Introduction: The rapid development of perinatal gynecology requires from the anatomists comprehensive studies of the patterns of prenatal morphogenesis and the development of topographic and anatomical relationships of female reproductive organs in the human fetuses of different age groups. The aim: To study the development and formation of the vaginal topography in the prenatal period of human ontogenesis. Materials and methods: The study has been conducted based on 23 series of histological and topographic-anatomical sections of human prefetuses aged 9-12 weeks with 31.0-80.0 mm of crown-rump length (CRL) and 83 specimens of female human fetuses aged 4-9 months with 81.0-345.0 mm of CRL by means of a complex of adequate morphological methods of investigation. Results and conclusions: Vaginal formation occurs during the 9th week of embryogenesis (prefetuses of 31.0-41.0 mm of CRL) due to the fusion of two different embryonic structures: mesodermal paramesonephral ducts and endodermal urogenital sinus. In this case, the caudal regions of the paramesonephral ducts are transformed into the uterus and the superior two thirds of the vagina, and the inferior third of the vagina develops from the urogenital sinus. Common uterovaginal canal, divided into right and left cavities by mesenchymal septum, is formed in the female prefetuses of 38.0-43.0 mm of CRL due to the fusion of the caudal regions of the paramesonephral ducts in the area of the posterior wall of the urogenital sinus. Complete dissolving of the septum of the uterovaginal canal occurs in prefetuses of 55.0-58.0 mm of CRL. The anterior and posterior vaginal vaults of the same depth are formed in 5-month-old fetuses. Canalization of vagina in the caudo-cranial direction is observed in the fetuses of 170.0-185.0 mm of CRL, with no clear boundary between the uterovaginal canal and the urogenital sinus. The vaginal epithelium in the upper third part originates from the uterovaginal canal, and in the lower two thirds of the vagina – from the urogenital sinus. In the 6-month-old fetuses there was detected the variability of the shape of the superior, middle and inferior third of the vagina, namely: oval (5 cases), elongated-oval (2 cases), stellate (1 case); in the lower third, the H-shaped form was predominantly found (6 fetuses). The proliferation of the hymen membrane occurs in fetuses of 220.0-245.0 mm of CRL. The absence of timely proliferation of the hymen membrane can lead to its atresia, and its premature proliferation causes the appearance of transverse vaginal septa.
Annually severe congenital abnormalities occur in 1 of 33 newborns or about 125.000 live births in the United States and are the leading cause of infant mortality. Craniofacial anomalies account for about one-third of all abnormalities. The prevalence of human congenital malformations is an important characteristic of public health. According to the World Health Organization, the birth rate of children with cleft lip and palate is on average 1:750 newborns, which is 20-30% of all human malformations and 86% of maxillofacial malformations. They contribute significantly to infant morbidity and disability as well as millions of dollars in health care costs each year. Development of the human skull begins about 23-26 days after fertilization, when a multipotent population of cranial neural crest cells migrates from the dorsal part of the neuraxis to the embryonic head region, giving rise to the frontal bone and interparietal part of the occipital bone, while the rest of the cranial arch comes mainly from the mesoderm. A malformation is a deviation from the normal development of an organ or tissue. Among the causes are chromosomal abnormalities, single gene defects, teratogenic or multi-factor agents, that is, a combination of genetic and external factors; the smallest number of cases are idiopathic. Exogenous causes of human congenital abnormalities include: physical (mechanical, thermal, radiation); chemical (hypoxia, malnutrition, hormonal discordance, teratogenic poisons); biological (viruses, bacteria and their toxins, protozoa); mental factors. Endogenous causes are heredity (changes in hereditary structures, mutations); biological inadequacy of germ cells (endocrine disorders, “over-ripening” of germ cells); parents’ age. Congenital craniofacial abnormalities are caused by improper growth and/or development of the brain and facial parts of the skull and soft tissue. Craniofacial abnormalities affecting the skull include macrocephaly, microcephaly and unilateral deformities. Sometimes cranial sutures fuse too early and craniosynostosis occurs, which is accompanied by various cranial deformities. This leads to abnormal cranial development, which can cause dysmorphia, and in the most severe cases catastrophically affect brain development. Conclusion. Based on the analysis of the literature sources, an attempt has been made to summarize the existing information and classifications of congenital cranial abnormalities, as well as the interpretation of various anomalies of the brain and facial skull in alphabetic order. The most common stigmas and malformations of the skull bones are briefly characterized
Congenital abnormalities occur in 2-3% of all children and about 1% have hereditary syndromes or multiple malformations. About 30% of all cases have a cleft lip or palate. Genetic factors such as chromosomal abnormalities and gene mutations cause about 15% of congenital abnormalities; exogenous environmental factors cause about 10% of defects; a combination of genetic and environmental factors (multifactorial inheritance) cause 20-25%; multiple pregnancy causes 0.5-1% of congenital abnormalities. Craniofacial anomalies represent an important pediatric problem. They are among the leading causes of infant mortality and morbidity. Craniofacial anomalies mainly affect the development of the skull and facial bones. These defects range from mild to severe, which can be life-threatening and require immediate surgical intervention. Examination of patients with congenital cranial pathology is of particular importance, since a correct diagnosis can often be established only by taking into consideration all stigmas and malformations. The onset of pathology occurs during ontogenesis: normal embryonic development is disturbed under the influence of exogenous and endogenous factors, to which the body is particularly sensitive during critical periods. The consequences of various endogenous and exogenous factors are disruption of growth and development of the organism and occurrence of congenital malformations as an independent unit or occurrence of hereditary syndromes as a set of certain symptoms. Craniofacial syndromes can be divided into several groups. They are most often accompanied by premature fusion of cranial sutures (craniosynostosis) and syndromes with cleft formation. The most frequent syndromes in this group are: Crouzon syndrome, suture synostosis, microsomia, cerebral anomalies and midface clefts. These developmental disorders can lead to a variety of health consequences, namely affecting these patients’ respiratory health, appearance, brain development, hearing, vision, bite, speech, and mental development. Congenital malformations of the skull bones can be related to genetic mutations and environmental factors. Conclusion. Based on the analysis of the literature, a brief clinical characterization of the most common hereditary syndromes accompanied by cerebral and facial skull deformities is given, the type of inheritance and the gene mutation that causes these disorders are indicated
Anatomie foetale aberrante de la veine grande saphèneIntroduction. Le matériel factuel accumulé sur la topographie de la veine grande saphène est extrêmement controversé. Par conséquent, une approche individuelle de l'étude de la variabilité anatomique liée à l'âge de la veine grande saphène chez les foetus humains est nécessaire. Le but de l'étude est de découvrir les caractéristiques de la topographie de la veine grande saphène chez les foetus humains âgé de 4-10 mois. Matériel et méthodes. L'étude de l'anatomie variante de la veine grande saphène a été réalisée sur les préparations des extrémités inférieures de 80 foetus humains à longueur pariétale-coccygienne de 81,0-375,0 mm,par préparation macro-microscopique, injection de vaisseaux, coloration superficielle des vaisseaux et des nerfs préparés, radiographie morphométrie. Résultats. Dans les foetus humains étudiés, la grande veine saphène est une continuation de la veine marginale médiale qui court vers le haut dans le tissu sous-cutané le long de la marge antérieure de la malléole mediale. Sur le tibia, la veine grande saphène s'étend le long de la marge médiale du tibia et reçoit des veines superficielles de la surface antérieure médiale du tibia.
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