diseases of the pulp

Diseases of the PulpDr. Nithin Mathew

Diseases of the Pulp – Dr. Nithin Mathew

CONTENTS

• Introduction• Pathophysiology• Classification• Etiological Agents

• Mechanical• Thermal• Electrical• Bacterial

• Diseases of the pulp• Reversible Pulpitis• Irreversible Pulpitis• Chronic Hyperplastic Pulpitis

• Internal Resorption• Pulp Degeneration• Pulp Necrosis

• Conclusion• References

D i s e a s e s o f t h e P u l p 3

Introduction


• Dental pulp – formative organ of the tooth which produces• Primary dentin during development of the tooth• Secondary dentin after the tooth eruption• Reparative dentin in response to stimulation as long as the odontoblasts remain

intact.

• Pulp consists of• Tiny blood vessels• Lymph• Myelinated and unmyelinated nerve fibres, etc..



• Reacts to bacterial infection or other stimuli by an inflammatory response.

• Inflammatory response of the pulp is altered by some unique features of the pulp:

• Encased by a hard tissue (enamel/dentin)• Does not allow for usual swelling associated with exudate of acute inflammatory

response.

• Lack of collateral circulation• To maintain the vitality when primary circulation is compromised.

• Response to any stimuli only as pain• Temp. of 16-55°C is well tolerated by the pulp• Temp. above this is perceived as pain



• Referred pain• Localizing affected tooth is difficult as proprioceptive nerve fibres are absent in the

pulp.

• Relating clinical status of the tooth to histopathology is very difficult as there are no signsor tests that correlate the two.


Pathophysiology of Pulpal Disease

Diseases of the Pulp – Dr. Nithin Mathew 9

External Noxious Stimuli

Pulp

Mast Cells Vasculature Cells

Release of Inflammatory Mediators (Histamine, Prostaglandins, Bradykinins)

Degranulation Decreased Blood Flow

Cellular Damage


Release of Inflammatory Mediators (Histamine, Prostaglandins, Bradykinins)

Dilatation of Arterioles

Increased Pulpal Pressure & Secondary Compression of Venous Return

Vessel Damage, Pulpal Inflammation, Tissue Necrosis

Localized pulpal damage will spread to involve the entire pulp


Irritation to Clinical Crown

Localized Pulpal Inflammation

Increased Local Tissue Pressure

Venous Collapse – Ichemia – Local Necrosis

Release of Intercellular Inflammatory Agents

Circumferential Vascular Disturbances

Increases Tissue Pressure

Necrosis of Additional Tissue Total Pulpitis

Initial Insult

Localized Effect

Mechanism Spread

Classification of Pulpal Diseases


Grossman’s Classification

1. Pulpitis (Inflammatory Diseases)i. Reversible

a. Acute (symptomatic)b. Chronic (asymptomatic)

ii. Irreversiblea. Acute

i. Abnormally responsive to coldii. Abnormally responsive to heat

b. Chronica. Asymptomatic with pulp exposureb. Hyperplastic pulpitisc. Internal resorption

2. Pulp Degenerationi. Calcificii. Atrophiciii. Fibrous

3. Pulp Necrosis



Seltzer & Bender’s Classification

• Found little correlation between clinical symptoms and histologic appearance.

• They correlated the results of clinical tests of the pulp with the histologic diagnosis:

Treatable:• Intact uninflammed pulp• Transitional stage• Atrophic pulp• Acute pulpitis• Chronic partial pulpitis without necrosis

Untreatable:• Chronic partial pulpitis with necrosis• Chronic total pulpitis• Total pulp necrosis



Baume’s Classification

• Found no direct correlation between clinical symptoms and histologic findings.

• Based on clinical symptoms :

1. The symptomless, vital pulp which has been injured or involved by deep caries, forwhich pulp capping may be done

2. Pulps with a history of pain which are amenable to pharmacotherapy3. Pulps indicated for extirpation and immediate root filling4. Necrosed pulps involving infection of radicular dentin accessible to antiseptic root

canal therapy



F.J. Harty’s Classification

• Clinicians have rejected previous complex histopathological classification and hasdeveloped a simple classification of the state of the pulp.

1. Normal pulp2. Reversible pulpitis3. Irreversible pulpitis4. Pulp necrosis



Cohen’s Classification

1. Reversible Pulpitis2. Irreversible Pulpitis3. Asymptomatic Irreversible Pulpitis4. Hyperplastic Pulpitis5. Internal Resorption6. Symptomatic Irreversible Pulpitis7. Pulp Necrosis



WHO Classification

K04.0 : Pulpitis/pulpal hyperemia/pulpal abscess/pulp polyp, acute/chronichyperplastic/ulcerative pulpitis

K04.1 : Necrosed pulp/pulp gangrene

K04.2 : Pulp degeneration, Denticles/pulp calcification

K04.3 : Abnormal hard tissue formation in pulp secondary or irregular dentin.



Classification by Morse et al (1977)

• Vital asymptomatic• Hypersensitive dentin• Inflamed – reversible• Inflamed/degenerating without radiolucent periapical area - irreversible• Inflamed/degenerating with radiolucent periapical area - irreversible• Necrotic without radiolucent periapical area• Necrotic with radiolucent periapical area


Etiology


According to Grossman

Physical

I. Mechanical1. Trauma

i. Accidentalii. Iatrogenic

2. Pathologic Wear3. Crack tooth syndrome4. Barodontalgia


II. Thermal1. Heat from cavity preparation2. Exothermic heat from setting of cement3. Conduction of heat & cold through deep

filling without a protective base4. Frictional heat caused due to polishing

of restoration


Chemical

1. Phosphoric acid, acrylic monomer, etc2. Erosion (acids)

Bacterial

1. Toxins associated with caries2. Direct invasion of pulp from caries/trauma3. Microbial colonization in the pulp by blood borne micro-organisms (Anachoresis)



According to Ingle

Bacterial

• Coronal Ingress:1. Caries2. Fracture – complete and incomplete3. Non fracture trauma4. Anomalies of tooth development.

• Radicular Ingress:1. Caries2. Retrogenic infection – periodontal pocket

and infection3. Hematogenic


Traumatic• Acute :

1. Coronal fracture2. Radicular fracture3. Vascular stasis4. Luxation5. Avulsion

• Chronic :1. Attrition2. Abrasion3. Erosion


Iatrogenic

1. Cavity preparation: Heat of preparation, depth of preparation, dehydration, pulphorn extensions, pulp exposure, haemorrhage etc.

2. Restorations: Insertion, fracture – complete and incomplete forces of cementing, heatof polishing etc.

3. Intentional extirpation4. Periodontal curettage5. Orthodontic movement6. Electrosurgery7. Laser burn8. Rhinoplasty9. Osteotomy10. Intubation



Chemical• Filling materials – cements, etching agents, bonding agents etc.• Disinfectants – silver nitrate, phenol, sodium fluorides• Desiccants – alcohol, ether and others

Idiopathic• Aging• Internal resorption• External resorption• Hereditary hypophosphataemia• Sickle cell anaemia• Herpes zoster infection• HIV and AIDS



According to Nicholl

• Nicholl’s has given the causes of pulpal diseases as:

• Causes unassociated with dental procedures• Causes associated with dental procedures



Physical Causes – Mechanical Injuries

Trauma

• May or may not be accompanied by fracture of the crown or root• Injury may be Accidental / Iatrogenic

• Accidental• Violent blow during a fight, sports, automobile accident or household accident.• Habits like bruxism, nail and thread biting.

• Iatrogenic• During cavity preparation or excavation of caries.• Rapid orthodontic tooth movement.• Pins used to retain amalgam restorations.



Pathologic Wear

• Pulp may also become exposed or nearly exposed by pathologic wear of the teeth• Attrition• Abrasion• Bruxism• Abfraction

• Occlusal trauma may also injure the pulp because of repeated irritation to theneurovascular bundle in the periradicular area.



Cracked Tooth Syndrome

• Incomplete fractures - body of the tooth - pain of idiopathicorigin.

• Pain ranging from mild to excruciating at the irritation orrelease of the biting pressure.

• Diagnosis - made by reproducing the pain by asking the patientto bite on a rubber wheel or a tooth sloth.

• Cracked enamel is visualized using a dye or bytransilluminating the tooth with fiberoptic light.



Barodontalgia

• Pain experienced in the tooth due to low atmospheric pressure

• Irreversible Pulpitis• Symptomless at ground level• Pain at high altitude due to reduced pressure


During ascent, trapped gases may expand and enter the dentinal tubules which stimulate the nociceptors in the pulp.

Movement of the contents of the pulp chamber through the apex of the tooth causes pain


Physical Causes – Thermal Injuries

Heat from Cavity Preparation

• Temp. changes produced during cavity preparation

• Increase of 20°C in temperature 1mm from the pulp• Increase of 30°C, 0.5mm from the pulp during dry cavity preparation

• High speed tungsten carbide/diamond bur – reduce operating time but accelerates pulpaldeath if used without a coolant.

• Heat generated is sufficient to cause irreparable pulp damage.



• Degree of pulpal response is inversely proportional to Remaining Dentin Thickness (RDT)

• RDT – key factor – determining if the changes are reversible or irreversible.

• Pulp horn extensions must be considered during cavity preparation

• Constant drying can also cause pulpal inflammation and necrosis.



Heat Conduction by fillings

• Metallic fillings close to the pulp without an intermediate base may conduct thetemperature changes rapidly to the pulp and may destroy the pulp.

Frictional Heat during Polishing

• Enough heat may be generated during polishing of a restoration or during setting of acement. – Transient Pulpal Injury

• Usually Reversible in nature



Physical Causes – Electrical Agents

• Galvanic current produced from dissimilar metallic restoration may generate heat andcause pulpal damage.



Chemical Agents

• Pulpal damage arise as a result of chemical irritation of pulp caused by• Erosion or use of acidic restorative materials

• Key factors determining pulpal reaction to a restorative material :• Acidity (pH of the material)• Heat generated during setting reaction• Remaining dentin thickness• Absorption of water during setting reaction• Poor marginal adaptation of the material which contributes to bacterial leakage.

• Long term prognosis of a restorative material – determined by its ability to inhibit micro-leakage and pulpal bacterial contamination



Bacterial Agents

• Most common cause of pulpal injury.

• Bacteria enter the pulp through:• Break in the dentin (caries/accidental exposure)• From developmental grooves• From percolation around a restoration• From extension of infection• Through open blood vessels/lymphatics during infections diseases/bacteremia• From gingiva

• Presence or absence of bacterial irritation is the determining factor in pulp survival oncethe pulp has been mechanically exposed.



Anachoresis

• Microbial contamination of the pulp by blood borne micro-organisms

• Bacteria circulating in blood stream tend to accumulate at sites of pulpal inflammation(following a mechanical / chemical injury to the pulp)

• One probable cause for this phenomenon is increased capillary permeability in this area


Diseases of Dental Pulp


Sequelae of Pulpal Disesaes

39

Normal Pulp

Reversible Pulpitis

Irreversible Pulpitis

Chronic Hyperplastic

Pulpitis

Symptomatic Irreversible

Pulpitis

Asymptomatic Irreversible

Pulpitis

Internal Resorption

Pulpal Necrosis

Calcific Degeneration/Calcific Metamorphosis

Stimuli Causing Degenerating

pulpal changes

Noxius Stimuli


Reversible Pulpitis

Mild to moderate inflammatory condition of the pulp caused bynoxious stimuli in which the pulp is capable of returning to the uninflamed state followingremoval of the stimuli.

Etiology

• Trauma – blow / disturbed occlusal relation• Thermal shock• Excessive dehydration• Chemical irritation – sweet/sour food• Galvanism• Excessive orthodontic forces


R e v e r s i b l e P u l p i t i s


• Slow progressive chronic lesion• Local vascular congestion• Circulatory disturbances

• Irritant that causes hyperaemic or mild inflammation in one pulp may produce secondarydentin in another, if the irritant is mild enough or if the pulp is vigorous enough to protectitself.




Symptoms

• Short sharp pain lasting for a moment

• Does not occur spontaneously and does not continue when the cause has been removed.

• Most often brought on by cold than hot food or beverages and by cold air.




Diagnosis

Diagnosis is by a study of the patients symptoms and by clinical tests.

• Pain:• 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.

• Visual examination and history:• Examine for caries, restorations, fractures or traumatic occlusion.• A history of past dental treatment and history of subjective symptoms.




• Percussion:• Reacts normally to percussion, palpation and mobility

• Radiograph:• Periapical tissue is normal on radiographic examination.

• Vitality test:• Hyperalgesic pulp responds more readily to cold stimulation than normal teeth.• Electric pulp testing requires minimal current to initiate positive response, due to

increased excitability of Aδ- fibres.




Histopathology

Reversible pulpitis may range from hyperaemia to mild to moderate inflammatorychanges limited to the area of the involved dentinal tubules.

Histological changes:

• Reparative dentin• Disruption of odontoblasts• Dilated blood vessels• Extravasation of edema fluid• Chronic inflammatory cells




Differential Diagnosis

• Can be differentiated from irreversible pulpitis because of its characteristic symptoms ofsharp onset of pain lasting for a few seconds.

• Thermal tests are useful in locating the affected tooth as reversible pulpitis respondsreadily 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 restoration if a cavity has developed• Use of a cavity varnish or a cement base before insertion of a restoration• Care in cavity preparation and polishing

• Once the symptoms has subsided, tooth must be tested for vitality to make sure that pulpnecrosis hasn’t occurred.




Prognosis

• Favourable if the irritant is removed early enough.

• Otherwise, the condition may develop into irreversible pulpitis.




Irreversible Pulpitis

Persistent inflammatory condition of the pulp, symptomatic orasymptomatic in nature with the pulp becoming incapable of healing.

Types:• Symptomatic• Asymptomatic

Etiology• Most common - bacterial involvement of the pulp• Chemical, thermal or mechanical injuries• Reversible pulpitis, if not treated may deteriorate into irreversible pulpitis.


I r r e v e r s i b l e P u l p i t i s


Symptoms

• 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.

• Pain persists for several minutes to lingering after the removal of the stimulus.

• Pain is described as sharp, piercing or shooting and it is generally severe.

• Changes in position that is on bending or lying downexacerbates the pain because of changes in intrapulpal pressure.




• Referred pain to the adjacent teeth, to the temple or sinuses when an upper posterior toothis involved or to the ear when a lower posterior tooth is affected.

• Later stages, pain is severe, described as boring, gnawing or throbbing.

• Nocturnal pain, which is intolerable despite their efforts at analgesia.

• Apical periodontitis is absent except in the later stages, wheninflammation or infection extends to the periodontal ligament.




Diagnosis

Diagnosis is by a study of the patients symptoms and by clinical tests.

• Pain:• Pain may be mild to severe or even excruciating throbbing.• Is generally diffuse and readily not localized by the patient.• Pain lingers after the primary irritant has been removed.• Pain may be referred to other areas.

• Visual examination and history:• Deep cavity extending to the pulp.• Decay under a restoration.




• Percussion:• Tenderness implies an increased intrapulpal pressure, as a result of hyperactive

exudative (acute) inflammatory tissue.• Widening of the periodontal ligament space without percussion tenderness implies

a non-painful state.

• Radiograph:• May not show anything of significance.• May disclose an interproximal cavity or caries

under a filling threatening the integrity of the pulp.




• Vitality test:• Thermal test:

• May respond in the same as reversible pulpitis, but pain may persist after thestimulus is removed.

• As pulpal inflammation progresses, heat will intensify the responses because ithas an expansive effect on the blood vessels, tissue and gaseous products ofproteolysis.

• Cold will tend to relieve the pain in advanced stages of pulpits, because, it has a contractileeffect on the remaining central or apical functional vascular bed, reducing the intrapulpalpressure.




• Electric Pulp test:• A response to less current may be expected in early stages because of low

threshold of peripheral Aδ-fibres.

• As the tissue becomes more necrotic, more current is required.

• This test may not be diagnostic in advanced cases of acute pulpalgia, because of mixedresponses, particulary multirootd teeth.




Histopathology

• Has both acute and chronic inflammatory changes.

• Continuous vasodilatation

• Accumulation of edema fluid in the connective tissuesurrounding the tiny tissue

• White blood cell collection may be found beneath the area ofcarious penetration

• Odontoblasts are destroyed

• Localized destruction of the pulp by polymorphonuclearleucocyte cells and formation of micro-abscess.





• One must differentiate between reversible and irreversible pulpitis.

• Asymptomatic Stage:• Exposed pulp exhibits little/no pain except when food in packed.• Hence more current is required to elicit a response to EPT than in control tooth.

• Early symptomatic Stage:• Less current is required to elicit a response in EPT than normal.• Pulp is abnormally responsive to cold• Induced/spontaneous pain that occurs is sharp and piercing.




• Later Stages:• Symptoms may simulate those of acute alveolar abscess.

• Abscess is differentiated from irreversible pulpitis, such that abscess will have:• Swelling• Tenderness on percussion• Mobility• Lack of response to vitality tests• Systemic symptoms: fever or nausea




Treatment

• Complete removal of the pulp or pulpectomy and the placement of an intracanalmedicament to act as a disinfectant or obtundent

• Extraction should be considered if the tooth is unrestorable.




Prognosis

• Favourable if the pulp is removed and the tooth undergoes proper endodontic therapy andrestoration.




Chronic Hyperplastic Pulpitis

Productive pulpal inflammation due to an extensive carious exposure of ayoung pulp.

• Characterized by the development of granulation tissue, covered at times with epitheliumand resulting from long standing, low grade irritation.

Etiology• Slow, progressive carious exposure.• For the development of pulp polyp, 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.


C h r o n i c H y p e r p l a s t i c P u l p i t i s


Symptoms

• Symptomless, except during mastication, when pressure from the food bolus may causediscomfort.




Diagnosis

• Generally seen only in the teeth of children and young adults.

• Polyp tissue is clinically characteristic as a fleshy, reddish, pulpal mass which fills most ofthe 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 apicalend of the pulp does cause pain.

• Differentiated from gingival overgrowth by tracing the stalk of the polypoid tissue.




• Radiograph:• Show a large open cavity with direct access to the pulp chamber.

• Vitality test:• Thermal test:

• Tooth may respond feebly or not at all to the thermal tests unless extreme coldsuch as ethyl chloride spray is used.




Histopathology

• Surface is covered by stratified squamous epithelium.

• Tissue in the pulp chamber is transformed into granulation tissue.

• Granulation tissue is young vascular connective tissue containingpolymorphonuclear neutrophils, lymphocytes and plasma cells.

• Pulp tissue is chronically inflamed.





• Appearance of hyperplastic pulpitis is characteristic and should be easily recognized.

• The disorder must be distinguished from proliferating gingival tissue.




Treatment

• Hyperplastic pulpal mass is removed with a periodontal curette or spoon excavator andthe bleeding can be controlled with pressure.

• Pulp tissue of the chamber is then completely removed and a dressing of formocresol issealed 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

• Prognosis of the pulp is unfavourable but the prognosis of the tooth is favourable afterendodontic treatment and adequate restoration.




Internal Resorption

It is an idiopathic, slow or fast progressive resorptive process occuring in thedentin of the pulp chamber or root canals of teeth.

Etiology• The cause of internal resorption is not known, but such patients often have a history of

trauma.


I n t e r n a l R e s o r p t i o n


Symptoms

• Internal resorption in the root of a tooth is asymptomatic.

• Crown, it may be manifested as a reddish area called “pink spot”- Pink tooth of Mummery

• Reddish area represents the granulation tissue showing through the resorbed area of thecrown.




Histopathology

• Internal resorption is the result of osteoclastic activity.

• Resorptive process is characterized by lacunae which may be filled in by osteoid tissuewhich is regarded as an attempt at repair.

• Presence of granulation tissue accounts for the profuse bleeding when the pulp is removed.

• Multinucleated giant cells or dentinoclasts are present.

• Pulp is usually chronically inflamed.

• Metaplasia of the pulp that is transformation to another type of tissue such as bone orcementum, sometimes occurs.




Diagnosis

• May affect either the crown or the root of the tooth or it may be extensive enough to involveboth.

• May be slow, progressive extending over 1-2 years or it may develop rapidly and perforatethe tooth within a matter of months.

• Most readily seen in the maxillary anterior teeth.

• Radiograph:• Radiographs show changes in the appearance of the walls in the root

canal or pulp chamber with a round or ovoid radiolucent area.





• When internal resorption progresses into the periodontal space and a perforation of theroot occurs, it is difficult to differentiate from external resorption.

• Resorptive defect is more extensive in the pulpal wall than on the root surface.




Treatment

• Extirpation of the pulp stops the internal resorptive process.

• Routine endodontic treatment is indicated, but obturation of the defectrequires a special effort, preferably with a plasticized gutta perchamethod.

• In many patients, however, the conditions progresses unobservedbecause it is painless, until the root is perforated.

• In such a case, calcium hydroxide paste is sealed in the root canal and isperiodically renewed until the defect is repaired.

• Repair is completed when the calcific barrier is present, following whichthe canal with its defect is obturated with plasticized gutta percha.




Prognosis

• Prognosis is best before perforation of the root or crown occurs.

• If perforation occurs, prognosis is guarded and depends on the formation of a calcificbarrier or access to the perforation that permits surgical repair.




Pulp Degeneration

• Generally present in the teeth of older people.

• May also be seen in teeth of younger people as a the result of persistent mild irritation.

• Early stages of pulp degeneration shows no signs or symptoms.

• But as the degeneration progresses, the tooth may discolour and the pulp will not respondto stimulation.

Types:

• Calcific degeneration• Atrophic degeneration• Fibrous degeneration


P u l p D e g e n e r a t i o n


Calcific Degeneration

• Part of the pulp tissue is replaced by calcific material (pulp stones or denticles).

• Calcification may occur either within the pulp chamber or root canal, but it is generallypresent in the pulp chamber.

• Calcified material has a laminated structure, and lies unattached within the body of thepulp / even attached to the wall of the pulp chamber.

• It is not possible to distinguish one type from anotheron a radiograph.




• Classified according to :

• Position:• Free: pulp stones lie freely in the pulp tissue• Attached: pulp stones are attached to the dentinal walls• Embedded: pulp stones are encircled by dentin

• Structure:• True: pulp stones are similar to dentin having dentinal tubules and odontoblasts.• False: calcified masses arranged in lamellar fashion around a nidus and do not

contain dentinal tubules




• Degeneration of complete pulp space may occur as a sequelae to atraumatic injury - Calcific Metamorphosis.

• Such response to trauma is characterised by rapid deposition of hardtissue within the canal space.

• Teeth remains asymptomatic and may exhibit discoloration ofcrown.

• Obliteration is evident radiographically as an intracanal radio-opacity similar to surrounding dentin.




Atrophic 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.




Fibrous Degeneration

• Characterized by replacement of the cellular elements by fibrous connective tissue.

• Pulp has the characteristic appearance of a leathery fiber.

• No distinguishing clinical symptoms to aid in diagnosis.




Necrosis of Pulp

• Necrosis is death of the pulp.• May be partial or total, depending on whether part of or the entire pulp is involved.• Necrosis can be caused

• As the sequel to inflammation• Following a traumatic injury in which the pulp is destroyed before an inflammatory

reaction can take place.

Etiology:• Can be caused by any noxious insult injurious to the pulp

such as bacteria, trauma and chemical irritation.


N e c r o s i s o f P u l p


Types

• Coagulation Necrosis:• 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.

• Liquefaction Necrosis:• Necrosis which results when proteolytic enzymes convert the tissue into a softened

mass, a liquid, or amorphous debris.




• End Products of Pulp Decomposition:• Hydrogen Sulfide• Ammonia• Fatty Substances• Indicam• Water• Carbon Dioxide


• Intermediate Products of Pulp Decomposition:• Indole• Skatole• Putriciene• Cadaverine



Symptoms

• Necrotic pulp causes no painful symptoms.

• Discolouration of the tooth is the first indication that the pulp is dead.

• Tooth lacks its usual brilliance, lustre and translucency.

• Presence of a necrotic pulp may be discovered only by chance, because such a tooth isasymptomatic.

• Teeth with partial necrosis can respond to thermal changes, owing to the presence of vitalnerve fibres passing through the adjacent inflamed tissue.




Diagnosis

• Pain is absent in a tooth with total necrosis.

• Radiographs:• Thickened PDL space

• Swelling, mobility and response to percussion and palpation are negative.

• There is no response to vitality tests as well.

• Teeth with partial necrosis can respond to thermal changes, owing to the presence of vitalnerve fibres passing through the adjacent inflamed tissue.




Histopathology

• Necrotic pulp tissue, cellular debris and microorganisms may be seen in the pulp cavity.

• Periapical tissue may be normal or slight evidence of inflammation of the apicalperiodontal ligament may be present.




Treatment

• Proper treatment of necrosis is the thorough canal debridement.

• Obturation of the root canals.




Prognosis

• Prognosis of the tooth is favourable if proper endodontic therapy is done.



Features Reversible Pulpitis

Acute Pulpitis Chronic Pulpitis Hyperplastic Pulpitis

Pulp Necrosis

Pain &Stimulus

Mild pain lasting for a moment

Constant to severe pain caused by hot/cold stimuli

Mild and intermittent • No Pain• Bleeds profusely

due to rich vascularity

Not Present

Stimulus Heat, Cold or sugar Hot/cold/ spontaneous

Spontaneous

Pulp Test• Thermal Readily responds to

coldAcute pain to hot stimuli

No response No response No response

• Electric Normal response Normal to elevated response

More current is required

More current is required

In Liquefaction necrosis – positive response with EPT

Radiograph • Deep caries• Defective

restoration

• Deep caries• Defective

restoration

• Chronic apical periodontitis

• Local condensing osteitis

• Chronic apical periodontitis

• Local condensing osteitis

Sometimes Apical Periodontitis or Condensing osteitis

Treatment • Removal of Decay

• Restn with Pulp protection

• Pulpotomy• RCT

• RCT• Extraction of non-

restorable tooth

• Removal of polypoid tissue followed by RCT


Conclusion

• Pulp is also a formative and highly resistant organ of the tooth.

• Pulp is among the most densely innervated and vascularised tissues in the human body.

• The microcirculatory system serves several essential roles in maintaining the vitality of thepulp.

• Both these systems are critically important in maintaining the homeostasis of the dentalpulp.

• The value of the pulp as an integral part of the tooth, both anatomic and functional shouldbe recognised and every effort must be made to conserve it.



References

• Dental Pulp – Seltzer & Bender (2nd Edition)

• Endodontic Practice – Grossman (13th Edition)

• Endodontics – Ingle (6th Edition)

• Pathways of the Pulp – Stephen Cohen

• Endodontic Therapy – Franklin S. Weine (6th Edition)

• Textbook – Nageshwar Rao (1st Edition)

• Textbook of Endodontics – Nisha Garg


diseases of the pulp

Education