Diseases on Hair Follicles Leading to Hair Loss Part I: Nonscarring Alopecias

Katharina Wiedemeyer; Wolf-Bernhard Schill, MD; Christoph Löser, MD

Disclosures

Skinmed. 2004;3(4) 

In This Article

Abstract and Introduction

Hair follicles are unique structures with exceptional regenerative potential. They are believed to be crucial for epidermal homeostasis and reepithelialization after damage to human skin. Like other, more active and quickly proliferating organ systems, hair follicles may be easily disturbed in their normal growth cycle by systemic and local influences, including specific skin diseases. This may lead to hair loss, a very common complaint in men and women. The difficulties in reviewing the diseases of hair follicles lay in the long list of different etiologic factors (infectious, autoimmune, inflammatory, neoplastic, physical, chemical, congenital) and a still missing classification system according to etiopathogenetic principles. In this article (Part I of II), the structure and function of hair follicles, the diagnostic approach to diseases causing hair loss, and the most common nonscarring alopecias (telogen effluvium, anagen effluvium, androgenetic alopecia, and alopecia areata) are reviewed in regard to pathogenesis, clinical findings, and current options of treatment. Part II will focus on scarring alopecias.

Hair follicles are invaginations of the surface epidermis that can be divided into different units (infundibulum, isthmus, and inferior part). The infundibular part ends at the opening of the sebaceous duct. The isthmus includes the middle part until the insertion of the arrector pili muscle at the bulge region. The inferior unit consists of the follicular bulb, including the keratogenous zone. Possessing multiple receptors for a vast number of mediators, the dermal papilla, in particular, is target of systemic and local hormonal changes or alterations of cytokine patterns. Figure 1 shows the anatomy of a normal anagen follicle. In anagen, the scalp follicles reach into the subcutaneous fat and the hair is produced by rapidly dividing keratinocytes within the keratogenous zone. The matrix cells have the ability to differentiate into the numerous structures of the fiber (inner root sheath, cuticle, cortex, medulla). The active anagen stage lasts several years. Then the follicle starts to degenerate and enters the intermediate catagen stage. The papilla becomes thinner and shorter by induction of apoptosis within the keratogenous zone, including the melanocytes. The follicular papilla rises closer to the isthmus and infundibulum, the permanent parts of the follicle. The following resting stage is called telogen; the hair is finally shed and the growth cycle starts at the beginning.[1]

Scheme of a normal anagen hair follicle. a=infundibular part; b=isthmus; c=inferior unit; 1=sebaceous gland; 2=bulge (insertion of arrector pili muscle); 3=hair shaft; 4=inner root sheath; 5=outer root sheath; 6=adventitial sheath; 7=hair matrix; 8=follicular papilla

Exceeding hair loss (defined as more than 100 hairs/d) may be due to either changes of the physiologic cycle of hair growth or damage of the hair apparatus by systemic or local influences. Effluvium means the active shedding of hair, which may lead to alopecia, the visible result of hair loss. Telogen effluvium, for example, may result in androgenetic alopecia but may also come to a halt without causing alopecia. Also, there are several physiologic conditions that lead to hair loss, such as postpartum effluvium in women and increasing hair loss with age.[2]

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