DISEASES OF THE ORAL MUCOSA – MUCOSAL INFECTIONS.ppt

Oral pathology

1. DR M REDDY

2. It is very important to have a thorough
understanding of the causes and the
clinical and radiographic presentation
of the common and important oral
diseases and their effects upon both
the treatment and the patient

3. The common viral infections affecting the oral
cavity are:
•Herpes simplex –primary and secondary
•Herpes zoster –primary and secondary
•Hand, foot and mouth
•Herpangina
Of these, infections caused by herpes simplex
are the most common and important

4. Two major forms of herpes simplex virus exists –type1
and type 2. Oral infections are generally caused by
type 1 and genital infections are most commonly
caused by type 2.
Oral infections with the herpes simplex virus occurs in
an initial (primary) form and a recurrent (secondary)
form.
The HSV is one of a group of viruses called human
herpes virus (HHV). Other herpes virus includes
varicellazoster virus, Epstein barrvirus, cytomegalo
virus and HHV-8.
HSV has the ability to persist in the latent state. The
primary infection undergoes remission without the virus
being completely eliminated.

5. Definition
The primary disease is usually seen in children, although adults
who have not been previously exposed to HSV may be affected.
Aetiology
Primary infection is usually caused by the Type 1 HSV.
Transmission of herpes is by close contact (saliva)
It is common in the immunocompromised patient.
Features that help with diagnosis:
The patient will complain about feeling unwell
They usually have a fever and enlarged lymph nodes in
the neck (cervical lymphadenopathy)

6. Early lesions are painful blisters
known as vesicles affecting any
part of the oral mucosa.
The hard palate and dorsum of
the tongue are common sites.
Vesicles are dome shaped and
2-3mm in diameter.
Vesicles rupture leaving circular,
sharply defined, shallow ulcers
with yellowish or greyishfloors
and red margins.
Ulcers are painful and may
interfere with eating.
Gingival margins are frequently
swollen and red and regional
lymph nodes enlarged and
tender.

7. Oral lesions usually resolve within a week to 10
days but malaise may persist.
Lesions heal without scar formation.
In approximately a third of the patients the virus
may migrate to the trigeminal ganglion to
reside in a latent form.

9. Diagnostic Tests
Clinical picture is usually distinctive
A smear showing virus-damaged cells is additional diagnostic
evidence.
Rising titreof antibodies confirms diagnosis.
Differential Diagnosis
Systemic signs and symptoms together with oral ulcerations may
require differentiation from:
•streptococcal pharyngitis (does not involve lips or perioral tissues
and vesicles do not precede ulcers)
•erythema multiforme(ulcers are larger without a vesicular stage
and less likely to affect the gingiva) and
•ANUG (oral lesions limited to gingiva and are not preceded by
vesicles and there is pain).


10. Management and Treatment
Acyclovir is the treatment of choice and must be
used early to be effective.
Bed rest, fluids and a soft diet may sometimes be
required.
In mild cases, topical tetracycline suspension,
rinsed round the mouth several times a day
relieves soreness and may hasten healing by
controlling secondary infection.
Unusually prolonged or severe infections or failure
to respond to acyclovir, suggest immunodeficiency
and herpetic ulceration persisting for more than a
month is an AIDS defining illness.

11. Definition
It is secondary herpes where the latent virus is reactivated
to cause cold sores (fever blisters).
Aetiology
The dormant virus is reactivated by certain stimuli such
as sunlight, menstruation, fatigue, fever and emotional
stress.
The virus travels down the trigeminal nerve, replicates
and forms characteristic vesicles.

12. Prodromalsymptoms of tingling, burning or pain in
the site at which lesions will appear.
There is erythemaat the site of attack followed by
vesicle formation after an hour or two, usually in
clusters along the mucocutaneousjunction of the
lips and can extend onto the adjacent skin.
The vesicles enlarge, coalesce and weep
exudates.
After 2-3 days they rupture and crust over and heal
usually without scarring.
The whole cycle may take up to 10 days.
Secondary bacterial infection can sometimes leave
scars.

14. Differential Diagnosis
Aphthousulcers
Diagnostic Tests
Diagnosis based on clinical characteristics of the disease.
Viral culture can be performed to confirm diagnosis.
Management and Treatment
Treatment must start as soon as premonitory sensations are
felt.
Acyclovir effective if applied at this time.
The patient is infectious during this time and dental
treatment should be avoided

15. Feature Minor Aphthous ulcer Herpes simplex ulceration
Location Nonkeratinized mucosa Keratinized mucosa
Number One to several Multiple (crops)
Vesicle precedes ulcer No Yes
Pain Yes Yes
Size <1cm 1 –2mm
Borders Round to oval Crops of ulcers coalesce to form a large
irregular ulcer
Recurrent Yes Yes

16. Both primary and secondary herpetic infections are
contagious.
HSV can cause a painful infection of the fingers called
herpetic whitlow.
Pain, redness and swelling are prominent with herpetic
whitlow.
Vesicles or pustules eventually break and become ulcers.
Duration of herpetic whitlow may be as long as 4-6 weeks.
HS can also cause eye infection.
Routine barrier infection control procedures (masks, eye
protection and gloves) are important in preventing
transmission of the HSV to dental health care providers.

18. Definition
The varicella zoster virus causes both chicken pox
(mainly in children) and shingles (mainly in adults due to
reactivation of the latent virus).
Both are contagious

19. Respiratory aerosols and contact with
secretions from skin lesions transmit the virus.
Reactivation of the VZV follows
immunosuppressionfrom malignancy, drug
administration or HIV infection.
Radiation or surgery of the spinal cord or local
trauma may trigger secondary lesions.
Prodromalsymptoms of pain or paresthesia
develop and persist for several days as the
virus infects the sensory nerve of a dermatome
(usually of the trunk or head and neck).

20. Varicella
Vesicular and pustulareruptions on the skin and mucous membrane that
occur in crops and eventually ulcerate.
Usually occurs in children.
Systemic symptoms include headache, fever and malaise.
2 week incubation period.
Herpes zoster
Affects mainly middle age adults and occasionally children.
First signs are pain and irritation or tenderness in the dermatome
corresponding to the affected ganglion.
Vesicles are confluent and form on one side of the face and in the mouth
up to the midline.
Regional lymph nodes are enlarged and tender.
Acute phase lasts about a week.
Pain continues until crusting and healing.
Secondary infection can cause suppuration and scarring of the skin with
associated malaise and fever.

25. Differential Diagnosis
Varicella-Primary HSV and hand-foot-and-mouth disease.
Herpes zoster –recurrent HSV
Diagnostic Tests
Diagnosis made on clinical features.
Biopsy or a smear may be done.
Management and Treatment
Varicella–supportive –normal individuals and antiviral
drugs for immunocompromisedpatients.
Herpes zoster –systemic acyclovir intravenously if
necessary.

26. Definition
Common, mild viral infection
characterisedby ulceration of the
mouth and a vesicular rash on the
extremities.
Aetiology
Caused by the strain of the
Coxsackie A virus.
Highly infectious

27. Usually occurs in children less than 5 years.
Short incubation period –resolves spontaneously in 1-2 weeks.
Signs and symptoms are mild to moderate.
Low grade fever, malaise, lymphadenopathyand sore mouth.
Pain –chief complaint.
Oral lesions begin as vesicles that quickly rupture to become
ulcers that are covered by a yellow fibrinousmembrane
surrounded by an erythematoushalo.
Multiple lesions occur anywhere in the mouth especially the
palate, tongue and buccalmucosa.
Multiple maculopapularlesions that are found typically on the feet,
toes, hands and fingers appear with or shortly after the oral
lesions.
They progress to a vesicular state and eventually become
ulcerated and encrusted.

28. Differential Diagnosis
Primary HSV and varicella
Diagnostic Tests
History and clinical features.
Confirmation by serology if needed
Management and Treatment
No specific treatment available or needed.
Bland mouthrinsessuch as sodium bicarbonate in
warm water may be used to alleviate oral discomfort.
Complications are myocarditisand encephalitis

29. Definition
It is a highly contagious disease causing
systemic symptoms and a skin rash.
Aetiology
Caused by the paramyxovirus
Spread by airborne droplets through the
respiratory tracts.
Highly contagious

30. Occurs commonly in childhood.
7-10 day incubation period.
Prodromalsymptoms of fever, malaise, coryza,
conjunctivitis, photophobia and cough develop.
In 1-2days small erythematousmaculeswith white
necrotic centers appear in the buccalmucosa –
known as Koplik’sspots.
Koplik’sspots generally precede the skin rash by
1-2 days.
Rash initially affects the head and neck followed by
the trunk and then the extremities.
Secondary infection may develop as otitismedia or
pneumonia.

31. Diagnostic Tests
Diagnosis made on clinical basis.
Lab confirmation can be made through virus
culture or serologic tests for antibodies to
measles virus.
Management and Treatment
No specific treatment.
Supportive therapy of bed rest, fluids, adequate
diet and analgesics usually suffice.

34. Oral lesions are not commonly seen
Include tuberculosis, syphilis

35. Aetiology
Caused by Mycobacterium tuberculosis –oral
lesions follow lung infection.
Risk factors are overcrowding, debilitation,
immunocompromised patients.
Important public health disease.
It is curable and preventable

36. One of the top 10 causes of death worldwide.
In 2015, 10.4 million people fell ill with TB and 1.8
million died from the disease (including 0.4 million
among people with HIV).
TB is a leading killer of HIV-positive people: in 2015,
35% of HIV deaths were due to TB.
Globally in 2015, an estimated 480 000 people
developed multidrug-resistant TB (MDR-TB).
South Africa has the 6
th
highest incidence of TB in the
world and TB remains the leading cause of death in
SA.

37. Low grade signs and symptoms of fever, night sweats,
malaise and weight loss may appear.
With progression –cough, hemoptysis and chest pain
develop.
Ulcer –irregular, superficial or deep, increase slowly in size,
painful
Tuberculous gingivitis –diffuse, hyperaemic, nodular,
papillary, proliferative
Oral manifestations appear on any mucosal surface –
tongue and palate are favouredlocations.
Bony involvement of the maxilla and mandible may produce
tuberculous osteomyelitis.
Pharyngeal involvement results in painful ulcers and
laryngeal lesions may cause dysphagiaand voice changes.

40. Differential Diagnosis
Primary syphilis, squamouscell carcinoma, major
aphthousulcer and chronic traumatic ulcer
Diagnostic Tests
Diagnosis confirmed by biopsy, chest radiograph
and a sputum specimen.
Management and Treatment
Multidrug chemotherapy

41. Syphilis is a sexually transmitted disease
There is an increase in sexually transmitted diseases:
•Use of contraceptives.
•Effective antibiotic treatment
•Prostitution
•Population movements: rural to urban
High risk groups:
•18-24 years (girls16-17 years)
•Frequent travelers
•Sex workers
•Homosexuals
•Army and navy personnel
•Airline crew
•Entertainment industry

42. Aetiology
Caused by the spirochete Treponema pallidum.
Transmitted from one person to another by
direct contact, transfusion of infected blood or
by transplacentalinoculation of the fetus by an
infected mother.
3 Stages
•Primary
•Secondary
•Tertiary

43. Primary syphilis -Chancre
Oral chancre appears 3-4 weeks after infection and forms
on the lip or tip of the tongue.
Consists initially of a firm nodule about a centimetre
across.
The surface breaks down after a few days leaving a
rounded ulcer with raised indurated edges.
Painless.
Little bleeding
Regional lymph nodes are enlarged, rubbery and
discrete.
Highly infective.
Heals after 8-9 weeks without scarring.

46. Secondary syphilis
Develops 1-4 months after infection.
Causes mild fever with malaise, headache, sore throat and generalised
lymphadenopathyfollowed by a rash and stomatitis.
Rash –consists of asymptomatic pinkish (coppery) macules, symmetrically
distributed and starting on the trunk.
Lasts for few hours or weeks.
Oral lesions affect the tonsils, lateral borders of the tongue and lips.
Flat ulcers covered by greyishmembrane and may be irregularly linear
(snail track ulcers) or coalesce to form well-defined rounded areas
(mucous patches).
Elevated broad-based verrucalplaques known as condylomatalatamay
also appear on the skin and mucosal surfaces.
Saliva at this stage is highly infective and lesions at this stage are most
infectious.
Undergo spontaneous remission but can recur for months or years.

49. Tertiary syphilis -Gumma
Appear after many years.
There is a predilection for the CVS and CNS.
This stage is rare because of effective antibiotic treatment.
Palate affected and can lead to palatal perforation called Gumma
–non-infectious. Tonsils and tongue can also be affected.
Gummaappears as a firm mass that eventually becomes a ulcer
which is rounded with soft, punched out edges. Floor is depressed
and pale
Heals with severe scarring.
Generalisedglossitisand mucosal atrophy also seen.
Congenital syphilis
Hutchinsonstriad –inflammation of the cornea –blindness, eight nerve
deafness and dental abnormalities –notched or screwdriver shaped
incisors and mulberry molars.

52. Differential Diagnosis
Chancre must be differentiated from squamouscell
carcinoma, chronic traumatic lesions and TB ulcer.
Differential diagnosis for secondary syphilis will include
infectious and non-infectious conditions marked by a
mucocutaneouseruption.
Gummamay resemble T-cell lymphoma.
Diagnostic Tests
Lab tests (dark field examination), biopsy, serologic tests.
Management and Treatment
Penicillin is the drug of choice for all stages of syphilis.

53. Candidosisis a common opportunistic oral
mycotic infection that develops in the presence
of one of several predisposing conditions.
Clinical presentation is variable and is
dependent on whether the condition is acute or
chronic.

54. Aetiology
Most commonly caused by C.albicans.
Predisposing factors
Immunodeficiency
Immunologic immaturity of infancy
Acquired immunosuppression
Endocrine disturbances
Diabetes mellitus
Hypoparathyroidism
Pregnancy
Hypoadrenalism
Corticosteroid therapy –topical or systemic
Systemic antibiotic therapy
Malignancies and their therapies
Xerostomia
Poor oral hygiene

55. ACUTE
Pseudomembranous–Thrush (white colonies)
Erythematous(red mucosa)
CHRONIC
Erythematous(red mucosa)
Hyperplastic(white keratoticplaque)
MUCOCUTANEOUS
Localised(oral, face, scalp, nails)
Familial
Syndrome associated

56. Acute Pseudomembranous (Thrush) forms soft, friable
and creamy colouredplaques on the mucosa.
Distinctive feature is that they can be easily wiped off to
expose an erythematousmucosa.
Varies from isolated flecks to widespread confluent plaques.
Angular stomatitisis frequently associated.
Young infants and the elderly are commonly affected.
Common in patients being treated for radiation and
chemotherapy.
Can grow at any location but favouredsites are the buccal
mucosa and mucobuccalfolds, oropharynx, lateral aspects
of the tongue.
Intraoral lesions are generally painless. In severe cases
patients complain of tenderness, burning and dysphagia.

61. Acute Erythematous(Antibiotic stomatitis)
results due to loss of pseudomembrane.
Along the dorsum of the tongue, patches of
depapillationand dekeratinizationis noted.
Affected areas are shiny, fiery red and painful.
It is related to antibiotic treatment of acute
infections.
Mucosa is red and sore. Flecks of thrush may be
seen.
Resolves with withdrawal of antibiotic and lesions
disappear with antifungal treatment.

64. Chronic erythematous(Denture sore mouth)
seen in geriatric patients with maxillary dentures.
Chronic low grade trauma as a result of poor
prosthesis fit, less than ideal occlusalrelationship,
and failure to remove appliance at night all
contribute to the development of this condition.
Appears bright red, velvety to pebbly surface with
little keratinisation.
Bleeds easily.
Smoking increases susceptibility to this infection.
Usually symptomless, but patients may complain of
pain, burning, irritation or disturbance in salivary
flow.

68. Three clinical varieties of denture sore mouth:-
Newton’s Type 1 –Localized simple inflammation or pin point
hyperaemia.
Newton’s Type 2 –Generalisedsimple inflammation –diffuse
erythemaand oedemainvolving part of or the
entire denture area. Most common form.
Affected area appears bright red and is sharply
differentiated from surrounding mucosa at
margins of denture.
Newton’s Type 3 -Granular-papillary type results when Type 2 is
not treated. Mucosa is bright red with a white
fluid over it. Papillae give rise to the corn in the
wind phenomenon. Usually involves the central
hard palate and the alveolar ridge.

69. Angular cheilitismay also be seen in patients who have deep
folds at the commissuresas a result of overclosure.
Saliva accumulates at the commissural angles and are then
colonized by yeast organisms.
Lesions are moderately painful, fissured, eroded and encrusted.
Chronic hyperplastic(candidalleukoplakia) when it occurs in
the retrocommissuralarea the lesion resembles speckled
leukoplakia.
Affects adult males of middle age.
White leathery plaques are found on the cheeks, lips and tongue.
Plaque is variable in thickness and often rough or irregular in
texture, or nodular with an erythematousbackground (speckled).
Lesion may be speckled and cannot be rubbed off.
May be associated with angular stomatitis.
Lesion resistant to antifungal therapy.

75. May involve the dorsum of the tongue –median
rhomboid glossitis.
Asymptomatic
Found anterior to the circumvallatepapillae and
has an oval or rhomboid outline.
May have a smooth, nodular or fissured surface
and range in colourfrom white to red.
Chronic mucocutaneouscandidosisis less
common and andcharacterisedby chronic
superficial involvement of the skin, scalp, nails and
mucous membrane.
Resistant to treatment.

76. Differential Diagnosis
White Candidosisshould be differentiated from chemical burns, traumatic
ulcerations, mucous patches of syphilis and white keratoticlesions.
Red lesions should be differentiated from drug reactions, erosive lichen
planusand DLE
Diagnostic Tests
Mucosal smear or biopsy
Management and Treatment
Topical (Nystatin) and systemic (Fluconazoleand ketonazole) medications
are used.
Failure to respond to topical antifungalssuggests immune deficiency.
For patients with dentures –remove denture and allow tablet to dissolve
in the mouth. Eliminate C.albicansfrom the denture base by soaking the
denture in 0.1% hypochlorite or dilute chlorhexidineovernight.

77. Management and Treatment
Correct predisposing factors
Topical (Nystatin)
•Suspension: 1ml = 100 000 units 4X daily
•Tablets –1 tablet (500 000) units 4X daily
•Ointment –100u/g apply to denture
Amphotericin B –10mg tablets 4X daily
Systemic (Fluconazole and ketonazole) medications –200mg –1
tablet/day –10 days
Miconazole (Daktarin) tablets –250mg 4X daily
Mysteclintablets (tetracycline 250mg Amphotericin 50mg); syrup 5ml 4X
daily
Failure to respond to topical antifungalssuggests immune deficiency.
For patients with dentures –remove denture and allow tablet to dissolve
in the mouth.
Eliminate C.albicansfrom the denture base by soaking the denture in
0.1% hypochlorite or dilute 0.2% chlorhexidine overnight.