Transcript SOFT TISSUE TUMORS

BACTERIAL/FUNGAL/VIRAL
INFECTIONS
SYPHILIS
SYPHILIS
• Chronic infection caused by Treponema
pallidum
• Transmitted by sexual contact or from
mother to fetus
• Proceeds through three stages: primary,
secondary, and tertiary
• Patient is infectious in the primary and
secondary stages
SYPHILIS
• Primary syphilis
– Chancre
• Usually solitary; arises 3-90 days after
exposure
• Papular lesion with a central ulceration
• Most common on the lip
• Regional lymphadenopathy
• Heals in 3-8 weeks
SYPHILIS
• Secondary syphilis
– Occurs 4-10 weeks after initial infection
– Systemic symptoms: painless
lymphadenopathy, sore throat, malaise,
headache, weight loss
– Diffuse, painless, maculopapular
cutaneous rash
SYPHILIS
• Secondary syphilis
– Mucous patches (exocytosis and spongiosis)
in the oral mucosa
– Condylomata lata
– Multiple lesions are common
– Spontaneous resolution occurs in 3-12 weeks
SYPHILIS
• Tertiary syphilis
– Develops 1-30 years after a latent stage
(latent syphilis)
– Serious complications: cardiovascular
system and central nervous system
– Granulomatous inflammation of the
skin, mucosa, soft tissue, bones, and
organs
SYPHILIS
• Tertiary syphilis
– Gumma: active sites of granulomatous
inflammation
– Intraoral lesions involve the palate and
tongue: palatal perforation and luetic
glossitis
SYPHILIS
• Congenital syphilis
– Hutchinson’s triad:
• Hutchinson’s teeth (Hutchinson’s
incisors and mulberry molars)
• Ocular interstitial keratitis
• Eighth nerve deafness
SYPHILIS
• Histopathologic features
– Primary and secondary forms:
• Perivasculitis (lymphocytes and plasma cells)
• Corkscrew-like organisms
– Tertiary form:
• Granulomatous inflammation
• Organisms are hard to identify
SYPHILIS
• Diagnosis
– VDRL (Venereal Disease Research Laboratory)
and RPR (rapid plasma reagin): serologic
screening tests - nonspecific; only positive in
the first two stages
– FTA-ABS (fluorescent treponemal antibody) and
TPHA (T. pallidum hemagglutination assays):
serologic tests - specific; positive in all three
stages
SYPHILIS
• Treatment and prognosis
– Penicillin
– Erythromycin or tetracycline:
penicillin allergy
TUBERCULOSIS
TUBERCULOSIS
• Chronic infectious disease caused by
Mycobacterium tuberculosis
• Acquired by direct person-to-person spread
through airborne droplets from a patient with
active disease
• Primary tuberculosis:
– Occurs in a previously unexposed
individual
– Almost always involves the lungs
TUBERCULOSIS
• Primary tuberculosis:
– Chronic inflammatory reaction
– Fibrocalcified nodule at the initial site of
involvement
– Viable organisms may be present for life
• Secondary tuberculosis:
– Reactivation of organisms in a previously
infected person
– Causes active disease
TUBERCULOSIS
• Secondary tuberculosis:
– Usually associated with immunosuppression
• Old age, poverty, crowded living condition,
AIDS
• Clinical and radiographic features:
– Primary tuberculosis
• Asymptomatic
• Fever, pleural effusion
TUBERCULOSIS
• Clinical and radiographic features:
– Secondary tuberculosis
• Low-grade fever, malaise, weight loss, night
sweats, cough, hemoptysis
• Extrapulmonary lesions:
–Skin, skeletal system, CNS, kidneys,
cervical lymph nodes, larynx, middle ear
TUBERCULOSIS
• Clinical and radiographic features:
– Secondary tuberculosis
• Oral lesions
–Chronic painless ulcer
–Due to hematogenous spread or
exposure to infected sputum
–Gingiva, tongue, palate, lip
TUBERCULOSIS
• Clinical and radiographic features:
– Secondary tuberculosis
• Scrofula
–Enlarged oropharyngeal lymphoid
tissue and cervical lymph nodes
–Due to contaminated milk
–Fistulas of the overlying skin
–Calcified lymph nodes
TUBERCULOSIS
• Histopathologic features
– Granulomatous inflammation
– Central caseous necrosis
TUBERCULOSIS
• Diagnosis
– Mantoux or PPD skin test:
indicates exposure to the
organisms
– Culture of infected sputum or
tissue
TUBERCULOSIS
• Treatment and prognosis
– Multiagent therapy
• Isoniazid, rifampin, pyrazinamide,
ethambutol, streptomycin
ACTINOMYCOSIS
ACTINOMYCOSIS
• Acute, rapidly progressing or chronic, slowly
spreading infection associated with
Actinomyces israelii
• 55% of cases occur in the cervicofacial region
• Organisms enter the tissue through an area of
prior trauma: soft tissue injury, periodontal
pocket, nonvital tooth, extraction socket, or
infected tonsil
ACTINOMYCOSIS
• Organisms spread by direct extension through
soft tissue producing draining fistulas to the
skin surface
• Sulfur granules: yellowish flecks
• Most frequent site: skin overlying the angle of
the mandible
• Salivary gland involvement
ACTINOMYCOSIS
• Bone involvement
– Actinomycotic osteomyelitis; illdefined radiolucency
– Periapical involvement; anterior
maxillary teeth > mandibular first
molars
ACTINOMYCOSIS
• Histopathologic features
– Inflamed granulation tissue
– Colonies of organisms surrounded
by a collection of neutrophils
ACTINOMYCOSIS
• Diagnosis
– Culture
– Biopsy
ACTINOMYCOSIS
• Treatment and prognosis
– Prolonged high dose antibiotics
(penicillin)
– Abscess drainage and excision of
sinus tracts
– Early lesions respond in 5-6 weeks
– Deep seated infections may take 12
months to resolve
CAT-SCRATCH DISEASE
CAT-SCRATCH DISEASE
• Infectious disorder that begins in the skin
and spreads to the adjacent lymph nodes
• Most common cause of chronic regional
lymphadenopathy in children
• Arises after contact with a cat
• Causative organism is Bartonella henselae
• Papule or pustule along the initial scratch line
• Lymphadenopathy occurs within 3 weeks
CAT-SCRATCH DISEASE
• Fever and malaise
• Papule or pustule has often
resolved by the time the
lymphadenopathy is apparent
CAT-SCRATCH DISEASE
• Histopathologic features
– Stellate suppurative necrosis
surrounded by histiocytes and
neutrophils
CAT-SCRATCH DISEASE
• Diagnosis
– Serologic tests
• Indirect fluorescent antibody assay:
antibodies to B. henselae
• ELISA: IgM antibodies to B. henselae
• PCR: polymerase chain reaction
CAT-SCRATCH DISEASE
• Treatment and prognosis
– Self-limiting disease; resolves in 4
months
– Antibiotics: erythromycin or
doxycycline
– Local heat, analgesics
– Aspiration of the node
CANDIDIASIS
CANDIDIASIS
• Most common oral fungal infection in humans
• Majority of cases are caused by Candida
albicans
• 30%-60% of patients carry the organism in
their mouths
• 3 factors determine if clinical infection occurs:
– Immune status of the host
– Oral mucosal environment
– Strain of C. albicans
CANDIDIASIS
• Pseudomembranous candidiasis
– “Thrush”; milk curds
– Underlying mucosa is normal or erythematous
– Often caused by exposure to broad-spectrum
antibiotics or an impaired immune system
– Symptoms are mild and consist of burning or
an unpleasant taste
– Common on the buccal mucosa, palate, and
dorsal tongue
CANDIDIASIS
• Erythematous candidiasis
– Several subtypes:
• Acute atrophic or “antibiotic sore
mouth”
• Central papillary atrophy or median
rhomboid glossitis
• Chronic multifocal
• Angular cheilitis
• Denture stomatitis
CANDIDIASIS
• Acute atrophic candidiasis
– Occurs after the use of broad-spectrum
antibiotics
– Mouth feels as if a hot beverage has
scalded it
– Diffuse loss of the filiform papillae if the
dorsal tongue is affected
CANDIDIASIS
• Central papillary atrophy
– Median rhomboid glossitis
– Failure of the tuberculum impar to involute
– Midline, posterior dorsal tongue;
symmetrical
– Asymptomatic
– Loss of the filiform papillae
CANDIDIASIS
• Angular cheilitis
– Involvement of the angles of the mouth
– Erythema, fissuring, and scaling
– Older individuals with reduced vertical
dimension
– 20% caused by C. albicans alone
– 60% caused by C. albicans and S. aureus
– 20% caused by S. aureus alone
CANDIDIASIS
• Denture stomatitis
– Chronic atrophic candidiasis
– Localized to the denture-bearing areas
– Patient wears the denture continuously
– Must rule out improper denture design,
allergy to the denture base, or inadequate
curing of the acrylic
CANDIDIASIS
• Chronic hyperplastic candidiasis
– Candidal leukoplakia
– Cannot be removed by scraping
– Least common form of candidiasis
– Usually located on the anterior buccal
mucosa
CANDIDIASIS
• Histopathologic features
– Exfoliative cytology or tissue sections
– PAS stain
• Hyphae or pseudohyphae (elongated
yeast)
• Hyperparakeratosis, acanthosis,
neutrophilic abscesses, chronic
inflammation in the connective tissue
CANDIDIASIS
• Treatment and prognosis
– Topical antifungal medications
• Nystatin, clotrimazole
– Systemic antifungal medications
• Fluconozole, itraconozole
HISTOPLASMOSIS
HISTOPLASMOSIS
• Most common systemic fungal infection in the
United States
• Caused by Histoplasma capsulatum
• Organisms grows in soil enriched with bird or bat
excrement
• Common in the Ohio and Mississippi River valley
regions
• Organisms are inhaled and germinate in the lungs
HISTOPLASMOSIS
• Most cases are asymptomatic or produce
few symptoms
• Organisms are ingested by macrophages
and T-lymphocyte immunity develops in 2-3
weeks
• Antibodies against the organisms appear
several weeks later
• 3 forms: acute, chronic, disseminated
HISTOPLASMOSIS
• Acute histoplasmosis
– Self-limited pulmonary infection
– Fever, headache, myalgia, cough
– Patients are ill for 2 weeks
– Calcification of the hilar lymph nodes
HISTOPLASMOSIS
• Chronic histoplasmosis
– Primarily affects the lungs
– Elderly or immunosuppressed patients
– Similar to tuberculosis
– Cough, weight loss, fever, dyspnea,
hemoptysis
HISTOPLASMOSIS
• Disseminated histoplasmosis
– Progressive spread to extrapulmonary
sites
– Elderly and immunosuppressed patients
– Oral lesions: tongue, buccal mucosa,
palate
• Painful ulceration of several weeks’
duration
HISTOPLASMOSIS
• Histopathologic features
– Diffuse infiltrate of macrophages
containing organisms (yeasts)
– Granulomas
HISTOPLASMOSIS
• Diagnosis
– Tissue sections or culture
HISTOPLASMOSIS
• Treatment and prognosis
– Acute form: supportive
– Chronic and disseminated forms:
amphotericin B, ketoconazole, or
itraconazole
– Mortality is 7%-23% with the
disseminated form
ZYGOMYCOSIS
ZYGOMYCOSIS
• Opportunistic fungal infection caused by one of
four genera of Zygomycetes: Absidia, Mucor,
Rhizomucor, and Rhizopus
• Organisms are found in decaying organic
material
• Spores are liberated into the air and inhaled
• Common in uncontrolled diabetics and
immunocompromised individuals
ZYGOMYCOSIS
• Common symptoms include: nasal obstruction,
bloody nasal discharge, facial pain or headache,
proptosis
• Involvement of the cranial vault leads to
blindness, lethargy, seizures, and death
• Massive tissue destruction with palatal
perforation, swelling of the maxillary alveolar
process, opacification of the sinuses
ZYGOMYCOSIS
• Histopathologic features
– Extensive necrosis
– Large branching, nonseptate hyphae
ZYGOMYCOSIS
• Treatment and prognosis
– Radical surgical debridement
– Amphotericin B
– Control underlying disease
– Prognosis is poor
HERPES SIMPLEX VIRUS
HERPES SIMPLEX VIRUS
• Two types of HSV: HSV-1 and HSV -2
• Two patterns of infection: primary and
secondary or recurrent
• Primary infection
– Initial exposure to the virus
– No antibodies in the circulation
– Occurs at a young age
– Often is asymptomatic (80%)
HERPES SIMPLEX VIRUS
• Secondary or recurrent infection
– Reactivation of the virus via axons of
sensory nerves
– Precipitated by old age, UV light, stress,
pregnancy, allergy, or trauma
– 50%-60% of adults are HSV-1 seropositive
HERPES SIMPLEX VIRUS
• Acute herpetic gingivostomatitis
– Most common pattern of symptomatic
primary HSV infection
– Peak age: 2-3 years of age
– Cervical lymphadenopathy, chills,
fever, nausea, anorexia
– Resolves in 7-14 days
HERPES SIMPLEX VIRUS
• Pharyngotonsillitis
– Primary infection in adults
– Sore throat, fever, malaise, headache
– Vesicles and ulcerations on the tonsils and
posterior pharynx
– Resembles streptococcal pharyngitis or
mononucleosis
HERPES SIMPLEX VIRUS
• Secondary or recurrent infection
– Usually occurs at the site of primary
inoculation
– Herpes labialis: 15%-45% of the US
population
– Oral mucosa: keratinized mucosa
– Resolves in 7-10 days
HERPES SIMPLEX VIRUS
• Histopathologic features
– Acantholysis, nuclear clearing,
nuclear enlargement (ballooning
degeneration), multinucleation
– Tzanck cells
HERPES SIMPLEX VIRUS
• Diagnosis
– Clinical presentation
– Viral culture: 2 weeks for results
– Antibody titers: positive 4-8
days after exposure
– Cytologic smear
– Tissue biopsy
HERPES SIMPLEX VIRUS
• Treatment and prognosis
– Primary disease
• Acyclovir suspension
• Nonsteroidal anti-inflammatory medications
– Secondary disease
• Acyclovir, valacyclovir, famciclovir,
penciclovir, foscarnet
VARICELLA
VARICELLA
• Primary infection with VZV
• Virus is spread through air droplets or direct
contact
• 5-9 years of age
• Most cases are symptomatic: rash begins on
face and trunk and then spreads to extremities
• Erythema, vesicle, pustule, and crust
VARICELLA
• Oral lesions
– Common on palate and buccal mucosa
– Painless
• Complications
– Reye’s syndrome, skin infections,
encephalitis, pneumonia
VARICELLA
• Histopathologic features
– Same as HSV
VARICELLA
• Diagnosis
– Cytologic smear
– Tissue biopsy
– Viral culture
– Antibodies to VZV
VARICELLA
• Treatment and prognosis
– Supportive
– Acyclovir, valacyclovir, famciclovir
– VZIG: varicella-zoster immune
globulin
• Immunocompromised patients
– VZV vaccine
HERPES ZOSTER
HERPES ZOSTER
• Reactivation of VZV; 10%-20% of individuals
• Single recurrence
• Predisposing factors
– Cytotoxic drugs, radiation, malignancies,
old age, alcohol abuse
• Three phases
– Prodrome, acute, and chronic
HERPES ZOSTER
• Prodrome: 90% of patients
– Intense pain in the area innervated by
the affected sensory nerve
– Present 1-4 days before exanthem
– Fever, malaise, headache
• Acute
– Vesicles, ulcerations, crusts: midline
– Resolves in 2-3 weeks
HERPES ZOSTER
• Acute
– Oral lesions
• Movable or nonmovable mucosa
• In conjunction with skin lesions
• Maxillary involvement may cause
devitalization of teeth
HERPES ZOSTER
• Acute
– Ocular lesions
• May cause blindness
– Ramsay Hunt syndrome
• Lesions of the external auditory
canal and facial paralysis
HERPES ZOSTER
• Chronic
– Postherpetic neuralgia
• Neuralgia-associated pain persists
for more than 3 months
• 15% of patients
• 50% of patients over 60 years of age
• Most cases resolve in 1 year
HERPES ZOSTER
• Histopathologic features
– Same as varicella and HSV
HERPES ZOSTER
• Diagnosis
– Clinical presentation
– Viral culture
– Cytologic smear
– Antibodies to VZV
HERPES ZOSTER
• Treatment and prognosis
– Supportive
– Acyclovir, valacyclovir,
famciclovir
INFECTIOUS MONONUCLEOSIS
INFECTIOUS MONONUCLEOSIS
• Caused by Epstein-Barr virus (EBV)
• Children: contaminated saliva on fingers or toys
• Adults: direct salivary transfer such as kissing
or shared straws
• Childhood exposure is usually asymptomatic
• Adulthood exposure is symptomatic
INFECTIOUS MONONUCLEOSIS
• Fever, lymphadenopathy, pharyngitis, tonsillitis
• Hepatosplenomegaly
• Oral lesions
– Palatal petechiae (25% of patients)
– Necrotizing ulcerative gingivitis
INFECTIOUS MONONUCLEOSIS
• Diagnosis
– Clinical presentation
– WBC count is elevated
– Lymphocytosis, atypical lymphocytes
– Paul-Bunnell heterophil antibody (90%)
– EBV-specific antibodies
INFECTIOUS MONONUCLEOSIS
• Treatment and prognosis
– Resolves in 4-6 weeks
– Supportive
HERPANGINA
HERPANGINA
•
•
•
•
Caused by coxsackievirus A 1 to 6, 8, 10, or 22
Most cases arise in the summer or early fall
Fecal-oral route of transmission
Acute phase: may be transmitted through saliva
or respiratory droplets
• Infection confers immunity against reinfection
to that one strain
HERPANGINA
• Sore throat, dysphagia, fever
• Oral lesions
– Vesicles or ulcers on the soft palate
or tonsillar pillars
– Resolve in 7-10 days
HERPANGINA
• Histopathologic features
– Intracellular and intercellular edema
– Intraepithelial and subepithelial
vesicles
– Epithelial necrosis and ulceration
HERPANGINA
• Diagnosis
– Clinical features
– Viral culture
• Treatment and prognosis
– Self-limiting
– Supportive
HAND-FOOT-AND-MOUTH
DISEASE
HAND-FOOT-AND-MOUTH
DISEASE
•
•
•
•
Caused by coxsackievirus A 16
Most cases arise in the summer or early fall
Fecal-oral route of transmission
Acute phase: may be transmitted through saliva
or respiratory droplets
• Infection confers immunity against reinfection
to that one strain
HAND-FOOT-AND-MOUTH
DISEASE
• Skin rash and oral lesions are associated with
flulike symptoms: sore throat, dysphagia, fever
• Skin lesions: macular, vesicles, crusts
• Oral lesions
– Buccal mucosa, labial mucosa, tongue
– Vesicles and ulcers
– Resolve in 1 week
HAND-FOOT-AND-MOUTH
DISEASE
• Histopathologic features
– Intracellular and intercellular edema
– Intraepithelial and subepithelial
vesicles
– Epithelial necrosis and ulceration
HAND-FOOT-AND-MOUTH
DISEASE
• Diagnosis
– Clinical features
– Viral culture
• Treatment and prognosis
– Self-limiting
– Supportive
HIV INFECTION
HIV INFECTION
• HIV-associated periodontal disease
– Linear gingival erythema
– Necrotizing ulcerative gingivitis
– Necrotizing ulcerative periodontitis
– Necrotizing stomatitis
HIV INFECTION
• Linear gingival erythema
– Linear band of erythema involving
the free gingival margin
– Punctate or diffuse erythema of the
alveolar mucosa
HIV INFECTION
• Necrotizing ulcerative gingivitis (NUG)
– Ulceration and necrosis of one or more
interdental papillae
– No loss of periodontal attachment
– Gingival necrosis, bleeding, pain and
halitosis
HIV INFECTION
• Necrotizing ulcerative periodontitis (NUP)
– Gingival ulceration and necrosis associated
with rapidly progressing loss of periodontal
attachment
– Multiple isolated defects
– Edema, severe pain, hemorrhage
– No deep pocketing
– Does not respond to conventional
periodontal therapy
HIV INFECTION
• Treatment of NUG and NUP
– Debridement combined with
povidone-iodine irrigation
– Antimicrobial therapy:
metronidazole, chlorhexidine
– Follow-up care
– Long-term maintenance
HIV INFECTION
• Necrotizing stomatitis
– Massive areas of tissue
destruction
– May involve soft tissue or bone
– Results in sequestration
HIV INFECTION
• Oral hairy leukoplakia
– Associated with EBV
– White mucosal lesions that
do not rub off
– Lateral border of the tongue
HIV INFECTION
• Histopathologic features
– Parakeratosis with or without candidiasis
– Surface corrugations
– Acanthosis with “balloon cells”
– Nuclear beading
HIV INFECTION
• Treatment
– None
– Acyclovir, desiclovir
– Zidovudine (AZT)