Histološka procena odgovora odontoblastima-sličnih ćelija nakon direktnog prekrivanja pulpe pasa kalcijum hidroksidom i hidroksilapatitom

This study was conducted to observe the response of dog's dental pulp to hydrpxylapatite (Hap) and calcium hydroxide when used as pulp capping materials. After the pulps of 22 teeth were exposed, they were capped with either Hap or calcium hydroxide. Histological analysis was performed 8 weeks after treatment. Results showed that pulp exposure caused irreversible injury of odontoblasts, which were subsequently replaced by similar, odontoblast-like cells. These cells were able for reparative dentin bridge formation in 6 cases treated with calcium hydroxide and almost all the cases treated with hydroxylapatite. The presence of odontoblast-like cells seemed to be crucial for reparative dentinogenesis. The capping material was of less importance. In conclusion neither calcium hydroxide nor hydrxylapatite had completely satisfied all the requirements of an ideal capping material, although Hap can be recognized as a superior alternative to calcium hydroxide.Cilj ovog rada je bio ispitivanje odgovora zubne pulpe pasa nakon njenog direktnog prekrivanja hidroksilapatitom (Hap) ili kalcijum hidroksidom. U eksperimentu su korišćena 22 zuba kod kojih je nakon arteficijelnog otvaranja, zubna pulpa prekrivana Hap-om ili kalcijum-hidroksidom. Osam nedelja nakon prekrivanja, urađena je histološka analiza. Dobijeni rezultati su ukazali da je tokom arteficijelnog otvaranja pulpe došlo do ireverzibilnog oštećenja odontoblasta i njihove zamene ćelijama sličnim odontoblastima. Odontoblastima-slične ćelije stvorile su mostić reparativnog dentina u 6 uzoraka iz grupe tretirane kalcijum hidroksidom i skoro svim uzorcima tretiranih Hap-om. Uočeno je da je prisustvo odontoblastima- sličnih ćelija presudno za uspeh reparativne dentinogeneze, dok je vrsta korišćenog materijala za direktno prekrivanje, bila od manje važnosti. Pri tome ni hidroksilapatit ni kalcijum hidroksid ne zadovoljavaju sve zahteve koji se postavljaju pred idealne materijale za direktno punjenje. Hap ipak predstavlja superiorniju alternativu u odnosu na kalcijum hidroksid

Recent views on cytohistological characteristics and pathogenic mechanisms of atherosclerotic lesions types I, II and III

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Malignancy-related hyponatremia: Case report

Hiponatrijemija je čest elektrolitski poremećaj kod hospitalizovanih bolesnika. Nakon potvrđivanja laboratorijskog nalaza, potrebno je pojavu hiponatrijemiju etiološki razjasniti. Prikaz bolesnika: Bolesnica stara 56 godina, hospitalizovana je zbog evaluacije grčeva nogu i malaksalosti. U biohemijskim nalazima se registruje hipotona hiponatrijemija, te je posumnjano na SIADH (engl. Syndrome of Inappropriate Antidiuretic Hormone Secretion). Evaluacijom SIADH-a, nije nađen uzrok hiponatrijemije. Primenom simptomatske terapije i korekcijom hiponatrijemije, pacijentkinja je otpuštena lako poboljšana. Četiri meseca nakon hospitalizacije, javlja se konfuzna, sa gušenjem, sindromom hiperglikemije i teškim opštem stanjem. Pored toga, kod pacijentkinjw su laboratorijski potvrđene hipotone hiponatrijemije, ultrasonografijom abdomena su viđene metastatske promene na jetri. Ubrzo nakon prijema, dolazi do smrtnog ishoda. Rodbina je odbila obdukciju, te primarno ishodište malignoma nije utrvđeno. Hipotona hiponatrijemija zahteva ozbiljnu kliničku evaluaciju. SIADH je najčešći uzrok hipotone hiponatrijemije, a najvažniji uzrok SIADH-a je maligna bolest. Pažljiva korekcija hiponatrijemije i lečenje osnovne bolesti je osnova lečenja SIADH-a.Hyponatremia is a common electrolyte disorder in hospitalized patients. In the case of repetitive biochemically confirmed hyponatremia, it is necessary to find its cause. Case report: a 56-year-old woman was admitted to hospital due to leg cramps and malaise. Routine biochemical analysis revealed hypotonic hyponatremia and Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) was suspected. The cause of hyponatremia was not discovered by means of evaluating SIADH. The patient was simptomatically treated, and discharged in better general condition, with partially corrected hyponatremia. She was advised to restrict water intake and to repeat serum electrolytes and BUN regularly. Four months later, she presented with dyspnea and hyperglycemic syndrome, she was confused and her life was threatened. Beside severe hyponatremia and hyperglycemia, an urgent abdominal ultrasonography showed liver secondaries. Shortly after admission, the patient passed away. Unfortunately, the patient's family refused an autopsy, so the origin of neoplasia has remained unknown. It is necessary to do a thorough clinical evaluation of hypotonic hyponatremia. SIADH, as the most frequent cause of hypotonic hyponatremia, is often a paraneoplastic syndrome. Careful correction of hypotonic hyponatremia and management of the underlying disease is the mainstay of SIADH treatment

The team management of patient suffered of acute severe dyslipidaemic pancreatitis: The experience of one tertiary health centre

U okviru ovog rada prikazan je slučaj bolesnika sa komplikovanim akutnim dislipidemijskim pankreatitisom u čijem je zbrinjavanju učestvovao tim, koji su činili endokrinolozi, gastroenterolozi i transfuziolozi. Dislipidemija, prevashodno tip IV dislipidemije, predstavlja čest uzrok nastanka akutnog pankreatitisa u populaciji mladih ljudi, posebno u slučajevima nezadovoljavajuće komplijanse (neredovno uzimanje preporučenih fibrata i nepridržavanje higijensko-dijetetskog režima). Tretman akutnog pankreatitisa se nezavisno od etiologije, zbog težine stanja, kompleksnosti lečenja i monitoringa bolesnika, sprovodi u Jedinicama intenzivnog lečenja. U slučajevima kada je dislipidemija uzrok akutnog pankreatitisa, često se u sklopu akutnog zbrinjavanja sprovodi i terapijska izmena plazme, kojom se brzo i značajno koriguju nivoi lipida, prevashodno triglicerida. Terapijska izmena plazme zahteva aktivnost transfuzioloških ekipa, koje su u manjim centrima, često nedostupne.This article presents a case of patient with acute and complicated dyslipidaemic pancreatitis, managed by team, consisted of the endocrinologists, gastroenterologists and transfusiologists. Dyslipidaemia, predominantly type IV, is a common cause of acute pancreatitis in young patients, especially in the cases of poor compliance (irregular taking of recommended fibrates and failure to comply with the dietary regime). The treatment of acute pancreatitis, regardless of the aetiology, is due to the severity of the condition, the complexity of the treatment, and the monitoring of patients, in the Intensive Care Units. In cases where dyslipidaemia is the cause of acute pancreatitis, in the context of acute care, a therapeutic plasma exchange is often performed. It rapidly and significantly corrects lipid levels, primarily triglycerides. Therapeutic plasma exchange requires the activity of transfusiology team, which are often unavailable in smaller hospitals

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

Introduction. Fast and precise diagnostics of the disease from the large group of adult leukoencephalopathy is difficult but responsible job, because the outcome of the disease is very often determined by its name. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by the mutation of Notch 3 gene on chromosome locus 19p13. Beside the brain arterioles being the main disease targets, extracerebral small blood vessels are affected by the pathological process. Clinically present signs are recurrent ischemic strokes and vascular dementia. CADASIL in its progressive form shows a distinctive pattern of pathological changes on MRI of endocranium. The diagnosis is confirmed by the presence of granular osmiophilic material (GOM) in histopathological skin biopsies. Case reports. Two young adult patients manifested ischemic strokes of unknown etiology, cognitive deterioration, migraine and psychopathological phenomenology. MRI of endocranium pointed on CADASIL. Ultrastructural examination of skin biopsy proved the presence of GOM in the basal lamina and near smooth muscle cells of arteriole dermis leading to CADASIL diagnosis. The presence of GOM in histopathological preparation is 100% specific for CADASIL. The patients were not searched for mutation in Notch 3 gene on chromosome 19, because some other leukoencephalopathy was disregarded. Conclusion. Suggestive clinical picture, distinctive finding of endocranium MRI, the presence of GOM by ultrastructural examination of histopathological skin biopsies are sufficient to confirm CADASIL diagnosis

Ultrastructural analysis of small blood vessels in skin biopsies in CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited small- and medium-artery disease of the brain caused by mutation of the Notch3 gene. Very often, this disease is misdiagnosed. We examined skin biopsies in two members of the first discovered Serbian family affected by CADASIL. Electron microscopy showed that skin blood vessels of both patients contain numerous deposits of granular osmiophilic material (GOM) around vascular smooth muscle cells (VSMCs). We observed degeneration of VSMCs, reorganization of their cytoskeleton and dense bodies, disruption of myoendothelial contacts, and apoptosis. Our results suggest that the presence of GOM in small skin arteries represents a specific marker in diagnosis of CADASIL

Ultrastructural analysis of small blood vessels in skin biopsies in CADASIL

Abstract — Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited small- and medium-artery disease of the brain caused by mutation of the Notch3 gene. Very often, this disease is misdiagnosed. We examined skin biopsies in two members of the first discovered Serbian family affected by CADASIL. Electron microscopy showed that skin blood vessels of both patients contain numerous deposits of granular osmiophilic material (GOM) around vascular smooth muscle cells (VSMCs). We observed degeneration of VSMCs, reorganization of their cytoskeleton and dense bodies, disruption of myoendothelial contacts, and apoptosis. Our results suggest that the presence of GOM in small skin arteries represents a specific marker in diagnosis of CADASIL

Mitotic activity of smooth muscle cells of the myoma: Does hormonal stimulation have an effect on the number of mitoses?

Myomas develop as a result of increased mitotic (proliferating) activity of smooth muscle cells. In this study we examined the pathohistological samples of 176 myomas and their endometria that were obtained after hysterectomy from patients in the proliferative (follicular) and secretory (luteal) phase of the menstrual cycle. We examined the mitotic activity of the myoma cells in both phases and established that the average number of mitoses in the proliferative phase was significantly larger compared to the secretory phase, and that in the proliferative phase of the cycle there exists a statistically significant convergent association of the number of mitoses in the endometrium and in myomas. The number of endometrial mitoses is significantly larger than in myomas in both phases of the cycle

Mitochondrial myopathy, encephalopathy, lactate acidosis with stroke-like episodes syndrome (MELAS): A case report

Introduction. Mitochondrial encephalopathy, lactacidosis and stroke-like episodes (MELAS) represent a multisystemic dysfunction due to various mutations in mitochondrial DNA. Here we report a patient with genetically confirmed MELAS. Case Outline. A patient is presented whose clinical features involved short stature, easy tendency to fatigue, recurrent seizures, progressive cognitive decline, myopathy, sensorineural deafness, diabetes mellitus as well as stroke-like episodes. The major clinical feature of migraine type headache was not present. Neuroimaging studies revealed signs of ischemic infarctions localized in the posterior regions of the brain cortex. Electron microscopy of the skeletal muscle biopsy showed subsarcolemmal accumulation of a large number of mitochondria with paracristal inclusions in the skeletal muscle cells. The diagnosis of MELAS was definitively confirmed by the detection of a specific point mutation A to G at nucleotide position 3243 of mitochondrial DNA. Conclusion. When a relatively young patient without common risk factors for ischemic stroke presents with signs of occipitally localized brain infarctions accompanied with multisystemic dysfunction, MELAS syndrome, it is necessary to conduct investigations in order to diagnose the disease