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

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.

The diagnosis is confirmed by a skin biopsy and a positive culture for acid-fast bacilli. A PPD test may also result positive.

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.

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.

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

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.

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.

Therapy for cutaneous tuberculosis is the same as for systemic tuberculosis, and usually consists of a 4-drug regimen, i.e., isoniazid, rifampin, pyrazinamide, and ethambutol or streptomycin.

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.

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.

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.

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%".

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.

It is self limiting condition

1.reassurence

2.steriod cream for local application

3.moisterizer lotion

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.

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 for fiddler’s neck is unnecessary if it is painless and shows minimal swelling, particularly since minor cases are taken as a mark of pride. But fiddler’s neck may lead to worse disorders. The primary methods of treatment involve adjustments to playing of the instrument:

- good hygiene for the affected area and for the instrument

- use of a clean cotton cloth that is changed frequently

- use of a shoulder rest to reduce pressure below the jaw

- a suitable chin rest, especially one carved or molded for the individual

- Covering or changing potentially allergenic materials on the instrument.

- shifting the chin rest to the center of the body over the tailpiece

- smoothing coarse surfaces to reduce abrasion

- for males, growing a beard to avoid folliculitis

Surgery is necessary for sialolithiasis, parotid tumors, and cysts. Cervical lymph nodes that are larger than 1 cm must be biopsied. Connective tissue can be removed by excision when a non-inflamed mass is large, and there is generally little recurrence. Infections should be treated conservatively, and causative species should be identified through smear and culture for appropriate antibiotic selection. Reduction of playing time may be helpful for cases without inflammation, but in 30% of cases this did not improve the symptoms.

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..."

The bacteria staphylococci are present in the majority of cases. Treatment with systemic antibiotics and coal tar shampoo can completely clear the condition when Staphylococcus aureus bacteria are found. Fungal infections such as tinea capitis are known to mimic the symptoms of the condition and can be cleared with antifungal treatment.

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.

Lichen aureus (also known as "lichen purpuricus") is a skin condition characterized by the sudden appearance of one or several golden or rust-colored, closely packed macules or lichenoid papules.

Lichen scrofulosorum (also known as "Tuberculosis cutis lichenoides") is a rare tuberculid that presents as a lichenoid eruption of minute papules in children and adolescents with tuberculosis. The lesions are usually asymptomatic, closely grouped, skin-colored to reddish-brown papules, often perifollicular and are mainly found on the abdomen, chest, back, and proximal parts of the limbs. The eruption is usually associated with a strongly positive tuberculin reaction.

Of the three tuberculids, the incidence of lichen scrofulosorum was found to be the lowest (2%) in a large study conducted in Hong Kong. This highlights its rarity and significance as an important marker of undetected tuberculosis.