DISORDERS OF

THE PULP &

PERIPAICAL
TISSUES
Prepared by: Dr Sundeep Bhagwath
OVERVIEW
1. INTRODUCTION
2. ETIOLOGY OF PULPITIS
3. FACTORS AFFECTING RESPONSE OF PULP
4. CLASSIFICATION OF PULPITIS
5. TYPES OF PULPITIS
6. PERIAPICAL ABSCESS
7. PERIAPICAL GRANULOMA
8. PERIAPICAL CYST / RADICULAR CYST
9. CELLULITIS
10. LUDWIGS ANGINA
11. CAVERNOUS SINUS THROMBOSIS
12. OSTEOMYELITIS
INTRODUCTION
 Pulpitis is an inflammation of pulp tissue,
a response to surrounding environment
The vitality of the tooth depends on
defence response of pulp dentine
complex by:
- Sclerotic dentin
- Tertiary dentin
- Calcified bridge of dentinal tubules
ETIOLOGY
1. MECHANICAL: Trauma, iatrogenic damage and
barometric changes.
2. THERMAL: uninsulated metallic restorations and
dental procedures like cavity preparation,
exothermic chemical reactions of dental materials
etc.
3. CHEMICAL: Irritation from certain dental materials
or from erosion.
4. BACTERIAL: Through toxins or from direct
extension of caries
 FACTORS
AFFECTING
RESPONSE OF
PULP
1. Severity and duration of irritant.
2. Nature of irritant.
3. Health condition of the pulp or pre-
existing state of the pulp
4. Apical blood flow
5. Local anatomy of the pulp chamber
6. Host defence
CLASSIFICATION
I. According to pathological condition: -
- Focal or acute reversible pulpitis (Pulp
hyperaemia)
- Irreversible pulpitis
II. According to its duration: -
- Acute pulpitis
- Chronic pulpitis
III. According to presence of dentin covering the
pulp chamber: -
- Open pulpitis
- Closed pulpitis
IV. According to extension of
inflammation in pulp tissue: -
- Partial pulpitis
- Complete / total pulpitis

V. According to amount of pus

formation: -
- Exudative pulpitis
- Suppurative pulpitis
 ACUTE
REVERSIBLE
PULPITIS
(FOCAL REVERSIBLE PULPITIS, PULP
HYPERAEMIA)
 Acute reversible inflammation of pulp
tissue characterized by vascular
dilatation

AETIOLOGY: -
Any mild irritants
CLINICAL FEATURES: -
Signs and symptoms: painful

Duration: 10-15 minutes, severe and short

Precipitating factors of pain: hot and

cold agents

Nature of pain:
Throbbing, continuous and radiating.
Pain stops when precipitating factors are
removed
The pain depends on -
The size of exposed pulp (size of
dental caries)
Severity of pulp inflammation
Age of patient
Nature of covering dentine
HISTOLOGICAL
FEATURES: -
Inflamed pulp tissue
contains dilated
blood vessels of
various sizes and
are lined by
endothelial cells
Presence of normal
odontoblasts
indicate vitality of
the pulp tissue.
PROGNOSIS-:
It is a reversible condition.
If it is treated , pulp will return
back to its normal status.
If it is left untreated , it will not
return back to its normal status
but it will enter the next
phase....
 ACUTE
PROGRESSIVE
PULPITIS
CLINICAL FEATURES: -
Duration : - more than 10-15 minutes,
severe and continuous, especially at
night

Precipitating factors of pain : -

spontaneously as well as hot and cold
agents

Nature of pain : -
Throbbing continuous and radiating pain
The pain does not stop even when
precipitating factors are removed.
PROGNOSIS: -
If it is left untreated, it will
change to chronic pulpitis or
pulp necrosis
CHRONIC PULPITIS
 It is a chronic inflammation of
pulp tissue characterized by
specific clinical features.

CLINICAL FEATURES: -
Signs and symptoms: - painful

Duration: - long duration (few

days to months).
Precipitating factors of pain: - hot,
cold agents and during biting.

Nature of pain: -
Mild and intermittent pain
The pain stops when precipitating
factors are relieved and when the
tooth is treated
The pain depends on: -
The size of exposed pulp (size of
dental caries)
Severity of pulp inflammation
Age of patient
Nature of covering dentin
HISTOPATHOLOGICAL FEATURES: -
The pulp tissue
contains dilated
blood vessels with
varying sizes.
Degenerated
odontoblasts
seen.
Areas of chronic
inflammatory cells
and fibrosis can
be seen around
inflamed areas
PROGNOSIS: -
It is dependant on the
success of pulp capping.
CHRONIC OPEN
HYPERPLASTIC
PULPITIS
( PULP POLYP )
 It is a chronic inflammation of pulp
tissue characterized by hyperplasia of
connective tissue of pulp in the form of
polypoid mass which originates from
exposed pulp chamber
CLINICAL FEATURES : -
Site:
A grossly carious molar
(permanent/deciduous) where pulp
chambers are wide, having multiple
roots with highly vascular pulp tissue

Shape : nodular fungated mass fills pulp

chamber
Size : variable

Colour : reddish, bleeds readily

Covering surface : intact or

ulcerated
HISTOLOGICAL FEATURES: -
Mass consists of proliferation of
granulation tissue with newly formed,
dilated blood vessels of varying sizes,
chronic inflammatory cells and fibrosis
Generalized degenerated odontoblasts
also called Wheat Shafing of
Odontoblasts
The mass is covered by hyperplastic
stratified squamous epithelial surface
Source of epithelial cells are from saliva
or desquamated mucosa of cheeks or
gingiva
 PULP
CALCIFICATION
(PULP STONE OR DENTICLES)
It is a localized / generalized condition of pulp
tissue characterized by formation of pulp
stone in the form of calcified bodies
CLINICAL FEATURES : -
Site: coronal or radicular pulp
Size: variable
Signs and symptoms : painless
 RADIOGRAPHIC
FEATURES: -
Radiopaque mass /
masses with variable
sizes inside the pulp
chamber or pulp
canals.
HISTOLOGICAL TYPES: -
True pulp stone - consists of dentinal
tubules.
False pulp stone - consists of concentric
calcified rings
Free pulp stone - is freely located within
the pulp tissue
Attached pulp stone - is adherent to
dentin wall
Embedded pulp stone - is surrounded by
secondary dentin
COMPLICATIONS: -
It interferes with root
canal treatment.
Can cause pain if it
impinges on major pulp
nerves.
PULP NECROSIS
It is an irreversible condition of pulp
tissue characterized by dead pulp
tissue and degeneration ( necrosis )

AETIOLOGY : -Severely irritant

agents.

CLINICAL FEATURES : -
Signs and symptoms : painful
Duration : 10-15 minutes, severe and
short
Precipitating factors of pain: hot and
cold agents

Nature of pain:
Throbbing, continuous and radiating.
The pain stops when precipitating factors
are relieved.
 PERIAPICAL
GRANULOMA
 It refers to a mass of chronically
inflamed granulation tissue at the apex
of a non vital tooth.
May arise either after an acute condition
like periapical abscess becomes quiet
or it may arise de novo.
Important these lesions are not
static and may transform into
periapical cysts or undergo acute
exacerbation.
CLINICAL FEATURES: -
Mostly asymptomatic.
Pain & sensitivity can develop if
acute exacerbation occurs.
No mobility or sensitivity to
percussion of involved tooth.
Pulp vitality tests are negative.
RADIOGRAPHIC FEATURES: -
Lesion can be either well / ill
defined.
Variable sized from small to
large.
Loss of apical lamina dura.
Root resorption is common.
Cannot distinguish periapical
granulomas from periapical
cysts on a radiograph.
HISTOLOGICAL FEATURES:-
Lesion shows inflamed
granulation tissue containing
a dense lymphocytic infiltrate
mixed with PMNLs, plasma
cells and macrophages.

Epithelial rests of Malassez

may be seen within the
granulation tissue.
 Cholesterol clefts
may also be seen
along with associated
multinucleated giant
cells.
Areas of
extravasation of
RBCs and
hemosiderin
pigmentation is also
common.
 RADICULAR CYST
(PERIPAICAL CYST / APICAL PERIODONTAL
CYST)
 By definition, a radicular cyst arises
from epithelial rests of Malassez
located in the PDL as a result of
inflammation.

Often, radicular cyst remains behind

in jaws after removal of infected
tooth then called RESIDUAL
CYST.
CLINICAL FEATURES: -
Age incidence: peak in 3rd, 4th and
5th decades.
Sex incidence: Slightly more in
males.
Site predilection: Maxillary anterior
region.
Frequency: Commonest cystic lesion
of jaws.
Signs & symptoms:
Primarily symptom less.

Discovered accidentally
during routine dental X ray
exam.
 Slowly enlarging
hard bony swelling
initially. Later, if
cysts breaks through
cortical plates, lesion
becomes fluctuant.
Diagnostic criteria
associated teeth
are non vital
Rare in deciduous
teeth.
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.
DIFFERENTIAL DIAGNOSIS: -
Following lesions must be
distinguished from other
periapical radiolucencies
1. Periapical granuloma

2. Peripaical cemento osseous

dysplasia (early lesions)
PATHOGENESIS: -
1. PHASE OF INITIATION:
Accepted generally that rests of Malassez
included within a developing periapical
granuloma proliferates to form the lining of
radicular cyst.
How these cells are stimulated is not clear.
Some product of non vital pulp can be
responsible which simultaneously evokes an
inflammatory response in CT.
Immune factors also held responsible as
plenty of plasma cells are seen in a periapical
granuloma.
2.PHASE OF CYST FORMATION:
Can occur in two possible ways.
One theory states that epithelium
proliferates and covers the bare CT
surface of the abscess cavity.
Another theory cyst cavity forms
within proliferating epithelium as the
cells in center move away from their
nutrient source.
3. PHASE OF ENLARGEMENT: -
Enlargement occurs by collection
of fluid within the lumen of the
cyst.
Osmosis plays an important role
here as the cyst wall appears to
have the properties of a semi
permeable membrane.
HISTOLOGICAL
FEATURES:-
Lined partly / completely
by non keratinized
epithelium of varying
thickness.
Epithelium usually shows
arcading around the CT.
The CT wall shows
inflammatory infiltrate
mainly in the form of
lymphocytes and plasma
cells.
 Hyaline / Rushton
bodies are found in
epithelium and rarely in
CT wall.

These are curved or

linear structures with
eosinophilic staining
properties.
 Cholesterol crystals
in from of clefts are
often seen in the CT
wall, inciting a
foreign body giant
cell reaction.
Originate from
disintegrating RBCs
in presence of
inflammation.
Different types of
dystrophic
calcification are also
seen in CT wall.
 Mucus cell metaplasia
as well as respiratory
cells may be seen in the
epithelial lining.
Keratinization if found is
due to metaplasia and
must not be confused
with an OKC.
 PERIAPICAL
ABSCESS
(ACUTE DENTOALVEOLAR ABSCESS)
 Collection of acute inflammatory cells at
the apex of a non vital tooth is called
periapical abscess.

Acute lesions may arise either as in initial

pathosis or as an acute exacerbation of a
chronic periapical pathology (Phoenix
abscess).
CLINICAL FEATURES:-
Initial stages
tenderness of affected
tooth.
Later pain becomes
intense, with extreme
sensitivity to
percussion.
Extrusion of tooth in its
socket.
Systemic findings
fever, malaise, chills.
 Abscess may spread along
path of least resistance
through medullary spaces
resulting in Osteomyelitis.
Can also perforate cortical
bone and spread to soft
tissues Cellulitis.
It can also drain through an
intraoral sinus tract.
Opening of such a tract is
usually covered by a
granulation tissue
Parulis.
 Periapical abscesses
may also channelize
through the overlying
skin and drain via a
Cutaneous sinus.
If an abscess begins
to drain, it becomes
asymptomatic due to
lack of collection of
pus within the cavity.
RADIOGRAPHIC
FEATURES: -
In initial stages
thickening of
periodontal ligaments.

Later ill defined

radiolucency.
HISTOLOGICAL FEATURES: -
Microscopic sections are not
usually made as specimen is
fluid.
Abscess contains abundant
PMNLs mixed with
inflammatory exudate, cellular
debris and histiocytes.
Phoenix abscesses may also
contain soft tissue component
comprising of granulation
tissue mixed with areas of
abscess
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.
TYPES: -
Cellulitis arising from dental infection
and spreading through soft tissues of
head and neck can take various forms.
Mostly, infection spreads through tissue
spaces like canine space, infratemporal
space, pharyngeal space, buccal space,
submental and submandibular space
etc.
 Two especially dangerous forms
of cellulitis are
- Ludwigs angina
- Cavernous sinus thrombosis
Canine space infection

Infection involving multiple spaces

 LUDWIGS ANGINA
Cellulitis of submandibular region
involving sublingual, submandibular and
submental spaces.
In 70% cases develops from spread of
infection from mandibular teeth.
Increased prevalence in
immunocompromised patients like
AIDS, aplastic anemia, organ
transplantation etc.
CLINICAL FEATURES: -
After reaching submandibular
region, infection extends to
lateral pharyngeal and
retropharyngeal spaces.
LA causes massive swelling
of neck extending close to
clavicles.
There is posterior
enlargement and protrusion
of tongue.
Pain in neck and floor of
mouth.
 Other symptoms dysphagia,
dysphonia, drooling and sore throat.
Lateral pharyngeal space involvement
may cause respiratory obstruction due
to laryngeal edema.
In sever cases tachypnea, dyspnea,
tachycardia, stridor may also be noted.
General signs fever, malaise,
leukocytosis, and raised ESR.
 CAVERNOUS SINUS
THROMBOSIS
Occurs when infection from maxillary
premolars / molars perforates buccal
cortical plate and enters maxillary sinus,
pterygopalatine space or infratemporal
space and reaches the orbit.

From here, infection enters cavernous

sinus through cranial vault.
CLINICAL FEATURES: -
Periorbital edema including lateral border
of nose, protrusion and fixation of eyeball.
Pupil dilatation, lacrimation, photophobia
and loss of vision may also occur.
Pain along distribution of ophthalmic and
maxillary branches of Vth cranial nerve.
Proptosis, chemosis and ptosis seen in
90% cases.
Fever, chills, headache, sweating,
tachycardia, nausea and vomiting also
occur.
OSTEOMYELITIS
 Refers to acute / chronic
inflammatory process in medullary
spaces or cortical surfaces of
bones.

Various patterns recognized like

focal and diffuse sclerosing,
proliferative periostitis etc.
TYPES OF OSTEOMYELITIS: -
1. Acute osteomyelitis
2. Chronic osteomyelitis
3. Diffuse sclerosing osteomyelitis
4. Condensing osteitis (Focal sclerosing
osteomyelitis)
5. Osteomyelitis with proliferative
periostitis.
6. Alveolar osteitis
PREDISPOSING FACTORS: -
1. After odontogenic infections
2. Trauma to jaws
3. Presence of ANUG
4. Chronic systemic diseases
5. Immunocompromised states
6. Tobacco and alcohol abuse
7. Diabetes mellitus
8. Exanthematous fevers
9. Malignancy
10.Malnutrition
ACUTE OSTEOMYELITIS
Acute osteomyelitis occurs when acute
inflammation spreads through medullary
spaces of bone.

CLINICAL FEATURES: -
Age incidence: Any age
Sex incidence: Strong male predilection
Site predilection: Mostly in mandible.
Maxilla is involved primarily in children.
Signs & symptoms:
Fever, leukocytosis,
lymphadenopathy and soft
tissue swelling of affected
area.
X-rays can show an ill
defined radiolucency.
Occasionally, fragments of
necrotic bone can be seen
separating from surrounding
normal bone Sequestrum.
If sequestrum is surrounded
by vital bone Involucrum.
HISTOLOGICAL
FEATURES: -
Biopsy specimen usually
contains necrotic bone,
showing loss of
osteocytes from lacunae
and bacterial colonization.
Bone periphery shows
necrotic debris and
infiltration with PMNLs.
Specimen diagnosed as
sequestrum unless there
is good clinico-pathologic
correlation.
 CHRONIC
OSTEOMYELITIS
It can arise either de novo from the onset
or as a continuation of acute
osteomyelitis, if it is not resolved quickly.

CLINICAL FEATURES: -
Age incidence: Any age
Sex incidence: Strong male predilection
Site predilection: Mostly in mandible.
Signs & symptoms:
Pain, swelling, purulent
discharge, sinus formation,
sequestrum formation, tooth
loss.
Frequent acute
exacerbations may occur if
infection continues for a
long time.
X-rays reveal ill defined,
moth eaten radiolucency
often showing a central
radiopacity (sequestrum).
HISTOLOGICAL
FEATURES:
Biopsy material contains
significant soft tissue
component consisting of
chronically inflamed
fibrous CT filling
intertrabecular areas of
bone.
Scattered areas of
sequestrum may also be
noted.
 DIFFUSE SCLEROSING
OSTEOMYELITIS
Characterized by pain, inflammation,
varying degrees of periosteal
hyperplasia, sclerosis and radiolucency
of affected bone.
Can be confused clinically and
radiologically with certain other intrabony
pathoses like florid cemento-osseous
dysplasia or Paget's disease of bone etc.
CLINICAL FEATURES: -
Age incidence: Almost exclusively in
adults.
Sex incidence: Nil
Site predilection: Primarily in mandible
Signs & symptoms:
Pain and swelling are uncommon.
To make a definitive diagnosis of diffuse
sclerosing osteomyelitis, microbiological
cultures must be positive.
RADIOGRAPHIC
FEATURES: -
Increased radiopacity
around sites of chronic
inflammation like
periodontitis, pericoronitis,
periapical pathology etc.
Sclerosis occurs more in
alveolar crest regions of
tooth bearing areas.
HISTOLOGICAL FEATURES:-
Sclerosis and remodeling of
bone.
Significant inflammation of
bone is not seen even
though sclerosis occurs
adjacent to inflammation.
Necrosis of sclerotic bone
secondary to inflammation
may occur.
In this case, necrotic bone
separates and is surrounded
by granulation tissue
 FOCAL SCLEROSING
OSTEOMYELITIS
(Condensing osteitis)
This refers to a focal area of bone
sclerosis associated with apices of
pulpally involved (caries, deep
restorations or pulp necrosis) teeth.
To be diagnosed as condensing osteitis,
association with inflammation is
essential, as it resembles several other
intrabony pathoses.
CLINICAL FEATURES: -
Occurs mostly in children
and young adults.
Mostly occurs in mandibular
premolar/molar area,
associated with pulpitis /
pulp necrosis.
Localized, uniform zone of
increased radiopacity seen
adjacent to tooth apex.
No swelling / cortical
expansion noted clinically.
DIFFERENTIAL DIAGNOSIS: -
This lesion must be distinguished
from
1. Focal cemento osseous
dysplasia it shows a radiolucent
border.
2. Idiopathic osteosclerosis
here, the lesion is separated from
the tooth apex.
 OSTEOMYELITIS WITH
PROLIFERATIVE PERIOSTITIS
Also called Periostitis
ossificans or Garrs
Osteomyelitis.

It is a type of osteomyelitis
associated with periosteal bone
formation.
CLINICAL FEATURES: -
Age incidence: Children & young
adults

Sex incidence: Nil

Site predilection: Mostly in

premolar/ molar regions of
mandible.
Signs & symptoms:
Swelling may be noted on lower border of
mandible.
Pain may / may not be present.
Radiographs demonstrate radiopaque
laminations roughly parallel to each other and
the underlying cortical surface (onion skin
appearance).
HISTOLOGICAL FEATURES:
Shows parallel rows of higly
cellular, woven bone in
which the individual
trabeculae are oriented
perpendicular to surface.
Sometimes, trabeculae are
interconnected or they may
be scattered, resembling
fibrous dysplasia.
In between trabeculae,
fibrous CT is relatively non
inflamed.
 ALVEOLAR OSTEITIS
(Dry socket / Fibrinolytic alveolitis)

Sometimes, the blood clot at the

extraction site fails to organize which
eventually leads to delayed healing and
causes a condition called Dry socket.
Research shows it is due to
transformation of plasminogen to plasmin
with resultant lysis of fibrin and formation
of kinin (pain mediators).
PREDISPOSING FACTORS: -
1. Local trauma
2. Estrogens
3. Bacterial toxins
4. Inadequate irrigation of
surgery site
5. Tobacco abuse.
CLINICAL FEATURES: -
Age incidence: Between 20 40
years

Sex incidence: Nil

Site predilection: Posterior

mandibular teeth, especially
impacted third molars.
Signs & symptoms:
Affected extraction site filled with a dirty
gray clot, which is lost, leaving behind a
bare, bony socket (Dry socket).
Diagnosis is confirmed by probing of
socket which shows an exposed and
extremely sensitive bone.
Severe pain, foul smell and
lymphadenopathy develop within 3 4
days of extraction.
 BIBLIOGRAPHY
Soames JV, Southam JC. Oral pathology/. 3rd ed.
Oxford 2002.
Shafer WG, Hine MK, Levy BM. A text book of oral
pathology. 6th ed. W.B. Saunders Company. Phil,
London, Toronto, 2005.
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and
maxillofacial pathology. 2nd ed. WB Saunders Company.
Phil, London, Toronto, 2007.
Cawson RA, Odell EW, Porter S. Cawsons essentials of
oral pathology and oral medicine, 7th Ed, Churchill
Livingstone, 2002.
Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology:
Clinical Pathologic Correlations. 4th ed. Saunders
Company, 2003.
ACKNOWLEDGEMENT

All pictures in this presentation

are courtesy of the authors
mentioned in the bibliography.
THANKS FOR YOUR PATIENCE!