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) utritive because the vascular tree nourishes all the vital organs of
the pulpodentin comple!.
") #ensor$ because of the critical role that both the sensor$ and motor
nerves pla$ in pain transmission.
%) &efensive because of the protective role of the dentinoblasts against
harmful ph$sical, chemical and microbial irritants.
The desirabilit$ of maintaining a vital pulp and of protecting it from
in'ur$ was recogni(ed b$ the earliest practitioners of dentistr$. )n the
development of the dental art, the integrit$ of the pulp was fre*uentl$
violated in the e!ecution of a technicall$ satisfactor$ mechanical
restoration. Toda$, histor$ seems to be repeating itself. +estorative dentistr$
has made radical demands on the integrit$ of the pulp.
)nspite of these circumstances, studies have indicated that an in'ured
pulp has some capacit$ to recover, but the degree is uncertain. ,owever,
what is important to the clinician is, whether or not, the tooth re*uires
endodontic treatment or is amenable to pulp maintenance or preventive
therap$.
1
II) CAUSES OF PULP DISEASE
According to Grossman, the causes of pulp disease are ph$sical,
chemical and bacterial.
Physical
-h$sical causes include mechanical, thermal or electrical in'uries.
A) Mechanical
1) Trauma
Traumatic in'ur$ ma$ or ma$ not be accompanied b$ fracture of the
crown or root. )t 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. ,abits li.e bru!ism, nail and threadbiting
ma$ also cause pulpal in'ur$.
#ome avoidable and un/avoidable dental trauma li.e, accidental
e!posure of the pulp during cavit$ preparation or e!cavation of caries, too
rapid rate of tooth movement during orthodontic treatment, or pins used to
retain amalgam restorations ma$ cause pulpal in'ur$. &eh$dration of the
pulp b$ a continuous air stream ma$ cause aspiration of the odontoblastic
nuclei. &eh$dration ma$ also be caused b$ restorative materials such as
0avit, which is h$drophilic and absorbs fluid from the dentinal tubules as it
sets.
2) Pathologic wear
The pulp ma$ also become e!posed or nearl$ e!posed b$ pathologic
wear of the teeth from either abrasion or attrition if secondar$ dentin is not
deposited rapidl$ enough. 1cclusal trauma ma$ also in'ure the pulp because
of repeated irritation to the neurovascular bundle in the periradicular area.
2
3) Cracked tooth syndrome
)ncomplete fractures through the bod$ of the tooth ma$ cause pain of
apparentl$ idiopathic origin. -atients usuall$ complains of pain ranging
from mild to e!cruciating at the irritation or release of the biting pressure.
&iagnosis can be made b$ reproducing the pain b$ as.ing the patient to bite
on a cotton application or rubber 23urlew) wheel, b$ visuali(ing the crac.ed
enamel b$ using a d$e or b$ transilluminating the tooth with fiberoptic
light. #uch teeth ma$ be sensitive for man$ $ears because of an incomplete
fracture of enamel and dentin that produces onl$ mild pain. Eventuall$, this
pain becomes severe, when the fracture involves the pulp chamber.
4) Radiation
4aser radiation sufficient to cause cavitation in teeth also causes
severe degenerative changes in the pulp.
5) Barometric changes (Barodontalgia)
3arometric changes are the high altitude changes of the pulp. )t is
also .nown as aerodontalgia, which denotes toothache occuring at low
atmospheric pressure e!perienced during a flight, where there is increase in
the intrapulpal pressure from the normal pressure of 15/16mm of mercur$.
B] The!al In"#y
Thermal causes of pulp in'ur$ are not *uite common.
,eat from cavit$ preparation cavit$ preparation produces temperature
changes with an increase of 2570 in temperature during dr$ cavit$
preparation 1mm from the pulp. This heat generated is sufficient to cause
irreparable pulp damage. 3ut pulpal damage is repaired more rapidl$ when
cavit$ preparation is done under water spra$.
"
Frictional heat generated during polishing or heat generated during
setting reaction of cements can cause transient pulp in'ur$.
8etallic fillings close to the pulp without an intermediate base ma$
conduct the temperature changes rapidl$ to the pulp and ma$ destro$ the
pulp.
C] Elec$ical
9alvanic current produced from dissimilar metallic fillings ma$
generate heat and cause pulpal damage.
Che!ical
-robabl$ the least common of all the causes. 0ements such as
silicate are the most fre*uent cause for pulp death.
:cid etchants, when used on e!posed dentin preliminar$ to the
application of a composite resin, irritate the pulp without causing pain.
#low, progressive erosion on the labial or facial surfaces at the
crevices of the teeth b$ acidic beverages ma$ eventuall$ sub'ect the pulp to
irritation and ma$ cause permanent damage.
Bac$eia
The most common cause of pulp in'ur$ is bacterial. 3acteria and
their products ma$ enter the pulp through a brea. in dentin, either from
caries or from accidental e!posure, from percolation around the restoration
or from anachoretic effect.
Acc%&in' $% In'le
The causes of pulpal inflammation, necrosis and d$stroph$ can be
arranged in a logical se*uence beginning with the most fre*uent irritant
microorganisms.
%
;ithout *uestion, bacterial invasion from a carious lesion is the most
fre*uent cause of pulpal inflammation. :n increase in automobile and c$cle
accidents, as well as accidents from bod$ contact sports, has also brought
about an increase in pulp death due to trauma. -arado!icall$, an alarming
amount of pulp involvement is induced b$ the ver$ dental treatment
designed to repair the carious lesion.
Acc%&in' $% Nich%ll(s
icholl<s has given the causes of pulpal diseases as:
:) 0auses unassociated with dental procedures.
3) 0auses associated with dental procedures.
III) DISEASES OF THE DENTAL PULP
&isease is the state of discomfort of an organ. -ulp has been
described as a highl$ resistant organ and as an organ with little or no
resistance. )ts resistance depends on cellular activit$, nutritional suppl$, age
and other metabolic and ph$siologic parameters.
:ge causes important changes in the pulp. The continuous deposition
of secondar$ dentin throughout the life of the pulp and deposition of dentin
in response to stimuli, reduce the si(e of the pulp chambers and root canals
and thereb$ reducing the volume. The decrease in pulp volume reduces the
cellular, vascular and neural content of the pulp and the pulp undergoes
atroph$.
The first and foremost reaction of pulp tissue to irritation is
=)nflammation>, but the basic disease process that is involved in pulp and
periapical disease is =)nfection>.
6
8en.in defined inflammation as =the comple! vascular, l$mphatic
and local tissue reaction to an irritant>. ;hereas, infection is the reaction to
a viable irritant i.e. microorganism. The term inflammation and infection is
not interchangeable. The patient can have an inflammator$ response
without having an infection however, the converse is not valid.
I)) CLASSIFICATION
0linical classification of pulpal diseases is based primaril$ on the
diseases. 8ost of the authors have come to a conclusion that, little or no
correlation e!ists between histopathological findings and the e!isting
s$mptoms. The value of the clinical classification lies in its use b$ the
clinician to determine the appropriate care and treatment, the endodontic
prognosis and probabl$ the restorative needs of the tooth.
Acc%&in' $% G%ss!an
&iseases of the pulp has been classified as:
I] P#l*i$i&es +in,la!!a$i%n)
:. +eversible 1. :cute 2s$mptomatic).
2. 0hronic 2as$mptomatic)
3. )rreversible 1. :cute
a. :bnormall$ responsive to cold.
b. :bnormall$ responsive to heat.
2. 0hronic
a. :s$mptomatic with pulp e!posure
b. ,$perplastic pulpitis.
c. )nternal resorption.
?
II] P#l* De'enea$i%n
:. 0alcific 2radiographic diagnosis).
3. 1thers 2histopathologic diagnosis).
III] P#l* Nec%sis
Acc%&in' $% Fan-lin .eine
The inflammator$ disease of the pulp are:
I] In,la!!a$%y &iseases %, $he &en$al *#l*
:. ,$peralgesia 2+eversible pulpitis, h$peractive pulpalgia,
h$persensitivit$).
1. ,$persensitive dentin.
2. ,$peraemia.
3. -ainful pulpitis
1. :cute pulpitis.
2. #ubacute pulpitis.
0. on painful pulpitis
1. 0hronic ulcerative pulpitis 2due to caries).
2. 0hronic pulpitis 2carious lesion absent).
". 0hronic h$perplastic pulpitis 2pulp pol$peptide).
II] A&&i$i%nal P#l* Chan'es
:. ecrosis 2se*uela to inflammator$ or retrogressive changes).
3. +etrogressive changes 2degeneration).
1. :troph$ and fibrosis.
2. &$strophic calcification 2calcific degeneration).
@
0. )nternal resorption.
Acc%&in' $% F/0/ Ha$y
0linicians have re'ected previous comple! histopathological
classification and has developed a simple classification of the state of the
pulp.
1. ormal pulp.
2. +eversible pulpitis.
". )rreversible pulpitis.
%. -ulp necrosis.
Acc%&in' $% In'le
I] BACTERIAL
a. 0oronal )ngress : 1. 0aries.
2. Fracture complete and incomplete.
". on fracture trauma.
%. :nomalies of tooth development.
b. +adicular )ngress : 1. 0aries.
2. +etrogenic infection periodontal
poc.et and infection.
". ,ematogenic.
II] TRAUMATIC
:. :cute : 1. 0oronal fracture.
2. +adicular fracture.
". Aascular stasis.
B
%. 4u!ation.
6. :vulsion.
3. 0hronic : 1. :ttrition.
2. :brasion.
". Erosion.
III] IATROGENIC
:. 0avit$ preparation : ,eat of preparation, depth of preparation,
deh$dration, pulp horn e!tensions, pulp e!posure, haemorrhage etc.
3. +estorations : )nsertion, fracture complete and incomplete forces
of cementing, heat of polishing etc.
0. )ntentional e!tirpation.
&. -eriodontal curettage.
E. 1rthodontic movement.
F. Electrosurger$.
9. 4aser burn.
,. -eriradicular curettage.
). +hinoplast$.
C. 1steotom$.
D. )ntubation.
I)] CHEMICAL
:. Filling materials cements, etching agents, bonding agents etc.
3. &isinfectants silver nitrate, phenol, sodium fluorides.
0. &esiccants alcohol, ether and others.
)] IDIOPATHIC
:. :ging.
E
3. )nternal resorption.
0. E!ternal resorption.
&. ,ereditar$ h$pophosphataemia.
E. #ic.le cell anaemia.
F. ,erpes (oster infection.
9. ,)A and :)&#.
Acc%&in' $% Nich%lls1
3acterial
:. 0auses unassociated with dental procedures / 8echanical
0hemical
8echanical
3. 0auses associated with dental procedures / Thermal
Electrical
4et us discuss each individual pulpal pathologies
2) Re3esi4le *#l*i$is
Definition : )t is a mild to moderate inflammator$ condition of the pulp
caused b$ no!ious stimuli in which the pulp is capable of returning to the
uninflamed state following removal of the stimuli.
)t is one of the earliest form of pulpitis and at one time referred to as
=pulp h$peraemia>.
Ca#ses : +eversible pulpitis ma$ be caused b$ an$ agent that is capable of
in'uring the pulp. The causes could be:
a) trauma as from a blow or from a disturbed occlusal relationship.
15
b) thermal shoc. as from preparing a cavit$ with a dull bur or .eeping
the bur in contact with the tooth for too long or from overheating
during polishing of a filling.
c) e!cessive deh$dration.
d) galvanism.
e) chemical stimulus as from sweet or sour foods or from irritation of
a silicate or self curing acr$lic filling.
f) bacteria as from caries.
g) circulator$ disturbances during pregnanc$ ma$ also result in
transient periodic h$peraemia.
h) local vascular congestion/associated with common cold or with sinus
disease can cause a generali(ed transient h$peraemia of the ma!illar$
posterior teeth.
The irritant that causes h$peraemic or mild inflammation in one pulp
ma$ produce secondar$ dentin in another, if the irritant is mild enough or if
the pulp is vigorous enough to protect itself.
Symptoms
#$mptomatic reversible pulpitis is characteri(ed b$ sharp pain
lasting for a moment. )t is more often brought on b$ cold than hot food or
beverages and b$ cold air. )t does not occur spontaneousl$ and does not
continue when the cause has been removed. :s$mptomatic reversible
pulpitis ma$ result from incipient caries and is resolved on removal of the
caries and proper restoration of the tooth.
11
Histopathology
+eversible pulpitis ma$ range from h$peraemia to mild to moderate
inflammator$ changes limited to the area of the involved dentinal tubules,
such as dentinal caries. 1ne sees reparative dentin, dilated blood vessels,
e!travasation of edema fluid and the presence of chronic inflammator$
cells. :lthough chronic inflammator$ cells predominate, one ma$ also see
acute inflammator$ cells.
Diagnosis
&iagnosis is b$ a stud$ of the patients s$mptoms and b$ clinical
tests. The pain is sharp, lasts for a few seconds and generall$ disappears
when the stimulus is removed. 0old, sweet or sour usuall$ causes the pain.
#ometimes, the pain ma$ become chronic and ma$ continue for wee.s or
even months. )nflamed pulp is sensitive to thermal changes, particularl$
cold. :pplication of cold is the least method of locating and diagnosing the
involved tooth. Tooth with reversible pulpitis reacts normall$ to percussion,
palpation, mobilit$ and the periapical tissue is normal on radiographic
e!amination.
Differential Diagnosis
+eversible pulpitis can be differentiated from irreversible pulpitis
because of its characteristic s$mptoms of sharp onset of pain lasting for a
few seconds. Thermal tests are useful in locating the affected tooth as
reversible pulpitis responds readil$ to cold. Electric pulp test is an e!cellent
corroborating test.
Treatment
-revention is the best treatment for reversible pulpitis. -eriodic care
to prevent the development of caries, earl$ insertion of a filling if a cavit$
12
has developed, use of a cavit$ varnish or a cement base before insertion of a
filling and care in cavit$ preparation and polishing are recommended to
prevent pulpitis.
;hen reversible pulpitis is present, removal of the no!ious stimuli
usuall$ suffices. )nspite 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
earl$ enough. 1therwise, the condition ma$ develop into irreversible
pulpitis.
5) Ie3esi4le *#l*i$is
Definition )rreversible pulpitis is a persistent inflammator$ condition of
the pulp, s$mptomatic or as$mptomatic, caused b$ a no!ious structures.
:cute irreversible pulpitis e!hibits pain usuall$ caused b$ hot or cold
stimulus, or pain that occurs spontaneousl$. The pain persists for several
minutes to hours, lingering after removal of the thermal stimulus.
Causes : The most common cause of irreversible pulpitis is bacterial
involvement of the pulp through caries although an$ clinical factor,
chemical, thermal or mechanical, mentioned alread$ as a cause of pulp
disease ma$ also cause pulpitis. :s previousl$ stated, reversible pulpitis
ma$ deteriorate into irreversible pulpitis.
Symptoms
)n the earl$ stages, a paro!$sm of pain ma$ be caused b$ sudden
temperature changes, particularl$ cold, sweet or acid food stuffs, pressure
from pac.ing food into a cavit$ and on l$ing down, which results in
congestion of the blood vessels of the pulp. The pain often continues when
1"
the cause has been removed and it ma$ come and go spontaneousl$, without
an apparent cause. The patient ma$ describe the pain as sharp, piercing or
shooting and it is generall$ severe. )t ma$ be intermittent or continuous
depending on the degree of pulpal involvement and depending on whether it
is related to an e!ternal stimulus. 0hanges in position that is on bending or
l$ing down e!acerbates the pain because of changes in intrapulpal pressure.
The patient ma$ also have pain referred to the ad'acent teeth, to the temple
or sinuses when an upper posterior tooth is involved or to the ear when a
lower posterior tooth is affected. -atients are often .ept awa.e at night b$
the pain, which continues to be intolerable despite all their efforts at
analgesia. :pical periodontitis is absent e!cept in the later stages, when
inflammation or infection e!tends to the periodontal ligament.
Histopathology
This disorder has both acute and chronic inflammator$ changes.
There is a continuous vasodilatation, accompanied b$ the accumulation of
edema fluid in the connective tissue surrounding the tin$ tissue. The
pavementing of pol$morphonuclear leucoc$te cells becomes apparent along
the walls of the vascular channels and rapidl$ migrate through the
endothelium lined structures in increasing numbers. 4arge number of white
blood cell collection ma$ be found beneath the area of carious penetration.
1dontoblasts in this area are destro$ed.
There is a locali(ed destruction of the pulp b$ pol$morphonuclear
leucoc$te cells and formation of microabscess .nown as pulp abscess
containing pus arising from the brea.down of leucoc$tes and bacteria as
well as from digestion of tissue. )f the carious process continues to advance
and penetrate the pulp, the histologic picture changes. The area of
ulceration is seen 2chronic ulcerative pulpitis) that drains through the cavit$
1%
and reduces the intrapulpal pressure and thereb$ the pain. :ccording to
#elt(er and 3ender, a possible mechanism b$ which a high concentration of
antigens in the carious process ma$ induce the formation of
immunoglobulins. :n immune antigen antibod$ precipitate in the presence
of complement, attracts pol$morphonuclear leucoc$tes followed b$
phagoc$tosis and cell degeneration with the release of l$so(omes in pulp
tissue.
The liberation of proteases b$ l$so(omes results in the formation of a
pulp abscess. 0hanges in odontoblastic la$er var$ from disruption to total
destruction. )rreversible pulpitis progresses to necrosis.
Diagnosis
)nspection generall$ discloses a deep cavit$ e!tending to the pulp or
deca$ under a filling. The pulp ma$ alread$ be e!posed. The surface of the
pulp is eroded and an odour of decomposition is fre*uentl$ present in this
area. -robing into this area is not painful until the deeper areas of the pulp
are reached. :t this level, both pain and haemorrhage ma$ occur.
+adiographic e!amination ma$ not show an$thing of significance
that is not alread$ .nown clinicall$. )t ma$ disclose an interpro!imal cavit$
or caries under a filling threatening the integrit$ of the pulp.
)n the earl$ stages of irreversible pulpitis, the thermal test ma$ elicit
pain that persists after removal of the thermal stimulus. )n the late stages,
when the pulp is e!posed, it reacts feebl$ to heat and cold. The electric pulp
test induces a response with mar.ed variation in current from the normal.
+esults of e!amination for mobilit$, percussion and palpation tests are
negative.
16
Di,,een$ial Dia'n%sis
)rreversible pulpitis should be distinguished from reversible pulpits,
in that the pain produced b$ the thermal stimuli disappear as soon as the
stimuli is removed. ;hereas in irreversible pulpitis, the pain lingers after
the stimulus is removed or it can occur spontaneousl$.
Treatment
0onsists of complete removal of the pulp or pulpectom$ and the
placement of an intracanal medicament to act as a disinfectant or obtundent
such as cresatin, eugenol or formocresol. #urgical 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 therap$ and restoration.
6) Ch%nic Hy*e*las$ic P#l*i$is +P#l* P%ly*e)
Definition : 0hronic h$perplastic pulpitis or Fpulp pol$pe< is a productive
pulpal inflammation due to an e!tensive carious e!posure of a $oung pulp.
This disorder is characteri(ed b$ the development of granulation tissue,
covered at times with epithelium and resulting from long standing, low
grade irritation.
Causes: #low, progressive carious e!posure is the cause. For the
development of pulp pol$pe, a large, open cavit$, a $oung resistant pulp
and a chronic low grade stimulus are necessar$. 8echanical irritation from
chewing and bacterial infection often provide the stimulus.
1?
Symptoms
)t is s$mptomless, e!cept during mastication, when pressure from the
food bolus ma$ cause discomfort.
Histopathology
8icroscopicall$, the pulp pol$pe is a comple! of new capillaries,
proliferating fibroblasts and inflammator$ cells. The tissue in the pulp
chamber is often transformed into granulation tissue, which pro'ects from
the pulp into the carious lesion. The granulation tissue is $oung vascular
connective tissue containing pol$morphonuclear neutrophils, l$mphoc$tes
and plasma cells. The pulp tissue is chronicall$ inflamed. #upport for the
protruding mass is provided b$ the collagenous fibres rooted in the deeper
pulp tissue of the chamber. #ensor$ nerve elements are almost absent near
the surface in contrast to the rich innervation and e!*uisite sensitivit$ of an
e!posed pulp which is not h$perplastic. #urface of the pol$pe is usuall$
covered b$ stratified s*uamous epithelium more commonl$ found in
deciduous teeth.
Diagnosis
This disorder is generall$ seen onl$ in the teeth of children and
$oung adults. The appearance of pol$pe tissue is clinicall$ characteristic as
a flesh$, reddish, pulpal mass which fills most of the pulp chamber or
cavit$ or e!tends be$ond the confines of the tooth. :t times, the mass is
large enough to interfere with the comfortable closure of the tooth. 0utting
of this tissue does not cause pain but pressure thereb$ transmitted to the
apical end of the pulp does cause pain.
+adiographs show a large open cavit$ with direct access to the pulp
chamber. The tooth ma$ respond feebl$ or not at all to the thermal tests
1@
unless e!treme cold such as eth$l chloride spra$ is used. 8ore current than
normal ma$ be re*uired to elicit a response b$ means of electric pulp
testing.
Differential Diagnosis
The appearance of h$perplastic pulpitis is characteristic and should
be easil$ recogni(ed. The disorder must be distinguished from proliferating
gingival tissue.
Treatment
Efforts at treatment should be directed towards elimination of the
pol$pe tissue followed b$ e!tirpation of the pulp, provided the tooth can be
restored. ;hen the h$perplastic pulpal mass has been removed with a
periodontal curette or spoon e!cavator, the bleeding can be controlled with
pressure. The pulp tissue of the chamber is then completel$ removed and a
dressing of formocresol is sealed in contact with the radicular pulp tissues.
The radicular pulp is e!tirpated at a later visit. )f time permits, the entire
procedure of pulpectom$ 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 ade*uate restoration.
7) In$enal Res%*$i%n
Definition : )nternal 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 .nown, but such patients
often have a histor$ of trauma.
1B
Symptoms
)nternal resorption in the root of a tooth is as$mptomatic. )n the
crown, it ma$ be manifested as a reddish area called =pin. spot>. This
reddish area represents the granulation tissue showing through the resorbed
area of the crown.
Histopathology
Gnli.e caries, internal resorption is the result of osteoclastic activit$.
The resorptive process is characteri(ed b$ lacunae which ma$ be filled in
b$ 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. 8ultinucleated giant cells or dentinoclasts are
present. The pulp is usuall$ chronicall$ inflamed. 8etaplasia of the pulp
that is transformation to another t$pe of tissue such as bone or cementum,
sometimes occurs.
Diagnosis
)nternal resorption ma$ affect either the crown or the root of the
tooth or it ma$ be e!tensive enough to involve both. )t ma$ be slow,
progressive e!tending over 1/2 $ears or it ma$ develop rapidl$ and
perforate the tooth within a matter of months. :lthough an$ tooth in the
mouth can be involved, those most readil$ recogni(ed are the ma!illar$
anterior teeth. Gsuall$ internal resorption is recogni(ed during routine
radiographic e!amination. The appearance of =pin. spot> occurs late in the
resorptive process, when the integrit$ of the crown has been compromised.
+adiographs show changes in the appearance of the walls in the root canal
or pulp chamber with a round or ovoid radiolucent area.
1E
Differential Diagnosis
;hen internal resorption progresses into the periodontal space and a
perforation of the root occurs, it is difficult to differentiate from e!ternal
resorption. )n internal resorption, the resorptive defect is more e!tensive in
the pulpal wall than on the root surface, this defect is usuall$ recogni(ed b$
means of a radiograph.
Treatment
E!tirpation of the pulp stops the internal resorptive process. +outine
endodontic treatment is indicated, but obturation of the defect re*uires a
special effort, preferabl$ with a plastici(ed gutta percha method. )n man$
patients, however, the conditions progresses unobserved because it is
painless, until the root is perforated. )n such a case, calcium h$dro!ide paste
is sealed in the root canal and is periodicall$ renewed until the defect is
repaired. +epair is completed when the calcific barrie is present. ;hen the
repair is completed, the canal with its defect is obturated with plastici(ed
gutta percha.
Prognosis
The prognosis is best before perforation of the root or crown occurs.
)n 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.
8) P#l* De'enea$i%n
&egeneration of the pulp is seldom recogni(ed clinicall$ and is
generall$ present in the teeth of older people. &egeneration ma$ also be the
result of persistent mild irritation in teeth of $ounger people. )t ma$ not
necessaril$ be related to infection or caries, although a cavit$ or a filling
25
ma$ be present in the affected tooth. The earl$ stages of pulp degeneration
does not usuall$ cause definite clinical s$mptoms. The tooth is not
discoloured, and the pulp ma$ react normall$ to electric and thermal tests.
:s the degeneration progresses, the tooth ma$ discolour and the pulp will
not respond to stimulation.
The specific t$pes of pulp degeneration are:
1) 0alcific degeneration.
2) :trophic degeneration.
") Fibrous degeneration.
1) Calcific Degeneration
)n calcific degeneration, part of the pulp tissue is replaced b$ calcific
material, that is pulp stones or denticles are formed. The calcification ma$
occur either within the pulp chamber or root canal, but it is generall$
present in the pulp chamber.
The calcified material has a laminated structure, and lies unattached
within the bod$ of the pulp. #uch a denticle or pulp stone ma$ become large
enough to give an impression of the pulp cavit$ when the calcified mass is
removed. )n another t$pe of calcification, the calcified material is attached
to the wall of the pulp cavit$ and is an integral part of it.
)t is not possible to distinguish one t$pe from another on a
radiograph.
-ulp stones, are considered harmless, although referred pain in few
patients has been described. 0alcification ma$ prevent the clinician from
reaching the apical foramen and ma$ therefore prevent complete
instrumentation of the root canal.
21
2) Atrophic Degeneration
)n this t$pe of degeneration, observed histopathologicall$ in pulps of
older people, fewer stellate cells are present and intercellular fluid is
increased. The pulp tissue is less sensitive than normal. o clinical
diagnosis e!ists.
) !i"rous Degeneration
This form of degeneration of the pulp is characteri(ed b$
replacement of the cellular elements b$ fibrous connective tissue. 1n
removal from the root canal, such a pulp has the characteristic appearance
of a leather$ fibre. This disorder causes no distinguishing s$mptoms to aid
in clinical diagnosis.
9) Nec%sis %, P#l*
Definition : ecrosis is death of the pulp. )t ma$ be partial or total,
depending on whether part of or the entire pulp is involved. ecrosis is
normall$ the se*uel to inflammation but it can also occur following a
traumatic in'ur$ in which the pulp is destro$ed before an inflammator$
reaction can ta.e place. :s a result, an ischaemic infarction can develop and
ma$ cause a dr$ gangrenous necrotic pulp.
ecrosis is of two t$pes:
a) 0oagulation and b) 4i*uefaction.
1) )n coagulation necrosis, the soluble portion of tissue is precipitated or is
converted into a solid mass. 0aseation is a form of coagulation necrosis
in which the tissue is converted into a chees$ mass consisting chiefl$ of
coagulation proteins, fats and water.
22
2) 4i*uefaction necrosis results when proteol$tic en($mes convert the
tissue into a softened mass, a li*uid, or amorphous debris.
Cause: ecrosis of the pulp can be caused b$ an$ no!ious insult in'urious
to the pulp such as bacteria, trauma and chemical irritation.
Symptoms
ecrotic pulp causes no painful s$mptoms. &iscolouration of the
tooth is the first indication that the pulp is dead. The tooth lac.s its usual
brilliance, lustre and translucenc$. The presence of a necrotic pulp ma$ be
discovered onl$ b$ chance, because such a tooth is as$mptomatic. Teeth
with partial necrosis can respond to thermal changes, owing to the presence
of vital nerve fibres passing through the ad'acent inflamed tissue.
Diagnosis
-ain is absent in a tooth with total necrosis. #welling, mobilit$ and
response to percussion and palpation are negative. There is no response to
vitalit$ tests as well.
Histopathology
ecrotic pulp tissue, cellular debris and microorganisms ma$ be seen
in the pulp cavit$. The periapical tissue ma$ be normal or slight evidence of
inflammation of the apical periodontal ligament ma$ be present.
Treatment
-roper 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 therap$
is instituted.
2"
)I) C%ncl#si%n
To understand pulpal patholog$, we must have a thorough
.nowledge of what is considered as normal. The stud$ of pulpal diseases
and their causative factors provides the clinician with a scientific basis for
diagnosis and treatment which leads to successful endodontic therap$.
)II) Re,eences
1. Endodontic -ractice 211
th
Edition) 1EE1 4ouis ). 9rossman,
0arlos &el +io. 4ea and Febiger -ublications.
2. Endodontics in clinical practice 2"
rd
edition) 1EE5 F.C. ,art$
23utterworth and 0o.).
". Endodontics 2%
th
edition) 1EB6 Cohn ). )ngle 2;illiams and
;il.ins).
%. Endodontic Therap$ 26
th
edition) 1EE? Fran.lin #. ;eine
28osb$ -ublications).
2%
CONTENTS
)) )ntroduction
))) 0auses of -ulp &isease
)))) &iseases of the &ental -ulp
)A) 0lassification of -ulpal &iseases
A)
1) +eversible -ulpitis
2) )rreversible -ulpitis
") 0hronic ,$perplastic -ulpitis
%) )nternal +esorption
6) -ulp &egeneration
?) ecrosis of -ulp
A)) 0onclusion
A))) +eferences
26