Disorders of the pulp

DISORDERS OF THE PULP &
PERIAPICAL TISSUE
PREPARED BY:
MIMANSA THAKKAR
ROLL NO:84
FINAL BDS

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.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

 Acute reversible inflammation of pulp tissue
characterized by vascular dilatation
 Pulp returns to uninflammatory state after removal
of stimulus
AETIOLOGY: -
 Any mild irritants
 Trauma or blow to teeth
 Disturbed occlusal relationship(high points)
 Restorative procedures without thermal instulation
Chemical irritation to pulp(acid etching)
-Excessive pressure due to orthodontic appliance
-Attrition and abrasion
-Dehydration of tooth cavity
-Rapid separation of teeth by mechanical separators
CLINICAL FEATURES: -
Signs and symptoms: painful
Duration: 10-15 minutes, severe and short
Precipitating factors of pain: hot and cold agents
,especially cold.

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.

TREATMENT:
-Best treatment is prevention.
-Identify the cause and treat it.
-Treat incipient carious lesion.
-Reduce high point.
-Proper insulation of restorations
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

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.
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
TREATMENT:
Extirpation of pulp
PROGNOSIS: -
• It is dependant on the success of pulp capping

CHRONIC HYPERPLASTIC PULPITIS
.
• 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

• 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

TREATMENT:
Extirpation or removal of both coronal and radicular pulp
PULP CALCIFICATION:
It is a localized / generalized condition of pulp tissue
characterized by formation of pulp stone in the form of
calcified bodies
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.
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.

TREATMENT:
Root canal treatment
CLASSIFICATION OF PERIAPICAL PATHOLOGY
1.Diseases of endodontic origin
-Apical periodontitis
acute and chronic
-Periapical abscess
acute and chronic
-Apical granuloma
-Periapical cyst
-Osteomyelitis
-External root resorption

2.Diseases of non endodontic origin
APICAL PERIODONTITIS
ACUTE APICAL PERIODONTITS
It is an acute inflammation of periodontium due to
trauma,irritation or infection through root canal.
ETIOLOGY
VITAL TOOTH NON VITIAL TOOTH
Occlusal trauma Sequelae of pulpitis
Wedging of foreign body
between teeth
During root canal
therapy
Blow on teeth
Orthodontic pressure

SIGN AND SYMPTOMS
-History of pulpitis
-Inflammatory exudates in periodontal space cause slight
extrusion of tooth
-pain on mastication
-Tender on percussion
-Pain on palpation of affected tooth
RADIOGRAPHIC FEATURES
-Thickened periodontal ligament
-Pulpless tooth may show periapical rarefaction
-Vital pulp shows normal periradicular tissue
TREATMENT

if pulp is infected endodontic treatment of the affected
tooth is done
Radiogram of healthy periodontium and chronic apical
periodontitis
CHRONIC APICAL PERIODONTITIS
Clinical examintaion:
little or no pain on percussion
X-ray:
interruption of lamina dura or apical radiolucency
Treatment:
root canal treatment

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.
• 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 PMNL’s,
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 RBC’s and hemosiderin
pigmentation is also common.

RADICULAR 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.
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.
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.
• 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 RBC’s 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.
TREATMENT:
-Surgical enucleation
-Root canal therapy
-some cases where cyst is large and curettage can
endanger vitality of adjacent tooth there following
root canal therapy of affected teeth surgical
exterioration is done to collapse the cyst wall . When
the cyst is reduced in size then curretage is done
PERIAPICAL ABSCESS
ACUTE PERIAPICAL ABSCESS(CLOSED)

SUPPARATIVE APICAL PERIODONTITIS(OPEN)
• 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.
• In initial stages – thickening of periodontal
ligaments.
Later – ill defined radiolucency
• Microscopic sections are not usually made as
specimen is fluid.

• Abscess contains abundant PMNL’s 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
TREATMENT:
-ACUTE ABSCESS
Drainage of abscess and controlling the systemic
reaction
Endodontic tereatment of affected tooth

-CHRONIC ABSCESS
Root canal therapy
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.
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.
• Biopsy specimen usually contains necrotic bone,
showing loss of osteocytes from lacunae and
bacterial colonization.
• Bone periphery shows necrotic debris and
infiltration with PMNL’s.

• 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.
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.

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.
• Increased radiopacity around sites of chronic
inflammation like periodontitis, pericoronitis,
periapical pathology etc.
• Sclerosis occurs more in alveolar crest regions of
tooth bearing areas.

• 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.
• 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 Garrѐ’s
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.

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. Cawson’s 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.

Disorders of the pulp

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Disorders of the pulp

Similar to Disorders of the pulp (20)

Recently uploaded

Recently uploaded (20)

Disorders of the pulp