Visual diagnosis is made by the "stuck on" appearance, horny pearls or cysts embedded in the structure. Darkly pigmented lesions can be challenging to distinguish from nodular melanomas. Furthermore, thin seborrheic keratoses on facial skin can be very difficult to differentiate from lentigo maligna even with dermatoscopy. Clinically, epidermal nevi are similar to seborrheic keratoses in appearance. Epidermal nevi are usually present at or near birth. Condylomas and warts can clinically resemble seborrheic keratoses, and dermatoscopy can be helpful. On the penis and genital skin, condylomas and seborrheic keratoses can be difficult to differentiate, even on biopsy.

To date, the gold standard in the diagnosis of seborrheic keratosis is represented by the histolopathologic analysis of a skin biopsy.

Physicians can often diagnose keratosis pilaris simply by examining the skin; tests are usually not needed. However, a dermatologist can use dermoscopy to confirm the diagnosis and assess if a person with KP is responding to treatment. Physicians will often consider family history and the presence of symptoms when making the diagnosis. Those with this condition are generally encouraged to contact a physician if the bumps are bothersome and do not improve with over the counter lotions.

Alopecia areata is usually diagnosed based on clinical features.

Trichoscopy may aid in establishing the diagnosis. In alopecia areata, trichoscopy shows regularly distributed "yellow dots" (hyperkeratotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening).

A biopsy is rarely needed to make the diagnosis or aid in the management of alopecia areata. Histologic findings include peribulbar lymphocytic infiltrate ("swarm of bees"). Occasionally, in inactive alopecia areata, no inflammatory infiltrates are found. Other helpful findings include pigment incontinence in the hair bulb and follicular stelae, and a shift in the anagen-to-telogen ratio towards telogen.

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

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.

Commonly, alopecia areata involves hair loss in one or more round spots on the scalp.

- Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata.

- Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head.

- Alopecia areata multilocularis refers to multiple areas of hair loss.

- Ophiasis refers to hair loss in the shape of a wave at the circumference of the head.

- The disease may be limited only to the beard, in which case it is called alopecia areata barbae.

- If the person loses all the hair on the scalp, the disease is then called alopecia areata totalis.

- If all body hair, including pubic hair, is lost, the diagnosis then becomes alopecia areata universalis.

Alopecia areata totalis and universalis are rare.

A scalp biopsy is essential for the diagnosis of cicatricial alopecia and is the necessary first step, as it can be hard to know the diagnosis for sure without a biopsy. Findings of the scalp biopsy, including the type of inflammation present, location and amount of inflammation, and other changes in the scalp, are necessary to diagnose the type of cicatricial alopecia, to determine the degree of activity, and to select appropriate therapy.

Clinical evaluation of the scalp is also important. Symptoms of itching, burning, pain, or tenderness usually signal ongoing activity. Signs of scalp inflammation include redness, scaling, and pustules. However, in some cases there are few symptoms or signs and only the scalp biopsy demonstrates the active inflammation. The overall extent and pattern of hair loss is noted and sometimes photographed for future comparison. A hair "pull test" is performed to see if growing, or "anagen", where hairs are pulled out easily. The pulled hairs are mounted on a slide and the hair bulbs are viewed with a light microscope to determine how many are growing hairs and how many are resting hairs. In addition, if pustules are present, cultures are taken to identify which microbes, if any, may be contributing to the inflammation. A thorough evaluation that includes all of these parameters is important in diagnosing a cicatricial alopecia and in identifying features in individual patients that will help the selection of therapy.

New diagnostic techniques, such as trichoscopy may be used for non-invasive differential diagnosis of cicatricial alopecia.

Diagnosis and treatment of cicatricial alopecias is often challenging. For this reason, it is helpful to be evaluated by a dermatologist with a special interest or expertise in scalp and hair disorders, and who is familiar with current diagnostic methods and therapies.

Because they are not usually associated with an increased loss rate, male-pattern and female-pattern hair loss do not generally require testing. If hair loss occurs in a young man with no family history, drug use could be the cause.

- The pull test helps to evaluate diffuse scalp hair loss. Gentle traction is exerted on a group of hairs (about 40–60) on three different areas of the scalp. The number of extracted hairs is counted and examined under a microscope. Normally, fewer than three hairs per area should come out with each pull. If more than ten hairs are obtained, the pull test is considered positive.

- The pluck test is conducted by pulling hair out "by the roots". The root of the plucked hair is examined under a microscope to determine the phase of growth, and is used to diagnose a defect of telogen, anagen, or systemic disease. Telogen hairs have tiny bulbs without sheaths at their roots. Telogen effluvium shows an increased percentage of hairs upon examination. Anagen hairs have sheaths attached to their roots. Anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs.

- Scalp biopsy is used when the diagnosis is unsure; a biopsy allows for differing between scarring and nonscarring forms. Hair samples are taken from areas of inflammation, usually around the border of the bald patch.

- Daily hair counts are normally done when the pull test is negative. It is done by counting the number of hairs lost. The hair from the first morning combing or during washing should be counted. The hair is collected in a clear plastic bag for 14 days. The strands are recorded. If the hair count is >100/day, it is considered abnormal except after shampooing, where hair counts will be up to 250 and be normal.

- Trichoscopy is a noninvasive method of examining hair and scalp. The test may be performed with the use of a handheld dermoscope or a video dermoscope. It allows differential diagnosis of hair loss in most cases.

There are two types of identification tests for female pattern baldness: the Ludwig Scale and the Savin Scale. Both track the progress of diffused thinning, which typically begins on the crown of the head behind the hairline, and becomes gradually more pronounced. For male pattern baldness, the Hamilton–Norwood scale tracks the progress of a receding hairline and/or a thinning crown, through to a horseshoe-shaped ring of hair around the head and on to total baldness.

In almost all cases of thinning, and especially in cases of severe hair loss, it is recommended to seek advice from a doctor or dermatologist. Many types of thinning have an underlying genetic or health-related cause, which a qualified professional will be able to diagnose.

Lichen planus has a unique microscopic appearance that is similar between cutaneous, mucosal and oral. A Periodic acid-Schiff stain of the biopsy may be used to visualise the specimen. Histological features seen include:

- thickening of the stratum corneum both with nuclei present (parakeratosis) and without (orthokeratosis). Parakeratosis is more common in oral variants of lichen planus.

- thickening of the stratum granulosum

- thickening of the stratum spinosum (acanthosis) with formation of colloid bodies (also known as Civatte bodies, Sabouraud bodies) that may stretch down to the lamina propria.

- liquefactive degeneration of the stratum basale, with separation from the underlying lamina propria, as a result of desmosome loss, creating small spaces (Max Joseph spaces).

- Infiltration of T cells in a band-like pattern into the dermis "hugging" the basal layer.

- Development of a "saw-tooth" appearance of the rete pegs, which is much more common in non-oral forms of lichen planus.

There are several different types of keratosis pilaris, including "keratosis pilaris rubra" (red, inflamed bumps which can be on arms, head, legs), "keratosis pilaris alba" (rough, bumpy skin with no irritation), "keratosis pilaris rubra faceii" (reddish rash on the cheeks), and related disorders. Keratosis pilaris is commonly described in association with other dry skin conditions, such as ichthyosis vulgaris, xerosis and atopic dermatitis, including those of asthma and allergies.

Keratosis pilaris does not bear any known, long-term health implications, nor is it associated with increased mortality or morbidity. It is not related to goose bumps, which results from muscle contractions, except that both occur in the area where the hair shaft exits the skin.

Tissue biopsy is usually indicated to rule out other causes of white patches and also to enable a detailed histologic examination to grade the presence of any epithelial dysplasia. This is an indicator of malignant potential and usually determines the management and recall interval. The sites of a leukoplakia lesion that are preferentially biopsied are the areas that show induration (hardening) and erythroplasia (redness), and erosive or ulcerated areas. These areas are more likely to show any dysplasia than homogenous white areas.

Brush biopsy/exfoliative cytology is an alternative to incisional biopsy, where a stiff brush is scraped against the lining of the mouth to remove a sample of cells. This is then made into a smear which can be examined microscopically. Sometimes the biopsy site can be selected with adjunct methods which aim to highlight areas of dysplasia. Toluidine blue staining, where the dye is preferentially retained by dysplastic tissue, is sometimes used, but there is high false positive rate. Other methods involve the use of illuminescence, relying on either the property of normal autoflorescent molecules in mucosa such as collagen and keratin which is lost from areas of dysplasia or carcinoma under blue light, or by initially staining of the mucosa with toluidine blue or dilute acetic acid and examination under white light.

Lichen planus lesions are diagnosed clinically by their "lichen-like" appearance. A biopsy can be used to rule out conditions that may resemble lichen planus, and can pick up any secondary malignancies.

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

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.

HED2 is suspected after infancy on the basis of physical features in most affected individuals. GJB6 is the only gene known to be associated with HED2. Targeted mutation analysis for the four most common GJB6 mutations is available on a clinical basis and detects mutations in approximately 100% of affected individuals. Sequence analysis is also available on a clinical basis for those in whom none of the four known mutations is identified.

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.

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.

Though not as common as the loss of hair on the head, chemotherapy, hormone imbalance, forms of hair loss, and other factors can also cause loss of hair in the eyebrows. Loss of growth in the outer one third of the eyebrow is often associated with hypothyroidism. Artificial eyebrows are available to replace missing eyebrows or to cover patchy eyebrows. Eyebrow embroidery is another option which involves the use of a blade to add pigment to the eyebrows. This gives a natural 3D look for those who are worried about an artificial look and it lasts for two years. Micropigmentation (permanent makeup tattooing) is also available for those who want the look to be permanent.

Perifollicular erythema and scarring white patches are seen on dermoscopy. On scalp biopsy, lymphocytic and granulomatous perifolliculitis with eccentric atrophy of follicular epithelia and perifollicular fibrosis are visualized.

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.

The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to exclude other causes of hair loss, and histology would demonstrate perifollicular fibrosis.

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.

Leukoplakia has a wide range of possible histologic appearances. The degree of hyperkeratosis, epithelial thickness (acanthosis/), dysplasia and inflammatory cell infiltration in the underlying lamina propria are variable. In mucous membranes, hyperkeratosis can be defined as "an increase in the thickness of the keratin layer of the epithelium, or the presence of such a layer in a site where none would normally be expected." In leukoplakia, the hyperkeratosis varies in thickness, and may be either ortho- or para-keratosis, (depending upon whether cell nuclei are lost or retained in the superficial layers respectively), or a mixture of both in different areas of the lesion.

The epithelium may show hypertrophy (e.g. acanthosis) or atrophy. Red areas within leukoplakia represent atrophic or immature epithelium which has lost the ability to keratinize. The transition between the lesion and normal surrounding mucosa may be well demarcated, or poorly defined. Melanin, a pigment naturally produced in oral mucosa, can leak from cells and give a grey color to some leukoplakia lesions.

Hyperkeratosis and altered epithelial thickness may be the only histologic features of a leukoplakia lesion, but some show dysplasia. The word "dysplasia" generally means "abnormal growth", and specifically in the context of oral red or white lesions refers to microscopic changes ("cellular atypia") in the mucosa that indicate a risk of malignant transformation. When dysplasia is present, there is generally an inflammatory cell infiltration in the lamina propria. The following are commonly cited as being possible features of epithelial dysplasia in leukoplakia specimens:

- Cellular pleomorphism, in which cells are of abnormal and different shapes.

- Nuclear atypia, in which the nuclei of cells varies in size, any may be increased in size relative to the cytoplasm, shape, and may stain more intensely. There may also be more prominent nucleoli.

- Increased number of cells seen undergoing mitosis, including both normal and abnormal mitoses. Abnormal mitosis may be abnormally located, e.g. occurring in suprabasal cells (cell layers more superficial to the basal cell layer) or of abnormal form, e.g. "tri-radiate mitoses" (a cell splitting into 3 daughter cells rather than only 2)

- Loss the normal organization of the epithelial layers. The distinction between the epithelial layers may be lost. Normally stratified squamous epithelium shows progressive changes in the form of cells from the basal to the superficial layers, with cells becoming more flat ("squames") towards the surface as a continuous maturation process. In dysplastic epithelium, cells may become vertically orientated rather than becoming flat towards the surface.

- There may be abnormal keratinization, where keratin is formed below the normal keratin layer. This can occur in individual cells or groups of cells, forming an intraepithelial keratin pearl. There may be an increase in number of basal cells, and they may lose their cellular orientation (losing their polarity and long axis).

- Alteration of the normal epithelial-connective tissue architecture - the rete pegs may become "drop shaped". wider at their base than more superficially.

Generally dysplasia is subjectively graded by pathologists into mild, moderate or severe dysplasia. This requires experience as it is a difficult skill to learn. It has been shown that there is high degree of inter-observer variation and poor reproducibility in how dysplasia is graded. Severe dysplasia is synonymous with the term carcinoma in situ, denoting the presence of neoplastic cells which have not yet penetrated the basement membrane and invaded other tissues.

Latanoprost and bimatoprost are specific PGF2a analogues applied topically, and have been found to lengthen eyelashes, darken hair pigmentation and elongate hair. Bimatoprost is available as treatment for eyelash growth. Latanoprost has shown ability to promote scalp hair density and pigmentation, and is theorized to function at the dermal papilla. A study found latanoprost ineffective on eyelashes in a patient with alopecia areata. It has also been found ineffective in treatment of eyebrow hair loss.

Causes of noncicatricial alopecia include:

- Alopecia areata

- Anagen effluvium

- Androgenetic alopecia

- Dermatopathia pigmentosa reticularis

- Telogen effluvium

- Trichotillomania (Trichotillosis)