Dermatology and Cosmetic Surgery

Author: Chief Editor: Yu Zong / et al
Publisher:
Publishing Date: 1999-03-01
Features: The abstract is designed to meet the needs of the development of dermatological cosmetology. We referred to relevant materials in Chinese, Japanese, English, French, and Russian to compile this book, "Dermatological Cosmetology." The content is divided into three parts: the upper, middle, and lower sections, respectively describing the basic biological knowledge of the skin and its appendages, the factors and methods of skin health, and the diagnosis and treatment of certain skin diseases. This book can be used as a reference for dermatological healthcare professionals, cosmetologists, students of cosmetology, cosmetic technologists, and individuals with a medium level of education.
Excerpt:
IV. Newborn Skin
Newborn skin is delicate and smooth, covered with varying amounts of vernix caseosa. This substance begins to shed 1–2 days after birth. The skin color changes over time after birth, progressing from purple-red → red → pale red. The surface pH value is usually above 6.0 (in older children and adults, the surface pH is around 5.5), which is neutral and related to the neutralization of vernix caseosa (pH 7.4). Within 1–2 weeks after birth, the surface pH value drops, typically to around pH 5.0. Shortly after birth, various transient and permanent bacteria colonize the skin. Within a few days, the frequency of bacterial detection is highest for Staphylococcus epidermidis and Micrococcus, and other bacteria such as non-hemolytic Streptococcus and diphtheroid bacilli may also be detected. The detection rate of Staphylococcus aureus increases in areas such as the nose, umbilicus, axillae, and perineum. The differentiation of the epidermis and appendages is immature both morphologically and functionally. The permeability of the stratum corneum is slightly higher than in older children, and the epidermis and dermis are loosely attached. Although melanocytes are present in the epidermis, their function is not fully activated, so the skin and hair color are lighter (compared to when melanocytes are fully activated). The eccrine sweat glands are morphologically developed but cannot fully function. Full-term infants do not sweat within 24 hours after birth, and it takes about 2–3 days for facial sweating to begin. Premature infants may delay sweating for 2–4 weeks. The apocrine sweat glands develop during the embryonic period and become fully developed and active during puberty. The sebaceous glands are stimulated to secrete by maternal androgens and fetal endogenous steroids. Vernix caseosa is composed of sebum and keratinized epidermal cells. Due to residual maternal androgen effects, newborn sebaceous glands are highly active, leading to neonatal acne and milia. Newborn skin is covered with fine, long vellus hairs, particularly prominent in premature infants. These vellus hairs soon fall out, replaced by terminal hairs. During the embryonic period, the hair cycle in humans is similar to that in rats and mice, with activity states synchronized across different body parts. After birth, these body parts also enter a resting phase and shed synchronously. After shedding, the scalp develops terminal hairs with medulla and cuticle, and the hairline gradually becomes distinct. Other body parts develop soft terminal hairs similar to lanugo, regulated by sex hormones. These hairs become terminal hairs during puberty, a secondary sexual characteristic.
V. Children and Adolescent Skin
Children's skin gradually improves in overall morphology and functional activity, differing significantly from infants and toddlers. As they age, melanocytes become more active, melanin increases, and the skin takes on a slightly brown hue. Due to increased fibrous components, the skin becomes firmer. However, during childhood, sebaceous gland activity temporarily weakens, and apocrine sweat glands do not yet function. Adolescence is a period of sex hormone secretion, during which the skin fully develops structurally and functionally. The "sexual characteristics" of the skin are prominent: male skin appears firm and straight, while female skin is fair and soft, exhibiting a curvaceous feminine beauty. The peak of adolescent beauty is around 20 years old, when sebum secretion increases, hair and body hair complete their characteristic development. Particularly in females, increased subcutaneous fat makes the skin appear plump, delicate, elastic, and curvaceous.
Section II: Skin Aging
The life of humans and animals is divided into growth, maturity, and decline over time, with the entire process called aging. The final decline phase is called aging (senescence). Aging due to aging is physiological aging (intrinsic aging), controlled by genetic factors, though inevitable, it can be delayed. Generally, women are considered middle-aged after 24 years old, and their skin care should follow middle-aged guidelines. Additionally, nutritional conditions, environmental factors, especially sun (UV) exposure, mental and physical overexertion, spicy foods, smoking, and improper use of cosmetics can cause the skin to lose moisture, degrade collagen and elastic fibers, and accelerate or promote the appearance of aging, known as pathological aging (extrinsic aging).
A. Mechanisms of Aging
The mechanisms of aging are not fully understood. There are various theories, such as programmed aging, error theory, free radical theory, cross-linking theory, and autoimmune theory.
1. Programmed Aging or DNA Theory
The basis is: ① The lifespan (rate of aging) of animals has a species-specific characteristic; ② The source of biological information is DNA, which programs and executes processes during aging, meaning that animals follow a certain program from occurrence, differentiation, maturity, aging, to death. However, the details of program are unclear. Additionally, certain DNA abnormalities can also lead to aging, such as DNA damage caused by radiation or UV exposure, which can break DNA strands. However, when DNA is damaged, it has the ability to cut, repair, amplify, and rearrange the damage. Animals with strong DNA repair capabilities have longer lifespans; among aging mice with chromosomal abnormalities, those that develop chromosomal abnormalities faster have shorter lifespans; as aging progresses, gene regulatory mechanisms also change. All of these indicate a close relationship between DNA changes and lifespan.
2. Error Theory
A slight increase in intracellular protein synthesis gradually leads to the accumulation of errors, ultimately causing cell aging and death. Physical, chemical, or microbial environmental factors can damage intracellular protein synthesis, leading to the accumulation of variant substances (e.g., variant enzymes) and further becoming harmful factors that cause cell aging and death.
3. Free Radical Theory
Free radicals produced within cells or tissues can cause changes in DNA, unsaturated fatty acids, and proteins. For example, DNA changes can lead to cell death or mutation (cancer); unsaturated fatty acids generate peroxides or lipofuscin, leading to cell death (especially in nerves and myocardium); protein molecules form cross-links and undergo degenerative changes in muscle fibers. Aging results from the accumulation of continuous harmful reactions caused by free radicals. Although the body has mechanisms to control or eliminate free radicals (antioxidants, DNA repair, cellular metabolism), a slight difference between the harmfulness of free radicals and the ability to resist them can lead to dysfunction and become the cause of aging.