Amalgam tattoo

Amalgam tattoo is the most common solitary focal pigmentation lesion of the oral mucosa. These lesions are generally less than 1 cm (rarely amalgam tattoos can be large) and appear as flat, gray-black to blue-black color macules. They are usually found in close approximation to a restoration. Majority of the lesions are located on the buccal mucosa, gingiva and alveolar mucosa with mandibular region being more affected as compared to the maxillary region (Figure 1). All these lesions are asymptomatic and are discovered during routine dental examination. If particles are large enough they can be viewed with help of a radiograph (taken with reduced exposure parameters for soft tissues). The amalgam granules and fragments are found mainly in the lamina propria but were sometimes also seen in the submucosa. Histopathologically, we may observe a giant cell reaction surrounding these amalgam particles.

Mercury poisoning

Mercury poisoning can be because of acute or chronic exposure of mercury vapors. Clinical features include gastric disturbances, diarrhea, excitability, headache and mental depression. Patients complain of gastric disturbances, diarrhea, excitability, headaches and mental depression. Patient may have tremors of lips and extremities, dermatitis and nephritis.

Oral manifestations include increased salivation (ptyalism) as mercury is excreted in saliva. Tongue may be enlarged and painful (glossodynia). There may be hyperemia and swelling of gingiva, ulcerative stomatitis, loosening and exfoliation of teeth.

Acrodynia (Swift disease, Pink disease) is idiosyncratic reaction to large doses of amalgam. It is an uncommon mercurial toxicity reaction in which skin is also involved. It usually occurs after ingestion of mercury from powder, ammoniated mercury ointment, calomel lotion. It is mainly seen in the children below the age of 5–6 years. Manifestations are widespread involving the hand, feet, nose and cheeks which become red or pink in color, cold and clammy like a raw beef. Skin may have maculopapular rashes with pruritis. Patients may complain of irritability, photophobia and muscular weakness. Children may be able to remove their hair in patches.

Oral manifestations include profuse salivation, gingiva is painful and ulcerated, teeth may become loose and exfoliate and bruxism is a common finding.

Arsenic

Arsenic in both organic and inorganic forms may produce acute or chronic symptoms. Oral manifestations may include increased salivation, gingivitis, and oral ulcerations. Exposure produces severe edema of the eyelids, gastrointestinal irritation, and both central and peripheral neuropathies.

Arsenic levels can be assessed by complete blood count, urine analysis and hair and finger nail clippings. The condition can be managed by removing the offending agent followed by gastric lavage and chelation therapy with d-penicillamine.

Bismuth

Bismuth is used in treatment of syphilis and dermatological disorders. Patients usually have systemic complaints and it is characterized by ‘bismuth grip’, muscular cramps in the abdomen.

Orally, we usually see bismuth line which is a bluish black line in marginal gingiva confined to gingival papilla. Bismuth may react with hydrogen sulfide produced by the bacteria to form bismuth sulfide that gets precipitated around periphery of an ulcer or erupting molar. Patient may also complain of burning sensation and metallic taste in the mouth.

Lead

Lead (plumbism) is an occupational hazard seen in plumbers due to acute or chronic exposure because of inhalation of lead vapors or dust. It is also seen among the children who chew wood painted with lead.

Clinical features include gastrointestinal symptoms like nausea, vomiting and constipation. Patients may have encephalitis or peripheral neuritis characterized by wrist drop or foot drop. Patients may have hypochromic anemia with basophilic stippling in red blood cells.

Oral manifestations include linear bluish black discoloration seen in the gingival margin called Burtonian line. Gingivitis, ulcerative stomatitis, excessive salivation, metallic taste, or rarely bismuth may get deposited in the deciduous teeth too.

Silver

Argyria (silver poisoning) is caused due to chronic exposure due to occupational hazard by silver nitrate. It can result in pigmentation of both the skin as well as the mucous membrane. Exposure to silver causes a violet marginal line, often is accompanied by a diffuse bluish-gray discoloration throughout the oral mucosa. It can also be associated with neurologic and hearing damage. Histologically we can observe silver particles staining the reticular fibers.

Racial/physiologic pigmentation

Physiologic pigmentation of the oral tissues is clinically manifested as multifocal or diffuse melanin pigmentation with variable prevalence in different ethnic groups. Gingiva appears darker in color among Africans, Asians, Caucasians and Hispanics and other dark skinned people. The variability in the color of the oral tissues is not due to the difference in the number of melanocytes is same but this color difference is due to the difference in the activity of the melanocytes. In dark skinned people melanocytes are more active as compared to the fair skinned people.

Physiologic pigmentation is seen as diffuse macular pigmentations that may be brown, gray or black in color and can appear anywhere in the mouth with buccal surface and gingiva being most commonly involved. On the gingiva it appears as well-demarcated, ribbon-like, dark brown continuous band that does not extend to involve the marginal gingiva. Occasionally pigmentation may also be seen on the tongue, lips and lingual gingiva as diffuse brown patches with ill-defined or diffuse borders (Figure 2).

Racial pigmentation mainly occurs in the childhood. However during early years it may not attract patient’s attention and may be observed after puberty. Racial pigmentation is asymptomatic and does not require any treatment.

Drug-induced pigmentation

Many medications when taken over a long period of time can cause oral mucosal pigmentation. Drug-induced pigmentation can be due to increased synthesis and accumulation of melanin pigments, deposition of the drug or its metabolites into the oral tissues or deposition of iron after damage to the dermal vessels (Table 3).

Chloroquine and other quinine derivatives which are usually used in the treatment of malaria and cardiac arrhythmia can cause pigmentation of oral tissues due to a direct stimulating effect on the melanocytes (Figure 3). According to some of the studies these drugs usually cause pigmentation of the palatal tissues.

Minocycline is another drug causing pigmentation of oral tissues. It is a synthetic tetracycline that is commonly used in the treatment of acne vulgaris. Tetracycline causes pigmentation of only the bones and teeth but minocycline can also cause pigmentation of soft tissues. It usually causes diffuse brownish discoloration of the hard palate, gingiva, mucous membranes and tongue.

Oral pigmentation can also be due to intake of birth control pills. Chloasma is the term which is used to describe perioral and periorbital pigmentation in such patients (Figure 4). The pigmentation usually occurs as a diffuse brown macular pigmentation which is asymptomatic and lesions resolve upon cessation of drug intake. These lesions usually occur due to the hormonal changes which influence melanocyte stimulation.

Smoker’s melanosis

Tobacco smokers have more intense pigmentation of oral mucosa as compared to non-smokers. Smoker’s melanosis is more common in females. Women are more commonly affected than men because of synergistic effect between the female sex hormones and smoking. Smoking may cause oral pigmentation in light-skinned individuals and accentuate the pigmentation in dark-skinned patients. Clinically, there may be multiple diffuse brown pigmented macules of less than 1 cm in diameter. These lesions can occur anywhere in the mouth but may be usually localized on the attached labial anterior gingiva and the interdental papillae of the mandible. These lesions are completely asymptomatic and benign in nature (Figure 5).

Microscopically there is evidence of basilar melanosis but there is no melanocyte proliferation. The increased melanin production may be a biologic defense mechanism against the noxious agents present in the tobacco smoke. The intensity of the oral pigmentation is directly related to the duration and amount of smoking. Smoker’s melanosis usually disappears within 3 years of smoking cessation. Biopsy must be advised whenever there is a surface elevation or increase in the pigment intensity or rapid increase in the size of the lesion.

Endocrine disorders

Adrenal cortical insufficiency can occur secondary to pathologic processes such as neoplasms that may cause damage to the adrenal glands. Due to the deficiency of the adrenocortical hormones in the blood there is an increased production of ACTH by the anterior pituitary gland. But ACTH stimulates the production of melanocyte-stimulating hormone which results in diffuse pigmentation of all the tissues. As a consequence the skin darkens and becomes bronzed. Also multifocal diffuse pigmentations appear in the mucous membranes of the oral cavity, conjunctiva, and genital regions.

In the oral cavity pigmentation may appear as diffuse brown patches on the gingiva, buccal mucosa, palate and tongue (Figure 6). This may resemble physiologic pigmentation. Physiologic pigmentation can be differentiated from pigmentation caused by Addison’s disease as the later develops and progresses during adult life and not present since birth. It is also accompanied by systemic manifestations like weakness, nausea and vomiting, abdominal pain, constipation or diarrhea, weight loss and hypotension. Oral pigmentation may be the first sign of Addison’s disease. Therefore complete examination must be done for patients with diffuse pigmentation of oral cavity and associated with systemic signs and symptoms. Patients presenting with such features should be sent for medical evaluation and laboratory tests to assess levels of ACTH, plasma cor-tisol and serum electrolytes.

A biopsy of these oral lesions shows acanthosis with silver-positive granules in the cells of the stratum germinativum. Melanin pigment can be seen in the basal layer of the epithelium. Management involves treatment of the underlying cause and corticosteroid replacement therapy.

A tumor of the posterior pituitary or certain small cell carcinomas can also secrete excessive amounts of ACTH which can cause pigmentation of oral tissues. In ACTH secreting tumors (paraneoplastic syndromes) the patient manifests features of the Cushing’s syndrome. In both these conditions there occurs diffuse pigmentation of oral tissues along with associated systemic features.

Café au lait pigmentation

It manifests as bronze or tan diffuse multifocal macular pigmentations that appear on the skin as well as the oral mucosa. These pale brown macules may vary considerably in size. They have widespread distribution and can occur on the face, neck or the oral cavity. Because of the pale brown color these lesions are called as Café au lait spots. It is usually associated with neurofibromatosis (von Recklinghausen’s syndrome), Albright’s syndrome (polyostotic fibrous dysplasia) and Peutz-Jeghers syndrome.

Café au lait pigmentations in neurofibromatosis have smooth borders and are associated with axillary freckling. It is an autosomal dominant inherited disease with multiple skin nodules.

In Peutz-Jeghers syndrome patients have intestinal polyposis along with oral macular pigmentations that appear around the mouth (Figure 7) and on the fingers. When such lesions are observed, a detailed history of the patient should be taken about gastrointestinal complaints as well as the family history for intestinal polyps. These pigmented melanotic spots do not require any treatment and are not associated with any risk for malignant transformation. However, the patient should be monitored for the development of internal m/>