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| IMC Wiki | Brown, grey or black lesions

Brown, grey or black lesions

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Specified variants, lesions and diseases

Introduction

Brown or black stains on the oral mucosa can be caused by accumulation of endogeneous or exogeneous pigments in subepithelial connective tissue.

Endogeneous pigments
  • haemoglobin (red/blue)
  • haemosiderin (brown)
    • local: blood extravasation(trauma, haemorrhage)
    • generalised: e.g. haemochromatosis
  • melanin (brown/black)
    • excessive melanin production or
    • proliferation of melanocytes
Exogene Pigmente
mainly acquired by trauma, via iatrogenic-therapeutic ways or by heavy metal intoxication
  • amalgam (grey/black)
    • tattoo, or iatrogenic trauma
  • graphite (grey/black)
    • tattoo, trauma
  • lead, mercury, bismuth (grey)
    • drugs, intoxication
  • chromogenic bacteria (brown, black, green)
    • surface colonialisation

Racial gingiva pigmentation

Definition and clinical features

Streaky and spotty light- to middle brown (infrequently black) discoloration of oral mucosa (gingiva, lips, tongue, bucca) in dark-skinned individuals (also in light-coloured Mediterranean persons).
Not pathologic.

Diagnosis/ Histopathological features

Histologically, there is an increase of melanin pigment within keratinocytes without significant increase in the number of melanocytes

Differential diagnosis

Pigmentations of other aetiology (particularly, Addison’s disease)
  • Localised: amalgam tattoo, melanotic macule, melanocytic naevus, Peutz-Jeghers syndrome, malignant melanoma, Kaposi’s sarcoma
  • Generalised: Addison’s disease, drugs, infectious diseases (AIDS, among others)

Treatment and prognosis

No treatment is necessary

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Oral melanotic macula

Synonyms: labial melanotic macula, lentigo labiali

Definition and clinical features

Solitary or multiple flat, brown mucosal discolorations, predominantly on the lip vermilion (lower lip), bucca, border of tongue or gingiva. A few millimetres in diameter, well demarcated, uniformly pigmented. It is asymptomatic. If multiple, it is usually part of a syndrome.

Diagnosis / Histopathological features

Increase in melanin and melanocytes at the dermo-epidermal junction. Scattered dendritic melynocytes. No atypia. Few melanophages and mild chronic inflammatory infiltration subepithelial

Differential diagnosis

Particularly, amalgam tattoo and malignant melanom

Treatment and prognosis

If amalgam tattoo is not the clear diagnosis, excisional biopsy to differentiate from a malignant melanoma.
Innocuous.

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Addison’s disease

Synonym: primary adrenocortical hypofunctio

Definition and clinical features

Brown pigmentation of oral mucosa and skin due to adrenocortical insufficiency. In the aetiology, autoimmune processes, tuberculosis (rarely), histoplasmosis (sometimes in AIDS) and carcinosis (e.g. bronchial carcinoma metastasis) can play a role. Clinical symptoms are: hypotension, asthenia, weight loss, vomitus, electrolytic disorders and systemic, diffuse skin bronzing.

It is a rare disease, affects primarily young and middle-aged women except with AIDS. Oral pigmentation may be the first sign of disease that may precede skin discoloration by years (early diagnosis can be made by the dental practitioner!). Increased melanin pigmentation is caused by an increased release of melanocyte stimulating hormone (MSH) from the hypophysis stimulated by adrenocortical hypofunction. Oral mucosal pigmentation manifests as spotty or poorly demaracated, diffuse, multifocal, light- to medium brown discoloration of the buccal and gingival mucosa with involvement of the corner of mouth.

Diagnosis/ Histopathological features

Melanin pigment is localised in basal keratinocytes of the epithelium without significant increase in the number of melanocytes

Differential diagnosis

Multifocal brown pigmentations of other aetiology, e.g. physiological/racial, neurofibromatosis (perioral café au lait spots), haemochromatosis, lichen planus, Peutz-Jeghers syndrome, petechia

Treatment and prognosis

Treatment of underlying disease and substitution therapy.

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Peutz-Jeghers syndrome

Synonym: pigment freckle polyposi

Definition and clinical features

A rare hereditary disease, inherited as an autosomal dominant trait, presenting with gastrointestinal polyposis, intra-, und perioral freckle-like pigmentations. Pigmented maculae may by present already at birth, or appear within the first years after birth. Most common sites of frecklelike discolorations are: lip vermilion, perioral skin and intraoral mucosa, as well as skin of the hands. The freckles are 1-5 mm in diameter, dark to light brown, grey-reddish, on occasion. The multiple gastrointestinal polyps are mostly bening corresponding to hamartomatous growth of intestinal mucosa, especially within jejunum and ileum. Patients often develop intestinal obstruction because of intussusceptions of polyps into a distal portion of small bowel. Predisposition to develop cancer

Diagnosis/ Histopathological features

The clinical appearance is pathognomonic. Histologically, melanin deposition and retention in the melanocytes in skin and mucosal maculae

Differential diagnosis

Racial pigmentation, freckles (ephelis

Treatment and prognosis

The pigmented maculae do not require treatment, eventually light protection. Patients and their families should be monitored for intussusceptions or tumour formation. Genetic counselling is appropriate.

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Smoker’s melanosis

Definition and clinical features

Multiple, poorly demarcated brown spots on gingival and labial oral mucosa in association with typical black discoloration of tooth necks, especially in heavy smokers

Diagnosis/ Histopathological features

Microscopically, oedematous swelling of epithelium and mild chronic inflammation subjacent to epithelium with intermixed melanophages

Differential diagnosis

Brown pigmentations of different aetiology

Treatment and prognosis

Smoking cessation; the lesion in itself is harmless.

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Melanocytic naevi

Synonyms: naevocellular nevus, pigmented nevus, mole, birthmark

Definition and clinical features

Melanocytic naevi are benign, localised, hamartomatous proliferations of epidermal melanocytes that correspond to melanocytic naevi of the skin. They can occur intraorally but are not common. Congenital and acquired types are distinguished. Acquired melanocytic naevi evolve through several stages which are histologically classified according to the location of melanocytic proliferations in:
  • epithelium
    • junctional naevus (lentigo simplex)
  • epithelium and lamina propria (dermis)
    • compound-naevus
  • lamina propria (dermis)
    • intramucosal (intradermal) naevus
  • deep connective tissue
    • blue naevus (special form)
Intraoral naevi occur most frequently on the hard palate (40%), lips (25%) and buccal mucosa (16%); they are mostly pigmented (about 85%) with slightly elevated surface. Occurrence at all ages, most commonly between 20-40 years of age, predominantly in females. With increasing age, the degree of pigmentation decreases. Clinical features are variable. Lentigines are up to 3 mm, junctional naevi up to 6 mm in diameter, round/oval, sharply demarcated, homogeneously pigmented brown or black papules. Compound naevi represent small papules and nodules, intramucosal naevi are light brown, often nonpigmented, sometimes pedunculated nodules. Blue naevi appear most commonly as dark blue (steel blue), up to 5 mm in diameter, firm, dome-shaped papule on hard palate.

There is an association between acquired melanocytic naevi and the development of malignant melanoma. However, the exact relationship is unknown and malignant transformation of a naevus is extraordinarily rare.

Diagnosis/ Histopathological features

In lentigo simplex (the precursor of junctional naevus), small, round aggregates of ovoid naevus cells with hyperpigmentation can be found along the basal cell layer of the epithelium, especially at the tips of slightly elongated rete ridges. Mild proliferation of melanocytes, which are localised in single formations along the basal cell layer. In stratum papillare, mild, superficial, perivascular, chronic inflammatory infiltrate and single melanophages.

In junctional naevus, more expressed naevus cell proliferations as single cells or nested aggregates along the epithelial-connective tissue junction, especially at the tips of rete ridges with hyperpigmentation. Nests are uniform and sharply demarcated from keratinocytes. The nuclei of melanocytes are monomorph. Mild subepithelial chronic inflammation with scattered melanophages.

In compound naevi, single melanocytes as well as nests of proliferating melanocytes occur both within the epithelium and the underlying superficial connective tissue.

In intramucosal (intradermal) naevi, nests and cords of naevus cells, frequently multinuclear melanocytes, are located entirely in the connective tissue of the dermis.

Blue naevi are characterised by an ill-defined proliferation of elongated, spindle-shaped, or epithelioid, usually heavily pigmented melanocytic cells in deep connective tissue. No connection to surface epithelium.

Differential diagnosis

Pigmented lesions of different aetiology, especially amalgam tattoos, or malignant melanoma (!

Treatment and prognosis

All pigmented lesions of unknown origin shall be completely excised and examined histologically in order to exclude malignant melanoma!The only exceptions are: benign lentigines, amalgam tattoos and drug-related pigmentations.

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Malignant melanoma

Definition and clinical features

Malignant tumour of melanocytic origin; 90% cutaneous, 10% mucosal, including about 1% at intraoral location. Men are affected more frequently than women (particularly between 40 and 70 years of age); it never occurs under 20 years. The most common intraoral locations are: hard palate, bucca and gingiva (especially maxillary alveolus). Melanomas appear characteristically as heavily but irregularly pigmented brown to black maculae or nodules (non-pigmented/amelanotic forms are rare), of several cm in diameter, later with ulceration. They typically grow rapidly and metastasise in regional lymph nodes and blood stream. On the skin, melanomas evolve through different stages beginning with an in situ melanoma. The development of mucosal melanomas is unclear.

Five clinico-pathological variants are distinguished:
  • Superficial spreading melanoma
  • Nodular melanoma
  • Lentigo maligna melanoma (specific type in elderly patients on sun-exposed facial skin)
  • Acral-lentiginous melnoma (palmoplantar and subungual)
  • Mucosal melanoma
Clinical appearance (ABCD rule)
A =Asymmetry
B =Border irregularity
C =Colour variegation
D =Diameter > 6 mm

Diagnosis/ Histopathological features

In case of any suspicion of a mucosal melanoma, a complete excision with broad tumour-free margins is indicated to ensure or exclude diagnosis.
Incisional biopsy in contraindicated! Histological evaluation of the level of tumour invasion according to Clark and measurement of maximal tumour thickness according to Breslow (see pTNM).

Clark’s levels:

I Cells confined to epithelium (melanoma in situ)
II Cells penetrating papillary dermis (through basement membrane)
III Cells filling papillary dermis
IV   Cells extending into reticular dermis
V Cells invading subcutaneous fat


Histologically: large, polymorphic, atypical melanocytes in all epithelial layers and subepithelial connective tissue; scattered singly and in irregular, confluent groups. Asymmetric structure, variable pigmentation, abundant cellular atypia, pathological mitotic forms. Poor demarcation laterally and to deeper connective tissue. Basal nests are frequently larger than superficial ones; there is no „differentiation“ of tumour cells in the depth of dermis. Inflammation and degenerative signs in surrounding tissues.

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Postoperative classification (pTNM):

pTis Melanoma in situ (Clark’s-level I)
PT1 Tumour thickness (Breslow) < 0,75 mm and (Clark’s-level II)
PT2 Tumour thickness (Breslow) 0,76 - 1,5 mm and/or (Clark’s-level III)
PT3 Tumour thickness (Breslow) 1,51 - 3,0 mm and/or (Clark’s-level IV)
PT4 Tumour thickness (Breslow) 3,01 - 4,0 mm and/or (Clark’s-level IV)
PT4a Tumour thickness (Breslow) > 4,0 mm and/or (Clark’s-level V)
PT4b  Satellite tumours within 2 cm adjacent to primary tumour
N Regional lymph node metastasis
N0 No lymph node metastasis
to N2c Up to lymph node metastases > 3 cm
M Distant metastasis
M0 No distant metastasis
to M1b Up to visceral metastases


Differential diagnosis

Differentiate from melanocytic naevi and other pigmented lesions, i.e. amalgam tattoo, haemangioma

Treatment and prognosis

Radical excision with a broad tumour-free margin (at least 1 cm laterally). In advanced stages, regional lymph node dissection additionally. Intense monitoring (in all 3 months within the first and second postoperative years). The prognosis is poor.

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Black hairy tongue

Synonyms: lingua pilosa nigra, lingua villosa nigra, lingua villosa fusc

Definition and clinical features

Black or brown, hairy appearence in the midline on posterior dorsal tongue. Mostly middle-aged and older men are affected. The spectrum of discoloration can comprise all colours between white and black (see also: White lesions (White hairy tongue)). Aetiology is unknown, smoking and poor oral hygiene and medications (e.g. iron salts) can be predisposing factors. The proliferation of chromogenic bacteria can cause brown or black discoloration. The “hairs” are composed of elongated keratinised tips of filiform papillae.

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Diagnosis /Histopathological features

The diagnosis is clinically unequivocal, in most of the cases.
Histologically, the “hairs” are caused by elongation and hyperkeratosis of the filiform papillae. Coccoidal bacterial colonies are almost always found on the keratinised tips of filiform papillae.

Differential diagnosis

Unequivocal clinical diagnosi

Treatment and prognosis

Improved oral hygiene, tongue brushing evenings, discontinuation of causative medication.

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Amalgam tattoo

Definition and clinical features

It is the most common form of exogeneous pigment implantation in oral mucosa. Black, bluish-black, or grey, solitary maculae, occasionally slightly elevated lesions under normal appearing mucosa. The commonest locations are: the alveolar ridges and mucobuccal folds. Adults are mainly affected. Asymptomatic, sometimes visible on rtg film. Amalgam, which is an alloy containing silver, mercury, tin and other metals, can be incorporated into the oral mucosa in several ways, e.g. through injured mucosal areas which get in contact with amalgam. Several dental procedures (tooth extraction, root filling, apicectomy) may cause mucosal amalgam implantation. If dental floss becomes contaminated with amalgam particles of recently placed filling it can be implanted in gingival tissues via hygiene procedures

Diagnosis/Histopathological features

Excision in order to exclude malignant melanoma. Histologically, fine, black pigmentary infiltration can be observed between subepithelial collagenous fibres. Also the elastic fibres and basement membrane of vessels are brownishly impregnated. The particles are negative in iron staining (Prussian blue). The inflammatory reaction varies and depends on the size of fragments; it can be very pronounced with formation of foreign-body granulomas.

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Brownish-black impregnated elastic fibres and basement membrane of a blood vessel.

Differential diagnosis

The most important differential diagnosis is the mucosal malignant melanoma. Otherwise pigmentations of different origin, lentigines, melanocytic naevi

Treatment and prognosis

Excision for diagnosis; no further treatment is necessary.

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Pigmentation in systemic metallic intoxications

Definition and clinical features

Numerous organic and inorganic chemical agents cause occasionaly hyperpigmentation of oral mucosa via mainly unknown mechanisms.
Chronic, systemic heavy metal poisoning, commonly secondary to occupational exposure or certain medical preparations in the past, caused stomatitis with hypersalivation and asymptomatic metal deposition along the marginal gingiva. Blue-black „gingival lines“ may be caused by silver (argyria), bismuth (industrial or medicinal), lead, mercury, cadmium, copper and arsenic. Occupational exposition to these elements is rare nowadays – with the exception of lead and mercury.

Chronic lead poisoning (plumbism) occurs in special occupations, e.g. printers, workers in lead-contaminated mines and chemical factories, painters, potters and traffic policemen. The bluish-black lead line results from the action of bacterial hydrogen sulphide on lead in the gingival sulcus to produce a precipitate of lead sulphite along the gingival margin in dentulous, but not in toothless patients.

Also chronic intoxication by mercury and bismuth results in blue-grey gingival lines and greyish pigmentation, sometimes ulceration on oral mucosa. In severe cases, particularly with mercury poisoning, ulcerative stomatitis and loosening of teeth can occur.

Medications containing silver and gold can cause blue-violet, pearl-like discoloration of the gingival margin. The role of other drugs, e.g. anti-malaria drugs, Busulfan, Cisplatin, Phenotiazine, ACTH and oral contraceptives is currently discussed.

Diagnosis/ Histopathological features

History of medication and occupation.
Characteristic histological features are:
  • Argyria: fine granules in mesenchymal cells and vessel walls, no foreign-body reaction.
  • Lead poisoning: from green to black nuclear inclusion bodies in mesenchymal cells.
  • Bismuth: black granules in connective tissue, endothelium and macrophages, no foreign-body reaction.

Differential diagnosis

Pigmentation of different origin.

Localised   Amalgam tattoo
single ephelis
melanocytic naevi
Peutz-Jeghers-syndrome
Malignant melanoma
Kaposi’s sarcoma
 
Generalised   Addison’s disease
other rare causes
AIDS

Treatment and prognosis

Elimination of causative agents, if possible.
Prognosis depends on systemic secondary diseases.

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sources

  • Hornstein OP (Mohr W, Gorz E) (1996)   Erkrankungen des Mundes. Ein interdisziplinäres Handbuch und Atlas   Kohlhammer, Stuttgart - Berlin - Köln
  • Kerl H, Garbe K, Cerroni L, Wolff HH (Hrsg.) (2002)   Histopathologie der Haut   Springer, Berlin
  • Mittermayer C (1993)   Oralpathologie. Erkrankungen der Mundregion 3. Auflage   Schattauer, Stuttgart-New York
  • Mohr W, Gorz E (2001)   Association of silver granules with elastic fibers in amalgam reaction of mouth mucosa   HNO. 2001 Jun;49(6):454-7
  • Reichart PA, Philipsen HP (1999)   Oralpathologie. Farbatlanten der Zahnmedizin 14   Georg Thieme Verlag, Stuttgart, New York
  • Scully C, Cawson RA (1996)   Taschenatlas Oralpathologie   Heidelberg: Hüthing, 1996