This document discusses various types of oral pigmentation. It begins by defining pigmentation as the deposition of pigments in oral tissues. Pigmentation can be endogenous from increased melanin or melanocytes, or exogenous from introduced materials. The document then classifies pigmentation and discusses specific types in detail. Endogenous pigmentation includes freckles and melanotic macules. Melanosis can be associated with systemic diseases or medications. Exogenous pigmentation may result from substances like tattoos, metals, or drugs deposited in tissues. Overall pigmentation can have many causes and determining the exact cause requires a thorough history, exam, and sometimes biopsy.

1. GOOD
MORNING

2. MAHARANA PRATAP
DENTAL COLLEGE &
HOSPITAL
DEPARTMENT OF ORAL
MEDICINE,DIAGONSIS AND
RADIOLOGY

4. Oral Pigmentation
Pigmentation is defined as the deposition
of pigments in tissue or in oral mucosa.

5. • Augmentation of melanin production
• Increased no of melonocytes
• Deposition of accidently introduced
exogenous materials
Causes

6. • ENDOGENOUS PIGMENTATION
• FOCAL MELANOCYTIC PIGMENTATION
• MULTIFOCAL/DIFFUSE PIGMENTATION
• MELANOSIS ASSOCIATED WITH SYSTEMIC OR
GENETIC DISEASE
• IDIOPATHIC PIGMENTATION
• TREATMENT OF MUCOCUTANEOUS MELANOSIS
• DEPIGMENTATION
• HEMOGLOBIN AND IRON-ASSOSIATED
PIGMENTATION
• EXOGENOUS PIGMENTATION
Classification

7. ENDOGENOUS
PIGMENTATION

8. According to Burket’s

9.  ORIGINATES FROM WITHIN THE BODY
A) MELANIN PIGMENTATION: ‘MELAS’– BLACK
• Endogenous, Derivative of tyrosine and is synthesized
by melonocytes ,which typically reside in the basal cell
layer of the epithelium.
• Composed of eumelanin which is a brown-black
pigment and pheomelanin which has red-yellow in
color.
• It may be physiologic or pathologic and focal,
Multifocal or diffuse in its presentation.
Endogenous Pigmentation

10. Freckle/Ephelis
• The cutaneous freckle,or ephelis is a commonly
occurring,asymptomatic,small(1-3mm),well –
circumscribed,tan-or brown-colored macule that is
often seen in sun exposed regions of the facial and
perioral skin.
• Freckle tends to become darker during periods of
prolonged sun exposure and less during the winter &
autumn month.
• Ephelis are most commonly observer in light skin
individuals and are quit prevelant in red or light blond
haired individuals.
• It is more abundant in no and darker in intensity during
childhood and adolescence.
FOCAL MELANOCYTIC
PIGMENTATION

11. EPHELIS
(EPHELIDES/FRECKLES)
Treatment:-With increasing age,the number of
ephelides and color intensity tends to diminish.In
general no therapeutic intervention is required.

12. • The Melanotic macule is a
unique,benign,pigmented lesion that has no
known dermal counterpart.
• Most common oral lesion of melanocytic
origin.
Oral/Labial Melanotic macule

13. • More frequent in females usually in the
lower lip and gingiva.
• Lesion develop at any age but generally
tends to present in adulthood.
• It tends to be small (<1 cm),well-
circumscribed,oval or irregular in outline
and often uniformly pigmented
• Overall,It is relatively innocuous lesion
doesnot represent a melanocytic
proliferation.
Clinical Features

14. Pathology
It is characterized by a
normal epithelial layer.
Basal cells contain an
abundance of melanin
pigment without an
increase in the number of
melanocytes

15. • melanocytic nevus
• Malignant melanoma
• amalgam tattoo
• focal ecchymosis
Differential Diagnosis

16. • It is unsual,benign,melanocytic lesion.
• It is an innocuous melanocytic lesion that
may spontaneously resolve,with or without
surgical intervention.
• The term melanoacanthoma may imply a
neoplastic process.
• The lesion is reactive in nature.
• A biopsy is always warranted to confirm
the diagnosis,but once established no
further treatment is required.
Oral Melanocanthoma

17. Oral Melanocanthoma

18. • It is usually present as a rapidly
enlargement, ill defined, darkly pigmented
macular or plaque-like lesion.
• Most develop in black females
• It Occurs between 3rd
and 4th
decades of
life.
• Typically asymptomatic, any mucosal
surface is involved,buccal mucosa is the
most common site of occurrence.
• Borders are typically irregular.
Clinical Features.

19. • Oral melanocanthomas are
characterized by a poliferation of
bengin,
• Dendritic melanocytes through
out the full thickness of an
acanthotic and spongiotic
epithelial layer.
• A mild lymphocytic infilterate
with exocytosis is also
characterstics.
• Occasionally esonophils may be
seen.
Pathology

20. • Malignant melanoma
• Nevus and melanotic macule could also
be consideration.
Differential Diagnosis

21. • It is arise as a consequence of
melanocytic growth and proliferation.
• The intramucosal nevus is most frequently
observed.
• The lesion nevus cells are cytologically
and biologically distinct from melanocytes
that colonize the basal cell layer of the
epidermis and oral epithelium.
• Both genetic and environmental factors
play a role in nevogenesis.
Melanocytic Nevus

23. Clinical features
• Cutaneous nevi are a common occurrence.
• The total number of nevi tends to be higher in males than
females.
• Usually asymptomatic and often(<1cm),solitary,brown or
blue, well circumscribed nodule or macule
• Most identified in pateints over the age of 30.
• Common site followed by the buccal and labial mucosae
and gingiva.
Treatment:-Surgical excision is the treatment of choice for
oral lesions.Laser and intense pulse light therapies have
been used succesfully for the treatment of cutaneous nevi.

24. • It is the least common but most deadly of all primary
skin cancers.
• Mostly common and a history of multiple episodes of
acute sun exposure.
• Specially occurs at a young age, immunosuppression,
the presence of multiple cuteanous nevi.
• It is prone in families have a high incideneof germ line
mutations in the tumor supressor genes.
• Melanomas also frequently exhibit mutations in the
BRAF,HRAS,and NRAS PROTO ONCO GENES.
Malignant melanoma

26. • Whites are mostly involved
• High mortality rates are higher in blacks
and hispanics.
• Male predilection but melanoma is most
commonly occurring in females of child
bearing age.
• Cuteneous melanoma is more common in
the sunbelt regions of the world.
CLINICAL FEATURES

27. • Physiologic pigmentation is the most
common source of multifocal or diffuse oral
mucosal pigmentation
• Common seen in dark-complexioned
individuals,blacks ,asians and south africans.
• Generlized hyper pigmentation is seen.
• Physiologic pigmentation is seen by
increased amounts of melanin pigment within
the basal layer.
• Gingivectomy and laser therapy used to
remove pigmented oral mucosa.
MULTIFOCAL/DIFFUSE
PIGMENTATION

29. • Idiopathic
• Drug Induced
• Or Smoking-induced melanosis
Differential diagnosis

30. • Medication may induce a variety of
different forms of mucocutaneous
pigmentation,including melanosis.
• Cheif Drugs implicated in drug-induced
melanosis are the antimalarial,including
cholorquinone,hydroxychloroquine and
others.
DRUG INDUCED MELANOSIS

32. • Has been Estimated 10 to 20% of all the
acquired melanocytic pigmentation may
be drug induced.
• Pigmentation seen in one mucosal
surface,often the hard palate,or it can be
multifocal and involve multiple surfaces.
• Sun exposure may excerbate cutenous
drug induced pigmentation.
Clinical Features

33. • Diffuse melanosis of the anterior facial
maxillary and mandibular gingivae,buccal
mucosa ,lateral tongue,palate and floor of
the mouth is occusionally seen among
cigratte smokers.
• The mechanism by which smoking induce
pigmentation is unknown.
• The oral meanosis increases first year of
smoking and eventually it is reduced.
Smoker’s Melanosis

35. • Melasma is a relatively common,acquired symmetric
melanosis that typically develops on sun-exposed areas of the
skin and frequently on the face.
• Commonly affected areas forehead,cheeks,upper lips and
chin.
• Distint female prediliction and most cases arise in darker-
skkined individuals.
• The term melasma has been used to describe any form of
generlized facial hyperpigmentation.
• A biopsy reveals basilar melanosis with no increase in the
number of melanocyte.
• Melasma may spontaneously resolve after
parturition,cessation of the exogenous hormones,or regulation
of endogenous sex-hormone levels.
MELASMA(CHLOASMA)

37. • Hypoadrenocorticism(Adrenal
Insufficiency,Addison’s Disease)
• Cushing’Syndrome/Cushing’s Disease
• Hyperthyroidism(Graves’Disease)
• Primary Biliary Cirrhosis
• Vitamin B12(Cobalamin) Deficiency
• Peutz-Jeghers Syndrome.
• Cafe au Lait Pigmentation.
• HIV/AIDS-Assosiated Melanosis.
MELANOSIS ASSOSIATED WITH
SYSTEMIC OR GENETIC
DISEASE

38. Laugier-Hunziker Pigmentation
Laugier-Hunziker pigmentation was intially as an
acquired,idiopathic,macular hyperpigmentation of the
oral mucosal tissues specifically involving the lips and
buccal mucosae.
Patients typically present with multiple,discrete,irregularity
shaped brown or dark brown oral macules.
Treatment:-laser and chemotherapy have been used with
some sucess.
IDIOPATHIC PIGMENTATION

39. • Focally pigmented removal by diagonstic and therapeutic purposes.
• Cases assosiated with neoplasia,surgical intervention is less of an
option for the treatment of multifocal or diffuse pigmentation.
• Drug induced melanosis are subside after withdrawal of the
offending substance.
• Laser therapy use in the treatment of bothersome oral pigmentation.
laser used:-superpulsed CO2 ,Q –Switched ND-YAG, and Q-
Switched alexandrite lasers.
• First line of therapy is bleaching creams.
Such as azelaic acid or hydroquinone have been used.
Most common,Dual-or triple-combination therapy is used.
(combination of 4% hydroquinone-0.05% retinoic acid-0.01%
fluocinolone acetonide to be effective in greater than 90% of
pateint.)
TREATMENT OF
MUCOCUTANEOU MELANOSIS

40. Vitiligo
Vitiligo is a relatively common, acquired,
autoimmune disease that is associated with
hypomelanosis due to destruction of melanocytes.
Pathogenesis is multifactorial –genetic and
environmental.
There maybe a single nucleotide polymorphism in a
vitiligo-susceptibility gene that is also associated
with susceptibility to other autoimmune diseases,
including diabetes type 1, systemic lupus
erythematous, and rheumatoid arthritis.
DEPIGMENTATION

42. • Ecchymosis
• Purpura/Petechiae
• Hemochromatosis
HEMOGLOBIN AND IRON-
ASSOSIATED PIGMENTATION

43. • Traumatic Ecchymosis is common on the
lips and face yet is common in the oral
mucosa,except in cases related to blunt-
force trauma and oral intubation.
• Ecchymosis of the oral mucosa may also
be encountered in pateint with liver
cirrhosis,leukemia,and end-stage renal
disease undergoing dialysis treatment
Ecchymosis

44. Ecchymosis

45. • Oral Purpura/petechiae may develop as a
consequence of trauma or viral or systemic
disease.
• The distinction between purpura and petechiae
is essentially semantic and based solely on the
size of the focal hemmorrhages.
• Petechiae are typically characterized as being
pinpoint or slightly larger than pinpoint and
purpura as multiple,small 2 to 4mm collection of
extravasated blood.
Purpura/Petechiae

47. • Hemochromatosis is a chronic,progressive
disease that is characterized by excessive
iron deposition in the liver and other
organs and tissues.
• A lower labial gland biopsy has been
shown to be easy and effective method for
the diagnosis of hemochromatosis
Hemochromatosis

48. • Amalgam Tattoo
• Graphite Tattoos
• Ornamental Tattoos
• Medicinal Metal-Induced Pigmentation
• Heavy-Metal Pigmentation
• Drug-Induced Pigmentation
• Hairy Tongue
EXOGENOUS PIGMENTATION

49. Source of Exogenous oral and perioral
Pigmentation.
According to Burket’s

50. Microscopically, particles are typically aligned
along collagen fibers and around blood
vessels
Amalgam Tattoo

51. • Occurs on the palate one to treatment
implantation of lead pencil
• Lesions are macular, focal gray or black
• Microscopically resembles amalgam.
Graphite Tattoo

52. Ornamental mucocutaneous tattooing is
considered a rite of passage and
esthetically pleasing. Female members of
certain tribes are more likely to exhibit this
form of exogenous pigmentation.
Ornamental Tatoos

53. A variety of metallic compounds have been
used medicinally for the treatment of
various systemic diseases.
Medicinal Metal-Induced Pigmentation

54. • Diffuse oral pigmentation may be assosiated
with ingestion of heavy metals.Yet it remains an
Occupational and health hazard for some
individuals who work in certain industrial plant
and for those who live in the environment in and
around these types of facilities.
• Lead,mercury,bismuth,and arsenic have all been
shown to be deposited in oral tissue if ingested
over a extended period of time.
Heavy–Metal pigmentation

55. Heavy – Metal Pigmentation

56. Minocycline,which is a tetracycline
derivative used in treatment of acne is a
relatively cause of drug induced non-
melanin-associated oral pigmentation.It
causes pigmentation of developing teeth.
developing teeth
Drug-Induced Pigmentation

57. Hairy tongue is a relatively common condition of unknown etiology.
Involves dorsum,especially middle and posterior one third of the tongue
Papillae are elongated which becomes pigmented
1) Colonization of chromogenic bacteria that imparts a variety of
colors ranging from green,brown,black
2) Various foods – Coffee, Tea
TREATMENT :
Patient is advised to brush the tongue and keep it clean.
Hairy Tongue

58. Hairy Tongue

59. Oral Pigmentation may be focal,mutifocal,or
diffuse.The lesion may be
blue,purple,brown,gray,or black. Some are
Localized harmless accumulations of
melanin,hemosiderin,or exogenous metal;orthers
are systemic or genetic diseases,and some can
be medical assosiated with life –threatening
medical conditions.
Although Biopsy is a helpful and necessary aid in the
diagnosis of focally pigmented lesions,the more
diffuse lesions will require a through history and
laboratory studies to arrive at a defintive
diagnosis.
CONCLUSION

61. • Burket’s Oral Medicine 11th
Edition.
• www.google.com.
Reference