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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