When a conception fails to become a pregnancy.
Other contributors to this symposium have analysed in great detail the many components that go to make up reproductive success, so it is fitting to conclude with some thoughts about the aetiology of reproductive failure. Firstly, there are occasions when reproduction can be too successful, so that a density-dependent mechanism for inducing early embryonic mortality may be a most valuable protective mechanism. This is particularly true for polytocous species, where it may be necessary to achieve some regulation of litter size by differential embryonic mortality. Even in monotocous species some degree of embryonic mortality may also be advantageous as a way of prolonging the interval between successive births, for if one infant follows too hard upon the heels of another, the normal growth and development of both offspring will be permanently impaired. Embryonic mortality is also likely to be an effective insurance mechanism against the production of genetically defective offspring, because the absence of haploid gene expression will protect the spermatozoon from maternal immunological surveillance systems. With these concepts in mind, it is interesting to look at the nature and extent of embryonic loss in man and animals.
D000818:Animals; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D004622:Embryo, Mammalian / Q000502:physiology*; D005260:Female; D005298:Fertility; D005313:Fetal Death; D006801:Humans; D007621:Karyotyping; D011247:Pregnancy; D011270:Pregnancy, Animal; D012729:Sex Chromosome Aberrations