There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.

Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.

Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair. The laser targets the melanin color in the lower 1/3 of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able treat all colors of hair.

Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.

Improving environmental factors will reduce damage to the hair. Gentle brushing with a soft brush should replace more aggressive brushing, ratting, or other procedures. Harsh chemicals such as hair straightening compounds and permanents should be avoided. The hair should not be ironed. Excessively harsh shampoo should be avoided. Hair conditioners should be used.

Several medications can cause generalized or localized acquired hypertrichosis including:

Anticonvulsants: phenytoin

Immunosuppressants: cyclosporine

Vasodilators: diazoxide and minoxidil

Antibiotics: streptomycin

Diuretics: acetazolamide

Photosensitizes: Psoralen.

The acquired hypertrichosis is usually reversible once these medications are discontinued.

Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.

There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.

Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.

Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.

Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits.

2008 and 2012 reviews found little evidence to support the use of special lights or lasers to treat hair loss. Additionally none are approved by the FDA in America for this use. Both laser and lights appear to be safe.

A 2014 and 2016 review found tentative evidence of benefit for lasers. While another 2014 review concluded that the results are mixed, have a high risk of bias, and that its effectiveness is unclear.

Estrogens are indirect anti-androgens and can be used to treat androgenetic hair loss in women with oral contraceptives. Systemic estrogen increases SHBG, which binds androgens, including testosterone and DHT, in turn reducing their bioavailability. Topical formulations are available in Europe. Hair follicles have estrogen receptors and it is theorized that topical compounds act on them directly to promote hair growth and antagonize androgen action. Large clinical studies showing effectiveness are absent. Topical treatment is also usually unavailable in North America.

There is tentative evidence for cyproterone acetate in women.

The most simple treatment for PFB is to let the beard grow. Existing razor bumps can often be treated by removal of the ingrown hair. Extrafollicular hairs can usually be pulled gently from under the skin with tweezers. Using the fingernails to "break" razor bumps can lead to infection and scarring, and should be avoided. Complete removal of the hair from its follicle is not recommended. Severe or transfollicular hairs may require removal by a dermatologist.

Medications are also prescribed to speed healing of the skin. Clinical trials have shown glycolic acid-based peels to be an effective and well-tolerated therapy which resulted in significantly fewer PFB lesions on the face and neck. The mechanism of action of glycolic acid is unknown, but it is hypothesized that straighter hair growth is caused by the reduction of sulfhydrylbonds in the hair shaft by glycolic acid, which results in reduced re-entry of the hair shaft into the follicular wall or epidermis. Salicylic acid peels are also effective. Prescription antibiotic gels (Benzamycin, Cleocin-T) or oral antibiotics are also used. Retin-A is a potent treatment that helps even out any scarring after a few months. It is added as a nightly application of Retin-A Cream 0.05 - 0.1% to the beard skin while beard is growing out. Tea tree oil, Witch Hazel, and Hydrocortisone are also noted as possible treatments and remedies for razor bumps.

The topical antifungal medications ketoconazole and ciclopirox have the best evidence. It is unclear if other antifungals are equally effective as this has not been studied.

Keratosis pilaris is medically harmless, but many individuals may seek treatment as the condition can cause emotional distress. Topical creams and lotions are currently the most commonly used treatment for keratosis pilaris, specifically those consisting of moisturizing or keratolytic treatments, including urea, lactic acid, glycolic acid, salicylic acid, vitamin D, or topical retinoids such as tretinoin. Corticosteroid creams can also be used as a treatment for KP. Improvement of the skin often takes months and the bumps are likely to return. Limiting time in the shower and using gentle exfoliation to unplug pores can help. Many products are available that apply exfoliation and alpha or beta hydroxy acids.

Some cases of keratosis pilaris have been successfully treated with laser therapy, which involves passing intense bursts of light into targeted areas of the skin. Depending on the body's response to the treatment, multiple sessions over the course of a few months may be necessary.

The most effective prevention is to grow a beard. For men who are required to; or simply prefer to shave, studies show the optimal length to be about 0.5 mm to 1 mm to prevent their hair growing back into the skin. Using a beard trimmer at the lowest setting (0.5mm or 1mm) instead of shaving is an effective alternative. The resulting faint stubble can be shaped using a standard electric razor on non-problematic areas (cheeks, lower neck).

For most cases, completely avoiding shaving for three to four weeks allows all lesions to subside, and most extrafollicular hairs will resolve themselves in about ten days.

Permanent removal of the hair follicle is the only definitive treatment for PFB. Electrolysis is effective but limited by its slow pace, pain and expense. Laser-assisted hair removal is effective. There is a risk of skin discoloration and a very small risk of scarring.

Exfoliation with various tools such as brushes and loofahs also helps prevent bumps.

Some men use electric razors to control PFB. Those who use a razor, should use a single blade or special wire-wrapped blade to avoid shaving too closely, with a new blade each shave. Shaving in the direction of hair growth every other day, rather than daily, may improve pseudofolliculitis barbae. If one must use a blade, softening the beard first with a hot, wet washcloth for five minutes or shave while showering in hot water can be helpful. Some use shaving powders (a kind of chemical depilatory) to avoid the irritation of using a blade. Barium sulfide-based depilatories are most effective, but produce an unpleasant smell.

Seborrhea is recognized as an androgen-sensitive condition – that is, it is caused or aggravated by androgen sex hormones such as testosterone and dihydrotestosterone – and is a common symptom of hyperandrogenism (e.g., that seen in polycystic ovary syndrome). In addition, seborrhea, as well as acne, are commonly associated with puberty due to the steep increase of androgen levels at that time.

In accordance with the involvement of androgens in seborrhea, antiandrogens, such as cyproterone acetate, spironolactone, and flutamide, are highly effective in alleviating the condition. As such, they are used in the treatment of seborrhea, particularly severe cases. While beneficial in seborrhea, effectiveness may vary with different antiandrogens; for instance, spironolactone (which is regarded as a relatively weak antiandrogen) has been found to produce a 50% improvement after three months of treatment, whereas flutamide has been found to result in an 80% improvement within three months. Cyproterone acetate is similarly more potent and effective than spironolactone, and results in considerable improvement or disappearance of acne and seborrhea in 90% of patients within three months.

Systemic antiandrogen therapy should only be used to treat seborrhea in women, as these drugs can result in feminization (e.g., gynecomastia), sexual dysfunction, and infertility in males. In addition, antiandrogens theoretically have the potential to feminize male fetuses in pregnant women, and for this reason, should always be combined with effective contraception in sexually active women who can or may become pregnant.

Madarosis has different possible treatments and can be reversed if treated early enough. The treatments for madarosis are completely dependent upon the pre-existing condition. When suffering from blepheritis, antibiotics are used to combat the bacterial infection. People who are suffering from trichotillomania need to seek behavioral and psychological help. Many people look to hair transplant surgeries, especially in non-scarring cases. These surgeries are mainly used as a cosmetic reason rather than a medical one. There are also other treatments that can be used for cosmetic purposes.

There are restoration surgeries for the eyebrows in severe cases. Many surgeons opt for nylon implants, but have been banned in some countries due to infections. Follicular transplantation is now the procedure of choice. In this surgery, hair samples are individually taken for a donor area and transplanted into the thinning area. Small incisions are made and grafts are placed individually according to the amount of hair in each follicle, eyebrows single. In this procedure, there are no scars or stitches and hair begins to grow after a few months post surgery.

Most doctors consider this a normal physiological phenomenon and advise against treatment.

The United States Food and Drug Administration (FDA) has not approved any medications for trichotillomania treatment.

Medications can be used to treat trichotillomania. Treatment with clomipramine, a tricyclic antidepressant, was shown in a small double-blind study to improve symptoms, but results of other studies on clomipramine for treating trichotillomania have been inconsistent. Naltrexone may be a viable treatment. Fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) have limited usefulness in treating trichotillomania, and can often have significant side effects. Behavioral therapy has proven more effective when compared to fluoxetine or control groups. There is little research on the effectiveness of both behavioral therapy together with medication, and robust evidence from high-quality studies is lacking. Acetylcysteine treatment stemmed from an understanding of glutamate's role in regulation of impulse control.

Many medications, depending on individuality, may increase hair pulling.

There is no treatment for the disorder. A number of studies are looking at gene therapy, exon skipping and CRISPR interference to offer hope for the future. Accurate determination through confirmed diagnosis of the genetic mutation that has occurred also offers potential approaches beyond gene replacement for a specific group, namely in the case of diagnosis of a so-called nonsense mutation, a mutation where a stop codon is produced by the changing of a single base in the DNA sequence. This results in premature termination of protein biosynthesis, resulting in a shortened and either functionless or function-impaired protein. In what is sometimes called "read-through therapy", translational skipping of the stop codon, resulting in a functional protein, can be induced by the introduction of specific substances. However, this approach is only conceivable in the case of narrowly circumscribed mutations, which cause differing diseases.

Trichorrhexis invaginata (also known as "Bamboo hair" ) is a distinctive hair shaft abnormality that may occur sporadically, either in normal hair or with other hair shaft abnormalities, or regularly as a marker for Netherton's syndrome. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing for intussusception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft.

Technology can be used to augment habit reversal training or behavioral therapy. Several mobile apps exist to help log behavior and focus on treatment strategies. There exists wearable devices that track the position of a users' hands. They produce sound or vibration notifications to notify users of passive hair pulling and they can document rates of these events over time.

In 1937, Touraine and Solente first noted the association between hair-shaft defects (bamboo node) and ichthyosiform erythroderma. Còme first coined the term ichthyosis linearis circumflexa in 1949, although Rille had previously recorded the distinctive features of ichthyosis linearis circumflexa by 1922. In 1958, Netherton described a young girl with generalized scaly dermatitis and fragile nodular hair-shaft deformities, which he termed trichorrhexis nodosa. Later, this was more appropriately renamed as trichorrhexis invaginata (bamboo hair) for a ball-and-socket–type hair-shaft deformity at the suggestion of Wilkinson et al.

In 1974, Mevorah et al. established the clinical relationship between ichthyosis linearis circumflexa and Netherton syndrome, and an atopic diathesis was found to occur in approximately 75% of patients with Netherton syndrome.

The treatment of primary immunodeficiencies depends foremost on the nature of the abnormality. Somatic treatment of primarily genetic defects is in its infancy. Most treatment is therefore passive and palliative, and falls into two modalities: managing infections and boosting the immune system.

Reduction of exposure to pathogens may be recommended, and in many situations prophylactic antibiotics or antivirals may be advised.

In the case of humoral immune deficiency, immunoglobulin replacement therapy in the form of intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG) may be available.

In cases of autoimmune disorders, immunosuppression therapies like corticosteroids may be prescribed.

While there is no cure for HPS, treatment for chronic hemorrhages associated with the disorder includes therapy with vitamin E and the antidiuretic dDAVP.

The treatment of choice by dermatologists is a safe and inexpensive oral medication, griseofulvin, a secondary metabolite of the fungus "Penicillium griseofulvin". This compound is "fungistatic" (inhibiting the growth or reproduction of fungi) and works by affecting the microtubular system of fungi, interfering with the mitotic spindle and cytoplasmic microtubules. The recommended pediatric dosage is 10 mg/kg/day for 6–8 weeks, although this may be increased to 20 mg/kg/d for those infected by "T. tonsurans", or those who fail to respond to the initial 6 weeks of treatment. Unlike other fungal skin infections that may be treated with topical therapies like creams applied directly to the afflicted area, griseofulvin must be taken orally to be effective; this allows the drug to penetrate the hair shaft where the fungus lives. The effective therapy rate of this treatment is generally high, in the range of 88–100%.

Other oral antifungal treatments for tinea capitis also frequently reported in the literature include terbinafine, itraconazole, and fluconazole; these drugs have the advantage of shorter treatment durations than griseofulvin. However, concern has been raised about the possibility of rare side effects like liver toxicity or interactions with other drugs; furthermore, the newer drug treatments tend to be more expensive than griseofulvin.

On September 28, 2007, the U.S. Food and Drug Administration stated that Lamisil (Terbinafine hydrochloride, by Novartis AG) is a new treatment approved for use by children aged 4 years and older. The antifungal can be sprinkled on a child's food to treat the infection. Lamisil carries hepatotoxic risk, and can cause a metallic taste in the mouth.

Bone marrow transplant may be possible for Severe Combined Immune Deficiency and other severe immunodeficiences.

Virus-specific T-Lymphocytes (VST) therapy is used for patients who have received hematopoietic stem cell transplantation that has proven to be unsuccessful. It is a treatment that has been effective in preventing and treating viral infections after HSCT. VST therapy uses active donor T-cells that are isolated from alloreactive T-cells which have proven immunity against one or more viruses. Such donor T-cells often cause acute graft-versus-host disease (GVHD), a subject of ongoing investigation. VSTs have been produced primarily by ex-vivo cultures and by the expansion of T-lymphocytes after stimulation with viral antigens. This is carried out by using donor-derived antigen-presenting cells. These new methods have reduced culture time to 10–12 days by using specific cytokines from adult donors or virus-naive cord blood. This treatment is far quicker and with a substantially higher success rate than the 3–6 months it takes to carry out HSCT on a patient diagnosed with a primary immunodeficiency. T-lymphocyte therapies are still in the experimental stage; few are even in clinical trials, none have been FDA approved, and availability in clinical practice may be years or even a decade or more away.