Erythematous Oral Lesions: When to Treat, When to Leave Alone

ABSTRACT: requires followed by wide local excision, ing white and pigmented oral le- since about 50% of these lesions represent invasive . sions, respectively. In this article, Geographic and migrans are largely benign; treatment is I consider erythematous oral le- symptomatic if patients complain of pain. Red lesions caused by hyper­ sions, the appearance of which re- sensitivity to drugs, foods or, most commonly, dental materials (eg, denture flects the increased vascularity of the adhesives, toothpastes, and rinses) can arise anywhere in the oral local tissues. cavity. Treatment consists of discontinuing the offending substance; up to In some cases, the increased 40 mg/d of prednisone can promote healing. Biopsy is not necessary for vascularity results from denudation most vascular erythematous oral lesions, except Kaposi’s sarcoma. If or of mucosal or gingi- vascular lesions are traumatized, surgery or embolization may be needed val areas by such diverse causes as to control bleeding. Because and peripheral giant allergy; fungal infection; dermatolog- cell granuloma can resemble amelanotic melanoma, they require biopsy. ic, hematologic, metabolic, and im- Treatment is excision. munologic disorders; and neoplasia. The lesions associated with these erythematous mucosal alterations Key words: erythroplasia, erythroplakia, migrans, , are generally flat or atrophic; howev- , candidiasis, , plasma cell , er, epithelial hyperplasia is seen with pityriasis rosea, hemangioma, Kaposi’s sarcoma, Osler-Weber-Rendu disease, erythroplakia and . blue rubber bleb syndrome, mucoepithelial syndrome, Fabry’s In other erythematous oral le- disease, Sturge-Weber syndrome, pyogenic granuloma, peripheral giant cell granuloma sions, vascular hyperplasia occurs, such as in Sturge-Weber syndrome. This may also take the form of neo- WILLIAM LAWSON, MD, DDS f you know what to look for, the plastic proliferations (hemangioma Mount Sinai School of Medicine appearance of a puzzling oral le- and Kaposi’s sarcoma), vascular mal- sion can help you narrow the pos- formations, or ectatic vessels (he- sible causes. In previous issues of reditary hemorrhagic telangiecta- CONSULTANT (April 2012, page sia). Finally, hypervascularized I301, and May 2012, page 347), I pro- masses may appear on the gingiva in vided tips for identifying and manag- response to local trauma or irrita-

Dr Lawson is professor of otolaryngology at the Mount Sinai School of Medicine in Figure 1 – Erythroplakia generally appears as a solitary red patch. Histologic examination New York City. revealed this lesion to be an invasive . www.Consultant360.com june 2012 consultant 449 Erythematous Oral Lesions: When to Treat, When to Leave Alone

tion. The Table classifies the lesions Table – Erythematous oral lesions in detail.

Mucosal alterations MUCOSAL ALTERATIONS Erythroplasia, erythroplakia Erythroplasia, erythroplakia. Erythroplasia simply denotes a non- Stomatitis migrans (geographic tongue, erythema migrans) specific red patch. Although some Candidiasis authors employ the terms “erythro- Allergy (contact stomatitis, ) plasia” and “erythroplakia” inter- Denuded bullous lesions changeably, others consider erythro- Dermatologic disorders (psoriasis, pityriasis rosea) plakia analogous to , a specific histologic entity with a dis- Vitamin deficiencies tinct premalignant potential.1,2 In Hematologic disorders fact, erythroplakia is more ominous Vascular lesions than leukoplakia, since histologic Vascular tumors (hemangioma, Kaposi’s sarcoma) study shows that about 50% of eryth- Arteriovenous malformations roplakic lesions represent invasive carcinomas (Figure 1).3 Genodermatoses (Osler-Weber-Rendu disease, blue rubber bleb nevus Erythroplakia generally ap- syndrome, mucoepithelial dysplasia syndrome, Fabry’s disease) pears as a solitary red patch of vary- Sturge-Weber syndrome ing size, which may be slightly Reactive lesions raised. Although the lesion derives Pyogenic granuloma (pregnancy tumor) its color from the loss of surface Peripheral giant cell granuloma keratin, it is painless. The area in- volved may be homogeneous or mixed with small areas of leukopla- Figure 2 – Irregu­ kia (speckled form). It most com- lar, erythematous monly occurs on the floor of the areas that charac­ mouth and the retromolar triangle; terize geographic the gingiva is rarely involved. tongue, or benign migratory , The in- result from the loss cludes chronic inflammation second- of filiform papillae. ary to trauma, candidiasis, and ero- The patterns sive stomatitis. Peak incidence is change at intervals after the sixth decade, with a male that range from days to weeks or preponderance. Following biopsy, months. treatment is wide local excision. Stomatitis migrans. Migratory stomatitis may be encountered in both lingual and nonlingual forms. Geographic tongue. Benign mi- gratory glossitis, or geographic tongue (Figure 2), is seen primarily in young adults, especially women.4 There also seems to be a higher inci- dence among patients with psoriasis or type 1 mellitus.1 The le- sions develop on the lateral borders and dorsum of the tongue, where de- papillated areas appear as smooth, erythematous patches with a gray- white rim. The fungiform papillae become prominent because of the selective loss of filiform papillae. 450 consultant june 2012 www.Consultant360.com Figure 3 – Denture stomatitis is an ery­ thematous variant of in which Candida albicans colonizes the desquamated mucosal area beneath a dental prosthesis. As evi­ dent here, involved areas typically appear as bright red patches.

The patterns in geographic trates seen on microscopic examina- ical drug can arise anywhere in the tongue change at intervals ranging tion. Its migratory character points oral cavity. Other substances or from days to weeks or months, and to the diagnosis. If patients complain foods may also be culprits. recurrences are the rule. If patients of associated pain, prescribe an anti- Drugs and other agents. Sulfon- complain of burning (usually after histamine and an oral amides, barbiturates, and iodine they have eaten spicy or acidic antibiotic to forestall secondary bac- preparations are traditionally associ- foods), prescribe a bland diet and an terial infection. ated with allergic stomatitis, al- mouth rinse. Candidiasis. Oral candidiasis though the occurrence is rare. More Erythema migrans. Although characteristically presents as a pseu- often, contact allergy develops from geographic tongue is commonly rec- domembranous lesion that mimics denture adhesives, toothpastes, ognized as a migratory stomatitis, the .6 Nevertheless, the condi- mouth rinses, and dental materials. nonlingual form, stomatitis areata mi- tion may appear in several other Patients generally experience local grans (erythema migrans), is not. variations. The erythematous pain, burning, or itching. The latter appears as multiple, flat, ir- form—atrophic candidiasis—is Since the clinical appearance of regularly shaped, serpiginous red caused by the loss of surface epithe- the lesion is nonspecific, a thorough patches with raised keratotic rims lium, including filiform and fungi- drug history—including oral and that heal spontaneously and reappear form papillae. dental preparations—is required. in constantly changing patterns. The Involved areas appear as bright Fisher7 provides a list of the active lesions usually occur on the buccal red patches without evidence of ul- ingredients in dental mucosa and the labial and oral vesti- ceration. Sites of predilection are the and dentifrices. The topical allergic bule, but the floor of the mouth, ven- dorsum of the tongue and the . lesions have been broadly subdivid- tral tongue, , and gingiva Denture stomatitis is a variant ed into two types, erythema multi- may be also involved. Brooks and Bal- wherein Candida albicans colonizes forme and lichenoid, because of ciunas5 found that geographic tongue desquamated mucosal areas beneath their resemblance to the lesions and were frequently a dental prosthesis (Figure 3). Treat seen in and li- associated with this condition. patients with clotrimazole troches (5 chen planus, respectively: Erythema migrans is seen daily) or with nystatin oral suspen- •Erythema multiforme–type lesions mainly in young adults. The condi- sion, 400,000 U qid for 7 to 10 days. have been associated with a variety tion is generally painless, despite the Allergy. Red lesions caused by of antibiotics (eg, penicillin, clinda- acute and chronic inflammatory infil- hypersensitivity to a systemic or top- mycin, sulfonamides, rifampin, and www.Consultant360.com june 2012 consultant 451 Erythematous Oral Lesions: When to Treat, When to Leave Alone tetracycline) and with anti-inflamma- thematous lesions because the loss The presence of typical chronic tory agents (salicylates and nonste- of the surface leaves an skin lesions (principally involving roidal compounds).8 irregular, inflamed base. This is es- the elbows, knees, scalp, and nails) •Lichenoid lesions can be produced pecially true of such conditions as helps to establish the diagnosis. Pre- by NSAIDs, thiazides, penicillamine, systemic erythematosus (Fig- scribe emollient mouthwashes for systemic gold compounds, ß-blockers, ure 4), erythema multiforme, pem- patients with oral lesions. methyldopa, and lithium.8 phigus, and . According- Pityriasis rosea is a common, Plasma cell gingivitis. This enti- ly, search for residual mucosal frag- self-limited skin disorder that pres- ty, also known as atypical gingivosto- ments that point to the true nature of ents with an oval erythematous matitis, was first recognized in 1968.9 the disease. Moreover, the bullous plaque (typically on the trunk), As the name implies, it is character- disorders tend to have widespread which is termed the “herald patch.” ized by an intense and diffuse gingi- oral involvement, often with cutane- This is followed by a generalized val erythema that shows plasma cell ous lesions. body eruption 3 to 14 days later. The infiltration on biopsy. Patients may Dermatologic disorders. A rel- characteristic clinical presentation is also have lesions on the , buccal atively common inflammatory skin diagnostic. Intraorally, erythematous mucosa, and tongue (with loss of fili- disorder, psoriasis vulgaris is charac- patches may occur with punctate form papillae). terized by erythematous scaling areas of hemorrhage on the buccal This condition represents an al- plaques. In severe cases, the plaques mucosa, especially in children.12 No lergic reaction to an unknown anti- may extend from the facial skin onto treatment is necessary. gen in some chewing and the lips. Less frequently, similar ir- Vitamin deficiencies. Vitamin toothpastes.9 To treat plasma cell gin- regularly shaped, scaling lesions B deficiency produces loss of the fili- givitis, tell patients to discontinue use may appear on the buccal mucosa, form papillae, resulting in an atro- of the offending substance. Healing tongue, and palate.10 However, geo- phic and red tongue. With can be promoted with up to 40 mg/d graphic tongue and its ectopic buc- (B2) deficiency, the dorsum of the of prednisone.9 cal mucosal form occur in as many tongue becomes intensely colored Denuded bullous lesions. At as 10% of patients with psoriasis. An (magenta tongue); this is often ac- first glance, many vesiculobullous increased incidence of fissured companied by fissuring of the com- oral disorders may appear to be ery- tongue has also been reported.11 missures of the lips, or angular chei-

Figure 4 – In this patient with system­ ic lupus erythema­ tosus, the erythem­ atous patch on the lateral border of the tongue is pro­ duced by sloughing of the overlying epithelium. Many of these vesicu­ lobullous oral disor­ ders appear at first glance to be erythematous lesions.

452 consultant june 2012 www.Consultant360.com losis (Figure 5). With niacin defi- ciency, and reddening of the tongue also occur; however, painful ulcerations develop on the tongue and on all the oral mucous mem- branes, gingiva, and lips. Pyridoxine

(B6) deficiency produces glossitis and angular cheilosis. Vitamin C de- ficiency is characterized by painful hemorrhagic gingivitis. Diagnosis relies on a careful nu- tritional history, which is confirmed by serum vitamin assays. Treatment consists of dietary correction and vi- tamin supplementation. Hematologic disorders. Ane- mia is commonly associated with pal- lor of the mucous membranes; how- ever, the loss of filiform and fungi- form papillae on the dorsum of the tongue results in denuded areas, which are atrophic and erythema- tous. The process of depapillation begins along the lateral borders of the tongue and may involve the en- tire tongue in severe cases. This find- ing is nonspecific; it occurs in both Figure 5 – The depapillated, erythematous tongue (magenta tongue) shown here results microcytic () from riboflavin deficiency. Note the fissuring at the oral commissures (angular cheilosis). and macrocytic anemia (pernicious anemia), as well as after acute viral sion. Sites of predilection are the posi’s sarcoma, its cause remains un- infections. tongue, buccal mucosa, and lips. clear. Involvement of the oral cavity Conversely, excessive red blood Hemangiomas are classified micro- is most common in AIDS patients, es- cell formation, as seen in polycythe- scopically as capillary or cavernous pecially among homosexual men.13 In mia vera, produces a deep red color- based on the size of the endothelium- these patients, the oral cavity is often ation of the mucous membranes, lined blood vessels; these vessels are the initial site of occurrence and may which diffusely involves the oral cav- larger in the cavernous type (Figure even be the only site. Tumors may ity and lips. Thrombocytopenia pro- 6). Treatment, which depends on the develop anywhere in the mouth; duces discoloration of the oral cavity extent and location of the lesion, in- however, the palate is the predomi- by the development of mucosal ec- cludes embolization, injection of scle- nant site (over 90%), followed by the chymoses and petechiae. rosing solution, cryosurgery, laser gingiva (about 20% to 30%).13 The diagnosis is made by a com- therapy, and surgical excision. The purple-red lesions progress plete blood cell count. The appear- Kaposi’s sarcoma is a vascular from multiple macules to a nodular ance of the oral tissues normalizes that occurs in several clini- mass (Figure 7). Larger lesions when the blood disorder is corrected. cal forms: arise in severely immunosuppressed •Classic (a racial genetic lesion patients. They may be confused with VASCULAR LESIONS found predominantly in elderly, Med- other pigmented (melanoma), vascu- Vascular tumors. Hemangiomas iterranean men). lar (hemangioma), or infectious are produced by the disordered for- •Endemic (among African children (bacillary angiomatosis) lesions; bi- mation of blood vessels and may arise and adults). opsy is necessary for definitive diag- anywhere in the deep or superficial •Associated with a non-AIDS immu- nosis. Microscopic examination re- structures of the head and neck. nocompromised state (among pa- veals spindle cells that line irregular When close to the surface of the oral tients who are receiving immunosup- vascular spaces. cavity, they appear as red to blue, pressive therapy, especially those Pain occurs in about one quar- slightly elevated to exophytic, smooth with a renal transplant). ter of patients; bleeding is uncom- to lobulated masses that range widely •Associated with AIDS. mon. Treatment options include sys- in size. Their vascular nature can be While various viruses have been temic interferon alfa-2b, intralesional confirmed by blanching on compres- implicated in the pathogenesis of Ka- injection with vinblastine, injection of www.Consultant360.com june 2012 consultant 453 Erythematous Oral Lesions: When to Treat, When to Leave Alone sclerosing solution, radiation thera- capillaries.14 The signs and symp- and may produce local soft-tissue py, surgical excision, laser therapy, toms are related to the size, site, and discoloration, deformity, and gigan- and systemic . degree of shunting within the mass. tism. Ulceration of the overlying skin Arteriovenous malformations. Physiologically, the lesions may be may cause life-threatening hemor- In these congenital lesions, vascular classified as high-flow, high-shunting rhage. The principal sites of involve- shunting occurs through vessels that or low-flow, low-shunting. The latter ment in the oral cavity are the buccal may be predominantly arteries, resemble hemangiomas. The former mucosa and the floor of the mouth veins, arteriovenous channels, or are pulsatile—often with a bruit— and tongue. Multidisciplinary management involves angiography and emboliza- tion and radical surgery. Partial man- agement results in regrowth with bleeding or airway obstruction. Genodermatoses. In these he- reditary syndromes, a variety of le- sions can involve the skin, mucous membranes, and other ectodermal tissues, as well as mesodermally and endodermally derived structures. Syndromes that produce erythema- tous lesions in the mouth are vascu- lar except for mucoepithelial dyspla- sia, which can also be classified as a mucosal alteration. Hereditary hemorrhagic telangi- ectasia (Osler-Weber-Rendu disease). In this autosomal dominant heredi- tary disease, telangiectasis occurs in Figure 6 – This soft, lobulated, bluish lesion on the dorsum of the tongue is a cavernous the skin and mucous membranes, hemangioma. The vascular nature of hemangiomas can be confirmed by blanching and angiodysplasia is present in the when the lesions are compressed. viscera and the CNS.15 In the oral cavity, the lesions appear as multiple, small (1- to 5-mm), red macules and on the lips and anterior tongue (Figure 8). They are pro- duced by a defect in the wall of small venules. If the lesions are traumatized, bleeding can be controlled by elec- trocautery or laser therapy. Howev- er, the arteriovenous malformations that can occur in the lungs and liver—as well as other angiodysplas- tic lesions in the CNS, gastrointesti- nal (GI) tract, and other viscera— may produce serious hemorrhage. Epistaxis from nasal mucosal lesions is a common presentation. Blue rubber bleb nevus syndrome. In this autosomal dominant disorder that presents at birth or during early Figure 7 – Nodular, reddish purple lesions appear on the dorsum of the tongue of childhood, multiple, soft, compress- this patient with Kaposi’s sarcoma. Note that multiple lesions are also present on the ible, blue nodules appear on the perioral skin. skin.16 The lesions are often associ- 454 consultant june 2012 www.Consultant360.com Figure 8 – Multiple, punctate, red macules on the anterior dor­ Figure 9 – Erythematous hyperplasia of the maxillary and man­ sum and tip of the tongue occur in this patient with hereditary dibular gingivae and the alveolar mucosa is apparent in this hemorrhagic telangiectasia (Osler-Weber-Rendu disease). The patient with encephalotrigeminal angiomatosis (Sturge-Weber lesions result from a defect in the wall of small venules. syndrome). On the facial skin, a port-wine stain always occurs on the same side as the oral lesion. ated with pain and sweating. Venous ules and papules—hence, the name tive embolization of regional blood malformations also develop in the GI angiokeratoma corporis diffusum. Se- vessels. tract (especially the small intestine), vere burning pain develops before heart, lungs, and other viscera; these the skin lesions appear. In the oral REACTIVE LESIONS malformations may bleed and cause cavity, angiokeratotic lesions appear Pyogenic granuloma. This le- chronic anemia. In the oral cavity, on the lips and buccal and palatal sion arises as a reaction to local trau- cavernous hemangiomas typically mucosa. ma. It appears as a small (0.5- to 1.5- develop on the tongue. Traumatized This lipid storage disorder also cm), exophytic, red, friable mass with lesions may produce bleeding that involves the kidney, heart, GI tract, a predilection for the gingiva (espe- requires surgical control. eyes, CNS, and other organs. Renal cially of the anterior ) of young Mucoepithelial dysplasia syn- or cardiac failure often causes death adults, but it may also occur on the drome. This autosomal dominant in midlife. buccal mucosa, tongue, or lips. Micro- disease first appears in infancy and Encephalotrigeminal angioma- scopic examination reveals a mass of is characterized by severe erythema tosis (Sturge-Weber syndrome). In capillaries in a loose connective tissue of the mucous membranes of the this neurocutaneous disorder, a port- stroma with interspersed chronic in- mouth, nose, genitourinary tract, wine stain (nevus flammeus) occurs flammatory cells. With continued and anus.17 In the oral cavity, the along the distribution of the trigemi- trauma, the surface ulcerates and gingivae are intensely red. The skin nal nerve, and meningeal angiomas granulation tissue forms. Biopsy is is rough with follicular keratoses. and calcifications are present along necessary, since amelanotic melano- Noncutaneous manifestations in- the cerebral convolutions.19 Many ma may have an identical appearance. volve the hair (alopecia), eyes (cata- patients also have seizures, glauco- Treatment is excision. racts), and lungs (bullous lung dis- ma, and mental retardation. A variant of this lesion is the ease). Microscopic examination re- When the second and third divi- pregnancy tumor, which arises on the veals a lack of epithelial cohesion, sions of the trigeminal nerve are in- gingiva of gravid women in response dyskeratosis, and cytoplasmic inclu- volved, increased vascularity and to hormonal stimulation (Figure 10). sions. There is no tendency to ma- vascular hyperplasia may develop in These lesions are histologically iden- lignant transformation. the oral cavity, especially the buccal tical to pyogenic granulomas. If trou- Fabry’s disease. This X-linked re- mucosa, gingiva, and lips (Figure 9). blesome, they may be removed in the cessive disorder of glycosphingolipid Uncommonly, the increased regional second trimester or postpartum. metabolism presents in children as a blood flow may result in gigantism of Peripheral giant cell granulo- diffuse rash over the lower trunk.18 It the gingiva or underlying bone. If ma. This lesion also arises on the is formed by small angiokeratomas the oral lesions bleed, they may be gingiva in response to local trauma that appear as small red-blue mac- treated with cryosurgery or selec- (eg, dental restorations or calcu- www.Consultant360.com june 2012 consultant 455 Erythematous Oral Lesions: When to Treat, When to Leave Alone

lus).20 It is dark red and friable and CLINICAL HIGHLIGHTS may have a broad or narrow base. There is an increased prevalence in q Although oral candidiasis usually presents as a pseudomembranous women and in the posterior mandib- lesion, it may appear in an erythematous form that results from the loss ular region. of surface epithelium, including filiform and fungiform papillae. Denture These lesions are clinically in- stomatitis is a variant that consists of desquamated mucosal areas distinguishable from pyogenic gran- beneath a dental prosthesis. ulomas; however, on microscopic examination, the presence of multi- q At first glance, many vesiculobullous oral disorders may appear to be nucleated giant cells within the gran- erythematous lesions because the loss of the surface epithelium leaves ulation tissue is diagnostic. Treat- an irregular, inflamed base; residual mucosal fragments point to the true ment is excision. n nature of the disease. q Vitamin B deficiency produces loss of the filiform papillae, resulting in REFERENCES: an atrophic and red tongue, while vitamin C deficiency is characterized by 1. Wood NK, Goaz PW. Differential Diagnoses of painful hemorrhagic gingivitis. Diagnosis is based on a careful nutritional Oral Lesions. 5th ed. St Louis: Mosby–Year Book, Inc; 1997. history, which is confirmed by serum vitamin assays. 2. Shklar G, McCarthy PL. Diseases of the . 2nd ed. Philadelphia: Lea & Febiger; 1987. q Anemia is commonly associated with pallor of the mucous membranes; 3. Shafer WG, Waldron CA. Erythroplakia of the oral cavity. Cancer. 1978;36:1025-1028. however, the loss of filiform and fungiform papillae on the dorsum of 4. Schneiderman H. What’s Your Diagnosis?® the tongue results in atrophic, erythematous, denuded areas. Excessive Geographic tongue. Consultant. 1991;31(12):47-48. 5. Brooks JK, Balciunas BA. Geographic stomatitis: red blood cell formation, as seen in polycythemia vera, produces a deep review of the literature and report of 5 cases. red coloration of the mucous membranes, which diffusely involves the J Am Dent Assoc. 1987;115:421-424. 6. Lawson W. White oral lesions: how to distinguish oral cavity and lips. the benign from the deadly. Consultant. 2012;52: 301-307. q Peripheral giant cell granulomas are clinically indistinguishable from 7. Fisher AR. Contact stomatitis. Dermatol Clin. 1987;5:709-717. pyogenic granulomas; however, on microscopic examination, the 8. Zelickson BD, Rogers RS. Oral drug reactions. presence of multinucleated giant cells within the granulation tissue is Dermatol Clin. 1987;5:695-708. 9. Silverman S, Lozada F. An epilogue to plasma- diagnostic. cell gingivostomatitis (allergic gingivostomatitis). Oral Surg. 1977;43:211-217. 10. Pindborg JJ. Atlas of Diseases of the Oral Mucosa. 5th ed. Copenhagen: Munksgaard; 1993. 11. Ulmansky M, Michelle R, Azaz B. Oral psoriasis: report of six new cases. J Oral Pathol Med. 1995;24: 42-45. 12. Kay MH, Rapini RP, Fritz KA. Oral lesions in pityriasis rosea. Arch Dermatol. 1985;121:1449-1451. 13. Ficarra G, Bersin AM, Silverman S. Kaposi’s sarcoma of the oral cavity: a study of 134 patients with a review of the pathogenesis, epidemiology, clinical aspects and treatment. Oral Surg Oral Med Oral Pathol. 1988;66:543-550. 14. Erdman MW, Jackson JE, Davies DM, Allison DJ. Multidisciplinary approach to the management of head and neck arteriovenous malformations. Ann R Coll Surg Engl. 1995;77:53-59. 15. Flint SR, Keith O, Scully C. Hereditary hemor- rhagic telangiectasia: family study and review. Oral Surg Oral Med Oral Pathol. 1988;60:440-444. 16. Sumi Y, Tagughi W, Kaneda T. Blue rubber bleb nevus syndrome with oral hemangiomas. Oral Surg Oral Med Oral Pathol. 1991;71:84-86. 17. Schemen AJ, Ray DJ, Witkop CJ. Hereditary mucoepithelial dysplasia: case report and review of the literature. J Am Acad Dermatol. 1989;21:351-357. 18. Chesser RS, Gentry RH, Fitzpatrick JE, Harrington AC. Perioral telangiectases: a new cuta- neous finding in Fabry’s disease. Arch Dermatol. 1990;126:1655-1656 19. Sujansky E, Conradi S. Outcome of Sturge- Weber syndrome in 52 adults. Am J Med Genet. 1998;57:35-45. 20. Katsiteris N, Kakarania-Angelopoulou E, Angelopoulou AP. Peripheral giant cell granuloma: clinicopathologic study of 224 new cases and a Figure 10 – This exophytic, intensely erythematous lesion occurs on the maxillary gingiva review of 956 reported cases. Int J Maxillofacial of a gravid woman. Pregnancy tumors arise in response to hormonal stimulation. Surg. 1988;17:94-99.

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