INTRODUCTION

Etiologic factors in Pulpal Diseases1.According to Grossman1.Physical A. Mechanical i.Trauma ii. Pathologic Wear iii.Cracked tooth Syndrome iv.Barodontalgia

B.Thermal

2.Chemical A. Phosphoric Acid, Acrylic monomers B.Erosions

3.Bacterial A.Toxins B.Direct invasion of pulp C.Anachoresis

2.According to Ingle -5th editionI. Bacterial A. Coronal ingress 1. Caries

2. Fracture

a. Complete

b. Incomplete (cracks, infraction)

3. Non fracture trauma

4. Anomalous tract

a. Dens invaginatus (aka dens in dente)

b. Dens evaginatus

c. Radicular lingual groove

(palatogingival groove)

B. Radicular ingress 1. Caries

2. Retrogenic infection

a. Periodontal pocket

b. Periodontal abscess

3. Hematogenic

II. Traumatic A. Acute 1. Coronal fracture

2. Radicular fracture 3. Vascular stasis 4. Luxation 5. Avulsion B. Chronic 1. Adolescent female bruxism 2. Traumatism 3. Attrition or abrasion 4. Erosion

III. Iatral A. Cavity preparation 1. Heat of preparation 2. Depth of

preparation 3. Dehydration 4. Pulp horn

extensions 5. Pulp hemorrhage 6. Pulp exposure 7. Pin insertion 8. Impression taking B. Restoration 1. Insertion 2. Fracture a. Complete b. Incomplete 3. Force of cementing 4. Heat of polishingC. Intentional extirpation and root canal fillingD. Orthodontic movementE. Periodontal curettage

F. ElectrosurgeryG. Laser burnH.Periradicular curettageI. RhinoplastyJ. OsteotomyK. Intubation for general anesthesia

IV. ChemicalA. Restorative materials 1. Cements 2. Plastics 3. Etching agents 4.Cavity liners 5. Dentin bonding agents 6. Tubule blockage

agentsB. Disinfectants 1. Silver nitrate 2. Phenol 3. Sodium fluoride

C. Desiccants 1. Alcohol 2. Ether 3. Others

V. Idiopathic

A. Aging B. Internal resorption C. External resorption D.Hereditary hypophosphatemia E. Sickle cell anemia F. Herpes zoster infection G.Human immuno deficiency virus

(HIV) and Acquired Immuno Deficiency Syndrome

(AIDS)

Classification of Pulpal Diseases

1.Grossman’s ClassificationI) Pulpitis (Inflammation)A) Reversible pulpitis 1) Symptomatic (acute) 2) Asymptomatic (chronic)

B) Irreversible pulpitis 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

II) Pulp Degeneration A) Calcific (Radiographic diagnosis) B) Others (Histopathologic diagnosis)

III) Pulp necrosis

2. Ingle’s classification

1) Hyperreactive pulpalgia a) Hypersensitivity b) Hyperemia

2) Acute pulpalgia i) Incipient (reversible) ii) Moderate (referred) iii) Advance (relieved by cold)

3) Chronic pulpalgia

4) Hyperplastic pulpitis

5) Pulp necrosis 1) Atrophic pulposis 2) calcific pulposis

3. Seltzer and Bender classification(histological)

1) Intact pulp with scattered chronic inflammatory cells.

2) Acute pulpitis

3) Chronic partial pulpitis with partial necrosis

4) Chronic partial pulpitis with partial liquefaction necrosis

5) Chronic partial pulpitis (Hyper plastic form)

6) Pulp necrosis 1) Atrophic pulp 2) Dystrophic mineralization

4.According to Weine- 5th edI. Inflammatory diseases of the dental pulp.

a.Hyperalgesia(Reversible pulpitis,hypeactive pulpalgia, hypersensitive)

i.Hypersensitive dentinii.Hyperemia

b.Painful pulpitis/Irreversible pulpitisi.Acute pulpalgia(acute pulpitis)ii.Chronic pulpalgia(subacute pulpitis)

c.Non Painful pulpitisi.Chronic ulcerative pulpitis(due to caries)ii.Chronic pulpitis(carious lesion absent)iii.Chronic Hyperplastic Pulpitis

2.Additional pulp Changes

a.Necrosis (squeal to inflammatory/ retrogressive change)b.Retrogressive changes ( degeneration, pulposis)

i.Atrophy & Fibrosis ii.Dystrophic Calcification(calcific degeneration, Calcific pulposis)

c.Internal Resorption – which may be sequela to persistent chronic

inflammation.

Pulpitis

Open pulpitis

Closed Pulpitis

5.According to Shafer's:

Pulpitis

Acute

Partial pulpitis

Subtotal pulpitis

Chronic Partial/focal pulpitis

Total/generalized

Pulpitis1.Focal Reversible Pulpitis/ Initial pulpitis/ Pulpal

Hyperemia Earliest form Mild….., localized…..

Def:

H/P: Mild to moderate hyperemia, inflammatory changes restricted to area of

involved dentinal tubules

µ scopy- Reparative dentin Disruption of odontoblasts Dilated b/v Extravasations of edema fluid Few acute infl. cells along with chronic infl cells present

Etiology: Trauma Thermal shock Recent oral prophylaxis Dehydration/ desiccation of the cavity Deep caries or restorations Chemicals

Symptoms: Unilateral sharp stabbing pain, intermittent & of immediate onset on

application of the stimulus Pain only on stimulation, responds more to cold than hot stimuli Short duration & does not linger……….. Difficulty in localization

Signs: Large intra/ extra coronal restoration Carious lesion involving the pulp Pin placed close to the pulp/ involving

Diagnosis: Percussion Vitality tests Color Radiograph

Treatment: Removal of the cause Use of Ca(OH)2 liner, ZOE temp.filling Review repeat vitality tests Serial radiographs @ 3,6 & 12 months ,monitoring apical condition &

sclerosis!!.....

Prognosis: Favorable if irritant is removed early enough.

2.Acute PulpitisUsually a squeal of focal rev. pulpitisUsually irreversible & leads to suppurative pulpitis

Def:H/P: Presence of chronic &acute inflammatory cells

Congestion of post capillary venules

Acute Inflammation

Necrosis

chemotaxis

Attracts PMNL’s

Affects pulpal circulation

Etiology: Bacterial involvement of the pulp through caries Trauma / chemical / thermal irritation Progression of rev. pulpitis

Symptoms: Unilateral pain initially piercing, shooting, stabbing sharp pain becoming dull or

throbbing type with time. Exaggerated response to hot stimuli Longer duration & lasts >15 sec.,(even up to several Hours) after removal of the

stimulus. Radiation Spontaneous, worsens at night & on lying down…… Cold reduces …….temp relief! Sudden stoppage…..! Poorly localized until………!

Signs: Pain increases by heat & decreases by cold although………….! Large carious lesion/ restoration, # or discolored tooth Initially may not be tender to bite on…….!

Diagnosis: Diagnostic LA injection may be required for localization> Vitality tests: Exaggerated response to heat & initially….later……….!! Vitality in multiple root?? Percussion:----- periodontitis! Radiographs:

Treatment: Complete removal of pulp / Pulpectomy…… Posterior tooth……….. Extraction as the last resort!!!!

Differential DiagnosisOne must distinguish between Reversible & irreversible Pulpitis

Potentially Reversible

Probably Irreversible

Pain Momentary Continous, Throbbing

Stimulus External stimulus required Spontaneous, Intermittent

History Recent dental proc,cervical erosion, trauma

Extensive, pulp capping,deep caries,trauma

EPT May be premature response Premature / Delayed /mixed

Percussion -ve response unless……..! May respond in advanced stage of pulpitis…….!

Referred Negative Common finding

Lying down Negative Common finding

Potentially Reversible

Probably Irreversible

Color Negative May be present ….!

Radiograph Periapex – Negative Periapex, may be slight widening of PDL space

Prognosis:• Favorable if the pulp is removed & if the tooth undergoes proper endodontic therapy & restoration

A. Advanced caries.

B. No secondary dentine ,destruction of odontoblasts,

C. Inflammatory cell.

3.Chronic Pulpitis: May arise on occasion through quiescence of a previous acute pulpitis / more

commonly as the chronic type of disease from onset

Signs & Symptoms: Large restorations Pain is not a prominent feature Poorly localized, milder than the acute form On exploration bleeding may occur but pain is absent

H/P: Chronic infl. Cells Prominent capillaries, collagen bundle gathering towards an attempt to ward

off the infection

A.Carious exposure with necrosis.

B.Destruction of odontoblasts.

C.Bacterial toxins

in atubular dentin.

Ulcerative Pulpitis Granulation tissue formation on the surface of pulp tissue in a wide open

exposure µ organisms in pulp present.

Diagnosis: Vitality: A gradual reaction Reaction to thermal changes & electrical stimulus is dramatically reduced

Percussion: Radiograph:……sclerosis of alveolar bone!

Treatment & Prognosis: Similar to acute pulpitis Endodontic therapy / Extraction

4.Chronic Hyperplastic Pulpitis:Def:“Pulp Polyp” is a productive pulpal inflammation due to extensive carious

exposure of a young pulp.

Etiology: Slow progressive carious exposure A large open cavity ….. Mechanical irritation too acts as a stimulus. Dental neglect

Symptoms:

Signs: Seen in…………! Visible polyp in……….! Coronal tooth ………!

Diagnosis:C/F Appearance of the polyp Sensitiveness…….! Bleeding…..! Origin……! Tooth involved!

Radiograph: Large open cavity with direct access to pulp chamber Vitality: Thermal-feeble or no response EPT- more current required

Internal Resorption/ Pink tooth of MummeryDef:Etiology: Unknown, but majority of patients give a H/O Trauma

H/P: Result of osteoclastic activity Lacunae seen filled with osteoid tissue…! Profuse bleeding on removal of the pulp Multinucleated giant cells…..! Chronic infl. Cells & metaplastc cells

Symptoms: Asymptomatic usually “Pink Spot” in the crown

Diagnosis: May involve crown / root Usually max. ant tooth. Routine radiographic examination. Appearance of “Pink spot”

R/F: Change in the wall……….! A round/ oval radiolucent area

Treatment: Extirpation of the pulp stops the receptive process Routine endodontic therapy is indicated Difficulty in obturation of the defect thermo plasticized GP is

used. In perforation Ca(OH)2 paste calcific barrier complete

obturation .

Prognosis: Best before perforation In perforation cases it is guarded &depends on the formation of

calcific barrier.

Pulp Degeneration:

Usually seen in teeth of older people sometimes young teeth with persistent mild infection may show degeneration.

At an early stage- No definite clinical symptoms At a later stage discoloration of the tooth pulp does not respond to stimuli

Calcific Degeneration:

A part of the pulp tissue is calcified i.e. deposition of Ca salts in dead & degenerating tissues

Pulp chamber( denticles)

Root canal( diffuse calcifications)

Denticles/ Pulp stones

Larger, well outlined, more commonly in the pulp chamber, laminated, large enough at times……!

Classification: Freea. According to location Attached Embedded

b.According to structure true false Studies reveal around 60% of teeth have pulp stones

Signs & symptoms: Harmless concretions Referred pain may be seen in some cases

Diagnosis:R/F: calcified or radio opaque mass Difficult to distinguish 3 type R/f

Treatment: Usually pose problem in endodontic treatment Use of chelating agents like EDTA is recommended

Atrophic Degeneration:

Atrophy means ‘wasting away’ or decrease in the size of an organ. It is attributed to faulty nutrition Usually occurs as the teeth grow older Increase in collagen fibers & decrease in the no. of cells No clinical diagnosis exists

Fibrous degeneration:

Replacement of cellular elements by fibrous connective tissue On removal from root canal appears like a leathery fiber No distinguishing diagnostic features

Pulp Artifacts:

Vacuolization of odontoblasts was ounce thought to be a type of pulp degeneration

Empty spaces formed by odontoblasts Actually an artifact caused by poor fixation of the tissue

specimen Other Ex- Fatty degeneration, Reticular atrophy

Pulp Necrosis:

Def: Necrosis is death of the pulp partial / total Usually a squeal of inflammation May occur following a traumatic injury…….!

CoagulationNecrosis Liquefaction

Coagulation necrosis: The soluble portion of tissue is precipitated or is converted into a

solid material. Caseation is a type characterized by a cheesy mass.

Liquefaction Necrosis: Results when proteolytic enzymes convert the tissue into a

softened mass, liquid or amorphous debris.

Etiology: Any noxious stimuli / insult injurious to the pulp, Bacteria, chemicals or trauma.

Symptoms: No painful symptoms Discoloration is a first indication of pulpal death. Crown--……..!

Diagnosis: Mostly only by chance as no significant findings

Radiograph: Large cavity / filling or an open approach to the root canal H/O trauma or severe pain followed by complete cessation of

pain at times by patientsVitality tests: no response to thermal / cold or test cavity EPT may give minimum response to max. current due to moisture

content / viable apical nerve fibers at times.

H/P: Necrotic pulp tissue, cellular debris & microbes Periapical tissue may be normal / slight evidence of the

inflammation of apical PDL ligament .

A. Necrosis.

B. Inflammatory cells.

C. Monocytes.

Treatment: Proper Endodontic therapy

Prognosis: Favorable if proper endodontic therapy is

instituted

Conditions mimicking Pulpitis

Aerodontolgia/ Barodontolgia Dental pain occurring due to reduced atmospheric pressure

Symptoms: Acute pulpitic pain , only during decompression / flying at high altitude

Signs: Recently restored teeth Aerosinusitis may be a contributing factor if max. teeth are involved

Diagnostic tests: Radiograph : possible antral opacity on paranasal radiograph.

Treatment: Monitor: pulpitis might prove to be rev./ Irreversiblle. If irreversible institute endodontic therapy/ extract Refer for investigation & treatment of Sinusitis

Galvanism:Etiology:

Symptoms: Intermittent pain Occurs only after placement of a new metal restoration ,is well localized & does

not refer

Signs: Recent metallic restoration abutting/ opposing an existing metallic restoration. Corrosion deposits or damage may be evident.

Treatment: Application of varnish over the restoration May diminish over in a few days by formation of corrosion products

Diseases of the Periradicular Tissues

Acute periradicular disease

Acute alveolar abscess

Acute apical periodontitis

Vital

Nonvital

Chronic periradicular diseases with areas

of rarefaction

Chronic alveolar abscess

Granuloma

Cyst

Condensing osteitis

External root resorption

Diseases of the periradicular tissue of non

endodontic origin

Acute Alveolar Abscess

Definition:

An acute alveolar abscess is a localized

collection of pus in the alveolar bone at the

root apex of a tooth following death of pulp

Symptoms:

The first symptom - mere tenderness of the

tooth. Later, - severe throbbing pain,

attendant swelling of the overlying soft tissues.

As the infection progresses- The swelling

becomes more pronounced and extends

beyond the original site.

The tooth becomes more painful, elongated,

and mobile.

The pain may subside or cease entirely while

the adjacent tissue continuous to swell.

If left unattended, the infection may progress to

osteitis, periostitis, cellulitis, or osteomyelitis.

The contained pus may break through to form

a sinus tract, usually opening in the labial or

buccal mucosa.

At other times, it may exit anywhere near the

tooth, such as the skin of the patient’s face or

neck, or even the antrum or nasal cavity.

When swelling becomes extensive, the

resulting cellulitis may distort the patient’s

appearance grotesquely.

In addition to the localized symptoms of an

acute alveolar abscess, a general systemic

reaction of greater or lesser severity may occur

The patient may appear pale, irritable and

weakened from pain and loss of sleep.

Patients with mild cases may have only a slight

rise in temperature (90 to 1000 F).

Whereas in those with severe cases, the

temperature may reach several degrees above

normal (102 to 1030 F).

The fever is often preceded or accompanied by

chills.

Intestinal stasis can occur, manifesting itself

orally by a coated tongue and foul breath.

Diagnosis:

In the early stages, it may be difficult to locate

the tooth because of the absence of clinical

signs and the presence of diffuse, annoying

pain.

The tooth is easily located when the infection

has progressed to the point of periodontitis

and extrusion of the tooth;

a radiograph may help one to determine the

tooth affected by showing a cavity, a defective

restoration, thickened periodontal ligament

space,

A diagnosis may be confirmed by means of the

electric pulp test and by thermal tests.

The affected pulp is necrotic and does not

respond to electric current or to application of

cold.

The tooth may be tender to percussion, or the

patient may state that it hurts to chew with

the tooth, the apical mucosa is tender to

palpation, and the tooth may be mobile and

extruded.

PERCUSSIONPALPATION

Differential Diagnosis:

Acute alveolar abscess should be differentiated

from periodontal abscess and from irreversible

pulpitis.

A periodontal abscess is an accumulation of pus

along the root surface of a tooth that originates

from infection in the supporting structures of

the tooth.

It is associated with a periodontal pocket and is

manifested by swelling and mild pain. On

pressure, pus may exude near the edematous

tissue or through the sulcus, the swelling is

usually located opposite the root apex or

beyond it.

A periodontal abscess is generally associated

with vital rather than with pulp less teeth, in

contrast to an acute abscess, in which the

pulp is dead, tests for pulp vitally are useful

in establishing a correct diagnosis.

Treatment:

Treatment consists of establishing drainage and

controlling the systemic reaction. When

symptoms have subsided, the tooth has been

left open for drainage, one must perform careful

and through debridement by instrumentation

and irrigation before medicating and sealing the

root canal. Once the root canal is sealed,

endodontic treatment is completed

Acute Apical Periodontitis

Acute Apical Periodontitis:

Definition:

Acute apical periodontitis is a painful

inflammation of the periodontium as result of

trauma, irritation, or infection through the root

canal, regardless of whether the pulp is vital or

nonvital.

Cause:

Acute apical periodontitis may occur in a vital

tooth

That has experienced occlusal trauma

caused by abnormal occlusal contacts,

By a recently inserted restoration

extending beyond the occlusal plane,

By wedging of a foreign object between

the teeth such as a toothpick,

Acute apical periodontitis may also be

associated with the nonvital tooth.

It may be caused by the sequelae of

pulpal diseases. the diffusion of

bacteria and noxious products from an

inflamed or necrotic pulp,

Or its cause may be iatrogenic

Symptoms:

The symptoms of acute apical periodontitis are

pain and tenderness of the tooth.

The tooth may be slightly sore, some times only

when it is percussed in a certain direction, or the

soreness may be severe.

The tooth may be extruded, making closure

painful.

Diagnosis:

The diagnosis is frequently made from a known

history of a tooth under treatment.

The tooth is tender to percussion or slight

pressure, whereas the mucosa overlying the

root apex may or may not be tender to

palpation.

Differential Diagnosis:

A differential diagnosis should be made

between acute apical periodontitis and acute

alveolar abscess.

at times, the difference is only one of degree

because acute alveolar abscess represents a

further stage in development,

with breakdown of periapical tissue, rather than

merely an inflammatory reaction of the

periodontal ligament.

The patient;s history, symptoms and clinical test

results, symptoms and clinical test results help

one to differentiate these diseases.

Treatment:

Treatment of acute apical periodontitis

consists of determining the cause and

relieving the symptoms.

When the acute phase has subsided, the

tooth is treated by conservative means.

Acute Exacerbation of

a chronic Lesion:

Acute Exacerbation of a chronic Lesion:

Synonyms: Phoenix Abscess.

Definition: This condition is an acute

inflammatory reaction superimposed on an

existing chronic lesion, such as a cyst or

granuloma.

Cause:

The periradicular area may react to noxious

stimuli from a diseased pulp with chronic

periradicular disease. While chronic

periradicular diseases, such as granulomas and

cysts, are in a state of equilibrium, these apical

reactions can be completely asymptomatic.

At times, because of bacteria and their

toxins, these apparently dormant lesions

may react and may cause an acute

inflammatory response.

Symptoms :

At the onset, the tooth may be tender to the

touch.

As inflammation progresses, the tooth may be

elevated in its socket and may become

sensitive.

The mucosa over the radicular area may be

sensitive to palpation and may appear red and

swollen.

Diagnosis:

The exacerbation of a chronic lesion is most

commonly associated with the initiation of

root canal therapy in a completely

asymptomatic tooth.

In such a tooth, radiographs show well-

defined periradicular lesions.

The patient may have a history of a

traumatic accident that turned the tooth dark

after a period of time or of postoperative

pain in a tooth that had subsided until the

present episode of pain.

Lack of response to vitality tests points to a

diagnosis of necrotic pulp, although, on rare

occasions, a tooth may respond to the electric

pulp test because of fluid in the root canal; or

in a multirooted tooth.

DIFFERENTIAL DIAGNOSIS

Differential Diagnosis:

An acute exacerbation of a chronic lesion

causes symptoms similar to those of an acute

alveolar abscess. Because the treatment of

both lesions is the same, no differential

diagnosis is needed.

Treatment:

The treatment of acute exacerbation of a

chronic lesion, which is an emergency, is the

same as that of an acute alveolar abscess.

Prognosis:

The prognosis for the tooth is good once the

symptoms have subsided.

CHRONIC PERIRADICULAR DISEASES WITH

AREAS OF RAREFACTION

These diseases are chronic alveolar abscess.

Granuloma, and radicular cyst.

Chronic Alveolar Abscess

Synonym: Chronic supportive apical periodontitis.

Definition:

A chronic alveolar abscess is a long-standing,

low –grade infection periradicular alveolar

bone. The source of the infection is in the root

canal.

Cause:

Chronic alveolar abscess is a natural sequela of a

death of the pulp with extension of the infective

process periapically, or it may result from a pre-

existing acute abscess.

Symptoms:

A tooth with chronic alveolar abscess is generally

asymptomatic; at times, such an abscess is

detected only during routine radiographic

examination or because of the presence of a sinus

tract.

A radiograph taken after the insertion of a gutta-

percha cone into the sinus tract often shows the

the involved tooth by tracing the sinus tract to its

origin. When an open cavity is present in the

tooth, drainage may occur by way of the root

canal.

Diagnosis:

A chronic abscess may be painless or only mildly

painful. At times, the first sign of osseous

breakdown is radiographic evidence seen during

routine examination or discoloration of the

crown of the tooth.

When asked, the patient may remember a

sudden, sharp pain that subsided and has not

recurred, or he may relate a history of traumatic

injury.

The tooth does not react to the electric pulp test

or to thermal tests.

Differential Diagnosis:

Clinically, it is practically impossible to establish

an accurate diagnosis among the periradicular

diseases with radiographs alone.

As a result, a proper and accurate diagnosis can

be made only when tissue specimen has been

examined microscopically

A chronic abscess should be differentiated from

cementoma or ossifying fibroma, which is

associated with a vital tooth and requires no

endodontic treatment.

Treatment:

Treatment consists of elimination of infection in

the root canal.

GRANULOMA:

Definition:

A dental granuloma is a growth of granulomatous

tissue continuous with the periodontal ligament

resulting from death of the pulp and the diffusion

of bacteria and bacterial toxins from the root

canal in to the surrounding periradicular tissues

through the apical and lateral foramina.

A granuloma may be seen as a chronic, low-grade

defensive reaction of the alveolar bone to

irritation from the root canal.

Cause:

The cause of the development of a granuloma

is death of the pulp, followed by a mild

infection or irritation of the periapical tissues

that stimulates a productive cellular reaction. A

granuloma develops only some time after the

pulp has died.

Symptoms:

A granuloma may not produce any

subjective reaction, except in rare cases when it

breaks down and undergoes supuration. Usually,

a granuloma is asymptomatic

Diagnosis:

The presence of a granuloma, which is

symptomless, is generally discovered by routine

radiographic examination.

The area of rarefaction is well defined, with

lack of continuity of the lamina dura

Differential Diagnosis:

A granuloma cannot be differentiated from

other periradicular diseases unless the tissue is

examined microscopically.

Treatment:

Root canal therapy may suffice for the treatment

of a granuloma.

BAY AND TRUE CYSTS

A= True cyst

B= Bay cyst

C= Granuloma

D= Epithelium

E= Alveolar bone

F= Dentine

G= Root canal

H= Cementum

I= Periodontal ligament

Radicular Cyst:

Definition: A cyst is a closed or sac internally lined

with epithelium, the center of which is filled with

fluid or semisolid material.

A radicular or alveolar cyst is a slowly growing sac

at the apex of a tooth that lines a pathologic

cavity in the alveolar bone.

Cause:

A radicular cyst presupposes physical, chemical, or

bacterial injury resulting in death of the pulp,

followed by stimulation of the epithelial rests of

Malassez, which are normally present in the

periodontal ligament:

Symptoms:

No symptoms are associated with the

development of a cyst,

A cyst may become large enough, however, to

become obvious as a swelling.

The presence of the cyst may be sufficient to

cause movement of the affected teeth, owing to

accumulation of cystic fluid. In such cases, the

root apices of the involved teeth become spread

apart, so the crowns are forced out of

alignment. The teeth may also become mobile.

If left untreated, a cyst may continue to grow at

the expense of the maxilla or the mandible.

Diagnosis:

The pulp of a tooth with a radicular cyst does not react to electrical or thermal stimuli, and results of other clinical tests are negative, except the radiograph.

The radiolucent area is generally round in outline, except where it approximates adjacent teeth, in which case it may be flattened and may have an oval shape.

Neither the size nor the shape of the rarefied area is a definitive indication of a cyst

Differential Diagnosis:

A cyst is usually larger than granuloma and may

cause the roots of adjacent teeth to spread apart

because of continuous pressure from accumulation

of cystic fluid.

Treatment:

Resolution of these areas of rarefaction occurs

following root canal therapy in 80 to 98% of cases.

Prognosis:

The prognosis depends on the particular tooth,

the extent of bone destroyed, and the

accessibility for treatment

CHRONIC PERIRADICULAR DISEASE WITH AREA OF

CONDENSATION:

Condensing Osteitis:

Definition:

Condensing osteitis is the response to a low-

grade, chronic inflammation of the periradicular

area as a result of a mild irritation through the

root canal.

Cause: Condensing osteitis is a mild irritation

from pulpal disease that stimulates osteoblastic

activity in the alveolar bone.

Symptoms: This disorder is usually

asymptomatic. It is discovered during routine

radiographic examination.

Diagnosis: The diagnosis is made from radiographs.

Condensing osteitis appears in radiographs as a

localized area of radiopacity surrounding the

affected root.

Treatment: Endodontic treatment is indicated.

Prognosis: The prognosis for long-term retention

of the tooth is excellent if root canal therapy is

performed and if the tooth is restored

satisfactorily.

External Root Resorption:

Definition: External resorption is a lytic process

occurring in the cementum or cementum and

dentin of the roots of teeth.

Cause: Although unknown, the suspected cause

of external resorption is periradicular

inflammation due to trauma.

Symptoms: Throughout its development, external

root resorption is asymptomatic. When the root is

completely resorbed, the tooth may become

mobile. If the external root resorption extends

into the crown. It will give the appearance of

“pink tooth” seen in internal resorption

Diagnosis:

External resorption is usually diagnosed by

radiographs.

Differential Diagnosis:

External resorption needs to be differentiated

from internal resorption. In external resorption,

the radiograph shows a blunting of the apex, a

ragged area, a “scooped – out” area on the side

of the root, or, if the area is superimposed on

the root canal, the root canal clearly traverses

the area of resorption.

Treatment:

Internal resorption ceases when the pulp is

removed or becomes necrotic

Prognosis:

The prognosis of a tooth with external resorption

is guarded. If the etiologic factor is known and it

is removed, the resorptive process will stop, but

it may leave a weak tooth unable to sustain

functional forces.

Diseases of the Periradicular Tissues of

Nonendodontic Origin:

Periradicular lesions not only arise as extensions

of pulpal diseases, but they may also originate

in the remnants of odontogenic epithelium.

Such lesions may be manifestations of systemic

diseases, such as multiple neurofibromatosis or

they may have other causes, such as periodontal

diseases.