A Clinical and Biological Guide for Understanding Chemotherapy-Induced Alopecia and Its Prevention

Abstract

Chemotherapy-induced alopecia (CIA) is the most visibly distressing side effect of commonly administered chemotherapeutic agents. Because psychological health has huge relevance to lifestyle, diet, and self-esteem, it is important for clinicians to fully appreciate the psychological burden that CIA can place on patients. Here, for the first time to our knowledge, we provide a comprehensive review encompassing the molecular characteristics of the human hair follicle (HF), how different anticancer agents damage the HF to cause CIA, and subsequent HF pathophysiology, and we assess known and emerging prevention modalities that have aimed to reduce or prevent CIA. We argue that, at present, scalp cooling is the only safe and U.S. Food and Drug Administration-cleared modality available, and we highlight the extensive available clinical and experimental (biological) evidence for its efficacy. The likelihood of a patient that uses scalp cooling during chemotherapy maintaining enough hair to not require a wig is approximately 50%. This is despite different types of chemotherapy regimens, patient-specific differences, and possible lack of staff experience in effectively delivering scalp cooling. The increased use of scalp cooling and an understanding of how to deliver it most effectively to patients has enormous potential to ease the psychological burden of CIA, until other, more efficacious, equally safe treatments become available.

Implications for practice: Chemotherapy-induced alopecia (CIA) represents perhaps the most distressing side effect of chemotherapeutic agents and is of huge concern to the majority of patients. Scalp cooling is currently the only safe option to combat CIA. Clinical and biological evidence suggests improvements can be made, including efficacy in delivering adequately low temperature to the scalp and patient-specific cap design. The increased use of scalp cooling, an understanding of how to deliver it most effectively, and biological evidence-based approaches to improve its efficacy have enormous potential to ease the psychological burden of CIA, as this could lead to improvements in treatment and patient quality-of-life.

Keywords: Cell models; Chemotherapy; Chemotherapy‐induced alopecia; Hair follicle; Hair loss; Prevention; Safety; Scalp cooling; Side effects; Toxicity.

Conflict of interest statement

Disclosures of potential conflicts of interest may be found at the end of this article.

© AlphaMed Press 2017.

Figures

Figure 1.

Structure of the hair follicle (HF). The schematic illustrates the organization and structure of the human HF, including key areas of the organ, such as the bulge region, the ORS and IRS, and the hair bulb that includes the hair matrix keratinocyte compartment and the dermal papilla region. Abbreviations: DP, dermal papilla; HFPU, hair follicle pigmentary unit; HS, hair shaft; IRS, inner route sheath; ORS, outer route sheath. Reprinted with permission from [121].

Figure 2.

The hair “cycle.” Schematic diagram of the three main phases of hair cycle: the growth phase (anagen), the dystrophic phase (catagen), an extremely shortened resting phase (telogen), and the ‘shedding’ of the hair (exogen). In anagen, the hair bulb is located deep inside the skin and hair grows towards the skin surface. The dermal papilla survives catagen and moves upward to the lowermost portion of the bulge, which then forms the secondary germ at its base during telogen. In telogen, the hair falls out and the hair bulb relocates down again as the new hair grows. At their cycle end, telogen HFs can be activated through mechanical depilation, pharmacologically, and by specific signaling factors (e.g., Wnt signaling), which stimulates a return to anagen and the generation of the new lower follicle and hair shaft. As the new hair grows in, the old hair is shed during exogen. The duration of each phase depends on the type, site and specific genetic programming of the follicle.

Figure 3.

Molecular regulators of apoptosis in the hair follicle (HF). The diagram illustrates the expression pattern of proapoptotic (e.g., Fas, p53, Bax) and antiapoptotic (Bcl‐2, survivin) molecules in the different HF compartments.