Laser Hair Removal

Hair anatomy

The hair follicle is a complex, hormonally regulated structure with a cyclical growth pattern. Each follicle is formed through an interaction between dermal and epidermal components.

In the pre-germ stage, there is an accumulation of basal cells and associated mesenchymal cells, which form the primitive hair germ. A solid column of epidermal cells progressively penetrates into the dermis to form a rudimentary hair follicle. The broad tip becomes concave and encloses the dermal papilla, which is a neurovascular structure that supplies the cells of the rapidly dividing proliferating matrix forming the hair shaft.

Two swellings appear at the posterior edge of the follicle, with the upper swelling representing the future sebaceous gland and the lower bulge representing the site of attachment of the arrector pili muscle. The hair emerges from the surface at an angle such that the arrector pili muscle and bulge are on the deeper aspect of the follicle.

The first hair follicles are formed at the end of the 2nd and beginning of the 3rd month of gestation in the eyebrow, upper lip, and chin, with further hair growth in a cephalad to caudal direction during the 4th to 5th months' gestation. No further follicular neogenesis occurs after birth.

The hair follicle is divided into three anatomic units: infundibulum, isthmus, and inferior segment ( Fig. 31.1 ). The infundibulum includes the region from the hair follicle orifice to the sebaceous duct entrance. The isthmus includes the region between the entrance of the sebaceous duct and the arrector pili muscle. The inferior segment extends from the insertion of the arrector pili muscle to the base of the follicle, including the hair bulb.

The hair bulb is composed of matrix cells interspersed with melanocytes. The matrix cells differentiate along separate pathways and form, from the outside inward, the outer root sheath, the three layers of the inner root sheath (Henle, Huxley, and cuticle), and the three layers of the hair shaft itself (cuticle of the hair shaft, cortex, and medulla).

Hair growth

Each hair follicle consists of a permanent and non-permanent part, with the lowermost aspect of the permanent part at the level of the insertion of the arrector pili muscle (the follicular bulge).

All hair undergoes intrinsic cyclical growth, consisting of three phases ( Fig. 31.2 ). In periods of active growth (anagen), the rapidly developing bulbar matrix cells differentiate into the hair shaft and inner root sheath, both of which migrate outward as the hair lengthens. Anagen bulbs are 2–7 mm below the skin surface. A transition period follows in which the bulbar part of the hair follicle, including matrical melanocytes, is almost totally degraded through apoptosis (catagen). The follicle decreases to approximately one-third of its former length, with its lowermost part coming to lie at the level of attachment of the dermal papilla. A resting phase (telogen) ensues. With new regrowth in early anagen, new epithelial cell division occurs near the arrector pili insertion, a new matrix develops, and hair growth resumes.

The hair follicle is self-renewing, with a population of stem cells capable of regenerating the follicle within or near the hair bulb matrix. Another population of slow-cycling stem cells has been defined in the follicular bulge arising off the outer root sheath at the site of arrector pili muscle attachment, approximately 1 mm below the skin surface. This region represents the lower end of the permanent part of the hair follicle. It is postulated that during late telogen to early anagen, these follicular bulge stem cells are activated by dermal papillary signals to proliferate briefly to form more differentiated follicular cells before returning to their non-cycling state in mid-anagen.

The duration of each of these growth phases varies according to the body site ( Table 31.1 ). Body sites with long hair (e.g., scalp) have a prolonged anagen phase, whereas areas with short hair (e.g., female upper lip) have short anagen and prolonged telogen phases. The duration of anagen growth of the upper lip is typically 16 weeks, catagen 1 week, and telogen 6 weeks. The duration of anagen growth on the scalp is generally 150 weeks, catagen 1–3 weeks, and telogen 12 weeks. The rate of hair growth is approximately 0.44 mm/day on the scalp and 0.27 mm/day for the beard region. Seasonal variation does exist, with a higher rate of growth during the summer months and slower growth during the winter months. This variability correlates with fluctuations in androgen levels, with higher levels of testosterone noted during the summer. Any method of hair treatment that induces telogen can produce a prolonged absence of hair growth that may not represent permanent hair loss. It is critical in the management of patients with excess hair growth to understand the variability of these growth phases to provide effective treatment and follow-up expectations with predictable outcomes.

Hair type

Hair can be classified according to its texture and length, with the three main types being defined as lanugo, vellus, and terminal hairs. Hair features such as the amount of pigment and hair shaft diameter increase from lanugo to terminal hairs. Hair diameter is determined by the size of the papilla and hair bulb. Lanugo hairs are soft, fine hairs that cover a fetus and are shed before or shortly after birth. Vellus hairs are non-pigmented, with a diameter of 30 µm or less. Secondary vellus hairs represent miniaturized or hypoplastic terminal hairs and have the same diameter as vellus hairs, but are pigmented. Terminal hair shafts range from 200 to 300 µm in cross-sectional diameter. Both vellus and terminal hairs go through all stages of follicular growth, but the duration of anagen is much shorter for vellus hairs. The type of hair produced by an individual follicle may change, as observed by the replacement of vellus by terminal hairs at puberty or the conversion of terminal to secondary vellus hairs with androgenetic alopecia. Vellus hair bulbs extend to a depth of less than 1 mm into the skin, whereas telogen hair bulbs may extend 2–7 mm into the skin. The bulge maintains a constant depth throughout the hair cycle.

Hair color

Hair color is genetically determined and is dependent on the amount of pigment in the hair shaft. Follicular melanocytes produce two types of melanin – eumelanin, a brown–black pigment, and pheomelanin, a red pigment. They are biologically related and share a common metabolic pathway, in which dopaquinone is a key intermediate. Pheomelanin absorption is 30 times lower than eumelanin at 694 nm and is poorly absorbed at wavelengths longer than 700 nm. Melanocytes occur in the upper part of the hair bulb and outer root sheath of the infundibulum with a 1 : 5 ratio of melanocytes to keratinocytes. Melanogenesis is halted during catagen and reinitiated during early anagen. Pigment transfer is halted during telogen, resulting in an unpigmented telogen bulb. Hair varies in its type of melanin – black and brown hair contains ellipsoidal heavily melanized eumelanosomes; red hair contains spherical pheo­melanosomes; blond hair contains incompletely melanized melanosomes or fewer melanosomes; gray hair-producing follicles contain few melanocytes, with poorly melanized melanosomes; while white hair-producing follicles contain no dopa-positive melanocytes.

Classification of excess hair

The removal of unwanted hair is a daily challenge for many men and women. Two main groups of individuals seek hair removal – individuals with increased hair in undesirable locations secondary to an underlying medical condition or genetic predisposition, and individuals with hair in areas considered to be normal in density and distribution, but which for social, emotional, or other reasons, is not desired.

Individuals with increased hair density are classified as having hypertrichosis or hirsutism. Hypertrichosis is defined as localized or excessive hair at any body site in a male or female and may develop as a result of a drug interaction to certain medications such as cyclosporine, phenytoin, and anabolic steroids. Internal malignancy, trauma, malnutrition, patients with a hair-bearing skin graft, endocrine disturbance, and a genetic or ethnic predisposition have also been implicated.

Excessive terminal hair growth in androgen-dependent areas, including the upper lip, chin, chest, lower abdomen, and thighs, is classified as hirsutism. Other cutaneous signs that may be associated with hirsutism include acne, acanthosis nigricans, striae distensae, and androgenetic alopecia. Systemic signs of virilization such as a voice deepening, hypertension, increased muscle bulk, and clitoromegaly may indicate a hyperandrogenic state, such as polycystic ovarian syndrome, 21-hydroxylase-deficient non-classic adrenal hyperplasia, insulin-resistant acanthosis nigricans, androgen drug intake, or an androgen-secreting neoplasm. Laboratory tests for free testosterone and dehydroepiandrosterone sulfate (DHEA-S) should be obtained to exclude elevated androgen levels as a cause of hirsutism.

Traditional treatment modalities

Numerous treatment modalities exist for the removal of hair. Temporary hair removal is obtained by shaving, tweezing, bleaching, waxing, and employing chemical depilatories. Though inexpensive and easy to perform, many women loathe shaving because of the masculine connotations associated with the procedure or the mistaken belief that shaving will coarsen hair or make it grow faster. Tweezing and waxing provide temporary hair loss for several weeks; however, these techniques are painful and may result in undesired side-effects such as post-inflammatory hyperpigmentation, ingrown hairs, folliculitis, and scarring. Bleaching provides a lightening of treated hairs, masquerading their presence. This technique is most effective for light-skinned individuals. Chemical depilatories commonly contain thioglycolates that dissolve hairs by disrupting disulfide bonds. The resultant hair removal includes some of the hair shaft below the skin surface. Although effective for temporary hair removal, they are messy to use and can provide significant irritation, especially when used on the face.

Antiandrogenic medications, including oral contraceptives for hormonal suppression and spironolactone, flutamide, and cyproterone acetate for peripheral androgen blockade, have been employed for the treatment of hirsutism with variable success. They provide only partial and temporary hair loss and are associated with significant side-effects, which warrant monthly monitoring.

Attempts to delay hair growth have been performed. There are three ways to slow down hair growth: decrease the anagen phase, delay the onset of anagen, or prolong the telogen phase. To date, pharmacological prolongation of the telogen phase or anagen onset is not possible. It is, however, possible to decrease the anagen phase. Eflornithine hydrochloride 13.9% cream (Vaniqa, Bristol–Myers Squibb) was approved by the Food and Drug Administration (FDA) in August 2000, as the first topical prescription treatment for the reduction of unwanted facial hair in women. It acts as an irreversible inhibitor of ornithine decarboxylase (ODC), an enzyme that is critical for the biosynthesis of cationic polyamines which are necessary for cell growth. ODC is abundantly expressed in the proliferating bulb cells of anagen follicles. When ODC is decreased, anagen is reduced with subsequent hair growth delay. The mean percutaneous absorption for eflornithine 13.9% cream is less than 1%. It is not metabolized and is excreted unchanged in the urine. Two multicenter, double-blind, vehicle-controlled, randomized studies were carried out, with twice-daily application of the creams for 24 weeks, followed by 8 weeks of no treatment, to the chin and upper lip. Statistically and clinically significant hair growth delay was noted in the eflornithine group when compared with the vehicle. Hair growth was noted to approach pretreatment levels within 8 weeks of treatment withdrawal. Applied twice daily, eflornithine hydrochloride 13.9% cream is effective in slowing facial hair regrowth temporarily and may complement other hair removal methods. Skin-related side-effects include stinging, burning, tingling, acne, and folliculitis at the treatment site. It is classified as a pregnancy category C agent.

For several decades, electrolysis was the only available means of achieving safe, permanent hair removal. Two types of electrolysis have been employed for hair removal: galvanic electrolysis and thermolysis. During galvanic electrolysis, a needle carrying direct electric current is inserted into each individual hair follicle. The current destroys the follicle by producing sodium hydroxide within the follicle. Thermolysis generates a high-frequency alternating current through a needle inserted into the follicle, which destroys the hair follicle through heat production. Both forms of electrolysis can provide permanent hair removal. However, the process is tedious, time-consuming, costly, painful, and can result in post-inflammatory hyperpigmentation, hypopigmentation, and ice-pick scarring; and the results are variable, with efficacy of 30–40% for destroying individual hair follicles. It is not a practical means of hair removal for individuals with extensive hair or large areas to treat.

Chromophores

The endogenous chromophore targeted for selective destruction of hair follicles is melanin, although water has also been used as a chromophore with minimal success to date ( Box 31.2 ). Melanin is in the hair shaft, the outer root sheath of the infundibulum, and the matrix area. It functions as a natural chromophore over a wide range of wavelengths, up to 1100 nm ( Fig. 31.3 ). Most lasers and non-coherent light sources with cut-off filters used for hair removal deliver energy at red or near infrared wavelengths, which target melanin within the hair follicle. The amount and type of melanin within the follicle determines the amount of follicular damage possible. Red and near infrared wavelengths are poorly absorbed by competing chromophores such as hemoglobin, and are able to penetrate into the deep dermis.