Nevi are typically diagnosed clinically with the naked eye or using dermatoscopy. More advanced imaging tests are available for distinguishing melanocytic nevi from melanoma, including computerized dermoscopy and image analysis. The management of nevi depends on the type of nevus and the degree of diagnostic uncertainty. Some nevi are known to be benign, and may simply be monitored over time. Others may warrant more thorough examination and biopsy for histopathological examination (looking at a sample of skin under a microscope to detect unique cellular features). For example, a clinician may want to determine whether a pigmented nevus is a type of melanocytic nevus, dysplastic nevus, or melanoma as some of these skin lesions pose a risk for malignancy. The ABCDE criteria (asymmetry, border irregularity, color variegation, diameter > 6 mm, and evolution) are often used to distinguish nevi from melanomas in adults, while modified criteria (amelanosis, bleeding or bumps, uniform color, small diameter or de novo, and evolution) can be used when evaluating suspicious lesions in children. In addition to histopathological examination, some lesions may also warrant additional tests to aid in diagnosis, including special stains, immunohistochemistry, and electron microscopy. Typically; the nevi which exist since childhood are harmless

The management of a nevus depends on the specific diagnosis, however, the options for treatment generally include the following modalities:

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.

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.

Due to the rarity of different types of vascular conditions, angiokeratomas may be misdiagnosed. A biopsy of the lesion can produce a more accurate diagnosis.

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.

Due to its overwhelming incidence on the gingiva, the condition is often associated with two other diseases, though not because they occur together. Instead, the three are associated with each other because they appear frequently on gingiva—peripheral giant cell granuloma and peripheral ossifying fibroma. Detailed analysis can be used to distinguish these conditions.

Oral propranolol appears to be the most effective treatment for reducing the size of capillary hemangiomas in children and is more effective than placebo, observation without intervention, or oral corticosteroids.

In most patients, the number and size of cherry angiomas increases with advancing age. They are harmless, having no relation to cancer at all.

Angiokeratoma may be classified as:

- "Angiokeratoma of Mibelli" (also known as "Mibelli's angiokeratoma," "Telangiectatic warts") consists of 1- to 5-mm red vascular papules, the surfaces of which become hyperkeratotic in the course of time. The disease is named after Italian dermatologist Vittorio Mibelli (1860-1910).

- "Angiokeratoma of Fordyce" (also known as "Angiokeratoma of the scrotum and vulva," though not to be confused with Fordyce's spots) is a skin condition characterized by red to blue papules on the scrotum or vulva.

- "Solitary angiokeratoma" is a small, bluish-black, warty papule that occurs predominantly on the lower extremities.

- "Verrucous vascular malformation" (also known as "Angiokeratoma circumscriptum naeviforme") is a malformation of dermal and subcutaneous capillaries and veins, a congenital vascular malformation, which, over time, a verrucous component appears.

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.

Usually observed at birth or shortly thereafter in 94% of patients, in other reports, patients did not develop skin lesions until 3 months or even 2 years after birth. Females are typically affected more often than males (64%).

Prognosis is usually good, however recurrence may happen with rate up to 16%. Presence of myxoid structures in the pyogenic granuloma may be the main cause of recurrence.

Although pyogenic granulomas are not infectious or malignant, treatment may be considered because of bleeding or ulceration. Frequently, pyogenic granulomas are treated with electrodesiccation (cauterization) and curettage (excision), though laser treatment using pulsed dye laser or CO laser is often effective.

Several reports have demonstrated the efficacy of topical application of the beta-adrenergic antagonist timolol in the treatment of pediatric pyogenic granuloma.

There is usually no treatment if the pyogenic granuloma occurs during pregnancy since the lesion may heal spontaneously. Recurrent bleeding in either oral or nasal lesions may necessitate excision and cauterization sooner, however. If aesthetics are a concern, then treatment may be pursued as well. Usually, only minor surgery may be needed, along with a dental cleaning for oral lesions to remove any calculus or other source of irritation. For nasal lesions, nose-picking should be discouraged.

Verruciform xanthoma is uncommon, with a female:male ratio of 1:1.1

Some patients have a few or no histopathologic abnormalities. Histological examination of a biopsy may show an increase in the number and size of capillaries and veins (rarely lymphatics), dilated capillaries located in the deeper dermis, and hyperplasia and swollen endothelial cells with occasional dilated veins and venous lakes.

These lesions generally do not require treatment. If they are cosmetically unappealing or are subject to bleeding angiomas may be removed by electrocautery, a process of destroying the tissue by use of a small probe with an electric current running through it. Removal may cause scarring. More recently pulsed dye laser or intense pulsed light (IPL) treatment has also been used.

Future treatment based on a locally acting inhibitor of MEK1 and Cyclin E1 could possibly be an option. A natural MEK1 inhibitor is myricetin

Differential diagnosis includes seborrheic keratosis, verruca simplex, condyloma acuminatum, granular cell myoblastoma, vulvar intraepithelial neoplasia, bowenoid papulosis, erythroplasia of Queyrat, and verrucous carcinoma

Dermatofibromas are hard solitary slow-growing papules (rounded bumps) that may appear in a variety of colours, usually brownish to tan; they are often elevated or pedunculated. A dermatofibroma is associated with the dimple sign; by applying lateral pressure, there is a central depression of the dermatofibroma. Although typical dermatofibromas cause little or no discomfort, itching and tenderness can occur. Dermatofibromas can be found anywhere on the body, but most often they are found on the legs and arms. They occur most often in women; the male to female ratio is about 1:4. The age group in which they most commonly occur is 20 to 45 years.

Some physicians and researchers believe dermatofibromas form as a reaction to previous injuries such as insect bites or thorn pricks. They are composed of disordered collagen laid down by fibroblasts. Dermatofibromas are classed as benign skin lesions, meaning they are completely harmless, though they may be confused with a variety of subcutaneous tumours. Deep penetrating dermatofibromas may be difficult to distinguish, even histologically, from rare malignant fibrohistocytic tumours like dermatofibrosarcoma protuberans.

Dermatofibromas typically have a positive "buttonhole sign", or central dimpling in the center.

The treatment for CGCG is thorough curettage. A referral is made to an oral surgeon. Recurrence ranges from 15%–20%. In aggressive tumors, three alternatives to surgery are undergoing investigation:

- corticosteroids;

- calcitonin (salmon calcitonin);

- interferon α-2a.

These therapeutic approaches provide positive possible alternatives for large lesions. The long term prognosis of giant-cell granulomas is good and metastases do not develop.

A capillary hemangioma (also known as an Infantile hemangioma, Strawberry hemangioma, and Strawberry nevus) is the most common variant of hemangioma which appears as a raised, red, lumpy area of flesh anywhere on the body, though 83% occur on the head or neck area. These marks occur in about 10% of all births, and usually appear between one and four weeks after birth. It may grow rapidly, before stopping and slowly fading. Some are gone by the age of 2, about 60% by 5 years, and 90–95% by 9 years. Capillary hemangioma is a vascular anomaly.

Capillary hemangiomas occur 5 times more often in female infants than in males, and mostly in Caucasian populations. Additionally, low birthweight infants have a 26% chance of developing a hemangioma.

It is the most common tumor of orbit and periorbital areas in childhood. It may occur in the skin, subcutaneous tissues and mucous membranes of oral cavities and lips as well as in the liver, spleen and kidneys. While this birthmark may be alarming in appearance, physicians generally counsel that it be left to disappear on its own, unless it is in the way of vision or blocking the nostrils.

Linear verrucous epidermal nevus (also known as a "Linear epidermal nevus," and "Verrucous epidermal nevus") is a skin lesion characterized by a verrucous skin-colored, dirty-gray or brown papule. Generally, multiple papules present simultaneously, and coalesce to form a serpiginous plaque. When this nevus covers a diffuse or extensive portion of the body's surface area, it may be referred to as a systematized epidermal nevus, when it involved only one-half of the body it is called a nevus unius lateris.

Benign fibrous histiocytomas (also known as dermal dendrocytoma, dermatofibroma, fibrous dermatofibroma, fibrous histiocytoma, fibroma simplex, nodular subepidermal fibrosis, and sclerosing hemangioma) are benign skin growths.

Microvenular hemangioma (also known as "Microcapillary hemangioma") is an acquired benign vascular neoplasm that presents as an asymptomatic, slowly growing, 0.5- to 2.0 cm reddish lesion on the forearms or other sites of young to middle-aged adults.

Bowenoid papulosis is a cutaneous condition characterized by the presence of pigmented verrucous papules on the body of the penis. They are associated with human papillomavirus, the causative agent of genital warts. The lesions have a typical dysplastic histology and are generally considered benign, although a small percentage will develop malignant characteristics.

It is considered as a pre-malignant condition. Other terms used to describe the condition are: Erythroplasia of Queyrat, Squamous cell carcinoma in situ and Bowen’s disease. The term "Bowenoid papulosis" was coined in 1977 by Kopf and Bart and is named after dermatologist John Templeton Bowen.

The term “intraepithelial neoplasia” defines a premalignant intraepithelial change.

On the vulva it is termed VIN (vulvar or vulval intraepithelial neoplasia); on the penis, PIN (penile intraepithelial neoplasia); and on or around the anus, AIN (anal intraepithelial neoplasia). The terminology has been very confusing and it is now recommended that the terms Bowen’s disease, erythroplasia of Queyrat, and bowenoid papulosis should not be used for lesions in the anogenital area. However, dermatologists still recognize a distinct clinical variant, bowenoid papulosis, characterized by discrete papules in a younger age group and a tendency for spontaneous regression. Additionally, some authorities believe that erythroplasia of Queyrat and Bowen’s disease remain useful terms in men.

Reported treatments include topical agents, dermabrasion, cryotherapy, laser therapy, and surgical excision. These therapies have a high failure rate because of incomplete relief of symptoms, scarring, or recurrence .

Though similar in appearance, ILVEN will not respond to therapies known to affect psoriasis. ILVEN can be very difficult to live with but can be treated. The most effective method is full-thickness excision of the lesion. CO2 Laser Surgery can resurface the skin to give a flat, smoother and more normal appearance, but does not remove the lesion.