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Dermatology · Folliculitis Decalvans

What’s Happening in the Scalp: Symptoms and Biology

At a Glance

Folliculitis decalvans is a chronic inflammatory scalp condition—not a hygiene problem—that can cause pustules, pain, tufted hairs, and permanent scarring. An overactive immune response, skin biology, and sometimes bacteria may work together to damage follicles.

When you look at a scalp affected by folliculitis decalvans (FD), you are seeing the results of an internal “perfect storm.” It is not just an infection, and it is certainly not a matter of hygiene. Instead, it is a complex interaction where your immune system, your unique skin biology, and common bacteria all collide to cause chronic inflammation and permanent scarring [1][2].

The Physical Signs: What You See and Feel

FD most commonly affects the vertex (the crown of the head) and the occipital area (the back of the head) [1][3]. During an active phase, you might notice:

  • Pustules: Small, pus-filled bumps that often form around the base of hair follicles [1].
  • Erythema and Crusting: Intense redness (perifollicular erythema) around the hairs, often accompanied by yellow or brownish crusts and scales [4][2].
  • Discomfort: Many patients report a “burning” sensation, itching, or significant scalp pain [1].
  • Tufted Hairs: This is a hallmark of FD. Also known as polytrichia, it looks like several hair shafts (sometimes 6 to 10 or more) are emerging from a single follicle opening, resembling the tufts on an old-fashioned doll’s head [5][6].

The Mystery of Tufted Hairs

Tufted hairs are not actually “new” hairs growing together. Instead, they are a sign of deep structural remodeling [2]. As chronic inflammation destroys the upper part of the hair follicles, the skin tries to heal by forming scar tissue (fibrosis) [5]. This scar tissue can fuse several neighboring follicles together. When these fused follicles share a single widened opening, the hairs they produce are forced out through the same “tunnel,” creating the characteristic tufted appearance [2][5].

The Role of Bacteria: It’s Not “Just an Infection”

One of the biggest misconceptions about FD is that it is a simple infection caused by “dirty” skin. This is false [7]. While a bacterium called Staphylococcus aureus (S. aureus) is found in about 45% of cases, it is a common organism that lives harmlessly on the skin of many healthy people [8][7]. In many instances, the bacteria may simply be colonizing the scalp rather than acting as the sole driver of the disease.

In FD, researchers are investigating the problem of how your body reacts to them:

  • The Biofilm Hypothesis: Researchers propose these bacteria may form a biofilm—a protective, sticky shield that allows them to cling to the hair shaft deep within the follicle [9]. This proposed shield could make the bacteria much harder for the immune system and standard antibiotics to reach, fueling a cycle of chronic, relapsing inflammation [9][10]. (Note: There is no routine clinical test for biofilms, and this remains an area of investigation).
  • Dysregulated Immune Response: Your body’s “innate” immune system (its first line of defense) appears to be overreacting [11]. Research studies on biopsied tissues suggest patients’ cells may produce too much of certain inflammatory messengers called IL-1beta and IL-17 [11][12]. This keeps the scalp in a constant state of “emergency,” leading to the destruction of the hair follicle [11].

Why You? Genetics and Skin Barriers

Why does this happen to some people and not others? There are a few theories about individual susceptibility:

  • The Barrier Breach: Some evidence suggests that people with FD may have a subtle “leak” in their skin barrier [13]. This could allow bacteria and other triggers to penetrate deeper into the follicle than they should [13][10].
  • Genetic Factors: While not everyone has a family history, there are documented cases of FD appearing in several family members, suggesting that some people may be genetically predisposed to this specific immune overreaction [14][15].
  • Keratinization: Some patients also show signs of abnormal skin cell production (hyperkeratosis), which can further clog the follicles and contribute to the inflammatory environment [16][17].

Understanding that FD is a biological “mismatch” between your immune system and the environment on your scalp can help move the focus away from hygiene and toward the real goal: calming the overactive immune response and protecting the hair you have [18][11].

Common questions in this guide

What symptoms can folliculitis decalvans cause?
Folliculitis decalvans can cause pus-filled bumps, redness around the hairs, crusting, itching, burning, scalp pain, and scarring hair loss. It often affects the crown or back of the scalp, and tufted hairs may appear during active or chronic disease.
What do tufted or “doll’s hair” follicles mean?
Tufted hairs are not new hairs growing together. Chronic inflammation and scar tissue can join nearby follicles, causing several hair shafts to emerge through one widened opening; this appearance is also called polytrichia.
Is folliculitis decalvans caused by poor hygiene?
No. Folliculitis decalvans is not simply a problem of dirty skin or a straightforward infection. Staphylococcus aureus may be found on the scalp, but it can also live harmlessly on healthy skin, so the disease appears to involve the immune response and other features of skin biology.
How does the immune system contribute to folliculitis decalvans?
The scalp’s first-line immune response appears to become overactive in folliculitis decalvans. This can keep inflammation active and damage hair follicles, potentially leading to scarring and permanent hair loss.
Why might bacteria be involved in folliculitis decalvans?
Staphylococcus aureus is found in some people with folliculitis decalvans and may simply be colonizing the scalp rather than causing the disease by itself. Researchers are studying whether bacteria can form a protective biofilm in the follicle, but there is no routine clinical test for biofilms.
Can genetics or skin barrier problems increase susceptibility to folliculitis decalvans?
Some families have more than one person with folliculitis decalvans, suggesting that genetic susceptibility may contribute. A weakened skin barrier or abnormal buildup of skin cells may also allow triggers to affect the follicle more easily, but these factors do not explain every case.

Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.Is the 'doll's hair' appearance on my scalp the same thing as tufted hairs?
  2. 2.Based on my clinical exam and biopsy, what type of inflammation is driving my hair loss?
  3. 3.Should we perform a bacterial culture to see if Staphylococcus aureus or other bacteria are involved in my case?
  4. 4.How does the understanding of the immune response change the way we might use antibiotics or other treatments?
  5. 5.Do I have any signs of skin barrier issues or keratinization disorders that might be contributing to this?

Questions For You

Tap a prompt to share your answer — we'll use it plus this page's context to start a tailored conversation.

References

References (18)
  1. 1

    Successful Treatment with Fusidic Acid in a Patient with Folliculitis Decalvans.

    Pimenta R, Borges-Costa J

    Acta dermatovenerologica Croatica : ADC 2019; (27(1)):49-50.

    PMID: 31032795
  2. 2

    Histopathologic and dermoscopic features of 42 cases of folliculitis decalvans: A case series.

    Uchiyama M, Harada K, Tobita R, et al.

    Journal of the American Academy of Dermatology 2021; (85(5)):1185-1193 doi:10.1016/j.jaad.2020.03.092.

    PMID: 32272176
  3. 3

    Epidemiological, Clinical, and Therapeutic Insights into Folliculitis Decalvans in Skin of Color: A Retrospective Descriptive Study of 17 Cases.

    Loubaris Z, Taib HE, Benzekri L, Meziane M

    Skin appendage disorders 2025; (11(6)):482-487 doi:10.1159/000546565.

    PMID: 40584732
  4. 4

    Evaluation of a Handheld Dermatoscope in Clinical Diagnosis of Primary Cicatricial Alopecias.

    Karadag Köse Ö, Güleç AT

    Dermatology and therapy 2019; (9(3)):525-535 doi:10.1007/s13555-019-0304-3.

    PMID: 31190216
  5. 5

    Compound Follicles in Folliculitis Decalvans Do Not Contain Vellus and Retained Telogen Follicles-A Pilot Histopathologic Series on Polytrichia.

    Lee J, Miteva M

    Journal of cutaneous pathology 2025; (52(1)):29-32 doi:10.1111/cup.14735.

    PMID: 39435542
  6. 6

    Tufted hairs: A bouquet of flowers in different hair diseases.

    Starace M, Vezzoni R, Alessandrini A, et al.

    Journal of cosmetic dermatology 2022; (21(9)):3741-3746 doi:10.1111/jocd.14712.

    PMID: 35001495
  7. 7

    Epidemiological and Clinical Evidence for the Role of Toxins in S. aureus Human Disease.

    Bennett MR, Thomsen IP

    Toxins 2020; (12(6)) doi:10.3390/toxins12060408.

    PMID: 32575633
  8. 8

    Gram-negative infections in patients with folliculitis decalvans: a subset of patients requiring alternative treatment.

    Samrao A, Mirmirani P

    Dermatology online journal 2020; (26(2)).

    PMID: 32239885
  9. 9

    Comment on Topical Dapsone for Folliculitis Decalvans.

    Trüeb RM, Luu NC, Rezende HD

    International journal of trichology 2023; (15(3)):88-90 doi:10.4103/ijt.ijt_39_22.

    PMID: 38179006
  10. 10

    Folliculitis Decalvans Has a Heterogeneous Microbiological Signature and Impaired Immunological Response.

    Moreno-Arrones OM, Garcia-Hoz C, Del Campo R, et al.

    Dermatology (Basel, Switzerland) 2023; (239(3)):454-461 doi:10.1159/000529301.

    PMID: 36716709
  11. 11

    Inflammasome Activation Characterizes Lesional Skin of Folliculitis Decalvans.

    Eyraud A, Milpied B, Thiolat D, et al.

    Acta dermato-venereologica 2018; (98(6)):570-575 doi:10.2340/00015555-2924.

    PMID: 29542810
  12. 12

    Evidence of interleukin-17-secreting mast cells in scalp lesions of folliculitis decalvans points to new therapeutic targets in recalcitrant lesions.

    Franciozi AB, Sotto MN, Rivitti-Machado MCM, et al.

    Clinical and experimental dermatology 2025; (50(3)):629-631 doi:10.1093/ced/llae421.

    PMID: 39388582
  13. 13

    Folliculitis decalvans is characterized by a persistent, abnormal subepidermal microbiota.

    Matard B, Donay JL, Resche-Rigon M, et al.

    Experimental dermatology 2020; (29(3)):295-298 doi:10.1111/exd.13916.

    PMID: 30907453
  14. 14

    Folliculitis decalvans in two families.

    Bhoyrul B, Fahey V, Kho YC

    Clinical and experimental dermatology 2026; doi:10.1093/ced/llag385.

    PMID: 42697555
  15. 15

    Folliculitis decalvans: a multicentre review of 82 patients.

    Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al.

    Journal of the European Academy of Dermatology and Venereology : JEADV 2015; (29(9)):1750-7 doi:10.1111/jdv.12993.

    PMID: 25682915
  16. 16

    Epidermal psoriasiform hyperplasia, an unrecognized sign of folliculitis decalvans: A histological study of 26 patients.

    Matard B, Cavelier-Balloy B, Reygagne P

    Journal of cutaneous pathology 2017; (44(4)):352-357 doi:10.1111/cup.12892.

    PMID: 28067422
  17. 17

    Paediatric-Onset Folliculitis Decalvans and Lichen Planopilaris Phenotypic Spectrum: Is It a Different Disease?

    Awad A, Kho YC, Asfour L, et al.

    Experimental dermatology 2026; (35(1)):e70197 doi:10.1111/exd.70197.

    PMID: 41496469
  18. 18

    Cicatricial alopecia.

    Kanti V, Röwert-Huber J, Vogt A, Blume-Peytavi U

    Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG 2018; (16(4)):435-461 doi:10.1111/ddg.13498.

    PMID: 29645394

This page explains folliculitis decalvans symptoms and biology for informational purposes only and does not constitute medical advice. A dermatologist should interpret your symptoms, biopsy results, and any bacterial testing.

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