Oral Infections PDF

Oral Infections Dr. Dilara Kazan Department of Oral&Maxillofacial Surgery Coccal infections of perioral area (pyoderma) • Pyoderma • • Staphylococcus / streptococcus Infectious disease of the skin- rarely seen in oral mucosa too (streptococcus stomatitis) Etiology: -saprofitic cocci In case of...

Oral Infections Dr. Dilara Kazan Department of Oral&Maxillofacial Surgery Coccal infections of perioral area (pyoderma) • Pyoderma • • Staphylococcus / streptococcus Infectious disease of the skin- rarely seen in oral mucosa too (streptococcus stomatitis) Etiology: -saprofitic cocci In case of immunocompromising situations: diabetes, leukemia, virus infection. Especially in children, any predisposing infection can be triggering. Injury-pressure wound to the tissue: local loss of resistance. • • • coccal infections of perioral area (acute pyoderma) • • • • • • • Impetigo contagiosa The most common bacterial skin infection in children. Staphylococcus aureus and less often Streptococcus pyogenes are the causes. Clinically, two types have been described: bullous and nonbullous. The perioral area is a commonly affected site. The diagnosis is based on clinical examination. The infection is transmitted by direct skin contact. Predisposing factors are warm and wet weather, minor skin trauma, and states of immunosuppression. • • • • • • • Can easily inoculate to the surrounding tissues In pediatric population: generally streptococcus Adult population: staphylococcus Especially in the perioral area When bulla and pustulas are severed: scab formation With scratching, focuses may be disseminated over the face. In oral mucosa: ulcerous areas and sometimes widespread infection • • Clinical features Clinically, the nonbullous type appears as red macules, 2 to 4 mm in diameter, which quickly evolve into a vesicle or pustule, then rupture, leaving a superficial erosion covered with “honey-colored” yellow crust. The lesions extend to the surrounding healthy skin. The most frequently affected ar- eas are the face, around the mouth, and nose. Mild lymphadenopathy may be present. • • • • • • • • Differential diagnosis Herpetic infection Chickenpox Candidiasis Eczema Insect bite Pemphigus • Pathology • Usually, not required. Microscopically, spongiosis and neutrophilic vesicles and pustules develop within the epidermis, while the dermis exhibits infiltration by neutrophils, lymphocytes, and eosinophils. Microbiological testing may be necessary in some cases. • Treatment • Topical antibiotic treatment with mupirocin or fusidic acid, cream or ointment, is effective and consists the first line of treatment. In patients with extensive disease, oral antibiot- ics such as erythromycin and penicillinase-resistant penicillin (e.g., flucloxacillin) are indicated. Other choices are first- or second-generation cephalosporins. coccal infections of perioral area (acute) • Fronculus/fruncle • • • • Abscess in the hair follicles, Staph. aureus. Carbuncle: infection multiple fronculus Most frequently seen in arms, legs, hairy skin. Foliculitis coccal infections of perioral area (acute) • • • • • Acute lymphangitis Group A strep Rarely staph aureus Local erythema, fever, pain, general tiredness-lethargy Painful lymphadenopathy and erythema along the trajectory of lymph nodes. coccal infections of perioral area (chronic pyoderma) • • • • • Erysipelas Common cause is S. pyogenes (group A). The infection usually affects the face and the lower extremities. The oral mucosa is not involved. (rarely) The diagnosis is based on clinical criteria. • Erysipelas is an acute skin bacterial infection primarily involving the dermis and lymphatic vessels. The disease is nearly always caused by group A streptococci (S. pyogenes). The sites of predilection are the lower extremities and the face. • • • Clinical features The oral mucosa is not involved. However, in cases of facial erysipelas, the redness and edema may extend to the vermilion border and the lip mucosa After an incubation period of 3 to 5 days, abrupt onset of fever, chills, nausea, malaise, and headache usually occur. Soon after, the skin lesion appears. Clinically, erysipelas is characterized by a shiny, hot, edematous, bright red, and slightly elevated plaque, which is sharply demarcated from the surrounding healthy skin and may show small vesicles. The disease may recur and cause permanent edema of the lips. • • • • • Differential diagnosis Cellulitis Herpes zoster Angioedema Contact dermatitis • • • • Discoid lupus erythematosus Other facial infections • Pathology • There is usually no need for laboratory tests. Histologically, diffuse edema with neutrophilic and eosinophilic infiltra- tion of the dermis along with lymph vessels dilatation are the principal features. The detection of Streptococcus with direct immunofluorescence and latex agglutination tests or culture could prove helpful in some cases. The circulating antibodies against Streptococcus could be useful. • Treatment • Oral antibiotics, especially penicillin for 10 to 15 days, or alter- natively, erythromycin for 7 to 12 days are the first-line choice for treatment. bacterial mucosal infections • • • • • Necrotizing Ulcerative Stomatitis A rare complication of necrotizing ulcerative gingivitis. Fusiform bacillus, Borrelia vincentii, and other anaerobic microorganisms are the most common associated bacteria. It is more common in immunocompromised individuals and HIV-infected people. Necrotizing ulcerative gingivitis may on occasion extend be- yond the gingiva and involve other areas of the oral mucosa. In such cases, the term necrotizing ulcerative stomatitis is used. Rarely, the disease may occur in the absence of ulcerative gingivitis. • Clinical features • Clinically, the oral mucosa is red, ulcerated, with ulcers with irregular margins, and may be covered with a dirty, white- grayish smear • The buccal mucosa, opposite the third molar, is the most commonly affected area. Rarely, it may involve the tongue, lips, and palate. The onset of the disease can be sudden or insidious. Necrotizing ulcerative stomatitis can be a manifestation of HIV infection, but rarely appears in non–HIV-infected patients. The presence of gingi- val lesions is of diagnostic significance. The diagno- sis is based on the history and the clinical features. • Differential diagnosis • Agranulocytosis • Neutropenia • Leukemia • Major aphthae • Wegener’sgranulomatosis • Langerhans cell histiocytosis • • • • Syphilis,secondstage Tuberculosis Noma Scurvy • Pathology • Laboratory tests are not recommended. Relevant tests should be applied only if it is necessary to exclude other diseases. • Treatment • In addition to debridement of local deposits, systemic met- ronidazole 500 mg every 8 hours, for 6 to 7 days is the most common therapeutic scheme. Other antibiotics can be used. Mouthwashes with oxygenproducing elements are also help- ful. If the patients do not respond to antibiotics, an underlying systemic disease should be suspected and investigated. bacterial mucosal infections • Streptococcus gingivostomatitis • • • • A debatable infectious oral disease. The infection is usually caused by β-hemolytic Streptococcus. The gingiva and tongue are common oral sites of involvement. The oral lesions can be preceded by streptococcal tonsillitis. • Streptococcal oral infection is a debatable disease caused by βhemolytic Streptococcus. It is a rare entity. The causative role of streptococci is controversial because it is not clear whether streptococcal infection is the primary cause or whether it rep- resents a secondary infection of pre-existing lesions. • Clinical features • The disease is usually localized on the gingiva, tongue, and rarely in other oral areas • Frequently, the oral le- sions follow tonsillitis or upper respiratory tract infection. Clinically, redness, edema of the gingiva, and patchy superficial, round, or linear erosions covered with a white-yellowish smear are observed. The interdental papillae remain intact. The disease is localized and rarely involves the entire gingi- val tissues. Mild fever and submandibular lymphadenopathy are also present. The clinical diagnosis should be confirmed by laboratory tests. • • • • Differential diagnosis Herpetic gingivostomatitis Necrotizingulcerativegingivitis Staphylococcal infection • • • • Pathology Gram staining and culture may confirm the clinical diagnosis. Treatment It consists of oral antibiotics, primarily oral penicillin 500 to 750 mg/d for 6 to 8 days. Erythromycin 250 to 500 mg every 8 h/d or clarithromycin 250 to 500 mg twice a day for 4 to 6 days may be used. bacterial mucosal infections • Noma (Cancrum Oris) • • • • A multifactorial, rare, rapidly progressive disease. Spirochete and anaerobic infection together with local and systemic predisposing factors are the cause. Gangrenous necrosis is the presenting clinical feature. Occasionally, the lesions may perforate the facial skin and jaw bones. • Cancrum oris or noma is a rare, rapidly progressive, and severely destructive disease, usually involving the oral tissues. It more commonly affects children and rarely adults, particularly in socioeconomically deprived areas of Africa, Asia, and South America. It is extremely rare in Europe and North America. Fusospirochetal microorganisms, Staphylococcus aureus, Streptococcus species, and Pseudomonas aeruginosa are almost always present in the lesions. Predisposing factors may be local or systemic and include poor oral hygiene, severe protein malnutrition, systemic infections and parasitic diseases, diabetes mellitus, leukemia, HIV infection and AIDS, malignancies, and immune defects. • Clinically, cancrum oris frequently begins as acute necrotizing ulcerative gingivitis that quickly spreads to the neighboring oral tissues. Gangrenous necrosis involves the buccal mucosa, lips, and the underlying bone, producing catastrophic lesions of the face. The gangrenous ulcers have an irregular border and are covered with whitish-brown fibrin and debris. Hypersalivation, halitosis, malaise, fever, and regional lymphadenopathy are always present. The diagnosis is usually based on clinical criteria. • • • • Differential diagnosis Burkitt’s lymphoma Malignant tumors Leukemia • • • • Agranulocytosis Systemic fungal infections Tuberculosis Latesyphilis • Pathology • Microbiological culture of exudates may be necessary to determine the choice of antibiotics in resistant cases. • Treatment • Without treatment, the disease is frequently fatal. Antibiotics, e.g., high-dose penicillin IV (10–20 MIU daily) and metronidazole 2 to 3 g/d are the medications of choice. Hydration and a nutritious diet as soon as possible are important. Surgical reconstruction should follow after stabilization of tissue destruction. This may sometimes even be undertaken when there is acute disease. bacterial mucosal infections • • • • • • • Gonococcus stomatitis The most common sexually transmitted disease caused by the gramnegative diplococcus Neisseria gonorrhoeae. Primarily involves mucous membranes of genital tract, anus, and rectum. The pharynx and oral mucosa are less frequently affected. The microorganism is transmitted after direct sexual contact with an infected person. Currently, third-generation cephalosporins are the drugs of choice for gonococcal infection. Systemic dissemination may cause signs and symptoms in many other organs. • Clinical features • Gonococcal stomatitis is a rare disease without specific clinical signs. Clinically, the oral mucosa is red, inflamed, and the patient complains of itching and burning. Rarely, erosions covered with a whitish pseudomembrane may occur. The soft palate, buccal mucosa, and gingiva are more frequently affected • Gonococcal pharyngitis is more common than oral disease and can manifest as a sore throat, a diffuse or patchy erythema and edema, with or without tiny pustules on the tonsillar pillars and uvula. Notably, oral gonococcal infection may be asymptomatic. The clinical diagnosis should be confirmed by laboratory tests. • • • Differential diagnosis Streptococcal stomatitis Herpetic infection • • • Herpangina Candidiasis Infectious mononucleosis • Pathology • Identification of the microorganisms by Gram’s stain, or culture, or molecular biological techniques establishes the definitive diagnosis. • Treatment • Oral lesions are self-limited and colonization usually disappears within 3 months. Third-generation cephalosporins (e.g., ceftriaxone 125 mg injection in a single dose or ciprofloxacin, 500 mg as single dose or ofloxacin 400 mg as single dose) are the drugs of choice. bacterial mucosal infections • • • • • • Actinomycosis The cause is the gram-positive anaerobic bacterium Actinomyces israelii, which is part of the normal flora of the mouth. The disease is classified into three forms: cervicofacial, pulmonary, and abdominal. Characteristic clinical signs of the cervicofacial type are swelling, induration, and fistulas formation with outflow of pus containing the characteristic sulfur granules. The drug of choice is penicillin. Actinomycosis is a subacute or chronic granulomatous infectious disease due to A. israelii, a gram-positive anaerobic bacterium. With anatomical criteria, disease is classified into three forms: (a) cervicofacial, (b) pulmonary/thoracic, and (c) abdominal. Oral lesions develop in the cervicofacial form, which constitutes around 50 to 60% of cases. The infection is endogenous resulting from the bacterium of the normal oral flora entering to the soft tissues following injury, tooth extraction, open nonvital tooth, fracture of the jaw, or tonsillitis, etc. It may then be extended to the salivary glands, bone of the jaw, and skin of the neck and face. • Clinical features • Clinically, at the site of inoculation, there is an inflammatory swelling that grows slowly, is usually painless, and characteristically hard on palpation • As the lesion progresses, multiple abscesses and draining sinuses form, usually on the skin of the face and upper neck • Yellow purulent material that represents colonies of Actinomyces (sulfur granules) may discharge from these sinuses. As the disease becomes chronic, healing of old lesions results in scar formation, but new abscesses and sinuses develop. Mandibular or maxillary involvement may be severe and usually is associated with trismus. Common oral locations of actinomycosis are the tongue, lips, buccal mucosa, submandibular and submental area. The clinical diagnosis should be confirmed by histologic and microbiological examination. • Differential diagnosis • Tuberculosis • Systemic mycoses • Abscess of oral soft tissues • Dental and periodontal abscess and fistula • Other bacterial infections • Benign and malignant tumors • Pathology • The histologic examination reveals a granulomatous reaction with pus collection. Histiocytes, epithelioid cells, plasma cells, and neutrophils can be observed at the periphery of the abscess, while in the center, the characteristic granules of the Actinomyces colonies known as “sulfur granules” are seen. These granules exhibit basophilic staining centrally and peripherally eosinophilic, with the use of common hematoxylin-eosin stain • Treatment • Intramuscular penicillin G (e.g., 10–20 MU/d for 4–6 weeks) is the drug of choice for early cervicofacial actinomycosis. This regimen is usually followed by oral penicillin V (e.g., 500 mg four times daily for 1–3 months). Localized, limited disease usually responds well to a combination of surgical removal of the infected tissues and a 2- to 4-week course of penicillin. Tetracycline 500 mg three to four times daily for 2 to 4 months may be used as an alternative drug for patients allergic to penicillin. Intramuscular or intravenous ampicillin 50 mg/kg/d for 4 to 6 weeks, followed by oral amoxicillin 500 mg/d for 6 to 12 additional months can be given to prevent recurrences. Surgical procedures such as drainage and resection can be combined with drug therapy. Oral mucosa in specific infections • • • • • • Leprosy Chronic infectious disease caused by the bacillus Mycobacterium leprae. Slowly progressive disease characterized by granuloma formation and • neurotropism with a predilection for skin and the peripheral nerves. The mouth is affected at a rate of 10 to 20%, mainly in the lepromatous form. • The drug therapy has greatly improved the disease prognosis. Leprosy is a chronic, systemic granulomatous infectious disease caused by the bacillus M. leprae. It is transmitted from person to person and is endemic mainly in Africa, Asia, South America, Japan, and less in Mediterranean countries, including Greece. Transmission of the bacillus is difficult and requires a long • period of promiscuity with the patient, while the incubation period ranges from 4• to 10 years. Leprosy affects the skin, mucous membranes, nerves, bones, and • viscera. On clinical, bacteriologic, immunologic, and histopathologic criteria it is • classified into six forms: two main types with lepromatous at one end, • tuberculoid at the other end, and three borderline types (two with features close • to the two main types, and one with a mixture of features), and finally indeterminate leprosy (unspecified form). • • • Clinical features • There is a wide spectrum of clinical manifestations of leprosy. The disease primarily involves the peripheral nervous system and the skin. In the tuberculoid form, skin patches or plaques appear which are red or reddish-brown in color, • and stand out clearly from healthy skin due to their deep colored halo; they are • mainly located in the buttocks and legs. In this form, the main signs are neurologic disorders (loss of sensory, analgesia, neuralgia). The lepromatous form is characterized by patches and papules, but mostly reddish nodules, solitary or confluent, called lepromata and identified mostly on the face and ears, creating the characteristic lion-like faces “leonine facies.” Neurologic disorders are rarer in this form. The borderline forms are characterized by lesions of both the previous types, while the indeterminate leprosy manifests with discolored unspecified spots or patches on the skin and, neurologic disorders that are rarely present. The mouth is affected, usually in lepromatous form in 10 to 20% and especially in the end stages of the disease. Clinically, oral lesions appear as multiple small, red nodules (lepromas) that progress to necrosis and ulcerations which cause atrophic scars and tissue destruction. The palate, dorsum of the tongue, lips, and gingiva are most frequently affected. Rarely, in late stages, the anterior part of the maxilla may be involved resulting in loss of anterior teeth. Differential diagnosis Syphilitic gumma Nasal-type non-Hodgkin’s lymphoma from natural killer (NK)/T cells Systemic mycoses Malignant neoplasms Traumatic lesions Pathology Microbiological testing for bacillus in nasal secretion and a thick drop of blood will assure the diagnosis. Histologic examination and the lepromin or Mitsuda test may be useful. Treatment In the recent years, the World Health Organization (WHO) guidelines have been used with great success. A multidrug therapy scheme is used including dapsone, clofazimine, rifampin, ofloxacin, and minocycline. Oral mucosa in specific infections • • • • • • • • • • • • • Syphilis • Syphilis is a sexually transmitted infection caused by Treponema pallidum. The disease may be congenital or acquired. Syphilis is clinically classified into primary, secondary, and tertiary stages with a • • latent (early and late) period preceding the tertiary stage. Oral manifestations may occur in all clinical stages. The diagnosis is based on direct detection of T. pallidum and various serologic tests. Penicillin G is the treatment of choice for all stages of the disease. The modern classification of syphilis is based on epidemiologic, clinical, and • therapeutic criteria, and is as follows: early syphi- lis (which includes primary • • and secondary stages and clinical relapses due to incomplete treatment and lasts < 1 year), latent syphilis, which is subclassified into early stage (lasts a • year or less) and late stage (lasts more than a year), and late syphilis, also called• • tertiary syphilis because of untreated disease. • Primary Syphilis The primary lesion of acquired syphilis is the chancre. It is usually localized on • the genitalia, but in approximately 10% of the cases, it may occur extragenitally • and especially in the oral cavity. Direct orogenital contact is the usual mode of • acquisition of an oral chancre. After an incubation period of 10 to 90 days (average, 21 days), the chancre appears at the site of inoculation. Clinically, the chancre begins as an inflammatory papule that soon erodes. The classic chancre ap- pears as a round or oval painless ulcer with a smooth surface, raised border, and indurated base. It is often surrounded by a narrow red border and is covered by a grayish serous exudate teeming with T. Pallidum. The chancre is usually solitary, although multiple lesions may appear simultaneously or in rapid succession. It varies in size from a few millimeters to 3 cm in diameter. A constant finding is enlarged regional lymph nodes, which are usually unilateral and less often bilateral. The enlarged lymph nodes are discrete, mobile, hard, and nontender. Without treatment, the chancre heals spontaneously within 3 to 8 weeks. The diagnosis of primary syphilis is based on the history, clinical features, and bacteriologic and serologic tests. Pathology Dark-field microscopic identification of T. pallidum in smears taken from the surface of chancre is the most sensitive and specific test for the diagnosis of primary syphilis. Serologic tests for syphilis must always be performed, but it should be remembered that during the very early primary phase, these tests may be negative. Differential diagnosis Traumatic ulcer Angular cheilitis Aphthous ulcer Behçet’s disease Tuberculous ulcer Herpes simplex Eosinophilic ulcer Infectious mononucleosis Squamous cell carcinoma Oral mucosa in specific infections • Secondary syphilis • The signs and symptoms of secondary syphilis begin 6 to 8 weeks after the appearance • of the chancre, which may still be present at the time of initiation of this stage. • The clinical features of secondary syphilis are classified into two major groups: constitutional symptoms and signs and general- ized mucocutaneous manifestations. The• former may precede or accompany mucocutaneous lesions and include malaise, low• grade fever, headache, lacrimation, sore throat, loss of appetite, weight loss, polyarthralgias and myalgias, systemic lymphade- nopathy (which is a classic and constant finding), along with splenomegaly. The enlarged lymph nodes are painless, discrete, mobile, and hard-rubbery on palpation. Generalized mucocuta- neous manifestations include pruritus, nail involvement, macu- lar, papular, pustular, nodular, • follicular, and other lesions. • • Mucous membrane lesions are multiple and frequent and may appear alone or in • association with skin lesions. These lesions usually last for 2 to 10 weeks and disappear • without scarring. • • • Macular syphilides: Macular syphilides (roseolas) are the earliest manifestations of secondary syphilis; they last for a few days and usually go unnoticed. In the oral mucosa, • mac- ular syphilides are most frequently found in the soft palate. Clinically, they appear • as multiple red oval spots. • • Mucous patches: Mucous patches are by far the most fre- quent oral manifestation of • secondary syphilis. They are flat or slightly raised, painless, oval or round papules with ero- sions or superficial ulcers covered by a grayish-white membrane. They are teeming with spirochetes and are extremely contagious. Occasionally, mucous patches may be the only manifestation of secondary syphilis for a long period of time. • Papular syphilides: Papular syphilides are the most com- mon and characteristic lesions of secondary syphilis on the skin, but they are rare in the oral mucosa. Alopecia and nail involvement are common. The oral lesions usually coalesce, forming slightly raised, painless, firm, and round nodules with a grayish-white color. The le- sions have a tendency to ulcerate and are usually located on the commissures and buccal mucosa and rarely in other areas. Papular syphilides and mucous patches are always associated with bilateral, regional lymphadenopathy. • Condylomata lata: In moistened skin areas, the eroded papu- lar syphilides have the tendency to coalesce and hypertrophy, forming elevated, vegetating, or papillomatous lesions, the con- dylomata lata. The most frequent localizations of condylomata lata are the perigenital and perianal area, axillae, submammary and umbilical areas. Condylomata lata rarely appear in the oral cavity, usually at the corners of the mouth and the palate. They appear as painless, slightly exophytic, multiple lesions with an irregular surface and are contagious. Pathology Dark-field microscopic examination and immunofluores- cence for the detection of T. pallidum may be a helpful di- agnostic tool. In addition, serologic tests (Venereal Disease Research Laboratory [VDRL], rapid plasma reagin [RPR], fluorescent treponemal antibody absorption [FTA-ABS], T. pallidum immobilization [TPI], T. pallidum hemagglutination assay [TPHA]) give more distinctive results in secondary syphilis. Differential diagnosis Candidiasis Lichen planus Leukoplakia Aphthous ulcers Herpetic stomatitis Erythema multiforme Trauma Infectious mononucleosis A plethora of other oral lesions that may mimic secondary syphilis Oral mucosa in specific infections • Interstitial glossitis: Late syphilis of the tongue may occur either as a solitary gumma or most commonly as a diffuse gumma- tous infiltration, which heals spontaneously, leading to interstitial glossitis. This is the result of After a latency period of 2 to 10 years or more, untreated syphi- lis may progress to severe clinical contracture of the lingual musculature after the gumma has healed. The tongue appears smoothly lobular with manifestations of late syphi- lis. The main manifestations of late syphilis are mucocutaneous lesions, irregular deep figures. Leukoplakia and squamous cell carcinoma may be a complication. cardiovascular manifestations, central nervous system (CNS), and bone lesions. Late syphilis is rare in many • Differential diagnosis Western countries nowadays. The oral lesions of late syphilis include gummas, atrophic glossitis, and • Fissured tongue interstitial glossitis. • Amyloidosis Gummas: A gumma is a syphilitic granulomatous lesion that originates as a subcutaneous mass secondarily extending both to the epithelium and the deeper tissues. Gummas appear ini- tially as painless elastic swellings • Benign and malignant tumors that have a tendency to ne- crose, forming a characteristic stringy mass. A punched-out ulcer forms and finally heals, leaving a scar. The size varies from 1 to 10 cm. The sites of predilection are the legs, scalp, face, and chest. Gummas are frequently located on the hard palate, which they may destroy and perforate. The lesion • Treatment may also involve the soft palate and rarely other oral regions. • Penicillin G is the treatment of choice for all stages of syphilis. The schedules and dosages are internationally Differential diagnosis established and depend on the stage of the disease. If penicillin allergy exists, erythromycin or cephalosporins Squamous cell carcinoma or other malignant tumors may be administered. The treatment of syphilis should be left to appropriate specialists—as medication can Leprosy vary between units and regions. Extranodal natural killer (NK)-/T-cell lymphoma, nasal type Other non-Hodgkin’s lymphomas • Congenital syphilis • Congenital (prenatal) syphilis reflects vertical transmission in utero. It is classified as early if the disease manifests before the age of 2 years, late if it becomes apparent after 2 years, and stigmata, which are developmental changes without active infection. The most common stigmata are high-arched palate, short mandible, rhagades at the commissures, saddle nose, frontal bossing, Hutchinson’s teeth, and dysplastic molars. • The dysplastic permanent incisors, along with interstitial keratitis and eighth nerve deafness, comprise the classic Hutchinson’s triad, and are the most common findings of congenital syphilis. Clinically, the upper central permanent incisors are widely spaced and shorter than the lateral incisors. They are conical or barrel-shaped at the incisal edge and are usually smaller at the cervical margins. Notched areas of the incisal edge may be present. Similar changes may exist in the lateral incisors and the teeth may be irregularly spaced. Atrophic glossitis: The tongue is frequently involved in late syphi- lis. Clinically, there is atrophy of the filiform • The permanent first molars may be dysplastic (Moon’s molars, Fournier’s molars, mulberry molars). Usually, and fungiform pa- pillae, and the dorsum becomes smooth and atrophic. Vasculitis ending in an obliterative the first lower molars are affected. Affected molars are narrower on their occlusal surfaces and have endarteritis is the process of the underlying changes. Atrophic syphilitic glossitis may lead to the development supernumerary cusps. of leukoplakia and squamous cell carcinoma. Differential diagnosis Lichenplanus,atrophic form Leukoplakia Plummer-Vinsonsyndrome Megaloblastic anemia • Late syphilis • • • • • • • • • • • • •