Classification of pericardial effusion.
\r\n\t
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One study examining bovine pericardium for age-dependent differences in collagen alignment showed higher elasticity, higher tensile strength, and thin pericardium in neonatal compared to adult bovine pericardium [1]. Despite such noted anatomical changes in the pericardial structure with age, the spectrum of pericardial disease remains similar among younger and older populations. Although most guidelines have not discussed specific age-related pericardial disease management, diagnostic evaluation and treatment of pericarditis in the geriatric population should take comorbidities into consideration for optimal management [2].
\nThe pericardial space contains 20–50 mL of fluid in the pericardial sac which works as a lubricant between two layers of pericardium. Pericardial effusion is defined by an excess fluid collection over the normal physiological amount within this space. Pericardial fluid accumulation can be secondary to increased fluid production (i.e., any inflammatory condition) or from reduced fluid reabsorption (i.e., heart failure, pulmonary hypertension, and pericardial lymphatic obstruction). The fluid starts accumulating according to gravitational forces, initially in the posterior-inferior site then circumferentially resulting in moderate to large effusion.
\nPericardial effusion can be classified based on various characteristics such as size (mild, moderate, and large), onset (acute, subacute, and chronic), distribution (localized or circumferential), composition (transudate, exudate, blood, or rarely gas from bacterial infections), and hemodynamic effects (without tamponade, with tamponade, effusive-constrictive) [2, 3]. (Table 1).
\nSize of fluid collection in TTE* | \nLess than 10 mm—mild | \n
10–20 mm—moderate | \n|
More than 20 mm—large | \n|
Onset of fluid collection | \n<1 week—acute | \n
>1 week to <3 months—subacute | \n|
>3 months—chronic | \n|
Fluid distribution | \nLocalized | \n
Circumferential | \n|
Fluid composition | \nInfectious—exudative Non-infectious—transudate | \n
Hemopericardium—blood | \n|
Pneumopericardium—air | \n|
Chylopericardium—chylous | \n|
Hemodynamic effects | \nNo tamponade effect | \n
Tamponade effect | \n|
effusive-constrictive | \n
Classification of pericardial effusion.
TTE, transthoracic echocardiography.
The normal pericardium is made up of a high content of collagen fibers, which creates a relatively inelastic sac that contains the heart. The pressure-volume curve of the normal pericardium is a J-shaped curve, which allows a limited stretch of the pericardium in response to physiological events such as posture or volume status without significant change in the intrapericardial pressure; however, after reaching a certain intrapericardial volume, the intrapericardial pressure rises suddenly and can cause sudden systemic hemodynamic derangements. The rapid rate of the fluid collection also plays a role in the pressure-volume curve; a sudden rise in intrapericardial volume (such as with aortic dissection or trauma with hemopericardium) of 100–200 mL significantly raises the intrapericardial pressure, whereas the slow collection of fluid may allow the development of a large pericardial effusion (1–2 L) without signs of cardiac tamponade [3, 4].
\nAmong the elderly, the spectrum of etiologies for pericardial effusion does not differ significantly from the rest of the population. The underlying cause of effusion can usually be inferred from the clinical picture. One study in 322 patients has reported around 60% of cases had a known cause of pericardial effusion [5]. A varying amount of effusion can be seen in other conditions such as malignancy (with or without direct pericardial involvement), renal failure, pregnancy, aortic or cardiac wall rupture, trauma, heart failure, cirrhosis of the liver, nephrotic syndrome, autoimmune diseases, radiation, etc. One study incorporated demographics in their review of pericarditis etiology by comparing a younger patient population (age 15–65,
According to one study with a mean participant age of 56, when determining the cause of moderate to severe pleural effusions, it is important to consider three major factors: (1) size of effusion; (2) presence of tamponade; and (3) inflammatory signs (defined as two or more from: fever >37°C, pericardial friction rub, characteristic chest pain, and diffuse ST-segment elevation). The presence of inflammatory signs was associated with acute idiopathic pericarditis (likelihood ratio = 5.4, P < 0.001), a large effusion without any inflammatory signs or tamponade was found to be associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P < 0.001), and the features of tamponade without inflammatory signs were associated with malignant effusions (likelihood ratio = 2.9, P < 0.01) [5].
\nThe presentation of pericardial effusion varies according to the speed of accumulation, size of effusion, and etiology. The rate of fluid collection plays a critical role in clinical presentation as rapidly accumulating pericardial effusion causes a quick rise in intrapericardial pressure, which results in cardiac tamponade, while slowly accumulating fluid accommodates comparatively larger volume before signs of tamponade [2, 3]. The cases of isolated pericardial effusion can be asymptomatic or can have symptoms related to the underlying etiology or to the effusion itself. The classically reported symptom is dyspnea on exertion; however, the wide spectrum of symptoms related to compressive effect includes cough, weakness, fatigue, palpitations (from compressive effect of the pericardial fluid or reduced blood pressure), nausea (diaphragm), dysphagia (esophagus), hoarseness of voice (recurrent laryngeal nerve), etc. Patients may present with fever from underlying disease (infectious or systemic inflammatory disease), pleural effusion, ascites, or hepatic dysfunction from long standing pericardial constriction [2, 8].
\nPhysical examination may remain normal without any significant findings in patients with no hemodynamic compromise. Pulsus paradoxus is an inspiratory drop in systolic BP >10 mmHg due to the augmentation of right ventricular preload causing impaired left ventricular filling resulting in abnormal decrease in stroke volume [9] and is a phenomenon commonly seen with large pericardial effusion or cardiac tamponade. Pericardial friction rub is rarely heard but is a usual finding of pericarditis.
\nUpon clinical suspicion of pericardial effusion, the diagnostic approach should consider three major steps: (1) confirm the presence of effusion; (2) assess the hemodynamic impact; and (3) effort to identify the underlying etiology. Transthoracic echocardiography (TTE) is recommended in all patients with suspected effusion as a class I, level C recommendation. Further imaging modalities such as computed tomography (CT) scan, cardiac magnetic resonance imaging (CMRI), pericardial fluid analysis, or biopsy can be considered in cases where loculated effusion, masses, or thickening of the pericardium are suspected. Basic diagnostic work up, including blood counts, chemistry, thyroid function tests, cardiac biomarkers, inflammatory markers such as C-reactive protein (CRP) and sedimentation rate (ESR), electrocardiogram (ECG), and chest X-ray, should be done [2, 10]. ECG findings in pericardial effusion include low QRS voltage and electrical alternans, a finding of large pericardial effusion or tamponade that is usually associated with sinus tachycardia.
\nTTE is recommended as the first modality to determine the hemodynamic significance of pericardial effusion and is highly sensitive and specific. The pericardial fluid appears as echo-lucent space between the pericardium and epicardium on TTE. The semi-quantitative assessment for largest echo-free space in echocardiographic views provides an assessment of severity. Mild pericardial effusion is considered <10 mm, moderate between 10 and 20 mm, and large effusion is any collection >20 mm. The collection of effusion follows gravity initially in the inferolateral position close to right atrium in the apical four chamber view with the patient in a supine-left lateral position. The pattern of collection changes to circumferential in the pericardium with increasing amount of fluid (Figure 1). After the development of a large amount of effusion, the heart can be seen swinging in the pericardial cavity, a finding that correlates with electrical alternans on ECG [2, 3, 11].
\nLarge circumferential pericardial effusion.
Cardiac CT and CMRI are useful imaging modalities for the evaluation of pericardial effusion and tamponade especially for more detailed assessment and the localization of the effusion and associated abnormalities in the mediastinum, lungs, and adjacent structures. They are useful for the guidance of pericardiocentesis since loculated effusions or calcified pericardium can be identified. CMRI is superior to CT in differentiating fluids especially highly exudative fluid from thickened pericardium. CT detects a minimum amount of pericardial calcium and is relatively quick [2, 11].
\nPericardial fluid analysis is often performed when the patient requires pericardiocentesis. Routine fluid studies include measuring fluid protein level, protein fluid/serum ratio, lactate dehydrogenase (LDH), LDH fluid/serum ratio, glucose, cell counts, and specific gravity. Fluid cytology and tumor markers (carcinoembryonic antigen, cancer antigen 19-9, adenosine deaminase, and interferon gamma) are useful measures in malignancy. Polymerase chain reaction and fluid cultures help in infectious etiologies.
\nFor small-to-medium sized, asymptomatic pericardial effusion without signs of hemodynamic instability, regular outpatient follow-up with clinical examination and/or echocardiography should be preferred. Management of pericardial effusion with signs of inflammation (pericarditis) should follow the standard or treatment for pericarditis; however, in the absence of any inflammation, anti-inflammatory drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids, are generally not effective. Such cases as well as cases with large effusion that failed empiric anti-inflammatory therapy would require pericardiocentesis. Recurrence of effusion is fairly common and further management options include pericardial window formation or pericardiectomy. A study comparing patients age 15–65 to a group of patients age 66–88 years showed elderly people had more persistence of effusion (6.3 vs. 14%; P < 0.05) but no statistically significant difference in mortality (24 vs. 30%) or evolution of cardiac constriction (4 vs. 2%) during median follow up time of 11 months [6]. There is no standard guideline available for elderly patients regarding pleural effusions; however, the expert consensus suggests adjusting the type and dosages of medications with special attention to drug interactions and renal function given the prevalence of polypharmacy and renal dysfunction in the geriatric population [2]. A proposed management algorithm for pericardial effusion of unknown origin is depicted in Figure 2 [2, 3].
\nManagement algorithm for pericardial effusion with unknown origin.
The prognosis of pericardial effusion is related to its etiology and size. Moderate-to-large size effusions are more commonly associated with bacterial infection, systemic inflammatory disease, or malignancy. Idiopathic pericardial effusion has a good prognosis, but effusion related to bacteria, post-radiation, or pericardial injury has a higher rate of developing either early (cardiac tamponade) or late complications (constrictive pericarditis). Large effusion (>3 months) carries a 30–35% risk of progression to cardiac tamponade. The follow-up of pericardial effusion is mainly based on symptomatic evaluation with the follow-up of inflammatory biomarkers and echocardiography [3]. A recent meta-analysis regarding prognosis of pericardial effusion in an elderly population with mean age > 60 reported that pericardial effusion can be considered as a marker of severity of the underlying disease as evidenced by a higher hazard ratio (HR) in patients with pericardial effusion with myocardial infarction (HR 2.65, 95% CI: 1.4–4.99; P = 0.003, 15 months follow-up) versus those with chronic heart failure (HR 1.53, 95% CI: 1.22–1.92; P < 0.0001, 31 months follow-up) [12].
\nAcute pericarditis is a condition defined by the inflammation of the pericardial sac that can take place in the setting of a systemic disease (infectious, malignant, inflammatory, etc.) or independently of any other condition [2, 5, 13, 14, 15]. Among the elderly, it is important to consider malignancy in the evaluation of etiology as it is more common in this population and may prompt appropriate testing leading to a faster diagnosis and potential earlier intervention.
\nVarious infections (viral, bacterial, fungal, and tick-borne) have been known to cause the inflammation of the pericardium. In fact, prior to the widespread distribution of anti-retroviral medications, pericarditis was found to be the most common cardiovascular manifestation of human immunodeficiency virus/acquired immunodeficiency syndrome [16, 17] and, in conjunction with tuberculosis, remains the most common cause of pericardial inflammation in the developing world [18], whereas coxsackievirus maintains its status as the most common viral etiology of pericarditis overall. Malignancy, independent of other systemic diseases, has also been associated with acute pericardial disease and accounts for about 6% of cases without another explanation [19, 20]. Systemic diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), have been found to cause pericardial inflammation with approximately 50% of patients with SLE experiencing pericarditis. Other established etiologies of acute pericardial disease include post-myocardial infarction pericardial inflammation and/or effusion [21, 22, 23, 24], post-radiation pericarditis with or without pericardial effusion [25], and uremic pericarditis usually in the setting of advanced renal failure and inadequate dialysis [26, 27]. Hypothyroidism severe enough to result in myxedema can result in a large, slowly accumulating pericardial effusion but rarely causes acute pericarditis [28].
\nThere are four major distinctive features of acute pericarditis (at least two of which are required to make a clinical diagnosis): chest pain, pericardial friction rub, characteristic ECG changes, and pericardial effusion. The predominant presenting symptom is chest pain that is usually pleuritic in nature, sharp and alleviated by sitting up and leaning forward due to the positional shift of the pericardium, a feature which distinguishes it from the typical chest pain caused by myocardial ischemia [29, 30]. Pericardial chest pain is also often associated with nonproductive cough and dyspnea [29]. A scratchy, squeaking sound heard over the left sternal border upon auscultation known as a pericardial friction rub is the second of four major clinical features of pericarditis and is reported to be found in approximately 85% of patients with acute pericarditis in the absence of a pericardial effusion [20]. It is an extra heart sound resulting from the friction between the parietal and visceral pericardium coming into contact in the presence of inflammation. The presence of a pericardial effusion is the third of the four major signs of acute pericarditis and can best be appreciated on an echocardiogram. The last of the four major signs of pericarditis is new, diffuse ST-elevation, PR segment depressions, and PR segment elevation in lead aVR found on ECG (discussed further under
Various laboratory tests and imaging modalities play role in establishing the diagnosis of acute pericarditis. Inflammatory markers, such as white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) levels although nonspecific, may help distinguish pericarditis from a condition with overlapping features given appropriate clinical criteria. Troponin levels, usually elevated in acute coronary syndrome, may also be elevated in pericarditis indicating myocardial involvement [34].
\nThe chest X-ray may show cardiomegaly in the presence of a significant pericardial effusion but otherwise has limited utility in the diagnosis of pericardial disease. An echocardiogram can be similarly useful although the absence of pericardial effusion would not necessarily exclude the diagnosis of acute pericarditis. Cardiac CT imaging can serve a dual purpose in the diagnosis of acute pericarditis in that it may also help elucidate the underlying pathology responsible for the inflammatory changes. Pericardial thickening and effusion in the absence of calcification along with the enhancement of the visceral and parietal pericardium with intravenous contrast are indicative of active inflammation consistent with pericarditis [35]. CMRI can confirm inflammation but is likely not necessary in the diagnostic workup of acute pericarditis unless the presumed etiology is a systemic inflammatory or autoimmune disease with characteristic cardiac findings.
\nThe ECG may be perhaps the most useful diagnostic modality when considering acute pericarditis. The ECG progresses through a distinctive, four stage pattern although the evolution can be variable with up to 40% of patients showing atypical changes [30, 31, 32]. Stage 1 is characterized by widespread ST elevation with reciprocal ST depression in leads aVR and V1 as well as PR segment elevation in lead aVR accompanied by PR segment depression in the remaining limb leads and V5–6. Within 1 week of onset, normalization of ST and PR segments on the ECG comprises Stage 2. Stage 3 of the ECG is marked by diffuse T-wave inversions, while Stage 4 consists of normalization of the ECG. However, not all forms of pericarditis result in the characteristic ECG pattern as the pericardium itself is an inert tissue and only inflammatory changes involving the epicardium or myocardium would be reflected in acute pericarditis [36]. In fact, one review found that of 100 patients studied, only seven arrhythmias were identified all resulting from underlying heart disease [37], while a separate study comparing acute pericarditis to myopericarditis found arrhythmias more frequently associated with myopericarditis [38].
\nMedical treatment of acute pericarditis utilizes one or a combination of two out of three different medications: NSAIDs, colchicine, and glucocorticoids. Treatment duration is usually guided by the resolution of symptoms and etiology of disease in the absence of confounding factors such as acute kidney or liver injury.
\nA combination of NSAIDs and colchicine is the mainstay of therapy for acute viral or idiopathic pericarditis. NSAIDs alone have been shown through multiple studies to effectively treat up to 80% of pericarditis cases [20, 32, 39]. No one particular NSAIDs has been shown to be more effective than another except in the case of post-myocardial infarction pericarditis for which aspirin is recommended and other NSAIDs should be avoided in order to prevent the disruption of myocardial scar formation [40]. Patients taking NSAIDs for pericarditis should concurrently take a proton-pump inhibitor for ulcer prophylaxis in the absence of any direct contraindication to do so. Treatment can be tapered once the patient is symptom-free for at least 24 hours (typically 1–2 weeks). Alternatively, one study recommends following weekly CRP levels along with symptom resolution and beginning tapering, once the patient is symptom-free for 24 hours and CRP levels have returned to normal [41].
\nIn 2005, the Colchicine for Acute Pericarditis (COPE) trial suggested colchicine as an effective adjunct for treating acute pericarditis when combined with NSAIDs therapy for patients with non-bacterial, non-malignancy-related pericardial disease [39]. The addition of colchicine was further shown to reduce symptom burden and decrease the rate of recurrent pericarditis by a subsequent, randomized-control trial (RCT) [42], a finding, which was later supported by a meta-analysis in 2014, that demonstrated a reduced risk of recurrence at 18 months in patients undergoing treatment for acute pericarditis [43]. The management of acute pericarditis with a combination of NSAIDs and colchicine is also currently supported by the 2015 European Society of Cardiology (ESC) guidelines [2].
\nFor patients with contraindications to NSAIDs therapy (kidney failure, GI bleeding, pregnancy, etc.), glucocorticoids may be used in combination with colchicine for the initial treatment of acute pericarditis. Treatment duration is then guided by symptom resolution and the normalization of CRP levels with tapering usually started 2–4 weeks thereafter. Glucocorticoids have also been utilized in patients with pericarditis refractory to NSAIDs and colchicine though one study shows a trend toward higher rate of recurrent pericarditis with steroid use [44].
\nGeriatric patients appear to have a higher risk of mortality when admitted and treated for pericarditis in the hospital. Although data regarding treatment of specifically elderly patients are sparse, one study examined the relationship between pericarditis, age, hospital admission, and mortality. They analyzed 45,504 patients above the age of 65 from 1999 to 2012 and found that hospitalization for the treatment of pericarditis is associated with increased risk of 1-year all-cause mortality despite a decrease in 1-year mortality rate from 19.7% (95% confidence interval (CI) 18.8–20.8) in 1999 to 17.3% (95% CI 15.3–20) in 2012 [45]. While it is possible that this association is in part due to a higher prevalence of significant comorbidities and compromised immune systems among the elderly, it nevertheless remains an aspect of pericardial disease that warrants further investigation as advanced therapies and support devices continue to enable longer lifespans with time.
\nRecurrent pericarditis is a syndrome defined by the reemergence of pericarditis after the treatment of the initial inflammatory event [31, 46, 47, 48]. A minimum 4–6 week symptom-free interval post anti-inflammatory treatment is required to differentiate recurrent pericarditis from incessant pericarditis.
\nAcute pericarditis has been found to have recurrence rates as high as 30% in patients treated without colchicine [32, 39, 47, 49]. Some cases of recurrent pericarditis appear to reflect localized inflammation given the detection of certain cytokines (interleukin (IL)-6, IL-8, and interferon gamma) in the pericardial fluid and their absence in the serum [50]; however, most cases are considered to be of autoimmune etiology [2, 51].
\nChest pain appears to be the most common recurring symptom; however, the clinical diagnosis of recurrent pericarditis requires the presence of at least one of the following in addition to pleuritic chest pain: fever, pericardial rub, ECG changes, pericardial effusion, elevated WBC, ESR, CRP, or evidence of active pericardial inflammation on imaging [15]. Patients with previously treated pericarditis may experience multiple recurrences over the course of months to years following the initial event [52, 53, 54].
\nThe selection of the initial treatment regimen can directly impact the potential for the recurrence of acute pericarditis and may serve as an independent predictor of risk. For instance, a prior response to NSAIDs therapy is associated with the reduced risk of recurrence [32], whereas treatment with glucocorticoids is associated with increased recurrence [55]. It is difficult to rely upon ECG changes for the diagnosis for recurrent pericarditis as they are non-specific in the majority of cases. Chest X-ray and TTE also have limited utility as both will appear to be normal without a significant pericardial effusion. CT and CMRI imaging have proven to be of benefit in elucidating the diagnosis of recurrent pericarditis as contrast-enhanced CT can detect active pericardial inflammation while CMRI may reveal the evidence of edema via pericardial gadolinium enhancement [2, 35].
\nRecurrent viral or idiopathic pericarditis is typically managed with an outpatient medical regimen [2, 52, 54] initially consisting of an NSAIDs and colchicine [15] as glucocorticoids are known to increase the risk of recurrence despite multiple recurrences of pericarditis [56]. Glucocorticoid therapy is, therefore, reserved for patients who are either unable to tolerate NSAIDs or have failed NSAIDs therapy in the past [2].
\nIt is important to ensure an adequate trial of NSAIDs was given prior to labeling a patient as refractory. Common agents such as Aspirin and Ibuprofen should be attempted first followed by Indomethacin for treatment resistant cases. Medication should be administered in three doses over 24 hours to ensure consistent therapeutic levels, and dosage should be titrated up as needed to achieve symptom control until the daily maximum is reached or symptoms have subsided [10, 32, 39, 52, 54, 57].
\nPatients with recurrent pericarditis are often times designated as refractory to colchicine therapy after having received inappropriate dosing or rapid tapers [43]. In addition, colchicine should be given twice a day in order to reduce the risk of poor compliance due to gastrointestinal discomfort [10, 57, 58].
\nIn cases of recurrent pericarditis refractory to treatment with NSAIDs, colchicine, and glucocorticoids, patients found to have the evidence of systemic inflammation may benefit from anti-interleukin-1 therapy. A recent trial in 2016 demonstrated a significant reduction of recurrence (90–18%) in patients with pericarditis resistant to colchicine and dependent on corticosteroids with the addition of anakinra, an IL-1B antagonist [59]. Although promising, this study’s results were limited by a small sample size and inconsistent colchicine dosing across trial participants warranting further investigation.
\nConstrictive pericarditis is a condition that occurs when a thickened or calcified pericardium loses elasticity resulting in the reduction of diastolic filling. It is a syndrome that is the end result of chronic pericarditis and pericardial effusion gradually progressing to fibrosis [2, 15, 29, 60]. Such impairment overtime causes the reduction of pericardial space, which in turn uncouples intrathoracic and intracardiac pressures generating increased interventricular interdependence visible on echocardiogram [2, 35, 61, 62].
\nConstrictive pericarditis can occur as a result of inflammation and effusion from any pericardial disease [2, 31, 63]. A combination of studies has found that 42 to 61% of cases were idiopathic or viral, 11 to 37% postcardiac surgery, 2 to 31% postradiation, 3 to 7% due to connective tissue disorders, 3 to 15% bacterial or tuberculous, and 1 to 10% related to malignancy, trauma, drug toxicity, sarcoidosis, or uremic pericarditis [64, 65, 66, 67, 68, 69]. Tuberculosis remains a major global cause of constrictive pericarditis especially in endemic nations [2, 70].
\nPatients with constrictive pericarditis usually present with symptoms of right heart failure in the absence of ventricular function impairment. Symptoms are consistent with volume overload, such as edema, pleural effusion, dyspnea, ascites, or low output states such as exertional dyspnea and fatigue [2]. As high as 93% of patients present with elevated jugular venous pressure (JVP) [65], while only approximately 20% of patients present with pulsus paradoxus or Kussmaul’s sign [64, 65, 71]. A pericardial knock has been noted in 47% of patients with constrictive pericarditis [65].
\nAlthough the diagnosis of constrictive pericarditis can be made by echocardiography [72], an ECG and chest X-ray should also be obtained as part of the initial evaluation. There are no specific ECG changes consistently indicative of constrictive pericarditis; however, an ECG may be helpful in ruling out other cardiac pathology. The chest X-ray may show the evidence of pericardial calcification in which the presence of right heart failure would be strongly suggestive of constrictive pericarditis; however, the absence of such a finding would not rule out the disease [2].
\nAll patients with suspected pericardial disease should be evaluated with echocardiography [2, 73]. Septal bounce and pericardial thickening on M-mode and 2-dimensional echocardiography would be suggestive of a constrictive pattern. On Doppler echocardiography, increased interventricular interdependence is associated with pericardial fibrosis, and the ratio of the right ventricular (RV) area to the left ventricular (LV) area, known as systolic area index (SAI), is virtually diagnostic of constrictive pericarditis when the SAI is >1.1 [74].
\nCT imaging can show pericardial thickening and calcification but is not necessary to diagnose constrictive pericarditis. However, the identification of important vascular structures on CT can prove useful if planning for pericardiectomy [75]. Positron emission tomography (PET)/CT can also be helpful in predicting response to corticosteroid therapy [76]. CMRI may show characteristic changes of constrictive pericarditis, such as pericardial thickening, dilation of the inferior vena cava, or ventricular interdependence, but is usually necessary unless investigating other related cardiac pathology.
\nTreatment of constrictive pericarditis is dependent on the course of the disease at the time of evaluation. For early subacute disease in patients who are hemodynamically stable, medical therapy similar to that used for acute pericarditis is recommended. Patients who present with the evidence of late chronic disease (cachexia, pericardial calcifications, and hepatic dysfunction) or those who have failed conservative management with anti-inflammatory therapy can be treated with pericardiectomy [63]. The majority of patients achieve symptomatic relief with early surgical removal of the inflamed pericardium [69] with one study reporting up to 69% of patients being symptom-free at 4 year follow-up [65].
\nCardiac tamponade is characterized by the accumulation of pericardial fluid causing significant impairment in cardiac function due to the pressure effect of external pericardial content causing compression of all cardiac chambers. Increase in intrapericardial pressure reduces the myocardial transmural pressure with a reduced ventricular wall diastolic compliance and a decrease in cardiac output and blood pressure. In cardiac tamponade, unlike constrictive pericarditis, most of the inspiratory decline in the intrathoracic pressure is transmitted through the pericardium to the right ventricle and results in increased venous return and right ventricular distention. The higher intrapericardial pressure limits the right ventricular free wall expansion, resulting in bulging of the right ventricular septum to the left ventricle. This bulge diminishes the compliance of the left ventricle, which results in decreased filling and cardiac output [4, 77]. A similar mechanism contributes to pulsus paradoxus, an abnormal decline in systolic blood pressure (>10 mmHg) with inspiration. Cardiac tamponade is a treatable cause of cardiogenic shock that can be rapidly fatal.
\nUsually, cardiac tamponade is seen after pericarditis, tuberculosis, iatrogenic (secondary to cardiac interventions), trauma, neoplasm, with other uncommon causes including, collagen vascular disorder, radiation therapy, post-myocardial infarction, uremia, aortic dissection, and a bacterial infection.
\nCardiac tamponade could be acute, subacute, low-pressure type, or regional. Acute cardiac tamponade is sudden in onset and acutely life-threatening if not treated. Subacute cardiac tamponade is less dramatic compared to acute, but once the intrapericardial pressure reaches the threshold, patients experience classical tamponade symptoms related to decreased cardiac function. Low-pressure tamponade is a condition that appears in hypovolemic patients (such as traumatic hemorrhage, over diuresis, etc.). Correction of volume status reveals a typical tamponade pattern. Regional tamponade occurs from loculated effusion or a localized hematoma causing compression of only selected chambers. It is usually seen after myocardial infarction or pericardiotomy [77].
\nDepending on the severity of the tamponade, a variety of clinical findings are seen. Sinus tachycardia as a physiologic response to maintain the cardiac output is common. Elevated jugular venous pressure, muffled heart sounds, and systemic hypotension together referred to as Beck’s triad is a pathognomonic sign for tamponade.
\nThe diagnostic approach and the evaluation of cardiac tamponade are similar to that for patients with suspected pericardial effusion. The ECG findings include sinus tachycardia, low voltage of QRS complex, and frequently electrical alternans, which is beat-to-beat changes in the position of the heart with relation to cardiac tamponade. The presence of total electrical alternans, including P wave, QRS complex, and ST segment alternans, is highly specific for cardiac tamponade, but sensitivity is very low with findings present in only 5–10% of cases. The presence of lone QRS alternans is more common but is not very specific for tamponade. The presence of QRS vector alternans (axis shift) is more specific than QRS amplitude alternans for the cardiac tamponade [77, 78].
\nTTE is the standard first-line imaging technique recommended for the evaluation of cardiac tamponade with excellent safety and efficacy. The size of the pericardial effusion does not indicate significance. Since respiration has an impact on intracardiac pressures, mainly on the right side of the heart, this respirophasic flow pattern becomes more evident in tamponade, which can be measured by Doppler echocardiographic variations in blood flow across the mitral (>25% variation) (Figure 3) and tricuspid valves (>40% variation) as well as pulmonary and systemic outflow. Right atrial collapse and RV collapse on diastole (Figure 4) are usual signs of cardiac tamponade, but in the setting of severe pulmonary hypertension, right-sided chamber collapse may be delayed and preceded by left atrial collapse. In most cases, the thickness of the left ventricular wall and lower compliance prevents LV collapse. As the tamponade worsens, there are progressive impairments in hemodynamics and intracardiac flows. Elevated pressures in the right atrium can be assessed from a plethora of the inferior vena cava (IVC) which is a lack of change in IVC caliber in response to respiratory flow pattern (<50% reduction in IVC diameter during inspiration). The swinging movement of the heart within the pericardial sac is another echocardiographic sign. These TTE findings in cardiac structural and functional change with a decline in cardiac function often occur well before the onset of pulsus paradoxus and significant clinical deterioration, and thus, they are an important indicator in cardiac tamponade [11, 79]. Cardiac CT and CMRI may provide valuable information about the functional and structural change of the heart and pericardium, but they are only required in special conditions such as localized tamponade, loculated pericardial effusion, or hematoma [61, 79].
\nDoppler echocardiographic variations in blood flow across the mitral valve.
Diastolic collapse of the right ventricular wall (top arrow) and diastolic period of cardiac cycle (bottom arrow).
The treatment of cardiac tamponade is decompression with pericardiocentesis which can be done by percutaneous catheter pericardiocentesis or open surgical drainage with or without a pericardial window or video-assisted thoracoscopic pericardiectomy. Catheter pericardiocentesis under echocardiographic or fluoroscopic guidance is a more rapid and less invasive technique. Surgical pericardiocentesis is usually performed in purulent pericarditis bleeding into the pericardium or when pericardial biopsies and pericardiectomy are needed [2, 77]. A triage system proposed by the ESC Working Group on Myocardial and Pericardial Diseases can be used to guide the timing of the pericardiocentesis in non-emergent cases [80]. Fluid removal and decompression of the pericardial cavity rapidly improve the clinical hemodynamic status. Positive pressure mechanical ventilation should be avoided as it increases the intrathoracic pressure that deteriorates cardiac filling. The use of vasodilators and diuretics that reduce the preload is not recommended in the presence of cardiac tamponade [2].
\nNone of the authors have any conflicts of interest to disclose.
\nOver the last year, COVID-19 has been the most widely spoken and researched disease worldwide and, inevitably, other existing pathologies were moved to the background. Amongst these, cardiovascular diseases (CVDs) should be highlighted because they still are by far the major contributor to global mortality [1]. CVDs are mainly caused by a blockage that prevents blood from flowing properly, known as atherosclerosis [2, 3]. This is a complex disease that affects medium and large size arteries and consists of a build-up of fatty deposits on the inner walls of the blood vessels, hampering the blood flow through the body [4]. The effect of atherosclerosis can be exacerbated by other diseases that affect blood circulation. Particularly, it has been shown that patients with COVID-19 are prone to develop blood clots on both arteries and veins [5], and thus atherosclerosis may be an even more important factor to global mortality.
Given the prevalence of this disease, atherosclerosis has been intensely studied through both cardiovascular modeling and experimental procedures, as reviewed elsewhere [6, 7, 8, 9]. Nevertheless, with the growing trend of greater computer power, computational approaches have become a valuable, cheaper, and efficient alternative for numerous researchers to predict blood flow behavior [10, 11, 12, 13].
There are two main approaches for simulating blood flow, computational fluid dynamics (CFD) and fluid-structure interaction (FSI). In the first one, the arterial wall is assumed as rigid, while in the second one, arteries are considered elastic and the interaction between the blood and the arterial walls are included in the simulation [14]. Although CFD has been widely applied in the study of blood flow under pathological conditions in virtue of lower computational cost [15, 16, 17, 18, 19, 20], since FSI provides a more realistic simulation of the human vasculature behavior, it has received increasing interest [21, 22]. Nonetheless, this approach requires significantly more computational effort, and the foremost difficulty is stability and convergence [23, 24].
In order to evaluate if the differences between CFD and FSI results are significant, some researchers have investigated and compared both. A commonly mentioned work was developed by Torii et al. [25]. The authors studied the effects of wall compliance on a stenotic patient-specific coronary artery and found noticeable differences in the instantaneous wall shear stress (WSS) produced by the FSI and rigid wall models. However, the effects of wall compliance on time-averaged WSS (TAWSS) and oscillatory shear index (OSI) were negligible. Malvè et al. [26] performed a similar study in the left coronary artery bifurcation and the conclusions regarding the WSS agreed with the previous study, but they observed significant differences in the TAWSS, especially on its spatial distribution. More recently, another similar study was performed on carotid bifurcation [10]. The authors found that the rigid model overestimates the flow velocity and WSS, but its influence on the TAWSS is minimal.
The differences between the CFD and FSI simulations have thus been the subject of several studies, however, as demonstrated, there is still a debate as to whether it is really necessary to use the most realistic approach, namely in computing WSS dependent variables, and sometimes the findings are contradictory. In this regard, this work presents the comparison of the results of both CFD and FSI simulations in an idealized stenotic coronary artery, with a degree of stenosis of 50%.
The first step necessary to study blood flow consisted in obtaining the three-dimensional geometry of the lumen of an idealized coronary artery as depicted in Figure 1. This geometry was previously adopted in other works by these authors [27, 28].
Geometry and mesh of the coronary artery for both solid and fluid domain with 50% of stenosis.
In the construction of the solid domain, a thickness of 0.8 mm was considered, according to an
Moreover, the fluid domain and the solid domain were discretized in 428,800 and 15,480 hexahedral elements, respectively, making a total of 444,280 elements for the FSI simulations. To ensure the quality of the mesh, the skewness and orthogonal quality were evaluated. The average skewness and orthogonal quality were approximately 8.3
Blood flow is governed by the incompressible Navier-Stokes and the continuity equations as described in Eqs. (1) and (2),
where
In the present study, blood was modeled as incompressible, laminar, and non-Newtonian fluid, having a density of 1060 kg/
where
The governing equation for the solid domain is the equilibrium equation (Eq. (4)) [30, 31]:
where
where
The arterial wall was modeled as a linear elastic, incompressible, isotropic, and homogeneous material with Young’s modulus of
The FSI simulations were performed using the Arbitrary-Lagrangian-Eulerian (ALE) methodology for the fluid flow. Taking into account that the interface between the lumen and the wall deforms, the equations governing fluid flow have to be expressed in terms of the fluid variables relative to the mesh movement. The ALE-modified Navier-Stokes momentum equation for a viscous incompressible flow is described as follows in Eq. (8) [30, 31]:
where
The displacement and equilibrium forces at the interface are represented by Eqs.(9) and (10) [30, 31]:
where
Regarding the boundary conditions used in this study, at the inlet, a physiologically accurate pulsatile velocity profile was set, which is depicted in Figure 2. At the outlet, a pressure of 80 mmHg was assumed [17, 36].
Velocity profile implemented in CFD and FSI simulations.
The solid and fluid wall-boundaries were defined as a fluid-structure interface, and the inlet/outlet adjacent solid boundaries were fixed in all directions.
For the CFD simulations, the Ansys Fluent software was used which applies the finite-volume discretization method. In this method, the fluid domain is divided into a finite number of control volumes, the conservation equations are applied to each control volume. Then, a system of algebraic equations for the variables is obtained. For the velocity-pressure coupling, the semi-implicit method for the pressure-linked equations (SIMPLE) scheme was used [37].
In FSI simulations, the same finite-volume method is applied in the fluid domain, and the computed forces in Fluent are transferred to the solid domain, through the interface. The finite element method (FEM) is used to solve the governing equations of the solid domain. Then, the computed displacements are transferred back to the fluid domain. This two-way coupling process was repeated until the difference of the displacements and forces for the last two iterations is below 1%. A time step of 0.01 s was used for every simulation.
The formation of atherosclerotic lesions has been widely associated with hemodynamic parameters, such as the wall shear stress (WSS) and its indices, time-averaged wall shear stress (TAWSS), and oscillatory shear index (OSI) [38, 39]. These have been very useful to predict and estimate disturbed flow conditions and the development of local atherosclerotic plaques [27, 40].
The spatial WSS,
The TAWSS index allows obtaining an average temporal evaluation of the WSS exerted during a cardiac cycle (
The OSI index is the temporal fluctuation of low and high average shear stress during a cardiac cycle (
The formulation developed in this section describes the models that couple the fluid dynamics and the mechanical interaction with the arteries’ wall which is treated as a deformable material. This methodology enables the computation of critical parameters for understanding the hemodynamics in the presence of a stenosis, such as the WSS. The advantages of this method are made evident by comparing it with a simple CFD analysis as detailed in the following section.
Figure 3 illustrates the velocity profiles measured along the center of the artery for both CFD and FSI simulations, in two different phases of the cardiac cycle: systole (0.4 s) and diastole (0.58 s).
Axial flow velocity profiles at the center line drawn across the artery at (a) systole and (b) diastole.
Looking at the results in Figure 3, it can be observed that the estimated velocity profiles are similar for both CFD and FSI modeling. Moreover, as expected, during diastole (Figure 3b) the velocities measured are higher than during systole (Figure 3a). This happens because, during systole, the coronary arteries are compressed by the contraction of the myocardium, and so, most of the coronary flow occurs during diastole, where the flow increases. In addition, the maximum velocities in both cases are measured in the stenosis throat (
It is also noted that the velocity is overestimated in the CFD model, particularly at and upstream of the stenosis throat. This is expected because the deformation of the elastic model provides a larger volume for the blood flow through and, as the inflow rate is equal for both models, naturally, the velocities will be higher when a rigid wall is considered. Downstream of the stenosis, at an
After evaluating the velocity profiles, velocity streamlines were created to better visualize and understand how blood flow behaves, as shown in Figure 4.
Velocity streamlines obtained during systole and diastole for both CFD and FSI simulations.
The results indicate the existence of fluid recirculation downstream of the stenosis for both CFD and FSI models, but the recirculation zones are longer in FSI simulations, and this is due to the considerable vessel expansion driven by the pulsatile blood flow.
The magnitude of the WSS predicted by FSI and rigid model along the artery wall for both systole and diastole are compared in Figure 5. In this case, it is observed that the differences between compliant and rigid-wall models are remarkable. In CFD simulations, WSS values estimated in the stenosis throat are approximately twice of those obtained with FSI simulations. This indicates that the WSS distributions were substantially affected by arterial wall compliance, which is in agreement with previous research [25, 26, 41].
Wall shear stress profiles obtained along artery wall at (a) systole and (b) diastole.
Taking into account that WSS-related hemodynamic parameters, such as OSI and TAWSS, play an important role in atherogenesis, these were also evaluated. Figure 6 depicts the TWASS profiles obtained in both CFD and FSI simulations.
Time-averaged wall shear stress profiles obtained in CFD and FSI simulations.
The results evidence high values of TAWSS at the stenosis throat, due to flow acceleration and high-velocity gradient near the wall, and, as expected the TAWSS is overestimated by the CFD model as previously explained for WSS distributions. In spite of these observations, the overall TAWSS distributions for the FSI and rigid-wall cases are identical.
Regarding the OSI profiles depicted in Figure 7, it can be observed that for both CFD and FSI simulations, the maximum values (
Oscillatory shear index obtained in CFD and FSI simulations.
In general, it was found that for both rigid and compliant models the post-stenotic region presents lower TAWSS and higher OSI values, which constitute risk factors for the incidence and abnormal plaque formation [16, 27].
Figure 8 represents the arterial wall displacement contours of the FSI simulations during systole and diastole.
Displacement profile at the arterial wall obtained in CFD and FSI simulations.
In the first place, it is noted that the displacements are similar for both cycle phases. This is a consequence of the assumption of the constant outlet pressure, which is a limitation of this work. In this case, the deformations are slightly bigger in the region upstream of the stenosis, and as there is a pressure drop in the throat, the displacements are somewhat lower in the downstream region.
It is also noteworthy that the displacements of the arterial wall are approximately 1.5–2% of the vessel thickness, which is in agreement with the hypothesis that arteries become stiffer with the development of atherosclerosis. Despite this order of magnitude of the displacement values, these still bring considerable differences in the calculations of the velocity and WSS-related variables.
The study of blood flow in stenotic arteries has been made mainly assuming the artery’s wall as rigid, however, in reality, they are naturally elastic. Given that there are some inconsistencies in the literature regarding the comparison between CFD and FSI simulations, in the present work, a comparative study between FSI and CFD modeling was performed in order to investigate the influence of artery compliance on stenotic coronary artery hemodynamics and wall shear stress distribution. The main conclusions obtained from this work are:
Comparing the rigid and compliant models, the velocities predicted differ slightly.
The difference between WSS profiles was remarkable. The CFD simulations overestimate the WSS values, which consequently indicates that when a more realistic WSS estimation is needed, is essential to consider the effect of the atrial wall on blood flow.
Insignificant differences were verified in the TAWSS and OSI measurements.
This work has been supported by FCT—Fundação para a Ciência Tecnologia within the R&D Units Project Scope: UIDB/00319/2020, UIDB/04077/2020, UIDB/04436/2020, and NORTE-01-0145-FEDER-030171 (PTDC/EMD-EMD/30171/2017) and EXPL/EME-EME/0732/2021, NORTE-01-0145-FEDER-029394 funded by COMPETE2020, NORTE 2020, PORTUGAL 2020. Violeta Carvalho, Diogo Lopes and João Silva would like to express their gratitude for the support given by FCT through the PhD Grants SFRH/UI/BD/151028/2021, SFRH/BD/144431/2019, and SFRH/BD/130588/2017, respectively.
The authors declare no conflict of interest.
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In general, the pyrolysis types are classified base on heating rate mainly either fast or slow pyrolysis. The characteristic and properties of wood vinegar are primarily influenced by the type of carbonaceous feedstocks as well as the production techniques. Wood vinegar is a complex mixture of polar and non-polar chemicals with various molecular weights and compositions. Its major constituent is water (80–90%). Some physical properties; such as pH, specific gravity, dissolved tar content are, respectively, within the range of 2–4, 1.005–1.016 g/mL, 0.23–0.89% wt, and color, odor and transparency have been reported. In addition, the degree of oBrix was ranged between 1.7 and 6.6. Besides water, the chemical compositions of wood vinegars consisted of acetic acid with the largest component (30.45–70.60 mg.mL−1). A high number of phenol derivatives have been found and those in higher concentrations were 4-propyl-2-methoxyphenol (5–11 mg.mL−1) followed by 2-methylphenol (2–4 mg.mL−1). Wood vinegar has been regarded as a natural product, which claimed to be capable in several fields of application. In agriculture, wood vinegar has been used in vegetable cropping in order to combat disease, pest control, improve growth and fruit quality, seed germination accelerator as well as herbicide. In pharmaceutical and medical applications, it is used for the preparation of detoxification pad while in veterinary and animal production, incorporation of the wood vinegar in feed could promote acidity in large intestine to inhibit growth of enteropathogenic microbes. In food processing, wood vinegar has a characteristic smoke flavor, and also exhibits microbial growth inhibition. In addition, several investigators reported that bio-oil and wood vinegar obtained from fast pyrolysis and carbonization showed a high potential on organic wood preservative. In summary, the wood vinegar prepared from the tropical wood and/or biomass waste is widely beneficial. The chapter attempts to provide essential knowledge relevant to physicochemical characteristics of wood vinegar and its applications.",book:{id:"6370",slug:"tropical-forests-new-edition",title:"Tropical Forests",fullTitle:"Tropical Forests - New Edition"},signatures:"Yongyuth Theapparat, Ausa Chandumpai and Damrongsak\nFaroongsarng",authors:[{id:"219997",title:"Dr.",name:"Yongyuth",middleName:null,surname:"Theapparat",slug:"yongyuth-theapparat",fullName:"Yongyuth Theapparat"},{id:"226821",title:"Dr.",name:"Ausa",middleName:null,surname:"Chandumpai",slug:"ausa-chandumpai",fullName:"Ausa Chandumpai"},{id:"398427",title:"Dr.",name:"Damrongsak",middleName:null,surname:"Faroongsarng",slug:"damrongsak-faroongsarng",fullName:"Damrongsak Faroongsarng"}]},{id:"66710",doi:"10.5772/intechopen.85804",title:"Deforestation in India: Consequences and Sustainable Solutions",slug:"deforestation-in-india-consequences-and-sustainable-solutions",totalDownloads:2062,totalCrossrefCites:13,totalDimensionsCites:17,abstract:"Deforestation is one of the most pressing environmental issues that the world is facing currently. It is the conversion of forested land to non-forested land by humans. Deforestation occurs when a land dominated by naturally occurring trees is converted to provide certain services in response to the human demand. The indiscriminate felling of trees has resulted in a reduction of 3.16% in the global forest cover from 1990 to 2015. Although India has seen an increment in the total forest cover of ca. 1%, still there are certain regions in the country that have sought a decrease in the forest cover. The main reasons attributed to the reduction in forest cover are shifting cultivation, rotational felling, other biotic pressures, diversion of forest lands for developmental activities, etc. Continuous illicit cutting of trees has impacted the microclimatic conditions, hydrological cycle, soil quality, biodiversity, etc. of the country, thereby making the country more vulnerable for any uneventful happening. Sustainable forest management practices, alternatives for shifting cultivation, promotion of plantation outside the forest and the usage of certified forest products, etc. are some of the measures that can be adopted to curb the rate of deforestation.",book:{id:"7629",slug:"forest-degradation-around-the-world",title:"Forest Degradation Around the World",fullTitle:"Forest Degradation Around the World"},signatures:"Rima Kumari, Ayan Banerjee, Rahul Kumar, Amit Kumar, Purabi Saikia and Mohammed Latif Khan",authors:[{id:"276688",title:"Prof.",name:"Mohammed Latif",middleName:null,surname:"Khan",slug:"mohammed-latif-khan",fullName:"Mohammed Latif Khan"},{id:"279797",title:"Dr.",name:"Purabi",middleName:null,surname:"Saikia",slug:"purabi-saikia",fullName:"Purabi Saikia"},{id:"279806",title:"MSc.",name:"Rima",middleName:null,surname:"Kumari",slug:"rima-kumari",fullName:"Rima Kumari"},{id:"279807",title:"BSc.",name:"Ayan",middleName:null,surname:"Banerjee",slug:"ayan-banerjee",fullName:"Ayan Banerjee"},{id:"285660",title:"Dr.",name:"Amit",middleName:null,surname:"Kumar",slug:"amit-kumar",fullName:"Amit Kumar"},{id:"285661",title:"Dr.",name:"Rahul",middleName:null,surname:"Kumar",slug:"rahul-kumar",fullName:"Rahul Kumar"}]},{id:"45219",doi:"10.5772/56279",title:"Potential Future Ranges of Tree Species in the Alps",slug:"potential-future-ranges-of-tree-species-in-the-alps",totalDownloads:4915,totalCrossrefCites:3,totalDimensionsCites:15,abstract:null,book:{id:"3403",slug:"management-strategies-to-adapt-alpine-space-forests-to-climate-change-risks",title:"Management Strategies to Adapt Alpine Space Forests to Climate Change Risks",fullTitle:"Management Strategies to Adapt Alpine Space Forests to Climate Change Risks"},signatures:"Niklaus E. Zimmermann, Robert Jandl, Marc Hanewinkel, Georges\nKunstler, Christian Kölling, Patrizia Gasparini, Andrej Breznikar,\nEliane S. Meier, Signe Normand, Ulrich Ulmer, Thomas\nGschwandtner, Holger Veit, Maria Naumann, Wolfgang Falk, Karl\nMellert, Maria Rizzo, Mitja Skudnik and Achilleas Psomas",authors:[{id:"165202",title:"Prof.",name:"Niklaus",middleName:"E.",surname:"Zimmermann",slug:"niklaus-zimmermann",fullName:"Niklaus Zimmermann"}]}],mostDownloadedChaptersLast30Days:[{id:"31959",title:"Structure, Diversity, Threats and Conservation of Tropical Forests",slug:"structure-diversity-threats-and-conservation-of-tropical-forests",totalDownloads:8044,totalCrossrefCites:2,totalDimensionsCites:5,abstract:null,book:{id:"902",slug:"tropical-forests",title:"Tropical Forests",fullTitle:"Tropical Forests"},signatures:"Madhugiri Nageswara-Rao, Jaya R. Soneji and Padmini Sudarshana",authors:[{id:"79318",title:"Dr.",name:"Padmini",middleName:null,surname:"Sudarshana",slug:"padmini-sudarshana",fullName:"Padmini Sudarshana"},{id:"120847",title:"Dr.",name:"Madhugiri",middleName:null,surname:"Nageswara-Rao",slug:"madhugiri-nageswara-rao",fullName:"Madhugiri Nageswara-Rao"},{id:"120848",title:"Dr.",name:"Jaya",middleName:null,surname:"Soneji",slug:"jaya-soneji",fullName:"Jaya Soneji"}]},{id:"66710",title:"Deforestation in India: Consequences and Sustainable Solutions",slug:"deforestation-in-india-consequences-and-sustainable-solutions",totalDownloads:2063,totalCrossrefCites:13,totalDimensionsCites:17,abstract:"Deforestation is one of the most pressing environmental issues that the world is facing currently. It is the conversion of forested land to non-forested land by humans. Deforestation occurs when a land dominated by naturally occurring trees is converted to provide certain services in response to the human demand. The indiscriminate felling of trees has resulted in a reduction of 3.16% in the global forest cover from 1990 to 2015. Although India has seen an increment in the total forest cover of ca. 1%, still there are certain regions in the country that have sought a decrease in the forest cover. The main reasons attributed to the reduction in forest cover are shifting cultivation, rotational felling, other biotic pressures, diversion of forest lands for developmental activities, etc. Continuous illicit cutting of trees has impacted the microclimatic conditions, hydrological cycle, soil quality, biodiversity, etc. of the country, thereby making the country more vulnerable for any uneventful happening. Sustainable forest management practices, alternatives for shifting cultivation, promotion of plantation outside the forest and the usage of certified forest products, etc. are some of the measures that can be adopted to curb the rate of deforestation.",book:{id:"7629",slug:"forest-degradation-around-the-world",title:"Forest Degradation Around the World",fullTitle:"Forest Degradation Around the World"},signatures:"Rima Kumari, Ayan Banerjee, Rahul Kumar, Amit Kumar, Purabi Saikia and Mohammed Latif Khan",authors:[{id:"276688",title:"Prof.",name:"Mohammed Latif",middleName:null,surname:"Khan",slug:"mohammed-latif-khan",fullName:"Mohammed Latif Khan"},{id:"279797",title:"Dr.",name:"Purabi",middleName:null,surname:"Saikia",slug:"purabi-saikia",fullName:"Purabi Saikia"},{id:"279806",title:"MSc.",name:"Rima",middleName:null,surname:"Kumari",slug:"rima-kumari",fullName:"Rima Kumari"},{id:"279807",title:"BSc.",name:"Ayan",middleName:null,surname:"Banerjee",slug:"ayan-banerjee",fullName:"Ayan Banerjee"},{id:"285660",title:"Dr.",name:"Amit",middleName:null,surname:"Kumar",slug:"amit-kumar",fullName:"Amit Kumar"},{id:"285661",title:"Dr.",name:"Rahul",middleName:null,surname:"Kumar",slug:"rahul-kumar",fullName:"Rahul Kumar"}]},{id:"68528",title:"Forest Biodiversity and Deforestation in Bangladesh: The Latest Update",slug:"forest-biodiversity-and-deforestation-in-bangladesh-the-latest-update",totalDownloads:1553,totalCrossrefCites:4,totalDimensionsCites:13,abstract:"Located in the Indo-Burma biodiversity hotspot, Bangladesh is a tropical country in Southeast Asia and a transitional point for flora and fauna between the Indo-Himalayan and Indo-Chinese subregions. About 11% land area (1,429,000 hectares) of the country is covered with four major forest types: mixed-evergreen forests, deciduous forests, mangrove forests, and freshwater swamp forests. Though Bangladesh is a small and densely populated country, it is the home of 1952 species of invertebrates, 653 fish, 50 amphibians, 147 reptiles, 566 birds, and 127 mammalian species of which many of them are globally threatened. We have discussed the latest status of all the major vertebrate groups in this chapter. Thirty-one species of vertebrates have gone extinct from Bangladesh over the last century. Many of the species are facing continuous threat of extinction due to deforestation and degradation of habitat caused by various anthropogenic activities. In this chapter, we are going to discuss about the current management and conservation practices and issues related to the forests and wildlife of Bangladesh.",book:{id:"7629",slug:"forest-degradation-around-the-world",title:"Forest Degradation Around the World",fullTitle:"Forest Degradation Around the World"},signatures:"Ahm Ali Reza and Md. Kamrul Hasan",authors:[{id:"281012",title:"Dr.",name:"Md. Kamrul",middleName:null,surname:"Hasan",slug:"md.-kamrul-hasan",fullName:"Md. Kamrul Hasan"},{id:"302258",title:"Dr.",name:"AHM Ali",middleName:null,surname:"Reza",slug:"ahm-ali-reza",fullName:"AHM Ali Reza"}]},{id:"61747",title:"Physicochemistry and Utilization of Wood Vinegar from Carbonization of Tropical Biomass Waste",slug:"physicochemistry-and-utilization-of-wood-vinegar-from-carbonization-of-tropical-biomass-waste",totalDownloads:2183,totalCrossrefCites:9,totalDimensionsCites:19,abstract:"Pyroligneous acid also called wood vinegar is an aqueous liquid produced from pyrolysis of lignocellulose waste and biomass. In general, the pyrolysis types are classified base on heating rate mainly either fast or slow pyrolysis. The characteristic and properties of wood vinegar are primarily influenced by the type of carbonaceous feedstocks as well as the production techniques. Wood vinegar is a complex mixture of polar and non-polar chemicals with various molecular weights and compositions. Its major constituent is water (80–90%). Some physical properties; such as pH, specific gravity, dissolved tar content are, respectively, within the range of 2–4, 1.005–1.016 g/mL, 0.23–0.89% wt, and color, odor and transparency have been reported. In addition, the degree of oBrix was ranged between 1.7 and 6.6. Besides water, the chemical compositions of wood vinegars consisted of acetic acid with the largest component (30.45–70.60 mg.mL−1). A high number of phenol derivatives have been found and those in higher concentrations were 4-propyl-2-methoxyphenol (5–11 mg.mL−1) followed by 2-methylphenol (2–4 mg.mL−1). Wood vinegar has been regarded as a natural product, which claimed to be capable in several fields of application. In agriculture, wood vinegar has been used in vegetable cropping in order to combat disease, pest control, improve growth and fruit quality, seed germination accelerator as well as herbicide. In pharmaceutical and medical applications, it is used for the preparation of detoxification pad while in veterinary and animal production, incorporation of the wood vinegar in feed could promote acidity in large intestine to inhibit growth of enteropathogenic microbes. In food processing, wood vinegar has a characteristic smoke flavor, and also exhibits microbial growth inhibition. In addition, several investigators reported that bio-oil and wood vinegar obtained from fast pyrolysis and carbonization showed a high potential on organic wood preservative. In summary, the wood vinegar prepared from the tropical wood and/or biomass waste is widely beneficial. The chapter attempts to provide essential knowledge relevant to physicochemical characteristics of wood vinegar and its applications.",book:{id:"6370",slug:"tropical-forests-new-edition",title:"Tropical Forests",fullTitle:"Tropical Forests - New Edition"},signatures:"Yongyuth Theapparat, Ausa Chandumpai and Damrongsak\nFaroongsarng",authors:[{id:"219997",title:"Dr.",name:"Yongyuth",middleName:null,surname:"Theapparat",slug:"yongyuth-theapparat",fullName:"Yongyuth Theapparat"},{id:"226821",title:"Dr.",name:"Ausa",middleName:null,surname:"Chandumpai",slug:"ausa-chandumpai",fullName:"Ausa Chandumpai"},{id:"398427",title:"Dr.",name:"Damrongsak",middleName:null,surname:"Faroongsarng",slug:"damrongsak-faroongsarng",fullName:"Damrongsak Faroongsarng"}]},{id:"54603",title:"Methodological Considerations in the Study of Earthworms in Forest Ecosystems",slug:"methodological-considerations-in-the-study-of-earthworms-in-forest-ecosystems",totalDownloads:1808,totalCrossrefCites:0,totalDimensionsCites:5,abstract:"Decades of studies have shown that soil macrofauna, especially earthworms, play dominant engineering roles in soils, affecting physical, chemical, and biological components of ecosystems. Quantifying these effects would allow crucial improvement in biogeochemical budgets and modeling, predicting response of land use and disturbance, and could be applied to bioremediation efforts. Effective methods of manipulating earthworm communities in the field are needed to accompany laboratory microcosm studies to calculate their net function in natural systems and to isolate specific mechanisms. This chapter reviews laboratory and field methods for enumerating and manipulating earthworm populations, as well as approaches toward quantifying their influences on soil processes and biogeochemical cycling.",book:{id:"5539",slug:"forest-ecology-and-conservation",title:"Forest Ecology and Conservation",fullTitle:"Forest Ecology and Conservation"},signatures:"Dylan Rhea-Fournier and Grizelle González",authors:[{id:"82355",title:"Dr.",name:"Grizelle",middleName:null,surname:"Gonzalez",slug:"grizelle-gonzalez",fullName:"Grizelle Gonzalez"},{id:"194800",title:"M.Sc.",name:"Dylan",middleName:null,surname:"Rhea-Fournier",slug:"dylan-rhea-fournier",fullName:"Dylan Rhea-Fournier"}]}],onlineFirstChaptersFilter:{topicId:"138",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:32,numberOfPublishedChapters:318,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:15,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{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"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. 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Vikhe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/323731/images/13613_n.jpg",biography:"Dr Deepak M.Vikhe .\n\n\t\n\tDr Deepak M.Vikhe , completed his Masters & PhD in Prosthodontics from Rural Dental College, Loni securing third rank in the Pravara Institute of Medical Sciences Deemed University. He was awarded Dr.G.C.DAS Memorial Award for Research on Implants at 39th IPS conference Dubai (U A E).He has two patents under his name. He has received Dr.Saraswati medal award for best research for implant study in 2017.He has received Fully funded scholarship to Spain ,university of Santiago de Compostela. He has completed fellowship in Implantlogy from Noble Biocare. \nHe has attended various conferences and CDE programmes and has national publications to his credit. His field of interest is in Implant supported prosthesis. Presently he is working as a associate professor in the Dept of Prosthodontics, Rural Dental College, Loni and maintains a successful private practice specialising in Implantology at Rahata.\n\nEmail: drdeepak_mvikhe@yahoo.com..................",institutionString:null,institution:{name:"Pravara Institute of Medical Sciences",country:{name:"India"}}},{id:"204110",title:"Dr.",name:"Ahmed A.",middleName:null,surname:"Madfa",slug:"ahmed-a.-madfa",fullName:"Ahmed A. Madfa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204110/images/system/204110.jpg",biography:"Dr. Madfa is currently Associate Professor of Endodontics at Thamar University and a visiting lecturer at Sana'a University and University of Sciences and Technology. He has more than 6 years of experience in teaching. His research interests include root canal morphology, functionally graded concept, dental biomaterials, epidemiology and dental education, biomimetic restoration, finite element analysis and endodontic regeneration. Dr. Madfa has numerous international publications, full articles, two patents, a book and a book chapter. Furthermore, he won 14 international scientific awards. Furthermore, he is involved in many academic activities ranging from editorial board member, reviewer for many international journals and postgraduate students' supervisor. Besides, I deliver many courses and training workshops at various scientific events. Dr. Madfa also regularly attends international conferences and holds administrative positions (Deputy Dean of the Faculty for Students’ & Academic Affairs and Deputy Head of Research Unit).",institutionString:"Thamar University",institution:null},{id:"210472",title:"Dr.",name:"Nermin",middleName:"Mohammed Ahmed",surname:"Yussif",slug:"nermin-yussif",fullName:"Nermin Yussif",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/210472/images/system/210472.jpg",biography:"Dr. Nermin Mohammed Ahmed Yussif is working at the Faculty of dentistry, University for October university for modern sciences and arts (MSA). Her areas of expertise include: periodontology, dental laserology, oral implantology, periodontal plastic surgeries, oral mesotherapy, nutrition, dental pharmacology. She is an editor and reviewer in numerous international journals.",institutionString:"MSA University",institution:null},{id:"204606",title:"Dr.",name:"Serdar",middleName:null,surname:"Gözler",slug:"serdar-gozler",fullName:"Serdar Gözler",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204606/images/system/204606.jpeg",biography:"Dr. Serdar Gözler has completed his undergraduate studies at the Marmara University Faculty of Dentistry in 1978, followed by an assistantship in the Prosthesis Department of Dicle University Faculty of Dentistry. Starting his PhD work on non-resilient overdentures with Assoc. Prof. Hüsnü Yavuzyılmaz, he continued his studies with Prof. Dr. Gürbüz Öztürk of Istanbul University Faculty of Dentistry Department of Prosthodontics, this time on Gnatology. He attended training programs on occlusion, neurology, neurophysiology, EMG, radiology and biostatistics. In 1982, he presented his PhD thesis \\Gerber and Lauritzen Occlusion Analysis Techniques: Diagnosis Values,\\ at Istanbul University School of Dentistry, Department of Prosthodontics. As he was also working with Prof. Senih Çalıkkocaoğlu on The Physiology of Chewing at the same time, Gözler has written a chapter in Çalıkkocaoğlu\\'s book \\Complete Prostheses\\ entitled \\The Place of Neuromuscular Mechanism in Prosthetic Dentistry.\\ The book was published five times since by the Istanbul University Publications. Having presented in various conferences about occlusion analysis until 1998, Dr. Gözler has also decided to use the T-Scan II occlusion analysis method. Having been personally trained by Dr. Robert Kerstein on this method, Dr. Gözler has been lecturing on the T-Scan Occlusion Analysis Method in conferences both in Turkey and abroad. Dr. Gözler has various articles and presentations on Digital Occlusion Analysis methods. He is now Head of the TMD Clinic at Prosthodontic Department of Faculty of Dentistry , Istanbul Aydın University , Turkey.",institutionString:"Istanbul Aydin University",institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"240870",title:"Ph.D.",name:"Alaa Eddin Omar",middleName:null,surname:"Al Ostwani",slug:"alaa-eddin-omar-al-ostwani",fullName:"Alaa Eddin Omar Al Ostwani",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/240870/images/system/240870.jpeg",biography:"Dr. Al Ostwani Alaa Eddin Omar received his Master in dentistry from Damascus University in 2010, and his Ph.D. in Pediatric Dentistry from Damascus University in 2014. Dr. Al Ostwani is an assistant professor and faculty member at IUST University since 2014. \nDuring his academic experience, he has received several awards including the scientific research award from the Union of Arab Universities, the Syrian gold medal and the international gold medal for invention and creativity. Dr. Al Ostwani is a Member of the International Association of Dental Traumatology and the Syrian Society for Research and Preventive Dentistry since 2017. He is also a Member of the Reviewer Board of International Journal of Dental Medicine (IJDM), and the Indian Journal of Conservative and Endodontics since 2016.",institutionString:"International University for Science and Technology.",institution:{name:"Islamic University of Science and Technology",country:{name:"India"}}},{id:"42847",title:"Dr.",name:"Belma",middleName:null,surname:"Işik Aslan",slug:"belma-isik-aslan",fullName:"Belma Işik Aslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/42847/images/system/42847.jpg",biography:"Dr. Belma IşIk Aslan was born in 1976 in Ankara-TURKEY. After graduating from TED Ankara College in 1994, she attended to Gazi University, Faculty of Dentistry in Ankara. She completed her PhD in orthodontic education at Gazi University between 1999-2005. Dr. Işık Aslan stayed at the Providence Hospital Craniofacial Institude and Reconstructive Surgery in Michigan, USA for three months as an observer. She worked as a specialist doctor at Gazi University, Dentistry Faculty, Department of Orthodontics between 2005-2014. She was appointed as associate professor in January, 2014 and as professor in 2021. Dr. Işık Aslan still works as an instructor at the same faculty. She has published a total of 35 articles, 10 book chapters, 39 conference proceedings both internationally and nationally. Also she was the academic editor of the international book 'Current Advances in Orthodontics'. She is a member of the Turkish Orthodontic Society and Turkish Cleft Lip and Palate Society. She is married and has 2 children. Her knowledge of English is at an advanced level.",institutionString:"Gazi University Dentistry Faculty Department of Orthodontics",institution:null},{id:"178412",title:"Associate Prof.",name:"Guhan",middleName:null,surname:"Dergin",slug:"guhan-dergin",fullName:"Guhan Dergin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178412/images/6954_n.jpg",biography:"Assoc. Prof. Dr. Gühan Dergin was born in 1973 in Izmit. He graduated from Marmara University Faculty of Dentistry in 1999. He completed his specialty of OMFS surgery in Marmara University Faculty of Dentistry and obtained his PhD degree in 2006. In 2005, he was invited as a visiting doctor in the Oral and Maxillofacial Surgery Department of the University of North Carolina, USA, where he went on a scholarship. Dr. Dergin still continues his academic career as an associate professor in Marmara University Faculty of Dentistry. He has many articles in international and national scientific journals and chapters in books.",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"178414",title:"Prof.",name:"Yusuf",middleName:null,surname:"Emes",slug:"yusuf-emes",fullName:"Yusuf Emes",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178414/images/6953_n.jpg",biography:"Born in Istanbul in 1974, Dr. Emes graduated from Istanbul University Faculty of Dentistry in 1997 and completed his PhD degree in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery in 2005. He has papers published in international and national scientific journals, including research articles on implantology, oroantral fistulas, odontogenic cysts, and temporomandibular disorders. Dr. Emes is currently working as a full-time academic staff in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery.",institutionString:null,institution:{name:"Istanbul University",country:{name:"Turkey"}}},{id:"192229",title:"Ph.D.",name:"Ana Luiza",middleName:null,surname:"De Carvalho Felippini",slug:"ana-luiza-de-carvalho-felippini",fullName:"Ana Luiza De Carvalho Felippini",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/192229/images/system/192229.jpg",biography:null,institutionString:"University of São Paulo",institution:{name:"University of Sao Paulo",country:{name:"Brazil"}}},{id:"256851",title:"Prof.",name:"Ayşe",middleName:null,surname:"Gülşen",slug:"ayse-gulsen",fullName:"Ayşe Gülşen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256851/images/9696_n.jpg",biography:"Dr. Ayşe Gülşen graduated in 1990 from Faculty of Dentistry, University of Ankara and did a postgraduate program at University of Gazi. \nShe worked as an observer and research assistant in Craniofacial Surgery Departments in New York, Providence Hospital in Michigan and Chang Gung Memorial Hospital in Taiwan. \nShe works as Craniofacial Orthodontist in Department of Aesthetic, Plastic and Reconstructive Surgery, Faculty of Medicine, University of Gazi, Ankara Turkey since 2004.",institutionString:"Univeristy of Gazi",institution:null},{id:"255366",title:"Prof.",name:"Tosun",middleName:null,surname:"Tosun",slug:"tosun-tosun",fullName:"Tosun Tosun",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/255366/images/7347_n.jpg",biography:"Graduated at the Faculty of Dentistry, University of Istanbul, Turkey in 1989;\nVisitor Assistant at the University of Padua, Italy and Branemark Osseointegration Center of Treviso, Italy between 1993-94;\nPhD thesis on oral implantology in University of Istanbul and was awarded the academic title “Dr.med.dent.”, 1997;\nHe was awarded the academic title “Doç.Dr.” (Associated Professor) in 2003;\nProficiency in Botulinum Toxin Applications, Reading-UK in 2009;\nMastership, RWTH Certificate in Laser Therapy in Dentistry, AALZ-Aachen University, Germany 2009-11;\nMaster of Science (MSc) in Laser Dentistry, University of Genoa, Italy 2013-14.\n\nDr.Tosun worked as Research Assistant in the Department of Oral Implantology, Faculty of Dentistry, University of Istanbul between 1990-2002. \nHe worked part-time as Consultant surgeon in Harvard Medical International Hospitals and John Hopkins Medicine, Istanbul between years 2007-09.\u2028He was contract Professor in the Department of Surgical and Diagnostic Sciences (DI.S.C.), Medical School, University of Genova, Italy between years 2011-16. \nSince 2015 he is visiting Professor at Medical School, University of Plovdiv, Bulgaria. \nCurrently he is Associated Prof.Dr. at the Dental School, Oral Surgery Dept., Istanbul Aydin University and since 2003 he works in his own private clinic in Istanbul, Turkey.\u2028\nDr.Tosun is reviewer in journal ‘Laser in Medical Sciences’, reviewer in journal ‘Folia Medica\\', a Fellow of the International Team for Implantology, Clinical Lecturer of DGZI German Association of Oral Implantology, Expert Lecturer of Laser&Health Academy, Country Representative of World Federation for Laser Dentistry, member of European Federation of Periodontology, member of Academy of Laser Dentistry. Dr.Tosun presents papers in international and national congresses and has scientific publications in international and national journals. He speaks english, spanish, italian and french.",institutionString:null,institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"171887",title:"Prof.",name:"Zühre",middleName:null,surname:"Akarslan",slug:"zuhre-akarslan",fullName:"Zühre Akarslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/171887/images/system/171887.jpg",biography:"Zühre Akarslan was born in 1977 in Cyprus. She graduated from Gazi University Faculty of Dentistry, Ankara, Turkey in 2000. \r\nLater she received her Ph.D. degree from the Oral Diagnosis and Radiology Department; which was recently renamed as Oral and Dentomaxillofacial Radiology, from the same university. \r\nShe is working as a full-time Associate Professor and is a lecturer and an academic researcher. \r\nHer expertise areas are dental caries, cancer, dental fear and anxiety, gag reflex in dentistry, oral medicine, and dentomaxillofacial radiology.",institutionString:"Gazi University",institution:{name:"Gazi University",country:{name:"Turkey"}}},{id:"256417",title:"Associate Prof.",name:"Sanaz",middleName:null,surname:"Sadry",slug:"sanaz-sadry",fullName:"Sanaz Sadry",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256417/images/8106_n.jpg",biography:null,institutionString:null,institution:null},{id:"272237",title:"Dr.",name:"Pinar",middleName:"Kiymet",surname:"Karataban",slug:"pinar-karataban",fullName:"Pinar Karataban",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/272237/images/8911_n.png",biography:"Assist.Prof.Dr.Pınar Kıymet Karataban, DDS PhD \n\nDr.Pınar Kıymet Karataban was born in Istanbul in 1975. After her graduation from Marmara University Faculty of Dentistry in 1998 she started her PhD in Paediatric Dentistry focused on children with special needs; mainly children with Cerebral Palsy. She finished her pHD thesis entitled \\'Investigation of occlusion via cast analysis and evaluation of dental caries prevalance, periodontal status and muscle dysfunctions in children with cerebral palsy” in 2008. She got her Assist. Proffessor degree in Istanbul Aydın University Paediatric Dentistry Department in 2015-2018. ın 2019 she started her new career in Bahcesehir University, Istanbul as Head of Department of Pediatric Dentistry. In 2020 she was accepted to BAU International University, Batumi as Professor of Pediatric Dentistry. She’s a lecturer in the same university meanwhile working part-time in private practice in Ege Dental Studio (https://www.egedisklinigi.com/) a multidisciplinary dental clinic in Istanbul. Her main interests are paleodontology, ancient and contemporary dentistry, oral microbiology, cerebral palsy and special care dentistry. She has national and international publications, scientific reports and is a member of IAPO (International Association for Paleodontology), IADH (International Association of Disability and Oral Health) and EAPD (European Association of Pediatric Dentistry).",institutionString:null,institution:null},{id:"202198",title:"Dr.",name:"Buket",middleName:null,surname:"Aybar",slug:"buket-aybar",fullName:"Buket Aybar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/202198/images/6955_n.jpg",biography:"Buket Aybar, DDS, PhD, was born in 1971. She graduated from Istanbul University, Faculty of Dentistry, in 1992 and completed her PhD degree on Oral and Maxillofacial Surgery in Istanbul University in 1997.\nDr. Aybar is currently a full-time professor in Istanbul University, Faculty of Dentistry Department of Oral and Maxillofacial Surgery. She has teaching responsibilities in graduate and postgraduate programs. Her clinical practice includes mainly dentoalveolar surgery.\nHer topics of interest are biomaterials science and cell culture studies. She has many articles in international and national scientific journals and chapters in books; she also has participated in several scientific projects supported by Istanbul University Research fund.",institutionString:null,institution:null},{id:"260116",title:"Dr.",name:"Mehmet",middleName:null,surname:"Yaltirik",slug:"mehmet-yaltirik",fullName:"Mehmet Yaltirik",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/260116/images/7413_n.jpg",biography:"Birth Date 25.09.1965\r\nBirth Place Adana- Turkey\r\nSex Male\r\nMarrial Status Bachelor\r\nDriving License Acquired\r\nMother Tongue Turkish\r\n\r\nAddress:\r\nWork:University of Istanbul,Faculty of Dentistry, Department of Oral Surgery and Oral Medicine 34093 Capa,Istanbul- TURKIYE",institutionString:null,institution:null},{id:"172009",title:"Dr.",name:"Fatma Deniz",middleName:null,surname:"Uzuner",slug:"fatma-deniz-uzuner",fullName:"Fatma Deniz Uzuner",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/172009/images/7122_n.jpg",biography:"Dr. Deniz Uzuner was born in 1969 in Kocaeli-TURKEY. After graduating from TED Ankara College in 1986, she attended the Hacettepe University, Faculty of Dentistry in Ankara. \nIn 1993 she attended the Gazi University, Faculty of Dentistry, Department of Orthodontics for her PhD education. After finishing the PhD education, she worked as orthodontist in Ankara Dental Hospital under the Turkish Government, Ministry of Health and in a special Orthodontic Clinic till 2011. Between 2011 and 2016, Dr. Deniz Uzuner worked as a specialist in the Department of Orthodontics, Faculty of Dentistry, Gazi University in Ankara/Turkey. In 2016, she was appointed associate professor. Dr. Deniz Uzuner has authored 23 Journal Papers, 3 Book Chapters and has had 39 oral/poster presentations. She is a member of the Turkish Orthodontic Society. Her knowledge of English is at an advanced level.",institutionString:null,institution:null},{id:"332914",title:"Dr.",name:"Muhammad Saad",middleName:null,surname:"Shaikh",slug:"muhammad-saad-shaikh",fullName:"Muhammad Saad Shaikh",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Jinnah Sindh Medical University",country:{name:"Pakistan"}}},{id:"315775",title:"Dr.",name:"Feng",middleName:null,surname:"Luo",slug:"feng-luo",fullName:"Feng Luo",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Sichuan University",country:{name:"China"}}},{id:"423519",title:"Dr.",name:"Sizakele",middleName:null,surname:"Ngwenya",slug:"sizakele-ngwenya",fullName:"Sizakele Ngwenya",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of the Witwatersrand",country:{name:"South Africa"}}},{id:"419270",title:"Dr.",name:"Ann",middleName:null,surname:"Chianchitlert",slug:"ann-chianchitlert",fullName:"Ann Chianchitlert",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"419271",title:"Dr.",name:"Diane",middleName:null,surname:"Selvido",slug:"diane-selvido",fullName:"Diane Selvido",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"419272",title:"Dr.",name:"Irin",middleName:null,surname:"Sirisoontorn",slug:"irin-sirisoontorn",fullName:"Irin Sirisoontorn",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"355660",title:"Dr.",name:"Anitha",middleName:null,surname:"Mani",slug:"anitha-mani",fullName:"Anitha Mani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"355612",title:"Dr.",name:"Janani",middleName:null,surname:"Karthikeyan",slug:"janani-karthikeyan",fullName:"Janani Karthikeyan",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"334400",title:"Dr.",name:"Suvetha",middleName:null,surname:"Siva",slug:"suvetha-siva",fullName:"Suvetha Siva",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}}]}},subseries:{item:{id:"1",type:"subseries",title:"Oral Health",keywords:"Oral health, Dental care, Diagnosis, Diagnostic imaging, Early diagnosis, Oral cancer, Conservative treatment, Epidemiology, Comprehensive dental care, Complementary therapies, Holistic health",scope:"\r\n This topic aims to provide a comprehensive overview of the latest trends in Oral Health based on recent scientific evidence. Subjects will include an overview of oral diseases and infections, systemic diseases affecting the oral cavity, prevention, diagnosis, treatment, epidemiology, as well as current clinical recommendations for the management of oral, dental, and periodontal diseases.
",coverUrl:"https://cdn.intechopen.com/series_topics/covers/1.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11397,editor:{id:"173955",title:"Prof.",name:"Sandra",middleName:null,surname:"Marinho",slug:"sandra-marinho",fullName:"Sandra Marinho",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRGYMQA4/Profile_Picture_2022-06-01T13:22:41.png",biography:"Dr. Sandra A. Marinho is an Associate Professor and Brazilian researcher at the State University of Paraíba (Universidade Estadual da Paraíba- UEPB), Campus VIII, located in Araruna, state of Paraíba since 2011. She holds a degree in Dentistry from the Federal University of Alfenas (UNIFAL), while her specialization and professional improvement in Stomatology took place at Hospital Heliopolis (São Paulo, SP). Her qualifications are: a specialist in Dental Imaging and Radiology, Master in Dentistry (Periodontics) from the University of São Paulo (FORP-USP, Ribeirão Preto, SP), and Doctor (Ph.D.) in Dentistry (Stomatology Clinic) from Hospital São Lucas of the Pontifical Catholic University of Rio Grande do Sul (HSL-PUCRS, Porto Alegre, RS). She held a postdoctoral internship at the Federal University from Jequitinhonha and Mucuri Valleys (UFVJM, Diamantina, MG). She is currently a member of the Brazilian Society for Dental Research (SBPqO) and the Brazilian Society of Stomatology and Pathology (SOBEP). Dr. Marinho's experience in Dentistry mainly covers the following subjects: oral diagnosis, oral radiology; oral medicine; lesions and oral infections; oral pathology, laser therapy and epidemiological studies.",institutionString:null,institution:{name:"State University of Paraíba",institutionURL:null,country:{name:"Brazil"}}},editorTwo:null,editorThree:null,series:{id:"3",title:"Dentistry",doi:"10.5772/intechopen.71199",issn:"2631-6218"},editorialBoard:[{id:"267724",title:"Dr.",name:"Febronia",middleName:null,surname:"Kahabuka",slug:"febronia-kahabuka",fullName:"Febronia Kahabuka",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRZpJQAW/Profile_Picture_2022-06-27T12:00:42.JPG",institutionString:null,institution:null}]},onlineFirstChapters:{paginationCount:7,paginationItems:[{id:"82405",title:"Does Board Structure Matter in CSR Spending of Commercial Banks? 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