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Filtering by Category: Scarring Alopecia

Hair loss of the beard: What are the considerations?


I have had beard alopecia areata/alopecia barbae since the age of 21, I am now 33. It began with one small bald patch under the chin and later in this period either simultaneously or after the bald batch grew back (which was within say the first couple of years) developed numerous very small bald patches throughout the entire beard (which on the cheeks appear slightly jagged) however are barely noticeable throughout. One bald patch larger than these very small patches developed on one cheek say 5 years ago and remains to this day. In summary, the condition has never dissipated however has remained static in its behaviour for a number of years to the present day.

My questions are as follows.

1. What is the likelihood of the condition progressing to other hair bearing areas? (I am aware of the study you quote at however this only followed up with patients after 12 months)

2. In the event that the condition did not progress to other hair bearing areas would hair transplantation surgery on the scalp (I have had male pattern hair loss since 2015/2016 and have been advised that it would be not until around age 35 when surgery could sensibly be considered - using FDA approved medications have only slowed down the condition rather than halted, or to any extent, caused its reverse) increase the risk of the condition (alopecia barbae) progressing to other hair bearing areas, especially the scalp?


The key here is …. what exactly is your diagnosis? It may or may not be alopecia areata and without actually seeing your scalp and beard up close myself, it would be a mistake to assume that it is. There are many mimickers of alopecia areata that need to be ruled out here - especially autoimmune cicatricial alopecia. If the areas are relatively unchanged for an extended period of time, the chances this is alopecia areata goes down.

Of course alopecia areata is on the list (and quite high up on the list of possibilities), but true classic alopecia areata of the beard does not stay unchanged over an extended period of time. You might consider seeing a dermatologist for expert review. A full review of your history and review of your hair loss pattern via dermoscopy is needed. A biopsy might be needed as well.

As far as chances of progression to other areas, it really depends on the precise diagnosis. If the disease has an immune basis, there is most certainly a chance of progression to the scalp. Hair transplantation of the scalp could be associated with an increased risk of the disease developing in the scalp - but it depends entirely on the precise diagnosis. For patients with isolated beard alopecia, my feeling is that there is about a 65-70 % risk over 10 years of alopecia areata being identified in the scalp. This too may be only one patch or may be more severe- but the presence of beard AA sets the stage for scalp AA to develop. Having a transplant is a small risk but only a small one. 2 % of the world will develop alopecia areata and so one generally expects 2 % of hair transplant patients to develop alopecia areata in their lifetimes. In 60-70 % of patients who do develop alopecia areata of the scalp in the years following their hair transplant regrowth happens quite readily with conventional treatments. Some do, however, have a more refractory course.

If the cause of the beard alopecia is actually a variant of immune based primary scarring alopecia (i.e. lichen planopilaris, folliculitis decalvans, lupus) or secondary scarring alopecias (sarcoid, scarring folliculitis etc), a hair transplant carries the risk of actually triggering scarring alopecia on the scalp. The concerns about proceeding with hair transplantation become magnified if the diagnosis actually turns out to be scarring alopecia.

All in all, alopecia areata is still at the top of the list here in the question that has been posed - but there are features of the story that are a bit unusual. You should be absolutely certain before moving on that this is alopecia areata and not something else. There is a risk over the next 10 years of alopecia areata developing on the scalp but in a majority of cases conventional treatments can help maintain the density. It largely comes down to understanding the risks and benefits (so called risk benefit ratio) …. and making an educated decision together with one’s dermatologist and surgeon. Making sure one has as much information as possible before moving forward with surgery is key.

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Frontal Hairine Loss in a 48 Year old Black Female


I'm a black female 48 years old with what I believe is CCCA. I started loosing my hairline in 2014, however in an 18 month period I lost my entire hairline. For the last 14 months I've been treating my scalp with natural oils/home remedies. The hair loss have stopped. I think my condition could be inactive. If the e disease is in fact inactive, without any medical treatment, can my hair grow back on its own or will I need a hair transplant?


Thanks for the great question. As a physician who sees a lot of women with CCCA, your brief story shouts out to me one main message: this may or may not be CCCA that you have and if it is CCCA, one or more other hair loss conditions might be present too.

Let me begin. Central centrifugal cicatricial alopecia (CCCA) usually starts in the middle of the scalp or in the crown. CCCA does not usually start in the front like you described. However several conditions can affect the frontal hairline just like you described including traction alopecia, cicatricial marginal alopecia and frontal fibrosing alopecia. What’s a bit unexpected from your story is the complete loss of the hairline that you described. That certainly favours a diagnosis of frontal fibrosing alopecia over traction alopecia but of course I would need to see your scalp myself to answer that. An entity called cicatricial marginal alopecia is also on the list.

Your story is not a typical story of CCCA although of course you could have CCCA back in the mid-scalp too. Many black women with hair loss in the frontal hairline also have some degree of CCCA too.

What you really need now is a diagnosis. An expert dermatologist who treats a lot of patients with hair loss might be able to make the diagnosis without a biopsy but if you are thinking of hair transplants down the road a biopsy is going to be helpful to secure the diagnosis and also determine for you (and your doctors) just how active or inactive the disease truly is right now. My advice to anyone with a story like yours would be to consider a sample from the frontal hairline area and also from the crown. Remember that a biopsy always needs to have a hair in it so don’t biopsy any bare area as that is useless.

I’m suspicious about your diagnosis of CCCA but a few things about your story are more definite. First, it’s unlikely you’ll get spontaneous growth if you haven’t had growth since 2014. Depending on the exact and precise diagnosis, you still could get a bit of regrowth with treatment but likely only a bit. Second, you are probably not a candidate for surgery yet. Whether you become a candidate depends somewhat in the diagnosis but also on the activity level of your primary disease. I like to have patients take photos once they feel their disease is quiet... and if there is absolutely no change in hair loss after two years of photography then a hair transplant might be possible. If you feel your scalp has now become quiet, take a picture today and plan to compare that same picture in 2 years. If the two pictures look 100 % identical you might be a candidate for surgery. The longer answer as to whether you are a candidate for surgery actually depends on several factors.

In summary, your story suggests a diagnosis of frontal fibrosing alopecia or traction alopecia much more than it does CCCA. A biopsy could be extremely important for you and your treating physicians right now.

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Hair Loss from Relaxers


Can my scalp be treated after severe damage from a hair relaxer?


Thanks for the great question. This is such an important question and also a very common one. There is a lot to discuss. As you’ll see, the answer to your question is ‘maybe.’ Some patients with hair loss form relaxers will grow back their hair. Some patients do not.

Let’s begin.

When a patient says to me they have hair loss from a relaxer, it’s important to keep in mind that there is not one type of hair loss that they might have. In fact, they might have one or more of many types of hair loss, including hair breakage, inflammatory scarring alopecias, hair loss from chronic inflammation, traction alopecia, telogen effluvium or androgenetic alopecia. Some patients just have one type of hair loss. Others have two or three.

Let’s take a look.

1. Hair breakage (Trichorrhexis nodosa)

Both chemical and heat relaxing of hair can cause breakage of the hair. The hairs simply break off because of the damage to the delicate strand. The heat or chemicals cause “micro tears” in the hair shaft which we call “trichorrhexis nodosa.”

The photo below shows a picture of a hair fibre that has such a tear.

Trichorrhexis nodosa of a hair fiber. This can occur from many agents including heat and chemicals used to relax hair.

Trichorrhexis nodosa of a hair fiber. This can occur from many agents including heat and chemicals used to relax hair.

If trichorhexis nodosa is the only reason for the hair loss, the hair will grow back. The damaged sections may need to be cut off, but the long term prognosis is good. It may take 6-9 months before hair returns back to the way it once was but it will return. Unfortunately, trichorrhexis nodosa as the ONLY and sole reason for a person’s hair loss from relaxers is not common. Ofter there is another reason present as well, and these are discussed below.

2. Telogen Effluvium

Many patients who come to see me with concern about their hair after using a relaxer also have a a diagnosis of telogen effluvium or “TE.” Telogen effluvium is a type of hair loss that occurs when the body feels some type of shock. This can occur from low iron (low ferritin), thyroid problems, anemias, crash diets, weight loss, stress, medications, and illness. Some of these issues such as anemia and low iron levels may make the hair slightly weaker and slightly more susceptible to hair damage. These issues must be addressed fully. For this reason, I always order blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA in all patients who come to see me with concerns about hair loss from a relaxer. Other causes must be fully evaluated.

3. Traction alopecia.

Traction alopecia is a type of hair loss that occurs from the chronic pulling of hair. Patients who use relaxers may be more susceptible to traction alopecia because their hair is subjected to many pulling forces during relaxers and the hair fibers may be weaker. Traction alopecia can occur anywhere on the scalp. The frontal regions near the temple are often a common site of traction.

Treatment for traction alopecia involves stopping the pulling forces that caused the traction in the first place. If traction alopecia is diagnosed and pulling is stopped immediately (within a few months of the new hair care practice), hair might grow back. However, if traction alopecia has been present many months, the hair may not fully return. Long standing traction alopecia is permanent and may even continue to progress once the hair pulling is stopped.

Traction alopecia of the frontal hairline.

Traction alopecia of the frontal hairline.

4. Scarring Alopecia and Chronic Inflammation .

It’s a little known fact but chronic use of relaxers, especially chemical relaxers, can create scalp inflammation. It may not be a type of inflammation that can be seen on the surface but rather a type of inflammation that is occurring deep under the scalp. In some people using relaxers (but certainly not all people), this chronic inflammation triggers the body to also create scar tissue beneath the scalp. The exact mechanism is not clear but micro injury to the skin creates microinflammation and chronic microinflamation may induce scar tissue to form.

This pattern of hair loss from relaxers has been most carefully studied in women with afro-textured hair but likely applies to all hair types. Chronic use of relaxers in women with afro-textured hair may be linked to the development of several types of hair loss including traction alopecia and central centrifugal cicatricial alopecia (CCCA). CCCA often affects the central scalp first. The diagnosis must be caught as early as possible to prevent progress and prevent irreversible loss of hair. Too often women with CCCA are told that their hair loss is simply from a relaxer and it will grow back. CCCA is a cause of permanent hair loss. If there is any doubt, a punch biopsy should be considered to properly evaluate for scarring alopecia. Treatment with agents such as topical steroids, steroid injections, and doxycycline can help stop the disease. Hair growth does not usually occur. A photo of a woman with CCCA is shown below.

Central centrifugal cicatricial alopecia (CCCA) in a woman initially misdiagnosed as having temporary hair loss from a relaxer. The correct diagnosis for this patient was CCCA which causes permanent hair loss.

Central centrifugal cicatricial alopecia (CCCA) in a woman initially misdiagnosed as having temporary hair loss from a relaxer. The correct diagnosis for this patient was CCCA which causes permanent hair loss.

Summary and Conclusion

Thanks again for the great question. Let’s now return to the original question regarding whether or not your scalp can be treated. As we’ve seen above, it really comes down the the exact cause of the hair loss. If the relaxer caused trichorrhexis nodosa, the damaged hair simply needs to be trimmed and hair density will eventually come back. If however, the relaxers have caused traction alopecia, it may or may not come back even if the relaxers are stopped. If the cause is CCCA, the hair is less likely to return and aggressive treatment with various anti-inflammatory medications are needed to stop the inflammation. If there is a telogen effluvium (from low iron for example) that predisposed to some fragility and hair loss, there could be some improvement with iron supplementation and stopping the relaxers as well.

Be sure to see a dermatologists as relaxer related hair loss can be complex sometimes. Blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA might be considered and if any doubt exists, a biopsy might be considered to rule out scarring alopecia.

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Seborrheic Dermatitis vs Lichen Planopilaris: Which do I have?


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My doctors can’t decide if I have seborrheic dermatitis or lichen planopilaris. My scalp does feel less itchy and becomes less red with anti dandruff shampoos. However, it also becomes less red and itchy with topical steroids. Overall my shedding has improved after 4 weeks of treatment. Does this information suggest one diagnosis over the other?


Thanks for the great question. The short answer is that the information provided here does not actually suggest one diagnosis over another. You may have scarring alopecia and you may have seborrheic dermatitis. The key point I would like to make is that you may have both! Up to 50 % of patients with lichen planopilaris have seborrheic dermatitis too. A scalp biopsy can fully answer your question.

Let’s take a closer look at both of these conditions and we’ll see why some patients with lichen planopilaris will benefit from anti-dandruff shampoos and we’ll see why some patients with seborrheic dermatitis benefit from topical steroids (the same ones used to treat lichen planopilaris.)

First, seborrheic dermatitis is closely related to dandruff. The exact cause is still being worked out but yeast such as Malassezia may have an important role. Patients with seborrheic dermatitis have many similar (and sometimes identical) symptoms to patients with lichen planopilaris. They have a red, itchy scalp! Seborrheic dermatitis however does not cause scarring for most people and usually only gives minor amounts of hair shedding. (Everything in medicine has exception and seborrheic dermatitis may cause scarring in some cases and may give excessive hair shedding when severe - see previous articles below).



Seborrheic dermatitis is an inflammatory condition which means there is inflammation in the scalp. Although the standard first line treatment for seborrheic dermatitis is topical anti-dandruff shampoos, treatment with anti-inflammatory agents like topical steroids can help reduce the inflammation which in turn reduces redness and itching. Many patients with seborrheic dermatitis feels better with use of both antidandruff shampoos and topical steroids. In fact, studies have shown that adding topical steroids to a patient’s seborrheic dermatitis treatment plan can greatly help.

To come back to your question for a moment, we would expect seborrheic dermatitis to improve with dandruff shampoos and topical steroids. However, fact that your scalp did improve does not rule out a scarring alopecia as we’ll see next.

Lichen planopilaris is a scarring alopecia that causes patients to experience itching and sometimes burning and tenderness in the scalp. The scalp is typically red. An important difference between lichen planopilaris and seborrheic dermatitis is that lichen planopilaris always associated with scarring. Biopsies of LPP show rings of scar tissue around hair follicles in early stages (called concentric perifollicular fibrosis) and deposits of large bits of scar tissue in the scalp in advanced stages.

Topical steroids are one of many agents used to treat LPP. They help reduce redness and scaling and help the patient feel better too with less itching, burning or pain.

Seborrheic Dermatitis in Patients with LPP: Is is More Common than We Realize?

Seborrheic dermatitis is present in a very large proportion of patients with LPP. In fact, a greater proportion of patients with LPP have seborrheic dermatitis compared to people in the general population. (About 5% of people in the general population have seborrheic dermatitis compared to nearly 50% of patients with LPP). On account of seborrheic dermatitis being so common in LPP, it makes sense that many people with LPP will feel better and gain some relief with use of antidandruff shampoos! The fact that a patient with LPP reports improvement with antidandruff shampoos does not rule out a scarring alopecia. It simply means they may have seborrheic dermatitis too!

Cleveland Clinic 2016 Study of Seborrheic Dermatitis in LPP

In 2016, Berfeld’s group at the Cleveland clinic studied the incidence of seborrheic dermatitis in patients with lichen planopilaris. This study is important to understand and relevant to the above discussion. It was one of the few studies to date which really documented the increased incidence of seborrheic dermatitis in patients with LPP.

The study I am referring to was a retrospective review of 246 patients seen over the period 2004-2015. Interestingly seborrheic dermatitis (SD) was present in 46.2 % of LPP cases. In 27.4 % of cases the SD was found outside the area affected by the LPP. On average the SD was diagnosed 7.8 months prior to the LPP diagnosis. Having SD seemed to delay an actual diagnosis of LPP. Patients with both SD and LPP diagnosis (LPP-SD) received their diagnosis with significantly more delay than patients with LPP who did not have SD (ie LPP). For example, patients with LPP-SD received their diagnose in 7.6 months on average comapred to 2.3 months for LPP alone.

Whether SD actually plays a role in the scarring process as well remains to be determined. It is interesting that there was a greater prevalence of late stage scarring alopecia in ptient with LPP-SD than LPP alone (41.5 % vs 15.7%). Patients with LPP-SD had greater rates of hyperandrogenism compared to patients with LPP alone.


Thanks again for the great question. One can’t determine if you are more likely to have SD or LPP from the information provided. It would be entirely within the realm of expected for a patient with LPP to improve with topical antidandruff agents since many have seborrheic dermatitis present as well. Likewise, it would be expected that a patient with seborrheic dermatitis would improve with topical steroids because this is an inflammatory disease just like LPP.

A biopsy can help distinguish if lichen planopilaris is truly present or not.

Ratnaparkhi et al. Association of lichen planopilaris with seborrheic dermatitis l: A retrospective case-control study. Poster 3727. JAAD May 2016.

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How long does it take to know if scarring alopecia treatments are working?



QUESTION: I was diagnosed with lichen planopilaris. My dermatologist put me on topical steroids (betamethasone diproprionate) and doxycycline (100 mg daily). How long does this treatment take before I know if I am benefiting?



Thanks for the question. The real answer depends on a few factors as you'll see below. It could be as early as a few days before your get a sense if you are on track or several months. Let me explain. 

As you've probably come to know from your own physicians, lichen planopilaris (LPP) is a type of scarring alopecia that causes permanent hair loss.  We don't typically expect to see hair regrowth to any significant degree (unless treatment is undertaken in the very earliest of stages). The goal of treatment is to stop the disease and prevent it from getting any worse. 

Lichen planopilaris (LPP) is often 'symptomatic', meaning that many patients have itching, burning or pain/tenderness and notice increased amounts of daily shedding.  Some have all four of these of these symptoms and some have two or three. Of course, about one-third or so of patients don't really have much in the way of symptoms and the scalp feels pretty normal to them. They may just notice a bit of increased shedding. 

The reason this concept is important to mention is because patients who do experience scalp symptoms with their LPP will know if a matter of a few days if they are benefiting from topical steroid treatments. Strong steroids like betmethasone dipropionate usually act to relieve symptoms very quickly and can help reduce shedding quite quickly as well. Oral immunomodulating medications like doxycycline take a bit long but also act within a few weeks. So, if a patient with LPP has considerable itching, burning and tenderness and finds that that the betamethasone is helping to relieve symptoms and shedding after a few days - this means the treatment is benefiting.

Now for a bit more involved discussion.


Difference between short term vs long term benefits

The "first step" for a patient with LPP who is symptomatic is to reduce their scalp symptoms and shedding. This is what we are watching for. This is what we are hoping for. If a patient has itching that they rate as 7 out of 10, we hope in future apportionments that it reduces to 1 out of 10 or maybe even 0 out of 10.  If they feel they once were losing 100 hairs daily and now feel it's under 50 hairs per day... this too is a good sign. 

What we don't know early on in the course of treatment is whether the reduction in symptoms actually correlates with a cessation of hair loss. In other words, a reduction in symptoms is terrific, but it's really the ability to prove that the hair loss is slowing down or stopping that is the most important thing. This comes with scalp examination and photography. 


Scalp examination and photography prove a treatment is benefiting

If a patient states that his or her itching is greatly improved, but a photograph at the 4-6 month follow up appointment shows that more hair loss has occurred, this means that the treatment is not working at all or not working well enough. If the treatment is not working at all, it needs to be stopped and another treatment started. If the treatment is not working well enough but is still helping to slow the rate of loss down a bit, one might consider continuing that treatment (as it is doing something) and adding a second treatment. Of course, this is a professional judgement, and something we stop treatments that are are only working a bit and bring on board treatments that have potential to stop the disease completely.  

Generally speaking if treatments are not working, a photograph will show more and more loss every 4-6 months. Some patients have very slowly progressing LPP and it will take 1 year to show that further hair loss is occurring. Nevertheless, carefully documented photographs will show whether the disease is progressing or stopping. The importance of photography can't be overemphasized. 

Up close examination of the scalp will also provide helpful signs for patients with LPP and so frequent examination by a dermatologist is important. The presence of redness and scaling in the scalp are all potential signs of disease activity. If the amount of redness or scale improves with treatment, this usually means the treatment is working. While the up close examination is important to judge whether a disease is active or not - the most important of all is the photograph of the scalp.



hanks again for the great question. I hope this clarifies things.  The real answer is that a patient will truly know in several months if the treatment is truly working by comparing photographs. There are some really helpful things to observe for in the first few weeks and months to give us hints that things are working. This includes a decrease in symptoms and shedding and a decrease in redness and scaling. The most valuable of all is the photograph. 


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What causes hair texture changes?




QUESTION: What causes hair texture changes? I used to have very soft and glossy hair. However, now after years of hairless (androgenetic, FFA & LPP) and treatments (injections, topical clobetasol & oral medications) my hair is very dry, dull, almost straw-like. Are these texture changes due to aging, the hair loss conditions or perhaps the treatments? Conditioners do not seem to help. Thank you.



Thanks for the great question. There are many causes of hair textural changes. In your case specifically, the causes are probably "multi-factorial" rather than a single cause.  Let’s take a look at some of the more common causes of textural changes and how they apply to the question you have raised. 


Consideration 1: Scarring alopecia

Many patients with scarring alopecia notice changes in their hair texture, especially a change to a drier, more brittle and slightly curlier hair texture. As the name suggests, scarring alopecia is associated with the development of scar tissue or ‘fibrosis’ under the scalp. Such fibrosis affects how hairs emerge from the scalp. Hair frequently twist and turn as they emerge from the scalp and sometimes even rotate 180 degrees. We call this twisting and turning ‘pili torti.’ Individuals with pili torti will notice a hair textural change.

Scarring alopecias are universally associated with loss of the oil glands (sebaceous glands) in the scalp. One can not have a scarring alopecia without having a reduction in the oil glands. These oil glands lubricate the hair follicle.  The destruction of sebaceous glands during the process of scarring alopecia contributes in part to the drier texture. 

Scarring alopecia also affects the quality of the hair that is produced. Commonly there is hair breakage on account of the much weaker fibers. 


Consideration 2: Hormonal changes

A variety of hormonal changes can lead to drier, coarser hair.  About 15 % of women are affected by thyroid disease and this a common cause of textural changes. The incidence fo thyroid disease is much more common in the conditions that you mention including lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) and so thyroid status should always be carefully evaluated in patients with scarring alopecia.

With approaching menopause, the declining estrogen levels and  imbalances in the ratio of androgens to estrogens also results in drier hair. Women who are predisposed to develop androgenetic alopecia may notice that the hair becomes finer and some may notice the texture changes too. About 40 % - 50% of women with frontal fibrosing alopecia (FFA) and lichen planopilaris (LPP) have androgenetic alopecia. 


Consideration 3: Heat and chemicals

A variety of products that are applied to the scalp can lead to the hair becoming drier, and more brittle. Products containing alcohol are frequently a culprit. This includes hairsprays but many other alcohol containing cosmetic products as well. Products such as minoxidil lotion, and topical steroids may contain alcohol-based ingredients which also dry out the hair.


Consideration 4: Inflammatory scalp diseases

A variety of scalp conditions that are associated with inflammation can lead to altered hair texture over time. Conditions such as seborrheic dermatitis and psoriasis can lead to drier duller hair. Many individuals with FFA and LPP have co-existent seborrheic dermatitis and if present, this should be treated. 


Consideration 5: Androgenetic alopecia (AGA)

Androgenetiic alopecia (AGA) is also a cause of hair textural changes. Although we discussed AGA in the context of hormonal changes above (see "Consideration 2"), androgenetic alopecia can also cause textural changes irrespective of any hormonal abnormalities. In fact, 85 % of women with androgenetic alopecia have normal hormone levels. In women, androgenetic alopecia is also known as female pattern hair loss and in men, male pattern balding. 

Women with AGA often notice the hair is finer and some notice the hair becomes curlier. Others notice the hair becomes flatter and less likely to hold it's original shape, curl or wave. 


Consideration 6: Aging

Hair "aging" is a poorly researched area and poorly defined in general.  Age-related changes in hair, independent of the hormonal changes that can occur with age, can also lead to textural changes in the hair. 



There are a variety of reasons for hair textural changes. One can usually determine the cause of the textural changes with a full review of one's story (i.e. the medical history) along with an up close examination of the scalp. Most of the time blood tests are also needed. 

Thanks again for the great question.  



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What causes scarring alopecias like FFA and LLP to reactivate?



QUESTION: What causes scarring alopecias like FFA and LLP to reactivate? After a period of approximately 6 months during which my hair loss from FFA & LPP seemed to stabilize and hair density actually improved, the shedding has now significantly increased again. What causes these scarring alopecias to reactivate months, or potentially even years, after a period of being quiet with no measurable hair loss? Thank you.



Thanks for the question. There are a number of reasons why a scarring alopecia can re-activate after it was once quiet. Here are the top 5 important points of discussion. 


Reason 1: We simply don't know the reason.

Although not the answer one would expect to hear as reason 1, we need to respect that we don't completely understand scarring alopecia in the present day and age. Often, we simply don't know the reason. Scarring alopecias can activate and become quiet for periods on their own. We often attribute the entry into a "quiet (inactive) phase" as proof that some type of treatment we are using is helping but scarring alopecias can become quiet other own. Similarly, we often attribute worsening as an indication that something we are doing is no longer working, or we're doing something 'wrong.' However, scarring alopecias can become active spontaneously for reasons that are not clear.


Reason 2: A second hair loss condition has developed.

Whenever there is worsening hair loss, we need to consider that the loss is actually due to another condition, and not the scarring alopecia. Such a condition is often in the form of a 'telogen effluvium," There is an increased incident of iron deficiency, low vitamin D and even thyroid dysfunction among patients with scarring alopecia. For example, a 2014 study from the Cleveland clinic showed that 29 % of patients with LPP develop thyroid dysfunction compared to 9 % of controls. A second study showed that there are also differences in vitamin D status. I've included these references below. 

Levels of vitamin D, TSH, ferritin, zinc should be checked in any patient who experiences a 'flare' following an extended period of quiescences. 


Reason 3: There has been increased life stress.

There's no doubt in my mind that increased life stress can trigger flares in patents with scarring alopecias. It's not clear why and the link seems more relevant for scarring alopecias such as lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) than many of the other scarring alopecias. Stress can increase a variety of neuromediators and nerve-related hormones in the scalp which impact inflammation.  


Reason 4: There has been injury to the scalp.

It continues to be an area of limited study, by injury can trigger a worsening or 'flare' of a scarring alopecia.  The medical literature documents injuries such as facelifts and hair transplants as triggering scarring alopecias to worsen. However, many types of injuries can cause the disease to reactivate. 


Reason 5: Medications have recently been started or stopped

A scarring alopecia can become active again on account of a) stopping a mediation that was helping, b) starting a medication that was not used before and c) rarely, changing the brand name of a medication that was helping .

If one has recently tapered or reduced a medication within the last one year and is now noticing a worsening of hair loss, they need to consider that the cessation  or reduction of medication could be responsible for the 'flare'. We see that with slow acting medications like hydroxychloroquine. 

Starting a new medication can sometimes trigger shedding. For example, the addition of minoxidil to the scalp in a patient who otherwise had stable disease, can trigger some shedding. Also some medications such as hydroxychoroquine can trigger shedding in some patients. 

Finally, we rarely encounter a situation where a pharmacy changes the brand of the mediation given to the patient. Instead of getting tablets form company X, they are dispensed tablets from company Y. It appears to be the same medication but for some reason a flare occurs. Even more rarely the wrong dose has been prescribed to the patient and they end up receiving less than intended. This of course can cause a flare.


Reason 6: The scarring alopecia has done from "very slightly active" to "slightly active"

To be truly confident a scarring alopecia is inactive, one needs to observe it for two years. After a period of 6 months of observation with a scarring it being "quiet", we can't actually conclude that it was truly inactive.

I often given an analogy of a car moving down the street as an analogy to understand the speed of hair loss. Suppose one's hair loss is moving forward at 6 miles per hour. For the sake of argument, let's say that particular speed is fast enough to see a change in hair density every 6 months. Now let's say the hair loss slows down to a rate of 2 miles per hour. That's really slow. It's not enough to see a change every 6 months but it is just enough to detect a change in density every 1-2 years. If a patient has hair loss moving forward a 2 mies per hour, and they don't see a change after 6 months, they can not conclude it is inactive. Rather there are two possibilities in such a case: either the scarring alopecia is inactive or it is still very slightly active. A clinical examination of the scalp by a dermatologist or time will declare which is correct.  



Thanks once again for the great question. When I teach doctors about the reasons for flares in an otherwise stable patient, I frequently use the memory tool "IM WORSE" to help remember the reasons for a flare. This is summarized below. I've also written about the topic in the attached link:





Atanaskova Mesinkovska N, et al. Association of lichen planopilaris with thyroid disease: a retrospective case-control study. J Am Acad Dermatol. 2014.

Conic RRZ, et al. Vitamin D Status in Scarring and Non-Scarring Alopecia. J Am Acad Dermatol. 2018.




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Do I need a scalp biopsy if I have scarring alopecia?


I have been diagnosed with frontal fibrosing alopecia, which I understand to be a type of scarring alopecia. My dermatologist wants to start me on treatment right away. Do I need a biopsy first?



Dermatologists have many different views as to whether every patient with potential scarring alopecia needs a scalp biopsy or not. These views fall in three main categories:

1) There are some dermatologists who believe that every single patient with hair loss (scarring or non-scarring) gets a biopsy.  

2) There are some dermatologists who conduct a scalp biopsy in every single patient with scarring alopecia. 

3) There are some dermatologists who perform a biopsy if the diagnosis is not certain and there is even the slightest ambiguity in the diagnosis.

I fall in the third category. My decision on whether a patient needs a biopsy comes during the final steps of a typical patient evaluation. First (step 1), I listen to the patient’s story about their hair loss (we call this a history). Second (step 2), I examine the scalp using a dermatoscope. Third (step 3) I review blood tests. Fourth, I decide whether a biopsy is needed given all the information I have collected during steps 1-3. If the diagnosis is clear and there simply can’t be another diagnosis possible, I don’t do a biopsy.

Here’s an example. Suppose a 56 year old female patient comes to see me. She started losing her eyebrows at age 51. At age 54 she started losing hair along her frontal hairline and it’s receded now about 1⁄2 inch. She’s lost her arm hair, pubic hair and leg hair. Examination shows a scarring alopecia along the frontal hairline. Her blood tests are normal. Based on steps 1-3 I’m confident in the diagnosis of a condition known as frontal fibrosing alopecia.

Will I do a biopsy? No. I will not recommend doing a biopsy in this situation. If the biopsy returns showing scarring alopecia, it’s true that I will have confirmed the diagnosis. Not a bad thing of course. But I will have caused the patient an unnecessary scar. Also, there is always the potential that biopsies (or any trauma) can further activate scarring alopecias, so I’d like to stay away from that.

But suppose the biopsy returns showing something else – such as androgenetic alopecia or alopecia areata. Biopsies are not 100 % accurate so once in a while a scenario like this does occur. In a situation like this, I won’t believe the biopsy results. I’ll simply put the biopsy results aside and move on with discussing treatment. In other words, I’d simply have to explain to the patient that biopsies are not perfect. The reality is that I have caused an unnecessary scar. There may also have been unnecessary expense for getting the biopsy done. There may have even been some pain and discomfort for a few days.

Suppose in the above example, we change things a bit. Suppose the patient is a 56 year old female patient like in the above example. She started losing her eyebrows at age 51. At age 54 she started losing hair along her frontal hairline and it’s receded now about 1⁄2 inch. She’s lost her arm hair, pubic hair and leg hair. She has joint pain in her wrists and ankles, unusual rashes, extreme fatigue and prominent lymph nodes enlarged in her neck. She is troubled by headaches and has had 2 seizures this year that nobody can figure out why. She has dry mouth and dry eyes. Examination shows a scarring alopecia along the frontal hairline. Her blood tests are abnormal with low white cells, abnormal kidney function tests, as elevated liver enzymes. Her ANA is borderline positive at 1:160. When I examine her scalp, I have the impression this is a scarring alopecia – resembling very close frontal fibrosing alopecia.

Here’s a good example of where I will do a scalp biopsy. Even though it seems the patient has frontal fibrosing alopecia, I want to rule out other conditions such as cutaneous lupus, discoid lupus, lymphomas, various infiltrative conditions, including some rare cancers.


You may wish to review these helpful articles (below) I've written in the past. Thanks again for the question. 

Top 25 Frequently Asked Questions about Scarring Alopecia

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What topical steroids are safe to use in FFA?


I was diagnosed with frontal fibrosing alopecia and prescribed a topical steroid by my dermatologist. I've been using it for 5 months. I am wondering if it's too strong because my skin seems thin in the area of the hair loss. What topical steroids are best to use for FFA?



Topical steroids can be mildly helpful for some patients with FFA. Generally speaking they are not as effective as steroid injections, and oral medications such as finasteride, doxycycline or hydroxychloroquine. Nevertheless, topical steroids do have a role in the treatment of FFA.

There are many classes of topical steroids and they range from class I to class VII. Class I steroids are the strongest and include agents like clobetsol. Class VII steroids include weak steroids like hydrocortisone.  Clobetasol is up to 600 times strong than  hydrocortisone and so has much more potent anti-inflammatory effects.  There's no doubt about it that stronger steroids suppress inflammation better- but that does not mean that stronger steroids are better, especially for FFA. In FFA, we need to consider side effects  - in particular the thinning of the skin that both the steroids and the disease itself can cause. 

Clobetasol, however, carries a greater risk of side effects including thinning of the skin. Patients with FFA already have thin skin to begin with (on account of their disease). So, one needs to be careful when treating FFA not to thin the skin further. Monitoring is needed and photographs are essential in this regard. 

Generally speaking, when someone with FFA notices thinner skin and blue veins appearing it's typically the disease itself that caused this - not the topical steroid. Nevertheless, to limit the side effects of topical steroids, dermatologists frequently prescribe weaker steroids to use on the frontal hairline for those with FFA. Instead of using clboetasol, steroids like fluocinonide or betamethasone are often used. Rather than using daily, these are frequently used every other day to limit side effects.  In addition, a non-steroid medication like pimecrolimus might be used as well. Pimecrolimus does not cause thinning of the skin but the trade off is they are not quite as consistently effective as the topical steroids. 

If clobetasol is going to be used, that is a decision that the dermatologist and the patient must both review together and be comfortable with. Daily use of clobetasol on the frontal hairline for a prolonged period is probably not a good idea when treating FFA. Some physicians might use it a few times per week or daily for a very short period of time. However, daily use of a strong steroid increases the risk of the patient experiencing further thinning of the skin.  

You may wish to review these helpful articles (below) I've written in the past. Thanks again for the question. 

Topical steroids and FFA

General articles on frontal fibrosing alopecia


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