GINGIVAL DEPIGMENTATION

INTRODUCTION :

            Pigmentation is a discoloration of the oral mucosa or gingiva due to the wide variety of lesions and conditions.  Oral pigmentation has been associated with a variety of endogenous and exogenous etiologic factors.  Most pigmentation is caused by five primary pigments. These include ; melanin, melanoid, oxyhemoglobin, reduced haemoglobin, and carotene.  Others are caused by bilirubin and iron.

Melanin : Melanin, a non hemoglobin derived brown pigment, is the most common of the endogenous pigments and is produced by melanocytes present in the basal layer of the epithelium.  Melanocytes have a round nucleus with a double nucleus membrane and clear cytoplasm lacking desmosomes or attachment plates.  Melanin accumulates in the cytoplasm, and the melanosome is transformed into a structureless particle no longer capable of melanogenesis. The number of melanocytes in the mucosa corresponds numerically to that of skin; however, in the mucosa their activity is reduced. Various stimuli can result in an increased production of melanin at the level of mucosa including trauma, hormones, radiation, and medications. Thyrosinase activity is present in premelanosome and melanosomes but absent in melanin granules.

Melanoid : Granules of melanoid pigment are scattered in the stratum lucidum and stratum corneum of the skin.  Initially it was assumed melanoid was a degradation product of melanin, but more recently it has been shown that such a relationship is highly improbable.  Melanoid imparts a clear yellow shade to the skin.

Oxyhemoglobin and reduced hemoglobin :  Oxyhemoglobin and reduced hemoglobin are pigments resulting from hemosiderin deposits. The skin color is affected by the capillary and venom plexues shining through the skin.

Carotene : Carotene is distributed in the lipids of the stratum corneum and stratum lucidum and gives a deep yellow color to the skin.  It is found in higher concentrations in more women than in men.

In several articles on oral pigmentation, Dummett and others implicate many systemic and local factors as causes of changes in oral pigmentation.

Epidemiology :

            Oral pigmentation occurs in all races of man. There were no significant difference in oral pigmentation between males and females. The intensity and distribution of racial pigmentation of the oral mucosa is variable, not only between races, but also between different individuals of the same race and within different areas of the same mouth.  Physiologic pigmentation is probably genetically determined, but as Dummett suggested, the degree of pigmentation is partially related to mechanical, chemical and physical stimulation.  In darker skinned people oral pigmentation increase, but thee is no difference in the number of melanocytes between fair skinned and dark skinned individuals. The variation is related to differences in the activity of melanocytes. There is some controversy about the relationship between age and oral pigmentation. Steigmann and Amir et al stated all kinds of oral pigmentation appear in young children.  Prinz, on the other hand, claimed physiologic pigmentation did not appear in children and was clinically visible only after puberty.

Clinical Characteristics :

            The gingiva are the most frequently pigmented intraoral tissues.  Microscopically, melanoblasts are normally present in the basal layers of the lamina propria. The most common location was the attached gingiva (27.5%) followed in decreasing order by the papillary gingiva, the marginal gingiva, and the alveolar mucosa.

            The total number of melanophores in the attached gingival was approximately 16 times greater than in the free gingiva.  The prevalence of gingival pigmentation was higher on the labial part of the gingiva than on the palatal / lingual parts of he arches. The shade of pigment was classified as very dark brown to black, brown, light brown yellow.  Melanin pigmentation of the oral tissues usually does not present a medical problem, but patients complain of black gums.

Melanin has been intensively studied, because it is the most important pigment of the skin. Chemical, melanin is a high molecular weight molecule that is insoluble in water and most organic solvents.  Melanin is formed only in the cytoplasm of melanin forming cells, or the melanocyte.  These are dendritic or branched cells found at the epidermal dermal junction of the skin and the mucous membranes, in the leptomeninges of the central nervous system, in the uveal tract and in the retina of the eye.  The melanocytes are located in the intercellular epidermal spaces and form intricate patterns by their long processes. The degree of pigmentation depends on a variety of factors, especially the activity of melanocytes.

            It also appears that the degree of gingival pigmentation of the gingiva and skin is reciprocally related.  Fair skinned individuals are very likely to have non pigmented gingiva, but, in darker skinned persons, the chance of having pigmented gingiva is extremely high. The highest rate of gingival pigmentation has been observed in the area of the incisors. The rate decreases considerably in the posterior areas.

Pigmentation  of the oral mucosa or gingiva is due to the wide variety of lesions and conditions.

Etiological factors

1. Endogenous
2. Exogenous

Most pigmentation is caused by 5 primary pigments.

1. Melanin
2. Melanoid
3. Oxyhemoglobin
4. Reduced hemoglobin
5. Carotene

Others include :

1. Bilirubin
2. Iron

Color of the gingiva is determined by several factors ;

1. Number and size of blood vessels
2. Epithelial thickness
3. Quality of keratinization
4. Pigments within the epithelium

Synthesis of Melanin :

• Once these granules are synthesized in melanocytes, these granules are phagocytosed and contained within other cells of the epithelium or connective tissue called “Melanophages or melanophores”.
• It is generally accepted that pigmented areas are present only when melanin granules synthesized by melanocytes are transferred to the keratinocytes.
• This close relationship between melanocytes and keratinocytes was tabelled as “Epidermal-melanin unit” (Fitzepatric and Breathnach 1963).

For the mechanism of this phenomenon few authors gave 2 possibilities.

  1. Dendritic process of the melanocytes are phagocytozed by keratinocytes or

  2. Melanin is secreted extracellularly from the melanocytes and engulfed by keratinocytes.

The melanocytes are dendritic cells, unattached to the surrounding epithelial cells (no desmosomes or tonofilaments). They almost always show well developed golgi regions and extensive areas of rough endoplasmic reticulum. The cells behave as unicellular exocrine glands and are located initially in the basal cell layer in a ratio of seven DOPA-positive cells per 100 keratinocytes or 1:4 to 1:18.  The melanin is then transferred outward to the basal and prickle cell layers.

            Active melanocytes, as components of the epithelial tissue, have special features. They convert tyrosine, via a series of intermediate stages mediated by the enzyme tyrosinase, to melanoprotein (melanin). According to the degree of maturation, melanosomes are classified into four stages.

I – membrane delineated vesicles containing tyrosinase and a proteic matrix;

II – Oval organelles with numerous membrane filaments, with or without cross-linking, but with a distinctive periodicity;

III – less periodicity and melanin deposition; and

IV – a dense uniform particle without any distinguishable internal structure (the melanin granules). These pigment particles can be released from the melanocytes and phagocytized by the keratinocytes.

            The cells carrying the pigmented material within their cytoplasm, plus the thickness and quality of epithelial keratinization, the extent of connective tissue vascularization, the presence of subcutaneous fat tissue, and the relative amount of reduced or oxidized hemoglobin, will dictate the clinical color variations of the mucosa and gingiva. The clinical color ranges from a light pink to a dark brown or bluish black, and overt melanosis varies from isolated posts to a band like distribution. Although more prevalent among blacks, oral melanosis has been demonstrated in other races. In general, individuals with fair skin will not demonstrate overt tissue pigmentation, although comparable numbers of melanocytes are present within their gingival epithelium. The melanocytes are generally inactive or hypoactive in melanin synthesis.

            Melanocyte division and multiplication have been described for the skin, scalp, and hair follicles of humans and animals by several authors, but little information is available about cell mitosis in the tissues of the oral cavity.  Miner and Gordon demonstrated one melanocyte undergoing mitosis and Squier and Waterhouse hypothesized the possibility of mitosis because a large number of centrioles were fond in the melanocytes.  Melanocytes are considered to be a self-replicating cell type of neuroectodermal origin, within epithelium, with distinctive morphology, function, mitotic potential, and relationships with adjacent epithelial cells

Mechanism of Melanin Hyperpigmentation :

            Melanocytic Stimulating Hormone (MSH) increases the skin pigmentation by stimulating the dispersion of melanin granules in melanocytes, thus causing darkening of the skin. Secretion of this hormone is stimulated by MSH stimulating factor. Glucocorticoids have an inhibiting effect on MSH, when there is adrenal insufficiency, there is reduced glucocorticoids secretion ® increase MSH ® increased melanin pigmentation.

Classification and Differential Diagnosis of Oral Pigmentation :

A. Localized pigmentation :

• Amalgam tattoo
  • Graphite or other tattoos
  • Nevus
  • Melanotic macules
  • Melanoacanthoma
  • Malignant melanoma
  • Kaposi’s sarcoma
  • Epitheloid  oligamatosis
  • Verruciform xanthoma

B. Multiple or generalized pigmentations :

1. Genetics – Idiopathic melanin pigmentation (racial or physiologic)

• Peutz-Jegher’s syndrome
  • Complex of Myxomas
  • Carney syndrome
  • Leopard syndrome etc

2. Drugs – Smoking, betal

• Anti-malarials
  • Anti microbials (minocycline)
  • Cloropromazine
  • ACTH
  • Zidovudine
  • Ketoconazole
  • Methyldopa
  • Heavy metals (Gold, Silver, Bismuth, Mercury, Lead, Copper)
  • Balulphan
  • Menthol

3. Endocrine

• Addison’s disease
  • Albright’s syndrome
  • Acanthosis Nigrecans
  • Pregnancy
  • Hyperthyroidism

4. Post-inflammatory

• Periodontal disease
  • Postsurgical gingival repigmentation

5. Others

• Hemochromatosis
  • Generalized neurofibromatosis
  • Goucher’s disease
  • HIV
  • Thalassaemia
  • Nutritional deficiencies

Gingival Depigmentation :

• Melanin hyperpigmentation usually does not present as a medical problem, but patients may complain their black gums are unaesthetic.
  • This problem is aggravated in patients with a gummy smile or excessive gingival display
  • Depigmentation is a periodontal plastic surgical procedure whereby the gingival hyperpigmentation is removed or reduced by various techniques.
  • Various techniques have been employed with similar results. The selection of a technique should be based on clinical experience and individual preference.

Different Technique Employed are ;

I. Methods aimed at removing the pigment layer

A. Surgical methods of depigmentation

1. Scalpel surgical technique (Ginnwall et al 1966)
   1. Slicing, or partial thickness flap technique
   1. Bone denudation
   1. Abrasion (Pal et al)
   1. Scraping (Manchandra 1979)
   1. Gingivectomy(Dummet and Bolden 1963)
2. Cryosurgery
3. Electrosurgery
4. Lasers
   1. Nd:YAG
   1. Er : YAG
   1. CO₂ lasers
      

B. Chemical method of depigmentation using caustic chemicals.

Eg. 90% phenol (Hirschfeld and Hirschfeld 1951)

II. Methods aimed at masking the pigmented gingiva with grafts from less pigmented areas

1. Free gingival grafts (FGG) (Tamizi et al 1996)
2. Acellular dermal matrix allografts (Novaas et al 2002).

Repigmentation is described  as “spontanoues” and has been attributed to the activity and migration of cells from surrounding areas.  Spontaneous repigmentation of depigmented areas of skin have also been reported following subtotal gastrectomy, exposure to ultraviolet light, or demabrasion. 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. 

Contributor- Dr. Priyanka Jairaj Dalvi