Key points

Introduction

Fetal and pediatric skin are commonly believed to have advantageous properties for wound repair, with the ability of fetal skin to undergo scarless wound repair and the inherent youthful appearance of pediatric skin. However, infant and pediatric skin are also considered to be more sensitive and prone to injury than adult skin with the cosmetic industry marketing an extensive line of delicate products exclusively for the care and hygiene of infants and children.

Introduction

Fetal and pediatric skin are commonly believed to have advantageous properties for wound repair, with the ability of fetal skin to undergo scarless wound repair and the inherent youthful appearance of pediatric skin. However, infant and pediatric skin are also considered to be more sensitive and prone to injury than adult skin with the cosmetic industry marketing an extensive line of delicate products exclusively for the care and hygiene of infants and children.

Skin development

The development of the dermal/epidermal layers is a continuous process starting early in pregnancy with discrete patterns related to gestational age, developing from the cranial to the caudal pole. At 4 weeks gestation, fetal skin can be visualized as 2 distinct layers: a basal cell layer covered by an outer layer, termed the periderm ( Fig. 1 ). The periderm is uniquely found in humans; there is no counterpart in animal models such as mice or rats. Keratinization begincs at 9 weeks gestation, and at 13 weeks gestation, stratification into different layers becomes apparent. Hair follicles begin to form as epidermal buds along the basal layer at 14 weeks gestation. In the subsequent 2 weeks, these epidermal buds are associated with local proliferation of mesenchymal cells associated with the epidermal bud as hair follicles rapidly develop. This is followed by continued elongation of the hair follicles. The development of eccrine sweat glands begins as epidermal buds in the basal layer at 20 weeks gestation and continue to develop over the next 10 weeks, first by elongating and then by coiling. At 24 weeks gestation, fetal skin continues to heal without scar, as keratinization and stratification into mature morphologic layers continues. After 24 weeks gestation, there is a transitional period when skin heals without characteristic scar deposition but fails to reconstitute the dermal appendages. This transitional period has been found in multiple animal models of fetal wound healing. The scarless wound healing phenotype is lost by the third trimester. At 34 weeks gestation, mature keratinocytes characterized by flattened, keratinized morphology are observed in conjunction with adult-type dermoepidermal undulations.

Fetal development of skin. ( A ) At 4 weeks’ gestation, skin is composed of 2 layers, the periderm and basal epidermis. ( B ) At 9 weeks gestation, keratinization becomes apparent. ( C ) At 14 weeks gestation, stratification of the epidermal layer is apparent along with budding of the basal layer as the primordial hair follicle develops. ( D ) At 16 weeks gestation, mesenchymal cells may be seen associated with the epidermal bud. ( E ) At 18 weeks, sebaceous glands become apparent, along with hair follicle elongation. ( F ) At 23 weeks, the hair follicles continue to elongate while the basal layer buds to form primordial eccrine glands. ( G ) At 30 weeks’ gestation, the eccrine glands continue to elongate and coil.

In later gestation, the fetal dermis is primarily thickened by an increase in collagen content. This dermis has higher levels of type III collagen, chondroitin sulfate, proteoglycans, and hyaluronan compared with adult dermis. Dermal elastin is also absent in fetal dermis.

During the last trimester, the fetus is covered by the vernix caseosa (VC), a protective coat secreted by the sebaceous glands and composed of protein (10%), lipids (10%), and water (80%). The VC is uniquely human, with no counterpart identified in animal models. This coat was initially posited to function as a lubricant in the birthing process. However, as the fetus continues to mature, part of the vernix sloughs from the skin surface into the surrounding amniotic fluid. This physiologic decrease of vernix with advancing gestational age renders this role unlikely. More recent studies of the VC suggest that the layer facilitates the transition from an aqueous in utero environment to the dry extrauterine environment. The vernix helps to protect the fetal epidermis from maceration while immersed in amniotic fluid and permits epidermal cornification and stratum corneum formation. The VC also contains high levels of lysozyme, lactoferrin, linoleic acid, as well as other antiinfective agents.

Full-term infants at birth have skin that is anatomically mature when examined histologically with all 5 layers present. These include from deep to superficial: stratum basale, stratum spinosum, stratum granulosum, stratum licidum, and stratum corneum. As epidermal cells mature, their morphology changes from the columnar stratum basale to the tightly overlapping squamous keratinocytes of the stratum corneum. The time to fully mature, keratinize, and form this protective horny layer varies depending on body site. This occurs more rapidly in facial skin than in the trunk and limbs. Neonatal skin has a relatively coarse texture compared with older infants and a more homogeneous smooth structure develops during the first 30 days of life. Infants have smaller corneocytes and a significantly thinner stratum corneum until 2 years of age.

During the next developmental period from infancy to puberty, there is little difference in skin between male and female patients. Both genders demonstrate a steady increase in dermal thickness, with boys developing thicker epidermal and dermal layers. At the onset of puberty, there is significant hormonal influence on the skin. After age 12 years, girls accumulate a thick layer of subcutaneous fat, which is absent in boys. On the other hand, boys exhibit a gradual thinning of their thick epidermal and dermal layers. These layers remain a constant thickness in females throughout adolescence and adulthood until menopause. In addition, dermal composition begins to change with advancing age starting at puberty; both sexes show similar rates of linear decrease in skin collagen content with age. Women start with a lower baseline collagen density and they seem to age earlier than men.

Skin function

Skin has multiple functions including regulation of body temperature and protection against physical, chemical, and biological insults. In full-term neonates at birth, the skin is histologically mature, however it remains functionally immature. Neonatal barrier functions are in a constant state of flux, in contrast to mature adult skin. It has been proposed that this changing infant skin barrier is not a deficit but a benefit because adaptive flexibility allows constant optimization, balancing growth, thermoregulation, water barrier, and protective functions.

Biophysical skin parameters

Skin can be defined by a variety of biophysical skin parameters, which permit the study of skin in a noninvasive manner. Multiple parameters, including transepidermal water loss, hydration, and skin acidity, are affected in skin diseases such as atopic dermatitis, psoriasis, and allergic or irritant contact dermatitis.