This document discusses gingival pigmentation and summarizes its key points in 3 sentences: Physiologic gingival pigmentation is caused by normal melanocyte activity and presents as symmetric pigmentation developing during ages 1-2 decades, while pathologic pigmentation can result from local factors like smoking, metals, drugs, or systemic conditions like Peutz-Jeghers syndrome and Addison's disease. Melanocytes produce melanin through melanogenesis within specialized organelles called melanosomes to protect against UV radiation, with types of pigmentation including melanin, iron, carotene and oxyhemoglobin. Evaluation of gingival pigmentation involves assessing its distribution, extent, color and changes over time to distinguish between

2. GINGIVAL
DEPIGMENTATION
PART-1

3. CONTENTS
Introduction
Etiology
Classification
Melanocytes, melanin and melanogenesis
Evaluation of gingival pigmentation
Gingival depigmentation
techniques Repigmentation
Conclusion
References
Physiologic pigmentation
Pathologic pigmentation

4. Introduction Etiology
PART 1
Classification Physiologic
pigmentation
Melanocytes, melanin
and melanogenesis
Evaluation of gingival
pigmentation
References
Conclusion

5. INTRODUCTION
❑Gingival tissue constitutes the macroelement of dentofacial esthetics along with face, lip, and
teeth.
❑Gingiva participates in the harmony of smile with its pigmentation playing a crucial role.
❑Pigmentation of gingiva is considered to be unaesthetic by patients, and it may have a
psychological impact on them
❑Gingival hyperpigmentation can be defined as a darker gingival color beyond what is
normally expected due to excessive melanin deposition by the melanocytes which mainly
locate in the basal and suprabasal cell layers of the epithelium
❑Dummett reported the occurrence of oral pigmentation as gingival tissues 60%, hard palate
61%, mucous membrane 22%, and tongue 15%

6. ETIOLOGY
❑ Dummet and Co in (1946) proposed the following explanation for gingival pigmentation.
❑The colour of healthy gingiva is variable ranging from a pale pink to a deep bluish purple hue.
Between these limits of normalcy are a large number of pigmentation which depend primarily
upon
❑More over colour variation may not be uniform and may exists as unilateral, bilateral, mottled,
macular or blotched and may involve gingival papillae alone or extend throughout the gingiva on
to other soft tissues
The number
and size of
vasculature
Epithelial
thickness
Degree of
keratinization
Pigments
within the
gingival
epithelium
•Dummett CO, Barens G. Pigmentation of the oral tissues: a review of the literature. Journal of periodontology. 1967; 38(5):369-78.

7. ❑Most pigmentation is caused by five primary pigments. These include:
❑Alex A Farnoosh in 1990 said that melanin deposits mainly in basal and suprabasal cell layers of
epithelium. The degree of pigmentation is attributed to melanoblastic activity and density of
melanophores in gingiva.
❑The gingiva is the most commonly affected intraoral tissue, which is responsible for an
unpleasant appearance. Melanin pigmentation often occurs in the gingiva as a result of an
abnormal deposition of melanin
❑Brown or dark pigmentation and discoloration of gingival tissue can be caused by a variety of
local and systemic factors
Melanin
bilirubin and iron carotene
melanoid oxyhemoglobin

8. MELANIN
Melanin is the end-product of complex multistep transformations of L-tyrosine, are polymorphous
and multifunctional biopolymers, represented by
Eumel
anin
(most
comm
on)
Pheo
melani
n
(Brow
n &
black,
red
hair)
Neuro
melani
n
(Brain
)
Melanocytes
Melanocytes constitute a heterogeneous group of cells.
These unicellular dendritic cells reside in the basal cell layer
of the epidermis and oral epithelium. Primitive melanocytes
originate from neural crest of ectoderm
• Round Nucleus
• Clear Cytoplasm
• Lack Desmosomes
•A. Patsakas, Melanin Pigmentation and Inflammation in Human Gingiva, J Periodontol 1981; 52(11)

9. FUNCTIONS
Synthesis of melanin pigment granules (melanosomes)
and transfer to surrounding keratinocytes
Protective function: Ultraviolet (UV) rays of the sun cause
damage of the skin called ultraviolet ray injury. Melanin
and the thick stratum corneum together prevents such
injury exposure to UV rays stimulate more melanin
production and melanin absorbs the light of all wave
lengths
Absence of enzyme melanocyte tryosinase leads to failure
of melanin formation from tyrosine and the person
develops albinism.
Dummett CO, Barens G. Oromucosal pigmentation: An updated literary review. Journal of periodontology. 1971; 42(11):726-36.

10. ⦿ 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.
⦿ According to the degree of maturation, melanosomes are classified in 4
stages.(Nordlund et al 1998)
•Type I
•melanosomes have intraluminal vesicles and resemble multivesicular bodies
•Type II
• characterized by an elongated, elliptical shape, with intralumenal fine fibrils giving a striated appearance
•Type III
•exhibits pigment deposition along the fibrils,
•Type IV
• has dense pigmentation filling the organelle and obscuring the fibrillar structure

11. MELANOGENESIS
ACTIVATION OF MELANIN SYNTHESIS OF MELANIN
EXPRESSION
OF MELANIN
Hedin CA. Smokers’melanosis. Occurrence and localization in the a ached gingiva. Arch Dermatol. 1977; 113:1533-8.

12. CLASSIFICATION
•Dummet et al. (1967)
•Primary oral melanin pigmentations
•Secondary oral melanin pigmentations
•Oral non-melanin pigmentations
•Oral melanoclasias.
•Meleti (2008)
•Melanin-associated lesions
• (e.g:- Racial pigmentations,
melanotic macules)
•Non melanin-associated lesions (e.g.- Blood-related pigmentations, metallic pigmentations)

13. Kauzman et al in 2004

14. Patil S, et al -2015

15. PHYSIOLOGIC PIGMENTATION
•Normal melanocyte activity
•Seen in all ages
•Symmetric distribution over many sites, gingiva most
commonly
•Surface architecture, texture unchanged
•develops during the first two decades of life
•asymptomatic and no treatment is required.
•Most common site: Attached gingiva
•intensity and distribution of racial pigmentation of the oral
mucosa varies between the races, between different
individuals of the same race and within different areas of
the same mouth

16. PATHOLOGIC PIGMENTATION
• Many systemic & local factors are responsible for causing gingival Pigmentation.
• Some of the important of them are:
•Michael Glick, Burket’s Oral medicine, 12th
edition

17. AMALGAM TATOO
✓ The pigmentation of the oral mucosa membrane by
tooth restoration material (amalgam) is a common
finding in dental practice.
✓ Amalgam pigmentation is generally called
“Amalgam Tattoo”.
✓ The lesions represents embedded amalgam particles
& usually manifests itself as an isolated bluish or
black macule in various areas of the mucosa.
✓ Color : Black, Blue, grey or a combination of these.

18. PIGMENTED NEVI
• Uncommon.
• The Pigmented Nevi are classified as
intramucosal, junctional compound or Blue
according to their histological features.
• Nevi are seen mostly on the vermillion border of
the lips & the gingiva.
• Color : Grey, Brown, or bluish macules and are
typically asymptomatic.

19. ORAL MELANOTIC MACULE
• Rare oral mucosal lesion.
• Synonyms : Ephelis, melonosis, lentigo, solitary
labial lentigo, labial melanotic macule & oral
melanotic macule.
• Common site: Vermillion Border of the lower
lip.
• Buccal mucosa, palate, and attached gingiva also
involved (mucosal melanotic macule)
•Usually brown, uniformly pigmented, round to
ovoid shape with slightly irregular border
•Usually < 1 mm in diameter

20. MELANOMA
• Cancerous condition of the melanocytes.
•Progression to deeply pigmented, nodular quality
with ulceration
•May arise de novo as a pigmented or amelanotic
nodule
•Rarely may be metastatic to the oral cavity as a
nodular, usually pigmented mass
• Great majority : On the palate, upper gingival &
alveolar mucosa.
• May exhibit early in situ phase: a macular,
pigmented patch with irregular borders

21. SMOKER’S MELANOSIS
•Melanin pigmentation of oral mucosa in heavy smokers
•May occur in up to 1 of 5 smokers.
•Melanocytes stimulated by a component in tobacco smoke
• Brownish discoloration of alveolar and attached labial
gingiva, buccal mucosa
• Pigmentation is diffuse and uniformly distributed;
symmetric gingival pigmentation occurs most often.
•Pigmented areas are brown flat and irregular.
•Increased melanin in basal cell layer
•Increased melanin production by normal numbers of
melanocytes
•Melanin incontinence
Hedin CA. Smokers’melanosis. Occurrence and localization in the a ached gingiva. Arch Dermatol. 1977; 113:1533-8.

22. HEAVY METAL PIGMENTATION
LEAD Plumbism (blue green line of pigment along gingival margin)
• MERCURY Acrodynia ( pink disease, swift disease )
• SILVER Argyria (generalised blue grey)
• ARSENIC Arsenical keratosis
• BISMUTH (blue black line of pigment along gingival margin)
• GOLD Chrysiasis (blue, grey or purple)
•LEAD INDUCED PIGMENTATION blue green bartonian line along
gingival margin
•BISMUTH blue black pigment due to bismuth sulfide formation

23. DRUG INDUCED PIGMENTATION
•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.
•Pigmentation that is caused by the soft tissue deposition
of drug metabolites or complexes and pigment associated
with deposition of lipofuscin or iron
•Minocycline induced soft tissue pigmentation may appear
gray, brown, or black
•Tetracycyline inducedcYellowish to gray (oxidized
tetracycline) color of enamel and dentin

25. PEUTZ JHEGHER SYNDROME
• 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
• Clinical manifestations include intestinal polyposis,
cancer susceptibility, and multiple, small, pigmented
macules of the lips, perioral skin, hands, and feet
• The macules may resemble ephelides, usually
measuring <0.5 cm in diameter

26. ADDISON’S DISEASE
•Results from atrophy of the adrenal cortices and
failure of secretion of cortisol and aldosterone.
•Oral manifestations due to secondary melanocyte
stimulation by increased levels of
adrenocorticotropic hormone (ACTH)
Clinical Presentation
•Brown macular pigmentation of local or diffuse
quality
•Pigmentation usually seen in association with
cutaneous bronzing, weakness, weight loss, salt
craving, nausea, vomiting, hypotension

27. EVALUATION
Dr. Shahna N, Gingival pigmentation: A review of literature International Journal of Applied Dental Sciences 2019; 5(2): 83-91

28. Melanin index: [HEDIN 1997]
This index has classified pigmentation as follows:
No pigmentation
One or two solitary unit(s) of pigmentation in papillary gingiva without the
formation of a continuous ribbon between solitary units
More than three units of pigmentation in papillary gingiva without the
formation of a continuous ribbon
One or more short continuous ribbons of pigmentation
One continuous ribbon including the entire area between canines
Melanin pigmentation index
Takashi et al. in 2005 have proposed another index to measure gingival melanin
pigmentation.
The index is as follows:
Score 0: No pigmentation
Score 1: Solitary unit(s) of pigmentation in papillary
gingiva without extension between neighboring solitary units
Score 2: Formation of continuous ribbon extending from neighboring solitary

29. Gingival pigmentation index
Score 0: Absence of pigmentation
Score 1: Spots of brown to black color or pigments.
Score 2: Brown to black patches but not diffuse pigmentation
Score 3: Diffuse brown to black pigmentation, marginal, and
attached gingiva.
Peteran et al, 2015

30. REFRENCES
•Dummett CO, Barens G. Pigmentation of the oral tissues: a review of the literature. Journal of periodontology.
1967; 38(5):369-78.
•Dummett CO, Barens G. Oromucosal pigmentation: An updated literary review. Journal of periodontology. 1971;
42(11):726-36.
•A. Patsakas, Melanin Pigmentation and Inflammation in Human Gingiva, J Periodontol 1981; 52(11)
•Dr. Shahna N, Gingival pigmentation: A review of literature International Journal of Applied Dental Sciences 2019; 5(2):
83-91
•Michael Glick, Burket’s Oral medicine, 12th
edition
•Hedin CA. Smokers’melanosis. Occurrence and localization in the a ached gingiva. Arch Dermatol. 1977;
113:1533-8.
•Hanioka T, Tanaka K, Ojima M, Yuuki K. Association of melanin pigmentation in the gingiva of children with parents who
smoke. Pediatrics. 2005; 116(2):186-90.
•Neville BW, Damm DD, Allen CM, Bouquot JE. Editors. Oral and maxillofacial pathology. 2nd ed. Toronto (ON):W.B.
Saunders Company, 2002