Ulcers

1. Ulcerative lesions of oral cavity
Presented by: ROSHNI MAURYA,2ND YEAR PGT
DEPT. OF PEDODONTICS & PREVENTIVE
DENTISTRY,GNIDSR

2. INTRODUCTION
• Injury to the oral mucosa may result in a localized defect of the
surface in which the covering epithelium is destroyed leaving an
inflammed area of exposed connective tissue.
• Such defects are called ulcers or erosions (term commonly used for
superficial ulcer)
• This may either follow molecular death of surface epithelium or its
traumatic removal.
• Ulceration is the most common lesion of oral mucosa and is the
manifestation for many local and genetic disorders.

3. What is an ulcer?
• Latin origin ULCUS means break in the skin.
• A mouth or oral ulcer is an open sore in the mouth, or
rarely a break in the mucous membrane or the epithelium
on the lips or surrounding the mouth.

4. • The surface of an ulcer is covered by mass of fibrin with
intermingled, dead and dying polymorphs which would dry on
the skin to form a crust or scab.
• A superficial ulcer with no evidence of significant fibrinous
exudation on the surface of polymorph exudation suggests the
possibility of bullous disorder.
• A heavy inflammatory infiltrate extends deep into the
underlying connective tissue n blood vessels may show slight
inflammatory vasculitis.
• Granulation tissue is formed with dilated blood vessels and
heavy infiltrate of plasma cells, lymphocytes and polymorphs.

5. PARTS OF AN ULCER
• Ulcer consists of:
1. Edge:- area between the margin and floor of ulcer.This
is an important finding of an ulcer which by itself not
only gives clue to diagnosis ulcer but also to the
condition of ulcer.
2. Floor:- this is the exposed part of an ulcer. The covering
of floor is important.
3. Base (on which the ulcer rests):- floor is the exposed
surface of an ulcer whereas the base is on which the
ulcer rests. Floor is seen but the base is felt.
4. Margin:- it’s the point where the ulcer joins the normal
epithelial tissue.

6. Parts of an ulcer :Davis et al. Symptom Analysis
and Physical Diagnosis (2nd edn), p. 309

7. The classic appearances of various ulcers are presented
. Infective ulcers due to Mycobacterium species, and bed sores, tend to have an undermined edge
while a trophic ulcer is punched out and typically round in surface shape. A raised firm ulcer edge
may indicate malignancy

8. • Histological examination
shows an ulcer covered
by thick layer of fibrous
exudate with a dense,
chronic inflammatory
cell infiltrate in its base
involving underlying
damaged muscle.
• The deeper parts
contain infiltrate rich in
histiocytes and
eosinophils.
• True granulomas are not
present.

9. CLASSIFICATION OF ULCERS
• TWO TYPES OF CLASSIFICATON OF ULCERS IS
POSSIBLE:-
1. CLINICAL:

10. PATHOLOGIC ULCERS
• Ulcerations are classified on the basis of etiology.
• CAUSES OF ORAL ULCERATIONS:-
1. Local Causes
2. Aphthae
3. Infections
4. Drugs
5. Systemic disease
6. Malignant disease

11. 1) Local Causes:
i) Trauma (physical)
- Appliances.
- Self-inflicted.
- Sharp teeth or restorations.
- Iatrogenic.
ii) Burns (chemical ant thermal )
- Chemical.
- Electric.
- Heat.
- Radiation.

12. 2) Recurrent aphthae
i) Minor ulcers
ii) Major ulcers
iii) Herpetiform type

13. 3) Infections
i) Viral
- Vesiculobullous diseases caused by viruses
- Human herpesvirus 8 (HHV-8)
- Human Immunodeficiency virus
ii) Bacterial
- Acute Necrotizing Ulcerative Gingivitis
(ANUG)
- Syphilis
- Tuberculusosis
iii) Fungal
- Chronic Mucocutaneous Candidosis (CMC)

14. 4) Drugs
i) Drug-induced neutropenia/anaemia (cytotoxics)
ii) Lichenoid drug reactions (e.g. β-blockers,
NSAIDs)
iii) Drug-induced mucositis (cyclophosphamide)

15. 5- Malignant diseases
i) Oral squamous cell carcinoma
ii) Kaposi’s sarcoma
iii) Non-Hodgkin’s lymphoma

16. 6) Systemic diseases
i) Mucocutaneous diseases
ii) Haematological disorders
iii) Gastrointestinal disorders

17. i) Mucocutaneous disease
- Behcet’s syndrome
- Lichen planus
- Vesiculobullous diseases

18. 6) Systemic diseases
ii) Haematological disorders
- Anaemia
- Leukemia

19. 6) Systemic diseases
iii) Gastrointestinal disorders
- Coeliac disease (Gluten-sensitive entropathy)
- Crohn’s disease
-

20. • The most widely accepted form divides them into acute
ulcers--sudden onset and short lasting—and
• chronic ulcers--insidious onset and long lasting.
• Commonest acute oral ulcers include traumatic ulcer,
recurrent aphthous stomatitis, viral and bacterial infections
and necrotizing sialometaplasia.
• On the other hand, oral lichen planus, oral cancer, benign
mucous membrane pemphigoid, pemphigus and drug-
induced ulcers belong to the group of chronic oral ulcers.

21. Epidemiology and Frequency
• Mouth ulcer is a very common oral lesion.
Epidemiological studies show an average
prevalence between 15% and 30%. Mouth ulcers
tend to be more common in women and those
under 45.
• The frequency of mouth ulcers varies from fewer
than 4 episodes per year (85% of all cases) to more
than one episode per month (10% of all cases)
including people suffering from continuous
recurrent aphthous stomatitis .

22. Epidemiology of the most common
oral mucosal diseases in children
• The lesions most frequently considered by authors and that most
often appear in the different studies are: recurrent aphthous
stomatitis (0.9-10.8%), labial herpes (0.78-5.2%), fissured tongue
(1.49-23%), geographic tongue (0.60-9.8%), oral candidiasis (0.01-
37%) and traumatic injury (0.09%-22.15%).
• {Med Oral Patol Oral Cir Bucal 2005 Nov-Dec;10(5):376-87}

23. Diagnostic Tools for Oral Mucosa Lesions
Andrea Santarelli, DDS; and Lorenzo Lo Muzio, PhD, MD July 2012 Issue -
Expires July 31st, 2015 Inside Dentistry -
• Lesions of the oral mucosa represent a diagnostic challenge for dental
practitioners, because similar appearances are the final common
manifestation of a wide spectrum of conditions, including autoimmune
diseases; neoplastic, traumatic, or infectious lesions; nutritional
deficiencies; and drug reactions, as well as oral manifestations of systemic
diseases. One of the roles of dental practitioners is the identification and
management of oral mucosa diseases. While the diagnosis of some oral
lesions can be made on the basis of the history and/or clinical findings, for
others, the definitive diagnosis requires the aid of some tools with which
the general dentist should be familiar. -

24. Tools for diagnosis:
• History
• Examination
• Further investigation
• Additional diagnostic methods – biopsy

25. Further investigation – questions
one should ask:
• How long have you had that ulcer?
• How many ulcers do you have?
• Is it painful?
• Can you relate them to any trauma, hot food or
another factors?
• Is it the first time or you had them before?
• Where are they located in the mouth?
• Do they start as ulcer or as vesicle/bulla?
• Do you get them anywhere else on the body?

26. Things one need to look for:
• Site
• Number
• Size
• Shape
• Base
• Edge

27. Differential diagnostic, based on history
• How long have you had the ulcer?
Long time – chronic
1. Chronic trauma (single, can identify the cause, and
should improve after removal)
2. Malignancy (single, painless)
3. TB (single ulcer in the tongue/palate, associated
symptoms – chronic cough)
4. Mucous membrane pemphigoid (multiple ulcers affect
mainly gingiva, blood filled blisters)
5. Primary or tetriary syphilis

28. Recent – acute
1. Acute trauma (single, can identify the cause, and
should improve after removal)
2. Viral infection (multiple, associated symptoms –
fever)
3. Immune mediated disease (Erythema multiforme,
RAS)

29. How many ulcers do you have?
• Single
1. Traumatic
2. Primary or tetriary syphilis
3. TB
4. Malignancy
• Multiple
1. Viral infection
2. Immune mediated disease

30. Is it painful?
• Yes
Acute causes (trauma, viral, immune mediate)
• No
Chronic causes (trauma, TB)

31. Can you relate them to trauma or hot food?
• Yes
1. Confirm traumatic ulcer
2. Remove the cause
3. Review after 1 week
• No
Look for other causes

32. Do you get them anywhere else on the body?
• No
Think of oral conditions
• Yes – where?
1. Skin – mucocutaneous disease (lichen planus,
pemphigus)

33. Traumatic ulcers:

34. Traumatic ulcers :
1- Physical Trauma:
- Physical traumatic ulcers are common oral lesions.
- Can be caused by a sharp or broken tooth, rough fillings, dental
instruments, biting, denture irritation, dental braces; sharp
foreign bodies, etc.
Ulcerative lesions
1) Local Causes:

36. Dental braces

37. 1- Physical Trauma:
Clinical features:
-They are clinically diverse, but usually appear as a single, painful
ulcer with a smooth red or whitish-yellow surface and a thin
erythematous halo. They are usually soft on palpation, and heal
without scarring within 6–10 days, spontaneously or after removal
of the cause.
Ulcerative lesions
Traumatic ulcers
1) Local Causes:

38. 1- Physical Trauma:
Clinical features:
- However, chronic traumatic ulcers may clinically mimic a carcinoma.
-The tongue, lip, and buccal mucosa are the sites of predilection.
-The diagnosis is based on the history and clinical features. However,
if an ulcer persists over 10–12 days a biopsy must be taken to rule
out cancer.
Ulcerative lesions
Traumatic ulcers
1) Local Causes:

39. Physical traumatic Ulcer

40. Ulcerative lesions
Traumatic ulcers
1- Physical Trauma:
Differential diagnosis Squamous-cell carcinoma and other
malignancies, aphthous ulcer, syphilis, tuberculosis.
Treatment Removal of traumatic factors. Topical steroids may be
used for a short time.

41. Ulcerative lesions
Traumatic ulcers
2- Chemical trauma:
-Oral ulcers may arise with local application of Aspirin (Salicylic Acid),
-Clinical features:
- It appears as a red, painful erythema that may undergo
desquamation, leaving erosions.
-The lesions heal spontaneously in about a week.
-The diagnosis is made exclusively on clinical grounds.

42. Chemical (Aspirin burn) ulceration:
-The photos show a patient who placed
an aspirin on her gums. Aspirin is an
acid and burned the oral tissues (gums
and cheek).
- Fortunately the mouth heals quickly
and within two weeks healing
occurred.

43. Ulcerative lesions
Traumatic ulcers
2- Chemical trauma:
Differential diagnosis
- Thermal burn, traumatic lesions, aphthous ulcers, drug reactions.
Treatment
- Discontinue the application of the causative agent.

44. RADIATION TRAUMATIC ULCERATION
• Oral mucosa may suffer immediate
damage due to direct effects of radiation
on cells or delayed effects due to
epithelial atrophy and damage to
underlying vascular bed during
radiotherapy of head n neck cancer.
• The immediate effects are erythema,
radiation mucositis and ulceration.
• Oedema due to obstruction of regional
lymphatics may occur.
• Radiation ulcers are painful.

45. EOSINOPHILIC ULCER
• Its also referred to as traumatic granuloma or
eosinophilic granuloma of tongue.
• It is particularly associated with trauma n injury
although the pathogenesis is unclear.trauma may
be due to missing,malposed teeth,partial denture
or more commonly,erupting teeth during nursing
which results in sublingual ulcerations in infants.
• It occurs most commonly on the tongue and
presents clinically as chronic, well demarcated
ulcer which may mimic a sq. Cell carcinoma.

47. 2-Recurrent Aphthous Stomatitis
Ulcerative lesions
- Recurrent aphthous ulcers are among the most common oral mucosal lesions, with
a prevalence of 10–30% in the general population.
-The cause remains unclear. Recent evidence supports the concept that cell-mediated
immune responses play a primary role in the pathogenesis.
- Several predisposing factors have been reported, such as trauma, allergy, genetic
predisposition, endocrine disturbances, emotional stress, hematological ,nutritional
deficiencies, and AIDS.
-Three clinical variations have been recognized: minor, major and herpetiform ulcers.
-They are very painful and cause the patient a lot of discomfort.

48. Herpetiform recurrent Aphthous Stomatitis
-The herpetiform variation is characterized by small, painful, shallow ulcers, 1–2 mm
in diameter, with a tendency to coalesce into larger irregular ulcers.
- Characteristically, the lesions are multiple (10–100), persist for one or two weeks,
and heal without scarring.
- usually in old age group, common in females.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis

49. Herpetiform aphthae

50. Minor recurrent Aphthous Stomatitis
-Minor aphthae are the most common form, and they present clinically
as small, painful, round ulcers 3–6 mm in diameter, covered by a
whitish-yellow membrane and surrounded by a thin red halo.
-The lesions may be single or multiple (two to six), and they heal
without scarring in 7–14 days.
- Mainly found in on the non-keratinized mobile mucosa, lips, cheeks,
floor of the mouth.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis

51. Minor aphthous ulcer

52. Major recurrent Aphthous Stomatitis
-The major form is characterized by deep painful ulcers, 1–2 cm in
diameter, that persist for 3–6 weeks and may cause scarring.
- The number of lesions varies from one to ten.
- Found in any area of the mucosa, including keratinized dorsum of
the tongue, palate.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis

53. Major aphthous ulcer

54. Aphthous Lesions
Clinical Types
• Minor (Lip) Minor (Tongue)
Major

55. CLINICAL FEATUERS OF RECURRENT
APHTHOUS STOMATITIS

56. Oral Aphthous Lesions
Treatment Options
• Topical Therapy
- Topical Corticosteroids
• Intralesional
- Triamcinolone: 40 mg /ml (0.5 ml-1.0 ml injected
bid)
• Systemic Therapy
- Prednisone:
•
- Diet supplementation:
• Vit.B12,FOLIC ACID,IRON,ZINC SULFATE

57. Ulcerative lesions
3) Infections
i) Viral - Herpetic gingivostomatitis , herpangia , hand-foot
and mouth disease, varicella ,EBV
- Human herpesvirus 8 (HHV-8)
- Human Immunodeficiency virus
- Vesiculobullous diseases caused by viruses
ii) Bacterial - Acute Necrotizing Ulcerative Gingivitis
(ANUG)
- Syphilis
- Tuberculosis,
leprosy
iii) Fungal - Chronic Mucocutaneous Candidosis
(CMC)

58. Primary herpetic gingivostomatitis
• Most common cause of severe oral ulceration in
children.
• Caused by simplex type 1 virus
• Usually occurs after 6 months of age.
• Peak incidence: b/w 12 & 18 months of age
• Incubation time:3-5 days with a prodromal 48 hour
history of irritability, pyrexia and malaise
• Child is often unwell, has difficulty in eating and
drinking and typically drools.

59. Clinical features
• Stomatitis is present
• Gingival tissues becoming red & oedematous
• Intra-epithelial vesicles appear; rapidly breakdown to
form painful ulcers.
• Vesicles may form on any part of the oral mucosa,
including the skin around the lips
• Solitary ulcers are usually small (3mm);painful with
an erythematous margin, but larger ulcers with
irregular margins often result from the coalescence
of individual lesions.
• Disease is self –limiting and the ulcers heal
spontaneously without scarring within 10-14 days.

61. Diagnosis:
• History & clinical features
• Exfoliative cytology
• Viral antigen can be detected by PCR
amplification.
• Viral culture
• Viral antibody detection in blood samples

62. Management
• Symptomatic care
• Encourage oral fluids
• Analgesics
• Mouthwashes for older children : CHX gluconate
,0.2%, 10 ml 4- hourly.
• Topical anaesthetics: lidocaine viscous 2% or
lidocaine (xylocaine) spray
• Antiviral chemotherapy

63. Herpangina
By coxsackievirus
A4
Affect children from
3-10 years ,peak
from June to
October

64. Clinical features
• -prodrome ,milder than herpes simplex (fever
,anorexia ,malaise)
• -sore throat ,dysphagia
• -ulcers mainly at post .area of oral cavity (soft
palate ,fauces ,tonsils ,posterior pharynx)
• -ulcers smaller than herpes
• -at post area and more painful.
• -no marginal gingivitis
• -mainly in epidemics

65. -Hand- foot and mouth
disease
Caused by
coxsackie virus
A16,from 8
months to 33 years
,75%under 4 years.

66. Clinical features
• -low grade fever
• -oral vesicles and ulcers more extensive than
herpes(mainly palate ,buccal mucosa)
• -macules and papules on extensor surface of
hand and feet.
• -examine hands and feet for maculopapular
lesions and vesicles if there is acute
stomatitis and fever

67. Infectious mononucleosis
• Caused by Epstein –Barr virus (EBV)
• Mainly affects older adolescents and young adults.
• Disease is highly infective and is characterized by
malaise, fever and acute pharyngitis.
• In young children, ulcers and petechiae are often
found in posterior pharynx and soft palate.
• Disease is self limiting

68. Diagnosis
• History & clinical features
• Paul –Bunnell agglutination test and atypical
monocytes on blood film

69. Varicella
• A highly contagious virus causing chickenpox in younger
subjects and shingles in older individuals.
• There is prodromal phase of malaise and fever for 24
hours followed by macular eruptions and vesicles.
• In chickenpox, oral lesions occur in around 50% of cases
but only a small number of vesicles occur in the mouth
• These lesions may be found anywhere in the mouth in
addition to other mucosal sites such as conjunctivae,
nose or anus .
• Healing of oral lesions is uneventful

70. Diagnosis
• Clinical appearance and history

71. Human Herpes virus-8 (HHV-8)
-The causative microbe for Kaposi’s sarcoma (KS).
-Kaposi sarcoma is a malignant neoplasm of endothelial cell
origin.
-Four forms of KS are recognized:
Classic, African (endemic), Immunosuppression-associated
(iatrogenic) and
AIDS-related (epidemic): This has a high incidence among AIDS
patients, primarily involves the skin, lymph nodes, viscera, and
frequently the oral mucosa.

72. Human Immunodeficiency Virus (HIV)
- A minority of patients with severe HIV disease will develop
deep, necrotic ulcers of unknown aetiology.
- These ulcers are painful, cause profound dysphagia and can
arise on any oral mucosal surface, although the buccal and
pharyngeal mucosa are the more commonly affected sites.

73. Human Immunodeficiency Virus (HIV)
-The ulcers typically resolve with systemic thalidomide
(e.g. 200 mg daily)
- Small number of patients with HIV disease may have
ulcers similar to that of recurrent aphthous stomatitis
(RAS), although whether the frequency of RAS in HIV is
truly increased remains unclear.

74. HIV-associated ulceration

75. 2- Bacterial
i) Acute Necrotizing Ulcerative Gingivitis
(ANUG)
ii) Syphilis
iii) Tuberculusosis
iv) Leprosy

76. i) Acute Necrotizing Ulcerative Gingivitis (ANUG)
-This entity used to be called "Trench Mouth" because of its
prevalence in soldiers fighting in the trenches during world
war I.
- Etiology: Fusobacterium nucleatum, Treponema
vincentii, and probably other bacteria play an important
role.
- Predisposing factors are emotional stress, smoking, poor
oral hygiene, local trauma, and mainly HIV infection.

77. Clinical features
The characteristic clinical feature is painful necrosis of the
interdental papillae and the gingival margins, and the
formation of craters covered with a gray pseudomembrane.
- Spontaneous gingival bleeding, halitosis, and intense
salivation are common. Fever, malaise, and
lymphadenopathy are less common.
-Rarely, the lesions may extend beyond the gingiva
(necrotizing ulcerative stomatitis).
-The diagnosis is made at the clinical level.

78. ِAcute Necrotizing Ulcerative Gingivitis

79. - Differential diagnosis
- Herpetic gingivitis, Desquamative gingivitis,Agranulocytosis,
leukemia.
- Treatment
Systemic metronidazole and oxygen-releasing agents topically are
the best therapy in the acute phase, followed by a mechanical
gingival treatment.

80. ii) Syphilis
- Syphilis is a relatively common sexually transmitted disease.
- Etiology Treponema pallidum.
-Clinical features: Syphilis may be acquired (common) or
congenital (rare).
- Acquired syphilis is classified as primary, secondary and
tertiary.

81. Clinical features:
-The characteristic lesion in the primary stage is the chancre
that appears at the site of inoculation, usually three weeks after
the infection.
- Oral chancre appears in about 5–10% of cases, and clinically
presents as a painless ulcer with a smooth surface, raised
borders, and an indurated base.
- Regional lymphadenopathy is a constant finding.

82. Solitary chancre on the ventral surface of
the tongue
Two chancres on the tongue

83. - Differential diagnosis
Traumatic ulcer, aphthous ulcer, tuberculosis, herpes
simplex, candidiasis, erythema multiforme, lichen
planus.
-Treatment
Penicillin is the antibiotic of choice. Erythromycin or
Cephalosporins are good alternatives.

84. iii) Tuberculosis
-Tuberculosis is a chronic, granulomatous,
infectious disease that primarily affects the lungs.
- Etiology
-Mycobacterium tuberculosis.

85. •Clinical features
- The oral lesions are rare, and usually secondary to
pulmonary tuberculosis.
- The tuberculosis ulcer is the most common feature.
- Clinically, the ulcer is painless and irregular, with a
thin undermined border and a vegetating surface,
usually covered by a gray-yellowish exudate.
- The dorsum of the tongue is the most commonly
affected site, followed by the lip, buccal mucosa,
and palate.

86. -
- Differential diagnosis:
- carcinomas, syphilis, eosinophilic ulcer, necrotizing
sialadenometaplasia, malignant granuloma, major
aphthous ulcer.
- Treatment
- Antituberculous drugs.

87. Tuberculosis: typical ulcer on the dorsal surface of the tongue

88. Leprosy
• Children are deemed more susceptible to leprosy
because of their immature immune systems.
Mycobacterium leprae is a member of the same
family of organisms found to cause tuberculosis.
• The disease affects multiple systems and organs of
the body such as the nerves leading to muscle
weakness, the liver, kidneys, eyes resulting in
blindness, lymph nodes, bones, and joints. The bones
are resorbed and deformity occurs.

89. Oral Manifestations
• The oral manifestations of leprosy may be present in
19% to 60% of patients. Shambulingappa, et al. (2012)
states that the oral examination is neglected in most
leprosy clinics today.
• When oral lesions appear, they usually occur in the LL
form (disseminative and progressive lepromatous
form). This form presents with the most severe effects
on the body. The second form is the tuberculoid form
(TT), and this form is less contagious. Combinations of
both types may also occur. Oral lesions occur in the
palate intraorally, but may manifest as skin lesions
periorally affecting the lips. The lips present as
macrocheilia and exhibit flat-topped nodules.

90. • Other oral lesions may occur causing superficial ulcers,
candidiasis, fissured tongue, and loss of papillae,
glossitis, and swellings.
• Treatments for leprosy include antibiotics, anti-
inflammatory medications, steroids, thalidomide, or
combinations of MRD therapy, depending upon the
type and extent of the leprosy. Often, pain and
ulceration are treated as other complications would
be treated to relieve discomfort.

91. • The World Health Organization estimates
approximately 182,000 cases world wide in 2012,
with elimination of the disease in 119 countries out
of 122 since 1985. However, new cases have recently
been reported to have increased in India.

92. OTHER
INFEC-TIONS
CLINICAL FEATURE CAUSE SIGNIFICANCE
GONORRHEA GENITAL LESIONS WITH RARE ORAL
MANIFESTATIONS; ERYTHEMA OR
ULCERS
N.gonorrhea MAY BE CONFUSED WITH
OTHER ULCERATIVE DISEASES
TUBERCULOSIS INDURATED, CHRONIC ULCER THAT
MAY BEPAINFUL- ON ANY MUCOSAL
SURFACE
M.tuberculosis INFECTIOUS ORAL LESIONS
ARE ALWAYS RESULT OF LUNG
LESIONS
LEPROSY SKIN DISEASE WITH RARE NODULES
OR ULCERS
M.leprae COMMON IN SOUTHEAST
ASIA, INDIA, SOUTHAMERICA
ACTINOMYCOSI
S
TYPICALLY SEEN IN MANDINLE,
WOOD HARD NODULE WITH
SULFUR GRANULES
A.israelii INFECTION FOLLOWS ENTRY
THROUGH SURGICAL SITE,
PERIODONTAL DISEASE OR
OPEN ROOT CANAL
NOMA NECROTIC, NONHEALING ULCER OF
GINGIVA OR BUCCAL MUCOSA;
RARE; AFFECTS CHILDREN
ANAEROBES IN PATIENT
WHOSE SYSTEMIC HEALTH
IS COMPROMISED
OFTEN ASSOCIATED WITH
MALNUTRITION; MAY RESULT
IN TISSUE DESTRUCTION

93. 3- Fungal
Chronic Mucocutaneous Candidosis (CMC)
-Chronic mucocutaneous candidiasis (CMC) is the label
given to a group of overlapping syndromes that have in
common a clinical pattern of persistent, severe, and diffuse
cutaneous candidal infections.
-These infections affect the skin, nails and mucous
membranes
- Chronic oral candidiasis
-Related to denture stomatitis
-HIV-associated candidiasis
-Related to inhaled corticosteroid use

94. CMC

95. DRUG-INDUCED LESIONS
• A wide spectrum of drugs can occasionally cause
mouth lesions, by various mechanisms. Ulcers
• are common in those treated with cytotoxic drugs.
The more common examples of drug reactions
include:
• Cytotoxic agents, particularly methotrexate,producing
ulcers.
• Agents producing lichen-planus-like (lichenoid)
lesions, such as non-steroidal anti-inflammatory
agents, some antihypertensives, antidiabetics, gold
salts, antimalarials and other drugs.

96. • Agents causing local chemical burns (especially
aspirin held in the mouth).
• Agents causing erythema multiforme (especially
sulphonamides and barbiturates).
• Other drug reactions are uncommon or rare.
• Cytotoxic induced ulcers: these have a nonspecific
appearance, but are widespread and very painful.
• Lichenoid lesions: resemble lichen planus clinically
and histologically

97. Management
• Diagnosis of a drug reaction is made from the drug
history and sometimes by testing the effect of
withdrawal. Skin patch tests are, unfortunately,
rarely of real practical value.
• Treatment is to stop the causative drug and treat
the ulceration symptomatically with topical
benzydamine and, possibly, aqueous chlorhexidine.

98. Management
• Diagnosis of a drug reaction is made from the drug
history and sometimes by testing the effect of
withdrawal. Skin patch tests are, unfortunately,
rarely of real practical value.
• Treatment is to stop the causative drug and treat
the ulceration symptomatically with topical
benzydamine and, possibly, aqueous chlorhexidine.

99. Ulcerative Lichen Planus in
Childhood
• Lichen planus (LP) is an autoimmune, chronic, inflammatory
disease that affects mucosal and cutaneous tissues.
• The exact etiology is unknown, but it is believed to result
from an abnormal T cell-mediated immune response in which
basal epithelial cells are recognized as foreign because of
changes in the antigenicity of their cell surface
• Oral lichen planus (OLP) is a common disease in the middle
aged and elderly population and has a prevalence of about
0.5% to 2%.
• By contrast, oral lichen planus in childhood (OLP) is rare and it
was first reported in the 1920s.
• Oral mucosal involvement in adults itself accounts for 0.5% to
19%, while in children, it is very uncommon

100. • The oral lesions are more pleomorphic than those
of their cutaneous forms and subtypes are
categorized as reticular, papular, plaque-like,
atrophic, erosive, and bullous .
• The erosive form is extremely rare in children and
few reports on this subject have been published in
the literature.

101. • OLP in childhood was first described in 1920 and since
then only few articles have been published and most
of the studies have suggested that childhood LP is
more common in tropical countries like India(A. J.
Kanwar andD.De, “Lichen planus in childhood: report
of 100 cases,” Clinical and Experimental Dermatology,
vol. 33, pp.423–427, 2008.)
• Sharma and Maheshwari reported 50 children with LP
and with concomitant oral lesions in 15 of them and
they stated that the oral mucosa seems to be less
commonly involved in children with LP than in
adults.(R. Sharma and V. Maheshwari, “Childhood
lichen planus: a report of fifty cases,” Pediatric
Dermatology, vol. 16, no. 5, pp. 345–348, 1999.)

102. • Kanwar and Kumar reported only one case having
oral ulcerative lichen planus out of 25 patients with
cutaneous lichen planus [A. J. Kanwar andD.De,
“Lichen planus in childhood: report of 100 cases,”
Clinical and Experimental Dermatology, vol. 35, no.3,
pp. 257–262, 2010.]

103. • The difference in the prevalence of OLP in children
(0.03%) versus that of OLP in adults (0.5%–2%) is
understood by less number of associated systemic
diseases in children, autoimmune diseases, infections,
drug usage, and dental restorations in childhood; this
may reduce the risk for developing OLP in childhood [M.
Rybojad, I. Moraillon, S. Laglenne et al., “Lichen plan
del’enfant,”Annales de Dermatologie et de Venereologie,
vol. 125, no. 10, pp. 679–681, 1998.].
• Moreover, the diagnosis of OLP may be missed due to
irregular dental checkups, lack of symptoms, and
ignorance by clinicians in diagnosing the condition.[A.
Pakfetrat, A. Javadzadeh- Bolouri, S. Basir-Shabestari,
and F. Falaki, “Oral lichen planus: a retrospective study
of 420 Iranian patients,”Medicina Oral, Patologia Oral y
Cirugia Bucal, vol. 14,no. 7, pp. E315–E318, 2009.]

104. Dorsum of tongue showing ulcerative
lesion.

105. BEHÇET’S SYNDROME (Behçet’s
Disease)
• Aphthae of any of the RAS types described earlier
may rarely be a manifestation of Behçet’s syndrome
where they are associated with systemic disease,
manifesting usually with genital ulcers and uveitis.
• This rare condition affects mainly young adult males
and is most common in people from the Middle East,
Japan, China and Korea, along the ancient silk route
from Europe to the Far East.

106. Aetiology
• Behçet’s syndrome appears to have an immunogenetic
basis, with a specific association with HLA genetic type
HLA-B5101. Immuno-logical changes are like those in
aphthae. The precipitating factor is unknown but may
be Streptococcus sanguis.
• There appears to be a subset of T cells which react to
an immunostimulatory human heat shock protein with
cross-reactivity to streptococci, and produce tumour
necrosis factor (TNF) and interleukin 8 (IL-8). The
interleukin leads to the chemo-attraction of
neutrophils, which are also hyperactive and release
superoxide, leading to vasculitis.

107. Clinical Features
• Behçet’s syndrome is a multisystem disease affecting the
mouth in most cases and many other sites including,
commonly:
• Genitals: ulcers resembling oral aphthae
• Eyes: uveitis is one of the more important ocular lesions and
visual acuity is often impaired.
• Skin: erythema nodosum (painful red lumps on the shins),
various rashes may develop as well as pustules at the site of
venepuncture (pathergy).
• Joints: large joint arthropathy is not uncommon.
• Neurological system: headache, psychiatric, motor or
sensory manifestations.
• Vascular system: thrombosis of large veins may be life-
threatening.

108. Diagnosis
• Behçet’s syndrome is a clinical diagnosis, the cardinal features
being oral and genital ulceration, uveitis and erythema
nodosum. Other causes of this constellation of lesions, such as
ulcerative colitis, Crohn’s disease, mixed connective tissue
disease, lupus erythematosus and Reiter’s syndrome, must be
excluded.
• Diagnostic criteria for Behçet’s syndrome are not completely
agreed but include:
• recurrent oral ulceration
• plus two or more of the following:
• recurrent genital ulceration; eye lesions; skin lesions;
pathergy.

109. Management
• No test of reliable value, except HLA typing
• Oral ulcers: treat as for aphthae
• Systemic manifestations: immunosuppression
using, typically, corticosteroids, colchicines or
• thalidomide.
Behçet's syndrome, oral
ulceration.

110. Erythema multiforme, Stevens-Johnson
syndrome and Toxic epidermal necrolysis
• These conditions exist that present with similar
clinical signs & histological appearances.
• There is a now view that these are distinct
pathological entities and might be intiated by quite
distinct aetiological agents.
• Ailternative view: these disorders represent
different presentations of the same basic
disorder,distinguished by the severity and extent of
the lesions.

111. Erythema multiforme
• Original description of it was that of a self-limiting
but often recurrent and seasonal skin disease with
mucosal involvement limited to oral cavity.
• Lips are typically ulcerarted with blood staining and
crusting.
• Characteristics macules (‘target lesions’) occur on
the Limbs but with less involvement of the trunk or
head and neck.
• Lesions are concentric with a erythematous halo
and a central blister.

112. • Although lesions are extremely painful, th course of
illness is benign and healing uneventful.

113. Stevens-Johnson syndrome
• The condition presents with acute febrile
illness,generalized exanthema, lesions involvement the
oral cavity and a severe purulent conjunctivitis.
• Skin lesions are more extensive than those of erythema
multiforme.
• It is characterised by Vesiculobullous eruptions over the
body, in particular the trunk and severe involvement of
multiple mucuous membranes including the vulva,
penis and conjunctivia.
• Course of condition is longer and scarring may occur.

114. Toxic epidermal necrolysis (TEN)
• TEN or Lyell’s syndrome is a severe, sometimes
fatal, bullous drug –induced eruption where sheets
of skin are lost.
• It resembles third-degree burns or staphylococcal
scalded skin syndrome.
• Oral involvement is similar to SJS

115. AETIOLOGY
• Erythema multiforme is often initiated by herpes
simplex reactivation. there is some evidence that
Stevens-Johnson syndrome is initated by a
mycoplasma pneumonia infection or drug reaction.
TEN is drug-induced.

118. Management
• If there is a known precipating factor such as
herpes simplex infection then antivirals such as
topical acyclovir can be used as a form of
prophylaxis.
• Management is generally symptomatic and
supportive.
• Debridement of oral cavity with 0.2% CHX
gluconate or benzydamine hydrochloride and CHX
(Difflam C) is effective in removing much of the
necrotic debris from the mouth.

119. • Extensive areas of ulceration tend to be less
responsive to CHX and a minocycline mouthwash
may prove more effective.The role of systemic
steroids is controversial but they may be necessary
in severe cases requiring hospital admission.
• It also includes:
• Adequate fluid replacement and total parentral
nutrition if required.
• Pain control which may necessitate the use of
narcotics and sedation.

120. Oral manifestations of
gastrointestinal diseases
• Lesions within the jaws, oral mucosa or perioral
tissues may sometimes be seen as manifestations of
gastrointestinal (GI) diseases.
• The oral lesions may occasionally occur before the
onset of GI disease, be present during the disease
process or persist even after the disease has
resolved. Sometimes the oral lesions are similar to
GI lesions, while at other times, the oral changes are
caused by systemic alterations secondary to GI
disease, such as those related to malabsorption.

121. Crohn’s disease
• Dupuy et al (3) found that only 0.5% of their patients with Crohn’s
• disease developed oral lesions, and these patients were more likely
• to also have anal and esophageal lesions. There is a predilection for
• males and onset in youth. Occasionally, the oral manifestations
• may be the first indication that a patient has Crohn’s disease, but
• the oral lesions usually develop in patients with known bowel disease.
• The oral lesions are multifocal, linear, nodular, polypoid or diffuse
• mucosal thickenings, with a predilection for occurring in the
• labial and buccal mucosa, and the mucobuccal folds (Figure 1).
• They are characteristically firm, pink and painless to palpation
• unless there are ulcerations that may cause pain on touch, or when
• eating acidic, spicy or hot foods.

122. • These ulcers, which are typically persistent, linear and
deep (3), should not be confused with
• aphthous ulcers, which are shallow, round to oval
shaped lesions that heal spontaneously in approximately
seven to 14 days (4).
• On palpation, the lesions may feel granular below the
epithelium, reflecting the histological findings.
• Microscopically, the lesions exhibit subepithelial,
noncaseating granulomatous inflammation
characterized by epithelioid histiocytes, giant cells and
lymphocytes (Figure 2), identical to those seen in the
bowel. There is great variability in the severity of the
inflammation, which is worse if ulcers are present.

123. • Oral lesions are routinely subjected to special
histochemical stains to rule out infectious agents
such as deep fungal infections or tuberculosis, and
polarized to rule out foreign body reactions.
• Because granulomatous microscopic lesions are
seen in other diseases, including orofacial
granulomatosis and sarcoid (4), the definitive
diagnosis of Crohn’s disease cannot be made on oral
biopsy alone. However, the biopsy may direct the
clinician to investigate the GI tract for Crohn’s
disease lesions.

124. • Oral lesions of Crohn’s disease are typically
persistent, and remit and relapse over the years (3).
• Their response to systemic therapy is highly
variable and unpredictable, and they do not
necessarily parallel the activity of gut disease.
• Some oral ulcerating lesions may require topical
corticosteroid therapy or even intralesional
corticosteroid injections.

125. Ulcerative colitis
• Oral lesions of ulcerative colitis – termed
pyostomatitis vegetans (5,6) – are rare, and are far
less common than oral manifestations of Crohn’s
disease. There is a male predilection (5), and oral
outbreaks may occur at any age (6).
• The oral lesions may precede GI lesions but are
generally present synchronously. Clinically, the
lesions consist of scattered, clumped or linearly
oriented pustules on an erythematous mucosa at
multiple oral sites, with variable severity (Figure 3),
but usually sparing the dorsum of the tongue.

126. • Patient discomfort is proportional to the degree of
ulceration of the lesions, many of which remain
epithelialized.
• Long-standing lesions may become granular,
polypoid or fissured (6), clinically mimicking Crohn’s
disease.
• Some patients exhibit oral aphthous-like lesions (6)
in addition to the pustular lesions, an
approximately 10% of patients develop
inflammatory bowel disease-associated arthritis of
the temporomandibular joints (6).

127. • Microscopically, the lesions mimic the crypt
abscesses of colonic lesions, without evidence of
granulomatous inflammation.
• The oral submucosa shows edema with
neutrophils, eosinophils and lymphocytes, while
the epithelium shows spongiosis with neutrophilic
and eosinophilic abscesses (5) (Figure 4).
• The microscopic appearance in itself is not
diagnostic, because neutrophilic or eosinophilic
intraepithelial abscesses may be seen in other
conditions such as candidiasis, benign migratory
glossitis, or stomatitis areata migrans and
pemphigus vegetans (

128. • The clinical appearance and historical information must be
correlated with the microscopic findings; otherwise,
asymptomatic patients who receive an oral diagnosis of
pyostomatitis vegetans should be investigated by a
gastroenterologist for bowel disease
• The oral lesions usually respond to colonic disease treatment
(6). Topical or systemic corticosteroids (5) and dapsone (6)
have been used for recalcitrant oral lesions with variable
effectiveness.
• Because the severity of oral disease usually reflects the
severity of the bowel disease, the gasteroenterologist may
use oral manifestations, when present, as an additional gauge
to determine the severity of the bowel disease and/or the
response to therapy.

129. MALABSORPTION CONDITIONS
AFFECTING HEMATOPOIESIS
• GI diseases related to protein-caloric malnutrition (10) or
micronutrient malabsorption (11) may have an effect on the
oral tissues.
• The classical examples are iron malabsorption inducing iron
deficiency anemia and vitamin B12 malabsorption in
pernicious anemia [Field EA, Speechley JA, Rugman FR,
Varga E, Tyldesley WR. Oral signs and symptoms in patients
with undiagnosed B12 deficiency. J Oral Pathol Med
1995;24:468-70.]
• When the malabsorption is sufficiently severe, the first oral
manifestation is atrophic glossitis (Figure 6), in which the
filiform papilla and sometimes the fungiform papilla of the
dorsumof the tongue undergo atrophy, leaving a bald, red
tongue (

130. • In milder cases, the atrophy is patchy, but more
severe cases show involvement of the entire
dorsum. In very severe cases, there may be shallow,
round to oval-shaped, persistent ulcers with bright
red borders, clinically resembling aphthous ulcers
but often responsive to appropriate replacement
therapy.
• Overt tongue lesions are usually sore, but a more
common complaint is a burning sensation
(glossopyrosis) that may precede clinically
detectable oral lesions

131. • Other oral mucosa may also become involved with
atrophic zones, with or without aphthous-like
ulcers and the burning sensation, but these lesions
are not as dramatic as the bald tongue and often go
unnoticed. Affected patients are predisposed to
developing angular cheilitis, which is a candidal
infection that can be treated with antifungal
medication.
• The gastroenterologist may use atrophic glossitis as
an indicator of moderate to severe nutrient
malabsorption.

132. CYCLIC NEUTROPENIA
• THE CLINICAL FEATURES INCLUDE ORAL ULCERS
WITH PERIODICITY; INFECTIONS, ADENOPATHY;
PERIODONTAL DISEASE.
• THIS IS CAUSED BY MUTATIONS IN NEUTROPHIL
ELASTASE GENE.
• CYCLIC NEUTROPENIA RESULTS IN RARE BLOOD
DYSCRASIA.
• FEVER, MALAISE, ORAL ULCERS, CERVICAL
LYMPHADENOPATHY AND INFECTIONS CAN OCCUR.

133. • THE NEOPLASMS INCLUDE
1. SQUAMOUS CELL CARCINOMA
2. CARCINOMA OF MAXILLARY SINUS
3. OTHER CARCINOMAS
NEOPLASMS

134. • ORAL AND OROPHARYNGEAL SQUAMOUS CELL
CARCINOMAS REPRESENT ABOUT 3% OF CANCERS IN
MEN AND 2% IN WOMEN.
• OF ALL THE FACTORS, TOBACCO IS REGARDED AS THE MOST
IMPORTANT ESP THE CIGAR, PIPE AND REVERSE SMOKING.
• THE TIME-DOSE RELATIONSHIP OF CARCINOGENS FOUND
IN TOBACCO IS OF MUCH IMPORTANCE IN THE CAUSE OF
ORAL CANCER.
• MICRO ORGANISMS SUCH AS CANDIDA ALBICANS
PRODUCES N-NITROSOBENZYLMETHYLAMINE CARCINOGEN
AND HPV SUBTYPES 16 AND 18 PRODUCES ORAL
SQUAMOUS CELL CARCINOMAS.
SQUAMOUS CELL CARCINOMA

135. • CARCINOMAS OF
LOWER LIPS ARE
MORE COMMON
THAN UPPER LIP
LESIONS BUT THE
GROWTH RATE IS
SLOWER.
• THEY APPEAR
COMMONLY IN
ELDERLY PATIENTS
MOSTLY AFFECTING
MEN
•THE SQUAMOUS CELL CARCINOMA CLINICALLY PRESENTS AS
CARCINOMA OF LIPS AND TONGUE

136. • SQUAMOUS CELL
CARCINOMA OF
TONGUE IS THE MOST
COMMON INTRAORAL
MALIGNANCY
• THESE PRESENT AS AN
INDURATED, NON
HEALING ULCER, AS A
RED LESION, AS A
WHITE LESION OR AS
A RED-WHITE LESION.

137. Ischaemic ulcers: necrotising
sialometaplasia
• This is an uncommon disorder that gives rise to
large areas of deep ulcers on one side of the hard
and sometimes the soft palate. This condition is
probably associated with an ischaemic event and is
associated with factors such as smoking, alcohol
use, denture wearing, recent surgery and systemic
disease. It can also be a feature of bulimia nervosa.
The clinical and histopathological features may
mimic those of SCC.

138. • MALIGNANCIES OF PARANASAL SINUSES
OCCUR MOST COMMONLY IN MAXILLARY
SINUS.
• THIS AFFECTS ELDER PEOPLE AND GENERALLY
MEN.
• PAST HISTORY FREQUENTLY INCLUDES
SINUSITIS.
• AS THE NEOPLASM EXTENDS TOWARDS
APICES OF MAXILLARY POSTERIOR TEETH,
REFERRED PAIN MAY OCCUR.
• TOOTHACHE WHICH ACTUALLY REPRESENTS
NEOPLASTIC MOVEMENT OF SUPERIOR
ALVEOLAR NERVE IS THE COMMON
SYMPTOM OF MAXILLARY SINUS
MALIGNANCIES.
• OCCASIONALLY IT MAY PRESENT AS PALATAL
ULCER AND MASS REPRESENTING EXTENSION
THROUGH THE BONE AND SOFT TISSUE OF
PALATE.
CARCINOMA OF MAXILLARY SINUS

139. Pemphigus
• It is an important vesiculo-bullous disease mainly
affecting adults; however,children can also be
affected.
• Lesions are intra-epithelial ,rapidly break down so
that affected individuals are often unaware of
blistering, complaining instead of ulceration,mainly
affecting the buccal mucosa,palate and lips.

140. Diagnosis
• There may be positive Nikolsky’s sign and
cytological examination can reveal the presence of
Tzanck’s cells.
• Direct immunofluorescence usingfrozen sections
from an oral biopsy will reveal intracellular
immunoglobulin(igg)deposits in the epithelium,
which are diagnostic for this disease.
• Indirect immunofluorescence on blood samples is
sometimes used to monitor patients.

141. Management
• Systemic corticosteroid therapy
• Antiseptic or minocycline mouthwashes and
analgesia as necessary.

142. Epidermolysis bullosa
• It is aterm used to describe several hereditary
vesiculo-bullous disorders of the skin and mucosa.
• Blisters may form from birth or appear in the first
few weeks of life depending on the form of the
disease.
• Corneal ulceration may also may be present and
pitting enamel hypoplasia has been
reported,mainly in the junctional forms of the
disease.

143. Management
• Mangement is extremely difficult because of the
fragility of the skin and oral mucosa.intensive
preventive dental care is essential to prevent dental
caries,combined with treatment of early decay.
• Supportive care is required with the use of CHX
gluconate mouthwashes and possibly topical
anaesthetics such as lidocaine(Xylocaine viscous)

144. Systemic lupus erythematous
• It is a chronic inflammatory multisystem disease
occurring predominantly in young women.The
hallmark of SLE is the presence of antinuclear
antibodies which form circulating immune
complexes with DNA.
• Oral ulceration often occurs in SLE and treatment of
the condition usually involves systemic steroids.

145. leukemia
• The most frequently reported oral abnormalities
attributed to the leukemic process include regional
lymphadenopathy,mucous membrane petechiae
and ecchymoses, gingival bleeding,gingival
hypertrophy, pallor and nonspecific ulceration.
• Oral changes can be attributed to
anemia,granulocytopenia,and thrombocytopenia