In most patients, the condition lasts only a matter of weeks; in some cases it can last longer (up to six months). The disease resolves completely without long-term effects. Two percent of patients have recurrence.

Experienced practitioners may make the diagnosis clinically. If the diagnosis is in doubt, tests may be performed to rule out similar conditions such as Lyme disease, ringworm, guttate psoriasis, nummular or discoid eczema, drug eruptions, other viral exanthems.The clinical appearance of pityriasis rosea is similar to that of secondary syphilis, and rapid plasma reagin testing should be performed if there is any clinical concern for syphilis. A biopsy of the lesions will show extravasated erythrocytes within dermal papillae and dyskeratotic cells within the dermis.

A set of validated diagnostic criteria for pityriasis rosea is as follows:

A patient is diagnosed as having pityriasis rosea if:

1. On at least one occasion or clinical encounter, he / she has all the essential clinical features and at least one of the optional clinical features, and

2. On all occasions or clinical encounters related to the rash, he / she does not have any of the exclusional clinical features.

The essential clinical features are the following:

1. Discrete circular or oval lesions,

2. Scaling on most lesions, and

3. Peripheral collarette scaling with central clearance on at least two lesions.

The optional clinical features are the following:

1. Truncal and proximal limb distribution, with less than 10% of lesions distal to mid-upper-arm and mid-thigh,

2. Orientation of most lesions along skin cleavage lines, and

3. A herald patch (not necessarily the largest) appearing at least two days before eruption of other lesions, from history of the patient or from clinical observation.

The exclusional clinical features are the following:

1. Multiple small vesicles at the centre of two or more lesions,

2. Two or more lesions on palmar or plantar skin surfaces, and

3. Clinical or serological evidence of secondary syphilis.

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.

The differential diagnosis for OLP includes:

- Other oral vesiculo-ulcerative conditions such as Pemphigus vulgaris and Benign mucous membrane pemphigoid

- Lupus erythematosus, with lesions more commonly occur on the palate and appear as centrally ulcerated or erythematous with radiating white striae. In contrast, OLP and lichenoid reactions rarely occur on the palate, and the striae are randomly arranged rather than radial.

- Chronic ulcerative stomatitis

- Frictional keratosis and Morsicatio buccarum (chronic cheek biting)

- Oral leukoplakia

- Oral candidiasis

The classification of exfoliative dermatitis into Wilson-Brocq (chronic relapsing), Hebra or pityriasis rubra (progressive), and Savill (self-limited) types may have had historical value, but it currently lacks pathophysiologic or clinical utility.

Tinea versicolor may be diagnosed by a potassium hydroxide (KOH) preparation and lesions may fluoresce copper-orange when exposed to Wood's lamp.

The differential diagnosis for tinea versicolor infection includes:

- Progressive macular hypomelanosis

- Pityriasis alba

- Pityriasis rosea

- Seborrheic dermatitis

- Erythrasma

- Vitiligo

- Leprosy

- Syphilis

- Post-inflammatory hypopigmentation

A skin biopsy can be performed to test for EAC; tests should be performed to rule out other possible diseases such as: pityriasis rosea, tinea corporis, psoriasis, nummular eczema, atopic dermatitis, drug reaction, erythema migrans and other rashes.

To help with cradle cap, parents can gently massage their baby's scalp with their fingers or a soft brush to loosen the scales. They may want to shampoo the baby's hair more frequently (no more than once a day), and after shampooing gently brush the baby's scalp with a soft brush or a terrycloth towel. Oil remedies can be used by rubbing a small amount of pure, plant-derived oil (coconut oil, pure olive oil, almond oil) on the baby's scalp and leaving it on for 15 minutes. After 15 minutes, gently comb out the flakes with a fine tooth comb or brush. Be sure to wash out all of the oil to avoid making the cradle cap worse.

For infants: in cases that are related to fungal infection, such as Tinea capitis, doctors may recommend a treatment application of clotrimazole (commonly prescribed for jock itch or athlete's foot) or miconazole (commonly prescribed for vaginal yeast infections).

For toddlers: doctors may recommend a treatment with a mild dandruff shampoo such as Selsun Blue or Neutrogena T-gel, even though the treatment may cause initial additional scalp irritation. A doctor may instead prescribe an antifungal soap such as ketoconazole (2%) shampoo, which can work in a single treatment and shows significantly less irritation than over-the-counter shampoos such as selenium disulfide shampoos, but no adequate and controlled study has been conducted for pediatric use as of 2010.

For adults: see the article on seborrheic dermatitis (the adult version of cradle cap).

The disease often goes undiagnosed for several years, as it is sometimes not recognized and misdiagnosed as thrush or other problems and not correctly diagnosed until the patient is referred to a specialist when the problem does not clear up.

A biopsy of the affected skin can be done to confirm diagnosis. When a biopsy is done, hyperkeratosis, atrophic epidermis, sclerosis of dermis and lymphocyte activity in dermis are histological findings associated with LS. The biopsies are also checked for signs of dysplasia.

It has been noted that clinical diagnosis of LS can be "almost unmistakable" and therefore a biopsy may not be necessary.

The patches of pityriasis alba may last from 1 month to about one year, but commonly on the face last a year. However it is possible that the white patches may last for more than 1 year on the face.

No treatment is required and the patches in time will settle.

The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.

As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required.

Tacrolimus has been reported as speeding resolution.

In exceptionally severe cases PUVA therapy may be considered.

There is no standard treatment for PLC. Treatments may include ultraviolet phototherapy, topical steroids, sun exposure, oral antibiotics, corticosteroid creams and ointments to treat rash and itching.

One study identified the enzyme bromelain as an effective therapeutic option for PLC.

It is not contagious and currently there is no cure for the disease, although the lesions can be treated with ultraviolet therapy as well as topical steroids and antibiotics.

Treatment often involves multiple therapies that address the immune system and bacterial, viral, or dermatological causes.

You have to treat the primary cause or the exacerbation may persisist and reincide.

Topical steroids are the primary category of medications used to treat exfoliative dermatitis (ED). A sedative antihistamine may be a useful adjunct for pruritic patients, since it helps patients to sleep at night, thus limiting nocturnal scratching and excoriations. Antimicrobial agents often are used if an infection is suspected to be precipitating or complicating exfoliative dermatitis. Other drugs specifically indicated for management of underlying cause of exfoliative dermatitis may be necessary.

For demodectic mange, properly performed deep skin scrapings generally allow the veterinarian to identify the microscopic mites. Acetate tape impression with squeezing has recently found to be a more sensitive method to identify mites. It was originally thought that because the mite is a normal inhabitant of the dog's skin, the presence of the mites does not conclusively mean the dog suffers from demodex. Recent research, however, found that demodex mite can hardly be found on clinically normal dogs, meaning that the presence of any number of mites in a sample is very likely to be significant. In breeds such as the West Highland White Terrier, relatively minor skin irritation which would otherwise be considered allergy should be carefully scraped because of the predilection of these dogs to demodectic mange. Skin scrapings may be used to follow the progress of treatment in demodectic mange.

Alternatively, plasma levels of zinc and copper have been seen to be decreased in dogs suffering with demodicosis. This may be due to inflammation involved in the immune response of demodicosis which can lead to oxidative stress resulting in dogs suffering from demodicosis to exhibit higher levels of antioxidant productivity. The catalases involved in the antioxidant pathway require the trace minerals zinc and copper. Dogs with demodicosis show a decrease in plasma copper and zinc levels due to the increased demand for antioxidant activity. Therefore, this may be considered as a potential marker for demodicosis.

Assurances that this condition will clear as the baby matures are very common. However, studies have shown that the condition occasionally persists into the toddler years, and less commonly into later childhood. It tends to recur in adolescence and persists into adulthood. In an Australian study, about 15 percent of previously diagnosed children still had eczema 10 years later. Sometimes, cradle cap turns into atopic dermatitis. Rarely, it turns out to be misdiagnosed psoriasis.

Treatments for tinea versicolor include:

- Topical antifungal medications containing selenium sulfide are often recommended. Ketoconazole (Nizoral ointment and shampoo) is another treatment. It is normally applied to dry skin and washed off after 10 minutes, repeated daily for two weeks. Ciclopirox (Ciclopirox olamine) is an alternative treatment to ketoconazole, as it suppresses growth of the yeast "Malassezia furfur". Initial results show similar efficacy to ketoconazole with a relative increase in subjective symptom relief due to its inherent anti-inflammatory properties. Other topical antifungal agents such as clotrimazole, miconazole, terbinafine, or zinc pyrithione can lessen symptoms in some patients. Additionally, hydrogen peroxide has been known to lessen symptoms and, on certain occasions, remove the problem, although permanent scarring has occurred with this treatment in some sufferers. Clotrimazole is also used combined with selenium sulfide.

- Oral antifungals including ketoconazole or fluconazole in a single dose, or ketoconazole for seven days, or itraconazole can be used. The single-dose regimens, or pulse therapy regimens, can be made more effective by having the patient exercise 1–2 hours after the dose, to induce sweating. The sweat is allowed to evaporate, and showering is delayed for a day, leaving a film of the medication on the skin.

No treatment is usually needed as they usually go away anywhere from months to years. The lesions may last from anywhere between 4 weeks to 34 years with an average duration of 11 months. If caused by an underlying disease or malignancy, then treating and removing the disease or malignancy will stop the lesions. It usually doesn't require treatment, but topical corticosteroids may be helpful in reducing redness, swelling and itchiness.

Some supported and not supported methods of having an effect on EAC include:

- Photosensitive so it can be moved/reduced with appropriate sunlight.

- Vitamin D

- Immune system - hence it will increase in size/number when the immune system is low or overloaded.

- Hormone Drugs

- Disulone

- Stress reduction

- Topical calcipotriol - a topical vitamin D derivative has been known to be beneficial

It is commonly misdiagnosed as chickenpox or rosacea. Pleva is also often misidentified as a form of staph. The most accurate way to diagnose it is by biopsy. This disease has not been known to be life-threatening. However, there may be mutations of the disease that can cause ulcers on the exterior.

Diagnosis of tinea nigra causing fungus is made on microscopic examination of skin scrapings, mixed with potassium hydroxide (KOH). The KOH the nonfungal debris.

Dr. W.A.D. Griffiths, from Great Britain, classified six forms of PRP in the early 1980s. At this time, the causes of PRP are still unknown and symptoms can be difficult to diagnose. Frequently, more than one medical professional will be consulted before an accurate PRP diagnosis is made.

Dermatologists have identified both an acquired form and an inherited form (familial) of PRP and have described them in medical journals. The acquired form usually shows a spontaneous or gradual remission of symptoms within several years although long-term symptoms may continue for years. The inherited form starts early in childhood with persistent long-term symptoms into adulthood.

Although most people who develop PRP are over age 50, individuals of any age, race, and nationality can be affected. Women and men seem to be equally affected.

The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.

Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".

There is no consensus about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)≤10, a Psoriasis Area Severity Index (PASI) score ≤10, and a dermatology life quality index (DLQI) score ≤10. Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10. The DLQI is a 10 question tool used to measure the impact of several dermatologic diseases on daily functioning. The DLQI score ranges from 0 (minimal impairment) to 30 (maximal impairment) and is calculated with each answer being assigned 0–3 points with higher scores indicating greater social or occupational impairment.

The psoriasis area severity index (PASI) is the most widely used measurement tool for psoriasis. PASI assesses the severity of lesions and the area affected and combines these two factors into a single score from 0 (no disease) to 72 (maximal disease). Nevertheless, the PASI can be too unwieldy to use outside of research settings, which has led to attempts to simplify the index for clinical use.

A diagnosis of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly, erythematous plaques, papules, or patches of skin that may be painful and itch. No special blood tests or diagnostic procedures are usually required to make the diagnosis.

The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema, seborrhoeic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis). Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.

If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy will show clubbed epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions. The stratum granulosum layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin are also abnormal as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nucleus. Inflammatory infiltrates can typically be visualized on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells while a predominance of CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and the joints.

Pityriasis lichenoides chronica (PLC) is probably caused by a hypersensitivity reaction to infectious agents such as the Epstein–Barr virus. Other infectious agents include the adenovirus and Parvovirus B19.