BY: Silpa Gharami

roll no.-25
3rd yr B.D.S
dept. of oral and
maxillofacial surgery
HIDSAR
 INDEX
Definition
History
Causes
Classification
Examination
Treatment
 DEFINITION
 A break in the continuity of the covering epithelium of
skin and mucous membrane.
 It may either follow molecular death of the surface
epithelium or its traumatic removal.
 HISTORY
 Duration:
1. Acute : present for short time
2. Chronic : present for long time
 Mode of onset
1. Following trauma
2. Spontaneously e.g. following – swelling e.g. ulcerating lymph node in
tuberculosis or a scar of burn Marjolin’s ulcer.
3. Marjolin’s ulcers are the malignant transformation of chronic wounds.
 HISTORY………
 Pain
1. Painful: ulcers associated with inflammation
2. Slight painful: tuberculous ulcer

3. Painless: e.g. syphilitic, malignant ulcer

 Discharge
If yes: Note the nature of discharge- pus, bloody, serous.
 Associated diseases
If present: nervous disease such as; tabes dorsalis, transverse myletis and
peripheral neuritis may result an ulcer (trophic or perforating ulcer).Generalized TB,
nephritis or diabete may lead to ulcer formation. Syphilis at the primary stage gives
rise to chance and in the tertiary stage gives rise to a gummatous ulcer.
 cauSES
 Traumatic causes
* Mechanical
* Physical
* Chemical
 Vascular insufficiency
* Arterial
* Venous
 Neoplastic condition
*SCC
*BCC
*Malignant melanoma, etc.
CAUSES………..

 Metabolic diseases
*DM
 Malnutrition
*Tropical ulcer
 Inflammatory processes
*cellulitis
 Infective processes
*TB
*Syphilis
*Fungal infection
CLASSIFICATION

A. Clinical
B. Pathological
 A. Clinical

 Spreading :(Edge -Inflamed & Edematous)

 Healing :(Edge is sloping with healthy red granulation
tissue & serousdischarge)
 Callous :(Floor contains pale unhealthy granulation
tissue with indurated edge)
B. PATHOLOGICAL

1.Nonspecific
2. Specific
3. Malignant
 1.NON SPECIFIC
 Traumatic ulcer: it may be due to mechanical, physical, chemical injury.
 Arterial ulcer: Atherosclerosis, TAO.
 Venous ulcer(gravitational ulcer, postphlebitic ulcer)
 Trophic ulcer
 Infective ulcer: pyogenic ulcer
 Tropical ulcer: it occurs in tropical countries. It is callous type of ulcer. e.g. Vincent’s ulcer
 Cryopathic ulcer: ulcers due to chilblains and frostbite.
 Diabetic ulcer
 Martoell’s hypertensive ulcer: it occurs due to obliteration of end arteries. It is observed in skin over
the back of calf region. Ulcer is severely painful with deep, non-healing ischemic look.
 Bazin’s ulcer: it is seen exclusively in legs, ankles of young females as erythematous purplish
nodules and non healing ulcer. It may be due to ischemic/ hypersensitive/ tuberculous etiology. It is
treated with anti tuberculous drugs, dressings, vasodilators and often by sympathectomy. It also
called as ERYTHROCYANOSIS FRIGIDA.
 2. SPECIFIC

 Tuberculous ulcer
 Syphilitic ulcer: it is punched out, deep ulcer, with “wash
leather” slough in the floor and with indurated base.
 Actinomycosis
 Meleney’s ulcer
 Soft sore
3.MALIGNANT

Carcinomatous ulcer
Rodent ulcer
Melanotic ulcer
 Traumatic ulcer

1.Mechanical- Dental ulcer on tongue (jagged tooth )

2.Physical- Electricalburn
3.Chemical- Application of caustics.
 Acute, Superficial, Painful, Tender
 Arterial Ulcer

 It is common in toes , feet or legs, often can occur in upper limb digits. It is due to poor blood supply
following blockage of the digital or medium size arteries.
 Atherosclerosis and TAO (thromboangitis obliterans) are common causes in lower limb.
 Cervical rib vasculities are common cause in upper limb.
 It occurs after trauma, soon becomes non healing, spreading with
scanty granulation tissue.
 It is very painful, tender and hyper esthetic.
 Ulcer is usually deep, destructs the deep fascia, exposing tendons,
muscles and underlying bones.
 Venous ulcer

 Medial aspect of lower 3rd of lower limb

 Ankle ( Gaiters Zone ) :Chronic Venous HTN
 Ulcers are Painless
 Varicose Veins or Post Phlebitic limb (PTS)
 Trophic Ulcer

• Pressure Sore or Decubitus Ulcer

• Punched out edge with slough on the floor
• Ex:Bed Sores & Perforatingulcers
• Develop as a result of Prolonged Pressure
• Sites :Ischial Tuberosity > Greater Trochanter
>Sacrum >Heel >Malleolus >Occiput
Pressure sore (Bed sore/
Decubitus Ulcer)

 Bedsore/ pressure sore is a trophic ulcer which

underlying bone as the base.
 It is non mobile, deep. Punched out ulcer.
 It is common in – old age, tetanus, diabetic, anemia,
comatose.
 Tropical Ulcer

• Tropical regions :Africa, India,S.America

• Trauma or InsectBite
• Fusobacterium fusiformis & Borrelia vincentii
• Abrasions, Redness, Papules &Pustules
• Severe Pain
 Diabetic Ulcer

 Itmay be caused due to:

• Diabetic Neuropathy: involving all sensory,
motor and autonomous components.
• Diabetic Microangiopathy: which affects
microcirculation .
• Increased Glucose :IncreasedInfection
 Sites: Foot ( Plantar ), Leg, Back,Scrotum,
Perineum Ischemia, Septicaemia, Osteomyelitis.
 Tuberculous ulcer

 This mostly results from bursting of caseous lymph nodes.

 This type of ulcer may also develop when cold abscess
from bone and joint tuberculosis breaks out on the surface.
 The ulcer is slightly painful.
 Such ulcer is usually seen in the neck,
axilla and groin acc. To frequency.
 Rodent ulcer

 It is ulcerative form of basal cell carcinoma which is common in face.

 Ulcer shows central area of dry scab with peripheral raised active and
beaded (pearly white) edge.
 It is common in face; rarely can it occur over tibia, external genitalia
mucocutaneous junction.
 Examination

 Inspection
 Palpation
 Examination of lymph nodes
 Vascular insufficiency
 Nervelesions
 Inspection
 Location of the ulcer
 Floor of the ulcer
 Discharge from the ulcer
 Edge
 Surrounding area
 LOCATION OF THEULCER

Arterial ulcer Tip of the toes, dorsumof

the foot
Long saphenous varicosity Medial side of theleg.
with ulcer
Short saphenous varicosity Lateral side of theleg.
with ulcer
Perforating ulcers Over the sole atpressure
points.
Nonhealing ulcer Over the shin
FLOOR OF THEULCER
This is the part of the ulcer which is exposed or seen.

Red granulation tissue Healing ulcer

Necrotic tissue, slough Spreading ulcer

Pale, scanty granulation Tuberculousulcer

tissue
Wash-leather slough Gummatous ulcer
 DISCHARGE FROM THE
ULCER
Serous discharge Healing ulcer

Purulent discharge Spreading ulcer

Bloody discharge Malignant ulcer

Discharge with bony Osteomyelitis

spicules
Greenish discharge Pseudomon
as infection
 EDGE

DEF:Thisisbetween the floor of the ulcer and the margin.

The margin isthe junction between the normal epithelium and the
ulcer.
These two parts represent areas of maximumactivity. 3STAGES
Stage of ex-tension.
Stage of transition.
Stage of repair.
 All healing ulcers like
A. Sloping edge
traumatic ulcers,
venous Ulcers
B. Punched out Gummatous ulcers
edge and trophic ulcers.
C. Undermined Tuberculous
edge ulcers
D. Raised edge Rodent ulcers or
(beaded edge) basal cell
carcinoma .
E. Everted edge Squamous cell
(Rolled out) carcinoma.
 SURROUNDING AREA

Thick and Varicose ulcer.

pigmented

Thin and dark Arterial ulcer.

Red and Spreading ulcers like

oedematous diabetic ulcer.
 PALPATION
 Edge
 Base
 mobility
 Bleeding
 Surrounding area
 TREATMENT
 Treat the cause like diabetes, anemia and malnutrition. Often needs
blood transfusion.
 Antibiotics are given depending on the culture and sensitivity.
 Regular dressing using EUSOL (Edinburgh University Solution
containing calcium hydroxide, boric acid, sodium hypochlorite)
 Wound excision/ slough excision/ debridement of the wound at
regular intervals.
 Once wound granulates well, split skin grafting is done to cover the
defect.
 If there is no adequate blood supply, or if bone is exposed then flap
is needed depending on the location of ulcer, either groin flap,
pectoralis major flap, etc.
 DEFINITION

 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)
 Ulceration is the most common lesion of
oral mucosa and is the manifestation for
many local and genetic disorders.
Recurrent Aphthous Stomatitis
(recurrent aphthous ulceration)
It is one of the most common oral
mucosal pathoses. The reported
prevalence in the general population
varies from 5% to 66% with a mean of
20%.
Etiology of Recurrent Apthous Stomatitis
• HEREDITARY PREDISPOSITION

• TRAUMA

• EMOTIONAL STRESS AND PSYCOLOGICAL FACTORS

• BACTERIALAND VIRAL INFECTIONS

• ALLERGIC DISORDERS

• HAEMATOLOGICALAND DEFICIENCY DISORDERS

• GASTROINTESTINAL DISORDERS
The clinical variations of aphthous
stomatitis:-

1.Minor
2.Major
3.Herpetiform
 Clinical features of RAS

MINOR MAJOR HERPETIFORM

AGE OF 10-19 10-19 20-29

ONSET
(YEARS)
NUMBER 1-5 1-10 10-100
OF ULCERS

PRINCIPA LIPS, CHEEKS, PALATE, PHARYNX FLOOR OF

L SITES TONGUE MOUTH, PALATE,
PHARYNX,
GINGIVA
SIZE OF <10 >10 1-2 BUT OFTEN
ULCERS(MM COALEASE
)
DURATION 7-14 >30 10-30
IN DAYS
 Minor aphthous ulceration
 This accounts for 80% or more cases of RAS.
 Its characterized by round or oval ulcers which affect non-
keratinized areas of oral mucosa and they have grey/ yellow
base with erythematous margin in association with prodermal
symptoms of burning, itching, stinging.
 The ulceration measure between 3&10 mm in diameter.
 They heal without scarring and tend to recur at 1-4 month
intervals, which is variable.
 The buccal and labial mucosa are affected most frequently,
followed by the ventral surface of the tongue, mucobuccal fold,
floor of the mouth and soft palate.
 Major aphthous ulceration
 These ulcers are larger than minor aphthae and demonstrate the longest
duration per episode.
 They occur anywhere in mouth including the keratinized oral mucosa
but the lips, soft palate, tonsillar areas and oropharynx are common
sites.
 The ulcerations are deeper than the minor variant , measure from 1-3cm
in diameter. They heal with scarring and tend to recur at 2-6 weeks and
may be associated with severe discomfort and with difficulty in eating
and speaking.
 The extension is deeper and may present as crater like ulcers with
rolledmargins which are indurated on palpation because of underlying
fibrosis.
 The onset of major aphthae is after puberty and recurrent episodes may
continus to develop for upto 20yrs. Or more.
 Herptiform Aphthous Ulcerations
 Its characterized by multiple, small, pin- headed ulcers that can
occur in any part of oral mucosa. The non-keratinized, movable
mucosa is affected most frequently. There is a female
predominance and typically the onset is inn adulthood.
 When hundreds of ulcers are clustered together, they
confluence , which results in larger areas of ulceration with
irregular outline. The individual lesions are small, averaging 1-
3 mm in diameter.
 They heal within 2-3weeks with scarring
 The ulcers tend to recur at less than monthly interval and may
be associated with severe discomfort.
 Histopathological Features
 The early ulcerative lesion demonstrate a central zone of
ulceration, which is covered by a fibrinopurulent membrane.
 Deep to the area of ulceration, the connective tissue exhibits
and increased vascularity and mixed inflammatory cellular
infiltrate that consist of lymphocytes, histiocytes and
polymorphonuclear leukocytes.
 The epithelium at the margin of the lesion demonstrates
spongiosis and numerous mononuclear cells in the basilar
one-third.
 Treatment and prognosis
Most mouth ulcers don't need treatment. However, if you get mouth ulcers
often or they are extremely painful, a no. of treatments can decrease pain and
healing time. This includes:-
 If patients with mild disease, the mainstay of therapy is the use of tropical
corticosteroids.
 Most patients with diffused minor or herpitiform aphthae respond well to
dexamethasone solution (0.5mg/5ml) used in a rinse- and- expectorate
method.
 Patients with localized ulcerations treated successfully with 0.05%
augmented betamethasone dipropionate gel or 0.05% fluocinoxide gel.
 The individual lesion may be injected with triamcinolone acetonide or
covered with 0.05% clobethasole propionate gel or halobetasole propionate
0.05% ointment. Triamcinalonetablets also can be dissolved directly over the
lesions.
 In hard to reach areas, such as the tonsillar pillars, beclomethasone
dipropionate aerosol spray can be used.
 Furthermore, some of the treatment may have significate side effects or
may be quiet expansive. So other treatments are:-
1. Using a rinse of salt water and baking soda.
2. Placing milk of magnesia on the mouth ulcer.
3. Covering mouth ulcer with baking soda paste.
4. Applying ice on canker sores.
5. Using topical paste.
6. Placing damp tea bags on your mouth ulcer
7. Taking nutritional supplements like folic acid, vita. B-6, vita. B-12 and
zinc.
8. Using a mouth rinse that contains a steroid to reduce pain and swelling.