LSC is typically diagnosed by careful observation and history taking. It is easily recognized (see "signs and symptoms", and "gallery"). Biopsies are not necessary, and cannot be used to distinguish LSC from psoriasis.

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.

Diagnosis is based on visual examination and the presence of itching. A skin biopsy is often performed to exclude other diseases. Lesion biopsies will typically show a high level of eosinophils in PN. A culture of at least one lesion will rule out staphylococcus infection, which has been significantly linked to atopic dermatitis.

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

Pemphigus is a group of autoimmune blistering diseases that may be classified into the following types:

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.

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.

Treatment is aimed at reducing itching and minimizing existing lesions because rubbing and scratching exacerbate LSC. The itching and inflammation may be treated with a lotions or steroid cream (such as triamcinolone or Betamethasone) applied to the affected area of the skin. Nighttime scratching can be reduced with sedatives and antihistamines. SSRIs can effectively reduce the scratching associated with obsessive psychosomatic behaviors.

Pemphigus defines a group of autoimmune interepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug induced pemphigus, Senear Usher syndrome and endemic pemphigus foliaceus exist;recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons and eye doctors, as lesions can affect the eyes and mucous membrane of the oral cavity. Intraorally it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone appearance".

Definitive diagnosis also requires the demonstration of anti-desmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire. Anti-desmoglein antibodies can also be detected in a blood sample using the ELISA technique.

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.

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.

There are four classic types of onychomycosis:

- Distal subungual onychomycosis is the most common form of "tinea unguium" and is usually caused by "Trichophyton rubrum", which invades the nail bed and the underside of the nail plate.

- White superficial onychomycosis (WSO) is caused by fungal invasion of the superficial layers of the nail plate to form "white islands" on the plate. It accounts for around 10 percent of onychomycosis cases. In some cases, WSO is a misdiagnosis of "keratin granulations" which are not a fungus, but a reaction to nail polish that can cause the nails to have a chalky white appearance. A laboratory test should be performed to confirm.

- Proximal subungual onychomycosis is fungal penetration of the newly formed nail plate through the proximal nail fold. It is the least common form of "tinea unguium" in healthy people, but is found more commonly when the patient is immunocompromised.

- Candidal onychomycosis is "Candida" species invasion of the fingernails, usually occurring in persons who frequently immerse their hands in water. This normally requires the prior damage of the nail by infection or trauma.

To avoid misdiagnosis as nail psoriasis, lichen planus, contact dermatitis, nail bed tumors such as melanoma, trauma, or yellow nail syndrome, laboratory confirmation may be necessary. The three main approaches are potassium hydroxide smear, culture and histology. This involves microscopic examination and culture of nail scrapings or clippings. Recent results indicate the most sensitive diagnostic approaches are direct smear combined with histological examination, and nail plate biopsy using periodic acid-Schiff stain. To reliably identify nondermatophyte molds, several samples may be necessary.

Prurigo nodularis is very hard to treat, but current therapies include steroids, vitamins, cryosurgery, thalidomide and UVB light. In the event that staphylococcus or other infection is present, antibiotics have proven effective, but tend to cause more harm than good for this particular disease.

A physician may administer a strong dose of prednisone, which will almost immediately stop the itch/scratch cycle. However, cessation of steroids allows relapse to occur, usually within a few weeks. Horiuchi "et al" recently reported significant improvement in PN with antibiotic therapy.

Another drug a physician may administer is Apo-Azathioprine. Azathioprine, also known by its brand name Imuran, is an immunosuppressive drug used in organ transplantation and autoimmune diseases and belongs to the chemical class of purine analogues.

Generally, lichen nitidus is asymptomatic and self-limited; therefore, no treatment is required. However, if persistent pruritus is present, or the appearance “...interferes with daily activities or outlook...” topical glucocorticoids may be tried. If the disease process is symptomatic, generalized and extensive, oral glucocorticoids may be indicated. Other reported treatments include PUVA, UVA/UVB phototherapy, astemizole, acitretin, and etretinate.

When appears with sun/humidity; air conditioning (cool dry air) reduces swelling and discomfort.

It is self limiting condition

1.reassurence

2.steriod cream for local application

3.moisterizer lotion

Frequent, chronic contact of instruments to skin may make it callous by the thickening of stratum corneum. Use of 'thumb position' in cellists may cause callosity of left thumb. Garrod's pads are seen on the dorsal left second and third fingers over the proximal interphalangeal joints in violinists. Drummer's digit is the callosity seen on the lateral phalynx of the left finger. Callosities need treatment only when they are excessive or symptomatic.

The diagnosis is normally made based upon the clinical appearance and history. Tissue biopsy is not usually indicated unless there are areas of ulceration or localized erythroplakia (red patches). The differential diagnosis is with other causes of white lesions (see leukoplakia for a more complete discussion). Specific conditions which can produce a similar appearance include Darier's disease, discoid lupus erythematosus, oral candidiasis, and oral lichen planus.

If a biopsy is taken, the histopathologic appearance is one of hyperkeratosis and acanthosis. There may be squamous metaplasia of excretory ducts, which results in the visible papules if the ducts become hyperplastic. Neutrophils may fill some ducts. It is characterized as a "fissured" or "dried mud" appearance from excess keratin production by cells. Dysplasia is rarely seen.

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%".

Patients with high concentration of antibodies show intercellular, intraepidermal antibodies as well as along the dermoepidermal junction. Patients with low concentration of antibodies only present with them inside the cells (intercellular).

If the results are negative, perform the additional assays regardless. Cases have been confirmed that reported with initial negative DIF and IDIF tests.

Immunoprecipitation, immunoblotting and enzyme-link immunosorbent assay (ELISA)

Poot et al. 2013 determined that immunoprecipitation for antibodies against envoplakin and periplakin or alpha2-macroglobulin-like–1 is the most sensitive test. However, alpha2-macroglobulin-like-1 can also be detected in patients with toxic epidermal necrosis.

Rosin, the material commonly used to wax string instruments is known to cause allergic contact dermatitis in musicians. Nickel, a metal found in musical instruments causes allergic contact dermatitis on the fingers and hands of string instrumentalists and in the lip and neck of wind instrumentalists. Wind instrumentalists with lip and neck infection should switch to gold or plastic mouthpieces if allergic dermatitis occurs. (R)-4-methoxydalbergione present in rosewood may cause allergic contact dermatitis in violinists. Cane reed (causing chelitis in saxophone players), propolis (a wax used to close structural gaps in musical instruments), paraphenylenediamine (used to polish musical instruments) and potassium dichromate (tanning agent to the skin of the harp) also cause allergic contact dermatitis in musicians.

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.

The histology of lichen nitidus is significant for a "...localized granulomatous lymphohistiocytic infiltrate in an expanded dermal papilla with thinning of overlying epidermis and downward extension of the ridges at the lateral margin of the infiltrate, producing a typical 'claw clutching a ball' picture..."