ORAL MEDICINE ORAL MEDICINE

Orofacial Disease: Update for the Dental Clinical Team: 4. Red, Brown, Black and Bluish

Crispian Scully and Stephen Porter

velvety red plaque typically seen on the Abstract: This article discusses coloured lesions of the orofacial region. soft or ventrum of the tongue/floor of mouth of elderly men (Figure 1). It is Dent Update 1999; 26: 169-173 usually level with or depressed below surrounding mucosa, and sometimes is Clinical Relevance: Red lesions may signify dysplastic as well as inflammatory associated with white patches—speckled conditions. Hyperpigmented lesions, unless confidently diagnosed as amalgam or erythroleukoplakia. tattoos, should also be taken seriously. Virtually every case of erythroplasia has areas of dysplasia, carcinoma in situ, or invasive carcinoma. Carcinomas are seen ost red lesions are inflammatory in and treatment which should be borne in 17 times more frequently in erythroplasia Morigin but it is important to appreciate mind in relation to this article. than in leukoplakia and erythroplasia is that others are associated with mucosal therefore the most potentially malignant of atrophy . Erythroplasia is one of the more all oral mucosal lesions—but erythroplasia important, since it is often dysplastic. Other RED LESIONS is far less common than leukoplakia. causes of red lesions include burns, While most red lesions are inflammatory in telangiectasia (after irradiation; in origin, it is important to appreciate that Diagnosis and Management hereditary haemorrhagic telangiectasia; or others are due to burns, telangiectasia (after Clinically it is important to differentiate scleroderma), haemangioma, purpura, or irradiation; in hereditary haemorrhagic erythroplasia from inflammatory and neoplasms. Generalized mucosal erythema telangiectasia; or scleroderma), atrophic lesions, such as those seen in may be caused by inflammatory lesions or haemangiomas, purpura, neoplasms, or deficiency anaemias, , mucosal atrophy. Central cyanosis associated with mucosal atrophy; see . Biopsy is indicated. produces a blue-red discoloration. Table 1. Erythroplasia is one of the more Treatment is by scalpel or laser excision The most usual cause of brown oral important red lesions to be considered. but the prognosis is often poor. mucosal pigmentation is ethnic origin. Generalized mucosal erythema may be Localized brown, blue or black caused by inflammatory lesions or mucosal hyperpigmentation may be caused by atrophy. Central cyanosis produces a blue- Mucositis amalgam tattoo, naevus, Kaposi’s sarcoma, red discoloration. Mucositis is common after irradiation of or malignant . Generalized tumours of the head and neck, if the hyperpigmentation may be caused by radiation field involves the . localized irritation (e.g. smoking), drugs Erythroplasia () Arising within 3 weeks of the irradiation, such as antimalarials, Addison’s disease, Erythroplasia is a rare condition mainly of or other rare causes. elderly men, defined as ‘any of the The first article in this series presented oral mucosa that presents as bright red several general observations on diagnosis velvety plaques which cannot be characterized clinically or pathologically as any other recognizable condition’. Crispian Scully, PhD, MD, MDS, FDS RCPS, FFD RCSI, FDS RCS, FDS RCSE, FRCPath, FMedSci, Professor, Aetiology and Stephen Porter, PhD, MD, FDS RCSE, FDS RCS, Professor, Eastman Dental Institute for The aetiology is unclear. Oral Health Care Sciences and International Centre for Excellence in Clinical Features , University of London. Erythroplasia is an uncommon, painless, Figure 1. Erythroplasia.

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● HIV disease; ● infectious mononucleosis; ● rubella; ● thrombocytopenia; ● performing fellatio. Diagnosis and Management The diagnosis is mainly clinical. Petechiae and ecchymoses do not blanch on pressure (cf. haemangioma). It may be necessary to take a blood and platelet count and assess haemostatic function. Treatment is of the underlying cause.

Figure 2. Candidosis; median Figure 3. Candidosis; rhomboid . erythematous lesion in palate. Localized Oral Purpura Blood blisters in the mouth are not uncommon in elderly people. there is painful generalized erythema, and of the tongue and palate (kissing lesions) Aetiology sometimes ulceration. There is no specific (Figures 2 and 3). Unclear. No bleeding tendency appears treatment but oral hygiene should be to underlie this condition. Corticosteroid improved and analgesics given. Chronic Atrophic Candidosis inhalers may sometimes predispose. (Denture-induced ) Chronic atrophic candidosis is a painless Clinical Features Erythematous Candidosis candidal infection of the denture and Blood blisters are seen in the mouth or Candidosis may cause a sore red mouth, denture-bearing mucosa (this will be pharynx, mainly on the soft palate and is especially seen on the tongue of discussed further in a later article). (sometimes termed angina bullosa patients taking broad-spectrum haemorrhagica) and occasionally on the antimicrobials. Erythematous candidosis, lateral border of the tongue in elderly especially on the palate or tongue, may Purpura people. There is rapid onset, with also be a feature of HIV disease (see Dent Purpura (see Table 2) is bleeding into the breakdown in a day or two to a large round Update 1999; 26: 73-80). skin and mucosa, usually because of ulcer (Figures 5 and 6). Median rhomboid glossitis is a painless trauma, suction or a blood platelet defect red patch occurring in the middle of the or deficiency. Diagnosis and Management dorsum in the posterior area of the anterior It is necessary to differentiate this two-thirds of the tongue. Some patients Aetiology condition from pemphigoid and other have lesions in the centre of the dorsum Trauma, such as that caused by the vesiculobullous disorders, trauma, and vomiting in bulimics, or suction and purpura. Confirm that haemostasis is trauma in performing fellatio are not normal first and then perform biopsy to Localized red patches: uncommon causes. Old people may suffer exclude pemphigoid if that is likely. ● Denture-induced stomatitis from senile purpura, and corticosteroids There is no specific treatment other than ● Geographic tongue may also produce purpura. Idiopathic reassurance. The blisters should be ● Lichen planus (autoimmune) platelet deficiency, carefully burst. Topical analgesics may ● Erythroplasia ● sometimes seen in HIV disease, infectious provide symptomatic relief. Purpura mononucleosis or rubella, is the other ● Telangiectases ● Angiomas main cause. Blood blisters may also arise ● Kaposi’s sarcoma in the palate, especially, for no apparent ● Burns reason—this is known as angina bullosa ● haemorrhagica (see below). ● Avitaminosis B12 ● Drugs Clinical Features Generalized redness: Red or brown pinpoint lesions (petechiae) ● Candidosis or diffuse bruising (ecchymoses) are seen ● Avitaminosis B complex mainly at sites of trauma (Figure 4). ● Irradiation mucositis Occasional small traumatic petechiae at the ● Mucosal atrophy occlusal line are seen in otherwise healthy ● Polycythaemia patients. Palatal petechiae may be seen after Table 1. Causes of oral red areas trauma and in: Figure 4. Purpura.

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regress spontaneously. Haemangiomas Management Trauma and suction Platelet disorders: may not need treatment but if they do for Excision biopsy is recommended, mainly ● Autoimmune thrombocytopenia aesthetic or functional reasons, laser or for cosmetic reasons, to exclude ● Bone marrow disorders: aplasia, cryosurgery or injection of sclerosing malignancy, and because of the malignant leukaemia agents are effective. Very large potential of some—particularly the Infections haemangiomas may need to be treated by junctional naevus. Referral to a specialist ● Infectious mononucleosis the surgeon with embolization (sclerosal may be necessary. ● Rubella or, rarely, arterial)—but only if bleeding is ● HIV infection troublesome. Localized oral purpura (angina Amalgam and graphite tattoos bullosa haemorrhagica) Amalgam or graphite incorporated into a Vascular disorders Lymphangioma wound may cause a tattoo. The features of Amyloidosis Lymphangioma is a rare hamartoma or these lesions are summarized in Table 4. Table 2. Causes of oral purpura. benign neoplasm of lymphatic channels, seen especially in the or tongue. Aetiology Although typically a colourless, sometimes Amalgam particles or dust can become Haemangiomas finely nodular, soft mass, bleeding into the incorporated in healing wounds after tooth lymphatic spaces causes sudden purplish extraction or apicectomy or beneath Aetiology discoloration. mucosa. Graphite may be introduced Haemangiomas are uncommon, benign Management is by excision biopsy. through accidents involving lead pencils. lesions of developmental origin— hamartomas. Clinical Features Kaposi’s Sarcoma Amalgam tattoos are common causes of Clinical Features This has been described in an earlier asymptomatic blue-black pigmented Most haemangiomas are seen in infancy. article, and will be discussed further at a macules, usually seen in the mandibular They appear most often on the tongue or later date. gingiva or at least close to the teeth (Figure lip, as painless reddish, bluish or purplish 9), in the floor of mouth, or in the scar of an soft lesions (Figure 7). The characteristic apicectomy where there has been a feature is that they blanch on pressure, or BROWN OR BLACK retrograde root filling. contain blood. PIGMENTATION There are many causes of hyperpigmented Diagnosis and Management Diagnosis and Management oral lesions (these are summarized in Table The diagnosis is usually obvious from the Diagnosis is clinical. 3). location and clinical appearance. Radio- Some 50% of those present in childhood opacities may or may not be seen on radiography. Biopsy may occasionally be Racial Pigmentation indicated to exclude a naevus or melanoma The most usual cause of brown oral but otherwise these lesions are innocuous. mucosal pigmentation is natural ethnic pigmentation, in Blacks, Asians and people of Mediterranean descent. The Addison’s Disease pigmentation is usually symmetrically Addison’s disease (adrenocortical distributed over the gingiva and palatal hypofunction; Table 5) is a rare disease, mucosa (Figure 8), though patches may seen typically in young or middle-aged be seen elsewhere. Pigmentation, if first women, due to damage to the adrenal noted by the patient in adult life, may cortex. It results in hypotension and a incorrectly be assumed to be acquired. feedback pituitary overproduction of Figure 5. Angina bullosa adrenocorticotrophic hormone (ACTH) haemorrhagica. Pigmented Naevi

Aetiology These lesions are genetic in origin. Clinical Features Pigmented naevi are seen particularly on the vermilion border of the lip and on the palate. They are usually asymptomatic Figure 6. Angina bullosa brown or bluish macules , usually less than haemorrhagica. 1 cm across, and do not change rapidly in size or colour. Figure 7. Haemangioma.

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Localized: adrenalectomy in the management of breast ● Amalgam tattoo cancer. ● Naevus Diagnosis and Management ● Kaposi’s sarcoma ● Malignant melanoma It may be necessary to differentiate from ● Pigmentary incontinence racial, drug-induced, and other causes of ● Peutz-Jegher’s syndrome hyperpigmentation, and to establish the Generalized: cause of the adrenal hypofunction. Blood ● Racial pressure, plasma electrolyte and cortisol ● Localized irritation, e.g. smoking levels and response to ACTH stimulation ● Drugs, e.g. antimalarials (Synacthen test) should be assessed, and Figure 8. Racial pigmentation. ● Addison’s disease thus a specialist referral is indicated. ● Other rare causes Addison’s disease is treated by Table 3. Causes of hyperpigmentation. replacement therapy (fludrocortisone and glucocorticoids). which produces hyperpigmentation of skin and mucosae. Drug-induced Aetiology Hyperpigmentation Addison’s disease is usually an autoimmune A variety of drugs can cause orofacial disease. Other causes include tuberculosis, hyperpigmentation, and often by unknown carcinomatosis and histoplasmosis. mechanisms: Figure 9. Amalgam tattoo. Clinical Features ● heavy metals (e.g. lead) cause pigmented Hyperpigmentation is generalized and lines because of sulphide deposits in ● change in colour; brown, but is most obvious in areas that are gingival pockets; ● ulceration; normally pigmented, such as: ● antimalarial agents; ● pain; ● busulphan; ● occurrence of satellite pigmented spots. ● areolae of nipples; ● cisplatin; ● genitalia; ● phenothiazines; Management ● skin flexures; ● zidovudine; The consensus of opinion is that lesions ● sites of trauma. ● minocycline; suspected of being malignant ● oral contraceptives. should not be biopsied until the time of The oral mucosa may show patchy brown definitive operation but the prognosis is poor hyperpigmentation (Figure 10). Diagnosis is usually from a history of Other features of Addison’s disease exposure to the drug. Treatment is to stop include: the drug if possible. Aetiology: ● Adrenocortical destruction and ● weakness; subsequent increased release of ● anorexia; Malignant Melanoma pituitary adrenocorticotrophic ● hormone (ACTH) weight loss; Melanoma is a rare malignant neoplasm of Clinical features: ● low blood pressure; melanocytes, with a poor prognosis. ● Hyperpigmentation, especially in ● collapse under stress. sites usually pigmented or Aetiology traumatized ● Oral: brown pigmentation of gingiva, Nelson’s syndrome is similar to Addison’s Malignant melanoma may arise in apparently occlusal line and elsewhere disease, but is iatrogenic and results from normal mucosa of a pre-existent pigmented ● Cutaneous: hyperpigmentation of naevus, usually in the palate. The incidence areolae and genitals, in flexures, of extra-oral melanoma is increasing as a and at sites of trauma Incidence: Aetiology: result of increased sun exposure. ● Rare; mainly seen in young or ● Particles or dust incorporated middle-aged women beneath mucosa or in wounds after Clinical Features Management: extraction or apicectomy or accident Melanoma typically appears as a heavily ● Blood pressure; plasma electrolyte Clinical features: pigmented (occasionally non-pigmented) and cortisol levels and response to ● Black or bluish-black small pigmented ACTH stimulation (Synacthen test). area macule or, later, nodule and ulceration, ● Idiopathic (autoimmune) Addison’s Incidence: usually in the palate. Spread is to regional disease: replacement therapy ● Common in adults mainly lymph nodes and then the bloodstream. (fludrocortisone and glucocorticoids) ● Others: treat cause, give Management: Features of a hyperpigmented lesion that replacement therapy ● May need to excise to exclude are suggestive of malignancy include: melanoma microscopically Table 5. Addison’s disease ● Table 4. Amalgam and graphite tattoos. rapid increase in size; (hypoadrenocorticism).

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● Lamey P-J, Carmichael F, Scully C. Oral mucosa. In: English GM, ed. Otolaryngology. pigmentation, Addison’s disease and the results Philadelphia: Lippincott, 1993; pp.1-28. of screening for adreno-cortical insuf ficiency. Br ● Scully C. Prevention of oral mucosal disease. Dent J 1985; 158: 297-298. In: Murray JJ, ed. Prevention of Oral and Dental ● Millard HD, Mason DK, eds. Perspectives on Disease, 3rd ed. Oxford: Oxford University 1993 World Workshop on Oral Medicine . Press, 1995; pp.160-172. University of Michigan, 1995. ● Scully C. The oral cavity. In: Champion RH, ● Moyer GN, Terzhalmy GT, O’Brian JT. Burton J, Ebling FJG, eds. Textbook of Nelson’s syndrome: another condition Dermatology, 5th ed. Oxford: Blackwells, 1991; associated with mucocutaneous pp.2689-2769. hyperpigmentation. J Oral Med 1985; 1: 13-17. ● Scully C. The oral cavity. In: Champion RH, ● Scully C. Handbook of Oral Diseases. Burton J, Burns DA, Breathnach SM, eds. Figure 10. Hyperpigmentation in London: Martin Dunitz, 1999. Textbook of Dermatology, 6th ed. Oxford: Addison’s disease. ● Scully C, Cawson RA. Medical Problems in Blackwells, 1998; pp.3047-3124. Dentistry, 4th edition. Oxford: Butterworth- ● Scully C, El-Kabir M, Samaranayake LP. Heinemann, 1998. Candida and oral candidosis. Crit Rev Oral Biol unless treatment is exceptionally early. ● Scully C, Flint S, Porter S. Oral Diseases. Med 1994; 5: 124-158. ● Specialist referral is thus usually indicated. London: Martin Dunitz, 1996. Stal S, Hamilton S, Spira M. Haemangioma, ● Scully C, Welbury R. Colour Atlas of Oral lymphangioma and vascular malformations of Disease in Children and Adolescents . London: the head and neck. Otolaryngol Clin North Am Further Reading Mosby-Wolfe, 1994. 1986; 19: 769-796. ● Burton J, Scully C. The . In: Champion RH, ● Scully C. The pathology of orofacial disease. ● Stephenson P, Lamey P-J, Scully C et al. Burton J, Burns DA, Breathnach SM, eds. In: Barnes IE, Walls AWG, eds. Gerodontology. Angina bullosa haemorrhagica: clinical and Textbook of Dermatology, 6th ed. Oxford: Oxford: Wright, 1994; pp.29-41. laboratory features in 30 patients. Oral Surg Oral Blackwells, 1998; pp.3125-3148. ● Scully C, Porter SR. Oral mucosal disease: a Med Oral Pathol 1987; 63: 560-565. ● Eveson JW, Scully C. Colour Atlas of Oral decade of new entities, aetiologies and ● Stephenson P, Scully C, Prime SS et al. Angina Pathology. London: Mosby-Wolfe, 1995. associations. Int Dent J 1994; 44: 33-43. bullosa haemorrhagica: lesional immunostaining ● Jones JH, Mason DK. Oral Manifestations ● Scully C. Diagnosis and diagnostic and haematological findings. Br J Oral Maxillofac of Systemic Disease, 2nd ed. London: Baillière, procedures: general and soft tissue diagnosis. Surg 1987; 25: 488-491. 1980 In: Pathways in Practice. London: Faculty of ● van der Waal RI, Snow GB, Karim AB et al. ● Kaban LB, Mulliken JB. Vascular anomalies General Dental Practice, Royal College of Primary malignancy melanoma of the oral cavity: of the maxillofacial region. J Oral Maxillofac Surg Surgeons of England, 1993; pp.25-33. a review of eight cases. Br Dent J 1994; 176: 1986; 44: 203-213. ● Scully C. Inflammatory disorders of the oral 185-188. Book Review

The Preservation and Restoration of Tooth readable textbook is a composite of practical authors, however, present cogent arguments Structure. By Graham J. Mount and W. R. and theoretical knowledge. It is filled with for the use of glass-ionomers to prevent Hume. Mosby-Wolfe Medical common sense backed up by scientific bacterial leakage and to act as a dentine Communications, London. (280pp., £49.95, evidence. There is a sensible progression replacement under composite restorations. £85 plus CD-Rom). from the basic sciences of tooth structure, The intention to maintain the maximum disease initiation and progression to clinical amount of original tooth tissue, whatever There has long been a need for a book of intervention. The scope of clinical restoration is being considered, runs ‘Operative Dentistry’ of this type. intervention is enormous including through the book and should be Traditionally, textbooks dealing with the prevention, endodontology, fixed commended. treatment of dental caries have been prosthodontics, relevant periodontology Chapter 11 is one of the most contentious mechanistic and oversimplified with the and occlusion, and the restoration of in that it proposes an alternative to the 100- result that they become redundant soon aesthetics. Incorporated in the clinical year-old Black’s Classification of Cavities. after the dental student has gained basic section are excellent chapters that review The logic in the proposed classification is operative skills. This new text begins from the key clinical properties of individual clear and useful. However, there appears a refreshingly biological basis and, even restorative materials and the concepts of to be a genetic predisposition to Black’s within the introduction, challenges dentine bonding of glass-ionomer, Classification (and cavity form) and I would dogmatic tenets. The beauty of this book composite and amalgam. be surprised if the new classification was is its ability to be used at different levels. It At each stage, traditional and newer, widely used — despite its advantages. will take the role of an instruction book for equally anecdotal, concepts are challenged. This is a wonderful book. It is well the early undergraduate but contains This is most notable in the chapters on ‘Pulp illustrated, well written and thought background and clinical knowledge that protection during and after restoration’, provoking. There is also an accompanying will be indispensable for Finals. It is, which supports the decreased use of setting CD-Rom, that was not available to me to however, unique in that it is also entirely CaOH as a base and ‘Basic principles for review but the quality of the book is such appropriate for use by postgraduate restorative dentistry’, which that it stands alone. I recommend it to students at all sorts of levels (e.g. DGDP/ comprehensively argues against the routine everybody who puts bur to tooth. MGDS/MSc/MRD). use of dentine pins in cuspal replacement. C. C. Youngson The main authors are highly respected. Believers in the infallibility of dentine- Senior Lecturer in Restorative Both are Australian with one an academic bonding systems will not accept the authors’ Dentistry and the other a practitioner. The eminently caution in recommending their use. The Leeds Dental Institute

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