Asalaam Alekum
8/03/2015
Diseases of the Pulp
Dr. Gaurav Garg, Lecturer
College of Dentistry, Al Zulfi
Majmaah University
•Learning Objectives
•At the end of lecture students should know:
Etiology of pulpal inflammation
Various diseases of the pulp, their clinical,
radiographic & histologic features
Differential diagnosis
Treatment
Etiology of Pulpal inflammation
1 .Physical
•
•
•
•
A. Mechanical
a. Trauma
b. Pathological wear
C. Cracked tooth syndrome
d .Barometric changes (Barodontalgia)
B. Thermal
• a. Heat from cavity preparation
• b. Exothermic heat from setting of cements
• c. Conduction of heat and cold through deep restorations
• d. Frictional heat produced during polishing
C. Electrical – Galvanic current
2. Chemical
- Acids from cements
- Erosion
3. Bacterial
-toxins associated with
caries
-direct invasion in
pulp
-by blood borne
microorganisms
(anachoresis)
Pulpal Diseases
Diseases of the pulp
1. Pulpitis (Inflammation)
A. Reversible Pulpitis
-Acute (symptomatic)
-Chronic (Asymptomatic)
B. Irreversible Pulpitis
-Acute
a. Abnormally responsive to cold
b. Abnormally responsive to heat
-Chronic
a. Asymptomatic with pulp exposure
b. Hyperplastic pulpitis
c. Internal resorption
2. Pulp degeneration
A. Calcific (radiographic diagnosis)
B. Others (histological diagnosis)
3. Necrosis
PULPITIS
Reversible pulpitis
Definition:-it is a mild to moderate
inflammatory condition of pulp caused
by noxious stimuli in which the pulp is
capable of returning to uninflammed
state following removal of the stimuli.
Clinical features
• Sharp/ shooting pain (in acute)
-which is often brought about by cold rather than
hot foods.
-does not occur spontaneously.
- subsides as soon as stimulus is removed.
- Pain is often localized.
Mild or no pain in case of chronic
• Tooth reacts to vitality tests at lower level than
normal ,indicating increased sensitivity.
Histopathology
• Slight disruption of
odontoblast layer
• Dilation of blood vessels
• Hyperemia
• Extravasation of odema fluid
• Presence of acute and Chronic
inflammatory cells
Radiographic features
• No changes in periradicular
tissues
• Usually one can see carious
lesion which is usually not
close to the pulp
Treatment
• Removal of cause ie: Caries etc.
Irreversible pulpitis
Definition:-It is
persistent
inflammatory
condition of pulp,
caused by noxious
stimuli.
Clinical features
• Sudden paroxysm of Pain which may be caused by
temperature changes, packing food into the cavity etc.
• Pain often continue even when the cause has been
removed.
• May occur spontaneously.
• May intermittent or severe continuous depending upon
the degree of pulpal involvement.
• Patient may also complain that change of position or
bending over and lying down exacerbates the pain.
• Pain may refer to adjacent teeth, temple region or to the
ear.
• In such cases patients are often kept awake at night by
the pain which continues to be intolerable despite all
analgesia.
• Pain is usually increased by the heat and relieved by the
cold.
• It gets decreased after the exposure and drainage
(becomes chronic).
Clinical examination
• Inspection generally discloses deep cavity or
decay under the filling.
• Pulp may already be exposed.
• Exposed pulp may be covered by a greyish,
scum like layer which is composed of food
debris, degenerated PMNs, microorganisms
and blood cells.
• On probing deep into the pulp , pain and
hemorrhage may be present.
• Drop of pus may be expressed on exposing
the pulp if it is already not exposed.
Histopathology
Series of events
• Inflammation
• congestion
• necrosis
• PMNs chemotaxis
• phagocytosis
• pus formation
Radiographic changes
• A deep interproximal cavity
that is not clinically seen can
suggest involvement of pulp
horn.
• May show caries under the
filling or deep caries
threatening the integrity of
pulp.
Differential diagnosis
From reversible pulpitis
• Pain
-onset
-type
-duration
• More response to cold than hot
• Vitality testing
Treatment
• RCT/Pulpectomy
Chronic Hyperplastic Pulpitis
synonym:-pulp polyp
Definition:-it is productive pulpal
inflammation due to extensive
carious exposure of young pulp.
• Characterized by development of
granulation tissue ,covered at
times with epithelium and
resulting from long standing, low
grade irritation.
Etiology
• Slow progressive carious exposure of the pulp is the
cause.
• For the development of Hyperplastic Pulpitis, a large
open cavity, a young pulp and a chronic low grade
stimulus are necessary.
Clinical features
• Usually seen only in teeth of children
and young adults.
• Characteristic appearance:- a fleshy
polypoid ,reddish pulpal mass fills
most of the pulp chamber or cavity or
even extends beyond the confines of
the tooth.
• At times mass may be large enough
to interfere with closure of teeth.
• Less sensitive than normal pulp.
• Usually symptomless except during
mastication when pressure of food
bolus may cause discomfort.
• Cutting of this tissue produces no pain but
pressure transferred to the apical end of pulp
may produce pain.
• Tissue bleeds easily because of rich network of
blood capillaries.
• Tooth may respond feebly or not at all to the
thermal test.
Histopathology
• Surface of polyp is covered by
epithelium.
• Epi. is usually stratified squamous
and is derived from gingiva or freshly
desquamated epi. cells of mucosa or
tongue.
• Tissue in pulp chamber is
transformed into granulation tissue
which is young vascular C.T
containing PMNs, lymphocytes and
plasma cells.
• Nerve fibers may be found in
epithelial layer.
Radiographic features
• Shows large ,open cavity
with direct access to the
pulp chamber.
Differential diagnosis
• Appearance is usually characteristic and is easily
recognized but must be distinguished from
proliferating gingival tissue.
• To differentiate it ,one should raise and trace
the stalk of the tissue back to its origin, the pulp
chamber.
Treatment
• RCT/Pulpectomy
Internal Resorption
• Definition:-it is an idiopathic
slow or fast progressive resorptive
process occurring in the dentin of
pulp chamber or root canals of
tooth.
 It is also known as:
•
Odontoclastoma
•
Pink tooth of mummery
•
Chronic proliferating hyperplasia
Etiology of internal resorption
• Exact cause is unknown.
• Possible contributing factors are:-trauma
-caries
-ortho treatment
-infection/pulpitis
-extreme heat
Clinical features
• Usually asymptomatic
• First evidence may be the pink
hued area on the crown of the
tooth so called Pink tooth which
represent the hyperplastic vascular
tissue.
• In root resorption ,perforation of
dentin and cementum may occur
which if left untreated results in
mobility of segment
Pathophysiology of
Histological features
• Resorption of pulpal surface
of dentin and proliferation
of pulpal tissue filling the
defect
• In coronal resorption,
enamel may also get
resorbed.
• Odontoclasts lining the
resorptive lacuna
Radiographic feature
Treatment
• RCT- Extirpation of pulp stops the
resorptive process.
• In case of root perforation,
Calcium hydroxide paste is placed
in canal until the defect is repaired
by calcific barrier & the canal is
finally obturated.
• Repair by MTA
Pulp degeneration
Usually present in teeth of older people.
Types:
• Calcific degenerations
• Atrophic degenerations
• Fibrosis
Calcifications
 In calcific degeneration part of pulp is
replaced by calcific material called Pulp
stones or Denticles
 Seen in functional as well as unerupted
embedded teeth.
• Pulp stones have been noted in patients
with systemic or genetic diseases such as
dentine dysplasia, dentinogenesis
imperfecta and in certain syndromes such
as Van der Woude syndrome
• Exact cause is unknown
MECHANISM OF FORMATION OF PULP STONES
Localized metabolic dysfunction
trauma
Hyalinization of injured cells
Vascular damage
fibrosis
mineralization (nidus formation)
Growth with time
Pulp stone
shafer:; textbook of oral pathology
Classification
Pulp stones are classified
1. According to structure:• True denticles
• False denticles
• Diffuse calcifications
2. According to location
• Free
• Attached
• Embedded
True Denticles
• Are comparatively rare
• Usually located close to apical
•
•
foramen.
Structure is similar to dentin, in
that they exhibit dentinal tubules
containing odontoblastic
processes.
True stones are formed by
inclusion of remnants of the epi.
root sheath with in the pulp which
in turn induce the cells of the pulp
to differentiate into odontoblasts
which then forms the denticles.
False Denticles
• Do not exhibit tubules but
appear as concentric layers of
calcified tissue.
• In centre of these calcified
masses there may be remnants
of necrotic and calcified cells.
• Some may arise from blood
vessels (Thrombi).
• All denticles begin as small
nodule but increase in size by
incremental growth on the
surface.
Diffuse calcifications
• Appear as irregular calcific deposits
in pulp tissue, usually following
collagenous fiber bundles and blood
vessels.
• Usually persists as fine calcified
spicules but may also develop into
large masses.
• Mostly found in radicular pulp
whereas pulp stones are more
frequent in coronal pulp.
• Incidence as well as size of pulp stones/
Calcifications increases with age.
• 10-30 yrs of age - 66 %
• 30-50 yrs of age- 80%
• over 50 yrs- 90%
• No treatment required
• Endodontic treatment is difficult in presence of
Pulp Stones
Necrosis of pulp
Definition :-death of pulp
Causes:-can be caused by any
noxious stimuli which is
injurious to the pulp such as
bacteria, trauma and
chemical irritation.
Clinical features
• Discoloration of tooth –
indicates dead pulp
• May be asymptomatic.
• Tooth with partial necrosis can
respond to thermal changes but
in case of total necrosis no
sensitivity to thermal or vitality
testing is there.
Radiographic changes
• Generally shows large cavity or
filling.
• Periapical tissue may be normal or
thickening of PDL can be there or
open apex.
• Some teeth have neither filling nor
cavity but pulp may have died
because of trauma.
Diagnosis
:-
• Proper history
• Vitality testing
• Thorough clinical examination
Histopathology :• pulp cavity contains necrotic pulp tissue,
cellular debris and microorganisms.
Treatment
• RCT
Pulpal Diseases
Pulpitis
Reversible
Acute/Chronic
Pulp
Degeneration
Calcific
Irreversible
Acute
Chronic:
1. Asymptomatic pulp exposure
2. Hyperplastic
3. Internal resorption
Others (Atrophic &Fibrous)
Necrosis
References
• Pathways of pulp; Stephen Cohen
• Endodontics; Franklin S. Weine
• Textbook of Endodontics; Ingle & Bakland