1. Pigmented lesion of oral mucosa

2.  PIGMENT•
Color or Coloring Agent
 NORMAL MUCOSA
• Pale pink to deep bluish purple sometimes even blackish

3. NORMAL RANGE DEPENDS UPON
 Melanogenesis and distribution of melanin
pigment
 Keratinization
 Depth of epithelization
 Vascularity

4. oral pigmentation physiologic (gray-brown)
Pathologic (brown, blue, gray, and black) .

6. Melanin
 primary pigment producing brown coloration
 Tyrosine – tyrosinase –melanin- this occurs in the melanosomes of
melanocytes
 Then the melanosomes are transferred from the melanocyte to a
group of keratinocytes called the epidermal melanin unit
 Variations in skin color is related to the number of melanosomes, the
degree of melanization, and the distribution of the epidermal melanin
unit

8. CLASSIFICATION
1. ENDOGENOUS PIGMENTATION
2. EXOGENOUS PIGMENTATION
3. DRUG RELATED PIGMENTED LESIONS
4. ASSOCIATED SYNDROMES
5. MISCELLANEOUS
- HIV INFECTIONS

9. Endogenous pigmentation
 Hemoglobin, hemosiderin, and melanin represent the most common
endogenous sources of mucosal color change
 A submucosal collection of hemoglobin or hemosiderin, produced by
extravasation and/ or lysis of red blood Common causes of endogenous
oral and perioral discoloration
 Melanin is the pigment derivative of tyrosine and is synthesized by
melanocytes
 keratinocytes control melanocytic growth.Yet the mechanisms by which
melanocytes are stimulated to undergo cell division remain poorly
understood

10. Endogenous pigmentation
 Melanin rolls
• protect against the damaging effects of actinic irradiation
• act as scavengers, protecting against cytotoxic intermediates
• the role of melanocytes in oral epithelium is unclear.
 Melanin is synthesized within melanosomes.
 It is composed of
1. eumelanin,( a brown‐black pigment)
2. pheomelanin, (a pigment of red‐yellow color)

11. Endogenous pigmentation
Melanin pigmentation may be physiologic or pathologic
The term melanosis is used to describe diffuse
hyperpigmentation
• sun exposure (commonly)
• Physiologic
• idiopathic sources
• neoplasia,
• Medications
• high serum concentrations of (ACTH),
• postinflammatory changes
• genetic or autoimmune disorders.
melanin may be associated with a variety of mechanisms,

12. Diagnosis
Biopsy
(If the etiology
of the oral
pigmentation
cannot be
clinically
established)
This is critical,
because
malignant
melanoma may
present with a
deceptively
benign clinical
appearance.
In addition to
biopsy various
laboratory and
clinical tests,
including
Diascopy
radiography
blood tests

14. Freckle or Ephelis
 A symptomatic macule is smaller than 1cm
 Associated with increasing production of melanin and the number of
melanocytes does not increase
 Color : brown / black
 Border : specific
 Sunlight : mostly in areas exposed to sunlight and people with blond hiar
 Ages : it is darker in children and teenage , it decrease with age progress

15. Oral/Labial Melanotic Macule
 Epidemiology
 The melanotic macule is a unique, benign,& common pigmented lesion.
 Over 85% of all solitary melanocytic lesions
 the etiology remains elusive but trauma has been postulated to play a role.
 Sun exposure is not a precipitating factor.

16. Clinical Features
 Melanotic macules develop more frequently in females,
 Common site : lower lip (labial melanotic macule) and gingiva & mucosa.
 Age :lesion may develop at any age, it generally tends to present in
adulthood.
 Size: (<1 cm), Once the lesion reaches a certain size, it doesnot tend to
enlarge further
 Border : well‐circumscribed, oval or irregular in outline, and often
uniformly pigmented
 Unlike an ephelis, a melanotic macule does not become darker with
continued sun exposure

17. Pathology
 Microscopically, melanotic macules are characterized
by the presence of abundant melanin pigment in the
basal cell layer without an associated increase in the
number of melanocytes

18. Differential Diagnosis
 melanocytic nevus
 malignant melanoma
 amalgam tattoo
 focal ecchymosis. (If such pigmented lesions are present after a two‐week
period, ecchymosis can usually be ruled out.)

19. Management
 Biopsy: specimen should be obtained to secure a definitive diagnosis.
Once the microscopic diagnosis is obtained,
 No further treatment is necessary.

20. Oral Melanoacanthoma
Etiology and Pathogenesis
 the term melanoacanthoma may imply a neoplastic process
but it’s an innocuous melanocytic lesion
 spontaneously resolve, with or without surgical intervention.
 actually it is allergic reaction
 It has rapid onset, with acute trauma or a history of chronic
irritation

21. Clinical Features
 Rapidly enlarging,
 ill‐defined
 Darkly pigmented
 Flat or slightly elevated
 A predilection for black females
 Occur between the 3rd and 4th decades of life.
 Typically: it’s a solitary lesion but nevertheless, bilateral and
multifocal lesions have been reported.
 generally asymptomatic but pain may be present

22. Clinical Features
 Site :Any mucosal surface may be involved, close to 50% arise on the
buccal mucosa.
 Size: is variable, small and localized to large, diffuse areas of
involvement, measuring several Cm in diameter
 Borders: irregular
 cutaneous melanoacanthoma, it is similarities with oral
melanoacanthoma

23. Diagnose and treatment
 D.D
 Malignant melanoma
 Melanotic macule
 Treatment
 spontaneously resolve, with or
without surgical intervention

24. Melanotic nevus
 Melanocytic nevi include a diverse group of clinically /microscopically
distinct lesions
 result from an increase in melanin pigment synthesis, Unlike ephelides and
melanotic macule
 Etiology : genetic and enviroments
 Risk factor : sun light

25. Clinical features
 Cutaneous nevi are common.
 adult may have several nevi
 occurring in males tends to be
higher than that seen in females
 In contrast, oral melanocytic nevi
are rare
 Solitary lesions that are more
common in females
 Oral melanocytic nevi
• Asymtomatic
• a small (<1 cm), solitary lesions
• brown or blue
• well‐circumscribed
• nodule or macule

26. Diagnosis & treatment
 Biobsy
 treatment
 conservative surgical excision ,
 Recurrence has only rarely been reported.
 Laser and intense pulse light therapies.

27. Malignant melanoma
 Melanomas arises from neoplastic transformation of either melanocytes or
nevus cells
 Age : 50
 Location: anterior labial gingiva and anterior aspect of hard palate
 Clinical features : appears as macular or nodular,
 Coloration varies ranging from brown black to black with zones of
depigmentation with jagged and irregular margins
 Commonly occurs on anterior labial gingiva and anterior aspect of hard
palate
 Sign and symptoms : unspecific
 Treatment : surgery and radiotherapy

29. Diffuse pigmentations
 Physiologic pigmentation
 Smokers melanosis
 Drug induced pigmentation

30. Physiologic pigmentation
 Due to greater melanocyte activity rather than a greater number of
melanocytes.
 This type of pigmentation is symmetric and persistent and does not alter
normal archaistic such as gingival stippling
 Blacks, Asians, dark skinned caucasians most frequently show diffuse
melanosis of facial gingiva
 In addition, lingual gingiva & tongue may exhibit multiple diffused and
reticulated brown macule
 Seen in patients at any age, no gender predilection

31. Physiologic pigmentation
 No further attention is required, in case of doubt, it should be excised and
sent for histopathological study.
 Lingual gingiva & tongue may exhibit multiple, diffuse & reticulated brown
macule
 Basilar melanosis, evolves in childhood
 Does not alter normal architecture
 Degree of intraoral pigmentation –may not correspond cutaneous
coloration
 No change in intensity

32. treatment
 Not necessary
 surgery and laser (If patient have any discomfort with this)

33. Drug induced pigmentation
Drugs associated with oral mucosal pigmentation
• Antimalarials: quinacrine, chloroquine,
• hydroxychloroquine
Oral contraceptives
• Quinidine
• Zidovudine (AZT)
• Tetracycline
• Minocycline
• Chlorpromazine

34. Cinical features
 Blue grey pigmentation of the gingiva from Minocycline

35. Clinical features
 10–20% of all cases of acquired melanocytic pigmentation may be drug
induced
 diffuse yet localized
 surface,: hard palate, or it can be , multifocal and involve multiple surfaces
 the lesions are flat and without any evidence of nodularity or swelling
 Sun Exposure may exacerbate cutaneous drug‐induced pigmentation.
 The sign and symptoms well remove after several month of drag not used

36. Smokers melanosis
 Diffuse macular melanosis of buccal mucosa, palate, lateral tongue, floor of
the mouth is usually seen among the smokers
 Tobacco smoke products stimulates the melanocytes and causes
hyperpigmentetion. increased production of melanin, which may provide a
biologic defence against the noxious agents present in tobacco smoke.
 Clinically lesions are brown, flat & irregular some are geographic or map like
in configuration
 Intensity of pigmentation appears to be time and dose related
 Histologically basilar melanosis with melanin is observed

37. Hyper pigmentation after inflammation
 Most common in black men and women
 Uncommon in oral cavity
 It occur in diffuse in these areas that have inflammation recently

38. Melasma (Chloasma)
 Melasma is a relatively common, acquired
symmetric melanosis
 Develops on sun‐exposed areas of the skin
and frequently on the face.
 More than 5 million people in the USA have
this condition
 Forehead chick lips and chin

39.  Most common in black women ,pregnant , and those who take
contraceptive drugs
 melasma tends to evolve rather rapidly over a period of a few weeks
 The term melasma has been used to describe any form of generalized
facial hyperpigmentation, including that related to postinflammatory
changes and medication use.
 the term is most appropriately used to describe the pigmentary changes
associated with sun exposure and hormonal factors,

40. Melanosis with systemic and genetic
diseases
 Addison diseases
 Cashing syndrome
 Hyperthyroidism
 Vitb12 deficiency
 Melanosis related to the HIV
 Peutz jegher’s syndrome

41. Hypoadrenocorticism (Adrenal Insufficiency,
Addison’s Disease)
 Hypoadrenocorticism is a potentially life‐threatening disease,
 It cased due to less activity of adrenal cortex in imunity diseases
 Have systemic signs and symptoms
 Clinically patient have
• felling Weakness and tired without any reason
• Depuration
• Mucosal and cutaneous hyperpigmentation
• Diffuse patch shaped mealnosis of oral cavity ( the first sign of Addison
diseases)

42. Cashing syndrome
 Due to high level of endogen & exogenous corticosteroid
 Common in wemen
 Systemic complacation
 High weight
 Moon face
 Diffuse mucosal and cutaneous pigmentation

43. Hyperthyroidism
Melanosis is a common complication
Specially in black people
40% of patients have cutaneous and mucosal hyperpigmentation
The mechanism of this hyperpigmentation is unknown

44. Vitb12 deficiency
 Associated with systemic features
 Megaloblastic anemia
 Neurologic disorders
 Oral disorder ( burning, erythema ,atrophy of oral mucosa)
 Cutaneous sign ( hyperpigmentation)
 Etiology : unknown

45. PEUTZ JEGHER’S SYNDROME
 Autosomal dominant condition associated with intestinal
 polyposis and pigmentation of oral mucosa, lips, skin.
 Pigmentation is distinctive with lesions on anterior part of tongue, buccal
mucosa
 Lesions are focal, multiple, melanotic brown macules less than
0.5cm in diameter

47. Vitiligo
 Vitiligo is a relatively common, acquired,
autoimmune disease that is associated with
 hypomelanosis due to destruction of melanocytes.
 • Pathogenesis is unkown
 Variable clinical presentation. Focal areas of depigmentation
or entire segment on one side of the body maybe involved.
Occasionally, vitiligo universalis.

48. Vitiligo
 Vitiligenous lesions often present as well circumscribed,
round, oval or elongated, pale or white-colored macules that
may coalesce into larger areas of diffuse depigmentation.
 Any age, before 3rd decade usually.
 No sex predilection.
 May also arise in patients undergoing
immunotherapy for malignant melanoma.

49. MANAGEMENT
 • Topical corticosteroids
 Topical/systemic photochemotherapies (PUVA)
 Medicinal depigmentation- cutaneous bleaching for unified
skin color.
 Labial vitiligo is more resistant to Rx.
 Surgical- autologous epithelial grafts, punch grafting,
micropigmentation

50. HEMOSIDERIN
BROWN HEME
ASSOCIATED LESIONS

51. ECCHYMOSIS
 Traumatic ecchymosis – most commonly on the lips and face
 Immediately after the trauma, erythrocytes extravasated into the
submucosa
 Clinically appear bright red macule or swelling if a hematoma forms
 The lesion then assume a brown discoloration within few days after
hemoglobin is degraded to hemosiderin
 TREATMENT : Observation for 2 weeks and look at BT,PTT

52. PETECHIAE
 Capillary hemorrhages will appear red initially, turning
brown in few days once the extravasated red cells have
lysed and degraded to hemosiderin
 Size: pin point for petechia (2-4mm for purura)
 It occur after trauma , systemic diseases,
viral infection.

53. PETECHIAE
 In viral diseases is common In oral cavity than cotaneous
 Mostly in soft plate
 If it causes by trauma , patient must be trained to avoid doing harmful
action
Observation for 2 weeks

54. HAEMOCHROMATOSIS
 Disorder in which excess iron is deposited into the body and results in
eventual sclerosis and dysfunction of the tissues/organs involved
 Iron is then stored as HEMOSIDERIN AND FERRITIN
 Cause of pigmentation is haemochromatosis i.e. an increase in melanin
production and not the deposition of hemosiderin in the skin
 Oral mucosal lesions - Brown to Grey, diffuse macules
 Usually seen on palate and gingiva
 HISTOPATHOLOGICALLY (lower labial gland Bx)- Basilar melanosis

55. HAEMOCHROMATOSIS
 HAEMOCHROMATOSIS complication:
 Liver cirrhosis
 Diabetes
 Anemia
 Hypertension
 DIAGNOSIS – Biopsy – stained with PRUSSIAN BLUE
 – Iron levels elevated in serum

56. AMALGAM TATTOO
 Small pieces of amalgam can break off, impregnate into
gingival and oral tissues during fabrication and removal
of restoration or extrication of teeth
 The lesions are macular and blushing gray of even black
and
 Usually seen in gingival and basement membrane and
palate
 Found in the vicinity of teeth with large amalgam rest or
crowned teeth
 D/D- nevus , early melanoma melanotic macule

57. AMALGAM TATTOO
 Microscopically, particles are typically aligned along collagen fibres
and around blood vessels
 Treatmet
 Surgery : if any aesthetic problems

58. GRAPHITE TATTOO
 Occurs on the palate one to treatment implantation of lead pencil
 Lesions are macular, focal gray or black
 Microscopically resembles amalgam