The pathogenesis of cleft palate. An animal study

Poswillo, David; Roy, L. J.

doi:10.1002/bjs.1800521115

Cited by 33 publications

(6 citation statements)

References 12 publications

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“…In animal experiments conditions similar to the PRS have been produced by preventing the mandibular growth in various ways (Poswillo & Roy, 1965;Locke, 1966).…”

mentioning

confidence: 99%

On the Pathogenesis of Cleft Palate in the Pierre Robin Syndrome

Rintala

Ranta

Stegars

1984

Scandinavian Journal of Plastic and Reconstructive Surgery

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In a series of Pierre Robin syndrome (PRS) and isolated cleft palate patients (ICP) both U- and V-formed clefts were observed with equal frequency, but the PRS clefts were in average slightly wider. There were totally submucous clefts among the PRS patients. There was no statistical difference between the groups in the prevalence of clefts in the relatives of the patients. The incidence of (genetically influenced) conical elevations in the lower lip was lowest in the noncleft subjects, high in ICP and highest in PRS children. The incidence of hypodontia, which acceptedly is genetically influenced, was also highest in the PRS group. Thus the foetal malposition with the tongue between the palatal shelves does not seem to play any decisive role in the pathogenesis of most PRS clefts. The cause for the PRS is more likely a genetically influenced growth disturbance in the maxilla and the mandible, which due to the organogenetic differences leads to diverging end results, micrognathia and cleft.

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“…In animal experiments conditions similar to the PRS have been produced by preventing the mandibular growth in various ways (Poswillo & Roy, 1965;Locke, 1966).…”

mentioning

confidence: 99%

On the Pathogenesis of Cleft Palate in the Pierre Robin Syndrome

Rintala

Ranta

Stegars

1984

Scandinavian Journal of Plastic and Reconstructive Surgery

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“…Fibroblasts found in wounds are a specialized form of cells named myofibroblasts, because they express elevated levels of Acta2 and, consequently, display a markedly enhanced ability to overexpress extracellular matrix. 11 Because the rat subjected to amniocentesis is used as an ABS experimental model, 7,12 it is ideal to identify the molecules involved in the fibrotic response.…”

Section: Discussionmentioning

confidence: 99%

The Amniotic Band Syndrome in the Rat Is Associated with the Activation of Transforming Growth Factor-β

Romero‐Valdovinos

Galván-Montaño

Olivo-Dı́az

et al. 2015

The American Journal of Pathology

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“…(2) funneling of the data pertaining to children with clefts from other health agencies into the records of the National 0009-9163/81/070013-12$02.50/0 0 1981 Munksgaard, Copenhagen Speech Institute; (3) exclusive surgical treatment for CP individuals by Dr. Fogh-Andersen in Denmark since 1940; and (4) a national medical health care system. Bifid uvula is commonly considered to be a microform of CP, although the histologic development of the uvula and the soft palate are different from that of the hard palate (Ferguson 1977, Poswillo 1974. This minor anomaly occurs with an incidence of 1.3 ' % in the Danish population (Lindemann et al 1977).…”

Section: Involved In the Study O F Cleft Palatementioning

confidence: 99%

Cleft palate: A genetic and epidemiologic investigation

1981

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An examination of kindred histories of 561 Danish probands who have non‐syndromic CP has indicated that neither a multifactorial‐threshold model nor a single major locus model is completely compatible with the data. This suggests etiologic heterogeneity for CP, which was tested with kindred data. As recommended by Smith (1976), an attempt to define partially this heterogeneity within the CP phenotype was undertaken by grouping and comparing the kindred data. It is both reasonable and heuristic to propose that CP, as defined in this investigation, is composed of three groups: (1) Syndromic CP; (2) Familial CP, which appears to have an autosomal dominant component to its etiology, and (3) Non‐familial CP which, by demonstrating an increasing frequency of CP and a maternal age effect, appears to be related to environmental factors which may cause CP or other malformations.

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The pathogenesis of cleft palate. An animal study

Cited by 33 publications

References 12 publications

On the Pathogenesis of Cleft Palate in the Pierre Robin Syndrome

On the Pathogenesis of Cleft Palate in the Pierre Robin Syndrome

The Amniotic Band Syndrome in the Rat Is Associated with the Activation of Transforming Growth Factor-β

Cleft palate: A genetic and epidemiologic investigation

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