Oral pigmentation

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Oral pigmentation is asymptomatic and does not usually cause any alteration to the texture or thickness of the affected area. The colour can be uniform or speckled and can appear solitary or as multiple lesions. [1] Depending on the site, depth, and quantity of pigment, the appearance can vary considerably. [2]

Contents

Oral pigmentation is found in the following places:

Oral pigmentation affects about 3% of the population [4] and is most likely seen in those with dark skin; [5] however people with light skin have, on average, 30 local pigmented areas and in some circumstances will present intra-orally. They are more often found in females than males [6] and the typical age at presentation is 40 years although they can appear at any age. [3]

Causes

Racial pigmentation

Oral pigmentation affects about 3% of the population [4] and is most likely seen in those with dark skin; [5] however people with light skin have, on average, 30 local pigmented areas and in some circumstances will present intra-orally. They are more often found in females than males [6] and the typical age at presentation is 40 years although they can appear at any age. [3]

Black hairy tongue

Black hairy tongue is a harmless condition which causes blackening pigmentation on the dorsum of the tongue. It is a very common oral condition and affects 13% of the world population. It is often due to poor oral hygiene which leads to accumulation of oral bacteria and build up of keratin on the tongue surface. Black hairy tongue can also be associated with the use of certain medications such as antibiotics, prolonged coffee/tea drinking habit, or smoking. [7]

Amalgam tattoo

The amalgam tattoo is mostly found on the alveolar or gingival mucosa (however can sometimes found on the buccal mucosa) and is more commonly found in females and older patients. It appears as painless, blue/gray/black, nonulcerated, soft macule without any erythematous reaction surrounding it. The tattoos greatest diameter is usually less than 0.5 cm and some lesions containing larger particles may be identifiable on certain radiographs.[ citation needed ]

Some patients exhibit a long-term inflammatory response and if so they may produce discoloured, small papules. The discoloured patch may enlarge over time in patients demonstrating a strong macrophage response

Amalgam deposits can be found within bone occasionally. This can be caused during a surgical procedure e.g. tooth extraction or endodontic surgery, which has caused the material to become inadvertently dislodged from a restoration in an adjacent tooth. These deposits become blackened and can lead to blackening of the adjacent bone. [8]

Peutz–Jeghers syndrome

The autosomal dominant disorder Peutz–Jeghers syndrome is characterized by 'intestinal hamartomatous polyps in association with mucocutaneous melanocytic macules'. These macules often vary in shades of brown, size and are confluent, Although any oral site can be affected, in almost all cases pigmented macules appear on the buccal mucosae, lips and around the mouth. Pigmented macules on the face are less common. The extent of oral involvement and degree of pigmentation varies between each individual case.[ citation needed ]

An individual who has this syndrome has a relative risk fifteen times greater of developing cancer in comparison to the general population.[ citation needed ]

In older patients, the main consequence of the syndrome is cancer. The sites mainly affected include the pancreas, stomach, lungs, colon, small intestine, uterus, breasts and the ovaries and breasts. Additionally, Peutz-Jeghers Syndrome can be associated with other reproductive site cancers including  sertoli cell tumours and adenoma malignum of the cervix.[ citation needed ]

In young patients, intussusception and obstruction of the small intestinal obstruction and are the main complications, these are caused by the small intestinal location of the polyps.[ citation needed ]

Addison's disease

Addison's disease can be caused by a variety of pathological processes. It is an endocrinal disorder where there is an increased amount of adrenocorticotropic hormone (ACTH) as a result of deficient amounts of hormones being produced from the adrenal cortex. [9] Due to this, dark pigmentation may be visible on the oral mucosa or skin. [10] Most common oral sites include: buccal mucosa, lips, gums, hard palate or tongue. Intraoral sites are usually seen as the first sign and they usually develop prior to the skin lesions. [11] In developing countries, this disease is often associated with tuberculosis, where the infection can lead to destruction of the adrenal gland. [12]

Systemically oral melanosis can also be associated with the following;

Kaposi's sarcoma

This is an intermediate neoplasm which affects the skin and mucous membranes; usually arising in patients with HIV. [15] The stages of this type of pigmentation start from an early patch stage, to become plaque-like which then develop into larger nodules- known as the tumour stage. [16] It is common to have oral involvement with this disease and frequently this is associated with a poor prognosis. [17]

Smoker's melanosis

Smoker's Melanosis, benign melanocytic pigmentation of the oral mucosa, [18] [19] most commonly seen in the lower labial gingiva and interdental papillae [19] of smokers. [20] Smoking results in an increase of melanin deposit in the oral mucosa [18] through physical thermal damage and chemical interaction between melanin and nicotine compounds, [19] but this is not the only risk factor towards the pigmentation, it is also associated with other aetiology factors. [21]

Oral melanoacanthoma

Oral melanoacanthoma are benign pigmented lesions due to dendritic melanocyte proliferation and superficial epithelium acanthosis. Clinically characterized by a rapidly growing macular brown lesion that appears suddenly. [22]

Melanocytic nevi

Oral nevi or oral melanocytic nevi, are result of benign proliferations of nevus cells present either in the epithelial layer, the submucosal layer or both. Most commonly seen presentation of oral nevi are intramucosal nevi, these are dome shaped brown papules accounting for 64% of all reported case of oral nevi. [23] Other presentation of oral nevi includes: Blue nevus, junctional nevus and compound nevus. [24]

Melanotic macules

Melanotic macules can be found on the buccal mucosa, lip, palate, alveolar ridge and gingiva. [8] Melanotic macules are benign pigmented lesions that are found in the oral cavity, caused by an increase in pigmentation in the basal cell layer of the epithelium and the lamina propria. Clinically presentation of melanotic macules are typically a brown, black, blue or grey area that is well circumscribed, lesions are usually less than 10 mm in diameter but can be larger in some cases. Vermillion border of the lips is the most common site to find melanotic macules. [25]

Oral melanoma

This type of oral malignancy is very rare. It's caused by proliferation of malignant melanocytes within the connective tissues. Most common oral sites include the hard palate and gums. [2] The presentation of oral melanoma can vary; some could be asymptomatic pigmented areas, whilst others could be rapidly growing areas of ulceration with symptoms such as, bone destruction, pain and bleeding.

To stage oral melanoma, the TNM clinical staging system is used. This stands for 'Tumor – Nodes – Metastasis'. It highlights the three stages: stage I is a primary tumor; stage II is a metastatic tumor which has spread to regional lymph nodes and; stage III is a  metastatic tumor which has spread to distant sites. [26]

Pathogenesis

Many different diseases can cause melanin pigmented lesions in the mouth through

  1. Increase in the number of melanocytes or melanocytosis
  2. Increased melanin production with or without melanocytosis

Melanin is an endogenous pigment synthesized by melanocytes that are located in the basal layer of epithelium. Melanin is then transferred to keratinocytes in melanosomes. Nevus cells in the skin and oral mucosa also produce melanin. Oral melanosis can present as black, gray, blue or brown lesions depending on the site and amount of melanin deposition in tissues. [12]

Physiological

Increased melanin production without increase in melanocytes [27]

Peutz-Jeghers syndrome

Increased production of melanin without increase in number of melanocytes [2]

Addison's disease

Decrease in blood adrenocortical hormone level causes increased levels of adrenocorticotropic hormone secreted by anterior pituitary gland. As a result, melanocyte-stimulating hormone is induced which causes oral melanosis [27]

Smoker's melanosis

Increased melanin production to defend against damage from tobacco smoke [27]

Oral melanoacanthoma

Increased number of dendritic melanocytes [27]

Melanocytic nevi

Accumulation of nevus cells at the basal layer of the epithelium or in the connective tissue or both [27]

Oral melanoma

Increased number of malignant melanocytes [27]

Diagnosis

Diagnosis of oral pigmentation is by a complete history taken by the clinician followed by a thorough clinical examination. [1] Management of such lesions is typically by close clinical monitoring, photographs and measuring tools. A biopsy may be indicated where the following features are present: large or new-pigmented lesions and those with a papular appearance or irregular colouration. [28]

Management

Physiological oral pigmentation

Physiological pigmentation is considered of normal variation. However, for some individuals, the brown/black discolouration may be aesthetically displeasing. It may cause embarrassment or discomfort for some, particularly when smiling or talking. Some methods used to eliminate or reduce this pigmentation include gingivectomy, laser therapy and cryosurgery. There are pros and cons for each type of management strategy.[ citation needed ]

Cryotherapy is one of the most successful and popular treatments for oral melanosis. Cryotherapy damages the tissue by freezing its internal components – thereby jeopardising the cells' optimum temperature; leading to denaturation of enzymes and proteins required for cell function. Minimum temperature needed for cell damage is cell specific, and melanocytes are very sensitive to low temperatures at −4 °C to −7 °C where cell death can occur. [29] This procedure is relatively pain free, so local anaesthesia is generally not needed. Immediately after, slight erythema of the gingiva becomes apparent. Superficial necrosis is observed over the next few days and a whitish slough could be separated from the underlying tissue leaving a clean pink ulcer bed. Within a week, the gingiva returns to normal and is fully healed in next few weeks minus the pigmentation. [30] In conclusion, cryotherapy has been described as the most suitable treatment options for physiological oral melanosis. It is simple yet effective method for treating oral pigmentation with minimal trauma to the patient. [31]

Alternatively, lasers can be used to treat physiological oral melanosis. There are many different lasers available on the market to purchase, each with their own individual benefits and disadvantages. These lasers are expensive therefore, not commonly available in a hospital or clinical setting. However, lasers allow for controlled cutting with a limited depth of necrosis. Studies have shown the diode laser is a safe method and is the preferred laser when no other short pulse lasers are available. [32]  The diode laser is specific and is absorbed only by the melanin meaning more selective destruction and less damage to surrounding normal tissue with comparison to CO2 lasers. [33]

Systemic conditions associated with oral pigmentation

Oral melanosis caused by systemic diseases may be the first sign a dentist or medical professional may pick up to cause suspicion for any underlying systemic disease. Most diseases are treated with the relevant medications which leads to a gradual decrease in oral melanosis. For example, Addison's disease causes hyperpigmentation in the mouth and may be noticed during an exam followed alongside other systemic symptoms. An oral biopsy alongside other relevant tests (i.e. bloods) should be taken and confirmed for diagnosis for any type of oral melanosis which you suspect to be caused by an underlying disease. For Addison's, the specific treatment option would be to treat with glucocorticoids and mineralocorticoids.[ citation needed ]

Alternatively, the continuous exposure to high concentrations of corticosteroids increases susceptibility to Cushing's syndrome which is also a cause of oral melanosis. The patterns of pigmentation are very similar to those with Addison's. The management of these depend on the severity and can be removed by surgical, radiation or drug therapy i.e. Pasierotide. [34]

With regards to oral melanosis caused by systemic diseases, the most important thing to do is to refer the patient to their GMP if there is a suspicion of any underlying systemic cause. If suitable, then it would be appropriate to carry out the relevant investigation to come to a definitive diagnosis. From here it will be easier to manage the cause with the relevant medication or therapy. [34]

Kaposi's sarcoma

There is a variety of different treatment options for Kaposi sarcoma. The appropriate therapy options may vary depending on the variation of disease and the patients immune status. [35] If the lesion is localised, usually found in classical Kaposi sarcoma, and not systemic treatments can be any from lasers, cryotherapy, non-intervention, chemotherapy and immune upregulation. [36] For generalized and systemic cases chemotherapeutic drugs are used. [35] HAART is also a recognised treatment if the patient is known to have AIDS-related Kaposi sarcoma. For cases of iatrogenic Kaposi sarcoma any immunosuppressive medication should be stopped or reduced if able.

Smoker's melanosis

Smokers melanosis may resolve over several years following smoking cessation. [2]

Oral melanoma

An initial biopsy of the lesion may be carried out first to determine correct diagnosis. Following this there is a number of different treatment options available. The combination used will be based on the individual patient and presenting melanoma. Surgical resection [37] is most commonly carried out. This involves cutting out the lesion and ensuring complete removal from the oral cavity. Chemotherapy and Radiotherapy are considered first line management [38] and they may be used in conjunction with surgery. Another option available is Immunotherapy. The aim of this is to target cells or molecules in the immune system in an effort to destroy tumours. [39] This can be done by suppressing or stimulating the patients immune system. After treatment has been carried out patients should be seen for regular follow ups [40] to manage any reoccurrence early and ensure complete healing following surgeries. If the melanoma has progressed extensively and metastasised, treatment, for example surgery, would be carried out in a palliative nature only. [41]

Epidemiology

Oral pigmentation also be classified as 2 categories, melanocytic or non-melanocytic. (Melanocytic being the genesis due to the increase in melanotic pigments and non-melanocytic origin being the genesis from non melanotic causes). The prevalence of melanocytic and non-melanocytic causes of oral melanosis was roughly 1:1. [42] [8]

Physiological

Oral pigmentation affects about 3% of the population [4] and is most likely seen in those with dark skin [5]

Peutz Jeghers syndrome

For Peutz Jeghers syndrome the frequency is approximately 1 case per 60,000-300,000 people in the USA. Equal occurrence in both sexes and all races. Average age of diagnosis being 23 years in men and 26 years in women. [25]

Smokers melanosis

Smoker's melanosis is present in all age groups, has no observed sex or race predilection. [8]

Melanotic macule

For hyperplastic or neoplastic processes, the mean age of oral melanotic macule (hyperplastic- increase in malanoticpigments without an increase in malanocytes)  is 43.1 years with the mean size of the lesion was about 6.8mm.  The female: male ratio is 2:1 and lower lip being the most common location. For oral melanoma (neoplastic) the mean age was 53.8 years with equal ratio of female:male and most common location being in the palate or gingiva. [25] [43]

Oral melanoma

For oral melanoma (neoplastic lesion), the mean age was 53.8 years with equal ratio of female:male and most common location being in the palate or gingiva. [25] [43]

Cumulative frequency

The occurrence of oral malanosis on the cheeks were (21%), alveolar mucosa (16.6%), gingiva (11.8%). Amalgam tattoo being majority of the cases (46.3%), malanotic macules (22.9%) and nevus (20.5%). [42]

See also

Related Research Articles

<span class="mw-page-title-main">Melanocytic nevus</span> Medical condition

A melanocytic nevus is a type of melanocytic tumor that contains nevus cells. Some sources equate the term mole with "melanocytic nevus", but there are also sources that equate the term mole with any nevus form.

<span class="mw-page-title-main">Melanocyte</span> Melanin-producing cells of the skin

Melanocytes are melanin-producing neural crest-derived cells located in the bottom layer of the skin's epidermis, the middle layer of the eye, the inner ear, vaginal epithelium, meninges, bones, and heart. Melanin is a dark pigment primarily responsible for skin color. Once synthesized, melanin is contained in special organelles called melanosomes which can be transported to nearby keratinocytes to induce pigmentation. Thus darker skin tones have more melanosomes present than lighter skin tones. Functionally, melanin serves as protection against UV radiation. Melanocytes also have a role in the immune system.

<span class="mw-page-title-main">Nevus</span> Mole or birthmark; visible, circumscribed, chronic skin lesion

Nevus is a nonspecific medical term for a visible, circumscribed, chronic lesion of the skin or mucosa. The term originates from nævus, which is Latin for "birthmark"; however, a nevus can be either congenital or acquired. Common terms, including mole, birthmark, and beauty mark, are used to describe nevi, but these terms do not distinguish specific types of nevi from one another.

<span class="mw-page-title-main">Acral lentiginous melanoma</span> Medical condition

Acral lentiginous melanoma is an aggressive type of skin cancer that is not caused by sunlight. Melanoma is a group of serious skin cancers that arise from pigment cells (melanocytes); acral lentiginous melanoma is a kind of lentiginous skin melanoma. Acral lentiginous melanoma is the most common subtype in people with darker skins and is rare in people with lighter skin types. It is not caused by exposure to sunlight or UV radiation, and wearing sunscreen does not protect against it. Acral lentiginous melanoma is commonly found on the palms, soles, under the nails, and in the oral mucosa. It occurs on non-hair-bearing surfaces of the body, which have not necessarily been exposed to sunlight. It is also found on mucous membranes.

<span class="mw-page-title-main">Hyperpigmentation</span> Darkening of an area of skin or nails caused by increased melanin

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

<span class="mw-page-title-main">Peutz–Jeghers syndrome</span> Medical condition

Peutz–Jeghers syndrome is an autosomal dominant genetic disorder characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis). This syndrome can be classed as one of various hereditary intestinal polyposis syndromes and one of various hamartomatous polyposis syndromes. It has an incidence of approximately 1 in 25,000 to 300,000 births.

<span class="mw-page-title-main">Café au lait spot</span> Type of birthmark caused by a collection of melanocytes

Café au lait spots, or café au lait macules, are flat, hyperpigmented birthmarks. The name café au lait is French for "coffee with milk" and refers to their light-brown color. Café au lait lesions with rough borders may be seen in McCune-Albright syndrome. In contrast, café au lait lesions of neurofibromatosis have smooth borders.

<span class="mw-page-title-main">Melasma</span> Medical condition

Melasma is a tan or dark skin discoloration. Melasma is thought to be caused by sun exposure, genetic predisposition, hormone changes, and skin irritation. Although it can affect anyone, it is particularly common in women, especially pregnant women and those who are taking oral or patch contraceptives or hormone replacement therapy medications.

Ocular melanosis (OM) is a blue-gray and/or brown lesion of the conjunctiva that can be separated into benign conjunctival epithelial melanosis (BCEM) and primary acquired melanosis (PAM), of which the latter is considered a risk factor for uveal melanoma. The disease is caused by an increase of melanocytes in the iris, choroid, and surrounding structures. Overproduction of pigment by these cells can block the trabecular meshwork through which fluid drains from the eye. The increased fluid in the eye leads to increased pressure, which can lead to glaucoma. In humans, this is sometimes known as pigment dispersion syndrome.

<span class="mw-page-title-main">Lentigo maligna</span> Medical condition

Lentigo maligna is where melanocyte cells have become malignant and grow continuously along the stratum basale of the skin, but have not invaded below the epidermis. Lentigo maligna is not the same as lentigo maligna melanoma, as detailed below. It typically progresses very slowly and can remain in a non-invasive form for years.

<span class="mw-page-title-main">Congenital melanocytic nevus</span> Congenital mole caused by genetic mutations

The congenital melanocytic nevus is a type of melanocytic nevus found in infants at birth. This type of birthmark occurs in an estimated 1% of infants worldwide; it is located in the area of the head and neck 15% of the time.

<span class="mw-page-title-main">Becker's nevus</span> Medical condition

Becker's nevus is a benign 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 on the torso or upper arm, 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).

<span class="mw-page-title-main">Blue nevus</span> Type of melanocytic tumor

A blue nevus is a type of coloured mole, typically a single well-defined blue-black bump.

<span class="mw-page-title-main">Smoker's melanosis</span> Medical condition

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.

Gum depigmentation, also known as gum bleaching, is a procedure used in cosmetic dentistry to lighten or remove black spots or patches on the gums consisting of melanin. Melanin in skin is very common in inhabitants in many parts of the world due to genetic factors. Melanin pigmentation in skin, oral mucosa, inner ear and other organs is a detoxification mechanism. Some toxic agents bind to melanin and will move out of the tissue with the ageing cells and are expelled to the tissue surfaces. Also in the gums and oral mucosa a visible pigmentation is most often caused by genetic factors, but also by tobacco smoking or in a few cases by long-term use of certain medications. If stopping smoking or change of medication do not solve the problem with a disfigurating melanin pigmentation, a surgical operation may be performed. The procedure itself can involve laser ablation techniques.

A benign melanocytic nevus is a cutaneous condition characterised by well-circumscribed, pigmented, round or ovoid lesions, generally measuring from 2 to 6 mm in diameter. A benign melanocytic nevus may feature hair or pigmentation as well.

Pseudomelanoma is a cutaneous condition in which melanotic skin lesions clinically resemble a superficial spreading melanoma at the site of a recent shave removal of a melanocytic nevus.

<span class="mw-page-title-main">Melanotic neuroectodermal tumor of infancy</span> Medical condition

Melanotic neuroectodermal tumor of infancy is a very rare oral cavity tumor that is seen in patients usually at or around birth. It must be removed to be cured. Definitions: A rare, biphasic, neuroblastic, and pigmented epithelial neoplasm of craniofacial sites, usually involving the oral cavity or gums.

<span class="mw-page-title-main">Neurocutaneous melanosis</span> Congenital disorder involving melanocytic tumours in the skin and brain

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.

<span class="mw-page-title-main">Amalgam tattoo</span> Common discoloration of tissue in the mouth

Amalgam tattoo is a grey, blue or black area of discoloration on the mucous membranes of the mouth, typically on the gums of the lower jaw. It is a healthcare caused lesion, due to entry of dental amalgam into the soft tissues. It is common, painless, and benign, but it can be mistaken for melanoma.

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