1. Or al ulcers

2. ULCER= defect or break in the continuity of
the epithelial component of skin or mucosa,
so that a depression or punched out area
exists with exposure of the underlying
.connective tissue

3. Important Causes of Oral
:Mucosal Ulcers
Vesiculo-Bullous Diseases:
Infective
• Primary and recurrent Herpes simplex.
• Herpes zoster and chickenpox
• Hand-foot-and - mouth disease
• Herpangina

4. Non-infective
Pemphigus vulgaris
Mucous membrane pemphigoid
Erythema multiforme
Contact allergy

5. Ulceration Without Preceding
Vesiculation (primary):
Infective
Cytomegalovirus-associated ulceration
Some acute specific fevers
Tuberculosis
Syphilis

6. Non-infective
Traumatic ulcers
Aphthous stomatitis
Behcet’s disease
Reiter’s syndrome
Lichen planus
Acute necrotizing ulcerative gingivitis/stomatitis
Some mucosal drug reactions
Carcinoma

7. :I) Herpes Virus Infections
Several herpes viruses cause human
disease:
Herpes simplex virus (HSV) 1 and 2
Varicella-Zoster virus
Cytomegalovirus (causes oral ulcers in
immunocompromised patients)
Epstein-Barr virus
Human herpes virus 6 (HHV6)

8. Herpes Simplex Virus Infection
Primary Herpetic
Stomatitis

9. :Clinical Features
Incidence : Children 2-10 years old
Non-immune adults
Infection is unexpected below 6 months
of age due to presence of maternal
antibodies gained by the enfant during
intrauterine life.

10. Prodrome
Fever, headache, malaise, lymphadenitis,
nausea and vomiting. These precede the
appearance of oral vesicles by 1-2 days.
The early lesions: vesicles 2-3 mm in
diameter. Rupture of vesicles leaves circular,
sharply defined, shallow ulcers with yellowish
or grayish floors and red margins. The ulcers
are painful and may interfere with eating.

11. The gingival margins: are frequently
swollen and red, particularly in children.
Sometimes labial and facial lesions
appear without intraoral involvement.
Oral lesions usually resolve within a
week to ten days (Self-limiting).

12. :Pathology
Intraepithelial vesicles.
Ballooning degeneration.
Multinucleated cells.
Intranuclear inclusion bodies
(lipschutz bodies) .

13. :Diagnosis
1-History:
History of prodromal symptoms 1-2 days
before oral lesions
Negative history of recurrent herpes
labialis
Positive history of contact with a patient
with primary or recurrent lesions.

14. 2-The clinical picture
3-Lab investigations:
A smear showing virus-damaged cells
A rising titre of antibodies reaching a peak
after 2-3 weeks provides absolute but
retrospective confirmation of the
diagnosis.

15. Treatment
Supportive measures sometimes are all that is
needed .
Acyclovir is a potent antiherpetic drug. It inhibits
DNA replication in HSV-infected cells but has no
effect on normal cells.
Dose: adult: 200 mg 5 times/day (5 days)
Children: 100 mg 5 times /day (5 days)

16. Recurrent Herpes Simplex
:Lesions
Due to reactivation of latent virus residing
in cells after a previous primary attack (not
a re-infection)
A) Recurrent Herpes Labialis
B) Recurrent Intra oral Herpes

17. :A) Recurrent Herpes Labialis
Prodromal paraesthesia
or burning sensations
then erythema.
Vesicles form after an
hour or two usually in
clusters along the
mucocutaneous
junction of the lips but
can extend onto the
adjacent skin.

18. The vesicles enlarge, coalesce and weep
exudates.
After two or three days they rupture and
crust over
Finally heal, usually without scarring. The
whole cycle may take up to 10 days.
Secondary bacterial infection may change
the lesions into pustules

19. :B) Recurrent Intra oral Herpes
Clusters of small
vesicles that break
into ulcers, 1-2
mm in diameter,
appear mainly on
keratinized oral
mucosa (gingival,
hard palate, …).

20. Treatment
Treatment must start as soon as the
premonitory sensations are felt.
Acyclovir cream may be effective if
applied at this time.

21. Chronic Herpes Simplex
:Lesions
It is a variant of recurrent herpes simplex lesion
occurring in immunocompromised patients
(AIDS, immunosuppressive therapy, leukaemia,
lymphoma, …..)
Lesions appear on skin or mucosal surfaces as
an ordinary recurrent herpetic lesion but: remain
for weeks or months and develop into large
ulcers (up to several centimeters in diameter).

22. :Treatment
Systemically administered acyclovir,
doubling the dose; i.e. 400 mg 5
times/day, till healing takes place.

23. :Herpetic Cross-infections
Both primary and secondary herpetic infections
are contagious.
Herpetic whitlow, which is an infection of fingers
after manipulation of herpetic lesions, is a hazard
to dental surgeons and their assistants.
Herpetic whitlows, in turn, can infect patients
In immunodeficient patients such infections can be
dangerous but acyclovir has dramatically improved
the prognosis in such cases .
Mothers applying antiherpetic drugs to children’s
lesions should wear gloves.

24. Herpetic whitlows

25. :Varicella –Zoster infection
A) Chicken Pox
B) Herpes Zoster
(1) H Zoster of Trigeminal Area
(2) Ramsay Hunt Syndrome

26. :A) Chicken Pox
A childhood disease
characterized by:
Mild systemic symptoms.
Generalized pruritic
eruption of
maculopapular lesions
that rapidly develop into
vesicles on
erythematous base.
Oral vesicles that rapidly
rupture giving ulcers.

27. B)Herpes zoster
:(1)The trigeminal area





Recurrence of VZV infection occurs typically
in the elderly
Pain precedes the rash (prodrome)
Facial rash accompanies the stomatitis
Lesions are localized to one side (absolutely
unilateral), within the distribution of any of the
divisions of the trigeminal nerve
Malaise can be severe

28. Sometimes pain occurs without rash or
oral lesions, (herpes sine eruption) which
leads to problems in diagnosis.

29. Herpes Zoster of maxillary nerve

30. Herpes Zoster of mandibular
nerve

31. Pathology
The varicella zoster virus produces similar
epithelial lesions to those of herpes
simplex, in addition to inflammation of the
related posterior root ganglion.

32. Complications
Sometimes followed by post-herpetic
neuralgia, particularly in the elderly.
Can be life-threatening in
immunocompromised patients.
Secondary infection may cause
suppuration and scarring of the skin.
When the ophthalmic division is involved,
blindness due to corneal scarring may
occur

33. Treatment
Oral acyclovir (800 mg five times daily, usually for 7
days) as early as possible.
Intravenous acyclovir :In immunodeficient patients.
Analgesics.
The addition of prednisolone (corticosteroids) may
accelerate relief of pain and healing and prevent postherpetic neuralgia in elderly patients.

34. :Ramsay Hunt Syndrome) 2(

35. Complications
Permanent facial paralysis.
Deafness

36. :Management
Corticosteroids or ACTH are given in
addition to antiviral drugs (acyclovir) to
avoid permanent fibrosis of the facial
nerve.

37. Hand-foot-and-mouth Disease
Common mild viral infection
Causes minor epidemics among school
children
Characterized by ulceration of the mouth
and a vesicular rash on the extremities.
Caused by strains of Coxsackie A virus.
The incubation period is 3-10 days.

38. Clinical Features
Small scattered oral ulcers usually with little
pain.
Intact vesicles are rarely seen
Gingivitis is not a feature.
Regional lymph nodes are not usually enlarged
and systemic upset is mild or absent.
The skin rash consists of vesicles, sometimes
deep-seated, or occasionally bullae, mainly seen
around the base of fingers or toes, but any part
of the limbs may be affected.

39. Hand-foot-and-mouth Disease

40. Treatment
No specific treatment available or needed.

41. Herpangina



Coxsackie virus A infection (usually A4).
Children 3-10 years are mostly affected (but
other ages are possible).
Frequently occurs in epidemics.

42. Clinical Features




Incubation period: 2-10 days
Prodrome: fever, chills, anorexia, sore throat,
dysphagia
Lesions (soft palate, tonsils, pharynx):
macules → papules and vesicles → small (12 mm) ulcers.
Ulcers heal without treatment in about 7 days.

43. Herpangina

44. Tuberculosis
Ulcer on the mid-dorsum or tip of the
tongue; the lip or other parts of the
mouth are infrequently affected.
The ulcer is typically angular with overhanging edges and a pale floor, but can
be ragged and irregular.
Ulcer is painless in its early stages
regional lymph nodes are usually
unaffected.

45. Pathology
Typical tuberculous granulomas are seen
in the floor of the ulcers.

46. Management
Diagnosis
Biopsy
Chest radiography .
Specimen of sputum. Mycobacterial
infection is confirmed by culture or PCR.

47. Treatment
Oral lesions clear up rapidly if vigorous
multi-drug chemotherapy is given for the
pulmonary infection. No local treatment is
needed.

48. Syphilis
Primary Syphilis:
An oral chancre appears 3-4 weeks after infection on the
lip, tip of the tongue or rarely, other oral sites.
It consists initially of a firm nodule about a centimeter
across. The surface breaks down after a few days, leaving
a rounded ulcer with raised indurated edges.
A chancre is typically painless but regional lymph nodes
are enlarged, rubbery and discrete.
Serological reactions are negative at first.
Treponema pallidum can be demonstrated by darkground illumination of a smear from the chancre.
Oral chancres are highly infective.
After eight or nine weeks the chancre heals, often without
scarring

49. Secondary Syphilis:
Develops 1-4 months after infection.
Mild fever with malaise, headache, sore throat and
generalized lymphadenopathy, soon followed by a rash
and stomatitis.
The rash consists of asymptomatic pinkish (coppery)
macules, symmetrically distributed and starting on the
trunk. It may last for a few hours or weeks
Oral lesions, which rarely appear without the rash, mainly
affect the tonsils, lateral borders of the tongue and lips.
They are usually flat ulcers covered by grayish membrane
and may be irregularly linear (snail track ulcers) or
coalesce to form well-defined rounded areas (mucous
patches).
Discharge from the ulcers contains many spirochaetes
and saliva is highly infective.
Serological reactions are positive and diagnostic at this
stage.

52. Tertiary Syphilis:
Develops in many patients about three or more
years after infection.
A characteristic lesion is the gumma.
Clinically, a gumma, which may affect the
palate, tongue or tonsils can vary from one to
several inches in diameter.
It begins as a swelling, sometimes with a
yellowish centre which undergoes necrosis,
leaving a painless deep ulcer. The ulcer is
rounded, with soft, punched-out edges. The floor
is depressed and pale.
It eventually heals with severe scarring which
may distort the soft palate or tongue, perforate
the hard palate or destroy the uvula.

54. Minor aphthous ulcer

55. Major aphthous ulcer

56. Herpetiform ulcers

57. Clinical Picture
Lesions are confined to oral mucosa ( no
extraoral manifestations).
Prodrome: burning sensation (2-48
hours) with the appearance of localized
erythema
Ulceration: single or multiple ulcers
appear within few hours. Ulcers are
surrounded by erythema and painful. No
tissue tags surround the ulcers.

58. Healing: in minor form it takes 7-14 days,
in major ulcers it may take several
months. No scar formation occurs except
in major form.
Healing is characterized by
disappearance of the surrounding
erythema.

59. Diagnosis and Management
Check-list for Diagnosis of Recurrent
Aphthae:
History
Examination
Special investigations

60. Treatment
In cases with underlying systemic
disease : remedy the cause
For minor aphthae: treatment is related
to the severity.

61. In mild cases:
Protective topical treatment as orabase
Topical anaesthetic
Non-steroidal anti-inflammatory
Benzydamine hydrochloride mouth wash.
In more severe cases:
Potent topical steroid asTriamcinolone
dental paste

62. Treatment of major aphthae.
Effective treatments include
Systemic or intralesional steroids,
Azathioprine,
Cyclosporine
Colchicines and
Dapsone.

63. Tetracycline mouth rinses. For
herpetiform aphthae particularly .
Chlorhexidine. A 0.2% solution has also
been used as a mouth rinse for aphthae.

64. Behcet's Disease
Behcet's syndrome was originally defined
as a triad of oral aphthae, genital
ulceration and uveitis. However, it is a
multisystem disorder with varied
manifestations.
Patients are usually young adult males
between 20 and 40 years old.

65. Patients suffer one of four patterns of disease:
Mucocutaneous (oral and genital ulceration)
Arthritic (joint involvement with or without
mucocutaneous involvement)
Neurological (with or without other features)
Ocular (with or without other features).
The oral aphthae of Behcet's disease are not
distinguishable from common aphthae. They are
the most consistently found feature and
frequently the first manifestation.

66. Diagnosis
Pathergy Test:
The test is positive if there is an
exaggerated response to a sterile needle
puncture of the skin, where such puncture
is followed by pustule formation.

67. Diagnostic criteria for Behcet's
disease
Major Criteria
Recurrent oral aphthae
Genital ulceration
Eye lesions (uveitis, retinal vasculitiz )
Skin lesions(Erythema nodosum, subcutaneous
thrombophlebitis, hyperirritability of the skin +ve
pathergy test)

68. Minor Criteria
Arthralgia or arthritis
Gastrointestinal lesions
Vascular lesions (mainly thrombotic)
Central nervous system involvement

69. Treatment
No specific treatment, but oral lesions can be
controlled by:
Topical or intralesional corticosteroids
Topical anaesthesia to alleviate pain
Systemic corticosteroids in resistant cases
(40-60 mg prednisone/day).
Combination of steroid and immunosuppressive
drugs (e.g. azathioprine).

70. Reiter’s Syndrome
A triad of urethritis, arthritis and conjunctivitis.
Oral manifestations:
Painless circinate white lesions that may
ulcerate giving aphthous-like ulcers.
Geographic tongue like lesions
Purpuric rash in palate

71. Treatment
Oral lesions are self limiting

72. Erythema Multiforme
This is an acute inflammatory
mucocutaneous disease but among dental
patients oral lesions are the most
prominent or the only ones present

73. Aetiology
Infections, particularly herpetic can be
triggering factors.
Drugs, particularly sulphonamides and
barbiturates.
In most patients no precipitating cause
can be found.

74. The histological appearance
Intraepithelial or subepithelial vesicle or
bulla formation due to widespread
necrosis of keratinocytes
Infiltration by inflammatory cells which
also involve the corium and may have a
perivascular distribution.

75. Clinical Picture
Erythema Multiforme Major-Stevens
Johnson Syndrome
Erythema Multiforme Minor

80. Typical cases show at least some target (or iris)
lesions. A typical target lesion is less than 3 cm
in diameter, rounded, and has three zones: a
central area of dusky erythema or purpura, a
middlepaler zone of oedema and an outer ring of
erythema with a well-defined edge.
Atypical target lesions have only two of the
zones
The kobner phenomenon

81. Localized vesiculobullous form
This form is intermediate in severity. The
skin lesions present as erythematous
macules or plaques, often with a central
bulla and a marginal ring of vesicles.
Mucous membranes are quite often
involved.

82. Erythema Multiforme Major:Stevens Johnson Syndrome
Stevens-Johnson Syndrome,
Toxic epidermal necrolysis

83. The onset is usually sudden
There may be a prodromal systemic
illness of 1-13 days before the eruption
appears.
Numerous organs are affected, changes
were found with the following frequency:
mouth 100% eyes, skin, male genitalia,
anal mucous membrane, bronchitis and
pneumonitis.

84. :Management
Systemic corticosteroids
Antibiotics are usually also given in severe
cases

85. :Pemphigus Vulgaris
Pemphigus is an uncommon autoimmune
disease causing vesicles or bullae on skin
and mucous membranes. It is usually fatal
if untreated

86. :Clinical Features
Females aged 40-60 years are predominantly affected.
Lesions often first appear in the mouth but spread widely
on the skin.
Vesicles are fragile . Residual erosions often have
ragged edges and are superficial, painful and tender.
Positive Nikolsky's sign.
Oral lesions show lack of inflammatory signs unless
secondary infection occurs.
Extension of lesions to the vermilion border may lead to
the formation of a crusted lesion.

89. :Pathology
Intra epithelial vesicles and bullae are
formed. Lesions result from the
destruction of desmosomal junction
between prickle cells and basal cells due
to the presence of autoantibodies against
desmoglein 3 which is an attachment
molecule in desmosomes.

90. Management
Diagnosis is confirmed by direct
immunofluorescence and by the demonstration
of circulating autoantibodies.
60-100 mg/day of predisolone alone or in
addition to azathioprine (1-1.5 mg/kg daily).
Azathioprine is given to allow doses of the
conrticosteroid to be lowered and reduce their
side-effects. Intralesional steroid application may
help.

91. Mucous Membrane (Cicatricial)
:Pemphigoid
Mucous membrane pemphiogoid is an
uncommon chronic disease causing bullae and
painful erosions.
Skin involvement is uncommon and often trivial.
In stead, mucous membranes all over the body
are affected. The term cicatricial pemphigoid is
sometimes used for this group of disease, but
particularly applies to ocular involvement where
scarring is prominent and impairs sight.

92. :Desquamative Gingivitis
The term desquamative gingivitis is a
clinical description, not a diagnosis. It is
used for conditions in which the gingivae
appear red or raw. Usually the whole of
the attached gingival of varying numbers
of teeth is affected

93. :Oral Reactions to Drugs
Many drugs can occasionally cause oral
reactions. They are varied in type but
frequently lichenoid or ulcerative. The
mechanisms of reactions to drugs are
often obscure