Oral pigmentation commonly affects various parts of the oral cavity.
Causes vary from iatrogenic factors like dental amalgam to complex disorders including Peutz-Jeghers syndrome and Addison disease.
Oral pigmented lesions arise from exogenous materials or excessive melanin.
Pigmented entities can originate from intrinsic or extrinsic sources. Color varies based on pigment source, quantity, and depth.
Melanin is brown but gives eyes colors like blue, gray, brown, or black due to light absorption and reflection properties explained by Tyndall effect.
Clinicians should inspect oral cavities and perform biopsies on undiagnosed pigmented lesions.
Patients with oral melanoma often remember previous pigmentation in the same area months to years before diagnosis.
Epidemiology
Oral pigmentation prevalence was 93.2% in black, 12.5% in white, 70% in native children.
A study of 1,300 Israeli Jewish schoolchildren showed 13.5% had physiological pigmentation in Middle Eastern children.
Diffuse pigmentations appear in about 92% of Addison patients. Amalgam tattoos are the most common oral pigmented lesions biopsied for histopathological examination.
Melanotic macule is a common pigmented oral mucosa lesion after amalgam tattoo. The average age at diagnosis of PJS is 23 years in men and 26 years in women.
Oral nevi occur in younger individuals, whereas malignant melanoma primarily affects those over 40 and is rare under 20.
Anatomy
Pathophysiology
Physiologic pigmentation is higher melanin production by melanocytes in individuals with darker skin.
Pigmentation arises from increased melanocytic activity but not more melanocytes. Flat and symmetrical lesions appear as even light-to-dark brown pigmentation.
It does not change normal tissue structure but can show as pinpoint pigmentation on the fungiform papillae of the tongue.
Pigmented macules vary in size and brown shades, appearing periorally, on lips, and buccal mucosae.
Addison disease results from adrenal cortex destruction to cause insufficient hormone production and increased ACTH levels.
Etiology
The causes of oral pigmentation are:
Physiological pigmentation
Systemic diseases
Oral mucosal insults
Developmental and neoplastic processes
Inflammatory causes
Pathologic Causes
Genetics
Prognostic Factors
Around 48% of PJS patients develop cancer by age 57, with intestinal polyps being the main morbidity cause.
The mean cancer diagnosis age is 42.9 years, with a 93% risk for PJS-related cancers in ages 15-64.
Amalgam tattoos have an excellent prognosis with no associated morbidity or sequelae in patients.
Oral nevi are benign, except junctional nevi that may lead to melanoma, which is frequently misdiagnosed until it becomes advanced and severe.
The oral mucosa’s lamina propria lacks distinct dermal layers that makes Clark levels unsuitable for describing mucosal melanomas due to architectural differences.
Mucosal melanoma staging relies on insights from more common cutaneous melanoma experiences.
Clinical History
Collect details including the chief complaint, history of present illness, medical and family history to understand clinical history of patients.
Oral pigmentation commonly affects various parts of the oral cavity.
Causes vary from iatrogenic factors like dental amalgam to complex disorders including Peutz-Jeghers syndrome and Addison disease.
Oral pigmented lesions arise from exogenous materials or excessive melanin.
Pigmented entities can originate from intrinsic or extrinsic sources. Color varies based on pigment source, quantity, and depth.
Melanin is brown but gives eyes colors like blue, gray, brown, or black due to light absorption and reflection properties explained by Tyndall effect.
Clinicians should inspect oral cavities and perform biopsies on undiagnosed pigmented lesions.
Patients with oral melanoma often remember previous pigmentation in the same area months to years before diagnosis.
Oral pigmentation prevalence was 93.2% in black, 12.5% in white, 70% in native children.
A study of 1,300 Israeli Jewish schoolchildren showed 13.5% had physiological pigmentation in Middle Eastern children.
Diffuse pigmentations appear in about 92% of Addison patients. Amalgam tattoos are the most common oral pigmented lesions biopsied for histopathological examination.
Melanotic macule is a common pigmented oral mucosa lesion after amalgam tattoo. The average age at diagnosis of PJS is 23 years in men and 26 years in women.
Oral nevi occur in younger individuals, whereas malignant melanoma primarily affects those over 40 and is rare under 20.
Physiologic pigmentation is higher melanin production by melanocytes in individuals with darker skin.
Pigmentation arises from increased melanocytic activity but not more melanocytes. Flat and symmetrical lesions appear as even light-to-dark brown pigmentation.
It does not change normal tissue structure but can show as pinpoint pigmentation on the fungiform papillae of the tongue.
Pigmented macules vary in size and brown shades, appearing periorally, on lips, and buccal mucosae.
Addison disease results from adrenal cortex destruction to cause insufficient hormone production and increased ACTH levels.
The causes of oral pigmentation are:
Physiological pigmentation
Systemic diseases
Oral mucosal insults
Developmental and neoplastic processes
Inflammatory causes
Pathologic Causes
Around 48% of PJS patients develop cancer by age 57, with intestinal polyps being the main morbidity cause.
The mean cancer diagnosis age is 42.9 years, with a 93% risk for PJS-related cancers in ages 15-64.
Amalgam tattoos have an excellent prognosis with no associated morbidity or sequelae in patients.
Oral nevi are benign, except junctional nevi that may lead to melanoma, which is frequently misdiagnosed until it becomes advanced and severe.
The oral mucosa’s lamina propria lacks distinct dermal layers that makes Clark levels unsuitable for describing mucosal melanomas due to architectural differences.
Mucosal melanoma staging relies on insights from more common cutaneous melanoma experiences.
Collect details including the chief complaint, history of present illness, medical and family history to understand clinical history of patients.
Oral pigmentation commonly affects various parts of the oral cavity.
Causes vary from iatrogenic factors like dental amalgam to complex disorders including Peutz-Jeghers syndrome and Addison disease.
Oral pigmented lesions arise from exogenous materials or excessive melanin.
Pigmented entities can originate from intrinsic or extrinsic sources. Color varies based on pigment source, quantity, and depth.
Melanin is brown but gives eyes colors like blue, gray, brown, or black due to light absorption and reflection properties explained by Tyndall effect.
Clinicians should inspect oral cavities and perform biopsies on undiagnosed pigmented lesions.
Patients with oral melanoma often remember previous pigmentation in the same area months to years before diagnosis.
Oral pigmentation prevalence was 93.2% in black, 12.5% in white, 70% in native children.
A study of 1,300 Israeli Jewish schoolchildren showed 13.5% had physiological pigmentation in Middle Eastern children.
Diffuse pigmentations appear in about 92% of Addison patients. Amalgam tattoos are the most common oral pigmented lesions biopsied for histopathological examination.
Melanotic macule is a common pigmented oral mucosa lesion after amalgam tattoo. The average age at diagnosis of PJS is 23 years in men and 26 years in women.
Oral nevi occur in younger individuals, whereas malignant melanoma primarily affects those over 40 and is rare under 20.
Physiologic pigmentation is higher melanin production by melanocytes in individuals with darker skin.
Pigmentation arises from increased melanocytic activity but not more melanocytes. Flat and symmetrical lesions appear as even light-to-dark brown pigmentation.
It does not change normal tissue structure but can show as pinpoint pigmentation on the fungiform papillae of the tongue.
Pigmented macules vary in size and brown shades, appearing periorally, on lips, and buccal mucosae.
Addison disease results from adrenal cortex destruction to cause insufficient hormone production and increased ACTH levels.
The causes of oral pigmentation are:
Physiological pigmentation
Systemic diseases
Oral mucosal insults
Developmental and neoplastic processes
Inflammatory causes
Pathologic Causes
Around 48% of PJS patients develop cancer by age 57, with intestinal polyps being the main morbidity cause.
The mean cancer diagnosis age is 42.9 years, with a 93% risk for PJS-related cancers in ages 15-64.
Amalgam tattoos have an excellent prognosis with no associated morbidity or sequelae in patients.
Oral nevi are benign, except junctional nevi that may lead to melanoma, which is frequently misdiagnosed until it becomes advanced and severe.
The oral mucosa’s lamina propria lacks distinct dermal layers that makes Clark levels unsuitable for describing mucosal melanomas due to architectural differences.
Mucosal melanoma staging relies on insights from more common cutaneous melanoma experiences.
Collect details including the chief complaint, history of present illness, medical and family history to understand clinical history of patients.
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