Oral

Pathology

Dr. Tasnim Hamdan

graduated from
University of Valencia
Unit 3.Periapical
lesions
 PERIAPICAL
LESIONS

Acute apical Acute alveolar Phoenix Chronic apical

periodontitis abscess abscess periodontitis
Chr. suppurative Cellulitis Persistent Periapical
apical periodontitis Lesion Apical Periodontitis Scars
Condensing Hypercementosis External Osteomyelitis
osteitis Root Resorption
Alveolar osteitis
Periapical Periapical
Granuloma Cyst

Periapical Periapical true

pocket cyst cyst
 PERIAPICAL LESIONS
Periapical tissue consists of cementum, PDL and alveolar process
Radiographically, these lesions appear as radiolucent areas around of
exit of the main canal or lateral and/or accessory canals.
 Histologic Features
Depending on their stage of development the lesions contain numerous
inflammatory cells:

1. PMNs
2. Macrophages
3. Lymphocytes
4. Plasma cells
5. Mast cells
6. Basophils
7. Eosinophils
The reaction of the periradicular
tissues to noxious products of
tissue necrosis, bacterial products,
and antigenic agents from the root
canal has been described by FISH.
4 well-defined zones of reaction

Zone of stimulation
Zone of irritation
Zone of contamination
Zone of infection
ZONE OF NECROSIS/ INFECTION
 Infection Is Present in the centre of the lesion
 Micro-organisms are found in this zone
 Characterised by polymorphonuclear leukocytes.

ZONE OF CONTAMINATION
 Characterized by round cell infiltration.
 Cellular destruction from the toxins discharged from central
zone is observed.
 Bone cells are dead & might go under autolysis which results
in empty appearance of lacunae.
ZONE OF IRRITATION:
 It is characterized by macrophages and osteoclasts.
 Small round cells, normal bone cells can be seen.
 Collagen framework is digested by phagocytic cells, i,e the
macrophages, while osteoclasts attack the bone tissue

ZONE OF STIMULATION:
 Characterized by fibroblasts and osteoblasts.
 At the periphery , toxin is mild enough to be a stimulant
 Response to this stimulation, collagen fibres get laid down by
fibroblasts, which acts both as a wall of defence around the
zone of irritation and as a scaffolding on which the osteoblasts
built new bone.
According to his concept, periapical lesion is not an infection
by itself but the reaction of body to infection in the canal.
 Clinical periapical tests

1.Percussion: indicates
inflammation of the
peridontium.

2.Palpation: determines how far

the inflammatory process has
extended periapically.
 3.Pulp Vitality
 Thermal tests
 Anesthetic testing
 Test Cavity
 Electrical pulp testing

4.Periodontal Examination
 Probing- determines the
level of connective tissue
attachment.
 Mobility- determines the
status of PDL.
5. Radiographic Examination
 Loss of lamina dura apically
 Radiolucency at apex regardless of cone angle and usually
resembles a hanging drop.
 Cause of pulp necrosis is usually evident.
CLASSIFICATION OF
PERIRADICULAR
TISSUES
 WHO classification of periradicular tissues
CODE NUMBER CATEGORY
K04.4 Acute apical periodontitis
K04.5 Chronic apical periodontitis (apical granuloma)
K04.6 Periapical abscess with sinus (dentoalveolar abscess with
sinus, periodontal abscess of pulpal origin)
K04.60 Periapical abscess with sinus to maxillary antrum
K04.61 Periapical abscess with sinus to nasal cavity
K04.62 Periapical abscess with sinus to oral cavity
K04.63 Periapical abscess with sinus to skin
K04.7 Periapical abscess with out sinus
K04.8 Radicular cyst(apical periodontal cyst, periapical cyst)
K04.80 Apical & Lateral cyst
K04.81 Residual cyst
K04.82 Inflammatory Paradental cyst
 GROSSMAN’S CLASSIFICATION

1.Acute Periradicular disease

1.1 Acute alveolar abscess
1.2 Acute apical periodontitis(symptomatic periodontitis)
1.2.1 Vital
1.2.2 Non Vital
1.3 Acute exacerbation of chronic apical periodontitis (phoenix
abscess)
2.Chronic periradicular diseases
2.1 Chronic apical periodontitis - chronic alveolar abscess - cystic
apical periodontitis
2.2 Persistent apical periodontitis
3.Condensing osteitis
4.External root resorption
5. Diseases of the periradicular tissues of non-endodontic origin
 WEINE’S CLASSIFICATION

1.Painful pulpoperiapical pathosis

1.1 Incipient acute apical periodontitis
1.2 Advanced acute apical periodontitis
1.2.1 Acute Periapical abscess
1.2.2 Phoenix abscess
1.2.3 Subacute Periapical abscess
2.Non painful Periapical pathosis
2.1 Condensing ostestis
2.2 Incipient chronic apical periodontitis
2.3 Advanced chronic apical periodontitis
2.3.1 Periapical granuloma
2.3.2 Chronic Periapical abscess
2.3.3 Periapical cyst
 INGLE’S CLASSIFICATION

1.Painful pulpoperiapical pathosis

1.1 Acute apical periodontitis
1.2 Advanced acute apical periodontitis
1.2.1 Acute apical abscess
1.2.2 Phoenix abscess
1.2.3 Suppurative apical periodontitis
2.Non painful pulpoperiapical pathosis
2.1 Condensing osteitis
2.2 Chronic apical periodontitis
2.2.1 Incipient
2.2.2 Advanced
2.3 Chronic apical periodontitis
2.3.1 Periapical granuloma
2.3.2 Apical cyst
2.3.3 Suppurative apical periodontitis
1.Acute apical periodontitis

Painful inflammation of the peridontium

as a result of trauma, irritation, or
infection through the root canal,
regardless of whether the pulp is vital or
nonvital.

Also referred to as symptomatic apical

periodontitis.
 1.1 Etiology

VITAL TEETH NONVITAL TEETH

Abnormal occlusal Diffusion of bacteria and

contacts necrotic pulp products
Recently inserted Iatrogenic
restoration extending  Forcing bacteria or debris
beyond the occlusal plane inadvertently through the AF
Wedging of a foreign  Forcing of irrigants or
object between the teeth medicaments through the AF
such as a toothpick or  Extension of obturating
food material through the AF
Traumatic blow to the  Perforation of the root
teeth  Overinstrumentation
 1.2 Signs & Symptoms
Tooth is tender on percussion
Dull, throbbing and constant pain
Tooth may feel extruded and patient
would have pain on closure and
mastication.

Negative or delayed vitality

test.
Radiographically, widening of
the PDL space.
 1.3 Histologic Features

PDL shows signs of inflammation

 Vascular dilation
 Infiltration of PMNs
Dilation of blood vessels .
Initiation of inflammatory
response due to presence of PMN ,
leukocytes and round cells.
Accumulation of serous exudate.
Distension of PDL and extrusion of
tooth, slight tenderness .
If continuous irritation occurs, loss
of alveolar bone.
 1.4 Treatment

Determining the cause and

relieving the symptoms.
Adjustment of high points
(in hyperocclusion cases).
Removal of irritatants (in
case of non vital infected
pulp)
When the acute phase has
subsided, the tooth is treated
by conservative means.
 1.5 Outcome of symptomatic
apical periodontitis
Spontaneous healing
Acute alveolar abscess
“Point” and open to
the exterior
(fistulation and sinus
tract formation)
Lesion becomes
asymptomatic and
enters chronic phase
 2. Acute alveolar abscess

Localized collection of
pus in the alveolar bone
at the root apex of a
tooth following death of
pulp with extension of
infection through apical
foramen into
periradicular tissue.
From its origin in the pulp, the inflammatory process extends into
the periapical tissues, where it may present as a granuloma or cyst
(if chronic) or an abscess (if acute). Acute exacerbation of a chronic
lesion may also be seen.
 2.1 Etiology

Trauma
Chemical & mechanical irritation
Bacterial invasion of dead pulp
tissue
Necrotic pulpal tissue debris, inflammatory cells, and bacteria,
particularly anaerobes and facultative anaerobes, all serve to
stimulate and sustain the periapical inflammatory process.
 2.1 Clinical Features

Common findings of inflammation- heat, redness, swelling and

pain.
Tenderness of the tooth relieved by continued slight pressure on the
extruded tooth.
Severe, throbbing pain, with swelling of the overlying soft tissue.
No reaction to cold, heat or EPT.
Percussion may produce dull sound instead metallic due to
granulation tissue at apex.
Swelling can extends and tooth becomes more painful, elongated
and mobile.
Systemic manifestations like lymphadenitis & fever may present
when confined to periapical region.
Rapid extension to adjacent bone marrow spaces produces acute
osteomyelitis or dentoalveolar abscess.
Max ant: swelling may extend to 1 or both the eyelids

Mand ant: swelling may involve the lower lip and chin

Max post: cheek may swell 2 an immense size, distorting the

facial structures

Mand post: swelling may extend 2 ear or round the border of

the jaw into the submaxillary region.
 2.2 Radiographic features

Thickening of PDL at root

apex.
As concomitent bone
resorption & proliferation
of granulation tissue
appears to be radiolucent
area.
Thin radiopaque line or
zone of sclerotic bone
sometimes seen outlining
lesion.
Long standing lesion may
show varying degrees of
root resorption.
 2.3 Systemic reactions

Pt may appear pale, irritable

and weakened due to pain and
loss of sleep.
Mild cases- slight rise in temp
Severe cases- temp above
normal
Fever often preceded or
accompanies by chills.
Intestinal stasis, manifesting
orally by a coated tongue &
foul breath.
Headache and malaise
 2.4 Histologic Features

PMN leukocytes infiltrate and initiate

inflammatory response and
inflammatory exudates
Distention of PDL and elongation of
tooth
If the process continues, separation of
PDL
Tooth becomes mobile
Bone resorption at apex
Localized lesion of liquefaction
necrosis containing PMN leukocytes,
debris, cell remanents, purulent
exudates (neutrophils)
 2.5 Treatment

Drainage and controlling the

systemic reaction.
LA is ineffective when injected
into acutely inflamed tissue
(conduction anesthesia)
If the swelling is extensive, soft
and fluctuant, an incision through
the soft tissue to the bone may be
necessary.
Antibiotics and analgesics can be
prescribed as needed.
 3.PHOENIX ABSCESS/ACUTE
EXACERBATION OF A CHRONIC LESION
An acute inflammatory reaction(exacerbation)
superimposed on an existing chronic lesion,
such as cyst or granuloma.
 3.1 Etiology

When state of equilibrium in

granuloma /cyst is upset by:

 Influx of bacteria/necrotic
products of high virulence
and antigenicity
 Lowering of host
defenses

Mechanical irritation during

RCT.
 3.2 Clinical Features

Often indistinguishable from periapical abscess.

Tooth may be tender on palpation, as inflammation
progresses, becomes sensitive.
Mucosa over the radicular area may appear red,
swollen and sensitive to palpation.
Most commonly associated with initiation of RCT.
Do not respond to vitality testing.
Radiographically, well defined periradicular lesion
may be present.
 3.3 Histologic Features
Shows areas of liquefaction necrosis with disintegrated
polymorphonuclear leukocytes and cellular debris surrounded by
macrophages, lymphocytes, plasma cells in periradicular tissues.
Should be differentiated from acute alveolar abscess through pt’s
history, symptoms and clinical tests results.
 3.4 Treatment

Establishment of drainage.
Once symptoms subside, complete root
canal treatment.
4.Chronic apical periodontitis / asymptomatic
apical periodontitis / periapical granuloma
Symptomless sequelae of acute
apical periodontitis.
May develop and enlarge
insidiously without any subjective
signs or symptoms.
Necrotic pulp gradually releases
noxious agents with low grade
pathogenecity or in low
concentration.
Develops after inadequate root
canal treatment.
 4.1 Etiology
Death of the pulp followed by mild irritation of periapical
tissue that stimulates a productive cellular reaction.
Some cases preceded by chronic alveolar abscess.
 4.2 Clinical Features
Asymptomatic, discovered on routine radiographic examination.
No pain on percussion.
Associated tooth has a necrotic pulp therefore should not respond
to the electrical or thermal stimuli.
 4.3 Histologic Features
Periradicular granuloma or cyst. The only accurate way to
distinguish these two entities is by histologic examination.
 4.4 PERIAPICAL GRANULOMA

A growth of granulomatous
tissue continuous with the
periodontal ligament
resulting from death of the
pulp and the diffusion of
bacteria and bacterial toxins
from the root canal into the
surrounding periradicular
tissues through the apical
and lateral foramina.
 4.4.1 Histologic Features
The periradicular granuloma consists predominantly of
granulation inflammatory tissue with many small capillaries,
fibroblasts, numerous connective tissue fibers, inflammatory
infiltrate, and usually a connective tissue capsule
Occasionally, needle-like spaces (the remnants of cholesterol crystals),
foam cells, and multinucleated foreign body giant cells are seen in these
lesions
4.4.2 Zones of well established granuloma
 4.4.3 Treatment
Root canal treatment is recommended.
Removal of cause of inflammation is usually followed by
resorption of Granulomatous tissue and repair with
trabeculated bone.
 4.5 Periapical Cyst / Radicular cyst
Pathological cavity containing fluid, semi fluid or gaseous material,
frequently but not always lined by epithelium
Direct sequelae of chronic apical periodontitis, not every lesion
develops into cyst
According to the studies 6-55% lesions are cyst.
 Hypothesis related wid this growth

Nutritional Deficient Theory

 Periradicular inflammatory changes cause the
epithelium 2 proliferate.
 As the epithelium grows into a mass of cells, the
center loses the source of nutrition from the peripheral
tissues.
 This leads to necrosis in the center and a cavity is
formed which is lined by stratified squamous
epithelium.

Abscess Theory
 An abscess cavity is formed within the connective
tissue and is then surrounded with proliferating
epithelial tissue, thereby producing a cyst.
 4.5.1 Etiology
Cyst develops from dormant epithelial cell rests that proliferate
probably under the influence of inflammatory cytokines & growth
factors released by various cells residing in the lesion.
When proliferation occurs within the body of the granuloma, it
plugs the body of the AF which limits the egress of the bacteria.
Sometimes, epithelial plugs protrude out of the apical foramen
resulting in a pouch connected to the root & continuous with the
root canal.
 There are 2 distinct
categories of radicular cyst
 4.5.2 Periapical pocket cyst

Originally designated as bay cyst.

Cyst contains an epithelial lined
cavity that is open towards the root
canal of the affected tooth.
Initiated by the accumulation of
neutrophils around the apical
foramen in response to the
bacterial presence in the apical root
canal.
This forms a microabscess, that
gets enclosed by the proliferating
epithelium, forming a collar with
epithelial attachment on contacting
the root tip.
4.5.3 Periapical true cyst

Characterized by
cavities that are
completely enclosed
in epithelial lining
and are totally
independent of the
root canal of the
affected tooth.
 4.5.4 Clinical features
No symptoms associated with
development of a cyst except
incidental to necrosis of the
pulp.
May become large enough,
however, to become obvious
as a swelling.
Pressure of the cyst may be
sufficient to cause movement
of the teeth, owing to
accumulation of cystic fluid.
If left untreated, may
continue to grow at the
expense of the max or mand.
Age incidence: peak in 3 rd , 4 th and 5 th decade
Sex incidence: Slightly more males.
Frequency: Commonest cystic lesion of jaws.
Primarily symptom less.
 Discovered accidentally during routine dental X ray exam.
 Diagnostic criteria – associated teeth are non vital
Rare in deciduous teeth.
 4.5.5 Histologic Features
Cavity is lined by
stratified squamous
epithelium.
Surrounded by connective
tissue that is infiltrated by
lymphocytes, plasma cells,
and polymorphonuclear
neutrophils.
Contains debris and
eosinophilic material.
Cholestrol clefts,
macrophages, giant cells .
 4.5.6 Radiological features

Classically presents as round

/ ovoid radiolucency with
sclerotic borders and
associated with pulpally
affected tooth / teeth.
If infection supervenes, the
margins become indistinct,
making it impossible to
distinguish it from a
periapical granuloma.
 4.5.7 Treatment

The treatment of choice is root canal therapy, followed by periodic

observation.
Surgery required when lesion fails to resolve or symptoms develop.
Extraction in case of severe bone loss.
 GRANULOMA
PERIAPICAL CYST
Radiographically, shows a well
Radiographically, shows a
circumscribed radiolucent
well-circumscribed
periapical lesion without a
radiolucent periapical lesion
sclerotic border, measuring less
with a partial sclerotic
than 1 cm in size.
border, measuring more than
Histologically, shows
1 cm in diameter.
fibrocellular connective tissue
Histologically, shows the
stroma consisting of chronic
presence of an epithelial
inflammatory cell infiltrate
lining with underlying dense
(mainly lymphocytes and plasma
fibrocellular connective
cells) and endothelium-lined
tissue stroma
blood capillaries with red blood
cells, fibroblasts, and collagen
fibers.
Granuloma

Cyst
5.Chronic alveolar abscess/ chronic suppurative
apical periodontitis/ asyptomatic apical abscess

Long standing, low

grade infection of the
periradicular alveolar
bone.

Characterized by
presence of an abscess
draining through a sinus
tract.
 5.1 Etiology

Source of infection is in
the root canal.
It is a natural sequelae of
death of the pulp with
extension of the infective
process periapically, or
may result from a
preexisting acute abscess.
 5.2 Clinical Features
Tooth is asymptomatic or mildly painful.
Detected only during radiographic examination or because of the
presence of a fistulous tract, which can be either intraoral or
extraoral.
Exudate can also drain through the gingival sulcus of the
involved tooth mimicking a periodontal lesion with a pocket.
Vitality test is negative.
 5.3 Radiographical Examination

A radiograph is taken after the insertion of GP cone into the

sinus tract which often shows the involved tooth by tracing
the sinus tract to its origin.
At times, the sinus tract is several teeth away from the cause.
Radiograph shows diffuse area of rarefaction which fade
indistinctly into normal bone.
The PDL is thickened.
 5.4 Histologic Features

Some of the periodontal

fibers at the root apex are
detached or lost followed
by destruction of apical
periodontal ligament.
Lymphocytes & plasma
cells are generally found
toward the periphery of
abscessed area, with
variable numbers of PMN
leukocytes at the center.
Fibroblast may start to
form a capsule at the
periphery.
 5.5 Treatment

Elimination of infection in root canal.

Once this is accomplished and root canal is filled, repair of
the periradicular tissues generally take place.
In case of smaller area of rarefaction, treatment is similar to
that of a tooth with a necrotic pulp.
 6.Cellulitis
It is a rapidly spreading inflammation of the soft tissues
characterized by diffuse pus formation.
This happens if an abscess is not able to establish
drainage through the skin surface or into oral cavity.
Infection spreads through canine space, infratemporal space,
pharyngeal space, buccal space, submental and submandibular
space etc.
Two dangerous forms of cellulitis are:
 Ludwig’s angina
 Cavernous sinus thrombosis
Cavernous sinus thrombosis
 6.1 Pathology

 Anaerobic bacteria are mainly

responsible and infection mainly
spreads from mandibular third molars
whose apices are closely related to
several fascial spaces.

 Fasciae covering muscles and other

structures are normally adherent but
can be spread apart by inflammatory
exudate.

 Spaces created in this way are almost

avascular and inflammatory exudate
carries bacteria widely through them.
 Involves the sublingual and submandibular spaces bilaterally, almost
simultaneously and readily spreads into the lateral pharyngeal and pterygoid
spaces and can extend into the mediastinum.

 The main features are rapidly spreading sublingual and submandibular

cellulitis with painful, brawny swelling of the upper part of the neck and the
floor of the mouth on both sides .

 With involvement of the parapharyngeal space, the swelling tracks down the
neck and oedema can quickly spread to the glottis.

 Swallowing and opening the mouth become difficult and the tongue may be
pushed up against the soft palate.

 The latter or oedema of the glottis causes worsening respiratory obstruction.

The patient soon becomes desperately ill, with fever, respiratory distress,
headache and malaise, and can dead for asfixia.
 6.2 Histological Features

Infection spreading through the tissues is accompanied by a

dense infiltrate of neutrophils, here separating muscle bundles in
a facial muscle.
 6.3 Treatment

Removal of the necrotic pulp.

Extraction of the infected tooth.
Incision and drainage of the swelling.
In severe cases hospitalization required.
Antibiotics and analgesics
 7.Persistent Apical Periodontitis

Post treatment apical periodontitis in

an endodontically treated tooth.

7.1 Etiology

Anatomical complexity
Apical biofilms
Cholestrol clefts
Foreign body reaction to
gp
Cellulose granuloma
Periapical scar tissue
 7.2 Bacteriology

E. Faecalis is the most

consistently reported organism
that can survive prolonged
starvation and can grow as a
monoinfection in
endodontically treated teeth.
Studies have shown presence
of yeast and candida albicans.
Gram+ cocci, rods, filaments,
Propioniobacterium have also
been implicated
 8.Periapical Scars

Apical scar is an area at the apex of a tooth that fails to fill in

with osseous tissue after endodontic treatment.
 8.1 Characteristic Features
Bone structures are recognized within the rarefaction.
The periphery of the rarefaction may be irregular and may be
demarcated by a compact bone border.
The rarefaction is often located asymmetrically around the apex.
The connection of the rarefaction with the periodontal space may
be angular.
 9.Condensing osteitis
Is a reaction of bone induced by inflammation.
It occurs mainly at the apex of a tooth from an infected pulp.
The infection from tooth caries reaches the pulp and progresses to
the apical tissues to produce a small periapical radiolucency called
RAREFYING OSTEITIS.
The small rarefying osteitis may be either a periapical granuloma, a
radicular cyst or an abscess.
 The bone surrounding this rarefying osteitis becomes dense in
order to prevent further spread of the lesion. This dense
radiopacity surrounding the rarefying osteitis is called
CONDENSING OSTEITIS.

A unusual reaction to mild bacterial infection entering the bone

through a carious tooth in persons who has high degree of tissue
reaction and tissue reactivity.
 9.1 Etiology

Infection of periapical tissues of a high immunity host by

organisms of low virulence which leads to a localized
bony reaction to a low grade inflammatory stimulus
Non- vital tooth
 9.2 Clinical Features

Usually asymptomatic but sometimes mild pain due to infected pulp

Discovered during routine radiographic examination.
Pulp of the involved tooth is non vital.
Commonly affects young adults and children
Mandibular molar is affected commonly
Large carious lesions
 9.3 Radiographic Examination
The tooth involved may exhibit a large carious lesion or a large
restoration close to the dental pulp.
Pathognomic ,well circumscribed radiopaque mass of sclerotic bone
surrounding and extending below the apex of one or both roots
It is the area of dense bone with reduced trabecular pattern.
PDL space widening
 9.4 Histologic Features

Appears as an area of dense

bone with reduced trabecular
pattern lined with osteoblasts.
If interstitial soft tissue is
present , it is generally fibrotic
and infiltrated with small
amount of lymphocytes,
plasma cells, are seen in the
scant bone marrow.
Many reversal and resting
lines giving pagetoid
appearance
Lacunae appears empty
 9.5 Treatment

Treatment consists of removing the infection either

through tooth extraction or root canal therapy.
 10.External Root Resorption
Process that leads to irreversible loss of bone, dentine, enamel
and cementum
Asymptomatic
Tooth can be vital or nonvital
Cervical area most commonly involved
 10.1 Classification

EXTERNAL
 External surface
resorption
 External inflammatory
root resorption
 External replacement
resorption or ankylosis

INTERNAL
 10.2 Etiology

Trauma
Excessive forces
Granuloma
Cyst
Central jaw tumors
Impaction of teeth
Bleaching
Systemic diseases
If no cause is evident, the
disorder is called as
idiopathic resorption.
 10.3 Clinical Features
Asymptomatic
On complete resorption, tooth may become mobile.
If extends into the crown, gives appearance of “pink tooth” as
seen in internal resorption.
In case of replacement resorption or ankylosis, root is
gradually replaced by bone, renders the tooth immobile, in
infraocclusion, and with a high mettalic percussion sound.
 10.4 Radiographical Examination
Concave or ragged areas on the root surface or blunting of the apex.
Inflammatory root resorption caused by the pressure of a growing
granuloma, cyst or tumor adjacent to the area of radiolucency.
Areas of ankylosis have a resorbed root with no PDL space and
with bone replacing the defects.
 10.5 Treatment

If extended by pulpal disease, root canal therapy.

If due to excessive orthodontic forces, treatment of
choice would be reducing those forces.
In case of cervical root resorption, surgical exposure of
the defect and restoration with a suitable restorative
material.
 11.Hypercementosis

Is an adaptive change in the periodontal ligament,

characterized by abnormal increased cementum thickness
on the root surface resulting with macroscopic changes in
shape.
 11.1 Etiology
Ageing
Functional Stress
Periapical periodontitis.
Functionless and unerupted teeth.
Systemic Disease
Paget’s disease.
Cementoblastoma and cemento-osseous
dysplasia
 11.2 Clinical Features

Asymptomatic
Incidental finding on radiographs
 11.3 Radiological features

Thickening of the
cementum layer along with
blunting or rounding of
the root tip.
The biological width
between the root surface,
the alveolar bone and the
periodontal ligament is
found intact on the
radiographs.
 11.4 Treatment
Asymptomatic; No treatment
Paget’s disease ; extractions become difficult
Inflamed or necrotic pulp; endodontic treatment of the
tooth is required, but it may pose great difficulty and might
necessitate surgical intervention.
 12. OSTEOMYELITIS

Acute or chronic inflammatory condition of the bone,

which begins as an infection of the medullary cavity or
cortical surfaces of the bone , rapidly involves the
haversian systems, and extends away from the initial site
of involvement, to involve the periosteum of the affected
area.
 12.1 Clasification
1. Acute suppurative
osteomyelitis
2. Chronic suppurative
osteomyelitis
3. Chronic focal sclerosing
osteomyelitis (Condensing
osteitis)
4. Chronic diffuse sclerosing
osteomyelitis
5. SAPHO syndrome
6. Chronic osteomyelitis with
proliferative periostitis
7.Sclerotic cemental masses
8.Alveolar osteitis / dry socket/
fibrinolytic osteitis
 12.2 Predisposing factors

Fractures due to trauma Systemic disease

Road traffic accidents
Gun shot wounds
Radiation damage
Paget`s disease
Osteoporosis
Malnutrition
Acute Leukemia
Uncontrolled diabetes
Sickle cell anemia
Chronic alcoholism
 12.3 Pathogenesis

Microorganisms may infect bone through one or more of

three basic methods

Contiguous
focus of Hematogenous
infection spread
Direct inoculation of
microorganisms into
bone
 12.4 Occurrence

Sex more common in men, than women.

Osteomyelitis in maxilla:
Rare occurrance due to
 Extensive blood supply
 Thin cortical plates
 Abundant medullary spaces

Osteomyelitis in mandible:
 An important factor in
establishment of osteomyelitis in
mandible is compromise of blood
supply
12.5 Microbiology
 12.6 Acute suppurative osteomyelitis

Serious sequela of periapical infection that often results in

diffuse spread of infection through out the medullary spaces ,
with subsequent necrosis of variable amount of bone.
Poly microbial- Staphylococcus aureus, S. albus,
Porphyromonas, Prevotella, Bacteriodes.
 12.6.1 Etiology
Most common cause : Dental infection
A periodontal pocket involved in a fracture
Acute necrotising gingivitis or pericoronitis (even more rarely)
Infection due to fracture of jaw, gun shot
Hematogenous spread
 12.6.2 Pathology
Acute inflammation of marrow tissues

Spread of exudate along the marrow spaces

Thrombosis of vessels due to compression

Necrosis of bone

Necrotic tissues, dead and dying cell, pus from bacteria → fill the
marrow space

Involves cortical bone → Lifting of periosteum causing further

necrosis

Osteoclastic activity >>>SEQUESTRUM

 Sequestrum
Piece of dead bone that has become separated during the
process of necrosis from normal or sound bone.
 12.6.3 Clinical features

Maxilla : localized
Mandible : Diffuse and widespread
In infants: NEONATAL MAXILLITIS
 Origin: Hematogenous spread or local oral infection
 Seriously ill and may not survive
In adults:
 Sever pain
 Trismus
 Parasthesia of lips in case
of mandibular
involvement
 Elevation of temperature
 Regional
lymphadenopathy
 Loosening of teeth and
exudation of pus from
gingiva
 No swelling and redness
till periostitis develops
 12.6.4 Radiographic feature

Progress rapidly → little evidence

Trabeculae becomes fuzzy and indistinct
Ill defined margins

Ill-defined area
of radiolucency
of the right body
of the mandible
 12.6.5 Histologic features

Necrotic bone- loss of

osteocytes from their lacunae,
peripheral resorption and
bacterial colonization.
Medullary space→ filled with
inflammatory exudates
The inflammatory cells are
chiefly PMNs but may show
occasional lymphocytes and
plasma cells
 Osteoblasts bordering the bony trabeculae are destroyed
Trabeculae may lose their viability and begin to undergo slow
resorption

Nonvital bone exhibits loss of the osteocytes from the lacunae. Peripheral resorption and
surrounding inflammatory response also can be seen
 12.6.6 Treatment and prognosis

Essential measures
Bacterial sampling and culture
Drainage
Analgesics
Give specific antibiotics based
on culture and sensitivities
Debridement
Remove source of infection, if
possible
Adjunctive treatment
Sequestrectomy
Decortication if
necessary
Hyperbaric oxygen
Resection and
reconstruction for
extensive bone
destruction
UNTREATED CASES
may proceed to
development of
periostitis , soft tissue
abscess or cellulitis
12.6.7 COMPLICATIONS
12.7 CHRONIC SUPPURATIVE OSTEOMYELITIS

Inadequately treated acute osteomyelitis

Rarely- complication of irradiation
Acute exacerbations of chronic stage may occur
Fistulous tract may form which open to surface
 12.7.1 Clinical Features

Swelling
Pain
Sinus formation
Purulent discharge
Sequestrum formation
Tooth loss
Pathologic fracture
 12.7.2 Radiological feature
Patchy, ragged & ill defined radiolucency.
Often contains radiopaque sequestra.
 12.7.3 Histology

Inflammed connective
tissue filling inter-
trabecular areas of bone.
Scattered sequestra.
Pockets of abscess.

Chronically inflamed and

reactive fibrousconnective tissue
filling the intertrabecular spaces.
 12.7.4 Treatment

Difficult to manage
medically :
Surgical intervention is
mandatory, depends on
spread of process.
Antibiotics are same as
in acute condition but
are given through IV in
high doses.
 SMALL LESIONS
Curretage, removal of necrotic bone and
decortication are sufficient.

EXTENSIVE OSTEOMYELITIS
Decortication combined with transplantation of
cancellous bone chips.

PERSISTANT OSTEOMYELITIS
Resection of diseased bone followed by
immediate reconstruction with an autologous
graft is required.
Weakened jaw bones must be immobilized.
12.8.CHRONIC FOCAL SCLEROSING
OSTEOMYELITIS
( CONDENSING OSTEITIS)

Condensing
Osteitis
slide.118
 12.9.CHRONIC DIFFUSE
SCLEROSING OSTEOMYELITIS
Clinical entity characterized by a nonsuppurative, inflammatory
process associated with recurrent swelling, trismus and pain
Common in edentulous mandible
Proliferative reaction of bone to a low grade infection.
Portal of entry is diffuse periodontal disease
 12.9.1 Clinical feature

Most common in edentulous mandibular jaws or edentulous

areas and does not exhibit any gender predominance.
On acute exacerbation results in vague pain ,unpleasant taste and
mild suppuration ,many times with the spontaneous formation of
a fistula opening onto the mucosal surface to establish drainage.
 12.9.2 Radiological feature
Diffuse patchy, sclerosis of bone (cotton wool appearance).
Sometimes bilateral involvement
Occationally involvement of both maxilla and mandible of same
patient.
Border between the sclerosed bone and normal bone is indistinct.
 12.9.3 Histologic features

Dense , irregular trabeculae of bone bordered by active layer

of osteoblasts ; focal osteoclastic area may be present
Trabecular bone with the presence of reparative and reactive
new bone formation. There was a marked abundant osteoid
and osteoblastic rim.
Mosaic pattern appearance- indicative of repeated periods of
resorption followed by repair
Interstitial soft tissue is fibrotic
Proliferating fibroblasts and occasional small capillaries as
well as small focal collection of lymphocytes and plasma
cells
Irregular trabeculae of bone bordered by active layer of osteoblasts.
Proliferating fibroblasts and occasional small capillaries as well as
small focal collection of lymphocytes and plasma cells
 12.9.4 Treatment

Intravenous antibiotics, oral antibiotics for long‐term use, cortisone,

nonsteroid anti‐inflammatory drugs
Surgical treatment with decortication to remove the infected bone or
resection to increase the blood flow in the area to improve healing
Complete pain relief with denosumab: regulates osteoclasts and
osteoblasts, resulting in increased osteoblast activity
 12.10 SAPHO syndrome
It was first described by Chamot et al. in 1987.
Rare and of unknown etiology.
The synovitis, acne, pustulosis, hyperostosis, and osteitis
In 1994, Kahn et al. (1994) reported three diagnostic criteria
for:
1) Multifocal osteomyelitis with or without skin
manifestations.
2) Sterile acute or chronic joint inflammation associated
with pustules or psoriasis on the palms and soles, acne,
or hidradenitis.
3) Sterile osteitis in the presence of one of the skin
manifestations
 12.11 CHRONIC OSTEOMYELITIS WITH
PROLIFERATIVE PERIOSTITIS
Garre’s osteomyelitis was first described by Carl Gaffe in 1893
as "a focal gross thickening of periosteum with peripheral
reactive bone formation resulting from infection”.
Non -suppurating type of osteomyelitis, with a reactive
periosteal thickening due to a low-grade irritation or dental
infection.
 12.11.1 Clinical feature
Young person before the age of 25 years
More common in mandible of children and young adults (most
cases occur in bicuspid and molar region)
Hard swelling over the jaw, producing facial asymmetry with little
or no pain.
This occur as a result of overlying soft tissue infection or cellulitis
subsequently involving periosteum.
The overlying skin was normal, but could occasionally be
inflammed
 12.11.2 Radiographic feature

Reveals an carious tooth near

the hard bony mass
Occlusal radiograph
→focal overgrowth of bone
on the outer surface of the
cortex ,which may be
described as duplication of
the cortical layer of bone .
 12.11.3 Histologic features

Subperiosteal mass is composed of much reactive new bone and

osteoid tissue , with osteoblasts bordering many of trabeculae
Trabeculae is perpendicular to cortex and parallel to each other
Connective tissue is fibrous and shows sprinkling of lymphocytes
and plasma cells
 12.11.4 Treatment

Extraction or endodontic
treatment of the teeth
No surgical intervention
except biopsy to confirm
diagnosis
After extraction the jaws
undergo remodeling and
facial symmetry is restored
Neoperiostitis or new
periosteum formation may
occur in certain conditions
 12.12 SCLEROTIC CEMENTAL MASSES

Multiple symmetric lesions producing pain, drainage or

localized expansion
Common in black females, unknown etiology
Large radiopaque mass usually involving several quadrants of
the jaws.
This condition has previously been described as chronic
sclerosing osteomyelitis, sclerosing osteitis, or gigantiform
cementoma, it appears more appropriate to consider these
lesions as part of the spectrum of the benign fibro-osseous
lesions of periodontal ligament origin
 12.12.1 Histologic features

Cemental masses have

tissues interrupted by
the cementum unlike
diffuse type which
mostly have sclerotic
bone
In some instances ,the
cementum is in the
form of large solid
masses with smooth,
lobulated margins
often with a globular
accretion pattern
 13. ALVEOLAR OSTEITIS / DRY SOCKET/
FIBRINOLYTIC OSTEITIS

Inflammation of the alveolar

bone in a post-extraction
socket that exhibits exposed
bone that is not covered by a
blood clot or healing epithelium
and exists inside or around the
perimeter of the socket or
alveolus for days after the
extraction procedure limited to
the lamina dura
Can be mistaken clinically for osteomyelitis which
can rarely follow. It is by far the most frequent
painful complication of extractions. Nevertheless, it
is uncommon overall.
 13.1 Aetiology

Excessive extraction trauma

Limited local blood supply
Local anaesthesia
Oral contraceptives
Osteosclerotic disease
Radiotherapy
Smoking
 13.2 Clinical features
The most common painful complication of dental extractions
Loss of clot may be due to excessive local fibrinolytic action or
bacterial enzymes or both
Bare, whitish lamina dura exposed in socket
Pain relieved by irrigation and repeated dressing of socket
Dead bone usually shed as crumb-like fragments
Eventual healing of socket from its base by granulation
 13.3 Pathology
The initial event is destruction of the clot which normally fills
the socket. This leaves an open socket in which infected food
and other debris accumulates in direct contact with the bone.
The dense bone of the lamina dura, dies. Dead bone is
gradually separated by osteoclasts and sequestra are usually
shed in tiny fragments.
 13.4 Treatment

Irrigation with antiseptic

Debridement; infected bone tissue
The opening filled with an dressing
containing some antiseptic to
prevent food and debris from
accumulating
Use of hot mouth rinses
Alvogel (absorbable,gives a
sensation of warmth)

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