Central centrifugal cicatricial alopecia (CCCA)

Key takeaways

• CCCA is the most common scarring alopecia in women of African descent. It begins at the crown and spreads outward in a circle, and lost follicles are replaced by scar (Sanz-Cabanillas 2026). It is mostly a condition of textured hair (roughly 3B to 4C), though men and children can be affected.
• Early signs are easy to dismiss: breakage in the centre of the scalp, tiny bumps, scale or a crusty feel, sometimes itching, burning, tenderness or pins-and-needles. Later a smooth shiny bald patch appears. Many people have no symptoms at all.
• Diagnosis is delayed. CCCA had a longer time to diagnosis than other scarring alopecias in a 2026 study (Issa 2026), and misdiagnosis of hair and scalp disorders in adults with skin of colour is documented (McMullen 2026).
• Genetics is now a leading explanation. Whole-exome sequencing of 75 biopsy-confirmed patients found 9 pathogenic variants in the PADI3 gene, plus variants in S100A3 and TCHH, which encode hair-shaft structural proteins (Keller-Rosenthal 2026). So it is not simply caused by relaxers or braids.
• The hairstyle story is unsettled. A 2024 review found mixed data on relaxers and heat (Geisler 2024). Gentle hair care still makes sense on an inflamed scalp, as a precaution rather than proven cause.
• Comorbidities: a 2026 meta-analysis (23 studies, 9,103 patients) found dyslipidaemia (OR 4.46), uterine leiomyoma (OR 2.25) and anxiety (OR 3.27) associated, while hypertension, obesity and thyroid disease were not consistently associated; the data were mostly retrospective and from the US (Sanz-Cabanillas 2026). A 2026 case-control study found no link with type 2 diabetes or hypertension (Ong 2026).
• There is no standard of care. A US expert Delphi (27 dermatologists) reached strong consensus on only 20 of 70 statements (Jackson 2024).

What it is

Chronic inflammation around the follicle, early loss of the inner root sheath and fibrosis lead to scarring. Researchers describe a fibrosis-prone tendency that overlaps with uterine fibroids. Under the scalp microscope, white or grey rings around follicles are more typical than redness or scale, and a biopsy from the active edge confirms the diagnosis (Geisler 2024).

What the studies show

Treatment evidence is low certainty.

• Potent topical steroids, steroid injections and anti-inflammatory antibiotics, topical or oral, are based on expert consensus with no randomized trials (Jackson 2024).
• Topical and oral minoxidil are used to thicken surviving hairs; a single case report paired oral minoxidil with topical ruxolitinib in someone with CCCA and traction alopecia (Soto-Canetti 2025).
• Low-level light, apremilast, JAK inhibitors and GLP-1 drugs have only small cohorts, pilots or case reports, and transplant is limited to burnt-out disease. See minoxidil, low-level laser therapy and PRP.

Hair type notes

• Tightly coiled hair is the highest-risk group. Coils shed breakage that hides crown thinning, so people often notice late. Check the crown with a mirror or have a partner photograph it monthly.
• Breakage from dryness or chemical damage does not leave a smooth shiny scalp. If the centre of the crown is losing density with tenderness or bumps, treat it as medical, not a moisturizing problem.
• Co-existing traction alopecia is common and can make diagnosis harder. See traction and hairstyles and brushing and detangling.
• In looser curl patterns (1A to 3A) CCCA is rare; crown thinning is far more likely to be pattern hair loss (see DHT and pattern hair loss).

Bottom line

Crown breakage, itching or burning, or a widening crown patch calls for a dermatologist who knows textured hair, and a biopsy. Do not wait for shiny skin: earlier treatment preserves more hair. Keep a monthly crown photo in the same light with the hair parted, and be cautious about unproven oils and devices, none of which has trial data for CCCA. See when to see a dermatologist. Discuss with a doctor.