Dandruff remains one of the most common scalp complaints encountered in primary care and dermatology. While often perceived as benign, its pathogenesis is multifactorial and clinically significant, particularly when symptoms persist or overlap with seborrheic dermatitis. Below is an evidence-based overview of the causes of dandruff.

1. Role of Malassezia Species

The predominant factor in dandruff pathogenesis is overgrowth of lipophilic yeasts in the genus Malassezia, especially M. globosa and M. restricta (Gupta & Madzia, 2018). These organisms metabolize triglycerides in sebum into free fatty acids (notably oleic acid), which disrupt the epidermal barrier and trigger an inflammatory response. This is supported by the efficacy of antifungal agents such as zinc pyrithione, ketoconazole, and selenium sulfide.

2. Epidermal Barrier Dysfunction

Patients with dandruff demonstrate increased transepidermal water loss and reduced stratum corneum integrity (Harding et al., 2002). Barrier impairment allows irritants and microbial byproducts to penetrate, amplifying inflammation and accelerating keratinocyte turnover.

3. Hyperproliferation of Keratinocytes

Compared to normal scalp skin, dandruff is characterized by a shortened epidermal turnover rate (~5–7 days vs. 28 days in healthy skin) (Piérard-Franchimont et al., 2006). This results in the shedding of immature corneocytes, clinically visible as flakes.

4. Sebum and Lipid Metabolism

Sebum is not increased in quantity among dandruff patients, but its composition plays a role. Lipid-rich environments favor Malassezia growth, and specific alterations in sebaceous lipid content (e.g., squalene peroxidation) may further impair barrier function (Ro & Dawson, 2005).

5. Host Susceptibility and Immune Response

Dandruff does not affect all individuals equally, despite near-universal colonization with Malassezia. Genetic predisposition, individual sensitivity to microbial metabolites, and variation in innate immune response are critical. Some studies have shown increased expression of proinflammatory cytokines such as IL-1α and IL-8 in dandruff-prone scalp (Kobayashi et al., 2011).

6. Environmental and Behavioral Triggers

• Climate: Low humidity and cold weather exacerbate flaking, while hot, humid environments may worsen seborrheic dermatitis overlap.

• Hair practices: Infrequent shampooing may allow accumulation of sebum and scale.

• Psychological stress: Known to modulate immune function and sebaceous activity, contributing to disease flares.

Conclusion

Dandruff arises from a dynamic interaction of Malassezia proliferation, barrier dysfunction, keratinocyte hyperproliferation, lipid metabolism, and host immune response. Recognition of its multifactorial etiology informs therapeutic strategies, emphasizing antifungal agents, barrier repair, and modulation of inflammation.

References

1. Gupta AK, Madzia SE. The role of Malassezia in dandruff and seborrheic dermatitis. J Eur Acad Dermatol Venereol. 2018;32(2):210–216.

2. Harding CR, Moore AE, Rogers JS, Meldrum H, Scott AE, McGlone FP. Dandruff: a condition characterized by decreased stratum corneum barrier function. Arch Dermatol Res. 2002;294(5):221–230.

3. Piérard-Franchimont C, Hermanns JF, Degreef H, Piérard GE. From dandruff to seborrheic dermatitis: exploratory immunocytochemical assessment of scalp hair follicles. J Eur Acad Dermatol Venereol. 2006;20(6):628–632.

4. Ro BI, Dawson TL. The role of sebaceous gland activity and scalp microfloral metabolism in the pathogenesis of seborrheic dermatitis and dandruff. J Investig Dermatol Symp Proc. 2005;10(3):194–197.

5. Kobayashi T, et al. Innate immune responses in dandruff and seborrheic dermatitis. J Dermatol Sci. 2011;62(1):1–7.