Infectious Diseases Affecting

Oral Cavity
Prof Dr Muhammad Rizwan
BDS, MSc, NBDE, NBDHE, ACMED
Pakistan
Infections of The Oral Mucosa
 Common oral mucosal infections are
caused by viruses, bacteria, and fungi.
Viral infections
 Laboratory confirmation of the diagnosis of
many viral diseses is slow and difficult and
diagnosis of most of the viral infections is
mainly based on the clinical features.
Laboratory diagnostic methods
 Three main laboratory methods available.
 Isolation of virus from lesion, and identification after
cultivation in tissue culture, fertilized eggs, or
laboratory animals.
 Viruses or characteristic histological changes may be
found in affected tissue using either light or electron
microscope.
 Viral antigens may be demonstrated in infected cells
by immunofluorescent or immunocytochemistry.
Viral infections
 Herpetic stomatitis
 Primary
 Recurrent (HSV)
 Chickenpox and shingles (herpes zoster) (Varicella-
zoster virus)
 Herpangina (coxsackie A Virus)
 Hand, foot, and mouth disease (Coxsackie A Virus)
 Infectious mononucleosis (EBV)
 Measles (Paramyxovirus)
 Hairy leukoplakia (EBV)
 Viral warts/epithelial heperplasia
 Oral manifestations of;
 HIV (HIV)
 Mumps (Paramyxovirus)
 Influenza (Influenza virus)
 Cytomegalovirus infecton(Cytomegalovirus)
Herpetic stomatitis
 HSV is a DNA virus and the most frequent
cause of viral infections in mouth.
 Two types of HSV
 Type 1 ; traditionally associated with
infections of skin and oral mucous
membranes
 Type 2 associated with infections of
genetalia.
Primary infection
 Caused by HSV type 1
 Frequently Involves oral mucosa and lips
 Presents as primary herpetic
gingivostomatitis.
 Transmitted by droplet spread or intimate
contact.
 Age: young children and young adults
Features
 Following incubation period of 5 days, patient
presents with prodromal symptoms of;
 Malaise
 fever, and
 within a day or 2 mouth become uncomfortable with
the development of of numerous small vesicles on
any part of the oral mucosa and lips.
 Vesicles soon ulcerate and become secondarily
infected accompanied by lymphadenitis.
Clinical features
 Widespread inflammation of gingiva which is
 erythematous and
 oedematous.
 Over next few days, fresh corps of vesicles
develop.
 Circumoral crusting lesions on the lips may be
seen due to coagulation of serum which exudes
from ruptured vesicles.
 Acute herpetic gingiva stomatitis
painful vesicle present in mandibular
and maxillary labial mucosa gingiva
swollen

Acute herpetic gingivitis

swollen with hemorrhage
VIRAL

Herpis Simplex Virus

 Tongue of a patient
acute herpetic
gingivitis. Note the
vesicular lesions and
coated tongue

Coated tongue of a patient

with herpetic
gingivostomatitis
Extraoral lesions
 Vesicles may occur on skin of the chin as
a result of drooling of saliva.
 On fingers as results of sucking.
 Infection involving nail-bed may be quite
painfull and may be transmitted to the
eyes by rubbing.
Resolution of lesions
 Symptoms begin to subside about sixth
day of fever with the oral lesions taking
10-14 days to resolve
Serological exam.
 Studies show a high incidence of
antibodies to HSV type 1 in adults,
although some give a history of primary
herpetic gingivostomatitis.
 Majority of primary herpetic infections are
subclinical and either pass unnoticed by
the patient or are diagnosed as teething or
tonsillitis in a young child.
Recurrent infection
 One in three persons having primary
infection, either clinical or subclinical, later
develop recurrent infections
Features
 These are characterized by marked local
symptoms unaccompanied by systemic
illness.
 Herpes labialis is the most frequent type.
 Appear as clusters of vesicles on the lips
and adjacent skin appearing a few hours
after prodromal symptoms of itching or
tingling.
Features
 These vesicles rupture within a short time
and become crusted.
 Ususlly heal within a week.
Recurrent Herpes – Dormant trigmenal ganglia

herpes labialis note

croppy vesicles at corner
of mouth

Herpetic whitlow of
skin 2ndry to contact
with active oral lesions
Recurrence
 It depends on various stimuli such as ;
 Common cold
 UV light
 Mechanical trauma
 Menstruation, and
 Stress
 Intra oral recurrence is rare and almost
always on hard palate or gingiva.
Histological features
 Vesicles appear to be intraepithelial
 Vesicles result from distension and rupture of
epithelial cells by intracellular oedema and
coalescence of disrupted cells.
 Some virus infected epithelial cells which show
ballooning degeneration. (swollen infected cells
with eosinophilic cytoplasm and large pale
vesicular nuclei with the chromatin distributed at
the periphery.)
Histological features
 Giant cells .
 Inflammatory infiltrate in the lamina propria
and epithelium (density of which depends
on the stage and severity of the disease.)
Diagnosis
 Balloon cells and multinucleate giant cells
can be identified in smears taken from an
intact vessicle or from recently ruptured
vesicle.
 Smear is stained with monoclonal
immunoflurescent antiserum to HSV give
spesific results which are useful in rapid
diagnosis.
Treatment
 No need for antibiotics
 Bed rest

 Analgia + fluids

 Anti pyretic

 Mouth rinses

Multinucleated giant
cell in a smear from
patient with primary
herpes simplex
Latent state of HSV
 Primary herpetic stomatitis is associated with the
replication of virus at the site of clinical infection,
but in many patients virus migrates by some
unknown mechanism, up the trigeminal nerve to
the sensory ganglion where it remains in a latent
state.
 Transcription of the virus HSV DNA is blocked in
latent state and so the virus is not affected by
anti viral drugs.
Latent state of HSV
 Sensory ganglion also apears to be
immunoprivileged site so that the virus is
effectively sequestrated from the immune
system.
 Various stimuli then may alter the latency state,
permitting the block in HSV transcription to be
overcome.
 The virus then migrate down the sensory nerve
axons to the nerve endings where it may be
eliminated by immune mechanisms.
Infection prone individuals
 Recurrent infections appear to be
associated with immunosupression, but
patients with generalized impairment of
cell-mediated immunity (those receiving
immunosupressive or cytotoxic therapy, or
infected with HIV) are particularly prone to
recurrent herpes and may develop
intractible infectons.
Chickenpox and herpes zoster
(shingles)
 Both are caused by the same DNA virus
called varicella-zoster virus.
 It is morphologically similar to HSV.
 Primary infection by the virus is
manifested as chickenpox and recurrent
by zoster.
Herpes Zoster (cont.)
 Affect all branches of trigeminal nerve affecting
face and oral cavity. Giving severe pain and
cramps appear- usually unilateral

herpes zoster linear herpes zoster of palate

distribution unilateral and
painful
Manifestations of chickenpox
 Lesions of chickenpox may be found in the
oral mucosa specially soft palate and
fauces, and may precede the
characteristis skin rash.
 Oral lesions present as small ulcers.
 Vesicles are seldom seen and if present ,
show histological features similar to the
HSV.
Herpes zoster (shingles)
 Following the infection by the chickenpox,
the virus remains latent in the sensory
ganglia probably for the whole of the life of
the host.
 Reactivation of the virus to cause zoster
may occur spontaneously or when the
host defences are depressed, such as in
patients with malignant lymphomas.
Features
 The lesions are localised to the distribution of one
or more sensory nerves.
 Unilateral vesicular eruptions
 These are followed by prodromal symptoms of
 pain and
 Paraesthesia, for up to two weeks.
 Involvement of trigeminal nerve may cause
toothache followed by the formation of vesicles in
the distribution of one or more branches of nerve.
Features
 Vesicles may be entirely intraoral, ulcerate
and become secondarily infected.
 Course of the disease is about 14 days.
Complication
 Most distressing complication is post-herpetic
neuralgia, caused by the fibrosis in and around
the sensory nerves and ganglia.
 It occasionally presents with lower motor facial
paralysis as the Ramsay-Hunt syndrome.
 Syndrome is due to extension of primary
involvement of the geniculate ganglion to affect
the facial nerve.
Differential Diagnosis
 Herpedtic gingivostomatitis
 Necrotizing ulcerative gingivitis
 Varicella
 Erythema multiforme
Herpangina
 Caused by Coxsackie A virus which is an RNA
virus.
 Mostly seen in children
 Clinically presented by sudden onset of mild
illness with fever, anorexia, dysphagia and sore
throat.
 Vesicles breaking down into 1-2 mm ulcers,
which are seen on the tonsils, soft palate and
uvula.
Clinical features
 sudden fever ( 38-40 C)
 Headache, malaise
 Sore throat, dysphagia
 Diffuse erythema and multiple vesicle formation
in the oropharynx, soft palate, and uvula
 Vesicles soon rupture leaving painful, shallow,
round ulcers
 Ulcers heal spontaneously in 7-10 days
Clinical features.
 Symptoms persist only for 2-3 days.
 Clinically it is difficult to distinguish from
herpes infection but
 It is an oropharangitis where as herpes is
a gingivostomatitis.
Differential Diagnosis
 Primary herpetic gingivostomatitis
 Aphthous ulcers
 FAPA syndrome
 Acute lymphonodular pharyngitis
 Gonococccal oropharyngitis
 Streptococcal pharyngitis
 Erythema multiforme
 Hand, foot, and mouth disease
Treatment
 Corticosteroids in low doses, e.g., prednisone
10-20 mg/day, for 4-6 days, reduce the
inflammation and pain dramatically.
 Analgesics for 3-6 days.
 Local use of antiseptic mouthwashes has
limited usefulness.
 Soft foods are recommended.
Hand, foot, and mouth disease
 Caused by coxsackie virus A, type 16
espaecially
 Occurs predominantly in children
 Transmitted by close association, living
within a house.
Features
 Characterized by development of shallow
ulers 2-8mm in diameter.
 Appear intraorally on
 Gingiva
 Tongue
 Cheeks
 Palate
Extra oral manifestations
 They appear On the palms of hands and
soles of the feet as
 Vesicles, and
 Ulcers
 The lesion may persist for upto 2 weeks.
 No specific histopathological changes
seen.
Diagnosis
 Estimion of specific IgM in acute sera is
helpful in doubtful cases
Differential Diagnosis
 Aphthous ulcers
 Herpetiform ulcers
 Primary herpetic gingivostomatitis
 Secondary herpes
 Herpangina
Treatment
 The treatment is symptomatic. Affected
children should stay in bed for 3-4 days.
 There is no specific antiviral therapy. The role
of acyclovir is debatable.
 Antipyretics, e.g. aspirin, for 4-6 days.
 Soft foods.
 The disease is self-limiting
Infectious mononucleosis
 Also called as glandular fever
 Caused by Epstein-Barr virus.
 Occurs predominantly in teenagers and
 Young adults.
 transmitted by kissing either from an
infected patient or a healthy carrier
Clinical features
The disease is characterized by
 Lymph node enlargement

 Fever, and

 Inflammation of pharynx

And may be associated with

 Prolonged periods of malaise lasting
months or years
Features
 Petechial haemorrages at junction of soft
and hard palate.
 Inflammation and
 Ulceration of oral mucoa
 Pericoronitis in association with bilateral
submandibular lymphadenitis.
Diagnosis
 Presence of IgM antibodies to EBV
antigen or specific monospot slide test in
acute serum.
 Paul-bunnell test.
Measles
 Occurs predominantly in children.
 In developed countries it is a mild disease
with low mortality rate compared to other
countries.
Features
 Prodromal symptoms resemble
 Common cold and
 Accompanied by koplik’s spots on oral
mucosa, specially buccal mucosa opposite
molar teeth
 Present as pin-point bluish white spots
against an erythematous background.
Features
 Occue in few numbers to hundreds.
 Likely to be overlooked as skin rash when
they start to disappear.
Gangrenous stomatitis (cancrum oris, noma)
may occur as complication of measles in
malnurished patients.
Human immunodeficency virus
 Transmission of HIV:
 It is transmitted by exchange of blood or
body fluids principally by sexuall contact
(both homosexual and heterosexual)
 Injection of blood or blood products (IV
drug abusers and haemophiliacs)
 Mother to child (perinatal infecton)
Transmission of virus
 Transmission may be followed by infection
which is detected by the HIV antibodies in
the blood. (seroconversion) occuring
within 3 month of exposure. And a few
having acute infecton at this time.
Clinical features of acute infection
These include,
 Pyrexia

 Skin rash

 Headache

 Diarrhoea

 Sore throat, and

 Erythema of buccal and palatal mucosa.

Clinical features
 Following seroconversion, patient may
remain HIV Seropositive for many years
(symptom free), but may develop PGL
(persistant generalized lymphadenopathy).
 In both PGL and Seropositive cases, there
may be progression to AIDS-related
complex (ARC).
AIDS Related Complex
It is characterized by,
 Lymphadenopathy

 Persistent pyrexia

 Diarrhoea

 Weight loss

 Fatigue, and

 Malaise.
Final stage of HIV infection.
It is fully developed AIDS characterized by,
 Opportunistic infections

 Kaposi’s sarcoma

 Non-hodgkins lymphoma

Patients may also develop

 Thrombocytopenia , and

 Neurological diseases
Oral manifestations of HIV
These are based on the strength of their
association with HIV infection.
 Group 1: Strongly associated with HIV infecton;

 Candidosis
 Erythematous
 Hyperplastic
 Pseudomembranous
 Hairy leukoplakia (EBV)
Oral manifestations of HIV
 HIV associated periodontal disease
 HIV-gingivitis
 Necrotizing ulcerative gingivitis
 HIV-periodontitis
 Necrotizing stomatitis
 Kaposi’s sarcoma
 Non-hodgkin’s lymphoma
Oral manifestations of HIV
Group 2: less commonly associated with
HIV infection ;
 Atypical ulceration (oropharyngeal)

 Idiopathic thrombocytopenic purpura

 Salivary gland disorders

 Dry mouth Decreased flow rate
 Swelling of major glands (uni- or bilateral).
Oral manifestations of HIV
 Viral infections (other than EBV)
 Cytomegalovirus
 HSV
 HPV
 Varicella-zoster virus
Oral manifestations of HIV
Group 3: lesions possibly associated with
HIV infection ;
 Bacterial infections (other than
gingivitis/periodontitis)
 Fungal infections (other than candidosis)
 Melanotic hyperpigmentation
 Neurologic disturbances like
 Facial palsy
 Trigeminal neuralgia
Pathogenesis of HIV
 Binding of virus to many target cells mainly to
CD-4 receptor of T-Helper lymphocytes.
 Infected T-helper cells die leading to reduction in
nos.
 This causes impairment of normal immune
response of body particulary of the T-cell
dependent antigens such as viruses, fungai, and
encapsulated bacteria causing most of
manifestations of the disease.
Cells where HIV may bind
Virus may bind to other cells in body but
generally does not kill them during infection. These
cells may include;
 Bone marrow stem cells

 Macrophages

 Endothelial cells

 Lymph node dendritic cells, and

 Langerhans cells
B-cell involvement in HIV infecton
 HIV infection may be characterized by the
polyclonal B-cell stimulation leading to
hyperglobulinaemia with antibodies
directed against HIV infected cells.
Bacterial infections
 A number of bacteria are normally present in the
oral cavity but only a few bacterial infections occur
in oral cavity.
 This all may be due to various defence
mechanisms present within oral cavity.
 Epithelial barrier.
 Saliva .. Cleansing action, lysozyme, antibodies
like IgA ( also IgG,IgM from gingival crevice)
 Phagocytosis by complement activation
(neutrophils from gingival crevice)
Acute ulcerative gingivitis
 Also called as acute necrotizing ulcerative gingivitis
(ANUG)
 Vincent’s gingivitis.
 Causative agents include
 Spirochaetes ,
 pleomorphic rods,and
 fusiform organisms
 It occurs mostly in young adults.
 Mostly seen in winter in Europe.
 More in males compared to females.
Clinical presentations
 It affects interdental papillae and may also
involve gingival margins and shows ,
 Necrosis
 Crater like, punched out ulceration
 All is of sudden onset
 Ulcers are covered with greyish-green
pseudomembrane demarcated from the
surrounding mucosa by a linear erythema..
BACTERIAL
Necrotizing Ulcerative Periodontitis
Clinical presentations
 Gingival bleeding either spontaneously or on minor trauma
 Pain
 Soreness of gums
 Marked halitosis
 Metallic taste (bad taste)

In advanced cases,
 Increased salivation
 Malaise
 Cervical lymphadenopathy, and
 Fever.
Role of bacteria in disease.
Precise role of various bacteria in the
disease is unclear but the disease is usually
regarded as
 Endogenous, and

 Opportunistic infection

The clinical response to antibiotic therapy

shows that bacteria are atleast involved in the
production of clinical symptoms.
Aetiological factors.
A variety of factors may disturb the normal
symbiotic host-parasite relationship And facilitate
the overgrowth of organisms of fusospirochaetal
complex.
These may include ;
 Reduced host resistance, and
 Pre-existing gingival tissue damage (in chronic
gingivitis .
It has high recurrence rate unless predispossing
factors are properly treated.
Predisposing factors
These may be local and general.
Local factors General factors
 Poor oral hygiene Fatigue
 Chronic gingivitis Stress
 Local trauma Illness
 Smoking
HISTOLOGICAL FEATURES
 Destroyed surface epithelium of papillary
and marginal gingiva.
 Epithelum is replaced by
pseudomembrane composed of fibrin,
necrotic epithelial cells, red and white
blood cells, bacteria and cellular debris.
 Connective tissue shows marked acute
inflammatory changes.
HISTOLOGICAL FEATURES
 Gram staining and electron microscope
shows multiplicity of organisms with great
preponderance of spirochaetes,
pleomorphic rods,and fusiform organisms
(fusospirochaetal complex)
NOMA (Cancrum oris)
 In some underdeveloped parts of thye
world, a severe form AUG presents in the
form of Noma in children.
 It has an acute onset
Clinical features
 Almost all cases appear in malnurishded
children, and children whose resistance has
been further lowered by intercurrent infection
like measles or herpetic stomatitis.
 Rapid spread of necrosis from gingival lesions
into the cheeks and development of demarcated
gangrenous area of orofacial tissues.
Aetiology and histology
 These features are alomost similar to
AUG.
Syphilis
 Its an infecton Caused by a spirochaete,
‘Treponema pallidum’.
 It presents its features as primary,
secondary, and tertiary infection
depending on site and nature of lesion.
Primary lesion
 Presents as chancre
 Usually occurs on the genitalia
 In minority of patients it may present on
the oral mucosa, usually the lips.
 It is typically described as a Clean-based,
Pain less, and Shallow ulcer with
induration of subjacent connective tissue.
 Enlarged regional lymph nodes.
Histology
 Chancre consists of ulcerated granulation
tissue.
 Dense mononuclear inflammatory cell infiltration
chiefly plasma cells.
 Inflammatory infiltrate is less dense I deeper
tissues and tends to be distributed around blood
vessels.
 Silver staining may show numerous
spirochaetes in the lesion.
Secondary lesion
 Chancre heals spontaneously over a
period of a few weeks and secondary
lesion develop about 6 weeks later, some
2-3 months later after initial exposure.
Features
 Predominant feature is a generalized skin rash
and it may be accompanied by oral lesions.
 In mouth, a diffuse erythema or the
characteristic mucous patch (necrotic slough
covering an area of ch. inflammation) may be
seen.
 Mucous patches may coalesce to produce an
irregular outline called snail track ulcers.
Histology
 Silver staining may show numerous
spirochaetes in the lesion.
 No other distinguish features seen.
Tertiary syphilis
 Here in this case a gumma may occur in
the tongue or palate.
 Initially it present as as indurated swelling.
 It subsequently may become necrotic and
ulcerated to form a deep painless ulcer.
Histology
Histologically gumma consists of a central
mass of coagulation necrosis surrounded by
granulation tissue infiltrated by
 Lymphocytes,

 Plasma cells

 Macrophages, and

 Giant cells (occasionally)

 Spirochaetes are very scanty or absent.

Lesion on the tongue
 Atrophic glossitis which is caused by endarteritis
obliterans.
 In this case, smooth surface of tongue is broken up by
fissures resulting from atrophy and fibrosis of tongue
musculature.
 Hyperkeratosis (syphilitic leukoplakia) frequently follows
and carcinoma of the tongue develops with great
frequency.

Tertiary syphlis is a rare factor in aetiology of oral

cancer.
Congenital syphilis
 It is associated with the infecton of developing
tooth germs of
 Permanent incisors called ‘Hutchinson’s
incisors’.
 First molars ‘moon molars or mulberry molars’
 Maxillary central incisors are most frequently
involved and characterized by central notching
of the incisal edge and a tapering ‘screw-driver’
appearance.
Mulberry molars
 Mulberry molars usually first molars are
characterized by hypoplastic defects of the
occlusal surface and defective
development with rounded, globular
masses of hard tissue producing mulberry
appearance.
Facial deformity
 Collapse of the bridge of nose due to
infection and destruction of the developing
nasal bones, produces saddle deformity of
the bridge and dished appearance of face.
Diagnosis
 Primary and secondary lesons show
presence of spirochaetes in the smears of
the lesion by dark-ground microscopy.
 In acquired syphilis, serology test for
syphilis becomes positive about 2-3 weeks
after appearance of the primary lesions,
and are also positive in congenital syphilis.
Actinomycosis
Always a mixed infection and caused by
 Actinomyces israelii; it was considered to
be principal cause of infection, but now
 A. viscosus, and

 A naeslundi, may also be associated with

the disease.
Sites of involvement
Mostly cervicofacial actinomycosis.and
mostly involves soft tissues of
 Submandibular area, and

 Neck
Characteristic lesions
 Infection is characterized by multiple foci of
chronic suppuration.
 Development of firm swellings (brawny-hard)
which often recur.
 These swellings eventually soften, and
accompanied by formation of pus discharging
from multiple sinuses.
 Pain is variable and swellings are often painless.
 Abscesses forming tend to point on to the
skin rather than mucosal surface and are
accompanied by marked fibrosis of the
surrounding tissue.
Portal of entry of infection
Infection is endogenous and portal of entry is
thought to be either a
 Tooth socket, most commonly lower third molar,
or
 Infected root canal

Infection is almost always confined to the

soft tissue but actinomycotic osteomylitis
may occur.
Treatment
 Surgical drainage and
 Prolonged antibiotic therapy
Pathogenesis of infection
 Its an opportunistic infection and other
organisms may provide improved conditions for
anaerobic growth of actinomyces and can lower
host or local tissue resistance leading to the
infection by actinomyces.
 It is thought to develop as areas of diffuse
oedema,
 Inflammatory cell infiltration manily mononuclear
cells, and
 Large no. of macrophages
 Granulomatous inflammation is surrounded by
abundent granulation tissue and fibrosis.
 Fresh foci of infection develop adjacent to
primary site following transport of some
organisms by phagocytis cells
 A central area of suppurative necrosis develops
in most of these foci.
Histological features
 Areas of diffuse oedema,
 Inflammatory cell infiltration manily
mononuclear and
 Large no. of macrophages
 Granulomatous inflammation is
surrounded by abundent granulation
tissue and fibrosis.
 Granules consisting of tangled meshes of
gram posivtive filaments of Actinomyces
seen in pus.
 Peripheral filaments are often gram
negative and may show terminal clubbing.
Diagnosis of lesion
 Organisms seen clinically as ‘sulphur
granules’ in pus form actinomycotic lesion
 And if these granules crushed between
two glass slides and stained by gram’s
method, can confirm the clinical diagnosis.
Tuberculosis
 An infection caused by mycobacterium
tuberculosis, but
 M. bovis and,
 Other atypical mycobacteria may also
cause disease in man.
 Oral tuberculosis is now rare in western
countries.
Oral lesions
 Primary lesions in the oral mucosa may
occur but secondary infection associated
with coughing up of infected sputum from
pulmonary tuberculosis are more likely.
 Classical feature of oral TB is painfull
undermined ulcer covered with a greyish-
yellow slough occuring most commonly on
the tongue.
 Other type of ulcers and
 Granulating gingival lesions also seen.
 Patients may present with tuberculous
lymphadenitis, frequently affecting the
cervical nodes.
 Intra- and extraparotid groups are
occasionally involved.
Diagnosis
 Usually follows a biopsy.
 Finding of typical tuberculoid granulomas.
 And tubercle bacilli.
Differential diagnosis
 Sarcoidosis
 Cat-scratch disease

These show same histological features but

both of these don’t show presence of
tubercle bacilli.
Leprosy
 Caused by mycobacteria, Mycobacterium
Leprae.
 Rare but endemic to certain typical areas.
 Two forms of infection depending on
immune response of host to the organism
Types of infection
Lepromatous type : Tuberculoid type :
 No cell mediated  Cell mediated
response to M. leprae responses are high
 Humoral response is  Humoral responses
high are low
 Wide spread infection  Infection remains
throughout the body. localized.
Oral lesions
 No lesions described in tuberculoid type
but 50% patients of lepromatous type
show oral features.
 Present as nodular inflammatory masses
 These masses tend to ulcerate.
 And heal with fibrosis.
Sites of lesion
 Hard palate
 Soft palate
 Anterior gingiva in maxilla, and
 Tongue are most often affected.
 Patients show varying degree of facial
deformity associated with bone lesions,
particularly naso-maxillary complex.
Gonorrhoea
 Mainly a venereal disease caused by
Neisseria Gonorrhoea.
 Though oral mucosa is highly resistant to
gonococcal infection but tonsillar and
oropharangeal lesions have been reported
in homosexuals.
Oral manifestations
These vary from generalized erythematous
stomatitis to vasiculation and ulceration
associated with
 Burning and

 Pain, on speaking and swallowing.

Lesions have been reported affecting all

areas of mucosa.
Reiter syndrome
 Aetiology is unknown but
 Causative factors may be
 Gonorrhoea
 Mycoplasmal infection
 Genetic predisposition
 Autoimmune mechanisms (HLA-B27).
Features
Mainly affects males
20-35 years of age group.
 Classical triad consists of
 Arthritis
 Conjunctivitis
 Urethritis
Oral lesions
 These may include slightly elevated areas
of erythema on the
 Buccal mucosa
 Lips, and
 Gingiva , and
 Purpuric spots on the palate
Kaposi’s sarcoma (KS)
 Idiopathic multiple pigmented sarcoma of
skin
 Mainly occurring on the skin of extremities.
 In 1960s it became apparent that tumour
is endemic in Southern Africa.(up to 10%
of all tumours in some areas)
Clinical Forms
 Four forms:
1- occurs in poland, russia and italy and
affects older male population.
2- Endemic form in africa
3- Iatroenic or transplant associated KS in
renal transplant patients.
4- AIDS associated form of KS.
Forms of KS (In endemic areas)
 Individuals up to 40  Occurs mainly in
years are involved. children.
 It Affects skin of arms  Spreads to lymph
and legs. nodes and visceral
 Tumour has good organs.
prognosis.  It has poor prognosis.
Features

 It is commonest tumour associated with HIV

infection.
 Occurs in up to 1 in 4 AIDS patients.
 Male to female ratio 20:1.
 Higher frequency in whites and homosexuals
than in blacks and IV drug abusers.
Aetiology
 There is association between KS and HIV.
 Its been suggested that KS results from
secondary viral infection in an
immunocompromised host.
 Cytomegalovirus has been implicated but
its isolation from KS lesion is unsuccessful.
 HHV8 is causative organism of KS.
Aetiology
 Recent evidence show that the vascular
proliferation in KS is caused by angiogenic
cytokines released by the action of HIV on
CD4 lymphocytes.
 Lesions in All four forms go through similar
histological evolvement.
 They progress from patch to plaque to
nodular stages.
 Patch stage normally seen in early
developing KS presents with flat macules.
 Lesions shows proliferation of new small
blood vessels around larger dilated
vascular spaces.
 In plaque lesions, the vascular
proliferation involves the dermis almost
completely with a bland spindle cell
proliferation limited around proliferating
vessels resulting in a slightly elevated skin
lesions.
 The nodular stage presents as a spindle
cell lesion with slit like vascular spaces.
Clinical features
 KS in AIDS presents on skin or mucosal
surfaces with single or multiple lesions.
 Lesions may be macules, papules or nodules.
 Colour of lesions may be pink, red, or violet.
 Skin lesions become darker and larger with time.
Tip of the nose is most frequent site on face.
Skin lesion
Oral lesions
 Frequently seen on palate.
 Less frequently on gingiva and tongue.
 Lesions present as blue, black, or red
macules which later become darker,
raised, and ulcerated.
 Lesions are painless unless ulcerated.
NEOPLASM

Kaposi Sarcoma (KS)

Histological features
 Early lesions consist of proliferating
endothelial cells and atypical, often cleft
like, vascular channels together with
extravasated erythrocytes, haemosiderin
and inflammatory cells.
 A few atypical spindle-shaped cells may
be seen in interstitial tissues.
Histological features
 Distinction from granulation tissue and
other vascular lesions such as
haemangiomas and pyogenic granulomas
may be difficult.
 In later stages vascular component
decreases and the atypical spindle cells
predominate.
Treatment
 No curative treatment
 Lesions may respond to radiotherapy or
chemotherapy.
Hairy leukoplakia
 Usually asymptomatic.
 Mostly occur bilaterally on the lateral
border of the tongue and occasionally
elsewhere on the oral mucosa.
 Clinically lesions are non-removable white
patches
 Variable in size, severity, and surface
characteristics.
 Lesions present as vertical white folds on
the lateral border of the tongue with raised
corrugated or hairy surface.
 Lesion may also have smooth flat surface.
Histological features
 Hairy leukoplakia shows
 Acanthotic, parakeratinized epithelium
with long, finger-like surface projections of
parakeratin producing the hairy or
corrugated appearance clinically.
 Candidal hyphae may be present in
parakeratin.
Oral Hairy Leukoplakia
 Absence of inflammatory cells both in epithelium
and the lamina propria.
 Swollen or balloon cells with prominent cell
boundaries are present as a band in the prickle
cell layer beneath the parakeratin.
 These swollen cells have small darkly staining
nuclei and perinuclear vacuoles.
 And also contain EBV.
Relation with HIV patients.
 It is seen in HIV-seropositive patients from
all risk groups and it has been suggested
that about 20-30 % of HIV-seropositive
patients may have HL.
 Some HIV-seronegative patients taking
immunosuppressive therapy have also
been described having few cases of HL.
Aetiological factors.
It may be due to opportunistic infection of
oral epith. by EBV in association with
 HIV infection or,

 Immunocompromised patients.
Pathogenesis
 A long term carrier of EBV generally follows
natural infection with EBV which in most people
ocurs subclinically during childhood or as acute
infectious mononucleosis (glandular fever) in
teenage years.
 Main reservoir for carrier state is thought to be
the circulating B lymphocytes but in oropharynx
and salivary glands the reservoir cells are
epithelial cells.
 EBV can be found in the saliva of most
EBV-seropositive individuals. A marked
depletion of langerhans cells has been
described in HL.
 Impaired antigen handling and impaired
immune response may allow EBV to enter
the oral eithelium and viral replication to
occur.
 The characteristic site distribution at the
lateral border may be due to the liability of
the area to trauma which could allow
access of EBV from saliva to viral
receptors on the prickle cells.
 Alternatively it may be a result of
endogenous infection from the EBV-
carrying B lymphocytes.
Relation with AIDS patients
 It is a common finding among patients with AIDS
or late –stage HIV infection and it is an
indication of declining immunocompetence.
 Size and appearance of HL are not correlated
with the subsequent development of AIDS and
long term behaviour of HL has not been
described.
 No evidence that it is a premalignant condition.