Bitot's spots are the buildup of keratin located superficially in the conjunctiva, which are oval, triangular or irregular in shape. These spots are a sign of vitamin A deficiency and are associated with conjunctival xerosis. In 1863, Pierre Bitot (1822-1888), a French physician, first described these spots.

In ancient Egypt, this was treated with animal liver, which is where vitamin A is stored.

Liver spots (also known as age spot, solar lentigo, "lentigo senilis", "old age spot", "senile freckle") are es on the skin associated with aging and exposure to ultraviolet radiation from the sun. They range in color from light brown to red or black and are located in areas most often exposed to the sun, particularly the hands, face, shoulders, arms and forehead, and the scalp if bald.

The spots derive their name from the fact that they were once incorrectly believed to be caused by liver problems, but they are physiologically unrelated to the liver, save for a similar color. From the age of 40 onward the skin is less able to regenerate from sun exposure, and liver spots are very common in this age group, particularly in those who spend time in the sun.

In the overwhelming majority of cases, liver spots pose no threat and require no treatment, though they occasionally have been known to obscure the detection of skin cancer. However, despite being a benign condition, liver spots are sometimes considered unsightly and some people choose to have them removed. This can be done by electrosurgery, laser treatment, cryotherapy, or the use of depigmentation agents, such as hydroquinone, tretinoin, topical cysteamine, azelaic acid or alpha hydroxy acids.

Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier's disease.

Also known as "true" leukonychia, this is the most common form of leukonychia, in which small white spots appear on the nails. Picking and biting of the nails are a prominent cause in young children and nail biters. Besides parakeratosis, air that is trapped between the cells may also cause this appearance. It is also caused by trauma. In most cases, when white spots appear on a single or a couple of fingers or toes, the most common cause is injury to the base (matrix) of the nail. When this is the case, white spots disappear after around eight months, which is the amount of time necessary for nails to regrow completely. The pattern and number of spots may change as the nail grows.

Freckles are clusters of concentrated melaninized cells which are most easily visible on people with a fair complexion. Freckles do not have an increased number of the melanin-producing cells, or melanocytes, but instead have melanocytes that overproduce melanin granules (melanosomes) changing the coloration of the outer skin cells (keratinocytes). As such, freckles are different from lentigines and moles.

Florida keratopathy, also known as Florida spots, is an eye condition characterized by the presence of multiple spots within both corneas. It is most commonly seen in dogs and cats, but is also rarely seen in horses and birds. The disease is found in the southeastern parts of the United States. In other parts of the world it is confined to tropics and subtropics, and it is known as tropical keratopathy.

Florida keratopathy appears as multiple cloudy opacities in the stromal layer of the cornea. The spots appear concentrated at the center and become more diffuse at the periphery. They can range in size from one to eight millimeters. There are no other symptoms, and there is no response to treatment with either anti-inflammatory or antimicrobial drugs. Histological analysis of affected corneas has found acid-fast staining organisms, suggesting Florida keratopathy may be caused by a type of mycobacterium. The disease may be induced by repeated stings to the eyes by the little fire ant, "Wasmannia auropunctata".

Nevus depigmentosus or nevus achromicus is a loss of pigment in the skin which can be easily differentiated from vitiligo. Although age factor has not much involvement in the nevus depigmentosus but in about 19% of the cases these are noted at birth. Their size may however grow in proportion to growth of the body. The distribution is also fairly stable and are nonprogressive hypopigmented patches. The exact cause of nevus depigmentosus is still not clearly understood. A sporadic defect in the embryonic development has been suggested to be a causative factor.

It has been described as "localised albinism", though this is incorrect. Those with nevus depigmentosus may be prone to sunburn due to the lack of pigment, and the patient should use good sun protection. Sunscreen should be applied to all exposed skin, since reduced tanning of normal skin will decrease the contrast with hypopigmented skin. Most patients with nevus depigmentosus do not pursue treatment for their lesion. There is no way to repigment the skin. If, however, the lesion is of cosmetic concern, camouflage makeup is effective. If the lesion is small one could also consider excision.

Mongolian spots (congenital dermal melanocytosis) are birthmarks that are present at birth and most commonly located in the sacrococcygeal or lumbar area. Lesions may be single or multiple and usually involve <5% total body surface area. They are macular and round, oval or irregular in shape. The color varies from blue to greenish, gray, black or a combinations of any of the above. The size varies from few to more than 20 centimeters. Pigmentation is most intense at the age of one year and gradually fades thereafter. It is rarely seen after the age of 6 years. Mongolian spots are considered a congenital anomaly because of the various causal mechanisms scientists believe they are linked to. Melanin production, metabolism problems, or family history of Mongolian spots are some of the various causes of Mongolian spots.

Differently from the melanotic nevi and the verrucous nevi on the skin, age spots change with time in color and in shape. Misrepair-accumulation aging theory proposes a hypothesis on the development of age spots. Firstly, the development of a flat spot is a result of accumulation of aged basal cells. When the skin is aged, some aged cells that contain lipofuscin bodies cannot be removed. An aged cell will affect the functionality of the local tissue and promote the aging of its neighbor cells. By a feedback loop, more and more neighbor cells become aged and lipofuscin-containing. They aggregate and form a spot with an irregular shape. Secondly, protruding of a flat spot is a result of the death of aged cells in the spot and release of lipofuscin bodies. Isolation of the un-digestible lipofuscin bodies in a fibrotic capsule is essential for maintaining the structural integrity of the tissue. Successive encapsulation of dead cells and lipofuscin bodies results in the growth of a spot in three dimensions. The dense lipofuscin bodies in the capsule make a protruding spot soft and dark in color.

The formation of freckles is triggered by exposure to sunlight. The exposure to UV-B radiation activates melanocytes to increase melanin production, which can cause freckles to become darker and more visible. This means that you may have never developed freckles before, but after extended exposure to sunlight, they may suddenly appear.

Freckles are predominantly found on the face, although they may appear on any skin exposed to the sun, such as arms or shoulders. Heavily distributed concentrations of melanin may cause freckles to multiply and cover an entire area of skin, such as the face. Freckles are rare on infants, and more commonly found on children before puberty.

Upon exposure to the sun, freckles will reappear if they have been altered with creams or lasers and not protected from the sun, but do fade with age in some cases.

Freckles are not a skin disorder, but people with freckles generally have a lower concentration of photo-protective melanin, and are therefore more susceptible to the harmful effects of UV radiation. It is suggested that people whose skin tends to freckle should avoid overexposure to sun and use sunscreen.

These white spots result from abnormalities in the function of melanocytes which produce little pigment thereby resulting in white spots in skin.

Mongolian spots, or Dermal melanocytosis, result from failure of complete melanocyte migration into the epidermis before birth with ensuing dermal nesting and melanin production. If there are many spots, or a spot covers a large area, it may be a sign of an underlying disorder, such as a metabolism problem called GM1 gangliosidosis Type 1. Recent data suggest that Mongolian spots may be associated with inborn errors of metabolism. Inborn errors of metabolism arise from single gene defect, most often involving an enzyme function, which leads to disruption of a specific metabolic pathway giving rise to abnormalities in the synthesis or catabolism or proteins, fats or carbohydrates. The most common condition associated with Mongolian spots is Hurler's disease followed by GM1 gangliosidosis Type 1. The clinical manifestations in Mongolian spots in inborn errors of metabolism are spots deeper in color and have a generalized distribution involving dorsal and ventral trunk in addition to sacral region and extremities. They are persistent and in some cases an indistinct feathery border has been described. Another possible cause is through genetic inheritance. Mongolian spots have been diagnosed on several occasions through family history, Mongolian spots were linked with an autosomal dominant inheritance. The majority of the neonatal cutaneous lesions are physiological and transient requiring no therapy. It is necessary to differentiate between benign and clinically significant skin lesions in newborn. Therefore, it is important to be aware of the innocent transient skin lesions in newborn and differentiate these from other serious conditions, which will help avoid unnecessary therapy to the neonates. Parents can be assured of good prognosis of these skin manifestations.

Bier spots are small, light macules usually found on the arms and legs of young adults, in which the intervening skin may seem erthematous but blanches with pressure so that these light macules disappear. This is a benign physiologic vascular anomaly of no significance clinically.

Café au lait spots are usually present at birth, permanent, and may grow in size or increase in number over time.

Cafe au lait spots are themselves benign and do not cause any illness or problems. However, they may be associated with syndromes such as Neurofibromatosis Type 1 and McCune-Albright syndrome.

The size and shape of the spots do not have any meaning or implications with regards to diagnosis of associated syndromes.

On the shaft of the penis, Fordyce spots are more visible when the skin is stretched, and may only be noticeable during an erection.

The spots can also appear on the skin of the scrotum.

Oral Fordyce granules appear as rice-like granules, white or yellow-white in color. They are painless papules (small bumps), about 1–3 mm in greatest dimension. The most common site is along the line between the vermilion border and the oral mucosa of the upper lip, or on the buccal mucosa (inside the cheeks) in the commissural region, often bilaterally. They may also occur on the mandibular retromolar pad and tonsillar areas, but any oral surface may be involved. There is no surrounding mucosal change. Some patients will have hundreds of granules while most have only one or two.

Occasionally, several adjacent glands will coalesce into a larger cauliflower-like cluster similar to sebaceous hyperplasia of the skin. In such an instance, it may be difficult to determine whether or not to diagnose the lesion as sebaceous hyperplasia or sebaceous adenoma. The distinction may be moot because both entities have the same treatment, although the adenoma has a greater growth potential. Sebaceous carcinoma of the oral cavity has been reported, presumably arising from Fordyce granules or hyperplastic foci of sebaceous glands.

In some persons with Fordyce spots, the glands express a thick, chalky discharge when squeezed.

Café au lait" spots or café au lait" macules are flat, pigmented birthmarks. The name "café au lait" is French for "coffee with milk" and refers to their light-brown color. They are also called "giraffe spots" or "coast of Maine spots".

They are caused by a collection of pigment-producing melanocytes in the epidermis of the skin.

These spots are typically permanent, and may grow or increase in number over time.

Café au lait spots are often harmless, but may be associated with syndromes such as neurofibromatosis type 1 and McCune–Albright syndrome.

Port-wine stains, also known as nevus flammeus and sometimes mistaken for strawberry marks, are present at birth and range from a pale pink in color, to a deep wine-red. Irregular in appearance, they are usually quite large, and caused by a deficiency or absence in the nerve supply to blood vessels. This causes vasodilation, the dilation of blood vessels, causing blood to pool or collect in the affected area. Over time, port-wine stains may become thick or develop small ridges or bumps, and do not fade with age. Such birthmarks may have emotional or social repercussions. Port-wine stains occur in 0.3% of the population, equally among males and females. They frequently express unilaterally, i.e., on only one side, not crossing the midline of the body. Often on the face, marks on the upper eyelid or forehead may be indicative of a condition called Sturge-Weber syndrome. Additionally, port-wine stains in these locations may be associated with glaucoma and seizures.

A "hemangioma of infancy", colloquially called a strawberry mark, is a benign self-involuting tumor (swelling or growth) of endothelial cells, the cells that line blood vessels. It usually appears during the first weeks of life and resolves by age 10. It is the most common tumor of infancy.

PHACES Syndrome, a rare condition that often involves brain, heart, and arterial abnormalities, is generally accompanied by the presence of large facial hemangiomas. In such cases, what appears to be a small bruise or birthmark may grow rapidly and take on a puffy appearance in the first days or weeks of life.

Normally, sebaceous glands are only found in association with a hair follicle.

They appear to be more obvious in people with oily skin types, with some rheumatic disorders, and in hereditary nonpolyposis colorectal cancer. In the latter, the most common site for Fordyce spots is the lower gingiva (gums) and vestibular mucosa.

Localised discoid lupus erythematosus typically presents with skin lesions localised above the neck, with favoured sites being the scalp, bridge of the nose, cheeks, above the lips and ears as well as the arms hair scratching glasses touching name="Andrews1"/> Another form of discoid lupus erythematosus includes oral discoid. Oral discoid lupus erythematosus results in oral lesions which present themselves as white spots, ulcers and central erythema lesions. Oral discoid lesions most commonly occur on the labial mucosa, vermillion border and buccal mucosa. Atrophy may be observed in some cases. Dentists may be important in establishing the diagnosis before the cutaneous lesions become apparent.

The only sign of vitiligo is the presence of pale patchy areas of depigmented skin which tend to occur on the extremities. The patches are initially small, but often grow and change shape. When skin lesions occur, they are most prominent on the face, hands and wrists. The loss of skin pigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Some lesions have increased skin pigment around the edges. Those affected by vitiligo who are stigmatized for their condition may experience depression and similar mood disorders.

Hyperpigmentation can be caused by sun damage, inflammation, or other skin injuries, including those related to acne vulgaris. People with darker skin tones are more prone to hyperpigmentation, especially with excess sun exposure.

Many forms of hyperpigmentation are caused by an excess production of melanin. Hyperpigmentation can be diffuse or focal, affecting such areas as the face and the back of the hands. Melanin is produced by melanocytes at the lower layer of the epidermis. Melanin is a class of pigment responsible for producing colour in the body in places such as the eyes, skin, and hair. As the body ages, melanocyte distribution becomes less diffuse and its regulation less controlled by the body. UV light stimulates melanocyte activity, and where concentration of the cells is greater, hyperpigmentation occurs. Another form of hyperpigmentation is post inflammatory hyperpigmentation. These are dark and discoloured spots that appear on the skin following acne that has healed.

Hyperpigmentation is associated with a number of diseases or conditions, including the following:

- Addison's disease and other sources of adrenal insufficiency, in which hormones that stimulate melanin synthesis, such as melanocyte-stimulating hormone (MSH), are frequently elevated.

- Cushing's disease or other excessive adrenocorticotropic hormone (ACTH) production, because MSH production is a byproduct of ACTH synthesis from proopiomelanocortin (POMC).

- Acanthosis nigricans—hyperpigmentation of intertriginous areas associated with insulin resistance.

- Melasma, also known as "chloasma"—patchy hyperpigmentation

- Acne scarring from post-inflammatary hyperpigmentation

- Linea nigra—a hyperpigmented line found on the abdomen during pregnancy.

- Peutz-Jeghers syndrome—an autosomal dominant disorder characterized by hyperpigmented macules on the lips and oral mucosa and gastrointestinal polyps.

- Exposure to certain chemicals such as salicylic acid, bleomycin, and cisplatin.

- Smoker's melanosis

- Coeliac disease

- Cronkite-Canada syndrome

- Porphyria

- Tinea fungal infections such as ringworm

- Haemochromatosis—a common but debilitating genetic disorder characterized by the chronic accumulation of iron in the body.

- Mercury poisoning—particularly cases of cutaneous exposure resulting from the topical application of mercurial ointments or skin-whitening creams.

- Aromatase deficiency

- Nelson's syndrome

- Grave's disease

- As a result of tinea cruris.

Hyperpigmentation can sometimes be induced by dermatological laser procedures.

The cause is unknown but is thought to be associated with diabetic neuropathy and vascular complications; because the lesions are more common on the shins, some suggest it represents an altered response to injury. It is seen more commonly in patients with longstanding diabetes and poor glucose control.

A lentigo () (plural lentigines, ) is a small pigmented spot on the skin with a clearly defined edge, surrounded by normal-appearing skin. It is a harmless (benign) hyperplasia of melanocytes which is linear in its spread. This means the hyperplasia of melanocytes is restricted to the cell layer directly above the basement membrane of the epidermis where melanocytes normally reside. This is in contrast to the "nests" of multi-layer melanocytes found in moles (melanocytic nevi). Because of this characteristic feature, the adjective "lentiginous" is used to describe other skin lesions that similarly proliferate linearly within the basal cell layer.

Lentigines are distinguished from freckles (ephelis) based on the proliferation of melanocytes. Freckles have a relatively normal number of melanocytes but an increased "amount" of melanin. A lentigo has an increased "number" of melanocytes. Freckles will increase in number and darkness with sunlight exposure, whereas lentigines will stay stable in their color regardless of sunlight exposure.

Lentigines by themselves are benign, however one might desire the removal or treatment of some of them for cosmetic purposes. In this case they can be removed surgically, or lightened with the use of topical depigmentation agents. Some common depigmentation agents such as azelaic acid and kojic acid seem to be inefficient in this case, however other agents might work well (4% hydroquinone, 5% topical cysteamine, 10% topical ascorbic acid).

Conditions characterized by lentigines include:

- Lentigo simplex

- Solar lentigo (Liver spots)

- PUVA lentigines

- Ink spot lentigo

- LEOPARD syndrome

- Mucosal lentigines

- Multiple lentigines syndrome

- Moynahan syndrome

- Generalized lentiginosis

- Centrofacial lentiginosis

- Carney complex

- Inherited patterned lentiginosis in black persons

- Partial unilateral lentiginosis

- Peutz-Jeghers syndrome

- Lentigo maligna

- Lentigo maligna melanoma

- Acral lentiginous melanoma

Discoid lupus erythematosus (DLE) is a chronic skin condition of sores with inflammation and scarring favouring the face, ears, and scalp and at times on other body areas. These lesions develop as a red, inflamed patch with a scaling and crusty appearance. The centre areas may appear lighter in colour with a rim darker than the normal skin.

Discoid lupus erythematosus can be divided into localised, generalised, and childhood discoid lupus erythematosus.