Normal and abnormal development of the anorectum

Putte, S. C. J. van der

doi:10.1016/s0022-3468(86)80515-2

Cited by 206 publications

(122 citation statements)

References 16 publications

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“…Many authors have mentioned that a shift of the dorsal cloaca or rectum is necessary to establish the anorectal canal (Bill and Johnson, 1958;Gans and Friedman, 1961;Van der Putte and Neeteson, 1983;Van der Putte, 1986). In the present study, from E11.5 to E12.5, ventral shift of the dorsal cloaca was observed.…”

Section: Observation Of Normal Cloacal Developmentsupporting

confidence: 57%

“…In contrast, Politzer (1931) had already rejected the separation into anal and urogenital membranes. Many authors later reported that the urorectal septum does not actively descend in the direction of the cloacal membrane, and neither fusion of this septum with the membrane nor fusion of two lateral ridges of the cloacal wall occur (Van der Putte and Neeteson, 1983;Van der Putte, 1986;Kluth et al, 1995;Nievelstein et al, 1998;Paidas et al, 1999).…”

Section: Observation Of Normal Cloacal Developmentmentioning

confidence: 99%

“…The most debated point is whether fusion of the urorectal septum with the cloacal membrane occurs in normal development (Keibel, 1895;Pohlman, 1911;Politzer, 1931;De Vries andFriedland, 1974a, 1974b;Van der Putte and Neeteson, 1983;Van der Putte, 1986;Stephens and Smith, 1988;Kluth et al, 1995;Miller and Briglin, 1996;Nievelstein et al, 1998;Kromer, 1999;Paidas et al, 1999;Qi et al, 2000aQi et al, , 2000bQi et al, , 2000c. In addition, discussion has also centered around whether the cloacal membrane is divided into urogenital and anal membranes by the urorectal septum.…”

mentioning

confidence: 99%

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Spatiotemporal distribution of apoptosis during normal cloacal development in mice

2004

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To understand normal cloacal developmental processes, serial sagittal sections of mouse embryos were made every 6 hrs from embryonic day 11.5 (E11.5) to E13.5. During cloacal development to form the urogenital sinus and anorectal canal, fusion of the urorectal septum with the cloacal membrane was not observed, and the ventral and dorsal parts of the cloaca were continuously connected by the canal until disappearance of the cloacal membrane to open the vestibule formed by the urogenital sinus and anorectal canal to the outside at E13.5. Ventral shifting of the dorsal part of the cloaca was observed until E12.5. The dorsal part was transformed in accordance with ventral shifting. In addition, apoptosis was seen to occur around the dorsal part. However, from E12.25, apoptotic cells are observed in a linear arrangement in the urorectal septum just ventral to the peritoneal cavity. Interestingly, extension of this line reaches the area of the cloacal membrane disintegrated by apoptosis. The present findings suggest that in the early stages (until E12.0), distribution of apoptosis in mesenchyme around the dorsal part of the cloaca might be strongly related to the transformation and ventral shifting of this part. Conversely, the apoptosis pattern in urorectal septum mesenchyme in later stages (from E12.0) might be involved in transformation of the urorectal septum and disintegration of the cloacal membrane.

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Section: Observation Of Normal Cloacal Developmentsupporting

confidence: 57%

Section: Observation Of Normal Cloacal Developmentmentioning

confidence: 99%

mentioning

confidence: 99%

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Spatiotemporal distribution of apoptosis during normal cloacal development in mice

2004

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“…This remained the basis of our understanding until 1986 when more extensive anatomical and histological works refuted this theory because of the absence of morphological evidence to suggest septum formation either by the descent of a septum caudally or the formation and fusion of lateral ridges in the cloaca. 18 More recently, studies of Sd mice noted that the most consistent finding in this animal model was the loss of the dorsal cloaca and the presence of a short cloacal membrane. 16,56 In our anorectal mouse models, we found no evidence of active septation or lateral ridges formation/fusion on transverse sections of our mutant embryos, and similar to the Sd mice, we also observed a lack of formation of a normal dorsal cloaca.…”

Section: Gli2mentioning

confidence: 76%

Anorectal Malformations Caused by Defects in Sonic Hedgehog Signaling

Kim

Zhang

et al. 2001

The American Journal of Pathology

213

179

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Anorectal malformations are a common clinical problem affecting the development of the distal hindgut in infants. The spectrum of anorectal malformations ranges from the mildly stenotic anus to imperforate anus with a fistula between the urinary and intestinal tracts to the most severe form, persistent cloaca. The etiology, embryology, and pathogenesis of anorectal malformations are poorly understood and controversial. Sonic hedgehog (Shh) is an endoderm-derived signaling molecule that induces mesodermal gene expression in the chick hindgut. However, the role of Shh signaling in mammalian hindgut development is unknown. Here, we show that mutant mice with various defects in the Shh signaling pathway exhibit a spectrum of distal hindgut defects mimicking human anorectal malformations. Shh null-mutant mice display persistent cloaca. Mutant mice lacking Gli2 or Gli3, two zinc finger transcription factors involved in Shh signaling, respectively, exhibit imperforate anus with recto-urethral fistula and anal stenosis. Furthermore, persistent cloaca is also observed in Gli2 Anorectal malformations encompass a broad spectrum of congenital defects that frequently necessitates urgent surgical treatment in the newborn period, most often because of intestinal obstruction and sepsis. One of the most common anomalies, imperforate anus, has an incidence of 1 in 5000 and carries with it significant chronic morbidity, particularly with fecal incontinence. The most severe form of anorectal malformation, the cloacae, where distal intestinal and genitourinary tracts remain in a common channel, is much less common than imperforate anus (1 in 50,000) but has more significant serious longterm medical problems including gender assignment.

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“…Anorektal malformasyonlar her 4000-5000 yemembran defektine bağlı gelişim hataları gibi çok nidoğanda bir gözlenen önemli bir konjenital anoçeşitli teoriler vardır (10). malidir (3).…”

unclassified

Anorektal Malformasyonlar: 40 Hastanin İncelenmesi̇

Turan;YAĞMURLU¹

1996

Ankara Üniversitesi Tıp Fakültesi Mecmuası

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Normal and abnormal development of the anorectum

Cited by 206 publications

References 16 publications

Spatiotemporal distribution of apoptosis during normal cloacal development in mice

Spatiotemporal distribution of apoptosis during normal cloacal development in mice

Anorectal Malformations Caused by Defects in Sonic Hedgehog Signaling

Anorektal Malformasyonlar: 40 Hastanin İncelenmesi̇

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