Skin & hair

Treating Alopecia Areata, From Injections to the New Pills

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Hair loss from alopecia areata does not follow the rules other hair loss follows: it can spread in weeks, and it can fill back in without any treatment at all. That makes choosing a treatment genuinely hard. Here is what sits on each tier, what the SALT score a dermatologist writes down actually means, and what the JAK inhibitor trials did and did not prove.

Last updated: July 2026

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What are the treatment options for alopecia areata?

Treatment sorts into three tiers, and which one applies depends less on how long you have had the diagnosis than on how much scalp is involved and how fast it is moving. A few discrete patches are usually approached with corticosteroid put directly into or onto the bare skin. Loss too widespread to treat patch by patch moves to specialist topical treatment. Severe disease is where the oral JAK inhibitors now sit.

Underneath all three is the same process. Alopecia areata is an autoimmune disease in which the immune system attacks the hair follicles, most often producing round patches of loss, and its course is unpredictable; treatments can promote regrowth, but there is no cure 1.

The tier is chosen by how much scalp is affected and how fast it is changing — not by how long you have had it.

Two consequences follow from that unpredictability, and they shape everything below. The first is that a treatment can look effective when the disease was going to remit anyway. The second is that regrowth is not the same as resolution: hair that returns can fall again, so most of what follows is managing an ongoing process rather than closing it.

Why this disease is unusually hard to treat by evidence

Because it can get better on its own. The course of alopecia areata is unpredictable and hair can regrow without any treatment at all 1. That single fact quietly undermines almost every uncontrolled account anyone will offer you — the supplement that worked, the diet that worked, the device that worked — because none of them can separate a treatment effect from a remission that was already on its way.

It also explains something odd about the shape of the evidence. The lower rungs here rest on decades of clinical practice with comparatively thin trial support behind them, while the top rung arrived attached to large randomised trials with placebo arms. That is an inversion of the usual pattern, in which the oldest treatment is the best studied one.

Spontaneous regrowth is common enough that it is a real possibility for a first, limited patch — not false hope.

None of this makes the lower tiers worthless. It means that when a dermatologist says a first-tier treatment is reasonable to try, they may be drawing on accumulated practice rather than on a study that proved it, and it is entirely fair to ask which of the two they are relying on. Clinicians answer that question willingly; most people simply never ask it.

What the SALT score is measuring

SALT stands for the Severity of Alopecia Tool, and it is a clinician's estimate of how much of the scalp has lost hair — not a questionnaire anyone fills in. The clinician looks at the scalp region by region, judges how much of each is bare, and combines those judgements into a single number. That number is then used two ways: to follow the same head across visits, and to define who qualifies for a trial or a treatment.

The tool was specified in the National Alopecia Areata Foundation's investigational assessment guidelines, which is where it became the consensus measure for quantifying scalp hair loss in this disease 2.

What that founding document does not contain matters, because it changes how much weight one score deserves. It is a consensus guidelines paper rather than a psychometric study, and it reports no minimal clinically important difference, no minimal detectable change, and no reliability statistics 2. A minimal clinically important difference is the smallest change in a score that a patient would actually notice. The severity and response thresholds now in circulation — the score at which disease is called severe, the ones used as endpoints in drug trials — come from later trial and consensus literature rather than from the paper that defined the tool 2.

So the score is a ruler, not a verdict. Its real value is longitudinal: a falling number across appointments means scalp is refilling, and a flat one across several months means the current plan has not moved the disease.

The first tier: a small number of patches

When the loss is a few defined patches, the standard approach is to deliver a corticosteroid to those patches — injected into the skin of the patch itself, or applied on top of it. The logic is deliberately local: suppress the immune attack where it is happening rather than across the whole body. Treatment at this level can promote regrowth, but it does not alter the disease's tendency to return 1.

Injection is the usual choice for adults with a countable number of patches, because it places the medicine at the depth of the follicle rather than on the surface above it. It is done in the office and repeated at intervals the dermatologist sets. Its characteristic side effect is a shallow dent where the treated tissue has thinned; that dent usually fills back in once injections stop, and its appearance is generally a reason to space treatments rather than to abandon them.

What a fair trial period looks like. Hair cannot answer quickly. A follicle that restarts still has to grow a shaft out to where anyone can see it, so the gap between a treatment working and a treatment visibly working is measured in months, not weeks. Most dermatologists set that expectation at the start; if that has not happened, the useful question is how long they intend to give this before calling it.

Minoxidil is often layered in at this stage. It is not an immune treatment, which is why it tends to be described as an addition to one rather than a treatment for alopecia areata in its own right.

The middle: when there is too much scalp to inject

Past a certain amount of loss, treating patch by patch stops being practical, and the options change shape rather than simply getting stronger. The principal one is topical immunotherapy: a sensitising chemical is applied to the scalp on purpose, to provoke a mild controlled dermatitis, on the reasoning that redirecting the immune response at the scalp lets hair grow. It is handled in specialist clinics, it takes months, and it makes the scalp itch and flake by design rather than by accident.

This is also the tier where honesty costs something. The treatments here predate the modern trial apparatus, they are difficult to blind, and they were never subjected to the sort of placebo-controlled study that later supported the systemic tier. They are used because clinicians have watched them work, which is a real form of knowledge and a weaker one.

A treatment being long-established is not the same as it being well proven, and in this disease the two frequently come apart.

Two practical filters end up mattering more than the choice between agents. The first is whether the loss is still advancing; active spreading disease is approached differently from a stable patch that has simply not refilled. The second is plain access — these treatments are compounded and administered at a limited number of centres, so for many people the real decision is not between this tier and the next but between this tier and waiting.

The systemic tier: what the JAK inhibitor trials showed

Two phase 3 trials, BRAVE-AA1 and BRAVE-AA2, tested oral baricitinib — a JAK1/2 inhibitor — against placebo in adults with severe alopecia areata. Baricitinib was superior to placebo for hair regrowth, with success defined as a SALT score of 20 or less at week 36, and those trials were the basis for the first systemic FDA approval in this disease 3. That is why jak inhibitors for alopecia became, more or less overnight, the phrase everyone with this diagnosis started hearing.

The endpoint repays reading closely. A SALT of 20 or less is a threshold for substantial regrowth, not for a full head of hair and not for cure 3. And the comparison was against placebo — which, in a disease that remits on its own, is exactly the comparison that needed making. It is the reason these results carry weight that decades of uncontrolled observation could not.

What the trials did not settle. They measured to week 36 3. They do not describe what happens to hair after the drug is stopped. They were run in adults with severe disease rather than in someone with two patches. And they do not rank one JAK inhibitor against another.

These are systemic immune drugs, and they are prescribed with the monitoring that implies: bloodwork before starting and on a schedule afterwards, and screening for infections that immune suppression can wake up. The class also carries boxed safety warnings in its labelling. Reading that label with the prescriber — rather than a summary of it, and rather than a forum thread about it — is the reasonable way to understand what is being weighed, because the size of that risk depends heavily on the person taking it.

Alopecia areata is not pattern hair loss, and the treatments do not swap

This is the most consequential confusion in hair loss, and it routinely costs people months. Alopecia areata is autoimmune — the immune system attacking follicles, typically in round smooth patches 1. Androgenetic alopecia, the male- and female-pattern thinning most people picture when they hear "hair loss," is a different process with a different pattern, a different timeline, and a separate body of evidence that does not carry across.

You can watch the non-transfer happen in the literature. Platelet-rich plasma injections have a systematic review and meta-analysis supporting improved hair density and thickness in androgenetic alopecia, with the authors themselves flagging substantial heterogeneity and variable protocol quality across the studies pooled 4. That is evidence about pattern hair loss. It is not evidence about alopecia areata, and a clinic offering the same injection for both without distinguishing them is telling you something useful about the clinic.

The caution runs in the other direction too, toward a drug class that looks like it ought to cross over. Topical ruxolitinib, a JAK1/2 inhibitor in cream form, was tested in two phase 3 trials in nonsegmental vitiligo and produced significantly greater facial and total-body repigmentation than vehicle 5. Vitiligo is also autoimmune and it also answers to JAK inhibition — but the vitiligo treatment options those trials established are for vitiligo. A cream that reaches pigment cells near the skin surface is not automatically a cream that reaches the base of a hair follicle.

Two kinds of hair loss can look alike in a mirror and share almost no evidence base. Which one you have decides which studies apply to you.

Eyebrows, lashes, beard, and what a scalp score misses

A scalp score counts scalp. The disease does not confine itself there — it can take eyebrows, eyelashes, beard hair, and body hair, sometimes with relatively little scalp involvement, so someone with alopecia in brows and beard can carry a low number and a heavy day. The tool was built to quantify scalp hair loss 2, and that is simultaneously its purpose and its blind spot.

This has a practical edge, because access to the systemic tier is often written in terms of scalp involvement. The trials that established that tier enrolled adults with severe disease assessed on the scalp 3. When loss is concentrated where the score does not look, that mismatch is worth naming out loud in the appointment rather than assuming the number has told the whole story.

The parts nobody scores. Eyelashes are not only cosmetic — they keep dust and debris out of the eye, and losing them changes how eyes feel in wind, sun, and air conditioning. Nail changes, fine pitting or ridging, show up in this disease often enough to be worth mentioning and are easy to blame on something else.

Then there is the part no instrument touches at all. Visible hair loss is a public illness: people notice, people ask, and strangers sometimes assume cancer treatment. Medical wigs, documented for insurance purposes as a cranial prosthesis, are a legitimate component of care rather than a form of giving up — and so is asking for mental-health support, which dermatologists in this field are well used to being asked for. A condition being medically benign does not make it psychologically minor.

Common questions

It might. Regrowth without treatment genuinely happens in alopecia areata, and it happens often enough that a first limited patch is sometimes watched rather than treated. What nobody can do is predict it for an individual. The same unpredictability that makes spontaneous regrowth possible also means hair that returns can fall out again later.

The hair loss itself is not physically harmful, and it does not damage the scalp or shorten life. Dermatologists commonly check for other autoimmune conditions alongside it, which is why a first appointment may include bloodwork that seems unrelated to hair. The serious burden of this disease is psychological, and that burden is treated as real, not incidental.

Months, in almost every case. Hair has to be regrown before it can be seen, so even a treatment that switched the immune attack off today would take a long time to show it. Judging any tier before the dermatologist's stated review point mostly produces discouragement rather than information.

No. The phase 3 trials measured regrowth on continued treatment out to a fixed point and showed the drug beat placebo. They did not establish a cure, and there is no cure for this disease. What the pills changed was the existence of a systemic option with placebo-controlled evidence behind it, which had never been true before.

Many people date the first patch to a hard year, and that connection is reported too often to dismiss. But alopecia areata is an autoimmune disease, not a failure of composure, and no amount of stress management has been shown to regrow hair on its own. Reducing stress is worth doing for its own sake. It is not a treatment plan.

The names describe extent, not different diseases. Alopecia areata is the general term and usually means patchy scalp loss. Totalis describes loss of all scalp hair. Universalis describes loss of scalp and body hair, including brows and lashes. The underlying immune process is the same one, which is why the treatment tiers are shared.

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When hair loss is not alopecia areata

  • —Bare patches that look shiny and smooth with no visible pore openings, or scalp that is red, scaly, tender, or burning — scarring alopecias destroy follicles permanently and are treated urgently
  • —Sudden diffuse shedding across the whole scalp alongside unexplained weight change, fatigue, or heat or cold intolerance
  • —Hair loss appearing with a new facial rash, mouth ulcers, or joint pain and swelling
  • —Rapidly enlarging patches accompanied by pus, crusting, or swollen lymph nodes at the back of the neck

If hair loss has brought you to thoughts of not wanting to be alive, call or text 988 in the US, or go to an emergency department. This is a common enough response to visible hair loss that clinicians expect it and know what to do with it.

This page describes how alopecia areata is treated and what the published trials measured. It is not medical advice, it cannot tell you which kind of hair loss you have, and it does not replace an examination by a dermatologist who can look at your scalp.

References

  1. 1.National Institute of Arthritis and Musculoskeletal and Skin Diseases (2024). Alopecia Areata. NIH / NIAMS. link ✓The definitional statements on this page: that alopecia areata is an autoimmune disease in which the immune system attacks hair follicles, that it typically causes patchy hair loss, that its course is unpredictable and hair can regrow without treatment, and that treatments can promote regrowth but there is no cure.
  2. 2.Olsen EA, Hordinsky MK, Price VH, et al. (2004). Alopecia areata investigational assessment guidelines--Part II. National Alopecia Areata Foundation. Journal of the American Academy of Dermatology. doi:10.1016/j.jaad.2003.09.032 ✓That the Severity of Alopecia Tool was specified in the National Alopecia Areata Foundation's Part II investigational assessment guidelines and became the consensus clinician-rated measure for quantifying percentage scalp hair loss in alopecia areata. Also cited for what this consensus document does not establish: no minimal clinically important difference, no minimal detectable change, no reliability statistics, and no severity or response thresholds — those postdate it and derive from later trial and consensus literature.
  3. 3.King B, Ohyama M, Kwon O, et al. (2022). Two Phase 3 Trials of Baricitinib for Alopecia Areata. New England Journal of Medicine. doi:10.1056/NEJMoa2110343That the BRAVE-AA1 and BRAVE-AA2 phase 3 trials showed oral baricitinib, a JAK1/2 inhibitor, superior to placebo for hair regrowth in adults with severe alopecia areata, with success defined as a SALT score of 20 or less at week 36, and that these trials were the basis for the first systemic FDA approval in alopecia areata. Also cited for the limits of what they measured: severe adult scalp disease, to week 36.
  4. 4.Gupta AK, Bamimore MA, Foley KA (2020). Efficacy of non-surgical treatments for androgenetic alopecia: platelet-rich plasma systematic review and meta-analysis. Journal of Dermatological Treatment. PMID 32410524 ✓That platelet-rich plasma injections have systematic-review and meta-analysis support for improving hair density and thickness in androgenetic alopecia, with substantial heterogeneity and variable protocol quality across pooled studies — cited here to mark that this evidence belongs to pattern hair loss and does not transfer to alopecia areata.
  5. 5.Rosmarin D, Passeron T, Pandya AG, et al. (2022). Two Phase 3, Randomized, Controlled Trials of Ruxolitinib Cream for Vitiligo. New England Journal of Medicine. doi:10.1056/NEJMoa2118828 ✓That the TRuE-V1 and TRuE-V2 phase 3 trials showed topical ruxolitinib cream, a JAK1/2 inhibitor, produced significantly greater facial and total-body repigmentation than vehicle in nonsegmental vitiligo — cited here to mark that a topical JAK inhibitor's trial evidence belongs to vitiligo and is not evidence in alopecia areata.

5 sources, numbered by first appearance. General health information, not medical advice. AI-assisted editorial content — citations link their sources. Editorial policy

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