Embryology Of The Skin.
The human
skin develops from two special embryonic tissues, the ectoderm and the
mesoderm. Epidermal tissue is derived from the embryonic ectoderm. The dermis
and subcutaneous tissue are derived from the embryonic mesoderm. The
developmental interactions between mesoderm and ectoderm ultimately determine
the nature of human skin. Interestingly, neural tissue and epidermal tissue are
both derived from the ectoderm. It is believed that calcium signaling is
critical in determining the fate of the ectoderm and its differentiation into
either epidermis or neural tissue.
At approximately 4 weeks after conception, a single layer of ectoderm is
present, surrounding a thicker layer of mesoderm. Two weeks later, this
ectodermal layer has separated into two different components: an outer periderm
and an inner basal layer, which is connected to the underlying mesoderm. At 8
weeks after conception, the epidermis has developed into three separate layers:
the periderm, an intermediate layer, and the basal cell layer. The dermal
subcutaneous tissue is now beginning to develop, and a distinct dermal
subcutaneous boundary can be seen by the end of the eighth week. Between weeks
10 and 15 after conception, the beginning of the skin appendages can be seen.
The formation of hair follicles is initiated by a complex genetic
mechanism that causes the dermis to direct certain basal epidermal cells to
congregate and form the rudimentary hair follicle. This process occurs in a
highly organized fashion beginning from the scalp and working caudally to the
lower extremity. At the same time, the hair follicles are developing and the dermal
papillae are beginning to form. The hair follicles continue to differentiate
throughout the second trimester, and the hair of the fetus can be seen at
approximately 20 weeks after conception. This first hair is known as lanugo
hair and is almost always shed before delivery.
The fingernails and toenails develop from ectoderm that invaginates into
the underlying mesoderm by the fourteenth week after conception. By the fifth
month, the fetus has fully developed fingernails and toenails. The fingernails
fully develop slightly before the toenails.
Melanocytes are specialized cells derived from neural crest tissue. These
cells form along the neural tube. Melanocytes migrate in a specific pattern
laterally and then outward along the trunk. Melanocytes can be seen in the
epidermis by the middle of the first trimester, but they are not functional
until the end of the second trimester. The density of melanocytes is highest
during the fetal period and decreases thereafter until young adulthood.
Melanocytes are beginning to make their first melanosomes and are capable of
transferring melanin pigment to adjacent keratinocytes by approximately 5
months after conception. Melanocytes are not fully functional until birth.
Langerhans cells are specialized immune surveillance cells that appear within
the epidermis at approximately 40 days after conception. In contrast to
melanocytes, the density of Langerhans cells increases with time.
By late in the second trimester, the periderm begins to shed. This
shedding results in the vernix caseosa, a whitish, cheese-like material that
covers the fetus. It is believed to have a protective function. At the beginning
of the third trimester, the individual epidermal layers can be seen, including
the stratum basale, stratum granulosum, stratum spinosum, and stratum corneum.
Keratinization begins to occur during the second
trimester, first in the appendageal structures and then in the epidermis. The
thickness of the epidermis in a newborn closely approaches that in an adult.
The significant difference is that the skin barrier function in a newborn is
not as fully developed as in an adult and therefore is more vulnerable to
infection and external insults.
By studying the embryology of the skin, one can gain insight into the
mechanisms of certain genetic disorders.
For example, one of the more studied groups of genetic diseases are the
congenital blistering diseases. The various types of epidermolysis bullosa are
all caused by genetic defects in proteins responsible for adhesion of
keratinocytes. A firm understanding of the embryology of skin development is
essential for under-standing the pathogenesis of these diseases and ultimately
for developing a mechanism to detect and therapeutically
treat them.
