of vertebral osteomyelitis. Rettopharyngeal space infection also can follow penetrating trauma to the posterior pharynx (eg. from an endoscopic procedure). Infections are commonly polymscrobial, involving a mixture of acrobes and anaerobes: group A f-hemelytic sweptococei and 5. aureus are the most common pathogens. (Me tuberculosis was a common cause inthe past but now is rarely ‘nvolved inthe United States, Patients with rettopharyngeal abscess typically present with sore throat, fever, dysphagia, and neck pain and are often doa! ing because of diiculty and pain with swallowing, Examination may revel tender cervical adenopathy, neck evelling, and dice tythema and edema ofthe posterior pharynx ae well a¢ a bulge in the posterior pharyngeal wall that may not be obvious on routine Inspection, A ot Gesue mass se usually demonstrable by lateral, reck radiography or CI. Because ofthe risk of airway obstruction, ‘treatment begins with securing af the airway, followed by «combi nation of surgical drainage and TV antibiotic administration Initial ‘empirical therapy should cover streptococci, oral anaerobes, and S. aureus, ampicilin/subactam, clindamycin alone, ox clindamycin plus ceiratone is usualy effective. Compliations result primar- ily fom extension to other areas (eg, rupture into the posterior pharynx may lead to aspiration pneumonia and empyema). Extension may alo accut tothe lateral pharyngeal space and medi- astinum, resulting in mediastinitis and peicardis, or into nearby major blood vesiels, All these events are associated with a igh morality rte, GED Awantcas Acaemy or Petaraics Svacomamrres ow MaxAGEaant oF ACUTE Onrmis Mapta: Diagnosis and mas agement of acute otis media, Pediatrics 113:1451, 2004 Awentcas Acapeny oF Peotaraics Sumcomnrrres ow ManaGEaanr oF Sinvstris aND Cosotrtex on QUALITY Iuprovenens: Clinical practice sideline: Management of sini. Peditrice 108.798, 2001, ‘Cayton RM: Expand the pharyngitis paradigm for adolescents and young adults. Ann Intern Med 151:812, 2009 ‘Coorex Rj et ak: Principles of appropriate antibiotic use for acute ‘pharyngitis in adults: Background, Ann Intern Med 134509, 2001, Gowzaras R et ak: Principles of appropriate antibiotic use fr reat ment of nonspeciic upper respiratory tact infections in adult Background. Ann Intern Med 134:490, 2001 GaeAIVA CG eta: Anibotc presription rates for acute respiratory tract infections in US ambulatory settings. JAMA 302:758, 2008, Msnoror SB: Valuing reduced antibiotic use for pediatric acute ‘otitis media. Pediatrics 122659, 2008 [Rares K etal: Airway infectious disease emergencies. Pediatr Clin ‘North Am 53:215, 2006 Rosaxexin RM et al: Clinical practice guideline: Adult sinus, ‘Otolaryngol Head Neck Surg 137(3 Suppl}S1, 2007 ‘Scuwanr? B etal: Pharyngitis principles of judicious use of ant ‘microbial agents, Pediatrie 101171, 1998 “Tompson P etal: fect of antbiotics for oie media on mastitis in children A retrospective cohort study using the United Kingdom, general practice research datahase. Pediatrics 12324, 2009 ‘Wiztiasisow IG et al Antibiotics and topical nara steroid for reat ‘ment of acute mauillary sinusitis. JAMA 298.2487, 2007 ‘Youne Jet al: Antibiotic for adults with clinically diagnosed aeste shinosinusitis: A meta-analysis of individual patient data. Lancet 371-908, 2008 roe EIR LH} asvasiq jo suoneysayueyy [210CHAPTER @12 ‘Samuel C, Durso Janet A, Yellowitz ‘The health status of the oral cavity is linked to cadiovascula dis ‘ence, diabetes, and other systemic illnesses. Thus, examining the ‘oral cavity for signs of disease is a key part of the physical exam. “This chapter presents numerous outstanding clinical photographs ilusteating many of the conditions dicussed in Chip. 32, Oral ‘Manifestations of Diseate, Conditions affecting the teeth, priodan- taltiseues, and oral mucosa ae all represented. eseesiq yo suojesoyueyy jei0 Jo seny PA ET EDL) Figure 012-5. fiythomatosus anlass undo a denture (the pation Figure 612-2 Oral een planus. shou he teated fo this urgal tect). aerae) CI sesvasiq Jo vojewesold pue suoneysajueyy euIpIeD Figure e126 Sowre peogontis. Figure 012-7 Angular coils Figure e12-8 Sublingual lukooska, Figure ©12-9 A. Epuls (gingival mypervopy) under denture, 8 Epuls ‘ssuratumFigure 012-13. Healy mouth Figure e12-10 Traumate les inside of chee, ‘Sseasiq 40 suoneysoyuey (210 Jo seny ACR ERAN) Figure e12-11 Ora ledkotai,sbtype homogenous lukopiia. e nn a= 7 Figure e12-12 Ora carcnoma, Figure 012-18. Mederate gngitsrae) CI sesvasiq Jo vojewesold pue suoneysajueyy euIpIeD 124 Figure e12-16 Gingival ecession Figure 012-17 Hay cus ard inghaliitarmatin Figure 012-18 Severe gga ilanmaton ar hoary cleus Figure 612-20 User on aaa bord oftonquo—potontal carcrara. Figure e12-21 OsteonecasisFigure 012-22 Severe parodntal disease, missing toth, vey bile ‘wet, Figure 012-23 Salvay store. —— iat Figure 612-24 A Callus. 8 Teeth cleaned. Figure ©12-27 Whitaexatou tongue—tkaycandlass. De Jane Atkinson wa a c-author ofthis chapter in the 17th edition ‘Some ofthe materials have been cari over into this edition. eseesiq yo suojesoyueyy jei0 Jo seny PA ET EDL) 125This page intentionally left blankCHAPTER 32 Oral Manifestations of Disease ‘Samuel C. Durso As primary care physicians and consultants, intemists are often asked to evaluate patente with dicease of the oral soft tieues, teeth and pharynx Knowledge ofthe oral milieu and its uniguestuetures is necessary to guide preventive services and recognize oral mani festations of local or systemic disease (Chap. 12). Furthermore, internist frequently collaborate with dentists inthe cate of patients who ave a variety of medical conditions that affect eral health of ‘who undergo dental procedures that increase their risk of medical, complications TOOTH AND PERIODONTAL STRUCTURE Tooth frmaton begins during the sth week of embryonic i tdeoninues rough the nt 7 yes af ae Teath evelopment iin tro ancontinges untae the oth cups Norell A190 decidous eth ave ered by age 3 ana ate ee hed y age 13, Permanent teth, eventually totaling 32, begin to erupt by age 6 and have completly erupted by age 1, though thied molars (isdom teeth) may erup ater te erupted tooth consist of the visible crown covered with ‘enamel and the root submerged below the gum line and covered swith bonelike cementum. Dentin, a material that is denser than, boone and exquisitely sensitive to pain, forms the majority of the tooth substance. Dentin surrounde a core of myxomatous pulp con: taining the vascular and nerve supply. The tooth i hel femly 1 the alveolar socket by the periodontiune, supporting structres that ‘consist ofthe gingivee, alveolar bone, cementum, and period ligament, The periodontal ligament tenaciously binds the tooth’ ‘cementum to the alveolar bone. Above this ligament i «colar of attached gingiva just below the crown. A few millimeters of unat tached or fce gingiva (1-3 mm) overlap the base ofthe crown, forming shallow suleus along the gam-tooth margin, ‘Dental caries, pulpal and periapical disease, and complications Dental carter begin aaymptomatially at a destructive process of| the hard surface of the tooth. Sireptococeus mutans, principal, slong with other bacteria colonize the orgenic buffering film on the tooth surface to produce plague. Ifnot removed by brushing or the natural cleaning ation of saliva and orl sol tissues, baceral aids son than the chronic forms described above, However ifthe host Js stressed or exposed to a new pathogen, rapidly progressive and destructive disease ofthe periodontal tasue can occur virulent ‘example acute necrotizing ulcerative gingivitis (ANUG) or Vincent’ fection, Stress, poor oral hygiene, and tebacco and aleahol use are sk factors. The presentation inclades sudden gingival indamma- ion, ulceration, Bleeding, interdental gingival necrosis, and fetid haltosis. Localized juvenile periodontitis, sen in adolescents, $¢ partculssly destructive and appears to be arvociated with impaired ‘eutrophil chemotaxis, AIDS-related periodontit resembles ANUG sn some patients of a more destructive form of adult chronie per ont in others. IC may also produce a gangrene like destructive process ofthe oral soft tissues and hone that resembles noma, seen fn severely malnourished children in developing nations Prevention of tooth decay and periodontal infection Despite the reduced prevalence of dental civies and periodontal Aiseace in the United States due in large part (o water Muoridation and improved dental cae, respectively, both diseasse constitute & major public health problem worldwide and for certain groups. ‘The internist should promote preventive dental cae and hygiene as part of health maintenance, Special populations at high risk for dental aries and periodontal disease include those with xerostomia, diabetics, alcoholics, tobacco users, those with Down's syndrome, and those with gingival hyperplasia, Furthermore, patients lack- ing dental-care access (low socioeconomic status) and those with reduced ality to provide self-care (eg. nursing home residents and those with dementia ot upperextzemity disability) suer ala disproportionate rate Its important to provide counseling regarding regular dental hygiene and professional cleaning, use of Aluoride-containing toothpaste, professional fuoride treatments, and use of electric toothbrushes for patients with limited dexterity and to give instruction to caregivers for those unable to perform selfcare Internists caring for international students studying in the United States should be avvare of the high prevalence of dental decay in this population, Cost, fear of dental care, and language and cultural differences may create barvers that prevent some from sing preventive dental services Developmental and systemic di and periodontium ‘Malocelusonisthe most common developmental problem, which in ‘dition toa problem with cozmesis, can interfere with mastication unless corrected through orthodontic techniques. Impacted third molars are common and occasionally become infected. Acquired prognathism due to acromegaly may alo lead to malocclusion, ae may deformity ofthe maxilla and mandible due to Page's diease ofthe bone, Delayed tooth eruption, receding chin, and a protrud ing tongue are occasional features of eretinism and hypopituitarion Congenital syphilis produces tapering, aotched (Hutchinson's) incisors and finely nodular (mulberry) molar crowns, ‘Bnumelypoplasia results tn ezown defects ranging fom pits to deep fissures of primary or permanent teeth, Intrauterine infection (eyphils, abel), vitamin deficiency (A, C, or D), disorders of calcium metabolism (malabsorption, vitamin D-resstant rickets hypoparathyroidism), prematurity, high fever, or rare inherited defects (amelogencss imperfecta) are all causes. Tetracycline, given in suticiently high doses during the ict eight years, may produce enamel hypoplasia and discoloration, Fxposure to endogenous pig ments can discolor developing teeth: erythrblastossftalis (green or bluish-back), congenital liver disease (green or yellow-brown), and porphyria (red or brown that uoresces with ultraviolet light). ‘Mottled enamel occurs excessive uorde is ngested dusing deve ‘opment. Worn enamel is seen with age, bruxism, or excessive acid exposure (eg. chronic gastric reflux or bulimia) espature tooth loss resulting from periodontitis is seen with cyalie neutzopenta, Papilon-Lefevee syndrome, Chédiak Higaths syndrome, and leukemia. Rapid focal tooth loosening is most often due to infection, but rarer causes include Langerhans cll istiocy~ tosis, Ewing's sarcoma, osteosarcoma, or Burkit’s lymphoma. Easly loss of primary teeth ia feature of hypephosphatasa. a rare inborn crror of metaboliem. Pregnancy may produce severe gingivitis and localized pyogenic ganulomas, Severe periodontal disease occurs with Down's syn rome and diabetes melitus. Gingival hyperplasia may be caused by phenytoin, calcium chansel blockers (eg. nifedipine), and cfclosporine, Idiopathic familial gingival flbromatois and sever] synlrome-related disorders appear similar, Removal ofthe medica- tion often reverses the drug-induced form, though surgery may be 2 affecting the teethneeded to control both, Linear gingival erythema is variably seen tn patients wath advanced HIV infection and probably represents immune deficiency and decreased neutrophil activity, Dilfase of focal gingival welling may be a feature of ealy or lte acute myelo- rmonocyticleukemia (AMMI,) aswell as of ther Imphoprolifraive disorders. A rare, bu pathognomonic, sign of Wegener's granuloma tosis is a ed-purpish, granular gingivitis (strawberry gums) PAN Infection ‘Most oral mucosal disease lve microorganisms (Fable 321), Pigmented lesions See Table 32.2, Dermatologic diseases See Tables 32-1, 322 323 and Chaps 51-55. Diseases ofthe tongue See Table 32-4 HIV disease and AIDS. See Tables 32-1, 32-2, 32-3, and 32-5; Chap. 189:and Figures 181-1 and 205-1, ers Ueration is the most common oral mucosal lesion. Although there are many cause, thehost and pattern oflesions, including the presence of aystemic features, narow the diferental diagnosis (Table 32-1. ‘Most acute uleers are painful and self limited. Recarrent aphthous Ulcers and herpes simplex infection constiute the majority. Persistent and deep aphthous ulcers can be idiopathic of seen wth HIVIAIDS. Aphthous lesions aze often the presenting symptom in Behge syndrome (Chap. 327) Similar-appearing. though less painful lesions may occur with reactive arthritis (formesly know as Reiter's syndrome), and aphthous uleers are occasionally present during phases of discoid or systemic fupus erythematosus (Chap. 323) Aphthouslike ulcers are seen in Croba's disease (Chap. 295), bat unlike the common aphthour variety, they may exhibit granu- Tomatous inflammation histologically. Recurrent aphthae in some patient with celiac disease have been reported to remit with elimi nation of gluten. Of major concern are chronic relatively painless ulcers and mixed redivehite patches (eythroplakia and leukoplakia) of more than two ‘weeks’ duration. Squamous cll carinoma and premalignant dys plasa should be considered early and a diagnostic biopsy obtained ‘The importance is underscored because eatly-sage malignancy i= vastly more treatable than late-stage disease, High risk site include love lip, floor ofthe mouth, ventral and literal tongue, and soft palate-toneillar pillar complex, Significant risk factors for oral cancer in Western counties include sun exposure (lower lip) and tobacco and alcohol use. In India and some other Arian counties, smokeless tobacco mixed with betel nut, slaked lime, and spices is ‘common cause of oral cancer, Less common etiologies include syphilis and Plummer Vinson syndrome (ion deficiency) ‘Rarer cause of chronic oral ulcer such a¢ tberclosit,fengal infection, granulomatess with plyangitis (Wegener), and midine ‘granuloma may look identical to carcinoma, Making the coreect dhagnosis depends on recognizing aber dinical features and biopsy of thelesion. The syphilitic chaneteis typically painless and therefore easly _missed. Regional lymphadenopathy i invariably present. Confmation is achieved using appropriate bacterial and serologic tet, Disorders of mucosal fragility often produce painful oral wleers al to eal within two wosks. Mucous membrane pemphigoid and pemphigus vulgaris are the major acquired disorders. While inal features are often distinctive, immunohistachemicalexars nation should be performed for diagnosis and to distinguish these ‘entities from lichen planue and drug reactio Hematologic and nutritional disease Tterists are more likely to encounter patients with acquired, rather than congenital, Bleeding disorders. Bleeding aller minor trauma should stop after 15 min and within an bour of tooth ‘eiraction if local pressure i applied. More prolonged bleding, if not due te continved injury or rupture of a large vessel, should lead to investigation fora clotting abnormality. In addition to Bleeding, petechiae and ecchymoses are prone o occur atthe line of vibration ‘betieen the soft and hard palates in patients with platelet dysfunc tion or thrombocytopenia, All forms of leukemia, bst particularly acute myelomonocytic leukemia, can produce gingival bleeding ulcers and gingival enlarge ‘ment. Ora ueers ate a feature of agranulocytosis, and ulcers and mucositis are often severe complications of chemotherapy and rad ation therapy for hematologic and other malignancies. Plummer Vinson syndrome (ion deficiency, angular stomatitis, gloss, and dysphagia) raises the risk of oral squamous cell cancer and esopha geal cancer atthe postricoidal tissue web, Atopic papillae and a red, burning tongue may occur with pernicious anemia, B-grovp vitamin deficiencies produce many ofthese same symptoms a well, as oral ulceration and chedloss. Swollen, bleeding gums, lees, and loosening ofthe teth area consequence of teuryy. Most, but not all oral pain emanates from inflamed or injured tooth pulp or periodontal tissues, Nonodontogenic causes may be ‘overlooked. In most instances, toothache is predictable and propor tional to the stimulus applied, nd an identifiable condition (eg, ‘caries, abscess) is found: Local anesthesia eliminates pain original. ing from dental or periodontal structures, But not referred pains. The most common nondental origin is myofascial pain referred from muscles of mastication, which become tender and ache with increased use. Many sufferers exhibit bruxism (the grinding of teeth, often during sleep) that is secondary to stress and anxiety Temporomandibular disorder is closely relate, It affects both sexes with a higher prevalence in women, Features include pai, limited ‘mandibular movement, and temporomandibulat joint sounds, The ‘etiologies are complex and malocclusion doesnot ply the primary role once attributed to it. Osteoarthritis a common cause of mas tieatory pain. Ant-inflammatory medication, jaw rest, sft foods, and heat provide relief The temporomancibular joint is involved fn 50% of patients with hewmtoid artritie and t usualy a late {eaure of severe disease. Bilateral preauricula pain parsiculaly in the morning limits range of motion Migrainous neuralgia may be localized tothe mouth, Episodes of pain and remission without identifiable cause and absence of relief ‘with local anesthesia are important clues. Trigeminal neuralgia (6 douloureus) may involve the entire branch of pat ofthe mandi: lar or manillary branches of the fifth cranial nerve and produce pain in one ora few teeth. Pain may occur spontancously or be triggered by touching the lip or gingiva, brushing the teeth, of chewing. Glossopheryngeal neuralgia produces similar acute neu: ropathic symptoms in the distribution of the ninth cranial nerve. Swallowing, sneezing, coughing, or pressure on the tragus of the ‘ear tiggers pain that fel inthe base of the tongue, pharynx, and soft palate and may be referred tothe temporomandibslar joint. Neuritis involving the maxlary and mandibular divisions of the igeminal nerve (eg. maxilay sinusitis, neuroma, and leukemic infiltrate is distinguished from ordinary toothache by the neuropathic roe EIR LH} asvasiq jo suoneysayueyy [210 268TABLE 32-1 Vesicular, Bullous, or Ulcerative Lesions of the Oral Mucosa Viral Diseases Primary acute epee Up andra mucese Lal vestles hte ard cs and Hels sprtanansiyin 10-14 dav. Uiess dingvosomatis (ural gga Inquel_ ial estes at uch ura exromay secondary infect, sir sing >3 [herpes simplex virus mucosa) painful; acute gingivitis, fever, malaise, foul odor, weeks are not due to primary HSV infection (iS) pe trary Sd cael mpraderopa, oes mary ‘pe 2 ini, len and oun aes Reciranthepet Miccutanoisjncton Epson of ove vse that may Las tat wos, it cndton mayb pr > atl, ptr sk codes ten opie andes panlto angi sconly feces. evr ope = pressor py tods ovr an may eset te ESI ecu inrorl Plt and gingival vesicles on arated opel tat Hel spontaneous in aout? week. Reivers ripe and onlesce pal fever, oil ora antral may rece resin ie Chickenpox varcola- ing and oral‘ esins maybe aconpanied by smal__Leon hel spontaneous thin 2 woos rvs) mca Yescles on ol mucosa tht upto frm g al less may cabo fom ge S bull sons tat ert; mucosa may have a senerizdenteme = teres ostr(ea- Cheek ng, ging, nine vsiear erate an uleraton in Gaal hang witout searing unless that avr. orpalte lina atm alonng sensory dt of secondly tes: posherpet nari SF meervns) {geri nee orneefistaenes = fecommen Oral see amcor, oF g ‘anes ede hein te ana pst B herpeve neg a Infectious mono- Oral mucosa Fatigue, sore throat, malaise, fever, and cervi- Oral lesions disappear during convales- 8 ‘ucleasis (Epstein-Barr ‘cal lymphadenopathy: numerous small ulcers cence; no treatment though glucocorticoids S virus) usually appear several days before lymphade- indicated if tonsillar swelling compromises. z ropa gingival oedng and multiple ate- alway g Cheat uncton ot hard and so gli EE —_Herpangiacrscke- Oral mcot, pharynx, Sudden ose of fever, seta and _—Incbon pri 2-9 das fever or ES ——vuekeabo posse, tongue oropharyngeal esis. sal n chin To. recvery naven 3 corse 8 a echo- Under yer, crn summer mont use on Dhanrea congestion and eis (-2 mm), g trays srourded yee ae: 2 vestleseniarge andere 8 and, foot, and mouth Orel mucosa. pharynx, Fever. malaise, headache with oropharyngeal Incubation period 218 days; lesions heal ° disease (coxsackie- _ palms, and soles vesicles that become painful, shallow ulcers; spontaneously in 2~4 weeks vis Ais most ht inte; sual fet hen der commin 200 10 Primary HV infction Ging, pista and Acute gigi and aophayngealucsaton, _Folowedby HV sercsnversn,ssmnpton- nn desoate th ebro iesrsemting abc HV fect, and usualy at by ‘mononucecss and including ymohadenopathy HIV disease Bacterial or Fungal Diseases ‘cute necrotizing ——Gngiva Painfl, bleeding gingiva characterized by Debidement and dite (1.9) peroxide Ulcerative ging necrosis and ulceration of gingival papillae and lavage provie eit within 24h; anibiatis (trench mouth.” margins plus lmpradenopathy and ful odor in acutely il patents; elapse may occur Vincent’ infection) Prenatal (congenital) Palate, jaws, tongue, Gummatousivolament of palate, jaws, and Toth deforms in permanent dentiton sypbiis and teeth facil bones; Hutchinson's incisors, mulbery —_ievesile molar, gloss, mucous patches, and fissures fn cena ef mth Primary syphilis Lesion appears where Small papule developing rapidly into large, Healing of chancre in 1-2 months, allowed (chancre) ‘organism enters body; pines ulcer wit indurated border; unlterl by secondary syphilis in 6-8 weeks may occur on fips, iyphadengpathy, cancre ané lymph nodes tongue or fnsiar area containing spirochetes; serologic tess postive by tied to fourth weeks Secondary syphils Oral mucosa ftequenty Maculopapular lesions of oral mucosa $10 mm Lesions may pesist rom several weeks to invlved with mucous in dlametor wit conta ulcorstion covered by year gatches, primary on grayish membrane; eruptions occuring on val- alate also at commis- ous mucesal surfaces and skin accompanies by sures of auth fever, malaise, and sore that ‘contest 270TABLE 32-1 Vesicular, Bullous, or Ulcerative Lesions of the Oral Mucosa (Continued) cmd Tertiary syphilis Gonarrnea Tuberculosis Cervicoteilactino- mycosis Histoplasmosis Candas Table 32-3) Dermatologic Diseases Palate and tongue Lesions may occur in mouth a ste of inocu: Iation or secondary by hematogenous spread from a primary focus slsowhere Tongue, tonsa rea, soft palate ‘Swelings in region of face, neck a oor of mouth ‘Ary area ofthe mouth, partculaly tongue, ln- va, or palate ri Gummatous infitvaton of palate or tongue fl- Towed by ulceration and fibrosis: atophy of ‘onguepapilee produces characteristic bald tongue and goss ost pharyngeal infection is asymptomatic; may produce burn o ching sensation; oropharynx and tonsils may be ulcerated and cnytrematous; salva viscous ard fetid ‘painless, soltary 1-5 cm, regular ulcer covered with a persstnt exudate; ulcer has a fm undermined border Infection may be associated with an extrac tion, aw tact, of eruption of moar ‘ooh in acute form resembles an acute pyogenic. abscess, but contains yellow “slur granules” (gram-positive mycelia an tei hyphae) Nodular, verucous, or granulomatous lesions leas ate indurated and pall: usual source homatogenous or pulmonary, but may be primary om umma may destroy palate, causing com plete peroration or ificut to eradicate than urogenital infection, though pharyngitis usualy resohes with appropriate animicroial treatment ‘Autoinoculation from pulmonary infection usual lesions resolve with appropate ant: microbial therapy “Typical, swelng is hard and grows pain less multiple abscesses wit draining ‘raos develo: penclin first choice; surgery usualy necessary roe EIR LH} z Systemic aniungal therapy necessary toeat Mucous membrane pemphigoid Erythema mulifrme minor and major {Stovens-Johnson symdrome) Pemphigus vularis Lichen planus Other Conditions peal produces mated gingival en- ‘homa and Ulceration; ther areas of oral cavity, esophagus, and vagina may be affected Prima the ora mucosa an the skin of hands and fet (ral mucosa and ski ses of mechan'- al trauma (sonar palate, enum ps, buccal mucosa) (ral mucosa and skin Painful, gryish-white collapsed vesicles or bu leo fulthickness epithelium with peripheral entrematous zone: gingiva lesions desaus- rat, leaving ulcerated area Intraoral ruptured bullae surrounded by an intammatry ara; tips may show hemoragic trusts; the “is,” or “target,” lesion onthe skin is pathognomonic; patient may have severe signs of toxic Usual (70%) presents with orl lesions fag- ile ruptured bul and ulcerated oa reas; mostly in alder adits Wiitestiae in mouth; purplish nodules on skin at sites of fton; ocasionaly causes oa mucosal urs and erosive gingvts Protracted course with remissions and cxaceroatons: involvement of dferent sts ccurs slowly, glucocoricoids may tempo: ratlyrduce symptoms but donot contol the disease aseasiq yo suoneysoy Onset very rapt; usualy lepathi, but may be associated wih tigger such a drug reaction condion may lst 3-8 weeks rmortaly with EM major 5-159 i univetes With repeated occurence of ula, txicty may led to cachexia. infection, and death within 2 years; often controllable with oal lucocotcaids. Wiitestiae alone usally asymptomati: xosive lesions often dificult to treat, but may respond to glucocorteias Recurentaohthous uleers Behgets syndrome Traumatic ulcers Usually on nonkerati= rized oral mucosa (ou cal and labial mucosa, ‘oor of mau, sft pal sto, ateal and vor tongue) ral mucosa, eyes, genitalia gut and CNS Arynhere on oral mmucoss; dour tre- quently responsible for cer in vestule Single or listers of paint ulcers with sur- rounding enytematous border; esions may be 1-2 mm in dameter n crops (herpetior), 4-5 mm (ino, o 5-15 mm (majo) Multiple aphthous wears in mouty: lam rmatry ocular changes, ulcerative lsions on gontala; infammatory bowel cease and CXS Aisease Localize, ciscrete ulcerated lesion with Ted border produced by accidental iting of mucosa, penetation by a foreign object, or chronic itaton by a denture Leslons heal in 12 weeks but may recut monthly or several times a year, protective batter wih orabase and topical steroids gve symptomatic reli systemic glucocorcoids may be naoded in over cases Cal lesions often fst manietation; persist several wae and heal witout seareng Lesions usualy hel in 7-10 days when imtant is moved, unless secondary infected (continued) anrae) ‘saseasiq Jo uonewuasaig pue suonEIsoylueWY [eUIDIeD 22 TABLE 32-1 Vesicular, Bullous, or Ulcerative Lesions of the Oral Mucosa (Continued) 5 i ‘ny area inthe mouth, a User wit elevated, indurated borer: are to Invades and destoys undertying tissues; Squamous cel carcinoma most commonly oneal, pan ot prominent; esions tend to arse frequent metastasis to reional mph Toner i, tongue, and in areas of enytroveukoplekia orn smooth nodes for of mouth atrophic tongue ‘Acute myeloid Singva Gingival sweling and superficial ulceration fol- Usually respands to systomi treatment leukemia usualy lowed by hyperplsia of gingiva wih extensve of leukemia; occasionally requres local monocytic) necrosis and hemorthage: deep ulcers may radiation therapy ‘occur elsewhere onthe mucosa complicatod by secondary infection Lymphoma Singiva, tongue, palate Elvated, ulcerated area that may proliferate Fatal if untreated; may indicate underjing fandtonsiar area rapidly, ving the appearance of traumatic HIV infecton intamation Chemical or thermal Any area in mouth White slough ue to contact with corsive Lesion heals in severl weeks if not second- bums agents (9, asin, not cheese) applied ariyinfected locally removal of siough leaves raw, painful surface ote: 2, conta renave tr, ‘TABLE 32-2 Pigmented Lesions of the Oral Mucosa on Pe ft ct (ral melenote macule Any area of he mouth Dituse melanin ‘Any area ofthe mouth Pigmentation Nest ‘Any area ofthe mouth Malignant melanoma Any area ofthe mouth ‘Addison's disse Any area of he mouth but mostly buccal Poute-Jeghers syndrome fry area of the mouth Drug ingestion neurlep- Any area ofthe mouth tis, ral contacts, minooyane, zidovudine, auinine derivatives) ‘Amalgam tatoo Gingiva and alveolar Hayy metal pigmenta- Gingival margin tion (bismuth, mercury, eas) Black hay tongue Dorsum of tongue Fordyce “spots” Buccal and labial Kapos's sarcoma Palate most common, but may occur in any ober site Mucous retention cysts Buccal and labial Discrete or difuselocalzed, brown to black macule Diffuse pale to dark-brown pigmentation; may be physiologic (racial) or due to smoking Diseete, eal2ed, brown to back pigmentation ‘Can be fat and difuse, panes, brown to lack, or can be raised and nodular Bliches or spots of bluish-black to dark-brown pigmentation cccutng eal inte disease, accompanied by difuse pigmentation of skin other symptoms of adrenal insufficiency Datk-brown spots on ips, buccal mucosa, with cha. acteristic dstrbuto of pigment around lips, nose, ‘yes, and on hands; concomitant ints plposis Brown, black, or gray areas of pgmentation Small blue-back pigmented areas associated with ‘embedded amalgam particles in sot tissues; these i le eee Thin blue-black pigs sargis rarely soon xce to lead-based paint Elongation of form papa of tongue, which become stained by cof, tea tobacco, or pig ‘mentes bacteria Numerous smal yelowish sot just beneath mucosal surface; no symptoms; de to hyperplasia of sebaceous glands Red or blue plaques of variable size and shape: often enlarge, become nodular and may ulerate lin along gingival for children exposed Bhish-ear id-ed yst due to extravasated mucous from inured minor salivary gland Remain indeitly; no growth Bemains indefinitely Remain indetiitly Expands and invades eal; metastasis leads to death onion cone by adrenal sterid replacement (ral pigmented lesions remain indf- ‘ely; gastrointestinal polyps may ‘become malignant Gradual disappears feloingcesse tin of dug Bemains indefinitely Indicative of systemic absorption; no signicane for oral healt Improves within 1-2 weeks with gentle ‘rushing of tongue a discontinuation of antbiot if due to bacteral overgrowth Benign; remains witout apparent change Usual ndtv of HV infection or non- Hodekin'smphoma: rarely ft, but may ‘que treatment for comfort or cosmesis Benign: painless unless traumatized may be removed sugicalyTABLE 32-3 White Lesions of Oral Mucosa CT CIT = Ueten pana Be muna, inge, Stag, hl pag dans, arm, Protect: ponds oe als pe pee hoger eee Scant, ere eu aos ay ln Vie ogee vag Pan vie Hila of pl: adr? Brg nd pean ea ae cary tient an Sickle Any se ofr mucosa, Wt pat at may Became fen, gh, Mayor nay ote vincxsin fad tmtatce sitetes tend” leedsatolen ros my booms Sead TBI 7 ap eqn cl 2 tones oon benlnt abt pat apes cxcrana ety Deo seta 5 a a a Ec ie cewtautwnte” en ngs an l- pace roo wet ce os abet Fa patches ‘cal mucosa in women a candidiasis ‘ay area in mouth Pssusemambranous toe (tus) creamy white Rasponds favorably to antungal Ey Clr paces altel ara stacey an coecion et pdspsg shen sctge mandible dalled ety rae wre ose s pelts tig hgh dss of iste g brn ts ars wt) AS s Enters dete, onwiner oe weeshh Case saneastorpeeutmenin- = ecarereese las nas 2 Cand opts nonremovable white hckering Respond o prolonged antungal & stentabon de Cats tewy = Angular chsiltis: sore fissures at corner of mouth Responds to topical antifungal therapy a oy lokopaa Usa atl nq, ite reas angi tom sal an fai tense Du EV: ress igh se & oy bas ca ene vele aad tideame wel oho ican eee g ee ‘croup or ADS Eomiotuesr scapes = wh Cua g Wars apems- Aryan sin and Sin or mull psly eons, wi ck wiles ow py nd pod ‘s calms ferried urea ong my pote poee- cana saamous co eran ard tions; cauliflower lesions covered wih nrmalcalored rue out wit biopsy; excision o laser mucosa or multiple pink o pale bumps (ocal epithelial therapy; may regress in HI infected pela) patients on antiretroviral therapy Esai Bar vs TABLE 32-4 Alterations of the Tongue oo Sein Size or Morphology Changes Macrogtossia Enarged tongue that may be ar of syndrome fund n develpmental condtns suchas Down syndrome, Simpson Golab-Benmal syndrome, o Becket Wederannsynomme may be cue to unr themangoma or mphangioma), melabolidseas such as primary myiasis), o endocrine diurbance (such a acromegaly or eens) Fsured (seta) tongue Dorsal surface and sides of tongue covered by painless shallow or deep fissures that may collect debris and become inate Mean rhomboid glossis Congenital abnrmaliy of tongue with ovoid, denuded area in median poster parton af the tongue may be associated with candidiasis and may respond to antifungals Color Changes “Geographic” tongue Asymptomatic inlammetory condition ofthe tongue, wth rapid oss and regrowth of iform papillae, leading to (benign migratory ghosts) appearance of denuded red patches “wandering” across the surface of the tongue Hairy tongue Elongation of form pape of he media oral surface area de to flue of keratin lye ofthe pape to desquamate normaly; eounish-ck coloration may be dust ting by tobacco, fod, or chromogenic organisms *Stawbery” and ‘Appearance of tongue during scarlet fever due tothe hypertrophy of fungform papillae pus changes in the fifrm “raspbery’ tongue papilae Bald tongue ‘Avophy may be associated wih xerostamia, pernicious anemia, on-defiieney anemia. pallagra, or syphilis; may be accompanig by painful buming sensation; may bean expression of erythematous candace and expend 0 antifungals 273