embryonic development. It is the outermost layer, and is superficial to the mesoderm (the middle layer) and endoderm (the innermost layer).[1] It emerges and originates from the outer layer of germ cells. The word ectoderm comes from the Greekektos meaning "outside", and derma meaning "skin".[2]
Generally speaking, the ectoderm differentiates to form
skin, linings of the mouth, anus, nostrils, sweat glands, hair and nails,[3] and tooth enamel. Other types of epithelium are derived from the endoderm.[3]
In vertebrate embryos, the ectoderm can be divided into two parts: the dorsal surface ectoderm also known as the external ectoderm, and the neural plate, which invaginates to form the neural tube and neural crest.[4] The surface ectoderm gives rise to most epithelial tissues, and the neural plate gives rise to most neural tissues. For this reason, the neural plate and neural crest are also referred to as the neuroectoderm.
History
embryogenesis. Pander received his doctorate in zoology from the University of Würzburg in 1817. He began his studies in embryology using chicken eggs, which allowed for his discovery of the ectoderm, mesoderm and endoderm
. Due to his findings, Pander is sometimes referred to as the "founder of embryology".
Pander's work of the early embryo was continued by a
blastula. Baer published his findings, including his germ layer theory, in a textbook which translates to On the Development of Animals which he released in 1828.[5]
Differentiation
Initial appearance
The ectoderm can first be observed in
blastula. The blastula is polar, and its two halves are called the animal hemisphere and vegetal hemisphere. It is the animal hemisphere will eventually become the ectoderm.[2]
Early development
Like the other two germ layers – i.e., the mesoderm and endoderm – the ectoderm forms shortly after
epidermis,[6] the neuroectoderm is induced along the neural pathway by the notochord, which is typically positioned above it.[2][4]
Gastrulation
During the process of gastrulation,
blastopore, another process occurs termed convergent extension. During convergent extension, cells that approach the lip intercalate mediolaterally, in such a way that cells are pulled over the lip and inside the embryo. These two processes allow for the prospective mesoderm cells to be placed between the ectoderm and the endoderm. Once convergent extension and radial intercalation are underway, the rest of the vegetal pole, which will become endoderm cells, is completely engulfed by the prospective ectoderm, as these top cells undergo epiboly, where the ectoderm cells divide in a way to form one layer. This creates a uniform embryo composed of the three germ layers in their respective positions.[2]
All of the organs that rise from the ectoderm such as the nervous system, teeth, hair and many exocrine glands, originate from two adjacent tissue layers: the epithelium and the mesenchyme.
FGF, TGFβ, Wnt, and regulators from the hedgehog family. The specific timing and manner that the ectodermal organs form is dependent on the invagination of the epithelial cells.[9] FGF-9 is an important factor during the initiation of tooth germ development. The rate of epithelial invagination in significantly increased by action of FGF-9, which is only expressed in the epithelium, and not in the mesenchyme. FGF-10 helps to stimulate epithelial cell proliferation, in order make larger tooth germs. Mammalian teeth develop from ectoderm derived from the mesenchyme: oral ectoderm and neural crest. The epithelial components of the stem cells for continuously growing teeth form from tissue layers called the stellate reticulum and the suprabasal layer of the surface ectoderm.[9]
Clinical significance
Ectodermal dysplasia
Ectodermal dysplasia is a rare but severe condition where the tissue groups (specifically teeth, skin, hair, nails and sweat glands) derived from the ectoderm undergo abnormal development. This is a diffuse term, as there are over 170 subtypes of ectodermal dysplasia. It has been accepted that the disease is caused by a mutation or a combination of mutations in certain genes. Research of the disease is ongoing, as only a fraction of the mutations involved with an ectodermal dysplasia subtype have been identified.[10]
Dental abnormalities in a 5-year-old girl from northern Sweden who suffered from various symptoms of autosomal dominant hypohidrotic ectodermal dysplasia (HED) a) Intraoral view. Note that the upper incisors have been restored with composite material to disguise their original conical shape. b) Orthopantomogram showing absence of ten primary and eleven permanent teeth in the jaws of the same individual.
EDA gene.[12] This disease typically affects males more severely because they have only one X chromosome
, while in females the second, usually unaffected X chromosome may be sufficient to prevent most symptoms.
^Baer KE von (1986) In: Oppenheimer J (ed.) and Schneider H (transl.), Autobiography of Dr. Karl Ernst von Baer. Canton, MA: Science History Publications.
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