Lesions usually disappear between 3 months to 3 years for those who stop smoking. Smoker's melanosis is a benign, normal physiological reaction, and does not develop into cancer. If it does not disappear, however, a biopsy can verify the diagnosis. If Smoker's melanosis is destroyed by excessive smoking, as in the hard palate of reverse smokers, who smoke with the glowing part of the cigarette inside the mouth for different reasons, a pale depigmented surface is first seen, indicating the loss of the protecting melanin. Then a red inflammation sometimes occurs and cancer development may follow. In reverse smokers it is important to inspect regularly the areas with smoker's melanosis to detect any melanin destruction, in order to stop smoking in time and thus prevent a cancer to develop.

Smoker's melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, cheeks or palate as well as in larynx. It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation.

The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deep, some of the toxic substances due to the UV-light damage to the cells, are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and kerationocytes together protect the tissue with melanin serving as a toxic defence- and cleaning agent.

In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, but here acting to clean the mucosa from different toxic chemicals entering the mouth. Besides chemicals in tobacco also antimalaria-drugs cause an oral pigmentation. Smoker's melanosis is like the genetic melanin pigmentations a defence-system in action.

The microscope shows smoker's melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans". They are produced by the dendritic, octopus-like melanocytes, seen between the epithelial cells situated closest to the epithelium/connective tissue border.

In tobacco-users the melanocytes are stimulated to produce melanin granules and to distribute them out to the surrounding epithelial cells for further transport to the mucosal surface, like the mechanism in melanin-pigmented skin.

Small amounts of melanin-like granules together with other electrone-dense particles can also be seen within large melanosome complexes in the underlying connective tissue. If the granules derive from the epithelium, a phenomenon known as melanin incontinence, is not known. In Caucasians these granules are not expected to influence on the clinically observed degree of smoker's melanosis.

Most cases of leukoplakia cause no symptoms, but infrequently there may be discomfort or pain. The exact appearance of the lesion is variable. Leukoplakia may be white, whitish yellow or grey. The size can range from a small area to much larger lesions. The most common sites affected are the buccal mucosa, the labial mucosa and the alveolar mucosa, although any mucosal surface in the mouth may be involved. The clinical appearance, including the surface texture and color, may be homogenous or non-homogenous (see: classification). Some signs are generally associated with a higher risk of cancerous changes (see: prognosis).

Leukoplakia may rarely be associated with esophageal carcinoma.

In the context of lesions of the mucous membrane lining of the bladder, leukoplakia is a historic term used to describe a visualized white patch which histologically represents keratinization in an area of squamous metaplasia. The symptoms may include frequency, suprapubic pain (pain felt above the pubis), hematuria (blood in the urine), dysuria (difficult urination or pain during urination), urgency, and urge incontinence. The white lesion may be seen during cystoscopy, where it appears as a whitish-gray or yellow lesion, on a background of inflamed urothelium and there may be floating debris in the bladder. Leukoplakia of the bladder may undergo cancerous changes, so biopsy and long term follow up are usually indicated.

The palate may appear gray or white and contain many papules or nodules that are slightly elevated with red dots in their center. These red dots represent the ducts of minor salivary glands which have become inflamed by heat. The condition is painless. If a denture is normally worn while smoking, then the mucosa underneath the denture appears unaffected by the condition. In severe cases, the mucosa may show fissuring and develop a "dried lake bed" appearance. Other changes associated with tobacco use may be evident such as brown or black extrinsic staining of teeth from tar and other components of tobacco smoke.

Stomatitis nicotina (also known as nicotine stomatitis, nicotinic stomatitis, nicotine palatinus, stomatitis palatini, leukokeratosis nicotina palate, palatal leukokeratosis, smoker's keratosis, smoker's palate, and smoker's patches), is a diffuse white patch on the hard palate, usually caused by tobacco smoking, usually pipe or cigar smoking. It is painless, and it is caused by a response of the palatal oral mucosa to chronic heat. A more pronounced appearance can occur with reverse smoking, sometimes distinguished from stomatitis nicotina by the term reverse smoker's keratosis. While stomatitis nicotina that is caused by heat is not a premaligant condition (i.e. it does not carry an increased risk of transformation to oral cancer), the condition that is caused by reverse smoking is premalignant.

Melanosis is a form of hyperpigmentation associated with increased melanin.

It can also refer to:

- Melanism

- Ocular melanosis

- Smoker's melanosis

- Oral melanosis

- Riehl melanosis

The congenital melanocytic nevus appears as a circumscribed, light brown to black patch or plaque, potentially very heterogeneous in consistency, covering any size surface area and any part of the body.

As compared with a melanocytic nevus, congenital melanocytic nevi are usually larger in diameter and may have excess terminal hair, a condition called hypertrichosis. If over 40 cm projected adult diameter with hypertrichosis, it is sometimes called giant hairy nevus; more usually these largest forms are known as large or giant congenital melanocytic nevus. The estimated prevalence for the largest forms is 0.002% of births.

Melanocytic Nevi often grow proportionally to the body size as the child matures. As they mature, they often develop thickness, and become elevated, although these features can also be present from birth. Prominent terminal hairs often form, especially after puberty. With maturity, the nevus can have variation in color, and the surface might be textured with proliferative growths.

Neurocutaneous melanosis is associated with the presence of either giant congenital melanocytic nevi or non-giant nevi of the skin. It is estimated that neurocutaneous melanosis is present in 2% to 45% of patients with giant congenital melanocytic nevi. Neurocutaneous melanosis is characterized by the presence of congenital melanocytic nevi on the skin and melanocytic tumors in the leptomeninges of the central nervous system.

Mucosal lentigines (also known as "labial, penile, and vulvar melanosis", and "melanotic macules") is a cutaneous condition characterized by light brown macules on mucosal surfaces.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Congenital melanocytic nevi may be divided into the following types:

- "Small-sized congenital melanocytic nevus" is defined as having a diameter less than 2 cm.

- "Medium-sized congenital melanocytic nevus" is defined as having a diameter more than 2 cm but less than 20 cm.

- "Giant congenital melanocytic nevus" (also known as "Bathing trunk nevus," "Garment nevus," "Giant hairy nevus", and "Nevus pigmentosus et pilosus") is defined by one or more large, darkly pigmented and sometimes hairy patches.

Laugier–Hunziker syndrome ( ) is a cutaneous condition characterized by hyperpigmentation of the oral mucosa, longitudinal melanonychia, and genital melanosis.

Becker's nevus (also known as "Becker's melanosis", "Becker's pigmentary hamartoma", "nevoid melanosis", and "pigmented hairy epidermal nevus") is a skin disorder predominantly affecting males. The nevus can be present at birth, but more often shows up around puberty. It generally first appears as an irregular pigmentation (melanosis or hyperpigmentation) on the torso or upper arm (though other areas of the body can be affected), and gradually enlarges irregularly, becoming thickened and often hairy (hypertrichosis). The nevus is due to an overgrowth of the epidermis, pigment cells (melanocytes), and hair follicles. This form of nevus was first documented in 1948 by American dermatologist Samuel William Becker (1894–1964).

Nevus of Ota (also known as "congenital melanosis bulbi", "nevus fuscoceruleus ophthalmomaxillaris", "oculodermal melanocytosis", and "oculomucodermal melanocytosis") is a blue hyperpigmentation that occurs on the face. It was first reported by Dr. M.T. Ota of Japan in 1939.

Nevus of Ota is caused by the entrapment of melanocytes in the upper third of the dermis. It is found on the face unilaterally and involves the first two branches of the trigeminal nerve. The sclera is involved in two-thirds of cases (causing an increased risk of glaucoma). It should not be confused with Mongolian spot, which is a birthmark caused by entrapment of melanocytes in the dermis but is located in the lumbosacral region. Women are nearly five times more likely to be affected than men, and it is rare among Caucasian people. Nevus of Ota may not be congenital, and may appear during puberty.

"Smoker's face" describes the characteristic changes that happen to the faces of many people who smoke.

The general appearance is of accelerated aging of the face, with a characteristic pattern of facial wrinkling and sallow coloration.

A summary of a study published by the National Institutes of Health found that certain facial features appeared in about 8% of smokers who had smoked a full decade while those same features were absent in a control group of non-smokers.

Riehl melanosis is a form of contact dermatitis, beginning with pruritus, erythema, and pigmentation that gradually spreads which, after reaching a certain extent, becomes stationary. The pathogenesis of Riehl melanosis is believed to be sun exposure following the use of some perfumes or creams (a photocontact dermatitis).

A 1991 report documented the cases of nine patients with both Becker's nevus and malignant melanoma. Of the nine melanomas, five were in the same body area as the Becker's nevus, with only one occurring within the nevus itself. As this was apparently the first documented co-occurrence of the two diseases, there is so far no evidence of higher malignancy rates in Becker's nevi versus normal skin. Nonetheless, as with any abnormal skin growth, the nevus should be monitored regularly and any sudden changes in appearance brought to the attention of one's doctor.

Transient neonatal pustular melanosis (also known as "transient neonatal pustulosis" and "lentigines neonatorum") is a cutaneous condition that presents at birth with 1- to 3-mm flaccid, superficial fragile pustules, some of which may have already resolved in utero, leaving pigmented macules.

Neurocutaneous melanosis is associated with the presence of either giant congenital melanocytic nevi or non-giant nevi of the skin. It is estimated that neurocutaneous melanosis is present in 2% to 45% of patients with giant congenital melanocytic nevi. Patients with non-giant congenital melanocytic nevi seem to have a much lower, but undefined risk. Of these patients, only a small number are symptomatic, usually displaying symptoms before the age of 2.

These symptoms are the result of melanocytic lesions being present in the leptomeninges of the central nervous system.

Symptoms can include:

- Papilledema

- Cranial palsies

- Headache

- Vomiting

- Seizures

Others symptoms may also exist that are related to an increase in intracranial pressure. These symptoms seem to be present regardless of the malignancy of the melanin deposits within the central nervous system.

Approximately 10% of patient with neurocutaneous melanosis also present the Dandy–Walker syndrome and associated Dandy-Walker malformation. This malformation involves an enlargement of the posterior fossae and fourth ventricle along with agenesis of the cerebellar vermis. The abnormalities of the leptomeninges during fetal development due to neurocutaneous melanosis may be the cause of this increased incidence of the Dandy-Walker malformation. The development of hydrocephalus is the most common symptom associated with a combination of neurocutaneous melanosis and a Dandy-Walker malformation, occurring in about two out of three patients.

Also called smoker's palatal keratosis, this condition may occur in smokers, especially pipe smokers. The palate appears dry and cracked, and white from keratosis. The minor salivary glands appear as small, red and swollen bumps. It is not a premalignant condition, and the appearance reverses if the smoking is stopped.

Neurocutaneous melanosis is a congenital disorder characterized by the presence of congenital melanocytic nevi on the skin and melanocytic tumors in the leptomeninges of the central nervous system. These lesions may occur in the amygdala, cerebellum, cerebrum, pons, and spinal cord of patients. Although typically asymptomatic, malignancy occurs in the form of leptomeningeal melanoma in over half of patients. Regardless of the presence of malignancy, patients with symptomatic neurocutaneous melanosis generally have a poor prognosis with few treatment options. The pathogenesis of neurocutaneous melanosis is believed to be related to the abnormal postzygotic development of melanoblasts and mutations of the NRAS gene.

Hyperpigmentation is the darkening of an area of skin or nails caused by increased melanin.

The term "necrotizing ulcerative gingivostomatitis" is sometimes used as a synonym of the necrotizing periodontal disease more commonly termed necrotizing ulcerative gingivitis, or a more severe form (also termed necrotizing stomatitis). The term "necrotizing gingivostomatitis" is also sometimes used.

Early signs of melanoma are changes to the shape or color of existing moles or, in the case of nodular melanoma, the appearance of a new lump anywhere on the skin. At later stages, the mole may itch, ulcerate or bleed. Early signs of melanoma are summarized by the mnemonic "ABCDE":

- Asymmetry

- Borders (irregular with edges and corners)

- Color (variegated)

- Diameter (greater than , about the size of a pencil eraser)

- Evolving over time

These classifications do not, however, apply to the most dangerous form of melanoma, nodular melanoma, which has its own classifications:

- Elevated above the skin surface

- Firm to the touch

- Growing

Metastatic melanoma may cause nonspecific paraneoplastic symptoms, including loss of appetite, nausea, vomiting and fatigue. Metastasis of early melanoma is possible, but relatively rare: less than a fifth of melanomas diagnosed early become metastatic. Brain metastases are particularly common in patients with metastatic melanoma. It can also spread to the liver, bones, abdomen or distant lymph nodes.

While each type of cancer has its own distinctive symptoms, most of them can indicate their presence by the occurrence and the prolonged presence of any common symptom. Some of the general symptoms of cancer in cats are:

- Any lump that changes shape or size

- Any sore that does not heal

- Change in bowel or bladder habits

- Difficulty eating or swallowing

- Difficulty urinating or defecating

- Unexplained bleeding or discharge from body

- Loss of appetite

- Chronic weight loss

- Coughing or difficulty breathing

- Stiffness

- Oral odor

Note that ravenous hunger, while a sign of other diseases like hyperthyroid, can also be a sign of cancer.