This document discusses gingival pigmentation from a historical, physiological, and clinical perspective. It begins by covering the historical descriptions of pigmentation in various populations dating back to the early 1900s. It then describes the structure and function of melanocytes and melanin, as well as the genetic, hormonal, and environmental factors that regulate melanin synthesis. The document classifies different types of pigmentation and pigmented lesions that can occur in the oral mucosa. Finally, it reviews various surgical and non-surgical methods that can be used to depigmentate abnormal gingival pigmentation.

1. GINGIVAL
PIGMENTATION
Dr Nida Sumra

2. CONTENTS
• Introduction
• Historical aspects
• Physiology of pigmentation
• Normal racial variations
• Classification of oral pigmentation
• Pigmented lesions of the oral mucosa
• Methods of depigmentation
• Conclusion
• References

3. INTRODUCTION

4. Historical aspects
• 1912 - Bonnet and Laboef described physiologic
pigmentation of oral mucosa.
• 1914 - Brault and Monpellier and in 1923 - Lortat –
Jacob & Solente also reported the normal occurance of
pigmentation in the French people and fillipinos.
• 1924 - Reiche described the occurance of oral
pigmentation in Arabian, Chinese and East Indians.
• 1945 – Dummet C.O. reported pigmentation variations in
healthy oral tissues of more than 600 negros.

5. Physiology of pigmentation
• Melanocytes
• These are specialized unicellular dendritic cells residing in the
basal cell layer of the epidermis and oral epithelium.
• Primitive melanocytes originate from neural crest of ectoderm.
• In the epithelium they divide and maintain themselves as a
self- reproducing population

6. Structure
• Round cells with pale-
staining cytoplasm.
• Lack desmosomes and
tonofilaments but possess
long dendritic processes.
• Melanosomes.

7. • Melanocytes are cells capable of synthesizing
tyrosinase, which, when incorporated within specialized
organelles, the melanosomes, initiates events leading to
the synthesis and deposition of melanin.

8. • Routine hematoxylin
and eosin (H&E)
preparations
• Replicate throughout
their life, although at a
much slower rate

9. • According to the degree of maturation, melanosomes are
classified in 4 stages.
• Stage I. Membrane delinated vesicles containing
tyrosinase and a proteinateous matrix.
• Stage II. Oval organels with numerous membrane
filaments distinctive periodicity.
• Stage III. Less periodicity and melanin deposition.
• Stage IV. A dense uniform particle without any
distinguishable internal structure.

10. Melanin
Structure
• The exact structure of melanin has not been
determined.
• Melanin is defined as a biochrome of high
molecular weight formed by the enzymatic
oxidation of phenyl alanine.
• Insoluble polymer of tyrosine derivative formed
from tyrosine by the action of copper.

11. • The first step of the biosynthetic pathway for both eumelanins
and pheomelanins is catalysed by tyrosinase:
• Tyrosine → DOPA → dopaquinone
Dopaquinone can combine with cysteine - pheomelanins
• Dopaquinone + cysteine → benzothiazine intermediate →
pheomelanin
Also, dopaquinone can be converted to leucodopachrome -
eumelanins
• Dopaquinone → leucodopachrome → dopachrome →
quinone → eumelanin

13. Regulation of melanin synthesis
• Melanin synthesis can be controlled by three major
determinants:
Genes
Hormones
U-V Radiation

14. Endocrine control
• Melanocyte stimulating harmone (MSH)
• Adrenocorticotropic hormone (ACTH)
• Androgens

15. Normal racial variations
• Common characteristic of the darker races including
Caucasian brunettes.
• Most usual cases of brown oral pigmentation are ethnic.
• The pigmentation is usually symmetrically distributed
over the gingiva and palatal mucosa.

16. • Dumett examined 600 negroes of varying shades of
complexion to determine the relationship of oral to cutaneous
pigmentation and found that gingival pigmentation was directly
proportional to skin pigmentation
• Erica Amir et al (1991) studied the oral physiologic
pigmentation and found that it varied, according to the intensity
of the skin pigmentation.
• Patsakas et al (1991) conducted a study to determine the
distribution of melanin granules in different anatomical areas of
the gingiva and to relate the melanin granules to the degree of
gingival inflammation. The results showed positive correlation
between the density of melanin granules of the vestibular
epithelium and the severity of inflammation.

17. CLASSIFICATION OF ORAL
PIGMENTATION
• Endogenous pigmentation
• Exogenous pigmentation

18. PIGMENTED LESIONS OF
ORAL MUCOSA
Blue / purple vascular lesions
Brown melanotic lesions
Brown heme Associated lesions
Gray / black pigmentation

19. VASCULAR LESIONS.

20. Kaposi’s sarcoma
• Tumor of putative vascular origin
• Described by Morietz Kaposi (1872)
• Slow progressive growth.
• Diagnostic sign for AIDS
Clinical Appearance
• The oral mucosa is red, blue and purple and hard palate is
most favored site.
• Multifocal with numerous isolated and coalescing plaques.
Some will involve entire palate.
• Facial gingiva second most favored oral site

21. Management
Early plaque or macular lesions no treatment.
Nodular lesions are surgically excised.
Intra lesions injection of 1% sodium, tetradecyl
sulfate.

22. BROWN MELANOTIC LESIONS

23. NEVOCELLULAR AND BLUE NEVI
• Nevi are benign proliferation of melanocytes.
Nevo cellular nevi
• Arise from basal cell layer melanocyte early in life
• Called as junctional nevi when macular.
• Flat, brown and have a regular round or oval out line.
• Dome shaped navei

24. Blue nevus
• Not derived from basal
layer melanocytes
• Blue in color on the skin
• Biopsy necessary for
diagnostic confirmation.
Treatment
• Simple excision

25. • Dyer et al (1993) reported a case of pigmented naevus
of the gingiva which was a recurrent lesion. The
histological examination confirmed the presence of
junctional activity of melanocytes at the epithelio
mesenchymal interface.

26. MALIGNANT MELANOMA
Melanoma may arise from neoplastic transformation of either
melanocytes or nevus cells.
Clinical features
• Melanomas of oral mucosa less common than cutaneous.
• Oral lesions mainly in hard palate and gingiva followed by lips
and buccal mucosa.
• Mixture of color such as brown, black, blue and red
• Can be asymmetrical or irregular margins.
• Depending on radial and vertical growth sub classified
Nodular melanoma
– Superficial spreading melanoma
– Lentigo malignant melanoma
– Acral lentiguous melanoma

28. • Management
– Oral melanomas highly malignant and have high
mortality.
– Biopsy essential for diagnosis.
– Destruction of underlying bone or metastasis
indicate poor outcome.
– Excision with centimeter wide margins followed by
radical radiotherapy.
– Immunotherapy with interferon and gene therapy
is also under trial.

29. DRUG INDUCED MELANOSIS

30. • A variety of drugs can
induce oral mucosal
pigmentation.
• May be localized usually to
the hard palate or multifocal
throughout the mouth.
• Lesions are flat without any
evidence of nodularity or
swelling.
• Antimalarial therapy, tricyclic
antidepressants, Busulfan,
cyclophosphamide,
bleomycin and fluoracil

32. • Birek et al (1988) reported two cases of pigmentation of the
palatal mucosa due to quindine therapy both the clinical
appearances were those of melanin pigmentation and had
characteristic bluish black color.
• Siller et al (1994) reported oral mucosal pigmentation in two
patients taking the drug minocycline and demonstrated
minocycline deposition within teeth and bone by fluorescence
microscopy.
• Meyerson et al (1995) reported acquired isolated lingual
hyperpigmentation caused by minocycline in two women .They
had been receiving oral minocycline for approximately 4 weeks
to 4 months.

33. SMOKING ASSOCIATED MELANOSIS
Clinical features
• Diffuse macular melanosis
• Seen on the buccal mucosa,
lateral tongue, palate and
floor of the mouth.
• Lesions are brown, flat and
irregular.

34. • Hedin et al (1993) compared the frequency of oral
melanin pigmentation in a large number of former
smokers with that of non smokers. Results showed
that although clinically pigment free, the oral mucosa
may have elevated melanin content for a period of
time until the melanocyte activity declines.
• Brown et al (1991) found smoker’s melanosis to be
secondary to tobacco smoking as described by Hedin
and as such has an identifiable etiologic agent or
factor.

35. ENDOCRINOPATHIC
PIGMENTATION
• Addison’s disease
• Cushings syndrome

36. Bronzing of the skin and patchy
melanosis, of the gingiva, palate
and buccal mucosa are classical
signs
Oral melanotic pigmentation
accompanied by cutaneous
bronzing.
Serum steroid and ACTH
determination will aid in the
diagnosis
Treatment
• The pigment will disappear once
appropriate therapy for the
endocrine problem is initiated.

37. GENO DERMATOSES
• Peutz–Jeghers syndrome.
• Albright’s syndrome.
• Neurofibromatosis.

38. PEUTZ – JEGHERS
SYNDROME
CLINICAL FEATURES
Melanin pigmentation of the
lips and oral mucosa is
usually present from birth.
Buccal mucosa more
frequently involved
followed by gingiva and
hard palate.
Facial pigmentation tends to
fade later on, the mucosa
pigmentation persists.

39. ALBRIGHTS SYNDROME
• It is also called polyostotic fibrous dysplasia .
• Associated with skin lesions and endocrine
dysfunction
Clinical Features
• Bowing or thickening of long bones – unilateral /
bilateral
• Bone of face and skull are frequently involved.
• Skin lesions described as “Café au-lait” spots

40. NEUROFIBROMATOSIS
(Von- Reckling hausen’s Disease)
– Multiple neural tumors
Clinical Features
– “Café au-lait” spots.
– Oral lesions present as discrete nodules, which tend to be of
same colour as the oral mucosal,
– Palate, alveolar ridges, vestibules and tongue.

41. • Most sero positive patients present with diffuse,
multifocal macular, brown pigmentation of the buccal
mucosa
• Gingiva, palate and tongue may also be involved.
Histologically
• Characterized by basilar melanin pigment.
• Alangford et al (1989) reported six cases of oral
hyperpigmentation in HIV infected patients. The lesions
could be related to systemic clofazimine or ketoconazole
therapy.
HIV ORAL MELANOSIS

42. BROWN HEME ASSOCIATED
LESIONS

43. HEMOCHROMATOSIS
• Deposition of hemosiderin
pigment in multiple organs
and tissue
• Primary heritable disease or
secondary to variety of
disease
• Clinical features
– Mucosal lesions appear
brown to gray diffuse
macules.
– Seen on the palate and
gingiva.

44. GRAY BLACK
PIGMENTATIONS

45. AMALGAM TATTOO
• The lesions are macular and
bluish gray or even black.
• Buchner and Hansen (1990)
evaluated series of cases of
amalgam tattoo, which were
analyzed clinically and
histologically. The most
common location was the
gingiva and alveolar mucosa
followed by the buccal
mucosa. Histologically the
amalgam was present in the
tissues as discrete fine, dark
granules and as irregular solid
fragments.

46. GRAPHIC TATTOO
• Graphic tattoo occur on
the palate representing
traumatic implantation
from a lead pencil.
• The lesions are usually
macular, focal and gray
or black in colour.
Microscopically
• Graphite resembles
amalgam in tissue although
special stains can
segregate the two.

47. HEAVY METAL
INGESTION
• Ingestion of heavy
metals or metal salts can
be occupational hazard.
• In oral cavity found along
the free marginal gingiva
• Metallic line is gray or
black in colour.
• Bismuth, lead, mercury,
silver.

48. DEPIGMENTATION

49. Hanioka T et al. Association of melanin pigmentation in the gingiva of children with
parents who smoke. Pediatrics Aug 2005;116(2):186-90.

50. - Santosh Kumar et al

51. Oral Pigmentation Index –Dummett et al 1964
0: No clinical pigmentation (pink gingiva)
1: Mild clinical pigmentation (mild light brown
color)
2: Moderate clinical pigmentation (medium
brown or mixed pink and brown color)
3: Heavy clinical pigmentation (deep brown or
bluish black color)

52. METHODS OF DEPIGMENTATION
1. De-epithelization
• a. Scalpel technique
• b. Gingival abrasion technique using diamond bur
• c. Combination of the scalpel and bur
2. Gingivectomy
3. Free gingival autografting
4. Acellular dermal matrix allograft (ADMA)
5. Electrosurgery

53. 6. Cryosurgery
• a. Using liquid nitrogren
• Using a gas expansion system
7. Chemical agents
• a. 90% phenol and 95% alcohol
• b. Ascorbic acid
8. Laser[
• a. Nd:YAG
• b. Semiconductor diode laser
• c. CO2 laser
• d. Argon laser

54. SURGICAL METHODS
Criteria for patient selection
• Skin shade not very dark toned, but gingiva is deeply
pigmented.
• Periodontal health not compromised or is pretreated.
• Adequate thickness of the periodontal tissues.

55. Scalpel
• The procedure essentially involves surgical removal of
the gingival epithelium along with a layer of the
underlying connective tissue under adequate local
anesthesia and allowing the denuded connective tissue
to heal by secondary intention.

56. Split thickness epithelial excision
technique

58. Gingival abrasion technique using
diamond bur
• Similar to the scalpel technique.
• Comparatively simple, safe and non-aggressive method
that can be easily performed and readily repeated, if
necessary, to eradicate any residual repigmentation.
• Extra care should be taken to control the speed and
pressure of the handpiece bur so as not to cause
unwanted abrasion or pitting of the tissue.
• Minimum pressure with feather light brushing strokes
with copious saline irrigation should be used without
holding the bur in one place to perceive excellent results

59. Gingivo abrasion technique

61. Gingivectomy
• Removing the gingival margin by gingivectomy or the entire
attached gingiva by the “push back” procedure may also be
used.
• However, these procedures are associated with alveolar bone
loss, prolonged healing by secondary intention and excessive
pain and discomfort caused by exposure and denudation of the
underlying bone.
• Oswaldo Bergamaschi et al (1993) treated five patients with
gingival pigmentation by gingivectomy to remove band like
melanin pigmentation. They concluded that gingival resective
procedure is not of permanent value, because pigmentation
tends to return to baseline values.

62. Free gingival graft
• Tamizi et al (1996) used free gingival auto graft treatment of
pigmentation and obtained successful results.
• Nicholas (1981) reported a case of amalgam tattoo of the
labial gingiva in the maxillary anterior region treated by
palatal gingival auto graft successfully.
• Esthetic result was not always satisfactory due to color
differences between the palatal tissues and the gingiva
• The presence of a demarcated line commonly observed
around the graft in the recipient site may itself pose an
esthetic problem.

64. Acellular dermal matrix allograft
• Novaes et al. reported the use of ADMA for elimination
of the gingival pigmentation.
• These studies demonstrated the efficacy of the ADMA,
with the advantages of reduced surgical time, decreased
postoperative complications, unlimited amount of graft
material and a predictable and satisfactory esthetic
result.
• However, it is expensive and requires clinical expertise.

66. Electrosurgery
• According to Oringer’s “Exploding cell theory, it is predicted
that electrical energy leads to the molecular disintegration of
melanin cells of the operated and surrounding sites.
• Thus, electrosurgery has a strong influence in retarding
migration of melanin cells.
• However, it requires more expertise.
• Prolonged or repeated application of current to the tissues
induces heat accumulation and undesired tissue destruction.
• Contact of current with the periosteum and vital teeth should
be avoided.
• Hence, it is to be used in light brushing strokes and the tip
has to be kept moving.

68. CRYOSURGICAL DEPIGMENTATION
• It is a method of tissue destruction by rapid freezing
• The cytoplasm of the cells freezes, leading to
denaturation of proteins and cell death. It does not
require use of local anesthesia or periodontal dressing,
is relatively painless and has shown excellent results
lasting for several years.
• The cryotherapy procedure requires a special container
for storage of liquid nitrogen.
• The depth of penetration is difficult to control and
prolonged freezing may cause excessive tissue
destruction.

69. • The Dip-stick method utilizes a small cotton bud/swab
dipped in LN, which can be applied on the pigmented
area and maintained in contact for around 20–30 s as
described by Tal et al.
• It requires a separate sitting after about 5 days, during
which the residual pigmentation, if any, may be removed.
• It is followed by considerable swelling and accompanied
by increased soft tissue destruction

70. • Spray technique is the most popular method using open
end cryoprobes i.e. spray tip cone or cylinder.
• In this method, the cryogen is sprayed directly on to the
lesion. The spray tip is held 1 cm away from the lesion
and a steady spray of liquid nitrogen is directed at the
centre of the lesion.
• In the cryoprobe technique, liquid nitrogen is circulated
so as to cool the tip of the cryoprobe, which is to be
applied on to the lesion.
• It will be not possible to observe immediate tissue
changes after application of the cryogen

71. CRYOSURGER
Y
Pre-op
Post-op
Liq. N2O

74. Chemical agents (chemoexfoliation)
• It is a treatment method that destroys the epidermis
and/or dermis using a chemical peeling agent.
• A variety of chemical peeling agents are available;
phenols, salicylic acid, glycolic acid, trichloracetic acid,
etc.
• These agents have been classified into four types: Very
superficial, superficial, medium depth and deep, based
on their penetration

75. • Phenol penetrates the subepithelial connective tissue
and causes necrosis or apoptosis of melanocytes. It
result in incapacity of melanocytes to normally
synthesize melanin.
• Phenol does not seem to determine melanocyte
destruction; rather, it compromises its activity.
• Hirschfeld reported a series with 20 cases that were
treated for melanin pigmentation with the phenol–alcohol
method.
• It requires the area to be air-dried before application The
phenol pellet is applied and maintained for 1 min and the
area needs to be rinsed with 99% alcohol.

76. ASCORBIC ACID
• Ascorbic acid significantly inhibits tyrosinase activity

77. LASERS
• Lasers combine the advantages of rapid healing of the
scalpel surgery and the minimal bleeding of electrosurgery.
• A one-step laser treatment is usually sufficient to eliminate
the pigmented gingiva and does not require a periodontal
dressing.
• Easy handling, short treatment line, hemostasis, sterilization
effects and excellent coagulation.
• The treated area should be left exposed in the mouth. Few
myofibroblasts present in the base of the wound cause
minimal contraction and scarring, with little restriction in
movement of the soft tissues.

79. • Emin Essen et al (2004) used CO2 laser for gingival
depigmentation. Ablation of the hyperpigmented gingiva was
accomplished with minimal carbonization and almost no
bleeding and concluded that CO2 laser appears to be safe
and effective procedure.
• Yousuf et al (2000) - a semiconductor diode laser and it
was effective in removing melanin. Post operative
reevaluation showed continuous healing process with the
proliferation of squamous epithelial cells.
• Ishikawa et al (2004) The Er. YAG laser -possesses
suitable characteristics for oral soft and hard tissue ablation.
It had been applied for effective elimination of granulation
tissue and gingival melanin pigmentation.

82. REPIGMENTATION
• Repigmentation is described as "spontanoues" and has
been attributed to the activity and migration of cells from
surrounding areas..
• Although the exact mechanism of repigmetnation is not
known, it is suggested that the melanocytes from normal
skin proliferate and migrate into the depigmented areas.
• Further research is needed on gingival repigmentation
to study factors affecting the rate and length of time
required for reappearance of the pigmented areas.
• It should be noted, however, that the simplicity of the
technique prevents permanent damage, unlike many
other periodontal treatments, hence deepithelialization
can be done repeatedly in the same areas for a number
of times.

83. CONCLUSION.
• Gingival melanin pigmentations can occur as a consequence
of local, systemic, environmental or genetic factors.
• To ensure treatment success, the potential causative or
aggravating agent of the pigmentation should be identified
and eliminated, if possible, before the surgical treatment.
• Various techniques are available with some advantages and
some drawbacks.
• However, choice of the technique should be dependent on
individual preference, clinical expertise and patient
affordability.
• More data is required on comparative techniques to ensure
the long-term predictability and success.

84. • Clinical Periodontology – Carranza 9th edition.
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Kumara Ajeya et al Annals of Dental Research (2011) Vol 1 (1): 91-95
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Report-Shaeesta Khaleel Ahmed-Clin Adv Periodontics 2012;2:73-78.
• Complication of Cryosurgery Treatment of Gingival Melanin Pigmentation: A Case Report
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Shimada et al J Periodontol 2009;80:317-323.
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Research Vol.3(1), Jan 2010
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al International Journal of Laser Dentistry, January-Apri l2012;2(1):29-32.
• Split mouth de-epithelization techniques for gingival depigmentation: A case series and
review of literature. Kathariya et al. Journal of Indian Society of Periodontology - Vol 15,
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85. Thank You