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Introduction: There are still no guidelines about pediatric cardiac cancers. The purpose of this work is to provide new scientific data facilitating the differential diagnosis of a rare cardiac tumor with an unusual presentation, such as the cardiac inflammatory myofibroblastic tumor (IMT).Case Presentation: A 3-year-old male child presented with several symptoms including unconsciousness, vomiting, and drowsiness. A clinical and neurological examination revealed a unilateral (right) motor delay and positive unilateral Babinski sign. Electrocardiogram (ECG) was normal.Diagnostic Assessment: The total body computed tomography (CT) scans showed hypodensity in the left temporal–parietal lobe, a large hypodense area in the right frontal lobe, and a second area in the left frontal lobe were found with head CT. A magnetic resonance (MR) also noted cerebral areas of hypointensity. The echocardiographic images revealed an ovoid mass, adherent to the anterolateral papillary muscle. The histological exams, performed with hematoxylin–eosin, Masson's trichrome, Alcian blue PAS, Weigert and Van-Gieson stain, allowed observing the microscopic structure of the neoplastic mass. The immunohistochemical analysis was performed through subsequent antibodies: anti-vimentin, anti-actina, anti-ALK, anti-CD8, anti-CD3, anti-CD20, anti-kappa and lambda chains, and anti CD68 antibodies. The healthcare professionals diagnosed a cardiac IMT with brain embolism.Differential Diagnosis: The ventricular localization, observed through radiological exams, required a differential diagnosis with fibroma and rhabdomyoma, the presence of brain embolism with sarcoma, and its morphology with fibroma. Neurological symptoms might be attributed to encephalitis, primitive cerebral cancer, such as astrocytoma or neuroblastoma, cerebral metastases due to any malignancy, or embolic stroke.Conclusion: New studies are encouraged to better define IMT behavior and draw up guidelines confirming the crucial role of multidisciplinary approach and treatment protocol selected on the basis of the characteristics of the tumors, in the case of this rare type of cancer.

The aim of this case report is to share with the forensic science community the experience of a rare complication of sickle cell anemia: acute chest syndrome. In October 2016, at the port of the city of Trapani (Sicily, Italy), the landing of an ONG "Médecins Sans Frontières" ship took place with 548 non-EU citizens and a corpse on board. The man, in the hours before his death, complained of severe chest pain and respiratory difficulties, and, despite of the therapeutic aids and resuscitation maneuvers, lastly died. The Public Prosecutor ordered that autopsy be executed on the corpse of the young Ghanaian, and it was to be supplemented by histological, toxicological, genetic investigations, and the dating of the biological age. The autoptic examination findings were indicative of bilateral bronchopneumonia, and were also confirmed by the histological findings, which identified a condition of massive adipose pulmonary embolism, due to the presence of extramedullary hematopoietic tissue, site of endovascular thrombosis secondary to hemolysis of sickle cells. The spleen appeared of small volume, with fibrotic phenomena. The predisposition to infections, thrombosis, extramedullary hematopoiesis are all complications of sickle cell anemia. The severe pulmonary condition characterized by vaso-occlusive findings and pulmonary inflammation with infiltrate, symptoms like fever, chest pain and severe systemic hypoxia allowed to ascribe the plausible cause of death as acute chest syndrome, a rare complication of sickle cell anemia. The peculiarity of this clinical case is also related to the methods of medical intervention (boat with non-governmental medical support for assistance to migrants).

The gold standard for the diagnosis of foetal death is known to be the autopsy examination, which is sometimes supplemented by chromosomal and/or genetic studies. Nevertheless, autopsy rates are continuously declining, due to multifactorial and complex reasons, even anatomical, social and psychological ones, thus impacting the rate of radiological post-mortem foetal examinations.

Kawasaki disease (KD) is an acute, self-limited vasculitis of unknown etiology that primarily affects the coronary artery (CA) and presents in childhood. The characteristic coronary arterial lesion is an aneurysm, which may lead to thrombosis, dilatation, stenosis, and occlusion. Such an aneurysm is typically calcified and generally develops five or more years after the onset of acute KD. It becomes more noticeable after ten years. KD is sometimes difficult to diagnose because of the limited clinical features, especially in infants younger than 6 months old, where the clinical presentations often do not fulfill the diagnostic criteria for KD. We report a case of Incomplete Kawasaki Disease (IKD) causing unexpected death in infants. A seven-month-old male baby, apparently well nourished and without fever or exanthema that was unexpectedly found agonal in his bed by his parents. He died in an emergency room a few hours later in spite of aggressive resuscitation efforts. Postmortem Magnetic Resonance Images were obtained during the autopsy, with evidence of an occlusive thrombus in left and right coronary artery aneurysms. Laboratory findings were consistent with IKD. The crucial role of postmortem imaging is discussed here in order to improve diagnosis tools for preventable events.

BACKGROUND: Chronic constipation in children can be caused by cows' milk intolerance (CMI), but its pathogenesis is unknown. AIMS: To evaluate the histology and manometry pattern in patients with food intolerance-related constipation. PATIENTS AND METHODS: Thirty-six consecutive children with chronic constipation were enrolled. All underwent an elimination diet and successive double-blind food challenge. All underwent rectal biopsy and anorectal manometry. RESULTS: A total of 14 patients were found to be suffering from CMI and three from multiple food intolerance. They had a normal stool frequency on elimination diet, whereas constipation recurred on food challenge. The patients with food intolerance showed a significantly higher frequency of erosions of the mucosa, and the number of intra-epithelial lymphocytes and eosinophils. The rectal mucous gel layer showed that the food-intolerant patients had a significantly lower thickness of mucus than the other subjects studied. Manometry showed a higher anal sphincter resting pressure and a lower critical volume in food intolerance patients than in the others suffering from constipation unrelated to food intolerance. Both histology and manometry abnormalities disappeared on the elimination diet. CONCLUSIONS: Food intolerance-related constipation is characterized by proctitis. Increased anal resting pressure and a reduced mucous gel layer can be considered to be contributory factors in the pathogenesis of constipation.

OBJECTIVE: Chronic constipation in children can be linked to cow''s milk intolerance (CMI) but the existence of a food intolerance-dependent proctitis is still debated. The aim of this study was to evaluate the histologic data in patients with food intolerance-related constipation. MATERIAL AND METHODS: Fifty-two consecutive patients (22 M, median age 4 years) with chronic constipation unresponsive to common treatment were enrolled. All patients were put on a cow''s milk-free diet for 4 weeks and those uncured on this diet underwent a subsequent 4-week period of oligoantigenic diet. In the patients cured on elimination diet, a subsequent double-blind food challenge was performed to confirm the diagnosis of food intolerance. At entry to the study, routine hemato-chemical and immunologic assays, rectoscopy, and histologic study of the rectal mucosa were performed. In the patients cured on elimination diet, rectal histology was repeated when they were cured. RESULTS: Twenty-four patients were found to be suffering from CMI and 6 from multiple food intolerance. These patients had a normal stool frequency on elimination diet, while constipation reappeared on food challenge. The condition of the remaining 22 patients did not improve on elimination diet. The patients with food intolerance showed a significantly higher frequency of erosions of the mucosa, number of intraepithelial lymphocytes and eosinophils, and number of eosinophils in the lamina propria. Study of the rectal mucus gel layer showed that the food-intolerant patients had a significantly lower thickness than the other subjects studied. In the food intolerant patients, histologic abnormalities disappeared on elimination diet, when the patients were well. CONCLUSIONS: Food intolerance-related constipation is characterized by proctitis with eosinophil infiltrate of the rectal mucosa. A reduced mucus gel layer can be considered a contributory factor in the pathogenesis of the constipation.

Noncompaction of the ventricular myocardium is a disease characterized by an increase of the ventricular trabecular meshwork caused by arrest of the normal endomyocardial morphogenesis (Figs. 1, 2, 3). In accordance with the normal human anatomy, the left ventricular wall is well compacted with a few thin trabeculae; on the contrary, the normal right ventricular wall is furrowed by many trabeculae (the trabecula of the marginal septum as well as other ones). For this reason, the term ‘‘noncompaction’’ usually refers to an exclusive or prevalent disease of the left ventricle [1–16]. Recently Song and Aragona et al. [1–3] reported two cases of isolated right-ventricular noncompaction. According to the data coming from scientific literature and from our own experience, in some patients noncompaction is biventricular [5, 6], and an increase of the right ventricular meshwork is often evident in such cases, even more so than on the left side. The main diagnostic criterion of noncompaction, that is, the only one that is accepted and recognized, is evaluation of the ratio between the spongiosus and the compact thickness of the ventricular wall, which must be [2 [6–16]. This ratio is easy to calculate for the left ventricle; on the contrary, it is more difficult to calculate for the right ventricle. Only one case of right-ventricular noncompaction has been reported in the literature [7, 8]. In our personal clinical experience, we have found that many cases of biventricular noncompaction are reported in the register of Italian Society of Cardiovascular Echocardiography. Recently two patients with an inexplicable dilatation of the right ventricle caught our attention: Both of them showed a more prominent trabecular meshwork on

Cardiac contusion, usually caused by blunt chest trauma, has been recognized with increased frequency over the past decades. Traffic accidents are the most frequent causes of cardiac contusion resulting from a direct blow to the chest. Myocardial contusion is difficult to diagnose; the clinical presentation varies greatly, ranging from a lack of symptoms to cardiogenic shock and arrhythmia. Although death is rare, cardiac contusion can be fatal. The authors report a case of death due to a cardiac conduction system injury from a blunt chest impact following a car accident. The autopsy showed no external signs of thoracic trauma, no evident rib or sternum fractures. A small sub-endocardial hemorrhage was found in the region of the atrioventricular node. Histological examination revealed an injury of the atrioventricular node and His’ bundle. The cause of the death was attributed to the arrhythmia induced by contusion of the cardiac conduction system.

Aging has a striking impact on the heart and the vascular system, particularly on the large elastic arteries (i.e., aorta), resulting in a multitude of changes at different structural and functional levels. As result, medial degeneration (MD) occurs. A characteristic example of MD is sporadic thoracic aortic aneurysm (S-TAA), whose patho-physiological mechanisms remain unclear. In this study, typical MD morphological phenotypes were researched in S-TAA cases and control aorta specimens by histopathological and immunohistochemical analyses. Three phenotypes (I, II, and III) were detected, but mainly the phenotype III was observed. Elevated cystic MD, plurifocal medial apoptosis, and increased metalloproteinase-9 amount characterize it. In addition, it was significantly correlated with the severity of elastic fragmentation, hypertension, and smoking, and particularly with advancing age. Thus, phenotype III might represent the typical MD phenotype associated with S-TAA in old people that have a major risk of aorta rupture and dissection independently on aneurysm diameter. This might permit the assumption that phenotype III with its typical histological abnormalities is an optimal biomarker of rupture and/or dissection in aged individuals and is useful both for applying different surgical approaches and providing appropriate surgical indications

Gli autori segnalano un caso di propria osservazione riguardante il decesso di giovane uomo, sportivo, con anamnesi familiare e patologica negativa per patologie cardiache, coinvolto in incidente stradale autonomo; la cui causa del decesso veniva inizialmente attribuita (sulla scorta della sola ispezione cadaverica effettuata dal medico del 118 intervenuto sul luogo) ai gravi effetti contusivi cerebrali connessi al trauma cranico. Il successivo esame autoptico, disposto dall’A.G., completato dagli esami di laboratorio, consentiva di individuare la sussistenza di una ampia sostituzione fibro-adiposa del miocardio del ventricolo destro, comprendete la porzione epicardica e gli strati intermedi della parete, in soggetto con riscontro positivo per alcool all’esame tossicologico di screening. Le risultanze del caso in questione confermano l’importanza delle indagini medico-legali quale presupposto fondamentale per la valutazione del nesso causale, anche talora al fine di avere contezza del determinismo dell’evento che ha avuto il suo epilogo nel decesso. Ne deriva, in definitiva, la rilevanza della disciplina medico legale, talora anche a scopo clinico-preventivo in relazione alla potenziale sussistenza di patologie sconosciute di carattere familiare.

Thoracic aorta shows with advancing age various changes and a progressive deterioration in structure and function. As a result, vascular remodeling (VR) and medial degeneration (MD) occur as pathological entities responsible principally for the sporadic TAA onset. Little is known about their genetic, molecular, and cellular mechanisms. Recent evidence is proposing the strong role of a chronic immune/inflammatory process in their evocation and progression. Thus, we evaluated the potential role of Toll like receptor- (TLR-) 4-mediated signaling pathway and its polymorphisms in sporadic TAA. Genetic, immunohistochemical, and biochemical analyses were assessed. Interestingly, the rs4986790 TLR4 polymorphism confers a higher susceptibility for sporadic TAA (OR=14.4,P=0.0008) and it represents, together with rs1799752 ACE, rs3918242 MMP-9, and rs2285053 MMP-2 SNPs, an independent sporadic TAA risk factor. In consistency with these data, a significant association was observed between their combined risk genotype and sporadic TAA. Cases bearing this risk genotype showed higher systemic inflammatory mediator levels, significant inflammatory/immune infiltrate, a typical MD phenotype, lower telomere length, and positive correlations with histopatological abnormalities, hypertension, smoking, and ageing. Thus, TLR4 pathway should seem to have a key role in sporadic TAA. It might represent a potential useful tool for preventing and monitoring sporadic TAA and developing personalized treatments.

The authors present a singular case of an iatrogenic right vertebral artery injury, involving a 67 year-old man, who reported a type II odontoid fracture (Anderson and D'Alonzo Classification) and posterior atlantoaxial dislocation following a road traffic accident. A small injury involving the right vertebral artery occurred as a consequence of transoral odontoidectomy and posterior cervical stabilization. It was caused by bone spicules of spinal origin and their presence was confirmed by the histological section of the right vertebral artery at the level of C1–C2. The case confirms how iatrogenic vertebral artery injuries during cervical spine surgery may be potentially lethal, especially where complications arise some days after surgery.

OBJECTIVES: Patients with chronic constipation due to food hypersensitivity (FH) had an elevated anal sphincter resting pressure. No studies have investigated a possible role of FH in anal fissures (AFs). We aimed to evaluate (1) the effectiveness of diet in curing AFs and to evaluate (2) the clinical effects of a double-blind placebo-controlled (DBPC) challenge, using cow's milk protein or wheat. METHODS: One hundred and sixty-one patients with AFs were randomized to receive a "true-elimination diet" or a "sham-elimination diet" for 8 weeks; both groups also received topical nifedipine and lidocaine. Sixty patients who were cured with the "true-elimination diet" underwent DBPC challenge in which cow's milk and wheat were used. RESULTS: At the end of the study, 69% of the "true-diet group" and 45% of the "sham-diet group" showed complete healing of AFs (P

Whipple Disease is a rare chronic multi-systemic disease caused by the ubiquitous environmental Gram-positive bacterium Tropheryma whipplei . It can be fatal if untreated. Here we describe the fatal outcome in a 27-year-old Caucasian female patient with a three-month history of persistent fever, anemia, weight loss and diarrhea. The final resolution of the diagnostic process was only reached after the patient’s death thanks to autopsy. The case depicted is a classic Whipple Disease histologically characterized by digestive involvement based on positive periodic acid-Schiff (PAS) staining and immunohistochemical analysis for T. whipplei and systemic involvement (pericarditis, brain lipid storage, renal fat embolism). The case reported here is of interest because the patient was a woman and also young, characteristics which do not meet the classical epidemiological features of this elusive and troubling disease.

Type A aortic dissection (TAAD) is a severe cardiovascular disease with high mortality rates. Current evidence suggests inflammation as the main mechanism of its complex pathophysiology. Accordingly, in this study the eventual presence of inflammatory cells in aorta specimens and any contribution of these cells in both apoptosis and metalloproteinase levels were assessed. The potential relationship between plasma inflammatory molecules and TAAD was also detected. In addition, implication in TAAD susceptibility of ten common and functional single nucleotide polymorphisms (SNP)s of six candidate genes (CCR5, TLR4, ACE, eNOs, MMP-9 and −2) was determined. Thus, histo-pathological and immunoistochemical aorta examination, TUNEL testing, genotyping of ten SNPs were performed. Levels of plasma inflammatory molecules were also determined using ELISA technique. A significant inflammatory infiltrate was observed in the examined aortas. Consistent with these data, significantly higher plasma levels of systemic inflammatory mediators characterized the cases. In addition, a high risk genotype significantly associated with TAAD susceptibility was identified. Thus, inflammation producing MMPs, cytokines and death mediators seem to be the shared pathological mechanism for TAAD in the population examined.

La sindrome da rivascolarizzazione (SR) comprende un insieme di eventi metabolici ed emodinamici che insorgono in un arto rivascolarizzato dopo un periodo più o meno lungo di ischemia, caratterizzata da specifiche manifestazioni cliniche sia a livello locale che sistemico. Riportiamo qui di seguito un caso di SR occorsa in una giovane donna di anni 20 con Sindrome di Turner e tiroidite autoimmune la quale veniva sottoposta ad intervento di giuntopieloplastica sinistra Robot assistita, poiché affetta da stenosi del medesimo giunto ed idronefrosi sinistra.

OBJECTIVES: The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim of this study was to identify the different mechanisms involved in TAA development in patients with BAV vs TAV. METHODS: Aorta specimens and DNA samples were collected from 24 BAV (18 men and 6 women; mean age: 54.2 ± 14.39 years) and 110 TAV (79 men and 31 women, mean age: 66 ± 9.8 years) patients. A control group of 128 subjects (61 men and 67 woman, mean age: 61.1 ± 5.8 years) was also enrolled. Histopathological and immunoistochemical analyses were performed, as well as genotyping of 10 polymorphisms. RESULTS: In BAV-associated ascending aortas, significant severe plurifocal apoptosis of smooth muscle cells and matrix metalloproteinase- 9 (MMP-9) amounts were detected. In contrast, TAV-associated ascending aortas were characterized by a significant severity of elastic fragmentation, cystic medial necrosis, medial fibrosis and inflammation. In addition, in BAV cases, the −1562TMMP-9 and −735TMMP-2 alleles represent independent risk factors for TAA. The effects of these genotypes combined with hypertension and smoking in BAV cases result in an increase in both the apoptosis (P = 0.0001) and levels of MMP-9 (P = 0.001). In TAV cases, the D angiotensin-converting enzyme and +896A Toll-like receptor-4 alleles seem to be the predictive factors for TAA risk. They, combined with hypertension and age, significantly increase both the microscopic lesions and inflammation. CONCLUSIONS: Our data seem to suggest that TAA in BAV and TAV patients arises from different molecular, cellular and genetic mechanisms. They might help to identify the potential molecular and genetic biomarkers that are useful to detect BAV subjects at high TAA risk, to monitor and treat them differently from those with TAV, with approaches such as the complete removal of the ascending aorta, including the aortic root with or without dilatation.

Objectives: We aimed to identify a phenotype of ascending thoracic aortic aneurysm (TAA), which, more than others, evolves into type A dissection (TAD). Methods: Aortic specimens were obtained from patients undergoing surgical repair of TAA and TAD (108 and 26, respectively). Histopathological and immunohistochemical analyses were performed by using adequate tissue specimens, appropriate techniques and criteria. Results: We identified the three following TAA phenotypes: phenotype I (cystic medial degeneration balanced by a substitutive fibrosis, in absence of medial apoptosis and with a faint collagenase concentration), phenotype II (cystic medial degeneration of higher grade, respectively, than substitutive fibrosis, with focal medial apoptosis and moderate collagenase concentration), and phenotype III (elevated cystic medial degeneration without substitutive fibrosis, with plurifocal medial apoptosis and severe collagenase concentration). The same medial degenerative lesions of TAA phenotype III were observed in TAD tissue samples. Conclusions: The morphological identity of medial lesions observed in both the TAA phenotype III and in TAD aortas might be assumed to be the precursor—and consequently the optimal biomarker— of dissection, independently of aneurysm diameter or valvular disorder. Identification of genetic risk factors, useful both in diagnostics and in developing more targeted treatment for individual patients, might also be needed.

OBJECTIVES: Aneurysm diameter and growing rate does not represent a definite parameter for operation in bicuspid aortic valve (BAV), ascending aortic aneurysm and normal root patients. Thus, we investigated histological and immunohistochemical aspects of different segments of ascending aorta (precisely, aortic root without dilatation, aneurysmatic tubular portion, dissected ascending aorta) and genetic features of patients with BAV and ascending aorta complication (aneurysm or dissection). METHODS: Aorta tissue samples of 24 BAV patients were examined. The patients comprised of 18 men and 6 women; the mean age was 54.2 ± 14.3 years. All patients underwent composite aortic root replacement (button Bentall operation). Multiple histological sections were prepared from each aortic specimen. The evaluated features included elastic fibre fragmentation, cystic medial change, smooth muscle cell necrosis, medial fibrosis, and the markers of medial apoptosis and the metalloproteinases. Furthermore, genetic risk factors were also investigated. RESULTS: The same medial degenerative lesions in tissue samples of different aorta segments (precisely of aortic root without dilatation, and aneurysmatic ascending aorta portion) were observed. More significant associations between single nucleotide polymorphisms (�786T/C endothelial nitric oxide synthase enzyme, D/I angiotensin-converting enzyme, �1562C/T metalloproteinase-9 and �735C/T metalloproteinase-2) and aneurysm risk were detected in BAV patients than in controls. CONCLUSIONS: Based on our histological and genetic data, we underline that a surgical approach in patients with BAV, ascending aortic aneurysm and normal root, should consider not only the diameter of the aneurysmatic aortic portion but also the histological features of the whole ascending aorta and the genetic risk profile.

Turner's syndrome is a genetic partial or complete monosomy of sexual chromosome X; therefore women affected by Turner's syndrome have 45 (XO) caryotype. In 15% of the cases Trner's syndrome is associated with cardiac congenital malformations, the most frequent anomalies are the aortic coartaction and the defect of interventricular septum. The authors introduce two cases of deceased women affected by Turner's syndrome caused by intrapericardic dissection of the ascending aorta.

Oral lichen planus (OLP) is an autoimmune disease with an inflammatory pathogenesis. The angiogenetic phenomenon is a mechanism at the base of the pathogenesis of chronic inflammatory processes. The aim of this research is to evaluate the angiogenetic phenomenon, comparing an in vitro method with an in vivo one. Thirty OLP patients and 30 healthy subjects were enrolled in the study. Immunohistochemical analysis of the vascular-endothelial growth factor (VEGF) and vascular-endothelial adhesion molecules were carried out by the means of primary antibodies and anti-CD34, anti-VEGF, anti-CD106 antigen (VCAM-1) and anti-CD54 antigen (ICAM-1). Capillary density and others capillaroscopic parameters were tested in vivo using oral videocapillaroscopy. The results reveal the presence of a significant angiogenesis in OLP patients through the immunoexpression of VEGF, CD34, CD106 and CD54 (p

Background: Eosinophilic granuloma (EG) is a clinical variant of the Langerhans cell histiocytosis (LCH) characterized by unifocal or multifocal bone lesions which predominantly affects children, adolescents, and young adults. Case Report: A case is reported of a 13-year-old Caucasian boy who presented unifocal EG in the mandible as the first clinic manifestation. Radiographic examination and skeletal scintigraphy revealed a further localization with an osteolytic lesion in the right femur. The therapeutic protocol used for the mandibular lesion included causal periodontal therapy, extraction of the compromised teeth, alveolar curettage, and intralesional injections of corticosteroids, in correspondence with femoral and mandibular bone lesions. Conclusions: Early diagnosis of LCH is considered an important factor which can improve the patient's prognosis and quality of life and also the cost-effectiveness of therapy. Dentists could play a fundamental role in the diagnosis and management of EG. The aim of the treatment is to eradicate EG lesions and provide adequate oral rehabilitation after the tooth loss. A careful multidisciplinary follow-up program is mandatory to identify any signs of local recurrence or dissemination.

BACKGROUND: The jejunal mucosa is the major site involved in celiac disease, but modifications have also been found in the gastric, rectal and esophageal mucosa. Few studies have focused on the histomorphological features of the oral mucosa in celiac disease patients. Our objectives were: (i) to assess the presence, quality and intensity of lymphocytic infiltrate in clinically healthy oral mucosa and its relation to celiac disease severity (villous height to crypt depth ratio); and (ii) to detect any other histological features connected to celiac disease. METHODS: Twenty-one untreated celiac disease patients (age range 13-68 years) with clinically healthy oral mucosa were enrolled and compared with 14 controls. Intestinal and oral biopsies were carried out and specimens were evaluated after staining with hematoxylin and eosin. RESULTS: Intra-epithelial lymphocyte B and T infiltrates of the oral mucosa were found to be similar in both groups; likewise, intensity of the lymphocytic infiltrate in the lamina propria was similar in both groups and was not related to intestinal damage; important signs of spongiosis were found to be more significantly present in celiac disease patients compared with controls (P = 0.0002). CONCLUSIONS: Our study showed that the healthy oral mucosa of untreated patients does not reflect the intestinal damage by celiac disease, but it is unexpectedly affected by spongiosis, as being detected for the first time in the literature. This latter feature could be related to gliadin ingestion and could contribute to explain the higher susceptibility of celiac disease patients to suffering from oral mucosa lesions.

Primary tumors of the heart in infants and children are rare. The types of heart tumors in pediatric age groups are generally different from those in adults. Cardiac myxoma is by far the most common tumor in adults, but in infants and adolescents the prevalent tumor of the heart is rhabdomyoma. Among benign cardiac tumors, cardiac hemangiomas are rare and often diagnosed post-mortem due to the lack of specific clinical symptoms and signs. We report a case of sudden death due to cardiac hemangioma in an apparently healthy 15-year-old adolescent. The autopsy revealed a cardiac hemangioma located at the apex of the heart; the histopathological examination showed the tumor was a mixed capillary and arteriolar hemangioma, a very rare type of primary tumor in adolescents.

Objective: Oral Lichen Planus (OLP) is a chronic inflammatory disease with an autoimmune inflammatory pathogenesis. The aim of the research is to compare the vascular endothelial growth factor (VEGF) and adhesion of molecules in the biopsy samples of patients affected by OLP, in order to research the presence of the angiogenetic phenomenon and to understand its pathogenetic mechanism. Materials and Methods: Thirty OLP patients and thirty healthy subjects were enrolled in a study. The immunohistochemical analysis of the VEGF and vascularendothelial adhesion molecules was carried out by means of primary antibodies and anti-CD34, anti-VEGF, antiCD106 antigen (VCAM-1) and anti-CD54 antigen (ICAM-1). The statistical significance of the differences was checked with the Mann-Whitney test (MW test). The level of significance was set to P

Summary Background Scalp reconstruction after wide tumor excision is particularly challenging. Free tissue transfers, local flaps, or skin grafts can be used but present some disadvantages especially with old patients with local advanced cancers, systemic diseases and in patients with a prior history of recurring scalp skin cancers in which the risk of burying a recurring tumor with a flap is likely. The Authors expose their early experience with Integra ® dermal regeneration template for scalp reconstruction after scalp tumor excision. Methods Eight patients with primary or secondary scalp tumor underwent a first surgical procedure under local anaesthesia for tumor removal and Integra ® positioning followed by a second operation performed three weeks later to reconstruct the defect by removing the superficial silicon layer of Integra ® and by covering the defect with a split thickness skin graft. The average surface area of the defect was 143.27 cm 2 . The average operating time was 30.4 minutes for the first operation and 45.6 minutes for the second operation. In six cases Integra ® was grafted as a classic full-thickness skin graft. In the remaining two cases the Integra ® template was meshed. The artificial derma was attached to the edge of the wound by either sutures or staples. Results There was a full graft take on all cases. The mean follow-up was 24 months. In two cases we were able to detect early tumor recurrence two months after the operation. Satisfactory cosmetic and functional results were obtained in all patients. Conclusions In the scalp defect reconstructions after tumor excision, Integra ® allows to obtain a thicker and more durable coverage than skin graft on the skull, allowing to detect a tumor recurrence earlier than a flap reconstruction with no risk of burying an eventual underlying residual tumor. These operations are performed under local anaesthesia and are therefore suitable for elderly patients.

Obiettivo: valutare le alterazioni dello sviluppo e della struttura dei villi conati di placente di gravidanze con ritardo di crescita fetale asimmetrico idiopatico (IUGR) tardivo. Pazienti e metodi: sono state esaminate 45 placente di pazienti con IUGR idiopatico con parto, per via vaginale o addominale, espletato dal gennaio 2001 al dicembre 2007. L’esame istologico è stato condotto secondo le linee guida del Gruppo Italiano di Anatomia Patologica. La diagnosi di IUGR è stata posta sulla base dell’evidenza clinica ed ultrasonica di ridotta crescita fetale e basso peso neonatale in associazione a riduzione del liquido amniotico e a placenta “matura” all’esame USG. Risultati: l’esame istologico ha evidenziato lesioni dello sviluppo e della struttura dei villi tipici della ipoperfusione cronica placentare così definite: maturazione accelerata dei villi (ipermaturità villare), villite ischemica (equivalente a microinfarti) ed infarti. In 10 casi, insieme a tali lesioni, ne e stata identificata un ‘altra, definita “ipercapilla-rizzazione dei villi”, che si associa ad una condizione dÏ ipossia relativa del sangue materno che circola tra i villi. Conclusioni: il ritardo di crescita intrauterino asimmetrico idiopatico può essere ricondotto ad alterazioni dell’angiogenesi e vasculogenesi che avvengono nelle fasi iniziali della gravidanza. Ciò determina una condizione di ipossia placentare con alterazioni dello sviluppo dei villi tipici della ipoperfusione cronica placentare. Objective: to evaluate the structural and developmental abnormalities of villous tissue coming from placentas of fetuses with IUGR. Patients and methods: placental examination of 45 patients with idiopathic IUGR was carried out in accordance with the guidelines of the "Gruppo Italiano di Anatomia Patologica". The diagnosis of IUGR was made on the basis of fetal growth restriction, amniotic fluid reduction and placental US imaging. Results: the placental microscopic examination showed villous alterations tipical of chronic placental ipoperfusion: ischemic villitis, accelerated villous maturity and placental infarctions. There was evidence of enhanced villous capillarization maybe due to a relative hypoxia of maternal intervillous circulating blood in ten placentas. Conclusion: asymmetric idiopathic IUGR seems to be correlated with alterations of angiogenesis in the initial pregnancy steps with resulting chronic placental ipoperfusion in late pregnancy.

Eosinophilic granuloma is a proliferation of Langerhans cells in the bones that most commonly involving the skeletal system. The disease generally affects children or young adults with predominance in males and it is characterized by a single or multiple skeletal lesions. This study describes a few cases of mandibular Eosinophilic Granuloma and the effects of surgical curettage of lesions

In a retrospective investigation performed in the department of Surgical Odontostomatology of Palermo University Polyclinic from 1997-2006, the authors examined 12 cases of cervico-facial actinomycosis, taking into consideration age range, gender distribution, predisposing factors and symptoms. In concordance with reports in literature, they found that the disease was perimandibular in 65%, they also report the diagnostic methods and therapeutic approaches used in the study

Gli Autori presentano il caso di una donna giunta alla 39,4 settimana di gestazione, regolarmente sottoposta ad esami clinici e strumentali che evidenziavano un decorso regolare della gravidanza eccetto oligoamnios. La paziente espletava il parto con feto nato vivo ma non vitale. L'esame esterno del cadavere evidenziava esclusivamente cianosi generalizzata. L'esame autoptico ha evidenziato cardiomegalia con incremento di tutte le cavità cardiache con rapporto cardio-toracico 6.5/8.5 ed un aspetto porcellanaceo delle pareti ventricolari di sinistra. All'istologia tale ispessimento era causato da fibroelastosi diffusa dell'endocardio associata a marcata miocitolisi colliquativa del miocardio subendocardico. Si sottolineano gli emergenti possibili profili di responsabilità inerenti l'errore nella diagnosi pre-natale e nell'approccio terapeutico nella fase immediatamente successiva al parto.