25 research outputs found

    Morphological and immunohistochemical characteristics of human trigeminal ganglion neurons in the prenatal period of development

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    Introduction: Data related to the amount, size and morphological characteristics of cell elements of sensory ganglia at different stages of prenatal development has not been fully elucidated in recent scientific publications. At the same time publications considering the study of cell structure of trigeminal ganglion in the postnatal period confirm heterogeneity of its neurons. The aim of the research was to study morphological and immunohistochemical characteristics of human trigeminal ganglion neurons at 12-14 weeks of prenatal development. Material and Methods: The study was made on 24 trigeminal ganglions of 12 human fetuses at 12 to 14 weeks of prenatal development after abortion made on social and medical indications. Results: At the studied period of the intrauterine development nerve cells of the trigeminal ganglion significantly differed in size, tinctorial properties and degree of argentophility of the perikaryon. At the same time, the number of small nerve cells with an average diameter of less than 15 pm prevailed. Immunohistochemical study allowed detecting the apparent Bd-2 expression in the overwhelming number of small neurons; the expression of this marker has been observed in 50% of cells of the medium-sized neurons. No Bd-2 expression has been found in most of the large neurons. Almost all the neurons, regardless of the size, showed moderate Ki-67 expression, protein S-100. VEGF expression has also occurred in the vast majority of the nerve cells of all size groups. Conclusions: 1. Human trigeminal ganglion neurons both at 12-14 weeks of prenatal development and in postnatal period are represented by heterogeneous population. 2. Polymorphism of trigeminal ganglion neurons has been found by all applied techniques. 3. Detected polymorphism is the evidence of processes of maturation and differentiation of neurons in human trigeminal ganglion at 12-14 weeks of prenatal developmen

    Clinical manifestations of sarcoidosis on the prolabium and oral mucosa: management

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    Останніми десятиліттями спостерігається неухильне зростання захворюваності на саркоїдоз. Особливе значення має той факт, що уражує ця патологія людей молодого і середнього віку. Для встановлення правильного діагнозу при рідкісних хворобах стоматолог мусить мати високий професійний рівень, використовувати міждисциплінарний підхід у діагностиці та веденні пацієнтів із цією патологією; В последние десятилетия наблюдается неуклонный рост заболеваемости саркоидозом. Особое значение имеет тот факт, что поражает эта патология людей молодого и среднего возраста. Для установления правильного диагноза при редких болезнях стоматолог должен иметь высокий профессиональный уровень, использовать междисциплинарный подход в диагностике и ведении пациентов с данной патологией; The statistics indicates on the tendency of morbidity rate of sarcoidosis to increase. The pathology affects young and older people notably. Sarcoidosis becomes a common chronic disease, which is often difficult to diagnose. Insufficient experience in recognition of this disease leads to misdiagnosis and ineffective treatment. All mentioned above highlights the extreme relevance of this issue. Sarcoidosis is a multisystem inflammatory nature disease of unknown etiology. The hereditary predisposition is taken to be but the whole family cases are also known. An abnormal immune response is also considered among the theories of the development of the disease. The infectious factor is also regarded as the cause of the disease. The increasing activity of lymphocytes, which start to produce substances promoting the formation of the granulomas, which are considered to be the basis for the pathological process, can initiate the onset of the disease. The maximum morbidity rate of sarcoidosis is observed between the ages of 35 to 55 years. Two age periods of the peak in male population are 35-40 years and about 55 years. The rate of sarcoidosis morbidity among female population is 65%. Up to 700 new cases of sarcoidosis are registered in Ukraine annually. The clinical signs of sarcoidosis vary. This pathology is more often manifested by the bilateral lymphadenopathy of lung roots, eyes and skin lesions. The liver, spleen, lymph nodes, heart, nervous system, muscles, bones and other organs can also be affected. In dental practice sarcoidosis can be manifested on the prolabium, oral mucosa and salivary glands. Blood laboratory indices (the increased level of calcium) are changed in sarcoidosis. Chest X-ray, MRI and CT also demonstrate changes in the lungs. The test for detection of granulomas shows positive Kveim reaction (the formation of purple-red nodules due to administration of antigen). Biopsy and bronchoscopy facilitate detection of both direct and indirect signs of sarcoidosis of the lungs. A general treatment of sarcoidosis is provided by a pulmonologist, who can assess the severity of the lesion and provide appropriate treatment. The core of treatment is based on corticosteroids. In severe cases immunosuppressors, antiinflammatory drugs, antioxidants are prescribed. A dentist performs oral cavity sanation, professional hygiene. Mouth rinses with Dekasan solution, sublingual Lisobakt pills are prescribed to prevent inflammatory lesions. Patients with sarcoidosis are recommended to avoid solar radiation and contact with chemical and toxic substances harmful to the liver, reduction of the consumption of foods rich in calcium. Healthy life-style is crucial in prevention of exacerbations of sarcoidosis. In the remission period regular medical check-ups and oral cavity sanation are recommended. The correct diagnosis in rare diseases requires highly qualified dental professionals, the interdisciplinary approach in the diagnosing and management of patients with this patholog

    Characteristics of trigeminal ganglion capsule structure in human embryogenesis

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    В работе проведено изучение структурной организации капсулы тройничного узла человека на 14-21 неделях внутриутробного развития на основании гистотопографических шлифов. Установлено, что в изучаемый период эмбриогенеза капсула тройничного узла человека образована сращением периневрия ствола тройничного нерва и листков твёрдой оболочки головного мозга. В составе капсулы определяется два слоя - внутренний и наружный, отличающиеся плотностью компоновки клеточных и фибриллярных структур. На протяжении изучаемого периода происходит увеличение толщины капсулы тройничного узла, структурная организация её принципиально не изменяется; В роботі проведено вивчення структурної організації капсули трійчастого вузла людини 14-21 неділях внутрішньоутробного розвитку на основі гістотопографічних шліфів. Встановлено, що в досліджуваний період ембріогенезу капсула трійчастого вузла людини створюється шляхом зрощення періневрія ствола трійчастого нерва і листків твердої оболонки головного мозку. В складі капсули визначається два шари - внутрішній і зовнішній, які відрізняються щільністю компоновки клітинних і фібрілярних структур. Протягом досліджуваного періоду відбувається збільшення товщини капсули трійчастого вузла, структурна організація її принципово не міняється; This paper presents the study of the structure of trigeminal ganglion capsule in human fetus on the 14th-21 st weeks of gestation. The study is based on the analysis of histotopographic sections. It has been found out the capsule of trigeminal ganglion in human fetus is formed by the fusion of perineurium of trigeminal nerve trunk .and leaves of dura mater of brain. The walls of the capsule are composed of two layers: internal and external. They dіffer by the density of composition in the cellular and fibrillary structures. Within the period mentioned above we have noticed the thickening of the trigeminal ganglion capsule, while its structure is mainly unchanged

    Parameters for evaluating the main indicators of coloproctological care in the adult population in the subjects of the far Eastern Federal District in 2016–2018

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    Aim. To work out the unified model for description of coloproctological service at the level of federal district.Material and methods. The study is the summary analysis of data from the annual statistical observation “The Report of the Chief Coloproctologist of the Russian Federal District” in 2016–2018. The analysis included the following stages: the estimation of staff situation; the assessment of the main parameters of out- and inpatient coloproctological care in 2018 in the Far Eastern Federal District (FEFD) and in its federal subjects.Results. Staff number of doctors in federal subjects of the FEFD did not change significantly in 2016-2018, it was 0.7 per 100 thousand population. An extremely low availability of outpatient consultation of coloproctologist in all federal subjects of FEFD was found (550.2 per 100 thousand population vs 3000 per 100 thousand population in Russian Federation). The incidence of colonoscopy is the lowest among all Federal Districts of Russia as well – 5.5%. A mean number of endoscopists is above 7.0 per 100 thousand population, which can be considered as the minimal threshold parameter. The total average staffing of endoscopists in the far Eastern Federal district was 86.0% in 2016, 87.3% – in 2017, 85.8% – in 2018. The staffing situation improved in Khabarovsk Territory and in Sakhalin Region while other federal subjects showed negative trend.Conclusion. The analyzed parameters can be considered as an objective tool for the assessment of coloproctological care efficacy. In the FEFD it needs further development

    Central Mechanisms Mediating Thrombospondin-4-induced Pain States

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    Peripheral nerve injury induces increased expression of thrombospondin-4 (TSP4) in spinal cord and dorsal root ganglia that contributes to neuropathic pain states through unknown mechanisms. Here, we test the hypothesis that TSP4 activates its receptor, the voltage-gated calcium channel Ca-v alpha(2)delta(1) subunit (Ca-v alpha(2)delta(1)), on sensory afferent terminals in dorsal spinal cord to promote excitatory synaptogenesis and central sensitization that contribute to neuropathic pain states. We show that there is a direct molecular interaction between TSP4 and Ca-v alpha(2)delta(1) in the spinal cord in vivo and that TSP4/Ca-v alpha(2)delta(1)-dependent processes lead to increased behavioral sensitivities to stimuli. In dorsal spinal cord, TSP4/Ca-v alpha(2)delta(1)-dependent processes lead to increased frequency of miniature and amplitude of evoked excitatory post-synaptic currents in second-order neurons as well as increased VGlut(2)- and PSD95-positive puncta, indicative of increased excitatory synapses. Blockade of TSP4/Ca-v alpha(2)delta(1)-dependent processes with Ca-v alpha(2)delta(1) ligand gabapentin or genetic Ca-v alpha(2)delta(1) knockdown blocks TSP4 induced nociception and its pathological correlates. Conversely, TSP4 antibodies or genetic ablation blocks nociception and changes in synaptic transmission in mice overexpressing Ca-v alpha(2)delta(1). Importantly, TSP4/Ca-v alpha(2)delta(1)-dependent processes also lead to similar behavioral and pathological changes in a neuropathic pain model of peripheral nerve injury. Thus, a TSP4/Ca-v alpha(2)delta(1)-dependent pathway activated by TSP4 or peripheral nerve injury promotes exaggerated presynaptic excitatory input and evoked sensory neuron hyperexcitability and excitatory synaptogenesis, which together lead to central sensitization and pain state development

    Central Mechanisms Mediating Thrombospondin-4-induced Pain States.

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    Peripheral nerve injury induces increased expression of thrombospondin-4 (TSP4) in spinal cord and dorsal root ganglia that contributes to neuropathic pain states through unknown mechanisms. Here, we test the hypothesis that TSP4 activates its receptor, the voltage-gated calcium channel Cavα2δ1 subunit (Cavα2δ1), on sensory afferent terminals in dorsal spinal cord to promote excitatory synaptogenesis and central sensitization that contribute to neuropathic pain states. We show that there is a direct molecular interaction between TSP4 and Cavα2δ1 in the spinal cord in vivo and that TSP4/Cavα2δ1-dependent processes lead to increased behavioral sensitivities to stimuli. In dorsal spinal cord, TSP4/Cavα2δ1-dependent processes lead to increased frequency of miniature and amplitude of evoked excitatory post-synaptic currents in second-order neurons as well as increased VGlut2- and PSD95-positive puncta, indicative of increased excitatory synapses. Blockade of TSP4/Cavα2δ1-dependent processes with Cavα2δ1 ligand gabapentin or genetic Cavα2δ1 knockdown blocks TSP4 induced nociception and its pathological correlates. Conversely, TSP4 antibodies or genetic ablation blocks nociception and changes in synaptic transmission in mice overexpressing Cavα2δ1 Importantly, TSP4/Cavα2δ1-dependent processes also lead to similar behavioral and pathological changes in a neuropathic pain model of peripheral nerve injury. Thus, a TSP4/Cavα2δ1-dependent pathway activated by TSP4 or peripheral nerve injury promotes exaggerated presynaptic excitatory input and evoked sensory neuron hyperexcitability and excitatory synaptogenesis, which together lead to central sensitization and pain state development
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