pulpal pathology / orthodontic courses by indian dental academy
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PULPAL PATHOLOGY
I) INTRODUCTION
The pulp is the formative organ of the tooth. Encased within the rigid
walls of the root canal is the firm, cohesive and resistant unit, the dental
pulp organ. The dental pulp carries out four basic functions i.e.:
1) Formative – because it forms dentin.
2) Nutritive – because the vascular tree nourishes all the vital organs of
the pulpodentin complex.
3) Sensory – because of the critical role that both the sensory and motor
nerves play in pain transmission.
4) Defensive – because of the protective role of the dentinoblasts against
harmful physical, chemical and microbial irritants.
The desirability of maintaining a vital pulp and of protecting it from
injury was recognized by the earliest practitioners of dentistry. In the
development of the dental art, the integrity of the pulp was frequently
violated in the execution of a technically satisfactory mechanical
restoration. Today, history seems to be repeating itself. Restorative dentistry
has made radical demands on the integrity of the pulp.
Inspite of these circumstances, studies have indicated that an injured
pulp has some capacity to recover, but the degree is uncertain. However,
what is important to the clinician is, whether or not, the tooth requires
endodontic treatment or is amenable to pulp maintenance or preventive
therapy.
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II) CAUSES OF PULP DISEASE
According to Grossman, the causes of pulp disease are physical,
chemical and bacterial.
Physical
Physical causes include mechanical, thermal or electrical injuries.
A) Mechanical
1) Trauma
Traumatic injury may or may not be accompanied by fracture of the
crown or root. It is more common in children than in adults. Trauma to the
tooth could be due to a violent below during a fight, sports, automobile
accident or household accident. Habits like bruxism, nail and threadbiting
may also cause pulpal injury.
Some avoidable and un-avoidable dental trauma like, accidental
exposure of the pulp during cavity preparation or excavation of caries, too
rapid rate of tooth movement during orthodontic treatment, or pins used to
retain amalgam restorations may cause pulpal injury. Dehydration of the
pulp by a continuous air stream may cause aspiration of the odontoblastic
nuclei. Dehydration may also be caused by restorative materials such as
Cavit, which is hydrophilic and absorbs fluid from the dentinal tubules as it
sets.
2) Pathologic wear
The pulp may also become exposed or nearly exposed by pathologic
wear of the teeth from either abrasion or attrition if secondary dentin is not
deposited rapidly enough. Occlusal trauma may also injure the pulp because
of repeated irritation to the neurovascular bundle in the periradicular area.
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3) Cracked tooth syndrome
Incomplete fractures through the body of the tooth may cause pain of
apparently idiopathic origin. Patients usually complains of pain ranging
from mild to excruciating at the irritation or release of the biting pressure.
Diagnosis can be made by reproducing the pain by asking the patient to bite
on a cotton application or rubber (Burlew) wheel, by visualizing the cracked
enamel by using a dye or by transilluminating the tooth with fiberoptic
light. Such teeth may be sensitive for many years because of an incomplete
fracture of enamel and dentin that produces only mild pain. Eventually, this
pain becomes severe, when the fracture involves the pulp chamber.
4) Radiation
Laser radiation sufficient to cause cavitation in teeth also causes
severe degenerative changes in the pulp.
5) Barometric changes (Barodontalgia)
Barometric changes are the high altitude changes of the pulp. It is
also known as aerodontalgia, which denotes toothache occuring at low
atmospheric pressure experienced during a flight, where there is increase in
the intrapulpal pressure from the normal pressure of 10-15mm of mercury.
B] Thermal Injury
Thermal causes of pulp injury are not quite common.
Heat from cavity preparation – cavity preparation produces temperature
changes with an increase of 20°C in temperature during dry cavity
preparation 1mm from the pulp. This heat generated is sufficient to cause
irreparable pulp damage. But pulpal damage is repaired more rapidly when
cavity preparation is done under water spray.
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Frictional heat generated during polishing or heat generated during
setting reaction of cements can cause transient pulp injury.
Metallic fillings close to the pulp without an intermediate base may
conduct the temperature changes rapidly to the pulp and may destroy the
pulp.
C] Electrical
Galvanic current produced from dissimilar metallic fillings may
generate heat and cause pulpal damage.
Chemical
Probably the least common of all the causes. Cements such as
silicate are the most frequent cause for pulp death.
Acid etchants, when used on exposed dentin preliminary to the
application of a composite resin, irritate the pulp without causing pain.
Slow, progressive erosion on the labial or facial surfaces at the
crevices of the teeth by acidic beverages may eventually subject the pulp to
irritation and may cause permanent damage.
Bacteria
The most common cause of pulp injury is bacterial. Bacteria and
their products may enter the pulp through a break in dentin, either from
caries or from accidental exposure, from percolation around the restoration
or from anachoretic effect.
According to Ingle
The causes of pulpal inflammation, necrosis and dystrophy can be
arranged in a logical sequence beginning with the most frequent irritant
microorganisms.
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Without question, bacterial invasion from a carious lesion is the most
frequent cause of pulpal inflammation. An increase in automobile and cycle
accidents, as well as accidents from body contact sports, has also brought
about an increase in pulp death due to trauma. Paradoxically, an alarming
amount of pulp involvement is induced by the very dental treatment
designed to repair the carious lesion.
According to Nicholl’s
Nicholl’s has given the causes of pulpal diseases as:
A) Causes unassociated with dental procedures.
B) Causes associated with dental procedures.
III) DISEASES OF THE DENTAL PULP
Disease is the state of discomfort of an organ. Pulp has been
described as a highly resistant organ and as an organ with little or no
resistance. Its resistance depends on cellular activity, nutritional supply, age
and other metabolic and physiologic parameters.
Age causes important changes in the pulp. The continuous deposition
of secondary dentin throughout the life of the pulp and deposition of dentin
in response to stimuli, reduce the size of the pulp chambers and root canals
and thereby reducing the volume. The decrease in pulp volume reduces the
cellular, vascular and neural content of the pulp and the pulp undergoes
atrophy.
The first and foremost reaction of pulp tissue to irritation is
“Inflammation”, but the basic disease process that is involved in pulp and
periapical disease is “Infection”.
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Menkin defined inflammation as “the complex vascular, lymphatic
and local tissue reaction to an irritant”. Whereas, infection is the reaction to
a viable irritant i.e. microorganism. The term inflammation and infection is
not interchangeable. The patient can have an inflammatory response
without having an infection however, the converse is not valid.
IV) CLASSIFICATION
Clinical classification of pulpal diseases is based primarily on the
diseases. Most of the authors have come to a conclusion that, little or no
correlation exists between histopathological findings and the existing
symptoms. The value of the clinical classification lies in its use by the
clinician to determine the appropriate care and treatment, the endodontic
prognosis and probably the restorative needs of the tooth.
According to Grossman
Diseases of the pulp has been classified as:
I] Pulpitides (inflammation)
A. Reversible 1. Acute (symptomatic).
2. Chronic (asymptomatic)
B. Irreversible 1. Acute
a. Abnormally responsive to cold.
b. Abnormally responsive to heat.
2. Chronic
a. Asymptomatic with pulp exposure
b. Hyperplastic pulpitis.
c. Internal resorption.
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II] Pulp Degeneration
A. Calcific (radiographic diagnosis).
B. Others (histopathologic diagnosis).
III] Pulp Necrosis
According to Franklin Weine
The inflammatory disease of the pulp are:
I] Inflammatory diseases of the dental pulp
A. Hyperalgesia (Reversible pulpitis, hyperactive pulpalgia,
hypersensitivity).
1. Hypersensitive dentin.
2. Hyperaemia.
B. Painful pulpitis
1. Acute pulpitis.
2. Subacute pulpitis.
C. Non painful pulpitis
1. Chronic ulcerative pulpitis (due to caries).
2. Chronic pulpitis (carious lesion absent).
3. Chronic hyperplastic pulpitis (pulp polypeptide).
II] Additional Pulp ChangesA. Necrosis (sequela to inflammatory or retrogressive changes).
B. Retrogressive changes (degeneration).
1. Atrophy and fibrosis.
2. Dystrophic calcification (calcific degeneration).
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C. Internal resorption.
According to F.J. Harty
Clinicians have rejected previous complex histopathological
classification and has developed a simple classification of the state of the
pulp.
1. Normal pulp.
2. Reversible pulpitis.
3. Irreversible pulpitis.
4. Pulp necrosis.
According to Ingle
I] BACTERIAL
a. Coronal Ingress : 1. Caries.
2. Fracture – complete and incomplete.
3. Non fracture trauma.
4. Anomalies of tooth development.
b. Radicular Ingress : 1. Caries.
2. Retrogenic infection – periodontal
pocket and infection.
3. Hematogenic.
II] TRAUMATIC
A. Acute : 1. Coronal fracture.
2. Radicular fracture.
3. Vascular stasis.
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4. Luxation.
5. Avulsion.
B. Chronic : 1. Attrition.
2. Abrasion.
3. Erosion.
III] IATROGENIC
A. Cavity preparation : Heat of preparation, depth of preparation,
dehydration, pulp horn extensions, pulp exposure, haemorrhage etc.
B. Restorations : Insertion, fracture – complete and incomplete forces
of cementing, heat of polishing etc.
C. Intentional extirpation.
D. Periodontal curettage.
E. Orthodontic movement.
F. Electrosurgery.
G. Laser burn.
H. Periradicular curettage.
I. Rhinoplasty.
J. Osteotomy.
K. Intubation.
IV] CHEMICAL
A. Filling materials – cements, etching agents, bonding agents etc.
B. Disinfectants – silver nitrate, phenol, sodium fluorides.
C. Desiccants – alcohol, ether and others.
V] IDIOPATHICA. Aging.
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B. Internal resorption.
C. External resorption.
D. Hereditary hypophosphataemia.
E. Sickle cell anaemia.
F. Herpes zoster infection.
G. HIV and AIDS.
According to Nicholls,
Bacterial
A. Causes unassociated with dental procedures - Mechanical
Chemical
Mechanical
B. Causes associated with dental procedures - Thermal
Electrical
Let us discuss each individual pulpal pathologies
1) Reversible pulpitis
Definition : It is a mild to moderate inflammatory condition of the pulp
caused by noxious stimuli in which the pulp is capable of returning to the
uninflamed state following removal of the stimuli.
It is one of the earliest form of pulpitis and at one time referred to as
“pulp hyperaemia”.
Causes : Reversible pulpitis may be caused by any agent that is capable of
injuring the pulp. The causes could be:
a) trauma – as from a blow or from a disturbed occlusal relationship.
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b) thermal shock – as from preparing a cavity with a dull bur or keeping
the bur in contact with the tooth for too long or from overheating
during polishing of a filling.
c) excessive dehydration.
d) galvanism.
e) chemical stimulus – as from sweet or sour foods or from irritation of
a silicate or self curing acrylic filling.
f) bacteria – as from caries.
g) circulatory disturbances during pregnancy may also result in
transient periodic hyperaemia.
h) local vascular congestion-associated with common cold or with sinus
disease can cause a generalized transient hyperaemia of the maxillary
posterior teeth.
The irritant that causes hyperaemic or mild inflammation in one pulp
may produce secondary dentin in another, if the irritant is mild enough or if
the pulp is vigorous enough to protect itself.
Symptoms
Symptomatic reversible pulpitis is characterized by sharp pain
lasting for a moment. It is more often brought on by cold than hot food or
beverages and by cold air. It does not occur spontaneously and does not
continue when the cause has been removed. Asymptomatic reversible
pulpitis may result from incipient caries and is resolved on removal of the
caries and proper restoration of the tooth.
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Histopathology
Reversible pulpitis may range from hyperaemia to mild to moderate
inflammatory changes limited to the area of the involved dentinal tubules,
such as dentinal caries. One sees reparative dentin, dilated blood vessels,
extravasation of edema fluid and the presence of chronic inflammatory
cells. Although chronic inflammatory cells predominate, one may also see
acute inflammatory cells.
Diagnosis
Diagnosis is by a study of the patients symptoms and by clinical
tests. The pain is sharp, lasts for a few seconds and generally disappears
when the stimulus is removed. Cold, sweet or sour usually causes the pain.
Sometimes, the pain may become chronic and may continue for weeks or
even months. Inflamed pulp is sensitive to thermal changes, particularly
cold. Application of cold is the least method of locating and diagnosing the
involved tooth. Tooth with reversible pulpitis reacts normally to percussion,
palpation, mobility and the periapical tissue is normal on radiographic
examination.
Differential Diagnosis
Reversible pulpitis can be differentiated from irreversible pulpitis
because of its characteristic symptoms of sharp onset of pain lasting for a
few seconds. Thermal tests are useful in locating the affected tooth as
reversible pulpitis responds readily to cold. Electric pulp test is an excellent
corroborating test.
Treatment
Prevention is the best treatment for reversible pulpitis. Periodic care
to prevent the development of caries, early insertion of a filling if a cavity
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has developed, use of a cavity varnish or a cement base before insertion of a
filling and care in cavity preparation and polishing are recommended to
prevent pulpitis.
When reversible pulpitis is present, removal of the noxious stimuli
usually suffices. Inspite of treating the reversible pulpitis, if the pain still
persists, the pulpal inflammation should be regarded as irreversible.
Prognosis
The prognosis for the pulp is favourable, if the irritant is removed
early enough. Otherwise, the condition may develop into irreversible
pulpitis.
2) Irreversible pulpitis
Definition – Irreversible pulpitis is a persistent inflammatory condition of
the pulp, symptomatic or asymptomatic, caused by a noxious structures.
Acute irreversible pulpitis exhibits pain usually caused by hot or cold
stimulus, or pain that occurs spontaneously. The pain persists for several
minutes to hours, lingering after removal of the thermal stimulus.
Causes : The most common cause of irreversible pulpitis is bacterial
involvement of the pulp through caries although any clinical factor,
chemical, thermal or mechanical, mentioned already as a cause of pulp
disease may also cause pulpitis. As previously stated, reversible pulpitis
may deteriorate into irreversible pulpitis.
Symptoms
In the early stages, a paroxysm of pain may be caused by sudden
temperature changes, particularly cold, sweet or acid food stuffs, pressure
from packing food into a cavity and on lying down, which results in
congestion of the blood vessels of the pulp. The pain often continues when
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the cause has been removed and it may come and go spontaneously, without
an apparent cause. The patient may describe the pain as sharp, piercing or
shooting and it is generally severe. It may be intermittent or continuous
depending on the degree of pulpal involvement and depending on whether it
is related to an external stimulus. Changes in position that is on bending or
lying down exacerbates the pain because of changes in intrapulpal pressure.
The patient may also have pain referred to the adjacent teeth, to the temple
or sinuses when an upper posterior tooth is involved or to the ear when a
lower posterior tooth is affected. Patients are often kept awake at night by
the pain, which continues to be intolerable despite all their efforts at
analgesia. Apical periodontitis is absent except in the later stages, when
inflammation or infection extends to the periodontal ligament.
Histopathology
This disorder has both acute and chronic inflammatory changes.
There is a continuous vasodilatation, accompanied by the accumulation of
edema fluid in the connective tissue surrounding the tiny tissue. The
pavementing of polymorphonuclear leucocyte cells becomes apparent along
the walls of the vascular channels and rapidly migrate through the
endothelium lined structures in increasing numbers. Large number of white
blood cell collection may be found beneath the area of carious penetration.
Odontoblasts in this area are destroyed.
There is a localized destruction of the pulp by polymorphonuclear
leucocyte cells and formation of microabscess known as pulp abscess
containing pus arising from the breakdown of leucocytes and bacteria as
well as from digestion of tissue. If the carious process continues to advance
and penetrate the pulp, the histologic picture changes. The area of ulceration
is seen (chronic ulcerative pulpitis) that drains through the cavity and
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reduces the intrapulpal pressure and thereby the pain. According to Seltzer
and Bender, a possible mechanism by which a high concentration of
antigens in the carious process may induce the formation of
immunoglobulins. An immune antigen antibody precipitate in the presence
of complement, attracts polymorphonuclear leucocytes followed by
phagocytosis and cell degeneration with the release of lysozomes in pulp
tissue.
The liberation of proteases by lysozomes results in the formation of a
pulp abscess. Changes in odontoblastic layer vary from disruption to total
destruction. Irreversible pulpitis progresses to necrosis.
Diagnosis
Inspection generally discloses a deep cavity extending to the pulp or
decay under a filling. The pulp may already be exposed. The surface of the
pulp is eroded and an odour of decomposition is frequently present in this
area. Probing into this area is not painful until the deeper areas of the pulp
are reached. At this level, both pain and haemorrhage may occur.
Radiographic examination may not show anything of significance
that is not already known clinically. It may disclose an interproximal cavity
or caries under a filling threatening the integrity of the pulp.
In the early stages of irreversible pulpitis, the thermal test may elicit
pain that persists after removal of the thermal stimulus. In the late stages,
when the pulp is exposed, it reacts feebly to heat and cold. The electric pulp
test induces a response with marked variation in current from the normal.
Results of examination for mobility, percussion and palpation tests are
negative.
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Differential Diagnosis
Irreversible pulpitis should be distinguished from reversible pulpits,
in that the pain produced by the thermal stimuli disappear as soon as the
stimuli is removed. Whereas in irreversible pulpitis, the pain lingers after
the stimulus is removed or it can occur spontaneously.
Treatment
Consists of complete removal of the pulp or pulpectomy and the
placement of an intracanal medicament to act as a disinfectant or obtundent
such as cresatin, eugenol or formocresol. Surgical removal should be
considered if the tooth is unrestorable.
Prognosis
The prognosis of the tooth is favourable if the pulp is removed and
the tooth undergoes proper endodontic therapy and restoration.
3) Chronic Hyperplastic Pulpitis (Pulp Polype)
Definition : Chronic hyperplastic pulpitis or ‘pulp polype’ is a productive
pulpal inflammation due to an extensive carious exposure of a young pulp.
This disorder is characterized by the development of granulation tissue,
covered at times with epithelium and resulting from long standing, low
grade irritation.
Causes: Slow, progressive carious exposure is the cause. For the
development of pulp polype, a large, open cavity, a young resistant pulp
and a chronic low grade stimulus are necessary. Mechanical irritation from
chewing and bacterial infection often provide the stimulus.
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Symptoms
It is symptomless, except during mastication, when pressure from the
food bolus may cause discomfort.
Histopathology
Microscopically, the pulp polype is a complex of new capillaries,
proliferating fibroblasts and inflammatory cells. The tissue in the pulp
chamber is often transformed into granulation tissue, which projects from
the pulp into the carious lesion. The granulation tissue is young vascular
connective tissue containing polymorphonuclear neutrophils, lymphocytes
and plasma cells. The pulp tissue is chronically inflamed. Support for the
protruding mass is provided by the collagenous fibres rooted in the deeper
pulp tissue of the chamber. Sensory nerve elements are almost absent near
the surface in contrast to the rich innervation and exquisite sensitivity of an
exposed pulp which is not hyperplastic. Surface of the polype is usually
covered by stratified squamous epithelium more commonly found in
deciduous teeth.
Diagnosis
This disorder is generally seen only in the teeth of children and
young adults. The appearance of polype tissue is clinically characteristic as
a fleshy, reddish, pulpal mass which fills most of the pulp chamber or
cavity or extends beyond the confines of the tooth. At times, the mass is
large enough to interfere with the comfortable closure of the tooth. Cutting
of this tissue does not cause pain but pressure thereby transmitted to the
apical end of the pulp does cause pain.
Radiographs show a large open cavity with direct access to the pulp
chamber. The tooth may respond feebly or not at all to the thermal tests
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unless extreme cold such as ethyl chloride spray is used. More current than
normal may be required to elicit a response by means of electric pulp
testing.
Differential Diagnosis
The appearance of hyperplastic pulpitis is characteristic and should
be easily recognized. The disorder must be distinguished from proliferating
gingival tissue.
Treatment
Efforts at treatment should be directed towards elimination of the
polype tissue followed by extirpation of the pulp, provided the tooth can be
restored. When the hyperplastic pulpal mass has been removed with a
periodontal curette or spoon excavator, the bleeding can be controlled with
pressure. The pulp tissue of the chamber is then completely removed and a
dressing of formocresol is sealed in contact with the radicular pulp tissues.
The radicular pulp is extirpated at a later visit. If time permits, the entire
procedure of pulpectomy can be completed in a single visit.
Prognosis
The prognosis of the pulp is unfavourable but the prognosis of the
tooth is favourable after endodontic treatment and adequate restoration.
4) Internal Resorption
Definition : Internal resorption is an idiopathic, slow or fast progressive
resorptive process occuring in the dentin of the pulp chamber or root canals
of teeth.
Cause : The cause of internal resorption is not known, but such patients
often have a history of trauma.
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Symptoms
Internal resorption in the root of a tooth is asymptomatic. In the
crown, it may be manifested as a reddish area called “pink spot”. This
reddish area represents the granulation tissue showing through the resorbed
area of the crown.
Histopathology
Unlike caries, internal resorption is the result of osteoclastic activity.
The resorptive process is characterized by lacunae which may be filled in
by osteoid tissue which is regarded as an attempt at repair.
The presence of granulation tissue accounts for the profuse bleeding
when the pulp is removed. Multinucleated giant cells or dentinoclasts are
present. The pulp is usually chronically inflamed. Metaplasia of the pulp
that is transformation to another type of tissue such as bone or cementum,
sometimes occurs.
Diagnosis
Internal resorption may affect either the crown or the root of the
tooth or it may be extensive enough to involve both. It may be slow,
progressive extending over 1-2 years or it may develop rapidly and
perforate the tooth within a matter of months. Although any tooth in the
mouth can be involved, those most readily recognized are the maxillary
anterior teeth. Usually internal resorption is recognized during routine
radiographic examination. The appearance of “pink spot” occurs late in the
resorptive process, when the integrity of the crown has been compromised.
Radiographs show changes in the appearance of the walls in the root canal
or pulp chamber with a round or ovoid radiolucent area.
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Differential Diagnosis
When internal resorption progresses into the periodontal space and a
perforation of the root occurs, it is difficult to differentiate from external
resorption. In internal resorption, the resorptive defect is more extensive in
the pulpal wall than on the root surface, this defect is usually recognized by
means of a radiograph.
Treatment
Extirpation of the pulp stops the internal resorptive process. Routine
endodontic treatment is indicated, but obturation of the defect requires a
special effort, preferably with a plasticized gutta percha method. In many
patients, however, the conditions progresses unobserved because it is
painless, until the root is perforated. In such a case, calcium hydroxide paste
is sealed in the root canal and is periodically renewed until the defect is
repaired. Repair is completed when the calcific barrie is present. When the
repair is completed, the canal with its defect is obturated with plasticized
gutta percha.
Prognosis
The prognosis is best before perforation of the root or crown occurs.
In the event of a root crown perforation, the prognosis is generated and
depends on the formation of a calcific barrier or access to the perforation
that permits surgical repair.
5) Pulp Degeneration
Degeneration of the pulp is seldom recognized clinically and is
generally present in the teeth of older people. Degeneration may also be the
result of persistent mild irritation in teeth of younger people. It may not
necessarily be related to infection or caries, although a cavity or a filling
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may be present in the affected tooth. The early stages of pulp degeneration
does not usually cause definite clinical symptoms. The tooth is not
discoloured, and the pulp may react normally to electric and thermal tests.
As the degeneration progresses, the tooth may discolour and the pulp will
not respond to stimulation.
The specific types of pulp degeneration are:
1) Calcific degeneration.
2) Atrophic degeneration.
3) Fibrous degeneration.
1) Calcific Degeneration
In calcific degeneration, part of the pulp tissue is replaced by calcific
material, that is pulp stones or denticles are formed. The calcification may
occur either within the pulp chamber or root canal, but it is generally
present in the pulp chamber.
The calcified material has a laminated structure, and lies unattached
within the body of the pulp. Such a denticle or pulp stone may become large
enough to give an impression of the pulp cavity when the calcified mass is
removed. In another type of calcification, the calcified material is attached
to the wall of the pulp cavity and is an integral part of it.
It is not possible to distinguish one type from another on a
radiograph.
Pulp stones, are considered harmless, although referred pain in few
patients has been described. Calcification may prevent the clinician from
reaching the apical foramen and may therefore prevent complete
instrumentation of the root canal.
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2) Atrophic Degeneration
In this type of degeneration, observed histopathologically in pulps of
older people, fewer stellate cells are present and intercellular fluid is
increased. The pulp tissue is less sensitive than normal. No clinical
diagnosis exists.
3) Fibrous Degeneration
This form of degeneration of the pulp is characterized by
replacement of the cellular elements by fibrous connective tissue. On
removal from the root canal, such a pulp has the characteristic appearance
of a leathery fibre. This disorder causes no distinguishing symptoms to aid
in clinical diagnosis.
6) Necrosis of Pulp
Definition : Necrosis is death of the pulp. It may be partial or total,
depending on whether part of or the entire pulp is involved. Necrosis is
normally the sequel to inflammation but it can also occur following a
traumatic injury in which the pulp is destroyed before an inflammatory
reaction can take place. As a result, an ischaemic infarction can develop and
may cause a dry gangrenous necrotic pulp.
Necrosis is of two types:
a) Coagulation and b) Liquefaction.
1) In coagulation necrosis, the soluble portion of tissue is precipitated or is
converted into a solid mass. Caseation is a form of coagulation necrosis
in which the tissue is converted into a cheesy mass consisting chiefly of
coagulation proteins, fats and water.
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2) Liquefaction necrosis results when proteolytic enzymes convert the
tissue into a softened mass, a liquid, or amorphous debris.
Cause: Necrosis of the pulp can be caused by any noxious insult injurious
to the pulp such as bacteria, trauma and chemical irritation.
Symptoms
Necrotic pulp causes no painful symptoms. Discolouration of the
tooth is the first indication that the pulp is dead. The tooth lacks its usual
brilliance, lustre and translucency. The presence of a necrotic pulp may be
discovered only by chance, because such a tooth is asymptomatic. Teeth
with partial necrosis can respond to thermal changes, owing to the presence
of vital nerve fibres passing through the adjacent inflamed tissue.
Diagnosis
Pain is absent in a tooth with total necrosis. Swelling, mobility and
response to percussion and palpation are negative. There is no response to
vitality tests as well.
Histopathology
Necrotic pulp tissue, cellular debris and microorganisms may be seen
in the pulp cavity. The periapical tissue may be normal or slight evidence of
inflammation of the apical periodontal ligament may be present.
Treatment
Proper treatment of necrosis is the thorough canal debridement and
obturation of the root canals.
Prognosis
The prognosis of the tooth is favourable if proper endodontic therapy
is instituted.
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VI) Conclusion
To understand pulpal pathology, we must have a thorough
knowledge of what is considered as normal. The study of pulpal diseases
and their causative factors provides the clinician with a scientific basis for
diagnosis and treatment which leads to successful endodontic therapy.
VII) References
1. Endodontic Practice (11th Edition) 1991 – Louis I. Grossman,
Carlos Del Rio. Lea and Febiger Publications.
2. Endodontics in clinical practice (3rd edition) 1990 – F.J. Harty
(Butterworth and Co.).
3. Endodontics (4th edition) 1985 – John I. Ingle (Williams and
Wilkins).
4. Endodontic Therapy (5th edition) 1996 – Franklin S. Weine
(Mosby Publications).
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CONTENTS
I) Introduction
II) Causes of Pulp Disease
III) Diseases of the Dental Pulp
IV) Classification of Pulpal Diseases
V)1) Reversible Pulpitis2) Irreversible Pulpitis3) Chronic Hyperplastic Pulpitis4) Internal Resorption5) Pulp Degeneration6) Necrosis of Pulp
VI) Conclusion
VII) References
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