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Chapter Contents
Exogenous Pigmentation
Amalgam tattoos are by far the most common form of exogenous pigmentation seen in the oral cavity. A distant second is graphite tattoo from implanted pencil lead.
Amalgam Tattoo (Focal Agyrosis)
Clinical Findings
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This occurs in adults as a nontender, localized lesion (usually <1 cm), or less commonly as a diffuse slate or blue-gray macule of the oral mucosa that is evenly pigmented.
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It often occurs on the gingiva adjacent to an amalgam restoration or crown, or around an apicoectomy (root apex surgery) scar after an amalgam retrofill ( Fig. 9.1A–D ); however, any mucosal site may be affected; larger particles may be evident on radiograph ( Fig. 9.1E–F )
FIG 9.1 (A) Amalgam tattoo adjacent to a crown. (B) Amalgam tattoo related to apicoectomy (apical surgery) scar. (C) Amalgam tattoo on the floor of mouth. (D) Amalgam tattoo on the right buccal mucosa close to a crown. (E) Amalgam tattoo on the alveolar ridge after extraction. (F) Periapical radiograph of FIG 9.1E shows amalgam particles.
Etiopathogenesis and Histopathologic Features
Silver within amalgam restorations (a combination of silver, mercury, tin, and other metals) stains agyrophilic connective tissue fibers. It either leaches out of contacting amalgams or root canal fillings, or is traumatically implanted; the latter is the most often biopsied because it is not in direct contact with a restoration.
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Scarring and fibrosis are always present for traumatically implanted lesions with a variable lymphocytic infiltrate and may be the first clue that an amalgam tattoo is present ( Figs. 9.2A–B and 9.4A ).
Three patterns are recognized ( Figs. 9.2–9.4 ):
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Fine golden-brown particles are deposited in a “beaded” pattern along connective tissue fibers, the basement membrane of the epithelium and blood vessels, perineurium and endomysium ( Figs. 9.2C–D and 9.3 )
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Golden-brown staining of connective tissue fibers occurs with or without particulate deposits ( Figs. 9.2E and 9.4B )
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Larger particles are found within foreign body granulomas ( Figs. 9.2B and 9.3B ).
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Fine refractile crystalline foreign material likely represents fragments of dental cement placed with amalgams.
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Differential Diagnosis
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Medication-induced pigmentation exhibits fine particles that align in linear fashion between collagen fibers, but they do not stain the fibers; usually they are Fontana-Masson and/or iron positive (see later).
Management and Prognosis
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No treatment is necessary although surgical or laser removal may be performed for cosmetic reasons.
References
Amalgam Tattoo (Focal Agyrosis)
Clinical Findings
- •
This occurs in adults as a nontender, localized lesion (usually <1 cm), or less commonly as a diffuse slate or blue-gray macule of the oral mucosa that is evenly pigmented.
- •
It often occurs on the gingiva adjacent to an amalgam restoration or crown, or around an apicoectomy (root apex surgery) scar after an amalgam retrofill ( Fig. 9.1A–D ); however, any mucosal site may be affected; larger particles may be evident on radiograph ( Fig. 9.1E–F )
FIG 9.1 (A) Amalgam tattoo adjacent to a crown. (B) Amalgam tattoo related to apicoectomy (apical surgery) scar. (C) Amalgam tattoo on the floor of mouth. (D) Amalgam tattoo on the right buccal mucosa close to a crown. (E) Amalgam tattoo on the alveolar ridge after extraction. (F) Periapical radiograph of FIG 9.1E shows amalgam particles.
Etiopathogenesis and Histopathologic Features
Silver within amalgam restorations (a combination of silver, mercury, tin, and other metals) stains agyrophilic connective tissue fibers. It either leaches out of contacting amalgams or root canal fillings, or is traumatically implanted; the latter is the most often biopsied because it is not in direct contact with a restoration.
- •
Scarring and fibrosis are always present for traumatically implanted lesions with a variable lymphocytic infiltrate and may be the first clue that an amalgam tattoo is present ( Figs. 9.2A–B and 9.4A ).
Three patterns are recognized ( Figs. 9.2–9.4 ):
-
-
- •
Fine golden-brown particles are deposited in a “beaded” pattern along connective tissue fibers, the basement membrane of the epithelium and blood vessels, perineurium and endomysium ( Figs. 9.2C–D and 9.3 )
- •
Golden-brown staining of connective tissue fibers occurs with or without particulate deposits ( Figs. 9.2E and 9.4B )
- •
Larger particles are found within foreign body granulomas ( Figs. 9.2B and 9.3B ).
- •
Fine refractile crystalline foreign material likely represents fragments of dental cement placed with amalgams.
- •
-
Differential Diagnosis
- •
Medication-induced pigmentation exhibits fine particles that align in linear fashion between collagen fibers, but they do not stain the fibers; usually they are Fontana-Masson and/or iron positive (see later).
Management and Prognosis
- •
No treatment is necessary although surgical or laser removal may be performed for cosmetic reasons.
Clinical Findings
- •
This occurs in adults as a nontender, localized lesion (usually <1 cm), or less commonly as a diffuse slate or blue-gray macule of the oral mucosa that is evenly pigmented.
- •
It often occurs on the gingiva adjacent to an amalgam restoration or crown, or around an apicoectomy (root apex surgery) scar after an amalgam retrofill ( Fig. 9.1A–D ); however, any mucosal site may be affected; larger particles may be evident on radiograph ( Fig. 9.1E–F )
FIG 9.1 (A) Amalgam tattoo adjacent to a crown. (B) Amalgam tattoo related to apicoectomy (apical surgery) scar. (C) Amalgam tattoo on the floor of mouth. (D) Amalgam tattoo on the right buccal mucosa close to a crown. (E) Amalgam tattoo on the alveolar ridge after extraction. (F) Periapical radiograph of FIG 9.1E shows amalgam particles.
Etiopathogenesis and Histopathologic Features
Silver within amalgam restorations (a combination of silver, mercury, tin, and other metals) stains agyrophilic connective tissue fibers. It either leaches out of contacting amalgams or root canal fillings, or is traumatically implanted; the latter is the most often biopsied because it is not in direct contact with a restoration.
- •
Scarring and fibrosis are always present for traumatically implanted lesions with a variable lymphocytic infiltrate and may be the first clue that an amalgam tattoo is present ( Figs. 9.2A–B and 9.4A ).
Three patterns are recognized ( Figs. 9.2–9.4 ):
-
-
- •
Fine golden-brown particles are deposited in a “beaded” pattern along connective tissue fibers, the basement membrane of the epithelium and blood vessels, perineurium and endomysium ( Figs. 9.2C–D and 9.3 )
- •
Golden-brown staining of connective tissue fibers occurs with or without particulate deposits ( Figs. 9.2E and 9.4B )
- •
Larger particles are found within foreign body granulomas ( Figs. 9.2B and 9.3B ).
- •
Fine refractile crystalline foreign material likely represents fragments of dental cement placed with amalgams.
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References
Graphite and Other Foreign Body Tattoos
Clinical Findings
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Localized gray-to-black, nontender macule or nodule occurs on any mucosal site but often on the palatal mucosa (eg, child who falls when running with a pencil held between the teeth, puncturing the palate) ( Fig. 9.5A ); other foreign material (eg, glass) may elicit inflammation and may be painful.
FIG 9.5 (A) Graphite tattoo on the left lower lip. (B) Ritualistic tattoo of the gingiva. - •
Ritualistic tattooing of the skin and mouth (especially gingiva) is practiced in some cultures in the world (such as in Africa), as well as among incarcerated subjects; these are not usually biopsied ( Fig. 9-5B )
Etiopathogenesis and Histopathologic Features
This is caused by traumatic implantation of pencil lead (graphite) or other material.
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Graphite takes the form of coarse black granules of nonrefractile, slightly geometric, foreign material, some of which lie within multinucleate giant cells of foreign body granulomas; there are no distinguishing features so the history of traumatic implantation is important ( Fig. 9.6 ). There may be yellow birefringence under polarized light at the periphery of the particles.
FIG 9.6 Graphite tattoo. (A) Granulomatous reaction and fibrosis. (B) Irregular, geometric, large and small, black particles with surrounding macrophages.
Differential Diagnosis
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Unlike amalgam, graphite does not stain connective tissue fibers; it maintains birefringence after treatment with 10% ammonium sulfide, whereas amalgam may have weak birefringence that is quenched on treatment with ammonium sulfide.
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Other traumatically-implanted foreign bodies should be considered after a careful review of the history; dispersive spectroscopy may be employed to identify the foreign material.
Management and Prognosis
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No treatment is necessary although surgical or laser removal may be performed for cosmetic reasons.
References
Clinical Findings
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Localized gray-to-black, nontender macule or nodule occurs on any mucosal site but often on the palatal mucosa (eg, child who falls when running with a pencil held between the teeth, puncturing the palate) ( Fig. 9.5A ); other foreign material (eg, glass) may elicit inflammation and may be painful.
FIG 9.5 (A) Graphite tattoo on the left lower lip. (B) Ritualistic tattoo of the gingiva. - •
Ritualistic tattooing of the skin and mouth (especially gingiva) is practiced in some cultures in the world (such as in Africa), as well as among incarcerated subjects; these are not usually biopsied ( Fig. 9-5B )
Etiopathogenesis and Histopathologic Features
This is caused by traumatic implantation of pencil lead (graphite) or other material.
- •
Graphite takes the form of coarse black granules of nonrefractile, slightly geometric, foreign material, some of which lie within multinucleate giant cells of foreign body granulomas; there are no distinguishing features so the history of traumatic implantation is important ( Fig. 9.6 ). There may be yellow birefringence under polarized light at the periphery of the particles.
FIG 9.6 Graphite tattoo. (A) Granulomatous reaction and fibrosis. (B) Irregular, geometric, large and small, black particles with surrounding macrophages.
Differential Diagnosis
- •
Unlike amalgam, graphite does not stain connective tissue fibers; it maintains birefringence after treatment with 10% ammonium sulfide, whereas amalgam may have weak birefringence that is quenched on treatment with ammonium sulfide.
- •
Other traumatically-implanted foreign bodies should be considered after a careful review of the history; dispersive spectroscopy may be employed to identify the foreign material.
References
Medication-Induced Pigmentation
Clinical Findings
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Diffuse, painless, symmetric, bluish-gray macular pigmentation of the hard palatal mucosa (may be subtle) is typical and there may be concomitant melanonychia and skin lesions ( Fig. 9.7 ).
FIG 9.7 Imatinib-induced pigmentation of the palatal mucosa.(Courtesy Dr. Paul Kuo, private practice, Brookline, Mass.) - •
Minocycline, antimalarial medications (such as mepacrine or quinacrine), imatinib, birth control pills, and clofazimine may give rise to this condition.
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Tetracycline and its analogues are taken up by teeth and bone, which appear brown; discoloration is visible through the oral mucosa.
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Rare instances of pigmentation caused by leaching of metals from a denture have been reported.
Etiopathogenesis and Histopathologic Features
Medication-induced pigmentation occurs through several mechanisms. Break-down products of antimalarial drugs, minocycline and imatinib chelate with iron or melanin and deposit within the lamina propria. Birth control pills lower cortisol level and increase levels of adrenocorticotrophic hormone (ACTH), leading to stimulation of melanocytes while the breakdown product of clofazamine is itself red. It is unclear why medication-associated pigment deposits exclusively on the hard palatal mucosa in the mouth.
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Particles are brown, uniformly spherical, only a few microns in diameter and align in linear fashion between collagen fibers, although this likely represents pigment within dendritic processes of macrophages or other dendritic cells ( Fig. 9.8A–B ).
FIG 9.8 Quinacrine pigmentation. (A) Pigmented particles are noted in the lamina propria without tissue reaction. (B) Fine, spherical dark-brown pigment granules are present within macrophages or dendritic processes. (C) Granules stain for iron (Prussian blue stain). (D) Granules stain for melanin (Fontana-Masson stain). - •
Particles stain with Prussian blue for iron and Fontana-Masson stain for melanin, although the degree of staining is variable (see Fig. 9.8C–D ); they elicit no fibrosis or inflammation.
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Teeth and bone that are stained by tetracycline fluoresce under polarized light.
Differential Diagnosis
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Amalgam particles are not uniformly spherical, and they stain connective tissue fibers.
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Hemosiderin particles are larger, coarser, and more variable in size, and stain with Prussian blue stain ( Fig. 9.9 ); there may be inflammation and hemorrhage present.
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Melanotic macules exhibit melanophages in the lamina propria and melanin within basal cells.
FIG 9.9 Hemosiderin deposits. (A) Coarse, irregular brown granules associated with many plasma cells. (B) Granules stain for iron (Prussian blue stain). -
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Blue nevus exhibits spindled melanocytes that react with MART-1 and HMB45 (see later).
Management and Prognosis
- •
No treatment is necessary.
References
Clinical Findings
- •
Diffuse, painless, symmetric, bluish-gray macular pigmentation of the hard palatal mucosa (may be subtle) is typical and there may be concomitant melanonychia and skin lesions ( Fig. 9.7 ).
FIG 9.7 Imatinib-induced pigmentation of the palatal mucosa.(Courtesy Dr. Paul Kuo, private practice, Brookline, Mass.) - •
Minocycline, antimalarial medications (such as mepacrine or quinacrine), imatinib, birth control pills, and clofazimine may give rise to this condition.
- •
Tetracycline and its analogues are taken up by teeth and bone, which appear brown; discoloration is visible through the oral mucosa.
- •
Rare instances of pigmentation caused by leaching of metals from a denture have been reported.
Etiopathogenesis and Histopathologic Features
Medication-induced pigmentation occurs through several mechanisms. Break-down products of antimalarial drugs, minocycline and imatinib chelate with iron or melanin and deposit within the lamina propria. Birth control pills lower cortisol level and increase levels of adrenocorticotrophic hormone (ACTH), leading to stimulation of melanocytes while the breakdown product of clofazamine is itself red. It is unclear why medication-associated pigment deposits exclusively on the hard palatal mucosa in the mouth.
- •
Particles are brown, uniformly spherical, only a few microns in diameter and align in linear fashion between collagen fibers, although this likely represents pigment within dendritic processes of macrophages or other dendritic cells ( Fig. 9.8A–B ).
FIG 9.8 Quinacrine pigmentation. (A) Pigmented particles are noted in the lamina propria without tissue reaction. (B) Fine, spherical dark-brown pigment granules are present within macrophages or dendritic processes. (C) Granules stain for iron (Prussian blue stain). (D) Granules stain for melanin (Fontana-Masson stain). - •
Particles stain with Prussian blue for iron and Fontana-Masson stain for melanin, although the degree of staining is variable (see Fig. 9.8C–D ); they elicit no fibrosis or inflammation.
- •
Teeth and bone that are stained by tetracycline fluoresce under polarized light.
Differential Diagnosis
- •
Amalgam particles are not uniformly spherical, and they stain connective tissue fibers.
- •
Hemosiderin particles are larger, coarser, and more variable in size, and stain with Prussian blue stain ( Fig. 9.9 ); there may be inflammation and hemorrhage present.
-
Melanotic macules exhibit melanophages in the lamina propria and melanin within basal cells.
FIG 9.9 Hemosiderin deposits. (A) Coarse, irregular brown granules associated with many plasma cells. (B) Granules stain for iron (Prussian blue stain). -
- •
Blue nevus exhibits spindled melanocytes that react with MART-1 and HMB45 (see later).
References
Melanocytic Pigmentation
Physiologic pigmentation is very common on the gingiva and elsewhere in the mouth in dark-skinned races and is generally bilaterally symmetric and evenly pigmented ( Fig. 9.10A ).
The two most common melanocytic lesions in the oral cavity are oral melanotic macule (comprising more than 80% of melanotic lesions) and postinflammatory hypermelanosis. Some melanotic macules are likely to represent end-stage postinflammatory hyperpigmentation. The less common melanoacanthosis is likely to represent an uncommon form of postinflammatory pigmentation. Smoker’s melanosis are diffuse brown macules on the gingiva and may also represent postinflammatory hypermelanosis ( Fig. 9.11 ).
Oral Melanotic Macule (Labial Melanotic Macule)
Clinical Findings
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This occurs most frequently in the fifth decade with a 2–3 : 1 female predilection; rarely, macules may occur congenitally on the tongue sometimes associated with an epithelial choristoma.
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Discrete, usually solitary (sometimes multiple), tan-to-brown-to-black, painless macules are evenly pigmented, less than 1 cm, and occur frequently on the lower vermilion (labial melanotic macule, 33% of cases), gingiva and palatal, and mucosa, or buccal mucosa (see Fig. 9.10B–D ).
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Multiple mapules are seen in patients with increased levels of ACTH, such as Addison disease, and in syndromes such as the Laugier-Hunziker syndrome (with melanonychia), neurofibromatosis, Peutz-Jeghers syndrome, McCune-Albright syndrome, Carney syndrome complex, LEOPARD (Lentigines, Electrocardiographic abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retarded growth, Deafness) syndrome, and Bannayan-Ruvalcaba-Riley syndrome.
Etiopathogenesis and Histopathologic Features
Some solitary melanotic macules may represent postinflammatory hypermelanosis where the inflammatory infiltrate is no longer present, whereas others (especially multiple ones) may be idiopathic. It is unclear whether these resolve because it usually takes many months for postinflammatory hypermelanosis to resolve and most patients are not followed up after the diagnosis has been made. The fact that almost all solitary labial melanotic macules occur on the lower lip, a readily traumatized site, rather than the upper lip, supports this theory.
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There is mild acanthosis and increased melanin within basal cells in the absence of, or with minimal melanocytic hyperplasia, with melanin being most prominent in the lower half of the epithelium and at tips of rete ridges; incontinent melanin and melanophages are present in the lamina propria ( Figs. 9.12 and 9.13 ).
FIG 9.12 Oral melanotic macule of palatal mucosa. (A) Mild acanthosis and no inflammation. (B) Abundant melanin in basal cells at the lower half and tips of rete ridges without melanocytic hyperplasia. (C) Incontinent melanin and melanophages are noted in the lamina propria.
FIG 9.13 Melanotic macule. (A) Abundant melanin in basal cells at the tips of rete ridges. (B) Melanin within spinous cells forming a supranuclear cap. (C) Absence of melanocytic hyperplasia (Melan-A). - •
Variable vascular ectasia is usually present with absent-to-mild lymphocytic infiltrate.
Differential Diagnosis
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Postinflammatory hypermelanosis appears similar with obvious inflammation present and is often seen in interface stomatitides such as lichenoid stomatitis.
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Melanoacanthosis shows acanthosis with dendritic melanocytes present throughout the thickness of the epithelium.
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Lentigo exhibits benign melanocytic hyperplasia within the basal cell layer ( Fig. 9.14 ).
FIG 9.14 Lentigo simplex. (A) Brown macule on lower lip similar to melanotic macule, histology depicted in B–D. (B) Slight acanthosis with melanocytic hyperplasia, vascular ectasia, and mild chronic inflammation. (C) Melanocytic hyperplasia with slight reactive atypia. (D) Lentiginous melanocytic hyperplasia confined to the basal cell layer (Melan-A).
Management and Prognosis
- •
No treatment is necessary although laser ablation may be helpful if there are cosmetic concerns.
References
Oral Melanotic Macule (Labial Melanotic Macule)
Clinical Findings
- •
This occurs most frequently in the fifth decade with a 2–3 : 1 female predilection; rarely, macules may occur congenitally on the tongue sometimes associated with an epithelial choristoma.
- •
Discrete, usually solitary (sometimes multiple), tan-to-brown-to-black, painless macules are evenly pigmented, less than 1 cm, and occur frequently on the lower vermilion (labial melanotic macule, 33% of cases), gingiva and palatal, and mucosa, or buccal mucosa (see Fig. 9.10B–D ).
- •
Multiple mapules are seen in patients with increased levels of ACTH, such as Addison disease, and in syndromes such as the Laugier-Hunziker syndrome (with melanonychia), neurofibromatosis, Peutz-Jeghers syndrome, McCune-Albright syndrome, Carney syndrome complex, LEOPARD (Lentigines, Electrocardiographic abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retarded growth, Deafness) syndrome, and Bannayan-Ruvalcaba-Riley syndrome.
Etiopathogenesis and Histopathologic Features
Some solitary melanotic macules may represent postinflammatory hypermelanosis where the inflammatory infiltrate is no longer present, whereas others (especially multiple ones) may be idiopathic. It is unclear whether these resolve because it usually takes many months for postinflammatory hypermelanosis to resolve and most patients are not followed up after the diagnosis has been made. The fact that almost all solitary labial melanotic macules occur on the lower lip, a readily traumatized site, rather than the upper lip, supports this theory.
- •
There is mild acanthosis and increased melanin within basal cells in the absence of, or with minimal melanocytic hyperplasia, with melanin being most prominent in the lower half of the epithelium and at tips of rete ridges; incontinent melanin and melanophages are present in the lamina propria ( Figs. 9.12 and 9.13 ).
FIG 9.12 Oral melanotic macule of palatal mucosa. (A) Mild acanthosis and no inflammation. (B) Abundant melanin in basal cells at the lower half and tips of rete ridges without melanocytic hyperplasia. (C) Incontinent melanin and melanophages are noted in the lamina propria.
FIG 9.13 Melanotic macule. (A) Abundant melanin in basal cells at the tips of rete ridges. (B) Melanin within spinous cells forming a supranuclear cap. (C) Absence of melanocytic hyperplasia (Melan-A). - •
Variable vascular ectasia is usually present with absent-to-mild lymphocytic infiltrate.
Differential Diagnosis
-
Postinflammatory hypermelanosis appears similar with obvious inflammation present and is often seen in interface stomatitides such as lichenoid stomatitis.
-
Melanoacanthosis shows acanthosis with dendritic melanocytes present throughout the thickness of the epithelium.
-
Lentigo exhibits benign melanocytic hyperplasia within the basal cell layer ( Fig. 9.14 ).
FIG 9.14 Lentigo simplex. (A) Brown macule on lower lip similar to melanotic macule, histology depicted in B–D. (B) Slight acanthosis with melanocytic hyperplasia, vascular ectasia, and mild chronic inflammation. (C) Melanocytic hyperplasia with slight reactive atypia. (D) Lentiginous melanocytic hyperplasia confined to the basal cell layer (Melan-A).
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