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.

A lesion biopsy is performed if the diagnosis remains uncertain after a clinical physical exam. The most common tissue sampling techniques include shave or punch biopsy. When only a portion of the lesion can be removed due to its size or location, the biopsy should sample tissue from the thickest area of the lesion, as SCCs are most likely to be detected in that area. If a shave biopsy is performed, it should extend through to the level of the dermis in order to provide sufficient tissue for diagnosis; ideally, it would extend to the mid-reticular dermis. Punch biopsy usually extends to the subcutaneous fat when the entire length of the punch blade is utilized.

Physicians usually diagnose actinic keratosis by doing a thorough physical examination, through a combination of visual observation and touch. However a biopsy may be necessary when the keratosis is large in diameter, thick, or bleeding, in order to make sure that the lesion is not a skin cancer. Actinic keratosis and squamous cell carcinoma (SCC) can present similarly on physical exam, and many scientists argue that they are in fact simply different stages of the same condition. In addition to SCCs, AKs can be mistaken for other cutaneous lesions including seborrheic keratoses, basal cell carcinoma, lichenoid keratosis, porokeratosis, viral warts, inflammatory dermatoses, or melanoma.

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.

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.

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

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.

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 annual malignant transformation rate of leukoplakia rarely exceeds 1%, i.e. the vast majority of oral leukoplakia lesions will remain benign. A number of clinical and histopathologic features are associated with varying degrees of increased risk of malignant transformation, although other sources argue that there are no universally accepted and validated factors which can reliably predict malignant change. It is also unpredictable to an extent if an area of leukoplakia will disappear, shrink or remain stable.

- Presence and degree of dysplasia (mild, moderate or severe/carcinoma in situ). Dysplasia is the most important predictor of malignant change, and about 10% of leukoplakia lesions show dysplasia when biopsied.

- Leukoplakia located on the floor of the mouth, the posterior and lateral tongue, and the retromolar areas (the region behind the wisdom teeth) have higher risk, whereas white patches in areas such as the top surface of the tongue and the hard palate do not have significant risk. Although these "high risk" sites are recognized, statistically, leukoplakia is more common on the buccal mucosa, alveolar mucosa, and the lower labial mucosa. Leukoplakia of the floor of the mouth and tongue accounts for over 90% of leukoplakias showing dysplasia or carcinoma on biopsy. This is thought to be due to pooling of saliva in the lower part of the mouth, exposing these areas to more carcinogens held in suspension.

- Red lesions (erythroplasia) and mixed red and white lesions (erythroleukoplakia/"speckled leukoplakia") have a higher risk of malignant change than homogenous leukoplakia.

- Verrucous or nodular areas have a higher risk.

- Although smoking increases risk of malignant transformation, smoking also causes many white patches with no dysplasia. This means that statistically, white patches in non smokers have a higher risk.

- Older people with white patches are at higher risk.

- Larger white patches are more likely to undergo malignant transformation than smaller lesions.

- White patches which have been present for a long period of time have higher risk.

- Persons with a positive family history of cancer in the mouth.

- Candida infection in the presence of dysplasia has a small increased risk.

- A change in the appearance of the white patch, apart from a change in the color, has a higher risk. Changes in the lesion such as becoming fixed to underlying tissues, ulceration, cervical lymphadenopathy (enlargement of lymph nodes in the neck), and bone destruction may herald the appearance of malignancy.

- White patches present in combination with other conditions that carry a higher risk (e.g. oral submucous fibrosis), are more likely to turn malignant.

- Although overall, oral cancer is more common in males, females with white patches are at higher risk than men.

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.

Patient presents with the following signs.

1. Hyperkeratotic papules present over the seborrheic area of the body.

2. V - shaped nicking present at the tip of the nails.

3. Red and white longitudinal nail lines.

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

Keratosis (from "keratinocyte", the prominent cell type in the epidermis, and , abnormal) is a growth of keratin on the skin or on mucous membranes. More specifically, it can refer to:

- actinic keratosis (also known as solar keratosis)

- hydrocarbon keratosis

- keratosis pilaris (KP, also known as follicular keratosis)

- seborrheic keratosis

Actinic keratoses are pre-malignant growths. Seborrheic keratoses are not pre-malignant.

Vaccinating girls with HPV vaccine before their initial sexual contact has been claimed to reduce incidence of VIN.

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.

A 1992 study of 163 affected persons found that most patients had no other medical problems and most manage to lead a relatively normal life.

This skin disease commonly affects adolescents and young adults, especially in warm and humid climates. The yeast is thought to feed on skin oils (lipids), as well as dead skin cells. Infections are more common in people who have seborrheic dermatitis, dandruff, and hyperhidrosis.

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.

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.

The patient may have no symptoms, or local symptomatology including itching, burning, and pain.

The diagnosis is always based on a careful inspection and a targeted biopsy of a visible vulvar lesion.

The type and distribution of lesions varies among the two different types of VIN. In the Usual type VIN, seen more frequently in young patients, lesions tend to be multifocal over an otherwise normal vulvar skin. In the differentiated type VIN, usually seen in postmenopausal women, lesions tend to be isolated and are located over a skin with a vulvar dermatosis such as Lichen slerosus.

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.

Dandruff scale is a cluster of corneocytes, which have retained a large degree of cohesion with one another and detach as such from the surface of the stratum corneum. A corneocyte is a protein complex that is made of tiny threads of keratin in an organised matrix. The size and abundance of scales are heterogeneous from one site to another and over time. Parakeratotic cells often make up part of dandruff. Their numbers are related to the severity of the clinical manifestations, which may also be influenced by seborrhea.

Keratosis pilaris atropicans includes many forms of keratosis pilaris with cicatricial alopecia. Variants include keratosis pilaris atrophicans faciei, atrophoderma vermiculatum, keratosis follicularis spinulosa decalvans, and ichthyosis follicularis.

Lichenoid trikeratosis is a cutaneous condition that may be related to keratosis lichenoides chronica.

Clinical diagnosis can be made with the naked eye using the ABCD guideline or by using dermatoscopy. An online-screening test is also available to help screen out benign moles.