1. The document discusses various causes and types of oral ulcers including recurrent aphthous ulcers, gastrointestinal causes like Crohn's disease and ulcerative colitis, and mucocutaneous conditions like oral lichen planus, pemphigus, and pemphigoid. 2. Recurrent aphthous ulcers are small round ulcers with erythematous halos that can be caused by genetic or nutritional deficiencies. Management involves correcting deficiencies and using mouthwashes or pastes. 3. Crohn's disease can cause oral ulcers and other manifestations. Ulcerative colitis rarely causes oral lesions but may result in chronic ulceration. 4. Mucoc

1. ORAL
ULERATION
Thilanka Umesh Sugathadasa

2. Thilanka Umesh Sugathadasa Page 1
ORAL ULCERATION
Main causes
1. Mechanical/ Chemical
2. Infections
3. RAU
4. Hematological
5. GIT causes
6. Mucocutaneous
7. Drugs
8. Endocrine
9. Malignancies
10. Others
RAU
Small, round or ovoid ulcers which have circumscribe margins, Erythematous haloes & yellow or grey floor.
Predisposing factors
1. Genetic predisposition
2. Hematinic deficiencies(Folate/ Vit B12/ Iron)
3. Drugs causes malabsorption of folic
4. Crohn’s disease - Histamine H2 receptor antagonists (cimetidine/omeprazole) can also impede vitamin B12
absorption.
5. Cessation of smoking.
6. Stress
7. Trauma from biting.
8. Sodium lauryl sulphate – Detergent in some tooth pastes.
9. Allergies
10. Endocrine factors – fall in progesterone level/ Contraceptive pills.
Aphthous like ulcers
1. Immune deficiencies. – HIV , Cyclic Neutropenia
2. Behcet’s syndrome – With genital ulceration & uveitis.
3. MAGIC syndrome – Behcet disease variant.
4. Sweet syndrome – Conjunctivitis, Episcleritis, Inflamed skin papules or nodules
5. Periodic fever, Aphthous stomatitis, Pharyngitis, Cervical adenitis syndrome (PFAPA)
6. Drugs
Ix
1. Hb
2. Serum Ferritin / Total Iron binding capacity
3. Serum Vit B12/ Folate

3. Thilanka Umesh Sugathadasa Page 2
Mx
1. Correcting deficiency
2. Stress Reduction
3. Avoid allergens
So as supportive therapy
1. 0.2% Chlorhexidine mouthwash / Benzydamine mouthwash
2. Tetracycline Mouthwash(250mg capsule) if want add Nystatin
3. 5% Amlexanox paste
4. 0.2% Hyaluronic acid
Gastrointestinal Causes
Disease Other Oral Manifestation Clinical Features DD & Mx
Crohn’s
disease
 Inflammatory disease of
unknown cause.
 Heterogeneous group of
disorders caused by
commensal bacteria in
people with genetically
determined deregulations
of mucosal T lymphocytes.
 Inflammation mediated by
TNF.
 Sub mucosal Chronic
inflammation
 Non caseating granuloma
in sub mucosa
 Ulcers(Linear ulcers)
 Facial / Labial
swellings.
 Mucosal tags
 Cobblestone
proliferation of
mucosa (Irregular
swellings with fibrosis
in between)
 Angular cheilitis
 Melkerson Rosenthal
syndrome* & Cheilitis
granulomatosa may
be incomplete
manifestation of CD
 Common in
Iliocecal junction
but can affect any
part
 Ulceration/
Fissuring/ Fibrosis
 Weight loss
 Internal/ External
fistula
 Perianal fissures
 Abscesses
 Renal damage
 NSAID should
avoid.
 Antibiotics which
could aggravate
diarrheal situations
must avoid.( co-
amoxiclave,
Clindamycin)
 Mx may
complicated by
Steroids or
Malabsorption.
Features Minor Major Herpetiform
Size 1-2mm >1cm Initially 2mm then coalesce
Site Mostly non-keratinize
parts. Mainly anterior
mouth.
Any site including
keratinized posterior parts.
Same as Minor
No of ulcers 1-5 1-3 10-100
Sex F M F
Healing Within 2 weeks 1-3 Months Within 2 weeks

4. Thilanka Umesh Sugathadasa Page 3
Ulcerative
Colitis
 Inflammatory bowel
disease.
 Affecting part or whole
large intestine, frequently
lower colon & rectum.
 Cause inflammation &
ulcers in superficial layers
of large intestine mucosa
followed by pseudo polyp
formation.
 Diarrhea with mucus
+blood +pus
 Pain, fever, anorexia
 Extra abdominal signs
are minimal
 Commonest
complication is Iron
deficiency anaemia.
 Skin lesions present
like Erythema
nodosum.
 Carcinoma
 Oral
manifestations are
rare.
 Chronic ulceration
can be occur.
(Polystomatitis
gangrenosum)
 Polystomatitis
vegetans (Multiple
intraepithelial
micro abscesses)
 Lesions related to
anaemia.
 Antibiotics &
NSAIDS should be
avoided.
Oro-facial
granulomatosis
 Non- caseating
granulomatous
inflammation affecting
soft tissues of oral &
maxillofacial region
 Two types-
-Melkerson Rosenthal
Syndrome
-Cheilitis Granulomatosa
(Swelling restricted to lips,
Recurrent & persistent lip
swelling in the absence of
any other systemic
disease)
 Non tender recurrent labial swelling that
eventually become persistent.
 Lip hypertrophy
 Initially soft then become firm due to
fibrosis.
 Recurrent facial swelling(Chin/ Cheeks/
Periorbital region)
Intraorally may see hypertrophy/
Erythema/Non-specific erosions/ ulcerations
on mucosa or tongue.
Relapses are common though long term
treatment is needed.
D/D
 Angioedema
 Sarcoidosis
 Crohn’s disease
 Infections
(TB/Leprosy/ Deep
fungal infection)
 Amyloidosis
 Minor Salivary gland
tumor.
Mx
 Local/ Systemic
corticosteroids or
both
 Intra lesional
injection or
Triamcinolone.
 Local side effects-
hypopigmentation &
skin atrophy.
 Systemic not using
mostly due to side
effects.
Coeliac disease  Gluten sensitivity causes villous atrophy in the mucosa of small intestine.
*Melkerson Rosenthal Syndrome – Facial swelling
Facial palsy 3F
Fissured tongue
Difference between Crohn’s disease & Ulcerative colitis
Features CD UC
Site(Main) Ileum Colo- Rectum
Other sites Any part/ Skin lesion Terminal ileum
Iron deficiency Common Common
Fistula/ Abscess Possible Rare
Colonic cancer risk Present High

5. Thilanka Umesh Sugathadasa Page 4
Pathology Transmural Inflammation Superficial inflammation
Abdominal pain Prominent Not Prominent
Bloody diarrhoea Not prominent Prominent
Mucocutaneous Conditions
Condition Causes/Predisposing
factors
Aetiopathogenesis & other
factors
Clinical features D/D & Mx
Oral lychen
planus
(Inflammato
ry
Autoimmun
e
Type of
disease)
 Dental materials
Amalgam
Gold
 Diseases
grafts verses
hosts
Liver diseases
HIV
Hepatitis B Virus
 Stress
 Drugs
NSAIDS
Antihypertensives
Antidiabetes
Antimalarial
Many others
 Not a classic autoimmune
disease. Bcos It not having
specific Autoantibody.
 Early changes are close to the
basal epithelium
 Then band like dense
mononuclear inflammatory
cell infiltrate (Mainly CD8+
)
appears in the upper lamina
propria.
 Cell death occurs(Apoptosis)
due to TNF-α
 Due to those things thickening
of spinous cell
layer(Acanthosis)
 Then granular cell layer
become hyperkeratosis or
hyperorthokeratosis
 That account for the clinical
white lesions
 Rete ridges take saw tooth
appearance.
 Can be
Reticular
Plaque like
Papular
Atrophic
Erosive oral
Bullous ulcers
 Desquamative
gingivitis occur due
to gingiva involved by
Atrophic or erosive
LP
 In Erosive Lychen
Planus
irregular/painful &
yellowish slough
occur
 Typically posterior,
buccal, Tongue,
gingival mucosa
 Skin lesions (Flexor
surfaces)
 Vulvo-vaginal lesions
(Vulvo vaginal –
gingival syndrome)
 Mostly Burning
Sensation present.
D/D
1. Lupus
erythematosus
2. Chronic ulcerative
stomatitis
3. Keratosis
4. Carcinoma
5. Lichenoid lesions
Mx
Not really necessary
Remove causes
Rx for the diseases.
Mild LP
Topical
corticosteroids (Low
potency
hydrocortisone/
Triamcenalone
acetanoid 0.1%)
Moderate LP
Topical cyclosporine
Severe LP
Systemic
Pemphigus
(Potentially
life
threatening
chronic
autoimmun
e condition)
 Fairly strong
genetic
predisposition
 Mostly idiopathic
may triggered by
medications
(Captopril)
 Radiation
 Surgery
 Certain
foods(Garlic)
 Emotional stress.
 Serum Autoantibodies mainly
IgG.
 Directed mainly against
desmosomes in stratified
squamous epithelium
 Intercellular immune deposits
are detectable intra-
epithelially.
 Antigen- Antibody response
causes loss of cell- cell
contacts (Acantholysis) &
intraepithelial vesiculation.
Pemphigus vulgaris is the
commonest form
Commonly in middle aged to
elderly more common.
Female predisposition present.
 Mucosa of
Mouth
pharynx
Larynx
Esophagus
Rectum
Nose
Ano genital region
Conjunctiva
Blisters/Erosions/Ulc
ers can see
 Start by blister
formation in oral
mucosa & scalp.
Blisters are soft &
easily broken.
 Mainly go for the
systemic
immunosuppressi
on.
 Before
introducing
corticosteroids
we have to
consider its
complications
also (Dehydration
& secondary
systemic
infections.)
 Refer to the
Pulmonary
specialist Detect

6. Thilanka Umesh Sugathadasa Page 5
Pemphigus vulgaris is the most
severe form of the pemphigus.
 Nikolsky sign
present(Spreading of
the blister by
pressure)
 Erosions in the
mouth irregular &
initially red with
whitish surround
then yellowish slough
form.
 Mainly present in the
soft palate &
posterior hard palate,
Buccal mucosa,
Gingiva(Desquamativ
e gingivitis)
paraneoplastic
pemphigus
 Gastroenterologis
ts to detect
possible
esophageal
involvement.
 Systemically –
Prednisolone
60mg/day
Pemphigoid
(Chronic
autoimmun
e disease-
Vesiculobull
ous)
 Drugs
Furosemide
Penicillamine
 Genetic
predisposition
Sub epithelial
vesiculobullous
Disorders.
1. Pemphigoid
variants
2. Dermatitis
Herpetiformis
3. Acquired
epidermolysis
bullosa.
4. Toxic Epidermal
Necrolysis.
5. Erythema
Multiforme
6. Linear IgA disease
7. Chronic bullous
dermotosis in
childrens
 Auto antibodies &
complement components are
directed against BM (IgG
mostly others & C3 less)
 Autoantibodies are directed
against hemidesmosomal
components or components
of the Lamina lucida.
 Due to compliment mediated
sequestration of leukocytes
with resultant cytokines &
enzymes release by
leukocytes Detachment occur
in the BM zone
These immune deposits
cause subepithelial split &
blistering
Eye – Blindness
Genital
Skin
Laryngeal- stenosis
These are rare.
 Lesions- Oral mucosal
pemphigoid
- Bullous
pemphigoid(Mainly
in the skin)
- Ocular
pemphigoid
(Conjunctivae)
 Intact tense blisters
can see some times
like Angina bullosa
hemorrhagica.
 Nikolsky sign present.
 Persistent irregular
ulcer or erosions
present after the
blister burst.
 Then covered with
fibrinous yellowish
slough & surrounded
by inflammatory
Erythema.
 Though Resembles
Erosive LP but
without white
lesions.
 Scarring
 Desquamative
gingivitis in gingiva.
 Mostly pts with
mucous membrane
pemphigoid having
oral involvement
only.
 Systemic or
topical steroids.
 Ophthalmologist
referral.
Autoimmune
blistering
Mucocutaneous
disorders are
mainly two
types.
1. Pemphigoid
subset
Autoantibodies
are target the
extracellular
components that
links epithelial
BM components
either to lower
most epithelial
cell layer or LP
components
2. Pemphigus
Subset
Autoantibodies
are target the
extracellular
components that
link one epithelial
cell to another.

7. Thilanka Umesh Sugathadasa Page 6
Erythema
Multiforme
(Acute,
often
recurrent
hypersensiti
ve reaction)
Mostly
occur in
younger
adults. More
common in
Males.
 Genetic
predisposition
 HSV
 Drugs(Antimicrobi
als /
Antihypertensives
/NSAIDS /
Anticonvulsants)
 Also immune
conditions such as
Sarcoidosis , Hep B
immunization,
SLE, Graft versus
host reactions,
Polyarteritis
nodosa.
 Antigenic change induced by
HSV or drug
 Cytotoxic secretions by
lymphocytes/ Macrophages/
Neutrophils.
 Apoptosis of Keratinocytes.
 Satellite cell necrosis
 Sub & intraepithelial
vesiculation
Forms of EM
1. Minor EM – Affects only one
site the mouth, skin or other
mucosa
Rashes are various
but typically target or bullae
lesions.
2. Major EM – (Steven- Johnson
syndrome)
Begins with 1-3
weeks after starting a new
drugs.
Present with flu
like symptoms/ sore throat/
headache/ Arthralgia/ Myalgia
Almost invariably
involve the mucosa. Causes
widespread lesions
Eyes
Genitals
Pharynx
Larynx
Oesophagus
3. HSV induced EM – Usually
extremities.
4. Drug induced EM
5. TEN(Toxic epidermal
necrolysis) – Fatal very serious
condition.
 Can be vary in mild to
severe life
threatening
condition.
Oral lesions
 Diffuse widespread
macules that
progress for the
blister & ulcer
mostly.
 Lips become swollen,
bleeding & crusted,
cracked.
Serosanguinous
exudate mostly frm
lips.
 Lesions on the non-
keratinized mucosa
are more pronounced
& anterior region
 Recur mostly 25%
 Periodicity of attacks
varies from 10-20
days to years. But
mostly 10-20 days.
 Resolves after about
6 episodes.
Skin Lesions
 Mostly distal
extremities, Extensor
surfaces of arms/
legs/ Elbows/ Knees/
dorsum of the hands
& feets.
 Macules are
symmetrical/ Round/
Erythematous /
Pruritic or not
 Target lesions are
large annular(Ring
shape) & well
demarcated.
Diagnosis
 Nickolsky sign
present.
Mx
 Spontaneous
healing.
 No specific Rx
 Supportive care
 Increase oral
hygiene.
 Precipitating
factors should
remove.
 Antivirals to HSV.
Epidermolys
is
bullosa(Inhe
rited
Mucocutane
ous bullous
disease)
 Subtypes - Autosomal recessive non scarring letalis
type
- Autosomal recessive scarring dermolytic
type.
 Scarring follows may cause severe
microstomia
 Buccal sulcus get obliterated by scar tissues
 Tongue become fixed
 Tongue becomes depapillated.
Oral hygiene is difficult as tooth brushing cause
oral ulceration.

8. Thilanka Umesh Sugathadasa Page 7
Dermatitis
Herpetiform
is(Gluten
sensitivity
skin
disorder)
 Associated with coeliac disease
 Mostly males.
 Clinically
symmetrical papulovascular eruptions of extensor
surfaces.
Oral lesions are vesicles, erythematous, erosive
similar to the pemphigoid or like Desquamative
gingivitis.
 Take gluten free diet.
Lupus
Erythemato
us(Rare
Autoimmun
e disease
usually in
Females. )
 Genetic
Predisposition
 Drugs
 Hormone
 Viruses
 2 types
SLE – systemic condition Oral ulceration like DLE but
usually more severe ulceration May associated with
Sjogren syndrome Rarely TMJ arthritis occur.
DLE(Discoid Lupus Erythematosus) – Mucocutaneous
involvement Characterized by central erythema. White
spot or papules present, Radiating white striae at margins
& peripheral telangiectasia. It can ulcerate. Oral lesions
can see 25% of times mostly buccal mucosa, Gingiva & lips.
 DLE- Topical
corticosteroids.
Cryosurgery
Excision of
localized lesions.
 SLE – Systemic
corticosteroids.
Behcet
syndrome
 Foods(Pork/
walnuts)
 Genetic
predisposition
D/D
1. Sweet syndrome
2. Erythema
multiforme
3. Pemphigoid
4. Pemphigus
5. Reiter’s syndrome
6. Ulcerative colitis
7. HSV
8. Syphilis
9. Lupus
Erythematosus
10. Mixed CT disease.
 Triple symptoms present
Apthous like ulceration
Genital ulceration(Recurrent & painful)
Eye disease
 Necrotizing vasculitis also may can be seen.
 20-30 years mostly men’s are affected.
 CNS lesions are predominantly subtentorial
 Skin lesions include Erythema Nodosum.
 Involvement can be seen of joints, epididymis, heart,
intestinal tract & vascular systems.
 Diagnosis by
Aphthous like
ulcers + 2 or
more following
things
-recurrent genital
ulceration
-Eye lesions
-skin lesions
& mainly using
pathergy(A >2mm
diameter
erythematous
nodule or pustule
forming 24-48 hrs
after sterile
puncture of the
forearm skin)
 Mx – Topical Rx
of RAU,
Tetracycline
mouthwash &
topical cortico….

9. Thilanka Umesh Sugathadasa Page 8
Reiter’s
syndrome
 This follows shigella infection of the gut.
 Almost always affect mens & comprises arthritis, a non- gonococcal urethritis & eye lesions.
 In mouth it causes painless, red patches which may be granular or vesicular with a scalloped white line
surrounding them.
 These are similar to be lesions of Erythema Migrans(Geographic tongue)
 Mostly buccal mucosa & male genitalia can affect then erythema migrans like patches can ulcerate.
Sweet
syndrome
 Oral ulcers / Conjunctivitis / Episcleritis / Inflamed tender skin papules or nodules.
Viral Infections
Herpes
simplex virus
 Two types - Primary herpetic gingivostomatitis
Secondary infections (Recurrent herpes)
 Primary infection associated with widespread oral ulceration preceded by eruption of vesicles on all
areas of the oral mucosa & gingiva.
 Mostly accompanied with fever & often affects the children.
 Secondary infection occurs when the virus that had remain dormant in the gasserion ganglion become
activated causing limited ulceration either on the lips(Herpes labialis) or intraorally.
Varicella
zoster virus
 Produce chicken pox in the primary infections oral ulceration is very rare.
 In the recurrent infections after it dormant in the trigeminal ganglion.
 Blisters appears unilaterally on the skin/mucosa supplied by one or more branches of the trigeminal
nerve
 Ulcers are mostly unilateral
EBV  Produce occasional oral ulceration as part of the systemic infection of infectious mononucleosis
 Lesions having creamy exudates accompanied by palatal petechiae & sore throat.
Coxsackie A
virus
 Can cause oral ulceration & hand , foot , mouth disease or herpangina
Bacterial Infections
ANUG
 Combination of anaerobic fusiform bacteria & spirochetes
 Cause oral ulceration on the tips of the interdental papillae.
 Sometimes spreading along the gingival margins.
 Soreness/ Gingival bleeding / Halitosis present.
D/D
 Leukaemia
 Herpetic gingivostomatitis.
Mx
 Local debridement.
 Metronidazole accompanied by peroxide or perborate mouthwash.
TB
 Mostly who suffer from pulmonary TB.
 Occasionally the initial presentation.
 Usually a solitary chronic stellate ulcer is found on dorsum of the tongue.
Syphillis  Spirochetes(Treponima Pallidum)
 Primary syphilis
Painless indurated ulcers known as chancre may be proceeded by papule or noduleon the lip or tongue.
Heals spontaneously.
 Secondary syphilis * Tertiary syphillis
Snail track ulcers Ulcers in the tongue or palate known as the Gumma

10. Thilanka Umesh Sugathadasa Page 9
Parasitic infections
Leishmania
donovani
 Indolent ulcer(Non healing persisting ulcer on the lips)
Hematological conditions
Either due to problems in the blood cells themselves(RBC /WBC) or problems in the blood forming tissues.
RBC disease
Classifications - Morphological
Normocytic Anaemia Microcytic Anaemia Hypochromic microcytic
Anaemia
Macrocytic Anaemia
1. Acutely following blood
loses mostly.
2. Chronic disease
3. Endocrine disorders
Hypopituitarism
Hypothyroidism
Hypoadrenalism
4. Hematological disorders
Aplastic anaemias
Some hemolytic anaemias
1. Anaemia of the chronic
disease.
Tuberculosis
crohn’s disease
RA
SLE
Here decrease release of
the iron from the bone
marrow to developing
erythroblasts.
1. Iron deficiency anaemia
2. Chronic disease
3. Sideroblastic Anaemia
4. Thalassaemia
1. Megaloblastic anaemia
Vit B12 deficiency
Folic acid deficiency
Other defects of DNA
synthesis
Myelodysplasia due to
dyserythropoiesis
2. Non Megaloblastic
Alcohol excess
Liver disease
Hypothyroidism
Reticulocytosis
- Etiologically
Loss of blood Excessive destruction of RBC Impaired
production
Inadequate production of mature RBC
1. Extracorpuscular causes
Antibiotics
lypomas
Infections
Chemicals
2. Intracorpuscular causes
Hereditory – Disorders of
glycolysis/Abnormalities in the
RBC membrane.
Acquired – Pb poisoning
1. Deficiency of RBC
2. Infiltration of bone marrow
3. Endocrine abnormalities
4. Chronic renal failure
5. Chronic inflammatory disease.
WBC disorders
Quantitative disorders Qualitative Disorders
 Decrease in No -
Granulocytopenia
Agranulocytopenia
Leukopenia
Neutropenia – Familial/ Cyclic/ Chronic/ Hypoplastic/
1. Lazy leukocyte syndrome.
2. Chediack Higashi syndrome
3. Multiple myeloma

11. Thilanka Umesh Sugathadasa Page 10
Primary splenic
 Increase in No -
Granulocytosis
Neutrophelia
Basophilic leukocytosis
Eosinophilic leukocytosis
Lymphocytosis
Monocytosis
4. IM
5. Lymphoma
6. Leukemia
Platelet disorders
1. Idiopathic thrombocytopenic purpura
2. Secondary thrombocytopenic purpura
3. Thrombotic thrombocytopenic purpura.
4. Thrombocytosis
WBC disorders
Condition Causes Oral features Clinical features D/D & Mx
Granulocytope
nia(Marked
leukopenia
with reduction/
absence of
neutrophils
Mild(1000-
2000mm2
)
Moderate(500-
1000mm2
)
Severe(<500)
Agranulocytosis
– No
Neutrophiles
 Idiosyncrasy –
Sensitization to drugs
such as Chlorempenicol
 Deficiency- Vit B12 & folic
 Diseases – SLE
 Infections
 Hemodialysis
 Irradiation
 Necrotizing ulceration
in oral mucosa with
foul sense.
 Pain, excessive
salivation &
spontaneous oral
bleeding
 Most common sites
are Gingivae, Palate,
Tonsils, Pharynx
 Rapid spread can see
in the gingiva.
 Common in elderly
female.
 Sudden or gradual
onset.
 Begins with sore
throat, high fever &
rigors.
 Pale & Anaemic
skin.
 Rapidly advancing
necrotic ulceration
of throat & mouth.
 Most of the times
patients are dying
with in 3-5 days due
to toxemia &
septicemia.
 D/D
1. Leukemia
2. Cyclic
neutropenia
3. wegner’s
granulomatosis
4. ANUG
5. Necrotizing
sialometaplasia
6. Erythema
Multiforme.
 Mx
1. Removing
causative agents.
2. Transfusion
3. Antibiotics
4. Oral & Dental
Mx
Cyclic
Neutropenia
(Characterized
by peiriodic
reduction in
circulating
neutrophils due
to failure of
stem cells of
bone marrow)
 Episodes 2-4 weeks
3-5 days
21 days
 Severe gingivitis
 Painful ragged ulcers
with core like centre
on lips, buccal mucosa
 Heals with scarring.
 Sore throat
 Fever
 Stomatitis
 Lymphadenopathy
 Headache
 Arthritis

12. Thilanka Umesh Sugathadasa Page 11
RBC disorders
Condition Causes Clinical features Oral manifestations
Iron deficiency
anaemia(Normal
iron intake should
be 0.6mg/day)
But in pregnancy 1-
2mg/ day
 Inadequate intake
 Decrease absorption(Chelation/
gastrectomy/ Malabsorption).
 Increase requirements.(Growing child/
pregnancy/ surgery)
 Increase loss.- blood lose (Rapid-RTA/
chronic- hook warm disease/ increased
menstruation)
stages
1. Pre latent iron deficiency
Body storage is reduced. But circulating
HB & serum iron is normal.
2. Latent iron deficiency
Body storage is exhausted & serum iron
is reduced but HB is
3. Mild anaemia
Serum iron is low & also circulating HB
also reduced.
4.Marked anaemia
HB is below 10g/dl
 Brittle nails
 Koilonychia (Spoon
shaped nails)
 Neuropathy (Tingling,
pins & needle
sensation in
extremities)
 Dysphasia
 Tenderness &
headache
 Palpable spleen & liver
 CVS- Angina, MI,
Cardiac failure/ Cramps
 Pallor oral mucosa.
 Atrophy of oral
mucosa then
ulcerate.
 Recurrent ulceration
 Red/ atrophy of
papillae of the
tongue.
 Burning sensation
 Plummer – vinson or
Peterson- Brown-
Kelly
syndrome(Dysphagia
+ Glossitis)
Aplastic
anaemia(Rare
disorder
characterized by
pancytopenia-
Anaemia /
Leucocytopenia/
Thrombocytopenia)
due to bone
marrow
suppression
 Primary causes
Congenital(Common in young adults)
 Secondary causes
Chemicals(Hg)
Drugs(Carbamazepine/ Chlorampenicol)
Infections(HIV/ Hepatitis)
insectisides
paroxysmal nocturnal hemoglobinuria
Causes for Pancytopenia
 Aplastic anaemia
 Megaloblastic anaemia
 Drugs
 Bone marrow infiltration &
replacement(Hodgkin’s & Non-Hodgkin’s
lymphoma)
 SLE
 Weakness
 Pallor
 Breathlessness
 Headache
 Anginal pain
 Bleeding from various
sites
 Fever
 Recurrent infections
IX
 RBC/WBC/ Platelete
decrease
 Decrease reticulocytes
 Prolong BT with
normal CT because
clotting factors are not
affected.
 Normocytic Anaemia
 Pallor mucosa
 Spontaneous gingival
bleeding
 Petechiae
 Sub mucosal
ecchymosis
 Large ragged ulcers
covered by grey
necrotic membrane
Mx
 Withdrawal of
etiological agents
 Supportive therapy
 Stimulate
haemopoiesis by
androgens.
 Bone marrow
transplantation.
Leukemia
Impairment of normal haemopoisis resulting Anemia, granulocytopenia & Thrombocytopenia.
Neoplastic proliferation of WBC in bone marrow, circulating blood & sometimes in other organs likes spleen & liver.

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Causes
1. Viruses(EBV/HTLM)
2. Radiation
3. Chemical Agent
4. Anticancer drugs
5. Genetic & chromosomal factors
6. Immunological deficiency syndrome
Classification
Acute Chronic
 ALL
L1- Primarily pediatric
L2- Primarily adult
L3- Burkitt’s
 AML
M1-Without maturation
M2-With maturation
M3-Promyelocytic
M4-Myelomonocytic
M5-Monocytic
M6-Erythroleukemia
M7-Megakaryocytic
 CLL
 CML
Condition Clinical features & others Oral manifestations
ALL
 Mostly males
 Childrens & young adults
 Sudden onset of fever+ splenomegaly
 Weakness/ Headache
 Generalized Lymphadenopathy
 Petechiae
 Hemorrhage in to skin & mucosa
 Bone pain & tenderness
 Anaemic & thrombocytopenic features
 Increase susceptibility to infections
 Paresthesia of lower lip
 Cervical lymphadenopathy
 Toothache due to infiltration of leukemic
cells in to dental pulp
 Pallor mucosa with ulceration & necrosis
 Gingival hyperplasia with cyanotic
discolouration.
CLL  Over 45 years
 Anaemia
 Thrombocytopenia
 Moderate enlargement of lymph nodes
 Skin nodule
 Increase susceptibility to infection.
 Gingival hypertrophy with ulceration,
Necrosis & gangrenous degeneration
giving very foul smell
 Swollen dark tongue
 Regional lymphadenopathy
 Rapid loosening of teeth due to
periodontal breakdowns.
Multiple myeloma
Malignant neoplasm of plasma cells of bone
marrow with involvement of skeletal system
Commonly seen in the males.
 Pain/ swelling & numbness in the jaws
 Epulis formation & Mobility of teeth
 Ulcerated Intraoral swellings & gingival bleeding
 Oral amyloidosis & high susceptibility to oral infections

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Traumatic ulcers
Peripheral keratotic border present. If cause is persist Hyperkeratosis or hyperplasia may occur.
Malignant lesions
1. SCC
2. Salivary gland
3. Kaposi sarcoma
4. Malignant melanoma – rarely
Drugs
1. NSAIDS
2. Drugs causing Neutropenia- Cotrimoxazole
Endocrine conditions
1. DM
2. Glucogonoma
Chemical
1. Nelli burns
2. Aspirin Burns
Thermal
Radiation
Others
1. Eosinophilic ulcers
2. Angina bullosa hemorrhagica.
3. Necrotizing sialometaplasia

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RAU
herpetiform
minor
Major
Crohn’s

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Melkerson Rosenthal syndrome
Cheilitis granulomatosa (or granulomatous cheilitis) is a chronic swelling of the lip due to granulomatous inflammation.
Miescher cheilitis is the term used when the granulomatous changes are confined to the lip. Miescher cheilitis is
generally regarded as a monosymptomatic form of the Melkersson-Rosenthal syndrome
Labial swelling and angular cheilitis
OFG

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LP
Erythema Multiforme

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Steven – Johnson syndrome
Pemphigus
Pemphigoid Angina bullosa hemorrhagica

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SLE DLE
Geographic tongue Primary herpetic gingivostomatitis
Traumatic ulcers TB ulcer

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Primary herpetic gingivostomatitis: erythema and multiple ulcers on the
gingiva.
Primary herpetic gingivostomatitis: multiple ulcers on the tongue.
Secondary herpetic stomatitis: small round ulcers on the palate
Herpes zoster: clusters of vesicles on the palate.
Herpes zoster: vesicles and erosions on the lower gingiva
Herpangina: numerous shallow ulcers on the soft palate.

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Erythema multiforme: multiple erosions on the lips and tongue.
Erythema multiforme: typical target- or iris-like lesions of the skin.
Stevens–Johnson syndrome: severe erosions on the lips, tongue, and the
nose in an 8-year-old boy.
Stevens–Johnson syndrome: genital lesions.
Toxic epidermal necrolysis: severe erosions covered by hemorrhagic crusting
on the lips.
Pemphigus vulgaris: hemorrhagic cluster of bullae on the buccal mucosa

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Pemphigus vulgaris: erosions on the dorsum of the tongue.
Pemphigus vulgaris: severe lesions of the skin of the face.
Cicatricial pemphigoid: erosions on the buccosal mucosa.
Bullous pemphigoid: bullae on the buccal mucosa.
Bullous pemphigoid: skin lesions.
Pemphigoid gestationis, multiple small bullae on the skin.

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Pemphigoid gestationis, hemorrhagic bullae on the soft palate.
Linear IgA disease: erosion on the tongue, covered by a whitish
pseudomembrane
Linear IgA disease: early gingival lesions.
Dermatitis herpetiformis: intact bulla on the lower lip mucosa and small
erosions on the gingiva
Lichen planus of the buccal mucosa: bullous form.
Epidermolysis bullosa simplex: hemorrhagic bulla on the buccal mucosa.

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Epidermolysis bullosa, recessive dystrophic form: bulla and scarring on the
tongue.
Epidermolysis bullosa, skin scarring.
Epidermolysis bullosa, dystrophic: severe scarring and dystrophy of the
hands.
Epidermolysis bullosa acquisita, hemorrhagic bulla on the buccal mucosa.
Angina bullosa hemorrhagica, multiple hemorrhagic bullae on the buccal
mucosa.
Traumatic ulcer of the tongue.

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Traumatic ulcer of the tongue.
Eosinophilic ulcer on the lower lip and the commissure.
Necrotizing sialadenometaplasia: two ulcers on the palate
Necrotizing sialadenometaplasia on the palate.
Severe necrotizing gingivitis in a 32-year-old HIV-seropositive homosexual
man
.
Necrotizing gingivitis and stomatitis in a 30-year-old man with AIDS. Note
the extensive soft-tissue necrosis beyond the gingiva.

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Chronic ulcerative stomatitis, gingival lesions in the form of desquamative
gingivitis.
Chronic ulcerative stomatitis, erosions on the buccal mucosa identical to
lichen planus
.
Noma, early necrotic ulcer of the lower lip.
Solitary chancre on the ventral surface of the tongue.
Condylomata lata on the palate.
Tuberculosis: typical ulcer on the dorsal surface of the tongue.

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Cryptococcosis, abnormal ulceration on the tongue.
Aspergillosis, black necrotic ulceration on the palate.
Mucormycosis, black necrotic lesion on the upper lip.
Minor aphthous ulcer.
Major aphthous ulcer on the lower lip.

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Multiple herpetiform ulcers on the tongue.
Behçet disease: multiple ulcers on the labia majora.
Behçet disease: major aphthous ulcer on the buccal mucosa.
Behçet syndrome: conjunctivitis and iritis.
Graft-versus-host disease: superficial ulceration on the buccal mucosa.
Wegener granulomatosis: large ulcer surrounded by an erythematous zone
on the tongue.

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Malignant granuloma: nonhealing ulcer and necrosis on the palate.
Early squamous-cell carcinoma of the lateral border of the tongue.
Non-Hodgkin lymphoma: large ulcer on the soft palate.
quamous-cell carcinoma presenting as exophytic ulcerated tumor of the
lateral border of the tongue.
Cyclic neutropenia: ulcer on the labial mucosa.
Cyclic neutropenia: localized gingivitis.

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Agranulocytosis: ulcer on the tongue.
Agranulocytosis: severe periodontal destruction.
Myelodysplastic syndrome: persistent ulcerations on the upper lip.
Chronic lymphocytic leukemia: ulcer on the palate.
Acute myelocytic leukemia, ulcers on the tongue.
Chronic lymphocytic leukemia: severe gingival enlargement and ulcerations.

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Langerhans cell histiocytosis, ulcer on the palate.
Langerhans cell histiocytosis, gingival enlargement and periodontitis.
FAPA syndrome, major aphthous ulcer on the soft palate.
Sweet syndrome: vesiculobullous lesions and edema of the fingers.
Sweet syndrome, major aphthous-like ulcers on the lipmucosa.
Staphylococcal infection, necrotic ulcer of the tongue.

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Ulcerative conditions
 Traumatic ulcer
 Eosinophilic ulcer
 Necrotizing sialadenometaplasia
 Necrotizing ulcerative gingivitis
 Necrotizing ulcerative stomatitis
 Chronic ulcerative stomatitis
 Noma
 Syphilis
 Tuberculosis
 Systemic mycoses
 Recurrent aphthous ulcers
 Behçet disease
 Graft-versus-host disease
 Wegener granulomatosis
 Malignant granuloma
 Non-Hodgkin lymphoma
 Squamous-cell carcinoma
 Cyclic neutropenia
 Agranulocytosis
 Myelic aplasia
 Myelodysplastic syndrome
 Leukemias
 Langerhans cell histiocytosis
 Glycogen storage disease,
 FAPA syndrome
 Sweet syndrome
 Staphylococcal infection
 Congenital neutropenia
 Cytomegalovirus infection

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Mechanical / Chemical
Ulcers
Mucocutaneous
LP
GIT
Hematological
DrugsEndocrineRAUInfectionsMalignancyothers

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