Summary

This document provides a comprehensive overview of oral pigmentation, including both physiological and pathological causes. It examines the role of various pigments such as melanin, carotenoids in oral and skin pigmentation. It further discusses the classification of pigmentation into exogenous and endogenous types, complete with relevant examples.

Full Transcript

# ORAL PIGMENTATION Sumeia Werfalli 10/15/2024 ## ORAL AND SKIN PIGMENTS - There are four pigments which contribute to the normal color of the skin and mucosa. - Melanin, Carotenoids, Reduced HB, Oxygenated HB. - Melanin is the most important. Melanin is an endogenous nonhematogenous pigment. It is...

# ORAL PIGMENTATION Sumeia Werfalli 10/15/2024 ## ORAL AND SKIN PIGMENTS - There are four pigments which contribute to the normal color of the skin and mucosa. - Melanin, Carotenoids, Reduced HB, Oxygenated HB. - Melanin is the most important. Melanin is an endogenous nonhematogenous pigment. It is produced by melanocytes in the basal layer of the epithelium and is transferred to adjacent keratinocytes via membrane-bound organelles called melanosomes. - Melanin is also synthesized by nevus cells, which are neural crest derivatives and are found in the oral mucosa and skin. Depending on the location and amount of melanin in the tissues, melanin induced pigmentation can be either black, gray, blue or brown in color. ## Pigmentation - Pigmentation is defined as the process of deposition of pigments in tissues. - Various diseases can lead to varied colorations in the mucosa - Pigmented lesions of the oral cavity are due to: - Augmentation of melanin production - Increased number of melanocytes (melanocytosis) - Deposition of accidentally introduced exogenous material ## ORAL PIGMENTATION MAYBE PATHOLOGIC OR PHYSIOLOGIC - Physiological oral pigmentation: due to variations in the activity of melanocytes in the basal cell layer of the oral epithelium. It is common in darker-skinned people. - Pathologic pigmentation can be classified into exogenous and endogenous based on the cause. - Exogenous pigmentation could be induced by drugs, tobacco/smoking, amalgam tattoo or heavy metal. - Endogenous pigmentation can be associated with endocrine disorders, syndromes, infections, chronic irritation, reactive or neoplastic. ## EXOGENOUS PIGMENTATION OF THE ORAL MUCOSA | Source | Color | Disease process | |-------------------------|----------------|----------------------------------------------------| | Silver amalgam | Gray, black | Tattoo, iatrogenic trauma | | Graphite | Gray, black | Tattoo, trauma | | Lead, mercury, bismuth | Gray | Ingestion of paint or medicinals | | Chromogenic bacteria | Brown, green, black | Superficial colonization | ## ENDOGENOUS PIGMENTATION IN THE ORAL MUCOSA | Pigment | Color | Disease process | |-------------|---------------|----------------------------------------------------------------------------------| | Hemoglobin | Blue, red, purple | Varix, hemangioma, kaposi's sarcoma, angiosarcoma, hereditary hemorrhagic telangiectasia | | Hemosiderin| Brown | Ecchymosis, petechia, thrombosedvarix, hemorrhagic mucocele, hemochromatosis | | Melanin | Brown, black or gray | Melanotic macule, nevus, melanoma, basilar melanosis with incontinence | ## CLASSIFICATION OF ORAL PIGMENTATION - Physiologic-racial - Pathologic - Exogenous - Drug induced - Tobacco-chewed/smoking - Heavy metals induced - Amalgam tattoo - Endogenous - Endocrine disorders - Addison's disease - Diabetes - Pregnancy - Hyperthyroidism - Syndrome associated - Peutz-Jegher syndrome - McCune Albright syndrome - Neurofibromatosis - Hemochromatosis - Leopard syndrome - Infections - HIV - Tuberculosis - Candiasis - Chronic irritation - Posttraumatic - Postinflammatory (lichen planus, pemphigus) - Reactive - Oral melanocytic macule - Oral melanoacanthoma - Neoplastic - Benign (nevus) - Malignant (melanoma) HIV: Human immunodeficiency virus ## DRUG-INDUCED PIGMENTATION - Pigmentation can be produced by various drugs like, hormones, oral contraceptives, chemotherapeutic agents like cyclophosphamide, busulfan, bleomycin and fluorouracil, transquilizers, antimalarials like clofazamine, chloroquine, amodiaquine, anti-microbial agents like minocycline, anti-retroviral agents like zidovudine and antifungals like ketaconazole. - Palate and gingiva are most common sites affected. In addition to mucosal changes, teeth in adults and children may be bluish gray owing to minocycline/tetracycline use. ## The Pathogenesis Underlying Drug-Related Pigmentation - The pathogenesis underlying drug-related pigmentation can be categorized as that occurs because of drug or drug metabolite deposition in dermis and epidermis, enhanced melanin deposition with or without increase in melanocytes, drug-induced post-inflammatory changes to the mucosa especially if the drugs induce an oral lichenoid reaction and bacterial metabolism, alone or in combination, may result in oral pigmentations. ## TOBACCO-INDUCED PIGMENTATION - Heavy cigarette, cigar and pipe smokers stimulate the melanocytes to actively produce melanin in the area where most smoke comes in contact with the mucosa. - This is believed to be a protective effect against certain tobacco elements; for example, melanin is known to bind to chemicals such as nicotine. This phenomenon is also true of the melanin production when exposed to the sun; it also is a protective process against ultraviolet light and its oxidative effect on the skin cells. - Smoking-related melanin production produces flat light brown pigment, usually diffuse, and present on the facial anterior gingival. It is more commonly present on the mandible than the maxilla in heavy cigarette smokers, the commissure and buccal mucosa of heavy pipe smokers, and the hard palate in reverse smokers. - The histology of the brown pigment is due to excessive melanin production. ## SMOKERS MELANOSIS ## HEAVY METALS - Increased levels of heavy metals (e. g., lead, bismuth, mercury, silver, arsenic and gold) in the blood are commonly known to cause oral mucosal discoloration. Various metals cause various types of pigmentation. - For example, pigmentation due to lead poisoning also called as plumbism appears as a blue-black line along the marginal gingiva known as Burtonian line. - Occupational exposure to heavy metal vapors is the common cause of pigmentation in adults. ## AMALGAM TATTOO - Amalgam tattoo is one of the most common causes of intraoral pigmentation. - Amalgam tattoos are twice as common as melanotic macules and 10 times as common as oral nevi. - The gingiva and alveolar mucosa are most commonly involved. - It presents clinically as a localized, blue-gray lesion. - Biopsy should be performed to demonstrate the presence of amalgam particles in the connective tissue, in cases of doubt. - Reasons for amalgam tattoo are: 1. Previous areas of mucosal abrasion can be contaminated by amalgam dust within the oral fluids 2. Broken amalgam pieces can fall into extraction sites 3. If dental floss becomes contaminated with amalgam particles of a recently placed restoration, linear areas of pigmentation can be created in the gingival tissue as a result of hygiene procedures 4. Amalgam from the endodontic retrofill procedures can be left within the soft tissue at the surgical site 5. Fine metal particles can be driven through the oral mucosa from the pressure of high-speed air turbine drills. ## GRAPHITE - Graphite may be incorporated into the oral mucosa through accidental injury with a graphite pencil which in turn cause pigmentation. - Commonly occurs in children. - Clinically, it appears as an irregular gray to black macule in the anterior palate region. - Malignant lesions like melanoma should be differentiated from these lesions as melanoma too commonly occurs on the palate ## PRIMARY HYPOADRENOCORTICISM (ADDISON'S DISEASE) - Chronic adrenal cortical insufficiency - At least 90% of the functioning cells in the adrenal cortex are destroyed - Etiology, tuberculosis, autoimmune, massive hemorrhage, or metastasis - Primary- adrenal dysfunction; Secondary, disease pituitary or hypothalamus - Hyperpigmentation of the skin (bronzing) and mucous membrane early in the disease process due to the increase of the ACTH level, that in turn has a melanocyte stimulating hormone (MSH)-like effect on melanocytes leading to excessive production of melanin. ## ADDISON'S DISEASE PATHOLOGY - Adrenal failure - Reduction in adrenal hormones - Increase in ACTH - Melanocyte-stimulation - Increase in MSH - Hyperpigmentation ## ADDISON'S DISEASE SYMPTOMS - Symptoms include weakness, fatigability, nausea, vomiting, anorexia, hypotension and sometimes salt-craving. Dentists may be the first to discover it, but extremely unlikely. - Addison's disease presents as multiple brownish macules anywhere in the oral cavity. - Laboratory findings: ACTH level; high in primary and low in secondary - Prognosis: The overall prognosis is good. Complications include lack of tolerance to stress because patients are incapable of producing steroids. May undergo cardiovascular collapse as a result but this is very rare. ## ADDISON'S DISEASE LAB FINDINGS - Rapid ACTH stimulation test and measurement of serum cortisol levels and plasma ACTH levels. If serum cortisol levels are below 20 microgram/dl, then the patient has adrenal insufficiency - The plasma ACTH levels are high. ## TREATMENT OF ADDISON'S - Corticosteroid replacement therapy - Increase dose during stressful events - No dose increase is needed for dental procedures using local anesthesia and lasting less than 1 hour - But increased dose maybe needed for longer dental procedures or under GA ## POLYOSTOTIC FIBROUS DYSPLASIA - Fibrous dysplasia is a developmental tumor-like lesion in which the bone is replaced by dysplastic fibrous tissue intermixed with irregular bony trabaculae. - It occurs because of a genetic mutation. The undifferentiated stem cells during the early embryonic life, the osteoblasts, melanocytes and endocrine cells will carry that mutation and express the mutated gene. It is classified as monostotic (single bone) and polyostotic (multiple bones). - The polyostotic form can be a feature of McCune Albright syndrome (Café au lait pigmentation, fibrous dysplasia, and endocrine dysfunction). ## NEUROFIBROMATOSIS - Neurofibromatosis is an autosomal dominant disorder. - They are classified as neurofibromatosis 1 (NF1) and NF2. Café au lait pigmentation of the skin is commonly seen in NF1. - They appear as light brown, oval patches of size more than 5 cm in diameter, the borders of which are smooth. It is also known as von Recklinghausen's disease of the skin ## CAFÉ AU LAIT PIGMENTATION ## HEMOCHROMATOSIS - It is a homozygous-recessive inherited disorder that is caused by excessive iron absorption. - It is characterized by excessive accumulation of body iron most of which is deposited in parenchymal organs like liver and pancreas and also deposited in other organs. - Secondary hemochromatosis or acquired hemochromatosis or hemosiderosis occurs as a consequence of parenteral administration of iron, which results in accumulation of iron in tissues. ## PEUTZ-JEGHERS SYNDROME - Peutz-Jeghers syndrome is an autosomal dominant disorder. - The syndrome consisted of mucocutaneous macules, intestinal polyposis and increased the risk of carcinomas of the pancreas, gastro-intestinal tract, thyroid, and breast. - The macular melanin deposits often involve the lips, buccal mucosa, and fingers. Lesions may also develop on the gingiva, palate, and tongue. - Histologically, the oral lesions show an increase in melanin in the basal layer, without an obviously increased melanocyte count. ## PEUTZ-JEGHERS SYNDROME CLASSIC PERI-ORAL MACULES ## POSTTRAUMATIC PIGMENTATION - Discoloration that occurs due to hematoma secondary to trauma that leads to hemosiderin deposition, which gives a bluish black discoloration. - The color varies from red to blue to purple depending on the age of the lesion and the degree of degradation of the extravasated blood. - The clinical feature of these lesions occasionally may be confused with pigment deposition of hematogenous origin. - Soft tissue hemorrhagic lesions usually appear in areas accessible to trauma such as the buccal mucosa, lateral tongue surface, lips and junctional of the hard and soft palate. ## НЕМАТОΜΑ ## POSTINFLAMMATORY PIGMENTATION - Mucosal diseases in particular lichen planus can cause mucosal pigmentation. - These pigmented areas clinically present as multiple brown-black pigmented areas adjacent to reticular or erosive lesions of lichen plants. - These areas microscopically show increased production of melanin by the melanocytes and accumulation of melanin-laden macrophages in the superficial connective tissue ## POST-INFLAMMATORY ## MELANOTIC NEVUS/MELANOTIC MACULE - Melanocytic nevi (common moles) are rare in the mouth but are very common on the skin. - Melanotic nevi are benign proliferation of nevus cells (melanocytes). and may appear clinically similar to melanotic macules; however, histological examination shows an increased number of melanocytes in the basal epithelial layers or underlying connective tissue. ## BLUISH GRAY NEVUS OF THE HARD PALATE. CLINICALLY, THE LESION WAS SLIGHTLY RAISED. - They most commonly occur on the hard palate, buccal mucosa, gingiva and lips. Nevi vary in color, from colorless to dark blue, brown or black; some oral nevi lack the brown color. They can be flat, raised, smooth-surfaced or papillary. - Nevi are usually not removed unless they are chronically irritated. They are sometimes removed for aesthetic reasons. They should be removed if they change in appearance (ABCDE) ## ORAL MELANOTIC MACULE - Can present in multiples. It is important to rule out other diseases that may cause multiple pigmented spots such as Addison's disease. - Can occur at any age, with a 2:1 prevalence in females. - Histology: the basal cell layer shows excessive production and release of melanin. - Usually excised to rule out malignant melanoma. They have an excellent prognosis ## PIGMENTED MALIGNANT LESION - Melanoma is a malignant neoplasm of the epidermal melanocytes. Benign lesions like common acquired nevus, congenital nevus, dysplastic nevus and cellular blue nevus are said to undergo a malignant transformation to melanoma. - Hard palate is the most commonly involved site where it presents as a brown to black macule with irregular borders. ## ORAL MELANOMA - Criteria for clinical diagnosis of melanoma (ABCDE-rule). - Asymmetry - is when one-half of the lesion does not match the other half of lesion - Border irregularity - is when the edges are, notched, ragged or blurred - Color irregularity - pigmentation is not various colored pigmentation is seen ranging from black, brown, tan, red, blue and white - Diameter - more than 6 mm - Elevation - a rise in the surface is also sign. ## THANK YOU - Questions?

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