Hair Loss

Alopecia Areata

Alopecia Areata

Alopecia Areata is a common autoimmune skin disease that causes hair and bristle loss in scalp and sometimes other parts of the body (beard, eyebrow, eyelashes and body hair).

Alopecia Areata is a condition that constitutes 0.7% to 3.8% of all dermatoses encountered in dermatology practice. The lifetime risk of occurrence is estimated to be 1.7% -2%.

Alopecia Areata starts with 80% single plaque, 2.5% double plaque, 7.7% frequency with multiple hair loss areas. Alopecia Areata can begin from any hairy area. Respectively the frequencies of the involvement areas are 66.8% -95% scalp, 28% beard, 3.8% eyebrow, and 1.3% extremities.

Patchy Alopecia Areata: The most common shape is one or more coin-sized hairless patches on the scalp or other parts of the body. Alopecia Totalis: Loss of all hair. Alopecia Universalis: Loss of whole body hair.

What is Etiopathogenesis Autoimmune?

The hair follicle is the only cell with a lifelong frequency transformation. The cycle of the hair follicle includes rapid growth, pigmentation, hairline construction (anagen phase), short apoptosis, and the involution of the organ (catagen) and the resting period (telogen).

The life-long hair cycle and regeneration has a stem cell-dependent function. The construction and pigmentation of the hairline is directed by the precursor genes of these stem cells. Rapidly proliferating keratinocytes and melanocytes are located in the matrix of the anagen hair. The main target of the inflammatory attack in alopecia areata is the hair matrix. In other words, Alopecia Areata is also classified as an anagen hair loss.

The hair follicle has a protected immunological environment against autoimmunity; It provides this protection by suppressing the introduction of autoantigens to CD8 + T lymphocytes. MHC 1 molecules, TGF β-1, β β-2, α-MSH, reduce the risk of introducing follicle autoantigens to CD8 + T cells through the factor inhibiting macrophage migration.

Suppression of MHC 1 molecules causes hair follicles to be attacked by NK cells. NK cell and T cell causes auto-destruct in hair matrix.

Will my child get an Alopecia Areata inheritance from me?

It is understandable that adults with alopecia areata will be worried about the risk of passing the disease to their future children. However, it is almost impossible to predict whether your child will develop the condition because Alopecia Areata is a very complex condition.

I personally believe that not only family inheritance but also multiple factors (both genetics and environment) are necessary to trigger the disease.

Especially in severe forms of disease (16% -18%) family history is more common. It is also a remarkable finding that it can be detected in twin cases. Studies show that the rate of family history supports genetic inheritance.

Diseases associated with Alopecia Areata:

Disease Frequency (%)

  • Thyroid disease 14,6
  • Diabetes mellitus 11,1
  • Inflammatory bowel disease 6,3
  • Systemic lupus erythematosus 4,3
  • Rheumatoid arthritis 3,0
  • Psoriasis and psoriatic arthritis 2,0
  • Atopy 38,2
  • Contact dermatitis and other eczema 35,9
  • Mental issues 25,5
  • Hyperlipidemia 24,5
  • Hypertension 2,.9

Also Alopeasia Areta is frequently observed in Atopic Dermatitis, Vitiligo, Collagen-vascular diseases, Down syndrome, psychiatric disorders, anxiety, personality disorders, depression and paranoid disorders. Nail involvement accompanies 20% of all Alopesia Areta cases.


Alopesia Areata is a benign condition, spontaneous remissions and relapses are common. Treatment can be topical or systemic.

Intralesional corticosteroid therapy is generally recommended for alopecia areata with less than 50% involvement.

In intralesional treatment, the injection is administered intradermally using a 5 mL syringe and a 30 punch needle.

  • Triamcinolone acetonide (Kenalog) is most commonly used; concentrations range from 2.5-10 mg / mL.
  • In the face area the lowest concentration is being used
  • 5 mg / mL is sufficient on the scalp
  • Less than 0.1 mL per area is injected and the injections are spread to cover the affected areas, intradermally at 1 cm intervals
  • Injections are applied in every 4-6 weeks

Topical Corticosteroid therapy may be particularly beneficial in children who cannot tolerate injections. It is applied as follows;

  • Fluocinolone acetonide cream 0.2% per day (Synalar HP), betamethasone dipropionate cream 0.05% (beclozon) twice a day was used.
  • Treatment should continue for at least 3 months before regrowth can be expected, and maintenance therapy is often required.

Systemic corticosteroids (prednisone decode) are not the chosen agents for alopecia areata due to adverse effects associated with both short and long term therapy. Some patients may benefit in the beginning, but the dose required maintaining cosmetic growth is often too great, adverse effects are inevitable, and most patients relapse after cessation of treatment.


  • Topical immunotherapy is defined as the induction and periodic removal of allergic contact dermatitis by topical application of potential contact allergens.
  • Most common agents include cardiac acid dibutylester (SADBE) and diphencyprone (DPCP).


  • Both short-term contact and night treatments have been used.
  • Anthralin concentrations ranged from 0.2-1%


  • Minoxidil appears to be effective in treating common diseases (50-99% hair loss), but has little benefit in alopecia totalis or alopecia universalis.
  • 5% solution seems more effective.
  • A maximum of 25 drops is applied twice a day, regardless of the extent of the affected area.
  • The first hair growth can be seen within 12 weeks, but continuous application is needed to achieve cosmetically acceptable output.


  • Both systemic and topical PUVA treatments have been used.
  • In most cases 20-40 treatments are sufficient.
  • Most patients recur within a few months (4-8 months on average) after treatment is stopped.

Other Agents

  • Topical cyclosporine showed limited efficacy
  • Tacrolimus Topical
  • Methotrexate has shown mixed results with or without systemic corticosteroids.

Cosmetic Treatment

  • Dermatographia has been used to camouflage the eyebrows of patients with Alopecia Areata; On average, 2-3 sessions are required for each patient, each lasting 1 hour.

Congenital Triangular Alopecia

Congenital triangular alopecia, also known as triangular alopecia; It was first described by Sabouraud in 1905; Also known as Congenital Triangle Alopecia, this form of alopecia is localized in the frontotemporal scalp. It typically occurs in early childhood and can be found in a variety of shapes along its front and side lines, including triangular, lancet-shaped or oval. In this case, there is no inflammation or scarring. In scalp pathology, the number of hair follicles is normal, but most of them are miniaturized. The main treatment for adults is the hair restoration surgery.

It usually occurs at birth or early childhood, but there are also adult cases. It is routinely mixed with Alopecia Areata. In our clinic, we successfully apply cosmetic hair and beard transplantation in treatment-resistant and frequently recurring lesions.

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