PHYSICAL

&
CHEMICAL
INJURIES OF THE
ORAL CAVITY

PHYSICAL & CHEMICAL INJURIES

PHYSICAL INJURIES Iatrogenic- repair
restoration of
missing teeth
Self inflicted-Overzealous
oral hygiene practice,
caused by psychotic or
neurotic condition or
habitual.
Traumatic fall, fight,
accidents, sports injuries.

CHEMICAL INJURIES
Environmental elements
such as toxic levels of
chemicals in water, air, or
in consumables
Restorative materials used
in dental practice.

PHYSICAL
INJURY
Traumatic Bone
DIRECT

cyst
Sinus mucocele

BONE

HARD
TISSUE

Fractures of
jaws

RESTORATION

Ortho mov.

According to the material

Adhesive: GIC
Non-adhesive: Amalgam

TEETH
DIRECT

SOFT TISSUE

Preparation:
Type of bur
Heat
Smear Layer
Vibration
Acid etching

Bruxism
Ankylosis
Fracture

PHYSICAL
INJURIES OF THE
HARD TISSUES

PHYSICAL INJURIES OF
THE BONE

TRAUMATIC CYST

(Solitary Bone Cyst, Hemorrhagic Bone Cyst,

Simple Bone Cyst)
Term

Cyst is a Misnomer:
no epithelial lining

Definition:

It is an unusual benign, empty or fluid

filled lesion which occurs both in jaws as
well as in other bones of the skeleton.

Clinical features
Frequency

: 1% of jaw cysts

Age

:2nd D
(almost all cases <30 yrs)

Gender

: Equal to /slight male

Site

: Mandible>>>Maxilla

Buccal and labial>> lingual

Mandible: Body and

symphysis

Clinical presentation:

Presenting symptom:

Swelling > Pain > Labial paraesthesia

Completely symptom less>>>definite symptoms.

Thus, commonly an accidental finding

50%: significant trauma to the area

Radiological features

Most valuable in diagnosis

R/L area with irregular but definite

edge and slight cortication

Occlusal view: R/L extending

along cancellous bone

Radiological features

Cyst seen enveloping the roots of erupted teeth

Scalloping is a prominent feature--- between teeth

Lamina dura +/-

Occasional root resorption

Sometimes interpreted as multilocular

erroneous diagnosis

 If.R/L
2.

molar area,
round or ovoid cavity

3.

vital tooth

1.

Differential diagnosis:
To differentiate

Static bone cyst

Mandibular canal

The static bone cavity usually lies below and

the traumatic cyst usually lies above it.

ETIOLOGY

Not known

Pathogenesis based upon traumatic etiology:

Trauma to a bone
Intramedullary haemorrhage
Failure of early organisation of the haematoma
Subsequent liquefaction of the clot
Traumatic cyst
Trauma-hemorrhage theory: widely accepted

Size
increase

Breakdown products of haemolysis

Transudation into cyst fluid
Increased intra-osseous pressure
Resorption of bone

Slowly, fluid is diluted dropping intracystic pressure

Gradual absorption of the serous fluid
Cavity becomes empty

 For

some unexplained reasons there is

subsequent degeneration of the clot.

Hemolytic

capillary
resorption.
Slowly

products accumulation leads to

fluid transudation and bone

pressure goes down and eventually

producing an empty cavity within bone.

Few other theories proposed:

1.

Origin from bone tumors that have undergone cystic

degenerations.

2.

A result of faulty calcium metabolism such as that

induced by parathyroid disease.

3.

Origin from necrosis of fatty marrow due to

ischemia.

4.

The end result of chronic low-grade infection.

5.

Local disturbances in bone growth.

Pathology
Gross:

Frequently empty

Blood, serosanguineous or serous fluid

No visible lining to a very thin membrane,

granulation tissue or blood clot

Ultrastructurally, no epithelium

Histological features
Most of the histologic findings reveal fibrous
connective tissue and normal bone

Loose vascular fibrous tissue

membrane of variable thickness
with no epithelial lining,

May show fragments of fibrin

with enmeshed red cells,

Haemorrhage and haemosiderin

pigment and scattered small
multinucleate cells,

Longer standing, more densely fibrous

Necrotic tissue or myxoid degeneration in

cavities adjacent to areas of bone resorption

Loose fibrous tissue covering bone

The lining is composed of loose vascular fibrous

tissue with osteoclastic activity on the surface of the

Treatment & Prognosis

The surgeon should open the cavity (since definitive diagnosis

cannot be established without surgical exploration).

Treated as part of the diagnostic process

Cyst lumen is opened to reveal an empty cavity

Cyst wall is then curetted

Granulation tissue and eventually new bone proliferate and

replace the haemorrhage

Recurrence is unusual but has been reported

Orthodontic
tooth
movement Ability of teeth to be moved through bone, without their
subsequent extrusion or loss, by application of pressure or
tension under appropriate & controlled circumstances.
Mechanism- bone under pressure- resorbing
bone under tension- deposition
Movement Tipping
Extrusive
Intrusive
Movement- Degree of force
Direction of the force
Position of the fulcrum around which the
force acts

PRESSURE SIDE
Compression of PDL
Osteoclast migrate to site
Resorption of bone
Deposition of new spicules
of bone on outer surface of
labial plate maintaining the
thickness of already thin
labial plate preventing
perforation by the tooth.
Ischaemia,necrosis

TENSION SIDE
Tearing of PDL
New trabaculae of bone
appear arranged parallel to
periodontal fibres.
Osteoblast activity
Bone depostion
Gradually stabilization
occurs leading to formation
fo compact bone that
existed before tooth
movement

TIPPING MOVEMENT-

Extrussive movement

It is similar to normal tooth eruption.

Deposition or apposition of new bone spicules at
alveolar crest arranged parallel to direction of force.
Direction of spicules becomes parallel to long axis of
tooth & increased the height of alveolar crest.
Noraml width of apical PDL is maintained by new
bony spicules formed in the same direction.

INTRUSIVE TOOTH MOVEMENTTISSUE CHANGES ARE OPPOSITE TO THAT OF

EXTRUSSION.
RESORPTION FO BONE OCCURS AT THE APICAL
AREA & AROUND THE ALVEOLAR MARGIN.
NEW BONE FORMATION IS MINIMAL.

EFFECT OF DECIDUOUS TOOTH MOVEMENT

UPON PERMANENT TOOTH GERMS
Breitner & Tischler permanent tooth germ
followed the movement of the deciduous teeth.
Whenever a deciduous tooth was moved away
from a tooth germ, the permanent tooth followed
it.
These studied suggested that form of dental arch
may be modified by altering the deciduous arch
through orthodontic tooth movement of deciduous
teeth.

INJURIES OF THE TEETH

ASSOCIATED WITH RESTORATIVE
PROCEDURES
During preparation
of tooth for restoration

Due to restorative
material

REACTIONS TO PREPARATION OF TEETH FOR

RESTORATIVE PROCEDURES
Effect on dentin and pulp depends upon:
1.
2.
3.
4.
5.
6.
7.
8.

Type of instruments used: steel burs, diamond burs or

alternative cutting methods like air abrasion,
Thermal injury,
Pulp exposure,
Smear layer,
Vibrations,
Desiccation of dentin,
Acid etching,
Remaining dentin thickness (RDT).

SMEAR LAYER FORMATION

This microscopic layer is formed after the tooth is

cut/prepared.

< 2m thickness

Consists of cutting debris from tooth and contamination

from the oral cavity, i.e.,

Enamel,

Dentin and its parts: Intertubular, peritubular matrix mixed with water and
dentinal fluid,

Occasionally saliva along with bacteria.

Beneficial since it reduces:

1. Flow of fluid through dentin,
2. Permeability,
3. Entry of bacteria.
But
this layer has to be removed to obtain optimal chemical
& mechanical bonding between the restoration
& the tooth structure.

HEAT
This is influenced by:
1.

The size, shape & composition of the bur or stone.

2.

The speed of the bur or stone.

3.

The amount & direction of pressure on the cutting instrument.

4.

The amount of moisture in the field of operation.

5.

The length of time the bur is in contact with the tooth.

6.

The type of tissue being cut; enamel or dentin.

Effects of heat:
Separation of the odontoblastic layer, edema,
hyperemia & inflammatory cell infiltration.
In severe conditions, the pulp may develop blisters,
abcesses or may be destroyed.
The pulp only encounters a fraction of the heat applied to the tooth, as dentin
dissipates heat and has low thermal conductivity.
It is an effective insulating medium for low heat conditions.

EFFECT OF HIGH SPEED

INSTRUMENTATION
If inadequate cooling or excessive drying of the
dentin occurs after cavity preparation:
1.
2.
3.

Displacement of the odontoblastic nuclei

Disorganization of the organelles & nuclear membrane
Lysis of cellular elements

DEAD TRACTS formation.

Adequate cooling
4.

To prevent histological changes in dentin or injury to the

odontoblastic zone of the pulp.

EFFECT OF AIRBRASIVES
Airbrasive: Aluminum oxide is sprayed under
pressure for cavity preparation.
Pulp irritant

Imperfect sealing, pressure & heat involved.

Use:
Short period.
Cleaning pits & fissures prior to application of sealants

EFFECT OF LASERS
(Light Amplification by Stimulated Emission of
Radiation)
Uses:
1.
2.
3.

Desensitization of exposed root surfaces,

Roughening of hard tissues to promote bonding,
Vaporization of carious tissue & organic tissue in
endodontic preparation.

Disadvantage: Heat generation.

Thus Lasers should be used with caution.

EFFECT OF ULTRASONICS
Principle:
Converts electrical energy to mechanical energy in the form
of vibrations.
Disadvantages:
Immediate reaction:
Mild hyperemia/ hemorrhage
Slight lymphocytic infiltration

` Late reaction:
Formation of calciotraumatic line
A hematoxyphilic line between regular dentin
& post-op dentin showing disturbance in dentin

REACTIONS TO RESTORATIVE
MATERIALS, TOOTH RESTORATION
INTERFACES & ADHESIVE TECHNIQUES

Direct restoration

Indirect restoration

Direct(nonadhesive)
1.

Dental amalgam
proposed
alternatives,

and its
metallic

2.

Condensable gold,

3.

Different cements and liners,

e.g., zinc phosphate, silicate
and temporary restorations,
i.e., ZOE based .

Indirect
Resin based composite:

Glass ionomer materials,

Resin-modified glass
ionomer cements,

Polycarboxylate cements

AMALGAM
Injury due to:
Exothermic reaction
Compaction pressure

Deep cavities with amalgam:

1.
2.
3.

Decreases the number of odontoblasts,

Mild inflammatory cell infiltration,
Extra pressure can directly expose the pulp.

Zinc phosphate cement

Injury due to:
Phosphoric acid
Damage:
1.
Hyperemia/
hemorrhage
with
inflammatory cell infiltratrion
2.
Reduction in the size and number of the
odontoblasts

Silicate Cement
Injury due to:
Phosphoric acid
It requires more free acid during mixing
than zinc phosphate cement

Damage:
1.
2.

Mild to severe pulpitis,

Varying degrees of degeneration & necrosis, &
destruction of odontoblasts.

Zinc oxide Eugenol

This is almost universal agreement
that ZOE is least injurious of all
filling materials to dental pulp.

Palliative and sedative

effect on the mildly
damaged pulp

Resin based materials

These composites are classified based on their
acid- etching protocol:
1.
2.
3.

Acid etching with phosphoric acid,

Self etching primer,
All in One, etching, priming & bonding in one
procedure.

Phosphoric Acid removes the Smear layer

& demineralises the dentin forming the hybrid layer.

The hybrid layer exposes the organic matrix, which is

lost during washing.

The peri-tubular dentin demineralises faster than

intertubular matrix leading to a funnel shaped
demineralised area surrounded by a collagen mesh.

Resin infiltrates into this area into the collagen mesh.

This is required for optimal bonding of the resin with

dentin.

If the hybrid layer becomes too dry, the collagen mesh

will collapse & penetration of resin will be impaired.

Thus an adequate moisture content is essential to prevent

collapse of the collagen mesh & ensure a strong bond
between the restoration & the tooth.

Glass ionomer cements

Advantage over silicate cements, zinc
phosphate cement:
Bland, moderate and less irritating.
Absence of strong acids and toxic monomers
&
presence of high molecular weight polymers.

Weak acids include:

1.
2.

Polyacrylic acid
Polyacids

Higher molecular weight polymers:

Limited diffusion through the dentinal
tubules to the pulp

MINERAL TRIOXIDE AGGREGATES (MTA):

MTA is a powder that consists of tri-oxides combined
with other hydrophilic particles.
Mechanism:
It crystallizes in the presence of moisture and induces
hard tissue formation.
Uses:
Perforation repairs, root end fillings, pulp capping &
other endodontic procedures.

Advantage:
1.
2.
3.

Less inflammation, hyperemia & necrosis

Thicker dentinal bridges
More frequent odontoblastic layer in comparison to
Calcium Hydroxide.

Calcium Hydroxide
Advantage:
Promotes limited sclerosis, when applied to vital tissues, including
unaffected dentin in young teeth.
Mechanism:
1.
Precipitation of crystalline material (physico-chemical
mechanism) within the dentinal tubules.
2.
Dissolving growth factors & other components of the dentinal
matrix.
Use:
As liner: protects pulp from reactions of other restorative
materials.

PHYSICAL INJURIES
OF THE TEETH

BRUXISM
(Night-grinding,
Bruxomania)

BRUXISM (Night-grinding, Bruxomania)

Definition:
It is habitual grinding of the teeth, either during sleep or as an
unconscious habit during waking hours.

Habit:
Both clenching habit and tapping of the teeth.
Tissue affected:
Pressure is exerted on the teeth, and periodontium by
the actual grinding or clamping of the teeth.

Etiology
1)
2)
3)
4)

Local
Systemic
Psychological
Occupational

Local factors
Generally

associated with some form of

mild
occlusal
disturbance,
which
produces mild discomfort and chronic
tension.
In children, the habit is generally
associated with the transition from the
deciduous to the permanent dentition and
may result from an unconscious attempt
to place the individual tooth planes so
that the musculature will be at rest.

 Systemic

factors like GI disturbances, subclinical nutritional deficiencies, allergy,

endocrine disturbances have all been
reported as causative factors.
Also seen in cases of acrodynia.
Psychological

factors are believed to be the

most common cause of bruxism.
Emotional tension may be expressed
through a number of nervous habits, one
of which may be bruxism.

Thus when a person suffers from fear, rage,

rejection or a variety of other emotions which
he is unable to express, these become hidden in
the subconscious but are expressed periodically
by numerous means.
Bruxism is common in mental institutions.
Also Seen in nervous tension in children and
may be related to chronic biting or chewing of
toys.

 Certain

Occupations favor the development

of this habit.
Athletes engaged in physical activities
often develop bruxism.
Voluntary bruxism also recognized in those
persons who habitually chew gum, tobacco
or objects such as toothpicks or pencils.
Although voluntary, this too is nervous
reaction and may lead eventually to
involuntary or subconscious bruxism.
Occupations, in which the work must be
unusually precise such as that of the
watchmaker, are prone to cause bruxism.

CLINICAL FEATURES
Typical grinding or clenching motions during sleep or
subconsciously when awake, which may be associated
with grinding or grating noise.
Effects of this have been divided into 6 categories
1)On the dentition,
2)On the periodontium,
3)On the masticatory muscles,
4)On the TMJ,
5)Head pain, and
6)Psychological and Behavioral effects.

- Severe wearing or attrition of the teeth

may occur, not only occlusally but also
interproximally.
- On both surfaces, actual facets may be
worn in the teeth.
- Loss of integrity of periodontal structures,
resulting in loosening or drifting of teeth
or even gingival recession with alveolar
bone loss.

- TMJ disturbances are also reported to

occur as a result of the traumatic injury of
continuous tooth, impact without normal
periods of rest.
- Hypertrophy of the masticatory muscles,
pert masseter, may interfere with
maintenance of the rest position, cause
trismus, and alter occlusion
and the
opening & closing pattern of the jaws.
- Bruxism may give rise to facial pain &
headache.

Treatment & Prognosis

- If underlying cause is an emotional one, the
nervous factor must be corrected if the
disease is to be cured.
- Removable splints to be worn at night may
be constructed to immobilize the jaws or to
guide the movements so that periodontal
damage is minimal.
- The use of oral sensors too have helped
bruxism patients.

ORAL SENSOR
The extra pressure may be registered,
by securely inserting a strain gauge
between the teeth. When the pressure
exceeds a predetermined level, the
alarm goes off.
A commercially available new device,
the OralSensor, produces an audible
tone when bruxism occurs.

Before & After treatment of Bruxism with Porcelain Crowns

OF&THE
TEETH
isFRACTURES
a common injury
is a mainly
caused
due to severe trauma.
It could be a fall, accident, fights etc. & is
seen more often in children & most often in
anterior teeth.
The other possible reasons are:
Teeth with large restorations, leaving
unsupported enamel & thin walls which
fracture under masticatory stresses, or
Internal resorption or Structural defects.
It

Classification of Fractures of Teeth:

A detailed classification by Ellis is as
follows:
1) Simple fracture of the crown, involving
little or no dentin (Minor chipping of
teeth).
2) Extensive fracture of the crown, involving
considerable dentin but not the dental
pulp.
3) Extensive fracture of the crown, involving
considerable dentin & exposing the pulp.

4)
5)
6)
7)
8)
9)

The traumatized tooth becomes non-vital

with or without loss of crown structure.
Teeth lost as a result of trauma.
Fracture of the root, with or without loss
of crown structure.
Displacement of a tooth, without fracture
of crown or root.
Fracture of the crown en masse & its
replacement.
Traumatic injuries to deciduous teeth.

FRACTURES OF TEETH

ELLIS CLASSIFICATION
(Depending on pulpal involvement) -9 classes
CLASS 1 Simple # of crown (Enamel # involving little or no dentin
CLASS 2 Extensive # of crown(inv. Considerable dentin but no pulp)
CLASS 3 Extensive crown # inv. enamel, dentin & causing pulp
exposure
CLASS 4 Traumatized tooth becomes non vital with /without loss of
crown structure
CLASS 5 Tooth lost due to trauma
CLASS 6 Root # with/w. out loss of crown structure
CLASS 7 displacement of tooth without # of crown /root
CLASS 8 - # of crown EN MASSE & its replacement
CLASS 9 Traumatic injuries to deciduous tooth

Root Fractures

Horizon
tal

Obliq
ue

Clinical Features:
If there is crown fracture without pulp
involvement, tooth remains vital but may
have mild pulp hyperemia.
If the dentin over the pulp is exceedingly
thin, bacteria may penetrate the dentinal
tubules, infect the pulp & cause pulpitis &
eventually necrosis.
If tooth remains vital, secondary dentin
formation is observed but tooth may be
sore & slightly mobile because of the
injury.

fractured tooth exposing the pulp, is a

serious problem.
If the pulp remains vital inspite of the
injury, the exposure can be capped by
calcium hydroxide & a dentinal bridge
forms.
Pulpotomy or pulpectomy may often be
necessary as infection sets in as soon as
there is exposure.

Root fractures are rare in children as their roots

are not completely formed.
If roots are fractured in mature teeth, they are
mostly horizontal in the middle third of the root
or the apical 3rd of the root.
This leads to tooth non-vitality immediately.
Sometimes, the tooth may remain vital & may
heal by formation of secondary dentin or
granulation tissue. The latter at times leads to
resorption & tooth loss.
This can be avoided by immobilization.

CEMENTAL TEARS:
These

are small cemental fractures that is

seen in teeth where the traumatic event is
not forceful enough & no true fracture
line is present.
These may also be seen due to tooth
movement.
They are incidental findings may be
asymptomatic.

TOOTH ANKYLOSIS
Ankylosis

is the union of tooth to bone &

is a rare condition.
It is seen when the connective tissue of the
PDL is lost allowing cementum or dentin
to come in contact with alveolar bone.
This leads to fusion of two calcified
structures.

Possible reasons for ankylosis are:

Interruption of physiological resorption of the
roots of deciduous teeth, where the granulation
tissue fibroses & forms bone.
Acute
or Chronic trauma leading to
inflammation & destruction of PDL.
Autoimplanted / Replanted or Transplanted
avulsed teeth with loss of PDL.
Periapical inflammation, Irritation to the apical
PDL after endo treatment, rapid orthodontic
movement, occlusal trauma, or long standing
impacted teeth.

CLINICAL FEATURES:
Ankylosis

of the deciduous teeth leads to

submerged teeth.
If Permanent teeth are affected, it could
be due the possible etiologies mentioned
earlier.
The tooth gives a dull, muffled sound on
percussion when an extensive area of the
root surface is involved.

Radiographic Features:
It

is observed as a loss of the normal thin

PDL space.
Mild sclerosis, of the bone with blending
of the bone to the tooth root.

Histologic Features:
The

PDL is completely obliterated in the

region of ankylosis.
An area of root resorption is seen which
is replaced by cementum or bone and is
continuous with the alveolar bone.

Treatment
There

is no treatment for this in

particular.
If there is any infection it should be
treated appropriately & usually shows a
good prognosis.
PRECAUTIONS
If the tooth needs to be extracted, it
should be done with care as it may lead
to fracture and may need surgical
removal.

PHYSICAL
INJURIES OF THE
SOFT TISSUES

Linea Alba
This is mainly caused due to Pressure,
frictional irritation, or suckling trauma from
the facial surfaces of the teeth
It may result in a usually scalloped, white line,
on the buccal mucosa corresponding to the
occlusal plane of the adjacent teeth.
This is bilateral & restricted to the dentulous
areas, more prominent adjacent to post teeth.

 Histologically,

hyperorthokeratosis &
intracellular edema of the epithelium &
chronic inflammation of the underlying
C.T. may be noted.
No treatment is required.

Factitial Injuries
(Chronic cheek chewing, Morsicatio buccarum)
These

injuries are inflicted by the patient.

They may be consciously undertaken,
habitual or inadvertent, with a frequent
psychogenic background.
Thus they originate as a result of such
habits as chronic lip or cheek or tongue
biting, or gingival trauma from finger
nails.

 Biting

habits also known as pathomimia

mucosae oris.
Chronic chewing or lip biting usually
produces lesions on the buccal mucosa
(morsicatio buccarum), and sometimes on
lip (morsicatio labialis) and tongue
(morsicatio linguarum).
Also seen in people who are under stress
or who exhibit psychological conditions.
They also observed as a result of suction
and in glassblowers.

 Occurrence

is twice as prevalent in women

and more common after the age of 35 yrs.
The emotionally disturbed individuals also
resort to secretive and purposeful
production of oral lesions to obtain
continuous attention from family and
health care workers.
Patients often indicate that their habit was
initiated & perpetuated due to itchiness
in the area.

 Patients

with the Gilles de la Tourette

syndrome are prone to spontaneous
erratic behavior & incoherent facial
expressions & verbalizations & facial tics.
Part of syndrome is the tendency for self
mutilation, which is often directed to the
oral tissue through the use of the teeth or
finger nails.

Clinical Features
- Usually bilateral located typically in the
mid portion of the anterior buccal
mucosa along the occlusal plane.
- The lesions appear as thickened,
shredded white areas, with an irregular
ragged surface, sometimes combined with
areas of erythema, erosion, or focal
traumatic ulceration.

Frequent scaling & flaking of vermilion

border involving both the lips due to
chronic injury secondary to habits such as
lip licking, biting, picking or sucking. This
condition is known as Factitious Cheilitis.
This process arises from excessive
production & subsequent desquamation of
superficial keratin.
These patients however deny any chronic
self-irritation of the area & are commonly
associated with personality disturbances,
psychological difficulties, & stress.

- Usually younger individuals are more

affected, with a marked female
predilection.
- Lesions associated with finger nail injury
are characteristically seen on the gingiva
appearing as vertical clefts produced by
forcing the free gingival margin apically,
this often results in root exposure of one
or more teeth.
- In other areas of mucosa, a chronic non
healing ulcer is produced.

Histologic Features
- Extensive
hyperparakeratosis
often
resulting in an extremely ragged surface
with numerous projections of keratin with
typical surface bacterial colonization.
- Clusters of vacuolated cells present in the
superficial portion of the prickle cell layer
mimic the appearance seen in oral hairy
leukoplakia, uremic stomatitis or betel
chewers mucosa.

Treatment & Prognosis

Psychologic counseling.
5-10mg of diazepam.
Occlusal night guard.

DEFINITIONA well circumscribed depressed lesion over which the epidermal

layer has been lost.
or
A break in the continuity of the covering epithelium.
or
A deeper crater that extends through the entire thickness of surface
epithelium & involves the underlying connective tissue.

PARTS OF ULCERMARGIN
EDGE
FLOOR
BASE
MARGINIt is the junction between normal epithelium and the ulcer.
Therefore it is the boundary of ulcer.
EDGEIt is the area between the margin and floor of the ulcer.
FLOORExposed surface of the ulcer.
BASEOn which the ulcer rests.

FIVE COMMON TYPES OF ULCER EDGEUNDERMINED EDGEe.g. -Tuberculosis.

PUNCHED OUT EDGE

The edge drops down at right angle
to the skin surface.
e.g. Gummatous ulcer

SLOPING EDGEe.g. Healing traumatic or Venous

ulcers.

RAISED AND PEARLY-WHITE BEADED EDGEe.g. Rodent ulcer

ROLLED OUT(EVERTED EDGE)Characteristic feature of squamous cell carcinoma

TRAUMATIC ULCER
These

ulcers are either self induced or

may be caused due to some kind of
trauma.
They
are manifested as surface
ulcerations which heal within few days.
The source of irritation is usually seen
next to the ulcer & helps at arriving at a
diagnosis.
In case of a chronic ulcer, biopsy would
be required to rule out any grave lesions.

Possible Causes of Traumatic Ulcers:

Cheek

bite, Lip Bite etc.

Contact with sharp foodstuff, toothpick
etc.
Irritation from a sharp tooth, sharp
restorations, denture or any external
irritant.
Toothbrush injury or injury during a
surgical procedure.

Clinical Features:
Most

commonly occurs in sites like, the

tongue, lips, & buccal mucosa which are
injured by teeth.
Other causes as mentioned previously can
cause ulcerations on the palate, gingiva &
mucobuccal fold.
Another important injury is the cotton
roll injury that is iatrogenic in nature &
caused by the dentist when they forcefully
pull out the roll that is adherent to the
mucosa.

 In

case of excessive toothbrushing, the

free gingival margins are affected by
linear
erythematous
lesions
that
surround
a
central,
yellow
fibrinopurulent membrane that can be
scraped off.
Traumatic ulcerations due to denture
irritation are termed as Sore Spots.
These are seen within a day or two of
insertion of a new denture.

Sore Spots may be caused due to over extension

of flanges, sequestration of bony spicules under
the denture, or high spots on the inner
surface of the denture.
These ulcers are small, painful, and irregularly
shaped, covered by a grey necrotic membrane
surrounded by an inflammatory halo.
Untreated lesions may lead to proliferations
around the periphery of the lesions.

ACUTE ULCER
Painful

CHRONIC ULCER
Little or no pain

Yellow base, red halo

Yellow base, elevated margins

History of trauma

History of trauma if remembered

Heals in 7 to 10 days if cause is

delayed healing if irritated

eliminated

(Tongue lesions)

Histologic Features:
Traumatic ulcers are non-specific &
microscopically show loss of continuity of
the surface epithelium.
The underlying exposed connective tissue is
covered by a fibrinous exudate.
PMNLs are seen under the ulcer area in
acute lesions and are replaced by
lymphocytes & plasma cells in chronic
lesions.
Capillary dilatation & proliferation as well
as fibroblastic proliferation may be seen.

Treatment & Prognosis

Removal

of the source of irritation relieves

ulceration in cases where traumatic cause
is identified.
If it is related to denture, then the
underlying cause needs to be rectified.
Applying topical dyclonine HCl, or
hydroxypropyl cellulose films gives
symptomatic relief.
If lesion persists, biopsy is indicated.

DENTURE RELATED INJURIES

DENTURE STOMATITIS
EPULIS FISSURATUM
INFLAMMATORY PAPILLARY
HYPERPLASIA
REACTIVE OSSEOUS AND
CHONDROID METAPLASIA
DENTURE BASE INTOLERANCE

DENTURE STOMATITIS
(Denture Sore Mouth, Erythematous candidiasis)
- It is an uncommon condition manifesting

as areas of erythema confined to the

denture bearing areas of a maxillary
removable denture.
- The patient may give a history of
sleeping with dentures.

The intense erythema is not due to a true

acrylic sensitivity, since patch test with the
denture material gives negative results.
Chronic trauma to the oral mucosa
arising from poor design & fit of the
denture, inadequate curing of the acrylic,
continued denture wearing & poor oral
hygiene predisposes the oral mucosa to
microbial invasion.

- Candidal species act as an endogenous

infective agent on this vulnerable tissue
causing this condition which is also known
as erythematous or chronic atrophic
candidiasis.
- The important aspect of colonization is
the attachment of the yeast to the denture,
which is enhanced by mucus & serum &
decreased by the presence of salivary
pellicle (suggesting the severity of the
condition in xerostomic patients).

- Rarely found under mandibular

denture, this cud be due to the negative
pressure that forms under a maxillary
denture excludes salivary antibody from
this region, allowing the yeast to
reproduce undisturbed in the space
between the denture & mucosa.

Clinical Features
- Mucosa exhibits a varying degree of
erythema and appears smooth or
granular.
- Multiple pin point foci of erythema may
be seen.
- The redness of the mucosa is rather
sharply outlined & restricted to the
tissues in contact with the denture.

Histologic Features
- Numerous papillary projections made of
stratified
squamous
epithelium
characterised by pseudoepitheliomatous
hyperplasia.
- Each projection has a core made up of
chronically inflammed granulation &
fibrous tissue.

Treatment & Prognosis

> Correction of irregularities in the
denture.
> Rebasing of denture.
> Construction of new dentures.
> Instruction on hygiene care of dentures.
> Antifungal therapy to manage candidal
infection.

Epulis Fissuratum
Other

names are:
Denture injury tumor
Inflammatory fibrous hyperplasia
Redundant tissue
Denture epulis

 Epulis-

mucosa

it is applied to tumor of gingiva or alveolar

 Most

common tissue reaction to a

chronic ill fitting denture is the
occurrence of hyperplasia of tissue
along the denture borders.
It is not restricted to this area but
occurs in any area where chronic
irritation exists, such as on gingiva,
buccal mucosa & angle of the mouth.

CLINICAL FEATURES
Development

of single or multiple fold or

folds of hyperplastic tissue in the
mucolabial or mucobuccal fold area into
which the denture flange conveniently fits
The redundant tissue is usually firm &
fibrous, although there may be irritation
or even ulceration in the base of the fold
into which the denture flange fits.

 The

size of the lesion varies from as

small as <1cm to large lesions occupying
the entire part of vestibule.
Seen in middle age or older adults.
Pronounced female predilection.
Increased propensity to occur in the
anterior portion of the jaws.

 This

proliferation of tissue is usually slow

in developing & results from either
resorption of the alveolar ridge or trauma
of the loose dentures or both.
Alveolar resorption causes extension of
the denture flanges deeper into the sulcus,
abnormally impinging on the soft tissues.

less common variant of fibrous

hyperplasia is the leaf like denture
fibroma that occurs beneath a maxillary
denture.
It presents as a flattened pink mass
closely applied to the palate by a narrow
stalk and sits in a slightly cupped out
depression.
The edge of the lesion is serrated
resembling a leaf.

Histologic Features
- Excessive bulk of fibrous C.T. covered by a
layer of stratified squamous epithelium,
which may be of normal thickness or show
acanthosis.
- Pseudoepitheliomatous hyperplasia.
- Hyperortho or parakeratosis.
- The C.T. is composed of coarse bundles of
collagen fibres with few fibroblasts or
blood vessels unless there is an active
inflammatory reaction present.

The chronic inflammatory cells seen is

variable,
demonstrating
sometimes
eosinophils or showing lymphoid
follicles.
- Minor salivary glands (if included in the
section), show chronic sialadenitis.
- Mucopolysaccharide keratin dystrophy,
also referred to as plasma pooling is
seen in the surface epithelium of
inflammatory fibrous hyperplasia.
-

TREATMENT & PROGNOSIS

- Surgically excised
- New denture fabrication, or
- Rebasing of old dentures to provide
retention.

INFLAMMATORY PAPILLARY
HYPERPLASIA
Also

known as palatal papillomatosis.

It is a reactive tissue growth that usually
occurs beneath a denture.
It is of unknown etiology, though ill fitting
dentures, poor oral hygiene & wearing
dentures 24 hrs a day is suggested
responsible.

CLINICAL FEATURES
Usually

seen in patients with dentures, but

on rare occasions, it is also observed in
patients with full complement of teeth &
no prosthetic appliance.
When an appliance is present, the site of
lesion corresponds to the denture base.
Any age in adult, no gender predilection.

 The

lesion presents itself as numerous

closely arranged, red edematous papillary
projections, often involving nearly all of
the hard palate, imparting to it a warty or
pebbly appearance.
Papilla are seldom over 1 mm or 2 in
diameter.
Varying degree of inflammation is seen,
but seldom is there ulceration.

HISTOLOGIC FEATURES
Numerous,
small vertical projections each
composed of parakeratotic (sometimes ortho)
stratified squamous epithelium & a central core
of C.T.
Severe inflammatory cell infiltration is nearly
always present in the C.T.
As is chronic sialadenitis in the accessory palatal
glands,
Pseudoepitheliomatous hyperplasia
(sometimes so severe as to be interpreted as
epidermoid carcinoma)

Treatment & Prognosis

Discontinuing

the use of ill fitting dentures.

Construction of new dentures without surgical
removal of the excess tissue will generally result
in regression of the edema and inflammation,
but the papillary hyperplasia persists.
Surgical excision prior to new denture
fabrication.

Denture Base Intolerance or Allergy

This

is a rare condition.
Allergy is found to be mainly due to monomer
present in regular as well as self-curing acrylic
denture bases.
This is one type of contact stomatitis.

Clinical Features
The features are similar to denture sore mouth.
It is confirmed by a positive patch test.
This is carried out by strapping the denture or
acrylic shavings to the forearm by adhesive tape
for 48 hrs.
A control area is created by using plain adhesive
tape to rule out allergy to adhesives

 Other

possible reasons for allergy in

dentures could be the use of cobalt
chromium alloy base materials where
nickel is the main cause of allergy.

Treatment
Once the cause of allergy is confirmed, the
denture should be replaced. In case of
monomer allergy, care should be taken
during polymerization & curing of the
denture.

INJURIES RELATED TO
THE SALIVARY GLAND

MUCOCELE
(Mucous Extravasation Phenomenon)
Mucocele

is a common lesion of the oral

mucosa involving salivary glands & their
ducts.
They result from traumatic severance of a
salivary duct, which might be produced by
biting the lips or cheek, pinching the lip by
extraction forceps, leading to spillage of
mucin into the surrounding tissues.
As these lack epithelial lining, they are not true
cysts.

CLINICAL FEATURES
Most

common on lower lip.

Other sites are buccal mucosa, anterior
ventral tongue & floor of the mouth.
Seen in all decades of life, with increased
predilection for children & young adults.
It appears as raised, dome shaped vesicles,
ranging in size from 1mm or 2mm to few
cms.
There might may be a history of rupture,
collapse & refilling which may be repeated.

 They

may lie deep in tissues or be

superficial.
Clinical appearance vary depending
upon location.
Superficial lesions present with a bluish,
translucent cast, the blue color imparted
by the spilled mucin below the mucosal
surface.
The deeper lesions are of normal color
because of the thickness of the overlying
tissue.

 These

often arise within a few days, reach

a certain size, and may persist as such for
months unless treated.
Contents consist of thick, mucinous
material.
Some regress & enlarge periodically &
may disappear after injury which results
in their evacuation, however, they almost
recur invariably.

 Superficial

Mucocele, is commonly seen in

the soft palate, retromolar area & post
buccal mucosa, presenting as single or
multiple tense vesicles measuring 1-4 mm
in diameter.
The vesicular appearance is created by
the superficial nature of mucin spillage,
resulting in a separation of epithelium
from underlying C.T.

 These

vesicles often rupture, leaving

shallow, painful ulcers that heal within
few days.
These vesicular appearing mucocele
should
be
differentiated
from
vesiculobullous
lesions,
especially
cicatricial pemphigoid.

HISTOLOGIC FEATURES
Circumscribed

cavity in the C.T. &

submucosa, producing an obvious
elevation of the mucosa with thinning of
the epithelium as though it were
stretched.
The wall is made up of a lining of
compressed fibrous C.T. & fibroblasts.

 Lumen

is filled by with the spilled mucin

containing cells chiefly leukocytes &
foamy histiocytes (macrophages).
C.T. wall usually shows infiltration by
abundant PMNLs, lymphocytes &
plasma cells.

 Occasionally

the cyst shows a flattened

intact epithelial lining, which may be the
portion of the excretory duct that was
injured.
This lining is termed as epithelium of the
Feeder Duct.
Or else, if the mucocele is epithelium-lined
it is termed as mucous retention cyst.

The normal salivary gland around it shows

alterations like
- Interstitial inflammation or sialadenitis,
Dilatation of intralobular & interlobular
ducts with collection of mucus
- Breakdown of individual acinar mucous cell
leading to formation of tiny areas of pooled
mucosa.

TREATMENT & PROGNOSIS

Excision.
If

it is incised its contents will be

evacuated, but it will be rapidly filled
again as soon as the incision heals.
Excised tissue should be sent for
microscopic examination to confirm the
diagnosis & to rule out the possibility of a
salivary gland tumor.
Recurrence is rare if associated SG acini
also removed.

 It

RANULA

is a form of mucocele that specifically

occurs in the floor of the mouth.
Name derived from the latin word rana,
which means frog, because the swelling
may resemble a frogs translucent
underbelly.
Although the most common source of
mucin spillage is sublingual gland, ranulas
may also arise from the submandibular
duct or from the minor salivary glands in
the floor of the mouth.

CLINICAL FEATURES
Appear

as dome-shaped, fluctuant
swelling in the floor of the mouth with a
translucent blue color .
Deeper ranulas are normal in color.
This develops as a slowly enlarging
painless mass located lateral to the
midline of the floor of the mouth.

 This

differentiates it from a midline

dermoid cyst.
The larger ranulas may be several cms in
size filling the floor & elevating the
tongue.
A rare suprahyoid type of ranula, termed
plunging or cervical ranula occurs due to
herniation of spilled mucin through the
mylohyoid muscle, producing swelling
within the neck.

HISTOLOGIC FEATURES
Similar

to that of smaller mucoceles.

The spilled mucin elicits a granulation
type of response that typically contains
foamy histiocytes.

TREATMENT & PROGNOSIS

Same

as mucocele.
Few prefer only to unroof the lesion
rather than to excise it totally.
Sometimes it recur.

SALIVARY DUCT CYST

(Mucous retention cyst)
These

are epithelium lined cysts arising

from Salivary Gland tissue.
These are true cysts.
Etiology is not clear.

 Ductal

obstruction may lead to ductal

dilatation
resulting
in
increased
intraluminal pressure & thus in the
formation of an epithelium lined cavity,
otherwise most cases represent true
developmental cysts that are separate
from the adjacent normal salivary ducts.

CLINICAL FEATURES
Affects

adults more commonly.

Can arise within both major & minor
Salivary Glands but the Parotid gland is
most commonly involved.
Cystic lesions presents as slow-growing
asymptomatic swellings.
Intraoral cysts seen involving minor
Salivary Glands of the floor of the mouth,
buccal mucosa & lips.

 Multiple

mucous retention cysts that

involve the excretory ducts of many of
the minor Salivary Glands throughout
the mouth have also been seen.
These lesions may be 100 in no.
Individual lesions present as painful
nodules with dilated ductal orifices
expressing mucus or pus.

specific histologic subtype is oncocystic cyst,

seen in buccal mucosa and lips of older
patients.
Identified as painless, sessile, dome shaped
masses of normal coloration located just below
mucosal surface.

HISTOLOGIC FEATURES
True

cyst with a variable epithelial lining

of cuboidal, columnar, or atrophic
squamous cells surrounding the thin or
mucoid secretions in the lumen.
Some cysts show oncocytic metaplasia of
the epithelium, with papillary folds of the
epithelium into the lumen, which
resembles Warthins tumour but with
lack of lymphoid stroma.

 Oncocytic

cysts show epithelium lining

of columnar cells often pseudostratified,
with strikingly eosinophilic cytoplasm
which is typical of oncocytes.
Lumen
is filled with eosinophilic,
proteinaceous material which is thought
to be inspissated mucin.

TREATMENT & PROGNOSIS

Conservative surgical excision for isolated
cysts.
Partial or complete removal of the gland in
major Salivary Gland cysts.
Recurrences do not occur.
Surgical management not possible for multiple
ones, so local excision is preferred for more
problematic swellings.

SIALOLITHIASIS
(Salivary stones, Salivary calculi)

Occurrence

of calcareous concretions in the

salivary ducts or glands.
They form by deposition of calcium salts
around a central nidus, which may consist of
desquamated epithelial cells, bacteria,
foreign bodies, or products of bacterial
decomposition,
Cause unclear, but their formation may be
promoted by chronic sialadenitis & partial
obstruction.

CLINICAL FEATURES
Moderate

to severe pain particularly

before, during & after meals.
It is associated with salivary swelling.
The occlusion of the duct prevents free
flow of saliva.
Stagnation or accumulation of saliva
under pressure, produces pain &
swelling.

 Sometimes,

the swelling is diffuse.

Occasionally symptomless & presents as
firm, palpable mass in the duct or gland.
Can be located by sialography on
Radiographic examination.
Sialography is the retrograde injection of
a radiopaque material into the duct
system of a SG & study of its
distribution by a R/F.

 Occurs

at any age, but more common in

middle-age.
Most
commonly
associated
with
submandibular gland & duct, followed by
parotid & then sublingual gland & duct.
Reasons for more common occurrence in
submandibular gland is:
>Due to tenacity of submandibular saliva,
>High mineral content of saliva,
>Long, tortuous & upward course of
duct.

 Sialoliths

are also seen in minor Salivary

Glands, in the upper lip & buccal
mucosa mainly & less commonly in
lower lip, palate & tongue.
They usually present as solitary, firm,
freely movable, small masses of nodules
& may or may not be symptomatic.

CHEMICAL & PHYSICAL FEATURES

They

may be round, ovoid or elongated.

May measure from few mms to 2cms or
larger.
May be single or many in number.
Usually yellow in color.
The structure is similar to apatite and
mainly contains Calcium Phosphate &
Calcium Carbonate.

HISTOLOGIC FEATURES
Concentric laminations around a central
nidus of amorphous debris.
The associated duct exhibits squamous,
oncocytic, or mucous cell metaplasia.
Periductal inflammation may also be
seen.
The feeding gland usually shows features
of acute or chronic sialadenitis.

TREATMENT & PROGNOSIS

Small

calculi by manual manipulation.

Surgical exposure for larger ones.
Surgical extirpation of gland if many & present
inside the gland substance.

EFFECT OF RADIATION
ON THE TISSUES

 The

general term radiation is applied

for 2 different forms of energy:
- Derived
from
Electromagnetic
radiation.
- Derived from Particle radiation.

 Electromagnetic

radiation consists of a
spectrum
of
varying

continuous
wavelengths.
It
includes long Electrical waves,
Radiowaves to Infrared, UV light, Visible
light, X-rays & Gamma Rays.
Particle radiation is generated through
decay of natural & artificial radioactive
materials which mainly consists of alpha
& beta particles.

General Effects of Radiation

The

cellular injury could be due to the

following factors:
Toxic effects of protein breakdown products
Inactivation of enzyme systems
Coagulation or flocculation of protoplasmic
colloids, or
Denaturation of nucleoproteins.

 Although

very large doses of radiation

has fatal effects on cells, each cell
responds differently to radiation in low
or therapeutic doses.
In
general, some cells are more
radiosensitive than others.
Based on cell response, the cells have
been classified as:
- Radiosensitive
- Radioresponsive
- Radioresistant

Radiosensitive cells
(2500 rads or less Seriously injures or
kills cells)
Lymphocytes

& Lymphoblasts
Bone Marrow - (Myeloblastic & erythroblastic cells)
Intestinal & Stomach Epithelium
Germ cells (Ovary & Testis)

Radioresponsive cells
(2500 5000 r Seriously injures or
kills many cells)
Epithelium

of skin & appendages

Endothelium of blood vessels.
Salivary glands
Bone & Cartilage
Conjunctiva, Cornea & Lens of the Eye
Collagen & elastic tissue (excluding
fibroblasts)

Radioresistant
(Over 5000 rads necessary to cause
serious injury or death of the cell)
Kidney, Liver, Pancreas
Pituitary,

Adrenal,
Thyroid
Parathyroid Glands
Mature bone & Cartilage
Muscle
Brain & other nerve tissue

&

 In

general, embryonic, immature cells are

more susceptible to injury than mature or
differentiated cells.
Most of these cells are injured during
mitosis. If irradiated during resting phase,
mitosis may be delayed or inhibited.
Latent tissue injury is retained for years in
the cells & are susceptible to injury if
radiated again.
The biological effects of radiation are
cumulative in case of repeated exposure to
small doses.

Effect of X-rays on
Oral & ParaOral Structures
X-rays

are generally used for treatment

of neoplasms, especially head & neck.
It is also used in whole body radiation of
leukemia patients with relapse.
The adjacent structures too are radiated
inadvertantly at times.

 Radiation

effects depends on many

factors such as:
- Source of Radiation,
- Total
amount
of
Radiation
administered
- Period of time over which radiation
was
administered.
- Type of filtration used.
- Total area of tissue irradiated.

EFFECTS ON SKIN
The

earliest reaction is erythema which

begins within few days after radiation.
This fades away and reappears after 2-4
wks.
The secondary erythema fades slowly and
leaves a permanent pigmented light tan
shade.
After heavy radiation, the erythema may
be accompanied by edema with
desquamation of epithelial cells resulting
in denudation of the surface.

 Re-epithelization

occurs in 10-14 days.

Early effects are caused by direct injury of
the radiated cells & tissues.
The later effects occur due to the changes
in the vascular bed & intercellular
material.
Dryness of the skin with formation of
scales
may occur within a week of
radiation due to alterations in the
sebaceous & sweat glands.
There may be temporary or permanent
loss of hair follicles.

In the later stages, the skin becomes atrophic

with telangiectatic superficial blood vessels,
which remains for months/years.
The vascular damage may include thickening of
the intima which leads to thrombosis.
Sunintimal
fibrosis,
endophlebitis
&
phlebosclerosis is also observed.

EFFECTS ON ORAL MUCOSA

The

effects are similar to that of skin, but

develops at a lower dose of X-ray & the
Radiation Induced Mucositis appears
earlier than the dermatitis.
This is seen as a whitish discolouration
due to defective desquamation of keratin.
This is replaced by atrophic mucosa which
is erythematous, edematous & friable.

 This

is followed by denudation, ulceration

& covered with a removable, yellowish,
fibropurulent surface membrane.
Patient feels discomfort with spicy or
coarse foodstuff. Usually a lidocaine
mouthwash is used before mealtimes to
produce topical anasthesia.
These
lesions undergo spontaneous
remission with the termination of the
radiation therapy. It may persist for
several weeks after treatment stops if
secondarily infected.

EFFECTS ON SALIVARY GLANDS

The

earliest complaint is Xerostomia (dry

mouth).
Secretion may be diminished or may be
completely lost in the early stages.
The acinar cells are damaged, organelles
are reduced, interstitial C.T. is inflamed.
Serous glands are affected severely as
they are more radiosensitive than
mucous glands, thus, Parotid gland is the
worst affected.

 This

decreased flow leads to loss of

bactericidal action & self cleansing
properties of the saliva.
Another feature that is associated with
post irradiation sialadenitis is the
elevation of serum & urinary amylase
and is seen when the salivary gland is
directly exposed to radiation.

EFFECTS ON TEETH
The

effect of radiation on teeth develops

after few years after radiation therapy.
A peculiar destruction of tooth in the
cervical area develops, resembling dental
caries & is termed as Radiation Caries.
Teeth become brittle & may fracture,
due to lack or thickening of saliva,
increased debris collection & increased
cariogenic microbial flora.

The developing teeth are also radiosensitive.

There is disorganization of the odontoblasts &
formation of atypical dentin.
The ameloblasts are less radiosensitive in
comparison. Enamel formation may be
affected, if there any metaplasia.
Tooth eruption may be affected if radiation is
given in high doses and depending on the age,
there may be total cessation of odontogensis
resulting in anodontia.

EFFECTS ON BONE
Bone

in general is quite radio-resistant,

yet the osteoblasts are radiosensitive.
High doses of radiation can lead to
disturbance in the balance of between
bone
formation
and
resorption;
decreased vitality of bone & localized
osteoporosis.
Due to change in vascularity, the bone
loses its normal ability to react to
infection & inflammation.

 The

healing response is slow & poor & is

of concern after extraction of tooth due
to retardation of surface closure of
wound & an open pathway for infection.
Other infections too flare up & lead to
destruction of bone which leads to a
condition
termed
as
OSTEORADIONECROSIS.

OSTEORADIONECROSIS
It

is a radiation-induced pathologic
process characterised by a chronic &
painful
infection
&
necrosis
accompanied by late sequestration &
sometimes, permanent deformity.
It
is one of the most serious
complications of radiation to the head &
neck.

 Radiation

causes a proliferation of the

intima of the blood vessels (endarteritis
obliterans) leading to thrombosis of the
end arteries. This results in a nonvital
bone.
The altered bone becomes hypoxic,
hypovascular & hypocellular.
Histologically, there is destruction of
osteocytes, absence of osteoblasts & lack
of new bone or osteoid formation.

 The

walls of the regional blood vessels

are thickened by fibrous CT.
The loose CT, which usually replaces the
bone
marrow
is
infiltrated
by
lymphocytes,
plasma
cells,&
macrophages
OSTEORADIONECROSIS IS THE RESULT
OF NON HEALING, DEAD BONE.

 This

devitalized bone may undergo

sequestration, although there is no clear
line of demarcation between vital &
nonvital bone.
The
necrotic process may extend
throughout the radiated bone.
Pathogenesis suggest involvement of 3
factors,
- Radiation, Trauma and Infection

 Mandible

is affected more than Maxilla.

This may be due to the difference in
blood supply to the 2 bones.
After infection has gained entry to the
bone, following traumatic injury,
extraction, pulp infection or even sever
periodontitis, there is relatively a diffuse
spread of the process.

 There

is minimal localization of the

infection & necrosis of a considerable
amount of bone, periosteum & overlying
mucosa.
Sequestration eventually occurs, but this
may be delayed for many months or
several years, during which time the
patient usually suffers intense pain.
Patients
are more vulnerable to
OsteoRadioNecrosis of the jaws in the 2
yrs following radiotherapy.

R/F :
Affected areas of bone reveal ill-defined
areas of radiolucency that may develop
areas of relative radio-opacity as the
dead bone separate from the residual
vital areas.
Intractable pain, cortical perforation,
fistula formation, surface ulceration &
pathologic fractures are common.

 The

occurrence is unpredictable & may arise

even without gross infection or trauma.
The most important risk factor for the
development of OsteoRadioNecrosis is the
radiation dose to bone.

 Following

are the factors that could lead to

osteoradionecrosis:
Irradiation of an area of previous surgery
before adequate healing.
Irradiation of lesions in close proximity of
bone.
Surgery in the irradiated area.
A high dose of radiation with/without
fractionation.
Use of a combination of external radiation
& intraoral implants.

 Poor

patient cooperation in managing

irradiated tissues or fulfilling home care
programs.
Poor oral hygiene & continued use of
irritants.
Indiscriminate
use
of
prosthetic
appliances following radiation therapy.
Failure to prevent trauma to irradiated
areas.
Poor nutritional status & other physical
problems prior to therapy.

BURNS
&
OTHER INJURIES
RELATED TO THE
ORAL MUCOSA

ELECTRICAL BURNS
These

can be of the contact or the arc

type.
In the contact type, electric current
passes through the body from the point of
contact to the ground site & can cause
death due to cardiopulmonary arrest.
The arc type is seen in oral cavity, saliva
acts as a conducting medium & an
electric arc flows between the electric
source & the mouth.

CLINICAL FEATURES
Lips,

gingiva, tongue are affected.

Painless, charred yellow area, with little or no
bleeding.
Edema develops.
Area feels cold compared to adjacent tissues
due to ischemia.

 Necrosis

& sloughing with loss of tissue

(around the 4th day).
Later bleeding due to exposure of
underlying vasculature.
Adjacent teeth may become nonvital,
with or without necrosis of surrounding
alveolar bone.

 Developing

tooth germs or buds are

destroyed leading to permanent cosmetic
disfigurement.
Such wounds heals relatively slowly.
Lips & angle of mouth if untreated lead
to
microstomia,
mucosal-alveolar
adhesions & morphologic alterations in
the shape of the lips.

TREATMENT & PROGNOSIS

Interdisciplinary

efforts
Comprehensive care
Tetanus immunization
Prophylactic antibiotic.

THERMAL BURNS
These

result from intake of hot foods or

fluids. (e.g. Hot tea/coffee, Hot Pizza,
Foods heated in the microwave oven)
Thermal burns tend to be more severe
during dental procedures like:
1) Hot instruments contacting oral
tissues
2) Overheated hydrocolloid impression
material.

CLINICAL FEATURES
Zones

of erythema & ulceration.

Remnants of necrotic epithelium at the
periphery.
Pain & Burning sensation.
Anterior tongue, palate & posterior buccal
mucosa are the common sites involved.

 Burns

from dental instruments are

mainly on lips & commissures of the
lips.
Overheated impression materials cause
burns on the gingiva & can be diffuse &
painful.
Treatment
Mostly these all burns resolve without
treatment.

CERVICOFACIAL EMPHYSEMA

Emphysema

is a swelling due to the

presence of gas or air in the interstices of
the CT.
Emphysema
in
cervicofacial
&
mediastinal areas occur following few
dental & oral procedures, like:

 Dental

extraction,
Blowing of compressed air into a root
canal during endodontic treatment or
into a periodontal pocket,
Blowing of air from a high speed air-rotor
machine, or
Following middle-face fractures.
Breathing of the patient following a
surgery, with a break in the tissue
permitting air to enter into the connective
tissue.

CLINICAL FEATURES
Develops

either during surgery or within 1 st

postop hour.
Manifests as a unilateral soft tissue enlargement
of the face and/or neck.
It occurs very rapidly.
Pain is minimal.
Crepitus detected on palpation.

 Enlargement

increases & spreads due to

secondary inflammation & edema.
Associated with pain, facial erythema &
mild fever.
Spread into the mediastinum results in
dysphonia, dysphagia or dyspnea.
Crepitus synchronous with the heartbeat
(hammans crunch) is heard on cardiac
auscultation in mediastinal involvement.

TREATMENT & PROGNOSIS

Complications

are:
> venous air embolism
> bacterial infection in emphysematous
CT
Resuscitation for venous embolism if
detected promptly, else fatal.
Antibiotics for infection.
Condition generally resolve within a week.

CHEMICAL INJURIES OF
THE ORAL CAVITY

 Allergic

phenomenon is the most common

reaction to the drugs or chemicals,
Two main types of dental interest are:
1) Drug allergy or Stomatitis
Medicamentosa
2) Contact Stomatitis or Stomatitis
Venenata

NON ALLERGIC
REACTIONS TO DRUGS
&
CHEMICALS USED
LOCALLY

 Aspirin
Sodium

perborate
Hydrogen peroxide
Phenol
Silver nitrate
Trichloroacetic acid
Volatile oils.

ASPIRIN
(ACETYLSALICYLIC ACID)
Aspirin

is mistakenly used for the relief of

toothache as a local obtundant by keeping
the tablet against the offending tooth,
allowing the cheek or lip to hold in position
& let it dissolve slowly.
Harmful, if applied locally, thus within few
minutes it starts as burning sensation of the
mucosa with blanching/whitening of the
surface

 The

caustic action of the drug causes

separation & sloughing of the epithelium
and frequent bleeding.
The healing of this ASPIRIN BURN
usually takes a week or two.

HistoPathology of Aspirin Burn

Endodontic Materials

Some of the endodontic materials commonly used

can be dangerous to the soft tissues.
They can cause damage, deep spread of
inflammation of the soft tissues & necrosis of the
adjacent hard tissues.
They either leak from the pulp chamber or may
extrude from the root canal filling material or
may be used in excess during irrigation.
The most common of the materials that have
been recorded to cause injury are sodium
hypochlorite, paraformaldehyde, Formocresol &
H2O2.

Sodium Perborate
Uses:

Mouthwash as well as in dentifrices

for the therapeutic effect on gingiva.
But, it is seen to produce erythema of the
oral mucosa & sometimes may progress to
sloughing of the oral tissues.
Gingivitis may be aggravated & may be
accompanied with ulceration & edema.
Thus the use of this material needs to be
discontinued.

Phenols
Uses:

Cavity sterilising agent

Cauterizing agent.
It is extremely caustic & may produce painful
burns of the oral mucosa if used carelessly.
These lesions heal slowly.

Silver Nitrate
Uses:

Cavity Sterilizing Agent

Caries Preventive Agent Topically
Chemical Cautery (Aphthous Ulcers)
It is known to cause painful burns of the oral
mucosa, thus its use should be restricted.

TriChloroAcetic Acid
Uses:

Cauterizing agent for gingival

tissue during the preparation of
gingival or proximal cavities,
placing bands or taking a detailed
impression of the cavity.
Its caustic nature leads to serious injuries of
the oral mucosa & should be used very
carefully.

Volatile Oils
Clove

Oil, Oil of Wintergreen & Eucalyptus Oil.

Used by patients at times to relieve toothache as
it gives a palliative effect.
It
may cause mild burns when used
continuously or in excess.

NON-ALLERGIC
REACTIONS TO DRUGS
& CHEMICALS USED
SYSTEMICALLY

Arsenic
Used

in both organic & inorganic forms.

Causes acute or chronic poisoning.
Occupational hazard in metal industry.
Causes diffuse macular pigmentation,
palmer & plantar hyperkeratosis.
Premalignant
lesions
(arsenical
keratoses), may transform into basal cell
carcinoma & cutaneous squamous cell
carcinoma.

Oral Manifestations
Oral

Mucous Membrane is intensely

inflammed.
Severe gingivitis.
Oral mucosal tissues become Painful.
Local use causes ulceration.
Systemic
poisoning
produces
excessive
salivation.

Bismuth
Formerly used for treatment of Syphilis.
Presently
used for treating dermatologic
disorders.

Oral Manifestations
Pigmentation of gingiva & buccal mucosa.
Bismuth line, a thin blue-black line in the
marginal gingiva.
Pigmentation may be seen on buccal mucosa, the
lips, ventral surface of the tongue.

 Precipitated

granules of BiS produced by

action of H2S on the Bi compound in the
tissues.
H2S
is formed through bacterial
degradation of organic material or food
debris.
Seen in patients receiving prolonged Bi
treatment.
High occurrence with poor oral hygiene.
Other complaints are : Burning sensation
of mucosa & Metallic taste.

HISTOLOGICAL FEATURES
Granules

of sulphide seen as small,

irregular black collections of pigment.
May be Perivascular in location or Diffuse
without apparent appearance.
Mainly present in intercellular tissues.
Also can be in endothelial cells or in
mononuclear phagocytes.
Provoke no foreign body response.
May be present even in absence of
inflammation.

Treatment & Prognosis

No

specific treatment.
Can be bleached by concentrated H 2O2.
Prevention

by scrupulous oral hygiene is

recommended.
Line gradually disappears over a longer period
of time, after discontinuation of bismuth, if
untreated.

GOLD

Used in the management of rheumatoid arthritis.

Long term used leads to Dermatitis, preceded by
pruritis.
Generalized exfoliative dermatitis leading to alopecia.
Loss of nails.
Chrysiasis i.e. slate-blue discoloration of sun exposed
skin.
Metallic taste followed by severe oral mucositis in
buccal mucosa, lateral border of tongue, palate &
pharynx.

DILANTIN SODIUM
Also

known as Phenytoin Sodium, or

Sodium Diphenylhydantionate.
Anticonvulsant in epileptic seizures.
Side effect: Overgrowth of the gingiva or
the misnomer Gingival Hyperplasia.
No hyperplasia or hypertrophy of the
epithelial or C.T. but increased
production of extracellular matrix,
mainly collagen.

More occurrence with poor oral hygiene or local

irritants like ortho bands & brackets.
Probable cause is stimulation of fibroblastic
proliferation & increased collagen synthesis.
Also decreases the degradation of collagen.
Dilantin destabilize the walls of the gingival
mast cells, including excessive degranulation &
release of histamine & heparin that stimulate
fibroblasts to produce collagen.
Other drugs that cause
this kind of
enlargements are nifedipine & cyclosporine.

Oral Manifestations
First change: Painless increase in the size of
the gingiva with enlargement of 1 or 2
interdental papillae.
Can begin within 2-3 weeks or 2-3 months.
Gradually seen as increased stippling with a
cauliflower, warty or pebbled surface.
Later it becomes lobulated & clefts remain
between each enlarged gingiva.

Tissue is dense, resilient & insensitive with little

tendency to bleed.
Gingiva covers a portion or whole of crown.
Lingual & occlusal extension of overgrowth
interfere with mastication & speech.
Edentulous areas are normal, if any.
Occasionally palate may also be involved in
denture wearers due to its local irritant factor.

Histological Features
Stratified

squamous epithelium thick

with thin keratinized layer.
Rete pegs long & thin (test-tube pegs).
Bulk of tissue is made up of large bundles
of collagen fibres interspersed with
fibroblasts & fibrocytes.
If its chronic inflammation, plasma cells
& leukocytes seen.
Vascularity is not seen prominently.

Treatment & Prognosis

Surgical

excision.
Discontinuation of drug.

LEAD (Plumbism)
Inhalation

of lead vapor or dust in adults.

In infants, chewing on wood painted with lead
containing paint.
Lead poisoning (plumbism) can be acute or
chronic.
Mainly an occupational hazard.

 Acute:
Serious

Clinical Features

GI disturbances like nausea,

vomiting, abdominal colic & constipation,
Anemia (hypochromic with basophilic
stippling of RBCs),
Fatigue, irritability & weakness.
Peripheral
neuritis
producing
characteristic wrist-drop or foot-drop.
Encephalopathy & renal dysfunction.

 Chronic:
Dysfunction

of nervous system,
Kidneys, bone & joints,
Fatigue, musculoskeletal pain,
Headache,
Skeletal changes due to deposition of
lead in growing bone in children,
demonstrable on roentgenogram.

Oral Manifestations
Lead

line (halo saturninus or Burtonians line),

Gray
or bluish black line of sulfide
pigmentation, on the gingiva.
More diffuse than bismuth line,
Ulcerative stomatitis.

 Excessive

salivation, metallic taste.

Swelling of salivary glands,
Advanced periodontal disease,
Tremor of the tongue on thrusting.
Lead gets deposited in deciduous teeth of
children suffering from lead poisoning and
these teeth may serve as an index of the
body burden of lead.

Treatment & Prognosis

Secondary

to systemic treatment.

Mercury
Acute

or chronic.
Prolonged contact with mercurial compounds
(therapeutic/occupational).
Elemental Mercury may be harmless, but
Mercury vapor is very harmful.
This is due to its high rate of absorption &
systemic retention.

 Uses:

Teething powders, Cathartic

agents, Antihelminthic drugs
containing mercury.
Ingestion of mercury salts also causes adverse
rections.
Acute
form is so severe that oral
manifestations are not significant in front of
systemic ones.

Clinical Features
ACUTE MERCURIALISM

Abdominal pain,
Vomiting, diarrhoea,
Thirst,
Pharyngitis
Nephritis

CHRONIC MERCURIALISM
Gastric disturbances like diarrhoea,
Excitability, insomnia, headache.
Mental depression.
Fine tremors of fingers & limbs, as well as lips
& tongue

Oral Manifestations
Increased

flow of saliva (ptyalism),

Metallic taste,
Salivary Gland may be swollen,
Tongue at times is enlarged & painful,
Occasional hyperemia & swelling of the
gingiva.

 Ulcerations

on gingiva, palate & tongue.

Liberation of mercuric sulfide due to
bacterial action on metal.
Pigmentation of gingiva ,
Destruction of alveolar bone, loosening &
exfoliation of the teeth.

Treatment & Prognosis

Supportive

Rx for oral lesions as it is secondary

to systemic poisoning.
Prognosis is usually good if attended to in time,
but there may be severe periodontal destruction
& loss of teeth.

ACRODYNIA
(Pink disease, Swifts disease)
Uncommon

disease with striking cutaneous

manifestations,
Cause: Mercurial toxicity reaction,
Actual Hg poisoning/idiosyncrasy to metal.

Source of Hg:
Teething powder,
Ammoniated mercury ointment,
Calomel lotion,
Bichloride of Hg disinfectant

Clinical Features
Mostly

in young infants before the age of 2

yrs & Occasionally upto age of 5 to 6 yrs,
Areas affected: Hands, feet, nose, ears &
cheek.
Skin: Red or pink, Cold & clammy feeling,
resembling raw meat.
Skin
over the affected area peels
frequently.

 Pruritic

maculopapular rash.
Severe sweating.
Extreme irritability, photophobia with
lacrimation,
muscular
weakness,
tachycardia, hypertension, insomnia, GI
upset, stomatitis.
Children can tear their hair out in
patches.

Oral Manifestations
Profuse

salivation, often with dribbling.

Gingiva is extremely sensitive, painful.
May even exhibit ulceration.
Bruxism may lead to Loosening & premature
shedding of teeth.
Difficulty in mastication due to pain.

Treatment & Prognosis

Discontinuation

of exposure to Hg,
Administration
of BAL (British
lewisite/dimercaprol).

anti-

SILVER
(Argyria, Argyrosis)
Is

seen due to chronic exposure.

Occupational or therapeutic use of silver
compounds, e.g Ag arsenaphine /Ag
nitrate,
Gets deposited subepithelially in the skin.
Results
in diffuse grayish black
pigmentation, mainly in sun exposed
areas.

 Sclerae

& nails also pigmented.

One of the earliest signs of argyria is the
appearance of Slate blue silver line along
the gingival margins due to deposition of
metallic silver & silver compounds.
No local or systemic signs & symptoms
associated.

AMALGAM TATTOO
Accidental

implantation
of
silver
containing compounds into oral mucosal
tissues.
Mainly because of amalgam which is
bound to silver bound to mercury.
Permanent grayish-black pigmentation is
seen, thus it is named as TATTOO.
It may enter the oral mucosa by the
following ways.

 From

condensation in the gingiva during

restorative work.
Lodgement of particles into the mucosa
after laceration while removing old
restorations with high speed instruments.
From broken pieces which enter the
socket or beneath the periosteum during
extraction.
From particles entering the surgical
wound during root canal treatment with a
retrograde amalgam filling.

CLINICAL FEATURES
Appear

as macules, rarely as raised lesion,

Borders are well defined, irregular or diffuse.
Seen commonly on gingiva, buccal mucosa &
alveolar mucosa.
If embedded in bone, it may be mistaken for
foreign bodies.

HISTOLOGIC FEATURES
Larger

particles evoke granuloma formation,

consisting of Multinucleated Giant cells,
lymphocytes & increased fibrosis surrounding
foreign material.
Fine particles may be engulfed by macrophages.
Or found within cytoplasm of many cells &
tissues like muscle, nerve, collagen etc.

 Amalgam

fragments appear as black or

olive-brown granules.
These granules are arranged in a linear
fashion along collagen & around blood
vessels.
In paraffin embedded specimens, they
appear as silver-gray flecks in the tissue.
Electron microscopy has found that only
silver remains in extracellular sites, while
other components of amalgam corrode
after sometime.

TETRACYCLINE
It

is Broad spectrum antibiotic.

May be used as prophylactic & therapeutic
regimens
Discoloration of either deciduous & permanent
teeth, due to deposition of Tetracycline in
pregnant female or postpartum in infant.

 Selective

affinity for deposition in bone &

tooth substance.
Formation of a complex with calcium ions
in the surface of hydroxyapatite crystals.
It crosses placental barrier so it may
involve teeth developing ante partum.
Tooth portion discolored determines the
stage of tooth development during drug
administration.

 Discoloration

depends upon:

Dosage
Duration of drug administration
Type of Tetracycline

Critical period is:

For deciduous maxillary & mandibular
incisors - 4 months in utero to 3 months
postpartum,
For deciduous maxillary & mandibular
canines - 5 months in utero to 9 months
postpartum,
For permanent maxillary & mandibular
incisors & canines 3-5 months
postpartum to about 7 yrs of age.

 Doxycycline

or oxytetracycline in
pregnant females or first 6 to 7 yrs of age
in children should be preferred, if
Tetracycline is indicated.
These diminish discoloration of tooth.
Semisynthetic
derivative
of
Tc:
Minocycline Hydrochloride affects fully
developed teeth too & has an affinity for
the collagenous tissues of the teeth.
Ascorbic acid can block the formation of
this discolouration.

Clinical Features
Yellowish

or brownish gray diffuse bands of

discoloration that are located within tooth
structure & not on the surface.
Discoloration most pronounced at time of
eruption,
Turns more brownish after exposure to light,

 ChlorTetracycline OxyTetracycline

Brownish-gray color,
& Tetracycline

Yellowish color,
Tetracycline fluoresces under UV light so
teeth discolored by Tc also fluoresces.
Minocycline HCl staining is seen in skin,
nails, sclera, conjunctiva, thyroid, bone
& teeth.

Dark color of underlying bone show through the

thin, translucent oral mucosa, imparting a bluegray appearance to the palate or anterior
alveolar mucosa,
Teeth show varying patterns of discoloration,
Discoloration remains after discontinuance of
the drug, though cutaneous staining fades away.

Cancer chemotherapeutic agents

These

agents are a diverse group of drugs

used for the treatment of certain
neoplastic diseases.
Their main function is to destroy
malignant cells.
They attck the cells mainly during
mitosis.
Thus other than neoplastic cells, normal
cells, of the GIT, skin, bone marrow also
are targeted due to high mitotic activity.

Clinical
Features agents are
the
chemotherapeutic
categorised
into
different
groups
depending on their chemical composition
& mode of action, there are a few general
manifestations.
These are:
Alopecia, due to arrest of mitosis.
Stomatitis, which can be varied.
Radiation recall or sensitization.
Although

Oral Manifestations
erosion
& ulceration, which may
diffuse & multiple.
Lips, tongue & Buccal mucosa are affected
more commonly.
Thrombocytopenia secondary to drug
therapy leads to hemorrhage.
Due to immunosuppression, patient may
develop other infections e.g HSV, Thrush
Hyperpigmentation of the oral mucosa
seen occasionally.
Mucosal