\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
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The contents of the book will be written by multiple authors and edited by experts in the field.",isbn:null,printIsbn:null,pdfIsbn:null,doi:null,price:0,priceEur:null,priceUsd:null,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"2b02515d1c61e12ec5e988463063bc89",bookSignature:"",publishedDate:null,coverURL:"//cdnintech.com/web/frontend/www/assets/cover.jpg",keywords:null,numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"January 11th 2018",dateEndSecondStepPublish:"February 1st 2018",dateEndThirdStepPublish:"April 2nd 2018",dateEndFourthStepPublish:"June 21st 2018",dateEndFifthStepPublish:"August 20th 2018",remainingDaysToSecondStep:"3 years",secondStepPassed:!0,currentStepOfPublishingProcess:1,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"12",title:"Environmental Sciences",slug:"environmental-sciences"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:null},relatedBooks:[{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3621",title:"Silver Nanoparticles",subtitle:null,isOpenForSubmission:!1,hash:null,slug:"silver-nanoparticles",bookSignature:"David Pozo Perez",coverURL:"https://cdn.intechopen.com/books/images_new/3621.jpg",editedByType:"Edited by",editors:[{id:"6667",title:"Dr.",name:"David",surname:"Pozo",slug:"david-pozo",fullName:"David Pozo"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"19064",title:"Vascular Complications in Kidney Transplantation",doi:"10.5772/18672",slug:"vascular-complications-in-kidney-transplantation",body:'\n\t\tKidney transplantation evolved as the treatment of choice for end-stage renal disease. Accumulated expertise and experience along with refined surgical techniques resulted in excellent patient and graft survival. Despite the improvements in surgical techniques vascular complications consists a significant and sometimes life-threatening problem that occurs in 10-20% of patients. Vascular complication can be divided in general in three main categories. Graft renal artery thrombosis and stenosis, graft renal vein thrombosis and stenosis and arterial injury.
\n\t\tTransplant renal artery stenosis (TRAS) is a very common vascular complication following kidney transplantations. It is reported in a wide range of frequency occurring in 3-12% of patients (in some reports even up to 20% depending on the awareness and the available imaging means especially MDCT-angiography) (Akbar 2005, Sebastia, 2001)]. It is very difficult to have the definitive true incidence of TRAS by looking at the literature and this discrepancy is due to the different definitions, the surgeon’s experience and technical skills in avoiding or preventing the TRAS and different peri-operative management. If we try to classify all arterial stenosis in kidney transplantation, we could divide it into two main categories; TRAS and proximal or pseudo-TRAS. TRAS can be categorised by the level of stenoses and this includes anastomotic stenoses, stenoses of the proper transplant renal artery and finally segmental renal artery stenoses. Proximal-TRAS refers to pre-existing or developing atherosclerotic inflow stenoses in the native iliac arteries of the transplant recipient. The incidence of proximal-TRAS has been reported to be 0%-2.4% and may become more prevalent with increasing age. Predisposing factors for transplant renal artery stenosis, are cadaveric transplant, end-to-end anastomosis, surgical clamp injury, intimal dissection, and inadequate suturing technique, long or kinking artery, prolonged cold ischemia time, acute cellular rejection, and cytomegalovirus (CMV) infection (Audard, 2006).
\n\t\t\tPatients with TRAS in the immediate post-transplant period, present oliguria or anuria and are dialysis dependent. After the first week, patients with TRAS usually present with severe renovascular hypertension. Even though severe renovascular hypertension could be attributed to TRAS we should always keep in mind and all other causes like chronic rejection, steroid use, cyclosporine toxicity, recurrent glomerulonephritis and disease of native kidneys (Mangray, 2011, Tutone, 2005). If TRAS is not managed properly in due time, it could lead to renal dysfunction and graft deterioration.Non-invasive imaging is mandatory in the immediate post-transplant period to evaluate for possible transplant renal artery stenosis. Doppler ultrasound should be the initial diagnostic modality used because of its ability to reveal the location, length, and gross appearance of a stenosis. In addition, it is widely available, cost-effective, and does not use ionizing radiation and the nature of the transplanted renal arteries makes Doppler ultrasound an ideal screening modality (Baxter, 1995, Irshad, 2008, 2009). Whilst Doppler ultrasound is ideal in recognizing a possible lesion, categorisation and better characterisation of TRAS would be using magnetic resonance angiography with or without contrast medium (especially gadolinium-enhanced), MDCT-angiography, Radionuclide imaging that includes the administration of an angiotensin-converting enzyme inhibitor (captopril scan) shows findings similar to those of renovascular hypertension in native kidneys (Sebastia, 2001). Catheter-based angiography is the gold standard technique for diagnosing TRAS. The use of low- or iso-osmolar contrast material is recommended to reduce the risk of contrast material–induced nephropathy. When renal insufficiency is present, carbon dioxide may be substituted for an iodinated contrast agent during preliminary angiography to minimize the use of iodinated agents.
\n\t\t\tUnfortunately there is no consensus definition of TRAS and it would be difficult to have one in the future. Usually there is the classic presentation with refractory hypertension, deteriorating renal function, and congestive cardiac failure secondary to fluid retention. It is very impressive that marked reversal of symptoms occurs when stenosis is successfully treated (Garovic, 2005, Mangray, 2011). The timeline of TRAS usually begins at 2 months to 2 years after transplantation and hypertension is due to activation of the renin-angiotensin system (Basso, 2001, Mangray, 2011). Another important issue concerns asymptomatic normotensive patients with Doppler examination of at least 50% without evident graft dysfunction. The problem with those patients is the potential risk carrying from a procedure to treat a clinically insignificant TRAS in the short to medium term. It is unclear whether treating a non-clinically significant TRAS would have an impact in long term survival of renal grafts but since hypertension is an independent risk factor for long term renal graft survival, anything that could contribute to this direction would be beneficial. Close follow up of those patients, with significant expertise and experience of the transplant centre, along with availability of vascular interventional techniques is of paramount importance in decision making. Nevertheless, there are no reports of the long-term safety of this line of management, and the natural history of a 50% TRAS is unknown, and that conservative treatment is safe provided that there is no deterioration of kidney function (Audard, 2006, Buturovic-Ponikvar, 2003). This may not be the case for other causes, such as intimal hyperplasia, and the indication for angiography is strong when graft deterioration is revealed in the absence of other causes of graft dysfunction or chronic allograft nephropathy (CAN). Increased awareness with follow up observation should be in case of a stenosis of 80% on ultrasound examination, even in cases without suspicion of a hemodynamically significant TRAS. Due to increased susceptibility to occlusion in the presence of dehydration or cardiovascular instability, and in this case intervention should be considered.
\n\t\t\tSince Goldplatt et al published their study on the hypertensive role of partial reduced renal perfusion of the kidney back in 1934; there has been subsequent identification by various investigators of the role of the renin-angiotensin system, with renin being the hormone released in elevated blood levels from the ischemic kidney (Goldplatt, 1934). Angiotensin is being released enzymatically from angiotensinogen, and has various properties, including vasoconstriction, aldosterone secretion, renal sodium retention, and myocardium hypertrophy (Brewster, 2003). There is evidence that when there are two kidneys the above theory has been proven probably right, however it has been showed that this is not the case for the sole kidney or the transplanted kidney. Hypertension is also present but predominantly as a balance between volume regulation depending on salt and water retention and the renin-angiotensin dependent mechanism. It is the highly circulating volume and not the pressor effect from the renin-angiotensin system that is capable to keep a normal GFR rate with normal renin blood levels. In case that ACE inhibitors are prescribed there is a subsequent reduction in kidney perfusion and finally renal function deterioration. In patients with kidney transplantation, and in order to control hypertension, it is not uncommon to establish a diagnosis of TRAS, when an ACE inhibitor is introduced.
\n\t\t\tDoppler ultrasonography is considered as the best screening test TRAS assessment. There are many advantages in the use of Doppler ultrasound as initial approach over other imaging methods, especially iodine contrast media. The fact that Doppler ultrasound is a noninvasive method, does not expose the recipient to the risk of iodine contrast examination, is widely and promptly available in all hospital settings makes it an excellent first choice for TRAS evaluation. The most significant limitation of the method, as in other conditions, is the fact that ultrasonography is operator dependent.
\n\t\t\t\tDigital subtractive angiography (DSA), used to be the gold standard technique for establishing the diagnosis, but today tends to be replaced by MRI angiography and more recently Multi Detector CT-angiography. DSA is an invasive technique and potential complications are groin hematoma, renal artery dissection, thrombosis, perforation, and acute kidney injury caused by contrast-induced nephropathy. Doppler ultrasound can also be used to evaluate the hemodynamic changes due to TRAS. Doppler findings in TRAS include peak systolic velocity 2.0-2.5 m/s, low pulsatility index, and a parvus et tardus waveform with a systolic acceleration time of ≥ to 0.1 seconds (Snider, 1989, Irshad, 2009, Baxter, 1995). Snider et al compared Doppler ultrasonography with conventional angiography and showed 94% sensitivity and 87% specificity on US (Snider, 1989). A velocity ratio of the stenotic to pre-stenotic segments of greater than 2:1 is considered supportive of the diagnosis.
\n\t\t\t\tMultidetectors helical CT gives accurate assessment of the site and degree of TRAS and provides accurate and valuable imaging, requires less volume of iodinated contrast medium than DSA (Sebastia, 2001). The nature of the vascular contrast medium may be of consideration, rather than the volume. Risk of contrast nephropathy is probably not related to the volume of contrast medium or the degree of renal failure (Birck, 2003, Pannu, 2004). Protection of the allograft with sufficient volume and N-acetylcysteine is recommended when intravenous contrast medium is injected, regardless of renal function and contrast volume. The alternative is to perform MRI with gadolinium, a non-iodinated contrast medium even though there have been reports of nephrogenic systemic sclerosis.
\n\t\t\tTreatment options for TRAS include both surgical and endoluminal options. Primary treatment for TRAS involves Percutaneous transluminal angioplasty (PTA) with or without stent placement (Audard, 2006, Bruno, 2004). The type of arterial anastomosis that is present is the deciding factor in determining the angiographic approach utilized. The technical success rate of PTA has been reported to be as high as 94%, with a clinical success rate of 82% (Patel, 2001). Recurrent stenosis may occur in more than 10%, and allograft loss has been reported in up to 30% of cases (Fervenza, 1998). There have been reports correlating TRAS with acute cellular rejection and that long term survival is significantly higher in non-TRAS patients compared with the TRAS. Surgical revascularization is now considered rescue therapy and generally has been reserved for patients with disease unsuitable for PTA
\n\t\t\tSince the introduction and the evolution of the endovascular interventions there has been a shift in TRAS treatment option with Percutaneous Transluminal Angioplasty (PTA) with or without the use of stent (Beecroft, 2004) being now the gold standard and the initial option of treatment. The method is considered very efficient especially in experienced hands and technical success has been reported to be greater than 90%. However when we consider the clinical impact that has on hypertension or improvement of allograft function, this is significantly lower.
\n\t\t\t\tAs we have already pointed out, the results in clinically insignificant TRAS can be evaluated only on the degree of the radiological success. PTA with or without stenting, is carrying a significant risk for the allograft and unless a significant pressure decrease exists across the TRAS, PTA should not be undertaken. Unfortunately there is no consensus as to the appropriate value of stenosis measurement beyond which intervention is warranted, and it would be very difficult to obtain one in the future since radiological success does not always results in clinical improvement. A cut off point proposed by Schoenberg et al (Schoenberg, 2000), could be pressure decrease at least 10 mm Hg across the stenosis.
\n\t\t\t\tThe type of arterial anastomosis that is present is the deciding factor in determining the angiographic approach utilized. If there is an end-to-end anastomosis with the internal iliac artery, commonly done in living donor allografts, then a contralateral femoral approach is utilized to make access to the downward sloping artery as easy as possible. However, if there is an end-to-side anastomosis with the external iliac artery, then an ipsilateral femoral approach is preferred by some authors to access the cephalad sloping artery (Bruno, 2004).
\n\t\t\t\tResults after PTA depend largely on the radiologists or vascular surgeons experience and expertise, and should have smooth cooperation with the transplant surgeons. Most of the complications relate to puncture site, but there could be also more severe complication like hemorrhage, rupture of transplant renal artery, iliac artery and loss of the allograft, in those case there could be a need for “salvage” operation. Evolution in endovascular technology, with newer pre-mounted stents, has minimised complications especially the life threatening ones and the risk for allograft loss. Rate of re-stenosis are reported to be 10% to 50% and depends on the primary cause of the stenosis, length of follow-up, and use of stents (Voiculescu A 2005). Even though there are several reports on the topic, there are limitations provided by the retrospective nature of those manuscripts and the limited number of patients. In a french study of 29 patients with TRAS treated with PTA, the technical success rate was 93.1%, and there was 27.5% re-stenosis (Audard, 2006). In other study from the US, TRAS was found in 26 (3.1%) renal allografts, and 17 were treated with PTA with a success rate of 94%. Re-stenosis occurred in 12% of the patients [Patel NH 2001] In case of segmental branches, there is a lower success rate and the success rate is even lower for anastomotic strictures, and even though the incidence of stenosis is similar between end-to-side anastomosis to the external iliac artery and end-to-end anastomosis to the internal iliac artery, PTA in the latter situation is technically more difficult and results in a higher complication rate and more graft loss (Voiculescu, 2005).
\n\t\t\tSurgical correction of TRAS is regarded as a difficult operation with graft loss rates exceeding 20% (Bruno, 2004). A couple of risks existing; to the recipient and to the allograft, the latter is not a contraindication to surgery, since severe TRAS could deteriorate the transplanted kidney, the patient proceeds to renal failure, and finally to end up in heamodialysis. Surgery is now considered as rescue therapy for cases unsuitable for PTA.
\n\t\t\t\tIn general indications for surgery include: TRAS caused by kinking, anastomotic strictures and complex atherosclerotic disease. There are several options to treat TRAS; mostly excision of the stenosis with direct anastomosis to the external iliac artery and grafting with saphenous vein, recipient internal iliac artery, and preserved ABO blood group compatible deceased donor artery. Reported surgical success rates range from 63% to 92%, with recurrence in12% of patients (Roberts, 1989). A study comparing PTA vs. surgical repair of TRAS showed an immediate and long-term success rate of 92.1% and 81.5% and 69% and 40.5% for surgical repair and PTA respectively [Benoit G 1990]. Limitations of surgical procedure are access to the artery and most importantly the subsequent warm ischemia time. A warm ischemia of 60 minutes might be tolerated by a kidney allograft that has been heparinised even though the risk for Acute Tubular Necrosis (ATN) and cortical necrosis is increased due to diminished blood flow. An alternative option even though rarely used, is back table reconstruction of a complex arterial problem and autotransplantation of the allograft.
\n\t\t\tPositioning the allograft is sometimes tricky and the source of pitfalls in kidney transplantation and can result in allograft torsion. Allograft torsion can be an early or late complication. One of the main problems caused by improper positioning or torsion is the arterial kinking. Usually arterial kinks are formed due to long renal graft artery when there is a shift in the graft and/or pelvic contents that causes turn of the artery. Even though the differential diagnosis between TRAS and arterial kinking is often difficult to have, it is of paramount importance to identify an arterial narrowing due to a kink and not TRAS. Prompt diagnosis permits graft detorsion and possible salvage. The most suggestive imaging finding is a change in the axis of the transplanted kidney. CT and MR imaging can show changes in renal graft orientation and vascular pedicle kinking. Surgery remains the primary treatment for arterial kinks and only in cases where surgery is contraindicated or patients refuses surgery, we should proceed with endovascular treatment. TPA with or without stents, may increase the risk of arterial vasospasm and dissection and in addition, placing stents across kinks usually can be technically demanding.
\n\t\tThe thrombophilias, also referred to as hypercoagulable states, comprise hereditary or acquired conditions that predispose individuals to thrombosis. It was the third factor of Virchow’s triad that suggested that systemic alterations in the coagulability of blood, is a critical factor in thrombogenesis (Virchow, 1856). Thrombophilias are classified as congenital (inherited), acquired (secondary), or both (mixed) conditions (Schafer, 2007).
\n\t\t\tCongenital hypercoagulable states are caused by inherited thrombotic disorders due to mutations in genes encoding plasma proteins involved in coagulation mechanisms. They can be broadly classified into two categories: 1) quantitative deficiencies or qualitative defects of the physiologic anticoagulants: antithrombin, protein C and protein S deficiency, and 2) increased levels or function of the coagulation factors: factor V Leiden, prothrombin gene mutation, elevated levels of specific coagulation factors (Schafer, 2003). Congenital abnormalities of anticoagulant or procoagulant proteins result in an increased risk for venous thromboembolism (VTE) as well as arterial thrombosis with the risk to be higher in cases with decreased levels of antithrombotic proteins than in those with increased levels of prothrombotic proteins. The overall incidence of venous thromboembolism (per 100 patient-years) is found to be 1.07 for antithrombin deficiency, 0.54 for protein C deficiency, 0.50 for protein S deficiency, and 0.30 for activated protein C resistance or factor V Leiden (Bucciarelli, 1999). Half of the patients with inherited hypercoagulable state present with venous thromboembolism before the age of 45 years, particularly in the absence of well recognized risk factors, and often have a family history of thrombosis (Anderson, 2010). The secondary hypercoagulable states encompass a variety of heterogeneous disorders that have been associated with an increased risk of thrombotic complications (Schafer, 2003). Acquired hypercoagulable states include antiphospholipid antibody syndrome, cancer, heparin-induced thrombocytopenia, pregnancy and estrogen therapy, and a prior history of venous thromboembolism. Acquired coagulation defects are particularly common in patients with endstage renal disease (Wagenknecht, 1999). The prevalence of antiphospholipid antibodies in patients awaiting renal transplantation is more than 10%, but the rate of clinical events is far less than the frequency of thrombophilic states. Hyperhomocysteinemia is the typical hypercoagulable state that occurs due to a combination of inherited and acquired factors. Elevated serum levels of homocysteine have been associated with an increased risk of arterial thrombosis (myocardial infarction, stroke, and peripheral arterial disease) and venous thromboembolism (Cattaneo, 1999).
\n\t\t\tAfter renal transplantation the donor kidney endothelium is conditioned to exhibit a prothrombotic state as a consequence of reperfusion injury, tissue trauma, inflammation and expression of tissue factor, in addition to the recipient immune response (Key, 1992, Irish, 1999). The combination of a conditioned endothelium and a genetic or acquired predisposition to a hypercoagulable state increase the risk of thrombosis. Factors specific for the renal transplant patients that have been suggested to contribute to this thrombotic risk include the use of calcineurin-inhibiting drugs, high levels of homocysteine, diabetic nephropathy, antiphospholipid syndrome, cytomegalovirus infection, and the presence of proteinuria or nephrotic syndrome (Kujovich, 2004).
\n\t\t\tIt has been proposed that inherited risk factors of venous thromboembolism, such as factor V-Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T, might be associated with poorer survival rates of transplanted kidneys, attributed to the context of graft perfusion defects, venous thromboembolic complications, and acute graft loss by vascular rejection, possibly reflecting immunological injury upon the vascular wall exacerbated or induced by the prothrombotic state (Heidenreich, 2003, Wuthrich, 2001). Later study with larger number of patients, did not find a statistically significant association of polymorphisms factor V-Leiden G1691A and MTHFR C677T with renal graft survival Meyer, 2007).
\n\t\t\tFactor V-Leiden mutation or activated protein C resistance is the most common inherited thrombophilic disorder, found in 5% to 8% of the general population, in 20% of patients with a first venous thrombosis, and in up to 50% of patients with a personal or family history of recurrent thrombosis (Kujovich, 2004). In renal transplant recipients, factor V Leiden has been associated with a variety of complications after renal transplantation and a significantly higher incidence of venous thromboembolism which occurred in up to 39% of FVL carriers (Wuthrich, 2001, Irish, 1997). Also FVL carriers had 12-fold higher risk of an early graft perfusion defect (Wuthrich, 2001). A higher risk of vascular rejection was found in FVL carriers, which was linked to the presence of endotheliolitis or fibrinoid necrosis on histopathology of renal grafts lost within the first year after transplant (Ekberg, 2000).
\n\t\t\tThe reported prevalence of prothrombin gene heterozygous mutation in renal transplant recipients is 3.7%, similar to that in the general population. The mutation was associated with a nearly threefold increased risk of graft failure, which was attributable to arterial, venous, or microvascular thrombosis in the majority of carriers (Fischereder, 2001, Kujovich, 2004).
\n\t\t\tA polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene coding for an enzyme that degrades the endothelium toxic product homocysteine have been associated with ESRD (Girndt, 2007).This mutation occurs in 50% to 90% of chronic dialysis patients presenting with mild hyperhomocysteinemia and have been associated with cardiovascular disease and vascular access thrombosis in this population (Mallamaci, 2005, Mallamaci, 2002). Additionally hyperhomocysteinemia can be acquired, such as in renal failure and in deficiencies of folate, vitamin B12, or vitamin B6. Even though many studies found that hyperhomocysteinemia is an independent risk factor for both first and recurrent venous thromboembolism (den Heijer, 1996, Cattaneo, 1999) and that hyperhomocysteinemia is an independent risk factor for cardiovascular disease (Ducloux D et al 2000), the effect of hyperhomocysteinemia on the risk of graft thrombosis is unknown. Antiphospholipid syndrome is the most common acquired blood protein defect associated with either venous or arterial thrombosis or both (Koniari, 2010). Antiphospholipid antibodies (APLA) are found in approximately 10% of patients awaiting renal transplantation. Since only a fraction of patients with antiphospholipid antibodies experience thrombotic complications, the description of antiphospholipid antibody syndrome (APAS), defines by the presence of antiphospholipid antibodies and a clinical history of thrombosis. Antiphospholipid antibodies include not only the lupus anticoagulant (LA) and anticardiolipin antibodies (ACLAs) but also more recently recognized subgroups of antiphospholipid antibodies (antibodies against beta-2-glycoprotein-I [B-2-GP-I]) and antibodies to phosphatidylserine,phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol, phosphatidylcholine, and anti-annexin-V (Bick, 2003). Patients with antiphospholipid antibodies in association with other autoimmune disease, most commonly lupus, are classified as having secondary antiphospholipid syndrome. Approximately 40% of patients with SLE have an antiphospholipid (anticardiolipin) antibody (lupus anticoagulant). The presence of antiphospholipid antibodies has been recognized as an important risk factor for early allograft failure (Wagenknecht, 1999. Patients with APAS are at high risk for renovascular thrombosis and renal allograft loss was reported to be universal in the absence of anticoagulation (Vaidya, 2000). Whereas, and despite the lack of anticoagulation, no allografts were lost to thrombosis, in patients with detectable anticardiolipin antibodies but no prior history of thrombosis. In a later report all patients with antiphospholipid antibodies were successfully transplanted using postoperative anticoagulation (Morrissey, 2002).
\n\t\t\tOther prothrombotic changes that have been reported in renal transplant recipients include decreases in antithrombin, protein C and protein S levels, markedly elevated factor VIII levels and over-expression of plasminogen activator inhibitor-1 by donor epithelium (suggestive of impaired regional fibrinolysis) (Irish, 1999).
\n\t\t\tIn vitro data suggest that immunosuppressive drugs like cyclosporine and OKT3 may increase the risk of thrombosis but an independent clinical association with allograft thrombosis is unproven (Gruber, 1989, Abramowicz, 1992). Specifically, the prothrombotic effects of cyclosporine include activation of monocytes to express tissue factor, increased platelet aggregation, endothelial dysfunction and activation of the intrinsic coagulation pathway, impaired fibrinolysis and impaired activation of protein C (Carlsen, 1988, Fishman, 1991, Bombeli, 1996, Evans, 1997, Levi, 1992).
\n\t\t\tThrombotic complications after renal transplantation are usually catastrophic. Inherited and acquired hypercoagulable states have to be considered prior to kidney transplantation and proper prophylactic treatment initiated for the purpose to improve transplant outcome. Andrassy et al. provided specified screening recommendations for thrombophilia prior to kidney transplantation (Andrassy, 2004). A general screening for thrombophilia, to include factor V Leiden, prothrombin gene G20210A polymorphism, antithrombin III, protein C and S activity, antiphospholipid antibodies and lupus anticoagulant, should be performed in all children and adolescents because they have the highest risk for thrombotic complications. Adults only with history of thrombotic events should be thoroughly screened (recurrent AVC fistula thrombosis should be taken into account). When risk factors are absent, screening only for antiphospholipid antibodies and lupus anticoagulant is recommended.
\n\t\t\tThere is also no consensus on the optimal management of renal transplant patients with thrombophilic disorders. Treatment strategies to reduce thrombotic risk including heparin, warfarin, and aspirin have been evaluated in several reports. While inadequate anticoagulation may place the patient at risk for thrombosis, preemptive or intense perioperative anticoagulation can result in postoperative bleeding (Morrissey, 2002, Murashima, 2010, Friedman, 2001). Morissey et al. (Morrissey, 2002) recommended management approach for renal transplant patients with thrombophilia. Patients with diagnosis or suspected to have thrombophilia is suspected, the risk for thrombotic complications should be stratified as low, intermediate or high. In high risk are patients with inherited thrombotic disorder and history of at least two thrombotic episodes. For the high risk patients indefinite oral anticoagulation has been advocated. In intermediate risk are patients with a known inherited thrombotic disorder who are asymptomatic or have experienced a single thrombotic event. They should receive adequate prophylaxis in high-risk situations such as surgery for a minimum of 6 months. For patients with no suspicion of thrombophilia, no anticoagulation or a short term postoperative anticoagulation may be given.
\n\t\tRenal transplantation is established as the preferred treatment for most cases of end-stage renal disease. Postoperative vascular complications include thrombosis of renal vein and artery, with a delay in the diagnosis and management of these complications leading to significant morbidity for the recipient, with a high risk of graft loss and mortality (Akbar, 2005). It consists of a rare complication that often results in graft loss, with reported incidence ranging from 0.4% to 6% (Rouviere, 2002, Giustacchini, 2002). Bakir et al reported that thrombosis represented 45% and 37% of renal allograft loss at 3 and 12 months (Bakir, 1996).
\n\t\t\tRenal vein thrombosis (RVT), although an unusual event, most often has graft loss as a result (Figure 1). The causes that may lead to this serious complication include compression due to hematomas or lymphoceles, angulation or kinking of the vein, anastomotic strictures, or an underlying state of deep venous thrombosis or hypercoaguability (Penny, 1994). RVT usually occurs suddenly and towards the end of the first week of an otherwise uncomplicated kidney transplantation. Specifically it occurs in the first 2 weeks post transplant, with 80% occurring in the first month and 93% within the first year (Kobayashi, 2007). Clinical presentation is initiated by oliguria and hematuria with a tender swollen graft, which if ruptured, is accompanied by life-treatening bleeding (Kobayashi, 2007).
\n\t\t\t\tSpecimen of renal allograft nephrectomy due to renal vein trhrombosis
This uncommon complication which may occur most often as an early but also as a late event after kidney transplantation consists a devastating clinical condition leading frequently to graft loss. Renal artery thrombosis (RAT) onset most often follows a technical problem such as intimal dissection, kinking or torsion of the vessels. Risk factors include poor cardiac output, hyperacute rejection, unresponsive acute rejection, and a hypercoagulable state. It presents with a rapid onset of oliguria. In cases of segmental infarct, there can be lack of symptomatology or a presentation of renal dysfunction and increased blood pressure. When RAT occurs as a late event, it could be attributed to renal artery stricture or its manipulation post-operatively e.g. during angiography, or usually due to graft rejection.
\n\t\t\tAn early clinical diagnosis is very important for both RVT and RAT, even during the morning ward round. Diagnosis of these complications is established by colour flow Doppler studies, demonstrating in RVT a swollen graft with a crescent of clot along the convex margin of the kidney. In this case it is essential that the patient is taken immediately to theatre. Under normal clinical conditions, the spectral Doppler renal arterial waveform shows high resistive index with reversal of diastolic flow. On the contrary, in RAT a lack of flow in the renal artery is demonstrated, with the presence of intraluminal filling defects. In RAT, diagnosis is set by Doppler studies or at time of surgical exploration, however by that time it is not possible for the graft to be saved due to the kidney’s low tolerance to warm ischemia (Rouviere, 2002).
\n\t\t\tFollowing establishment of diagnosis for RVT, the treatment of choice is urgent thrombectomy. However graft salvage may not be possible, in which case graft nephrectomy is usually required. In case thrombectomy is applied early, within 1 hour following the event, graft salvage can be achieved. The increased risk of swelling, edema and also a possible rupture of the kidney graft in such a condition, makes urgent exploration essential. Systemic anticoagulants can be applied as treatment only in cases of partial vein thrombosis.
\n\t\t\t\tThe surgical treatment for renal graft thrombosis includes laparotomy, thrombectomy and ultimately a possible graft nephrectomy. Several authors describe endoluminal therapy for renal graft thrombosis; however the exact role of interventional radiologic treatment is not yet well-defined (Obed, 2008). The technique for percutaneous treatment involves placing the tip of a catheter within the thrombus, 1 cm distal to the surgical anastomosis, with infusion of a thrombolytic agent (Rouviere, 2002). Because transcatheter thrombolysis revascularizes arteries at a slower rate than surgical thrombectomy, patients with a heavy clot burden should be primarily offered surgical treatment (Hedegard, 2009). Transcatheter thrombolysis should be limited to low clot burden, segmental artery thrombosis, or high-risk surgical candidates. Additionally catheter-directed thrombolytics should be avoided in the first 2 weeks following kidney transplant due to the immature anastomotic suture line. On the other hand RAT can be determined as a terminal event, which can be averted only if poor graft function can be attributed to arterial inflow and in this case intervention should be immediate. By the time the diagnosis is set, the transplanted kidney is lost.
\n\t\t\tAlthough in many cases of renal allograft vascular thrombosis, no cause can be identified, epidemiological studies have attempted to categorise risk factors as modifiable, including drugs and the surgical procedure among others, and nonmodifiable, including age, diabetes mellitus and vascular anomalies. Additionally studies have identified changes in coagulation or fibrinolysis promoting a more thrombotic state, as risk factors as well.
\n\t\t\t\tPrevention may hold an important role in avoiding the formation of vascular thrombosis. This requires of course a combination of different measures such as avoiding prolonged cold and warm ischemia. Attention to precise surgical technique, use of preservation solution such as University of Wisconsin solution and an immediate and effective management of rejection, should all be outlined as important in the prevention strategy.
\n\t\t\t\tAdditionally identification and management of thrombophilic states could act as a preventive measure against renal vascular thrombosis, with a possible need for routine screening and directed therapy to reduce the risk of thrombosis and graft loss, however no consensus for either strategy have been introduced. Previous reports indicate a possible laboratory investigation to potential recipients with a previous history or family history of thrombotic events, such as deep and superficial vein thromboses, pulmonary emboli, fistulas having been thrombosed or incidents of multiple occlusions of central venous dialysis catheters, as well as patients undergoing preemptive transplantation with a living donor kidney (Andrassy, 2004).
\n\t\t\t\tThe risk of thrombosis must be balanced against that of bleeding. For known thrombophilia and a history of clinical events, perioperative heparinization followed by long-term anticoagulation with warfarin has shown good results, including successful retransplantation. However since results of the few available, prospective randomized studies on heparin use in renal transplant patients, show conflicting conclusions, one understands that there is a great need for a preoperative classification of thrombotic and hemorrhagic risk among renal transplant candidates and for establishment of consensus guidelines.
\n\t\t\tExtrarenal arterial pseudoaneurysms in renal transplantation are rare, and their prevalence is less than 1% (Bracale, 2009). Extrarenal pseudoaneurysms are directly related to arterial anastomosis, percutaneous nephrostomy placement and infectious causes. It is usually asymptomatic and rarely can cause renal dysfunction or compression of adjacent structures (Bracale, 2009). When extrarenal pseudoaneurysms become large, there is a strong indication to be surgically removed to avoid spontaneous rupture and loss of the allograft (Figure 2).
\n\t\t\tExternal iliac artery pseudoaneurysm presented as a complication of renal vein thrombosis and allograph nephrectomy. The pseudoanurysm was formed at the stump of the arterial anastomosis due to inflammation. Preemptive treatment with double stent placement was successfully performed.
Arteriovenous fistula (AVF) is a well-recognized vascular complication of percutaneous biopsy. The reported incidence of AVF ranges between 0.5 and 16% (Martinez, 1998). An arteriovenous fistula (AVF) may be formed when both arterial and venous walls are punched by the biopsy needle. Mostly they are asymptomatic, rarely may cause persistent hematuria or recurrence of hematuria, hypertension and deterioration of renal function. Rarely, renal graft ischemia may be the result of steal phenomenon from a large AVF (Harrison, 1994, Matsell, 1992, Cruzado, 19990. Factors that may predispose to the development of arteriovenous fistula include early postransplant period, the presence of hypertension, sclerosis and interstitial fibrosis, the formation of intrarenal hematoma (Schwarz, 2008). About 70% of AVF cases resolve spontaneously within weeks or months (Matsell, 1992).
\n\t\t\tDoppler sonography allowing noninvasive diagnosis of AVFs is the diagnostic examination of choice (Ozbek, 1995). Angiography is the reference standard as it confirms the presence of the AVF, accurately assesses its size and location, and permits endovascular treatment (Loffroy, 2008). On Doppler, the AVF shows a focal area of turbulent flow and a localized region of disorganized color that extends outside the normal vessels on color Doppler. In the area of AVF, the duplex US shows a very high velocity with low resistive index in the feeding arterywith arterialization of the flow in the draining vein (Irshad, 2009).
\n\t\t\tIn most cases AVFs close spontaneously within a few months, but they warrant observation to exclude the need for therapeutic intervention. The likelihood of and time to spontaneous closure in renal allografts, and the optimal time for therapeutic intervention are not predictable (Loffroy, 2008). Treatment has been recommended when bleeding persists for more than 72 h, renal function deteriorates markedly, lesion enlarges and there is suspicion of steal phenomenon. Endovascular superselective embolization is the therapeutic procedure of choice, as loss of normal parenchyma is minimal, with success rate of approximately 88% with no significant loss of allograft function (Loffroy, 2008, Tarif, 2002). In the majority of cases, successful embolization can be achieved using coils or microcoils. Schwarz et al (Schwarz,2008) proposed a hemodynamic prognostic test to predict which AVF would probably profit from AVF coiling, by comparing Doppler sonographic resistive indices of the main renal artery and the non-AVF associated segmental arteries (Schwarz, 2008). The resistive index of the main renal artery should be at least 0.05 less than that of the non-AVF-associated segmental renal arteries indicating under-perfusion of the rest renal parenchyma.
\n\t\tRenal transplantation is regarded as an optimal treatment for End-stage renal disease. Improvements in surgical techniques and advanced immunosuppressive drugs have resulted in remarkable survival of patients and renal grafts. However complications occur in both the immediate postoperative period and later. Awareness for early post-operative complications, like renal vein and artery thrombosis could save allografts and patients. Cardiovascular disease remains the most frequent cause of death and transplant loss after kidney transplantation, with hypertension present in vast majority of kidney transplant recipients and a risk factor for cardiovascular disease. Improvements in imagining modalities and interventional techniques resulted in earlier identification and management of TRAS. It is of paramount importance for the transplant surgeon to keep in mind that early and late vascular complications after renal transplantation could be very challenging and potentially allograft and/or life threatening
\n\t\tThe mandibular central and lateral incisors have a single conical root. The root dimensions of both incisors vary corresponding to the crown. They are narrow in mesiodistal dimension and wide in labiolingual dimension and taper uniformly on both proximal sides from the CEJ to the apex. The apical end may curve slightly to the distal. Longitudinal root depressions can be seen in both incisors from the mesial and distal views. Multiple comparisons revealed that, among all permanent teeth, mandibular central incisor has the shortest root. Furthermore, in contrary to maxillary incisors, the root of mandibular lateral incisor is longer than that of mandibular central incisor [1]. It has been reported that the average lengths of mandibular central incisor and lateral incisor roots are 12.6 mm (7.7–17.9) and 13.5 (9.4–18.1), respectively [2]. Kim et al. [3] measured the mandibular incisor root lengths using CBCT in Korean population and found that no significant differences in crown and root lengths were noted between the CBCT-based and direct measurements. The R/C ratios were higher for the mandibular lateral incisors (1.4 ± 0.1) than mandibular central incisors (1.3 ± 0.1) [4]. Therefore, crown lengthening may not be possible in the case of traumatic fracture or iatrogenic orthodontic extrusion due to the short root length in these teeth. Variations in root length between males and females have been reported. According to Zorba et al. [5], it was observed that root length was greater in males than in females. Haghanifar et al. [6] found similar results when comparing crown and root lengths between males and females. He found that females had longer crowns while males had longer roots.
Many authors reported that the external crown and root morphology of mandibular central and lateral incisors are similar [2, 7, 8]. Mandibular incisors usually have a single root, which is wider buccolingually than mesiodistally and tapers toward the apex. The lateral incisor root is larger than that of the central incisor in mesiodistal and labiolingual directions [8, 9]. Variation in number of roots has not been reported in literature. However, Loushine et al. [10] have found two rooted mandibular lateral incisors. However, the shape may vary from conical to round in different populations. Sexual variation in the number and shape of roots has not been reported [9]. Mandibular incisor roots are commonly reported to be straight and in rare occasions curved in the apical region. Curvature can be in the mesial, distal, labial, or lingual direction [9].
Orban stated that the shape of the root canal “to a large degree, conforms to the shape of the root. A few canals are round and tapering, but many are elliptical, broad and thin” [11].
The internal anatomy of permanent mandibular incisors does not usually reproduce the simplicity of external anatomy. Its internal anatomy is complicated by the presence of lingual canals, lateral canals, isthmus, and apical deltas [12]. The pulp cavity is the central cavity within a tooth and is entirely enclosed by dentin except at apical foramen. It is divided into coronal portion (pulp chamber) and radicular portion. The pulp chamber is wide and ovoid labiolingually and it tapers incisally. The size of the pulp chamber is not constant throughout life. It decreases in size with aging as a result of secondary dentin deposition [13]. The pulp horn is well developed in this tooth. The root canal systems of these single-rooted teeth often have a single root with a single root canal. However, studies have shown that the root canal anatomy of these teeth is not simple. It may not be single and straight as it appears on the periapical radiograph. Indeed, these teeth have a high prevalence of bifurcation, second canals, lateral canals, and apical deltas which would complicate surgical and nonsurgical endodontic treatment. Mandibular incisor’s anatomy presents a challenge when an endodontic access is made, because of its small size and high prevalence of two canals. The main reason for failure in endodontic treatment of mandibular incisors is the inability to detect the presence of a second canal which can then not be prepared and filled during treatment [14]. In literature, the incidence of mandibular incisor teeth with more than one canal has been reported to range from 11 to 68% [15, 16, 17, 18, 19]. The differences between these morphology studies may be related to variations of examination methods, classification systems, sample sizes, and ethnic background of tooth sources. Many researchers have studied the prevalence of a second canal in mandibular permanent incisors on different populations and showed that the root canal morphology varies with race, sex, and age [20, 21, 22, 23, 24].
Routine clinical radiographs may mislead clinicians to be under an impression that all root canals are round in shape. A high prevalence of oval root canals in human teeth was reported [25, 26].
The pulp canal of the permanent mandibular central incisor is wider buccolingually than mesiodistally [9]. These dimensions are not constant along the root from the orifice till the apex. Oval canals and long oval canals are the most common canal shape seen in the coronal and middle third [27]. As we approach the apex, the canal shape becomes more rounded [28]. This canal shape morphology corresponds to the shape of the root.
The root canal morphology of mandibular central and lateral incisors is very similar. Although they have only one root and a high prevalence of Type 1 root canal morphology, surgical and nonsurgical root canal treatment may fail in these teeth if there is a lack of awareness in their internal anatomy which is complicated by the presence of the lingual canal, bifurcation, lateral anatomy, and isthmus [17, 29]. The morphological characteristics of the root canal system were studied using a number of techniques [18, 27, 30]. The prevalence of a second canal in mandibular permanent incisors is different between populations. Vertucci [18] reported that the incidence of the presence of a second canal was 25.7% among American population, whereas the incidence in Chinese population for the mandibular central and lateral incisors was 5.71 and 27.36%, respectively [31], 30% in Saudi population [32], 26.2% in north Jordanian population [33], and 36.25% in North-East Indian population [34]. In Iranian population, the incidence of mandibular central and lateral incisors having two canals was 27.3 and 29.4%, respectively [35]. The highest incidence (63%) of a second canal in mandibular incisors has been reported in a study in Turkish population [19].
Rankine-Wilson and Henry [36] filled the root canals of mandibular anterior teeth with radio-opaque material, sectioned them in a horizontal plane, and exposed radiographs. They reported two canals in 40.5% of mandibular incisors. Later, Vertucci [18] studied the root canal morphology of 300 extracted mandibular anterior teeth using the clearing technique. In 30% of mandibular central incisors and in 25% of mandibular lateral incisors, there was a second canal. On the other hand, higher prevalence of a second canal in Chinese population was reported in lateral mandibular incisors 25.5% compared with 10.9% in central mandibular incisors [37].
Many researches have shown that root canal systems also vary according to gender. In Turkish population, Sert and Bayirli [19] reported the incidence of second canal in central incisors in females (70%) was higher than in males (65%). Also in Turkish population, Arslan et al. [38] found the frequency of mandibular incisors with a second root canal in males (63%) was higher than in females (35%). The differences among both studies may be due to the fact that Sert and Bayirli examined the root canal morphology in vitro, whereas Arslan et al. studied the root canal anatomy in vivo. In Chinese population, Zhengyan et al. [30] found a significant difference between sex. The result of his study showed that 9.4% of the mandibular lateral incisors in males had a second canal, whereas this value was 11.9% in females. Among Iranian population, Haji et al. [39] reported that there was no significant difference between males and females in the incidence of a second canal in mandibular incisors.
It has become clear that teeth have complicated root canal systems rather than simplified canals [40]. Most investigators have shown that the root canal systems for most, if not all, permanent teeth are complex and canals may branch, divide, and rejoin. In addition to the complexity of root canal anatomy, root canal morphology varies from tooth to tooth. Concerning root canal treatment, these variations in root canal morphology of permanent teeth may result in missing root canals, nonsurgical endodontic treatment failure, and a need for surgical procedures. Weine et al. [41] classified root canal systems into four basic types, but Vertucci [18] subsequently classified them into eight configurations. The Vertucci classification may give consideration to the complex reality of canal systems in a way that the Weine et al. system did not.
Weine [42] described each of the canal types as below:
Type I: Single canal from pulp chamber to apex.
Type II: Two canals leaving the chamber and merging to form a single canal short of the apex.
Type III: Two separate and distinct canals from chamber to apex.
Type IV: One canal leaving the chamber and dividing into two separate and distinct canals.
Vertucci [24] classified canal configurations into eight types as described below:
Type 1: A single canal from the pulp chamber to apex [1].
Type II: Two separate canals leaving the pulp chamber before joining short of the apex to form one canal [2-1].
Type III: One canal leaving the pulp chamber before dividing into two in the root and then merging to exit as one canal [1-2].
Type IV: Two distinct canals that extended from the pulp chamber to the apex [2].
Type V: One canal leaving the pulp chamber and dividing short of the apex into two separate distinct canals with different apical foramina [1-2].
Type VI: Two separate canals leaving the pulp chamber, merging in the body of the root, and re-dividing short of the apex to exit as two distinct canals [2-1-2].
Type VII: One canal leaving the pulp chamber, dividing and then rejoining in the body of the root, and finally re-dividing into two distinct canals short of the apex [1-2-1-2].
Type VIII: Three separate, distinct canals that extended from pulp chamber to apex [3].
Although mandibular incisors are usually single-rooted teeth, their root canal system cannot be predicted not only between different populations but also between the same population, with respect to the Vertucci’s configuration. Studies reported that Vertucci’s Type I configuration has the highest prevalence among the other Vertucci configurations [43, 44, 45]. When a second canal is present, Vertucci’s Type III configuration is the most common for central and lateral incisors. Scarlatescu [46] found Type III has higher incidence than Type II, of 25 and 6.3% respectively in a Romanian population. de Almeida [47] reported that Vertucci’s Type I and III configurations represented 92% of the sample. Leoni investigated the root canal anatomy of mandibular central (n = 100) and lateral (n = 100) incisors and founded that Vertucci’s Type I (50 and 62%, respectively) and Type III (28%) were the most prevalent canal configurations in incisors [48]. However, researchers found high prevalence of Vertucci’s Type II than Vertucci’s Type III when a second canal is present. For example, Al-Qudah and Awawdeh [33] reported that the most common root canal configurations were Vertucci’s Type I, II, III, IV, and V with a prevalence of 73.8, 10.9, 6.7, 5.1, and 3.6% of mandibular central and lateral incisors respectively in a Jordanian population. Another study done in an Iranian population conducted by Yazdi and Jafari [49] using in vitro radiography, staining, and sectioning technique reported 88, 3.5, 0.5, and 8% prevalence of canal types I, II, IV, and V respectively in mandibular incisors. A similar study done by Miyashita et al. [17] among Japanese population founded central and lateral incisors with prevalence of Vertucci’s Type I, II, III and IV as 87.6, 9.3, 1.4, and 1.7% respectively. These configurations may have an implication in endodontic treatment outcome. A properly executed root canal treatment will lead to success in Type I, II, IV, and VIII canal configurations while the same treatment might lead to unfavorable treatment outcome in Type III canal configuration. Apically dividing systems like Type V, VI, and VII are the most difficult systems to prepare and obturate and may have an influence on the outcome of root canal treatment. Miyashita et al. [17] studied the relationship between canal configuration and external dimension, and found that Type II and III root canal configurations of mandibular incisors were larger in tooth length, and crown width labiolingually and mesiodistally. In cases of nonsurgical root canal procedure, disinfection and obturation of Type I and IV canal systems are relatively simple owing to that each of these configurations having definite canals with separate orifice and apex. Contrarily, Type II, III, and V systems are different because there are areas in the root where the two canals share space and others where the canals are separate. This requires an individualized procedure for preparation and filling in each of these conditions to obtain the most desirable results. Although the incidence of two separate canals is low, ribbon-like canals are detected in cases that were classified as Type I (simple root canal) based on their canal configuration, and this results in enabling the file to touch a large area of the canal walls.
Lateral canals are accessory canals located in the coronal or middle third of the root, extending horizontally from the main canal to the external surface of the root. Their formation is due to the entrapment of periodontal vessels in Hertwig’s epithelial root sheath or when blood vessels running from the dental sac through the dental papilla persist during calcification [50]. Lateral canals communicate with the periodontal ligament space and this increases risk of spread of periodontal disease into the pulp canal. According to their location, Vertucci classified lateral canals into coronal, middle, apical, or furcation. He observed lower occurrence of canal ramifications in the middle 11.4% and coronal 6.3% thirds compared to the apical 73.5% third [18, 24]. Recent micro-CT studies on root canal morphology of mandibular anterior teeth reported that lateral canals are rare [48, 51]. Miyashita et al. [17] reported that out of mandibular incisors with lateral branches, single lateral branch had the highest prevalence (82.2%) and multiple branches were extremely narrow. Al-Qudah and Awawdeh [33] found that there was an increasing prevalence of lateral canals toward the apical third of the root with approximately 64% occurring in the apical part of the roots. On the other hand, other studies reported that lateral canals were frequently found in the middle of the canal [34, 46]. Clinically, lateral canals are not usually visible in preoperative radiographs, but its presence can be suspected when there is a localized thickening of the periodontal ligament or a lesion on the lateral surface of the root [50]. It is also important to note that lateral canals cannot be instrumented. Its contents can only be neutralized by the action of effective irrigation with appropriate tissue dissolvent properties and antimicrobial activity solution or with the addition of use of intracanal medications.
Apical deltas are defined as an intricate system of spaces within the root canal that allows free passage of blood vessels and nerves from the periapical compartment to the pulp tissue [52, 53]. The apical delta is different from the accessory canal in which the main pulp canal is still distinguishable. The prevalence of apical deltas in human permanent teeth varies among populations, and the type and locations of tooth and methods of study. High prevalence of apical deltas is found in maxillary second premolars, mandibular lateral incisors, and mandibular second premolars [22]. Among American population, Vertucci [18] reported that the incidence of apical deltas was 5, 6, and 8% in the mandibular central incisors, lateral incisors, and canines, respectively. However, Çalişkan et al. [22] reported that the prevalence of apical deltas in those teeth was 9.8, 23.5 and 7.8% in a Turkish population. Apical deltas have been reported to be of great importance in endodontics because they are difficult to be instrumented during chemical-mechanical preparation. Furthermore, their long vertical extension may cause failure of the apical surgery if not involved during apical resection [54]. Gao et al. [55] reported that the median vertical distance of the apical delta was 1.87 mm with 13% of them more than 3 mm. Therefore, resection of the apical 3 mm of a root may include the whole apical delta and residual microorganisms from 87% of roots with apical delta.
A thin communication can occur between two or more canals in the same root or between vascular elements in tissues [56]. Green [23] described this corridor as a “ribbon shaped passage.” He found this corridor in 22% of mandibular incisors. An isthmus is formed when an individual root projection is unable to close itself off. Any root that contains two root canals has the potential to contain an isthmus [57]. It may contain tissue remnants and necrotic debris, which participate in microorganisms’ growth resulting in root canal treatment failure [58]. Therefore, knowledge of the root canal anatomy is essential for complete cleaning of the root canal and successful endodontic treatment [11]. Isthmus classification was described by Hsu and Kim et al. [59]. They classified isthmus into five types: Type I—two canals with no notable communication; Type II—a hair-thin connection between the two main canals; Type III—differs from Type II because of the presence of three canals instead of two; Type IV—an isthmus with extended canals into the connection; and Type V—there is a true connection or wide corridor of tissue between two main canals. Mauger reported that isthmus was present in 20% of the teeth at the 1-mm level, 30% at 2 mm, and 55% at 3 mm [27]. Estrela et al. [60] demonstrated high prevalence of both partial and complete isthmii in mandibular lateral incisors (47.6%) compared with mandibular central incisors (33.3%). On the other hand, Arslan et al. [38] found a low incidence (3.7%) of intracanal communication among Turkish population. A similar study done by Haghanifar [61] found the prevalence of complete isthmus in the mandibular anterior teeth ranged from 3 to 5%.
As a result of large width of the root canal buccolingually than mesiodistally, mandibular incisors have oval and flattened canals [25]. The overall prevalence of long oval root canals in the apical region in mandibular incisors is >50% [25]. When using rotary files, these oval-shaped canals are a challenge for proper shaping of the canal. This is because rotary instrumentation cannot touch all the canal walls, leaving behind untouched area. To improve mechanical apical debridement, the use of instruments up to an ISO size 100 is required to avoid leaving untouched area on the buccal and/or lingual walls of the canal [62]. However, using files with large taper or tip may cause lateral or apical perforation of the root as the root has a narrower diameter in the mesiodistal direction. Therefore, it stresses the use of good chemical disinfection protocol on these teeth. Canals are considered as oval, long oval, and flattened when the ratio between the maximum and the minimum cross-sectional diameter is <2:1, 2–4:1, and >4:1, respectively. Apical foramina are the main apical opening of the root canal. It is the main exit of the root canal onto the external root surface. Variation in the number and position of apical foramina is especially seen in mandibular incisors with two canals. The apical foramen coincides with the anatomical apex in 17–52.2% of the cases [19, 22, 33, 57, 63].
A number of studies (17.33%) reported that the position and the number of the apical foramen vary according to the race. Al-Qudah and Awawdeh [33] reported that more than half of the roots (52.2%) had centrally located foramina and 47.8% had laterally located foramina. Apical deltas were observed in only eight teeth (1.8%), and among mandibular incisors with two canals, single foramen was more prevalent than two apical foramina. Miyashita et al. [17] reported that only 3% of the mandibular incisors containing two canals had two foramina. He also found that 67.9% of mandibular incisors with curved root had eccentrically located foramina toward the labial direction and none of the canals were curved lingually.
According to Walker [63], the distance between the apical foramen and the most apical end of the root ranges between 0.2 and 2.0 mm. The diameter of the apical foramen of mandibular incisors has been reported to be as 262.5 μm.
Anomaly (Gk, anomalos; irregular) is a deviation from what is regarded as normal [64]. These abnormalities may occur, in terms of size or shape, to either crown or root. WHO listed the following dental anomalies: concrescence, fusion, gemination, dens evaginatus, dens in dente, dens invaginatus, enamel pearls, macrodontia, microdontia, peg-shaped teeth, taurodontism, and tuberculum paramolare [65]. Anomalies of permanent mandibular incisors regarding the crown and root shape are extremely rare. However, few case reports have registered anomalies associated with mandibular incisors. As an example, dens invaginatus, a deep surface invagination of the crown or root, which is lined by enamel and resulting from the invagination of the enamel organ into the dental papilla during odontogenesis, can be seen in these teeth [66]. Dens invaginatus has been classified into three categories according to the depth of invagination and communication with the periapical tissue or periodontal ligament [67].
Type 1: The invagination ends as a blind sac confined to the crown.
Type 2: The invagination extends apically beyond the external CEJ, ending as a blind sac and never reaching the periapical tissues.
Type 3: The invagination extends beyond the CEJ and a second “apical foramen” is found in either the periapical tissues or the periodontal ligament.
The prevalence of this anomaly has been found to range from 0.25 to 5.1% of the population [66]. More commonly, dens invaginatus occurs in the maxillary permanent lateral incisors. Also, it may occur in maxillary central incisors, premolars, canines, and molars. It usually occurs unilaterally, but bilateral cases have also been reported [68]. Occurrence of dens invaginatus in mandibular teeth is very rare. When it occurs in mandibular incisors, the central incisor has a higher incidence compared with lateral incisor [69, 70].
Talon cusp is also a rare developmental anomaly defined as an additional cusp that projects predominantly from the labial or lingual surface of primary or permanent anterior teeth [71]. Mellor and Ripa [72] named this anomaly “talon cusp” as it resembles the shape of an eagle’s talon. Talon cusp was classified by Hattab [73] as follows:
Type 1: True talon cusp—this is a morphologically well-delineated additional cusp that prominently projects from the palatal surface of a primary or permanent anterior tooth and extends at least half the distance from the CEJ to the incisal edge.
Type 2: Semi talon cusp—this is an additional cusp of size a millimeter or more but extending less than half the distance from the CEJ to the incisal edge.
Type 3: Trace talon—this is enlarged or prominent cingula and their variations (i.e., conical, bifid, or tubercle-like).
Radiographically, the talon cusp may appear typically as a V-shaped radiopacity, starting from the cervical third of the crown. Most of the talon cusps occur in the maxillary lateral incisors (55%), followed by maxillary central incisors (32%) and maxillary canines (9%) [71]. Although it is rarely seen in mandibular teeth [74], Gündüz and Celenk [43] studied the site distribution of talon cusp among Turkish population and found only 3% of talon cusp was seen in the mandibular right central incisors.
Another rare developmental anomaly that has been reported to occur in mandibular central incisor is “Gemination” [75]. It is a rare anomaly that arises when the tooth bud of a single tooth attempts to divide. The structure most often presents as two crowns, either totally or partially separated, with a single root and one root canal [76]. In the anterior region, gemination can cause poor esthetic appearance due to irregular morphology. In addition, these teeth are more susceptible to periodontal disease and caries, if deep groove is present [77, 78].
Fusion is another developmental anomaly which can occur in these teeth. Contrary to gemination, fusion is defined as the union of two or more separately developing tooth germs during odontogenesis, when the crown is not yet mineralized at the dentinal level, yielding a single large tooth [79]. Depending on the stage of development at the time of union, the pulp might be merged or separated [80]. Fusion is more frequently seen in primary dentition, but it may occur in both dentitions. If it occurs in permanent dentition, the vast majority of permanent teeth fusion cases are seen in maxillary teeth. Although, the incidence of fusion of mandibular incisors is rare, mandibular central incisors have been reported to fuse with a supernumerary tooth [81] and bilaterally with the adjacent lateral incisor [82].
It should be emphasized that special attention is required during root canal treatment owing to the abnormal morphology of the crown and the complexity of the root canal system in fused teeth.
Mandibular incisors are prone to endodontic treatment as a result of several reasons. Due to their location in the jaw, they are prone to traumas that result in tooth fracture which may necessitate root canal therapy. Moreover, their proximity to the opening of the sublingual and submandibular ducts increases the incidence of dental caries as a result of lingual deposition of calculus. Therefore, an accurate knowledge of the external and internal anatomy of these teeth is an essential prerequisite to carry out root canal treatment. They often have two canals that are buccolingually located and the lingual canal usually is missed. Therefore, the dentist should extend the access preparation in lingual direction to locate the lingual canal which is usually below the cingulum. In case of two canals, Type II canal is the most prevalent configuration where the buccal canal is the most straight and easiest to be located. Consequently, it is recommended to instrument and fill these canals till the apex whereas the lingual canal merges with the labial canal. Presence of an isthmus may complicate the root canal disinfection as it may contain tissue remnants and necrotic debris, hence irrigation and activation are very essential to overcome these anatomical difficulties.
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\\n\\nAuthors are required to declare all potentially relevant non-financial, financial and material Conflicts of Interest that may have had an influence on their scientific work.
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\n\nA Conflict of Interest is a situation in which a person's professional judgment may be influenced by a range of factors, including financial gain, material interest, or some other personal or professional interest. For IntechOpen as a publisher, it is essential that all possible Conflicts of Interest are avoided. Each contributor, whether an Author, Editor, or Reviewer, who suspects they may have a Conflict of Interest, is obliged to declare that concern in order to make the publisher and the readership aware of any potential influence on the work being undertaken.
\n\nA Conflict of Interest can be identified at different phases of the publishing process.
\n\nIntechOpen requires:
\n\nCONFLICT OF INTEREST - AUTHOR
\n\nAll Authors are obliged to declare every existing or potential Conflict of Interest, including financial or personal factors, as well as any relationship which could influence their scientific work. Authors must declare Conflicts of Interest at the time of manuscript submission, although they may exceptionally do so at any point during manuscript review. For jointly prepared manuscripts, the corresponding Author is obliged to declare potential Conflicts of Interest of any other Authors who have contributed to the manuscript.
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\n\nEditors can also have Conflicts of Interest. Editors are expected to maintain the highest standards of conduct, which are outlined in our Best Practice Guidelines (templates for Best Practice Guidelines). Among other obligations, it is essential that Editors make transparent declarations of any possible Conflicts of Interest that they might have.
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