11,editor:{id:"35854",title:"Prof.",name:"Tomasz",middleName:null,surname:"Brzozowski",slug:"tomasz-brzozowski",fullName:"Tomasz Brzozowski",profilePictureURL:"https://mts.intechopen.com/storage/users/35854/images/system/35854.jpg",biography:"Prof. Dr. Thomas Brzozowski works as a professor of Human Physiology and is currently Chairman at the Department of Physiology and is V-Dean of the Medical Faculty at Jagiellonian University Medical College, Cracow, Poland. His primary area of interest is physiology and pathophysiology of the gastrointestinal (GI) tract, with the major focus on the mechanism of GI mucosal defense, protection, and ulcer healing. He was a postdoctoral NIH fellow at the University of California and the Gastroenterology VA Medical Center, Irvine, Long Beach, CA, USA, and at the Gastroenterology Clinics Erlangen-Nuremberg and Munster in Germany. He has published 290 original articles in some of the most prestigious scientific journals and seven book chapters on the pathophysiology of the GI tract, gastroprotection, ulcer healing, drug therapy of peptic ulcers, hormonal regulation of the gut, and inflammatory bowel disease.",institutionString:null,institution:{name:"Jagiellonian University",institutionURL:null,country:{name:"Poland"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:4,paginationItems:[{id:"10",title:"Animal Physiology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/10.jpg",isOpenForSubmission:!0,annualVolume:11406,editor:{id:"202192",title:"Dr.",name:"Catrin",middleName:null,surname:"Rutland",slug:"catrin-rutland",fullName:"Catrin Rutland",profilePictureURL:"https://mts.intechopen.com/storage/users/202192/images/system/202192.png",biography:"Catrin Rutland is an Associate Professor of Anatomy and Developmental Genetics at the University of Nottingham, UK. She obtained a BSc from the University of Derby, England, a master’s degree from Technische Universität München, Germany, and a Ph.D. from the University of Nottingham. She undertook a post-doctoral research fellowship in the School of Medicine before accepting tenure in Veterinary Medicine and Science. Dr. Rutland also obtained an MMedSci (Medical Education) and a Postgraduate Certificate in Higher Education (PGCHE). She is the author of more than sixty peer-reviewed journal articles, twelve books/book chapters, and more than 100 research abstracts in cardiovascular biology and oncology. She is a board member of the European Association of Veterinary Anatomists, Fellow of the Anatomical Society, and Senior Fellow of the Higher Education Academy. Dr. Rutland has also written popular science books for the public. https://orcid.org/0000-0002-2009-4898. www.nottingham.ac.uk/vet/people/catrin.rutland",institutionString:null,institution:{name:"University of Nottingham",institutionURL:null,country:{name:"United Kingdom"}}},editorTwo:null,editorThree:null},{id:"11",title:"Cell Physiology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/11.jpg",isOpenForSubmission:!0,annualVolume:11407,editor:{id:"133493",title:"Prof.",name:"Angel",middleName:null,surname:"Catala",slug:"angel-catala",fullName:"Angel Catala",profilePictureURL:"https://mts.intechopen.com/storage/users/133493/images/3091_n.jpg",biography:"Prof. Dr. Angel Catalá \r\nShort Biography Angel Catalá was born in Rodeo (San Juan, Argentina). He studied \r\nchemistry at the Universidad Nacional de La Plata, Argentina, where received aPh.D. degree in chemistry (Biological Branch) in 1965. From\r\n1964 to 1974, he worked as Assistant in Biochemistry at the School of MedicineUniversidad Nacional de La Plata, Argentina. From 1974 to 1976, he was a Fellowof the National Institutes of Health (NIH) at the University of Connecticut, Health Center, USA. From 1985 to 2004, he served as a Full Professor oBiochemistry at the Universidad Nacional de La Plata, Argentina. He is Member ofthe National Research Council (CONICET), Argentina, and Argentine Society foBiochemistry and Molecular Biology (SAIB). His laboratory has been interested for manyears in the lipid peroxidation of biological membranes from various tissues and different species. Professor Catalá has directed twelve doctoral theses, publishedover 100 papers in peer reviewed journals, several chapters in books andtwelve edited books. Angel Catalá received awards at the 40th InternationaConference Biochemistry of Lipids 1999: Dijon (France). W inner of the Bimbo PanAmerican Nutrition, Food Science and Technology Award 2006 and 2012, South AmericaHuman Nutrition, Professional Category. 2006 award in pharmacology, Bernardo\r\nHoussay, in recognition of his meritorious works of research. Angel Catalá belongto the Editorial Board of Journal of lipids, International Review of Biophysical ChemistryFrontiers in Membrane Physiology and Biophysics, World Journal oExperimental Medicine and Biochemistry Research International, W orld Journal oBiological Chemistry, Oxidative Medicine and Cellular Longevity, Diabetes and thePancreas, International Journal of Chronic Diseases & Therapy, International Journal oNutrition, Co-Editor of The Open Biology Journal.",institutionString:null,institution:{name:"National University of La Plata",institutionURL:null,country:{name:"Argentina"}}},editorTwo:null,editorThree:null},{id:"12",title:"Human Physiology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/12.jpg",isOpenForSubmission:!0,annualVolume:11408,editor:{id:"195829",title:"Prof.",name:"Kunihiro",middleName:null,surname:"Sakuma",slug:"kunihiro-sakuma",fullName:"Kunihiro Sakuma",profilePictureURL:"https://mts.intechopen.com/storage/users/195829/images/system/195829.jpg",biography:"Professor Kunihiro Sakuma, Ph.D., currently works in the Institute for Liberal Arts at the Tokyo Institute of Technology. He is a physiologist working in the field of skeletal muscle. He was awarded his sports science diploma in 1995 by the University of Tsukuba and began his scientific work at the Department of Physiology, Aichi Human Service Center, focusing on the molecular mechanism of congenital muscular dystrophy and normal muscle regeneration. His interest later turned to the molecular mechanism and attenuating strategy of sarcopenia (age-related muscle atrophy). His opinion is to attenuate sarcopenia by improving autophagic defects using nutrient- and pharmaceutical-based treatments.",institutionString:null,institution:{name:"Tokyo Institute of Technology",institutionURL:null,country:{name:"Japan"}}},editorTwo:null,editorThree:{id:"331519",title:"Dr.",name:"Kotomi",middleName:null,surname:"Sakai",slug:"kotomi-sakai",fullName:"Kotomi Sakai",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000031QtFXQA0/Profile_Picture_1637053227318",biography:"Senior researcher Kotomi Sakai, Ph.D., MPH, works at the Research Organization of Science and Technology in Ritsumeikan University. She is a researcher in the geriatric rehabilitation and public health field. She received Ph.D. from Nihon University and MPH from St.Luke’s International University. Her main research interest is sarcopenia in older adults, especially its association with nutritional status. Additionally, to understand how to maintain and improve physical function in older adults, to conduct studies about the mechanism of sarcopenia and determine when possible interventions are needed.",institutionString:null,institution:{name:"Ritsumeikan University",institutionURL:null,country:{name:"Japan"}}}},{id:"13",title:"Plant Physiology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/13.jpg",isOpenForSubmission:!0,annualVolume:11409,editor:{id:"332229",title:"Prof.",name:"Jen-Tsung",middleName:null,surname:"Chen",slug:"jen-tsung-chen",fullName:"Jen-Tsung Chen",profilePictureURL:"https://mts.intechopen.com/storage/users/332229/images/system/332229.png",biography:"Dr. Jen-Tsung Chen is currently a professor at the National University of Kaohsiung, Taiwan. He teaches cell biology, genomics, proteomics, medicinal plant biotechnology, and plant tissue culture. Dr. Chen\\'s research interests include bioactive compounds, chromatography techniques, in vitro culture, medicinal plants, phytochemicals, and plant biotechnology. He has published more than ninety scientific papers and serves as an editorial board member for Plant Methods, Biomolecules, and International Journal of Molecular Sciences.",institutionString:"National University of Kaohsiung",institution:{name:"National University of Kaohsiung",institutionURL:null,country:{name:"Taiwan"}}},editorTwo:null,editorThree:null}]},overviewPageOFChapters:{paginationCount:17,paginationItems:[{id:"81751",title:"NanoBioSensors: From Electrochemical Sensors Improvement to Theranostic Applications",doi:"10.5772/intechopen.102552",signatures:"Anielle C.A. Silva, Eliete A. Alvin, Lais S. de Jesus, Caio C.L. de França, Marílya P.G. da Silva, Samaysa L. Lins, Diógenes Meneses, Marcela R. Lemes, Rhanoica O. Guerra, Marcos V. da Silva, Carlo J.F. de Oliveira, Virmondes Rodrigues Junior, Renata M. Etchebehere, Fabiane C. de Abreu, Bruno G. Lucca, Sanívia A.L. Pereira, Rodrigo C. Rosa and Noelio O. Dantas",slug:"nanobiosensors-from-electrochemical-sensors-improvement-to-theranostic-applications",totalDownloads:4,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Biosignal Processing",coverURL:"https://cdn.intechopen.com/books/images_new/11153.jpg",subseries:{id:"7",title:"Bioinformatics and Medical Informatics"}}},{id:"81766",title:"Evolution of Organoids in Oncology",doi:"10.5772/intechopen.104251",signatures:"Allen Thayakumar Basanthakumar, Janitha Chandrasekhar Darlybai and Jyothsna Ganesh",slug:"evolution-of-organoids-in-oncology",totalDownloads:6,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Organoids",coverURL:"https://cdn.intechopen.com/books/images_new/11430.jpg",subseries:null}},{id:"81678",title:"Developmental Studies on Practical Enzymatic Phosphate Ion Biosensors and Microbial BOD Biosensors, and New Insights into the Future Perspectives of These Biosensor Fields",doi:"10.5772/intechopen.104377",signatures:"Hideaki Nakamura",slug:"developmental-studies-on-practical-enzymatic-phosphate-ion-biosensors-and-microbial-bod-biosensors-a",totalDownloads:3,totalCrossrefCites:0,totalDimensionsCites:0,authors:[{name:"Hideaki",surname:"Nakamura"}],book:{title:"Biosignal Processing",coverURL:"https://cdn.intechopen.com/books/images_new/11153.jpg",subseries:{id:"7",title:"Bioinformatics and Medical Informatics"}}},{id:"81547",title:"Organoids and Commercialization",doi:"10.5772/intechopen.104706",signatures:"Anubhab Mukherjee, Aprajita Sinha, Maheshree Maibam, Bharti Bisht and Manash K. 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