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.

Improvement or stabilization of the condition has been reported with topical and intralesional corticosteroids, antibiotics, hydroxychloroquine, topical and oral immunomodulators, tacrolimus, and most recently, 5-alpha-reductase inhibitors. In one study, the use of anti-androgens (finasteride or dutasteride) was associated with improvement in 47% and stabilization in 53% of patients

The objective assessment of treatment efficacy is very difficult and spontaneous remission is unpredictable, but if the affected area is patched, the hair may regrow spontaneously in many cases. None of the existing therapeutic options are curative or preventive.

In cases of severe hair loss, limited success has been achieved by using the corticosteroids clobetasol or fluocinonide, corticosteroid injections, or cream. The cream is not as effective and it takes longer in order to see results. Steroid injections are commonly used in sites where the areas of hair loss on the head are small or especially where eyebrow hair has been lost. Whether they are effective is uncertain. Some other medications that have been used are minoxidil, Elocon (mometasone) ointment (steroid cream), irritants (anthralin or topical coal tar), and topical immunotherapy ciclosporin, sometimes in different combinations. Topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target, and small lesions typically also regrow spontaneously. Oral corticosteroids decrease the hair loss, but only for the period during which they are taken, and these drugs can cause serious side effects.

When alopecia areata is associated to celiac disease, the treatment with a gluten-free diet allows complete and permanent regrowth of scalp and other body hair in many people, but in others there are remissions and recurrences. This improvement is probably due to the normalization of the immune response as a result of gluten withdrawal from the diet.

As mentioned above, primary cicatricial alopecias are classified by the predominant type of inflammatory cells that attack the hair follicles: i.e., lymphocytes, neutrophils, or mixed inflammatory cells. Treatment strategies are different for each subtype and detailed treatment options are beyond the scope of this discussion. However, certain general principals are reviewed below.

Treatment of the lymphocytic group of cicatricial alopecias (including lichen planopilaris, frontal fibrosing alopecia, central centrifugal alopecia, and pseudopelade (Brocq) involves use of anti-inflammatory medications. The goal of treatment is to decrease or eliminate the lymphocytic inflammatory cells that are attacking and destroying the hair follicle. Oral medications may include hydroxychloroquine, doxycycline, mycophenolate mofetil, cyclosporine, or corticosteroids. Topical medications may include corticosteroids, tacrolimus, pimecrolimus, or Derma-Smoothe/FS scalp oil. Triamcinolone acetonide, a corticosteroid, may be injected into inflamed, symptomatic areas of the scalp.

Treatment of the neutrophilic group of cicatricial alopecias (folliculitis decalvans, tufted folliculitis) is directed at eliminating the predominant pathogenic microbes that are invariably involved in the inflammatory process. Oral antibiotics are the mainstay of therapy, and topical antibiotics may be used to supplement the oral antibiotics. In dissecting cellulitis, pathogenic microbes are not usually present. Isotretinoin in small doses may be helpful in treating dissecting cellulitis.

Treatment of the mixed group of cicatricial alopecias (folliculitis keloidalis) may include antimicrobials, isotretinoin, and anti-inflammatory medications.

You should discuss any treatment with your dermatologist, who will also explain potential side effects, as well as laboratory tests that are needed before starting treatment and sometimes are monitored during treatment.

The course of cicatricial alopecia is usually prolonged. Treatment is continued until the symptoms and signs of scalp inflammation are controlled, and progression of the condition has been slowed. In other words, itching, pain, tenderness, and burning have cleared, scalp redness, scaling, and/or pustules are no longer present, and the progression of the hair loss has been stopped or slowed. Treatment may then be stopped. Unfortunately, the cicatricial alopecias may reactivate after a quiet period and treatment may have to be repeated.

Surgical treatment for cosmetic benefit is an option in some cases after the disease has been inactive for one to two or more years. Hair restoration surgery or scalp reduction may be considered in these instances.

Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

Hair will not regrow once the follicle is destroyed. However, it may be possible to treat the inflammation in and around surrounding follicles before they are destroyed, and for this reason it is important to begin treatment as early as possible to halt the inflammatory process. Minoxidil solution (2% or 5%) applied twice daily to the scalp may be helpful to stimulate any small, remaining, unscarred follicles. The progression of hair loss is unpredictable. In some cases, progression is slow and there is always sufficient hair remaining to cover the affected scalp areas; in other cases, progression can be rapid and extensive.

Treatments for the various forms of hair loss have limited success. Three medications have evidence to support their use in male pattern hair loss: minoxidil, finasteride, and dutasteride. They typically work better to prevent further hair loss, than to regrow lost hair.

- Minoxidil (Rogaine) is a nonprescription medication approved for male pattern baldness and alopecia areata. In a liquid or foam, it is rubbed into the scalp twice a day. Some people have an allergic reaction to the propylene glycol in the minoxidil solution and a minoxidil foam was developed without propylene glycol. Not all users will regrow hair. The longer the hair has stopped growing, the less likely minoxidil will regrow hair. Minoxidil is not effective for other causes of hair loss. Hair regrowth can take 1 to 6 months to begin. Treatment must be continued indefinitely. If the treatment is stopped, hair loss resumes. Any regrown hair and any hair susceptible to being lost, while Minoxidil was used, will be lost. Most frequent side effects are mild scalp irritation, allergic contact dermatitis, and unwanted hair in other parts of the body.

- Finasteride (Propecia) is used in male-pattern hair loss in a pill form, taken 1 milligram per day. It is not indicated for women and is not recommended in pregnant women. Treatment is effective starting within 6 weeks of treatment. Finasteride causes an increase in hair retention, the weight of hair, and some increase in regrowth. Side effects in about 2% of males, include decreased sex drive, erectile dysfunction, and ejaculatory dysfunction. Treatment should be continued as long as positive results occur. Once treatment is stopped, hair loss resumes.

- Corticosteroids injections into the scalp can be used to treat alopecia areata. This type of treatment is repeated on a monthly basis. Oral pills for extensive hair loss may be used for alopecia areata. Results may take up to a month to be seen.

- Immunosuppressants applied to the scalp have been shown to temporarily reverse alopecia areata, though the side effects of some of these drugs make such therapy questionable.

- There is some tentative evidence that anthralin may be useful for treating alopecia areata.

- Hormonal modulators (oral contraceptives or antiandrogens such as spironolactone and flutamide) can be used for female-pattern hair loss associated with hyperandrogenemia.

Many different treatments have been reported for cutaneous lichen planus, however there is a general lack of evidence of efficacy for any treatment. Treatments tend to be prolonged, partially effective and disappointing. The mainstay of localized skin lesions is topical steroids. Additional treatments include retinoids, such as acitretin, or sulfasalazine. Narrow band UVB phototherapy or systemic PUVA therapy are known treatment modalities for generalized disease.

Reassurance that the condition is benign, elimination of precipitating factors and improving oral hygiene are considered initial management for symptomatic OLP, and these measures are reported to be useful. Treatment usually involves topical corticosteroids (such as betamethasone, clobetasol, dexamethasone, and triamcinolone) and analgesics, or if these are ineffective and the condition is severe, the systemic corticosteroids may be used. Calcineurin inhibitors (such as pimecrolimus, tacrolimus or cyclosporin) are sometimes used.

No treatment of seborrheic keratoses is necessary, except for aesthetic reasons. Since a slightly increased risk of localized infection caused by picking at the lesion has been described, if a lesion becomes itchy or irritated by clothing or jewelry, a surgical excision is generally recommended.

Small lesions can be treated with light electrocautery. Larger lesions can be treated with electrodesiccation and curettage, shave excision, or cryosurgery. When correctly performed, removal of seborrheic keratoses will not cause much visible scarring except in persons with dark skin tones.

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.

Dietary supplements are not typically recommended. There is only one small trial of saw palmetto which shows tentative benefit in those with mild to moderate androgenetic alopecia. There is no evidence for biotin. Evidence for most other produces is also insufficient. There was no good evidence for gingko, aloe vera, ginseng, bergamot, hibiscus, or sorphora as of 2011.

Many people use unproven treatments. Egg oil, in Indian, Japanese, Unani (Roghan Baiza Murgh) and Chinese traditional medicine, was traditionally used as a treatment for hair loss.

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.

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.

Surgical removal of the lesion is the first choice of treatment for many clinicians. However, the efficacy of this treatment modality cannot be assessed due to insufficient available evidence. This can be carried out by traditional surgical excision with a scalpel, with lasers, or with eletrocautery or cryotherapy. Often if biopsy demonstrates moderate or severe dysplasia then the decision to excise them is taken more readily. Sometimes white patches are too large to remove completely and instead they are monitored closely. Even if the lesion is completely removed, long term review is still usually indicated since leukoplakia can recur, especially if predisposing factors such as smoking are not stopped.

Many different topical and systemic medications have been studied, including anti-inflammatories, antimycotics (target Candida species), carotenoids (precursors to vitamin A, e.g. beta carotene), retinoids (drugs similar to vitamin A), and cytotoxics, but none have evidence that they prevent malignant transformation in an area of leukoplakia.Vitamins C and E have also been studied with regards a therapy for leukoplakia. Some of this research is carried out based upon the hypothesis that antioxidant nutrients, vitamins and cell growth suppressor proteins (e.g. p53) are antagonistic to oncogenesis. High doses of retinoids may cause toxic effects. Other treatments that have been studied include photodynamic therapy.

There is no standard treatment for alopecia universalis. Many treatments have been explored, including immunomodulatory agents such as imiquimod. Tofacitinib citrate may also have benefits. In June 2014, it was reported that a 25 year old man with almost no hair on his body grew a full head of hair, and eyebrows, eyelashes, facial, armpit and other hair, following 8 months of treatment.

Minoxidil is a growth stimulant that stimulates already-damaged hair follicles to produce normal hair. Minoxidil does not, however, provide any protection to the follicles from further DHT damage. When a follicle is destroyed by DHT, minoxidil will no longer be able to have any more regrowth effects on that follicle. Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, spironolactone, alfatradiol, and topilutamide (fluridil).

Methotrexate and corticosteroids are proposed treatments.

Scalp cooling has specifically been used to prevent alopecia in docetaxel chemotherapy, although it has been found prophylactic in other regimens as well. Treatment effects may take time to resolve, with one study showing breast cancer survivors wearing wigs up to 2 years after chemotherapy.

Finasteride is a medication of the 5α-reductase inhibitors (5-ARIs) class. By inhibiting type II 5-ARI, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp. Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use. Treatment with finasteride more effectively treats male-pattern hair loss at the vertex than male-pattern hair loss at the front of the head and temples.

Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase. Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States. However, it is commonly used off-label to treat male-pattern hair loss.

Treatment of manifestations: special hair care products to help manage dry and sparse hair; wigs; artificial nails; emollients to relieve palmoplantar hyperkeratosis.

Many medications are being studied, including abatacept, MEXIS/M6S, triamcinolone, secukinumab, tralonkinumab, apremilast, botulinum toxin, INCB018424, bimatoprost, clobetasol, AS101, autologous platelet-rich plasma, topical minoxidil, and nitric oxide gel. Some of these medications are approved for other diseases, others are not available outside of studies.

In 2014, preliminary findings showing that oral ruxolitinib, a drug approved by the US Food and Drug Administration (FDA) for bone marrow disorder myelofibrosis, restored hair growth in three individuals with long-standing and severe disease. The medicine costs almost USD $10,000 a month.

When the appearance is caused by heat, the lesion is usually completely reversible within a few weeks if the smoking habit is stopped. This is the case even if the condition has been present for decades. Without stopping smoking, spontaneous remission of the lesion is unlikely. If the lesion persists despite stopping smoking, this is usually then considered to be a true leukoplakia rather than a reactionary keratotis, and may trigger the decision to carry out a biopsy to confirm the diagnosis. Since this condition almost always develops in the setting of long term heavy smoking, it usually indicates the need for regular observation for cancers associated with smoking, e.g. lung cancer.

Recent research has used induced pluripotent stem cells to study disease mechanisms in humans, and discovered that the reprogramming of somatic cells restores telomere elongation in dyskeratosis congenita (DKC) cells despite the genetic lesions that affect telomerase. The reprogrammed DKC cells were able to overcome a critical limitation in TERC levels and restored function (telomere maintenance and self-renewal). Therapeutically, methods aimed at increasing TERC expression could prove beneficial in DKC.

Trachyonychia, sometimes called sandpapered nails, is a condition characterized by rough accentuated linear ridges (longitudinal striations) on the nails of the fingers and toes. When the condition occurs on all the twenty nails of the fingers and toes, it is known as twenty-nail dystrophy, most evident in childhood, favoring males.

Trachyonychia causes the nails to become opalescent, thin, dull, fragile, and finely longitudinally ridged, and, as a result, distally notched. It can be a manifestation of lichen planus, psoriasis, alopecia areata, immunoglobulin A deficiency, atopic dermatitis, and ichthyosis vulgaris.

"The longitudinal striations can occur as a normal part of the aging process", and not until the nails start to thin and get a sandpaper look is the condition called trachonychia. The nails are opalescent and frequently are brittle and split at the free margin. There has been evidence of the condition as a cutaneous manifestation of lichen planus. It has also been associated with other diseases such as eczema, psoriasis, alopecia areata, and atopic dermatitis. Trachonychia is often seen in vitiligo patients – suggesting that they are more susceptible to this condition.