Download - Diseases of the pulp
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DISEASES OF THE DENTAL PULP- Part IIDeepthi P.R.1st year MDSDept of Conservative Dentistry & Endodontics
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CONTENTS Introduction Irritants Inflammatory process Immunologic responses Lesion progression Classification of diseases
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INTRODUCTION Etiologic factors causing pulp
inflammation Mechanism of spread of inflammation Mediators of pulpal inflammation Classification & features of diseases
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IRRITANTS
Living • Micro organisms
• Viruses
Non Living• Mechanical• Thermal• Chemical
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Microbial irritants Main source Numerous species: S. mutans,
Lactobacilli, Actinomyces Toxins: deep penetration to pulp Local infiltration of pulp- chronic
inflammatory cells Progression: intensity & character
changes
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Microbial irritants Actual exposure: PMN infiltration &
liquefaction necrosis Long periods of inflammation/ necrosis-• Virulence• Release of inflammatory fluid: avoiding intrapulpal pressure• Host resistance• Circulation• Lymphatic drainage
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Microbial irritants Yamasaki et al : pulpal necrosis in rats Exposed pulp: bacteria & by products Temporary impeding of spread &
destruction Persistence: extensive destruction –
spread throughout pulp- periapical spread & inflammatory lesions
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Microbial irritants Kakehashi et al : pulp exposures in
conventional & germ free rats Mӧller et al: sealed infected & non
infected canals in monkeys Sundqvist et al: traumatised teeth with
and without apical pathosis
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Microbial irritants Viruses: symptomatic apical pathoses Periapical lesions: CMV & EBV-
symptomatic
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Mechanical irritants Deep cavity preparations Removal of tooth structure without
proper cooling Impact trauma Occlusal trauma Deep periodontal curettage Orthodontic movement
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Mechanical irritants Extensive restorative procedures: pulpal
inflammation Dentin permeability closer to pulp
Operative procedures without coolant- more pulpal irritation
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Mechanical irritants Impact injuries : severity of trauma &
degree of apical closure – pulpal recovery
Orthodontic forces beyond physiologic tolerance: cellular atrophy, alteration of nerve axons, apical resorption
Deep scaling & curettage
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48 hours after crown preparation through enamel & 1mm into dentin
Aspiration of odontoblasts into tubules & pulpal infiltration by PMNs & Lymphocytes
M Torabinejd. Endodontics
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Chemical irritants Dentin sterilizing :
Silver nitrate, phenol, eugenol & desensitizing substances
Cleansers: Alcohol, chloroform, H2O2, various acids
Restorative materials & liners
Periapical extrusion of filling materials causing periapical
inflammation M Torabinejd. Endodontics
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Pulpal pathosis Injury: cell death & inflammation Slight: little or no inflammation Incipient caries, shallow cavity
preparations More damaging: severe inflammation Deep caries, extensive operative
procedures, persistent irritants
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Pulpal pathosis
Severity & duration of illness Host capacity
Reversible pulpitis
Irreversible pulpitis
Total necrosis
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Inflammatory process Irritation of dental pulp – mediators:
Histamine, Bradykinin, Arachidonic acid metabolites
Lysosomal granule products: Elastase, Cathepsin G, Lactoferrin
Protease inhibitors: Antitrypsin, CGRP, Substance P
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Inflammatory process Mast cells: Histamine, Leukotrienes, PAF Released: Physical injury to mast cells or
bridging of IgE
Bradykinin, Substance P, Neurokinin A
Plasma/ Tissue
kallikreinsKininogens Kinins
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Inflammatory process iCGRP release : PGE2
Pulpal nerve fibers: SP, CGRP- protective Mild- moderate injuries: iCGRP Severe: iCGRP
Cellular damage
Arachidonic acid
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Immunologic Responses Bacteria & by products: Antigen Immunocompetent cells – Normal pulp
Ig levels in inflamed pulps Arthus reaction Delayed hypersensitivity reactions Necrotic foci & pulpal necrosis
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Healthy pulp Pulp : vital; free of inflammation Prosthetic reasons First hours after traumatic pulp
exposure
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Pulpitis Vital & inflamed No info on:
Degree of inflammation Reversible/ irreversible
Two clinical diagnoses for inflamed pulp Symptomatic pulpitis
Asymptomatic pulpitis
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Pulpitis Symptomatic Vital, inflamed Symptoms of
pulpitis Exacerbation of
chronic pulpitis Acute
Asymptomatic Vital, inflamed &
no symptoms Knowledge of
etiology of pulpitis & reaction pattern of pulp
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Lesion Progression Moderate to severe injuries: localized
inflammation & mediators Increase in protease inhibitors: natural
modifiers Increased vascular permeability,
vascular stasis, migration of WBCs- injury site
CGRP: increased blood flow during inflammation
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Accumulation of inflammatory cells within the pulp horn
Beer. Pocket Atlas of Endodontics
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Neutrophilic granulocytes in Predentin layer & Dentin tubules
Beer. Pocket Atlas of Endodontics
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Lesion Progression capillary pressure & permeability
Exudation tissue pressure: passive compression & complete collapse of venules Increased pressure Inablity to expand Lack of collateral circulation
Pulpal necrosis
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Lesion ProgressionInflammatory
mediators
IndirectDirect
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PULPITIS Acute/ Chronic: Clinical differentiation Partial/ Total Infected/ Sterile: smear or culture Acute: Precipitous short course Violently painful Chronic: Practically symptomless Slightly painful Longer durationExposed
pulp: caries/ trauma
Hyperplastic pulpitis
Ulcerative pulpitis
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CLASSIFICATION OF PULPAL DISEASES
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CONTENTS Introduction Different classifications Normal pulp Reversible pulpitis Irreversible pulpitis Chronic hyperplastic pulpitis Necrotic pulp Pulp degeneration Previously treated pulp Previously initiated therapy
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CLASSIFICATION OF PULPAL DISEASES *No correlation between histologic
findings & symptoms Clinical classification: Signs & symptoms Helps: appropriate treatment, prognosis,
restorative needs Indistinct demarcation between the
classes
Garfunkel et al: direct correlation -49%, partial correlation- 46%.
Wegner & Knorr: Correlation- 40%
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CLASSIFICATION OF PULPAL DISEASES Grossman Baume Seltzer & Bender Wiliam T. Johnson American Board of Endodontics (ABE)- 2007 Reit, Petersson & Molven Walton & Torabionejad Torabinejad & Shabahang Tronstad Ingle & Beveridge Castelucci Beer & Baumann Abbott WHO- 1995
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Grossman1. Inflammatory diseases of the dental
pulpa. Reversible pulpitis (i) Symptomatic (acute) (ii) Asymptomatic (chronic)b. Irreversible pulpitis (i) Acute - Abnormally responsive to cold - Abnormally responsive to heat
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Grossman(ii) Chronic - Asymptomatic with pulp exposure - Hyperplastic pulpitis - Internal resorption2. Pulp degenerationa. Calcific (radiographic diagnosis)b. Others (histopathologic diagnosis)
3.Necrosis
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Baume Symptomless vital pulp: Deep caries-
pulp capping done History of pain: Amenable to
pharmacotherapy & restorative rehabilitation
Infected pulps: Extirpation & immediate RCT
Infected & necrosed pulps: Intracanal serous drainage- medicament prior to RCT
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Seltzer & Bender(a) Treatable without
pulp extirpation and RCT:
Intact, uninflamed pulp
Transitional stage Atrophic pulp Acute pulpitis Chronic partial pulpitis
without necrosis
(b) Untreatable without pulp extirpation and RCT:
Chronic partial pulpitis with necrosis
Chronic total pulpitis Total pulp necrosis
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William T.Johnson Normal Reversible pulpitis Irreversible pulpitis
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American Board of Endodontics (ABE)- 2007 Normal pulp Reversible pulpitis Irreversible pulpitis Symtomatic Asymptomatic Pulp necrosis Previously treated Previously initiated therapy
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Reit, Petersson & Molven Pulpa sana Pulpitis Necrosis pulpae Periodontitis apicalis chronica/ acuta
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Walton & Torabinejad Normal Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis
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Torabinejad & Shabahang Normal pulp Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis Previously treated pulp
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Tronstad Healthy pulp Asymptomatic pulpitis Symptomatic pulpitis Necrotic pulp
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Ingle & Beveridge Incipient acute pulpalgia Moderate & advanced acute pulpalgia Chronic pulpalgia Hyperplastic pulposis Necrosis
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Castelucci Healthy pulp Hyperemia Pulpitis Necrosis
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Beer & Baumann Asymptomatic pulp pathology Reversible pulpitis Irreversible pulpitis Pulpal necrosis
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Abbott a.Clinically normal pulpb.Reversible pulpitisTypes: Acute, Chronicc. Irreversible pulpitisTypes: Acute Chronic, Necrobiosisd. Pulp necrosisTypes: Necrosis without infection, Necrosis with infection
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Abbott e. Pulpless CanalsTypes: Pulpless and no signs of infection Pulpless and infectedf. Degenerative ChangesTypes: Atrophy, Pulp canal obliteration(calcification)- Partial, Total Hyperplasia Internal resorption- Inflammatory, Replacement
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Abbott g. Previous Root Canal TreatmentTypes : Satisfactory – No signs of infection - InfectedTechnically inadequate - No signs of infection - Infectedh. Endodontic- Periodontal Lesions
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Abbott h. Endodontic- Periodontal LesionsClassification based on the origin of the periodontal defect: - Lesion of endodontic origin- Lesion of Periodontal origin- Combined Endo- Perio Lesions Types: Separate endo & perio lesions that do NOT communicate endodontic and periodontal lesions that DO communicate
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Application of the International Classification of Diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995
K04 DISEASES OF PULP AND PERIAPICAL TISSUES K04.0 Pulpitis K04.00 Initial (hyperaemia) K04.01 Acute K04.02 Suppurative [pulpal abscess] K04.03 Chronic K04.04 Chronic, ulcerative K04.05 Chronic, hyperplastic [pulpal polyp] K04.08 Other specified pulpitis K04.09 Pulpitis, unspecified
Gutmann et al. JOE — Volume 35, Number 12, December 2009
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Application of the International Classification of diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995
K04.1 Necrosis of pulp Pulpal gangrene K04.2 Pulp degeneration Denticles Pulpal calcification Pulpal stones K04.3 Abnormal hard tissue formation in pulp K04.3X Secondary or irregular dentineExcludes: pulpal calcifications (K04.2)pulpal stones (K04.2
Gutmann et al. JOE — Volume 35, Number 12, December 2009
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Application of the International Classification of diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995
K04.4 Acute apical periodontitis of pulpal origin Acute apical periodontitis K04.5 Chronic apical periodontitis Apical granuloma K04.6 Periapical abscess with sinusIncludes: dental abscess with sinus dentoalveolar abscess with sinus periodontal abscess of pulpal origin K04.60 Sinus to maxillary antrum K04.61 Sinus to nasal cavity K04.62 Sinus to oral cavity K04.63 Sinus to skin K04.69 Periapical abscess with sinus, unspecified
Gutmann et al. JOE — Volume 35, Number 12, December 2009
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K04.7 Periapical abscess without sinus Dental abscess } Dentoalveolar abscess } without sinus Periodontal abscess of pulpal origin } K04.8 Radicular cystIncludes: cyst apical periodontal periapical K04.80 Apical and lateral K04.81 Residual K04.82 Inflammatory paradentalExcludes: developmental lateral periodontal cyst (K09.04) K04.89 Radicular cyst, unspecified K04.9 Other and unspecified diseases of pulp and periapicaltissues
Gutmann et al. JOE — Volume 35, Number 12, December 2009
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Normal pulp A clinical diagnostic category in which
the pulp is symptom-free and normally responsive to pulp testing*.
Asymptomatic Mild to moderate response: stimuli Subside immediately on removal
AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009
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No painful response: palpation & percussion
Radiographs: clearly delineated canal- tapers to apex, intact lamina dura, no calcification/ resorption.
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Reversible Pulpitis 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
*Pulpal inflammation which should resolve once the etiology is removed (defective restorations or caries).
Dabuleanu M. J Can Dent Assoc 2013;79:d90
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Reversible Pulpitis Clinical condition associated with
subjective & objective findings indicating presence of mild inflammation in pulp tissue
A clinical diagnosis based on subjective and objective findings indicating that the
inflammation should resolve and the pulp return to normal*.*AAE Consensus Conference.JOE — Volume 35, Number 12, December
2009
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Reversible Pulpitis - Causes Incipient caries Cervical erosion Occlusal attrition Thermal shock: Operative procedures Deep periodontal curettage Enamel fracture
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Causes Trauma: Occlusal / Blow Fresh amalgam filling: contact with cast
restoration Circulatory disturbances Local vascular congestion
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Reversible Pulpitis- Histopathology Reparative dentin Disruption of odontoblast layer Dilated blood vessels Extravasation of oedema fluid Immunologically competent chronic
inflammatory cells & occasional acute cells
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Reversible Pulpitis- Symptoms Thermal stimuli: quick, sharp
hypersensitive response- subsides on removal of stimulus
More often by cold than hot Asymptomatic- incipient caries No spontaneous pain
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Diagnosis Patient’s symptoms Momentary sharp
pain, disappearing on removal of stimulus
Cold, sweet, sour Chronic pain-
paroxysm of short or long duration
Complete recovery or shorter relief
Clinical tests Application of cold Normal reaction to
percussion, palpation, mobility
Normal on radiographic examination
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Treatment Prevention Early restoration Desensitization – marked gingival
recession Cavity varnish/ cement base Care in cavity preparation & polishing Sedative dressing- ZOE dressing Vitality tests
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Treatment & Prognosis Sealing & insulating exposed dentin/
vital pulpContinuous / increased irritation- moderate to severe inflammation
Irreversible pulpitis Pulpal necrosis
Favorable: irritant removed early enough
Persistence: irreversible pulpitis
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Irreversible Pulpitis Persistent, inflammatory condition of
the pulp, symptomatic or asymptomatic, caused by a noxious stimulus
Clinical condition associated with subjective and objective findings indicating presence of severe inflammation in the pulp tissue
*Pulpal inflammation which will not resolve once the etiology is removed
*Dabuleanu M. J Can Dent Assoc 2013;79:d90
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Irreversible Pulpitis Acute/ Subacute/ Chronic Partial/ Total Infected/ Sterile Acute: pain by hot/ cold stimulus or
spontaneous Lingering pain Chronic quiescent to Acute symptomatic-
hours/ years Exudate: vented- quiescent, confined- painful
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Irreversible Pulpitis- Histopathology Chronic & acute inflammatory features Congestion of postcapillary venules Affect pulpal circulation : necrosis PMNs: acute inflammatory reaction Lysosomal enzymes + cellular debris of
PMNs: pus
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Areas of microabscesses: necrotic tissue + micro organisms+ lymphocyte, plasma cells, macrophages
Walled off by fibrous connective tissue No micro organisms in the centre of
abscess On pulpal penetration: area of ulceration Necrotic tissue+ PMN zone+ proliferating
fibroblasts: calcific masses
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Symptomatic Irreversible Pulpitis A clinical diagnosis based on subjective
and objective findings indicating that the vital inflamed pulp is incapable of healing. Additional descriptors: lingering thermal pain, spontaneous pain, referred pain*.
Spontaneous intermittent or continuous paroxysms of pain.
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Symptomatic Irreversible Pulpitis Prolonged painful response to cold:
relieved by heat Prolonged painful response to heat :
relieved by cold. Painful response to both Moderate/ severe Sharp/ dull
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Localized/ referred Continuous/ intermittent Later: ‘boring, gnawing, throbbing’ Triggered by change in posture Cavity with no outlet: intense pain Kept awake at night
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Asymptomatic Irreversible Pulpitis A clinical diagnosis based on subjective
and objective findings indicating that the vital inflamed pulp is incapable of healing. Additional descriptors: no clinical symptoms but inflammation produced by caries, caries excavation, trauma*
Progress to symptomatic/ necrotic Treatment as soon as possible
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009
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Diagnosis Grayish scum like layer: exposed pulp Odor of decomposition Probing painful & hemorrhage : deeper
areas of pulp Drop of pus: gaining access
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Diagnosis Radiographs Little use Helps identification of suspect teeth Advanced stages: thickening of PDL Mobility, percussion & palpation:
Negative
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Diagnosis Thermal tests Early: Persistent pain after removal of
stimulus Late: normal response, feeble EPT: marked variation from normal
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Differential diagnosis Reversible
Pain disappears on removal of thermal stimulus
EPT: responds with less current than on control
Irreversible Lingering/
spontaneous pain Asymptomatic:
little/ no pain EPT: more current
required
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Differential diagnosis Irreversible
Early symptomatic: less current with EPT
Abnormal response to cold- sharp, piercing
Later stage: diffuse dull constant pain
Abnormal severe response to heat
Acute alveolar abscess
Swelling Tenderness on
palpation, percussion
Mobility Lack of response
to vitality tests
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Differential diagnosis Pain of non-odontogenic origin: Musculoskeletal pain Neurovascular pain Neuropathic pain Pain caused by a distant pathology
(cardiovascular, cranial, throat, neck) Psychogenic pain
*Dabuleanu M. J Can Dent Assoc 2013;79:d90
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Treatment & Prognosis Pulpectomy Pulpotomy: emergency procedure Surgical removal: not restorable Favorable prognosis: Proper endodontic
therapy & post endodontic restoration
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Chronic Hyperplastic Pulpitis ‘Pulp polyp’ Productive pulpal inflammation due to an
extensive carious exposure of a young pulp
A form of irreversible pulpitis that originates from overgrowth of a chronically inflamed young pulp onto the occlusal surface
Granulation tissue – epithelial covering Long standing, low grade irritation
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Causes & Symptoms Slow progressive carious exposure Large open cavity Young resistant pulp Chronic low grade stimulus Symptomless: discomfort during
mastication
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Chronic Hyperplastic Pulpitis- Histopathology Surface covering: Stratified squamous
epithelium (deciduous) Gingiva/ mucosa/ tongue Young vascular connective tissue+
PMNs+ lymphocytes+ plasma cells Nerve fibers
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Diagnosis Fleshy, reddish pulpal mass filling
chamber & beyond confines of the tooth Size of a pin or upto interfering with
comfortable closure Sensitivity : < pulp, > gingiva No pain, easy bleeding Stalk traced back to pulp chamber
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Diagnosis Radiographs: Large, open cavity:
direct access to the pulp chamber Thermal test: no or feeble response EPT: more current than normal Distinguished from proliferating gingival
tissue
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Treatment & Prognosis Elimination of polypoid tissue; pulp
extirpation Bleeding controlled after tissue removal Temporary dressing after pulpotomy Radicular pulp extirpation later Favorable after adequate endodontic
treatment & restoration
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Necrotic pulp Clinical condition associated with subjective
and objective fndings indicating death of the dental pulp
A clinical diagnostic category indicating death of the dental pulp. The pulp is usually nonresponsive to pulp testing*.
Exudate: absorbed / drained- necrosis delayed & radicular pulp vital for long periods
Closure/ sealing of inflamed pulp- rapid & total necrosis & periradicular pathosis
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009
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Necrotic pulp Non vital/ necrotic Suspected on negative reaction to
sensitivity tests Confirmed on inspection of root canal
space only Total/ Partial Sequel to inflammation/ trauma- before
inflammation: Dry gangrenous necrotic pulp
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Necrosis- Types Coagulation : soluble portion precipitated/
converted to solid material Caseation : form of coagulation necrosis-
tissue converted to cheesy mass: coagulated proteins+ fat+ water
Liquefaction : softened mass/ liquid/ amorphous debris by proteolytic enzymes. Follows irrevrsible pulpitis
Ischemic : traumatic injury, disruption of blood supply
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Necrotic pulpIntermediate products- unpleasant odor Indole Skatole Putrecine Cadaverine
End products H2S NH3 Fatty substances Indican Protamines Water CO2
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Necrotic pulpHistopathology Necrotic pulp
tissue Cellular debris Microorganisms Normal/ slight
evidence of inflammation: peripaically
Cause Bacteria Trauma Chemical irritation
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Necrotic pulp- Symptoms No painful symptoms if otherwise
normal Discoloration: first symptom Dull/ Opaque: lack of normal
translucency Grayish/ Brownish discoloration By chance discovery
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Symptoms Usually asymptomatic Episodes of spontaneous pain/ discomfort,
pain on pressurePartial necrosis: Vital nerve fibers- positive thermal tests
Pain on heat application- thermal expansion of gases present in RC space
Unlikely Cold, heat, electric stimuli: no response
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Diagnosis Non responsive to vitality testing Presence of various degrees of
inflammatory response- teeth with multiple canals: confusion
Minimal response-EPT: conduction through moisture
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Diagnosis Spread of inflammatory reactions to
periradicular tissues: sensitive to percussion & palpation
Radiographs: large cavity/ filling , open approach to RC, thickening of PDL
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Treatment & Prognosis RCT Surgical removal Favorable: proper endodontic therapy
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Pulp Degeneration Seldom recognized clinically Generally: old; persistent mild irritation:
young Not infected/ restored always Early: no definite symptoms Late: discolored, no response to
stimulation Types: Calcific, Atrophic, Fibrous
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Calcific Degeneration/Hard tissue changes Pulp calcification Resorption
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Pulp CalcificationExtensive- pulp stones/ diffuse Trauma Caries Periodontal disease Other irritants Sources: Thrombi in vessels & collagen
sheaths around vessel walls
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Pulp stones Pulp chamber generally Laminated structure: Skin of an onion Source: True/ False Position: canal wall- Free - Attached/ Adherent - Embedded/ Interstitial
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Pulp CalcificationCalcific Metamorphosis: Extensive formation of hard tissue on
dentin walls Irritation/ death & replacement of
odontoblasts Partial/ complete radiographic
obliteration of pulp chamber & root canal
Yellowish discoloration of the crown
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Pulp Calcification Increased pain threshold to stimuli;
often unresponsive Palpation & percussion : WNL Various degrees of pulp space
obliteration- radiographic Reduction in coronal pulp space &
gradual narrowing of root canal Not pathologic, no treatment
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Internal/ Intracanal resorption Idiopathic slow or fast progressive
resorptive process occurring in the dentin of the pulp chamber or root canals of teeth
Resorption of dentin walls, advancing from centre to periphery
Asymptomatic mostly Advanced cases: pink spots in the crown
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Internal resorption- Histopathology Osteoclastic activity Lacunae- filled by osteoid tissue Granulation tissue MNGCs/ Dentinoclasts Chronic inflammation Metaplasia of pulp: Bone/ Cementum
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Internal/ Intracanal resorption Pulpal & periapical tests: WNL Radiographs: Radiolucency with
irregular enlargement of root canal compartment; round/ ovoid radiolucent area
Immediate removal of inflamed tissue, RCT
Progression & perforation to lateral periodontium-
necrosis & treatment difficult
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Treatment & Prognosis Routine endodontic therapy Obturation: Plasticized GP method Root perforation: MTA repair Prognosis: Best before perforation Guarded: perforation Surgical repair
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Atrophic Degenration Histopathological diagnosis Older people Fewer stellate cells, increased
intracellular fluid Less sensitive pulp tissue ‘Reticular atrophy’- delay of fixative
agent reaching pulp: artifact
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Fibrous degeneration Cellular elements replaced by fibrous
connective tissue Leathery fiber appearance on
extirpation No clinical diagnosis
Kouros et al Eur J Dent 2013;7 Suppl 1:s26-32
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Pulp artifacts Unsatisfactory
fixation: Fatty degeneration
of pulp Vacoulization
Tumor metastasis
Rare Terminal stages Direct local
extension from jaw
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PREVIOUSLY TREATED PULP A clinical diagnostic category in which
the tooth had had either partial or complete endodontic therapy
A clinical diagnostic category indicating that the tooth has been endodontically treated and the canals are obturated with various filling materials other than intracanal medicaments*
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009
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PREVIOUSLY TREATED PULP Symptomatic/ asymptomatic Completion of partial RCT Retreatment of failed RCT Endodontic surgery Extraction
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Previously Initiated Therapy A clinical diagnostic category indicating that
the tooth has been previously treated by partial endodontic therapy (eg, pulpotomy, pulpectomy)*
Pulpotomy/ Pulpectomy performed before presenting for RCT
Emergency procedure: Irreversible pupitis Vital pulp therapy Traumatic injuries Accurate pulpal diagnosis: Impossible
*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009
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Dental pulp in Systemic diseases Systemic viral infections Genetic & developmental disorders Endocrine disorders Cancer
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Genetic disorders Hypophosphatemic rickets Taurodontism Dens invaginatus Dentinogenesis imperfecta amelogenesis imperfecta Gaucher’s disease
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Systemic viral infections
Glick et al
HIV: dental pulp & periradicular tissues- reinforcing universal precautions
HSV-I &II: pain, pulpal necrosis & internal resorption
Gregory et al- 1975Solomon et al- 1986Sigurdsson & Jacoway- 1995
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Systemic viral infections Rubella:
cytopathic effects on ameoblasts
1st trimester
Paget’s disease: Measles virus –
Paramyxovirus family Pulpal obliteration Internal resorption Dystrophic
calcification Apical ending: difficult
to localize in treatment
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Diabetes mellitus Presence of large-vessel and small-
vessel angiopathies and a thickened basement membrane*
Extensive amorphous calcifications** Larger & more prevalent periradicular
lesions of endodontic origin***
*Russel B.Acta Pathol Microbiol Scand 1967; 70: 319-320
**Bissada et al. Egypt Dent J 1970; 283-296***falk et al. Scand J Dent Res 1989; 97:198-206
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Diabetes mellitus Limited dental collateral circulation Impaired immune response Increased risk of acquiring pulp
infection/ necrosis Hyperglycaemia- bone resorption,
inhibiting osteoblastic differentiation and reducing bone recovery.
Lima et al .International Endodontic Journal, 46, 700–709, 2013
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New investigation EphA7 genetic expression: marked in
inflamed human dental pulp Pathogenesis, diagnosis & therapy of
tumors: lymphoma & GITDong Y et al. JOE — Volume 39, Number 2, February 2013
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References Chandra BS, Gopi Krishna V. Grossman’s
Endodontic Practice. 12th Edition Beer R, Baumann MA, Kielbassa AM.
Pocket Atlas of Endodontics Tronstad L. Cinical Endodontics. A
textbook. 2nd revised edition Abbott PV. Endodontics and Dental
Traumatology. An overview of Modern Endodontics
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References Castelucci A. Endodontics. Volume 1 Hargreaves KM, Cohen S. Cohen’s Pathways of
the Pulp. 10th Edition Ingle JI, Bakland LK. Ingle’s Endodontics. 5th
Edition Hargreaves KM, Goodis HE. Seltzer and
Bender’s Dental Pulp. AAE Consensus Conference on Diagnostic
Terminology: Background and Perspectives. J Endod .2009;35(12):1634
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References Gutmann JL, Baumgartner GC, Gluskin AH,
Hartwell GR, Walton RE. Identify and Define All Diagnostic Terms for Periapical/
Periradicular Health and Disease States. J Endod 2009;35:1658–1674 Dabuleanu M. Pulpitis (Reversible/ Irreversible).
Can Dent Assoc 2013;79:d90 Lima SMF, Grisi DC, Kogawa EM. et al. Diabetes
mellitus and inflammatory pulpal and periapical disease: a review. Int End J. 46, 700–709, 2013
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Fernandes M, de Ataide I, Wagle R. Tooth resorption part I - pathogenesis and case series of internal resorption. J Conserv Dent 2013;16:4-8
Kouros P, Koliniotou-Koumpia E, Koulaouzidou E, Helvatjoglu-Antoniades M, Tziafas D. Pulp response to dentine adhesives: A study on mature human pulps. Eur J Dent 2013;7 Suppl 1:s26-32
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Thank You…..