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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](https://image.slidesharecdn.com/diseasesofthepulp-151031155704-lva1-app6892/85/Diseases-of-the-pulp-51-320.jpg)
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Diseases of the pulp
This document discusses various classifications of pulpal diseases. It describes classifications proposed by Grossman, Baume, Seltzer & Bender, Johnson, American Board of Endodontics, Reit et al., Walton & Torabinejad, Torabinejad & Shabahang, Tronstad, Ingle & Beveridge, Castelucci, Beer & Baumann, Abbott, and the World Health Organization. Many classifications divide pulpal diseases into categories such as normal pulp, reversible pulpitis, irreversible pulpitis, necrosis, hyperplastic pulpitis, and previously treated pulp. The classifications aim to help with treatment planning, prognosis determination, and assessing restorative needs based on the signs and symptoms of
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Diseases of the pulp
- 1. DISEASES OF THE DENTAL PULP-Part II Deepthi P.R. 1st year MDS Dept of Conservative Dentistry & Endodontics
- 2. CONTENTS Introduction Irritants Inflammatory process Immunologic responses Lesion progression Classification of diseases
- 3. INTRODUCTION Etiologic factorscausing pulp inflammation Mechanism of spread of inflammation Mediators of pulpal inflammation Classification & features of diseases
- 4. IRRITANTS Living • Micro organisms •Viruses Non Living • Mechanical • Thermal • Chemical
- 5. Microbial irritants Mainsource Numerous species: S. mutans, Lactobacilli, Actinomyces Toxins: deep penetration to pulp Local infiltration of pulp- chronic inflammatory cells Progression: intensity & character changes
- 6. Microbial irritants Actualexposure: PMN infiltration & liquefaction necrosis Long periods of inflammation/ necrosis- • Virulence • Release of inflammatory fluid: avoiding intrapulpal pressure • Host resistance • Circulation • Lymphatic drainage
- 7. Microbial irritants Yamasakiet 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
- 8. Microbial irritants Kakehashiet 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
- 9. Microbial irritants Viruses:symptomatic apical pathoses Periapical lesions: CMV & EBV- symptomatic
- 10. Mechanical irritants Deepcavity preparations Removal of tooth structure without proper cooling Impact trauma Occlusal trauma Deep periodontal curettage Orthodontic movement
- 11. Mechanical irritants Extensiverestorative procedures: pulpal inflammation Dentin permeability closer to pulp 𝑃𝑢𝑙𝑝 𝑑𝑎𝑚𝑎𝑔𝑒 ∝ 𝑎𝑚𝑜𝑢𝑛𝑡 𝑜𝑓 𝑡𝑜𝑜𝑡ℎ 𝑠𝑡𝑟𝑢𝑐𝑡𝑢𝑟𝑒 𝑟𝑒𝑚𝑜𝑣𝑒𝑑 + 𝑑𝑒𝑝𝑡ℎ 𝑜𝑓 𝑟𝑒𝑚𝑜𝑣𝑎𝑙 Operative procedures without coolant- more pulpal irritation
- 12. Mechanical irritants Impactinjuries : 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
- 13. 48 hours aftercrown preparation through enamel & 1mm into dentin Aspiration of odontoblasts into tubules & pulpal infiltration by PMNs & Lymphocytes M Torabinejd. Endodontics
- 14. Chemical irritants Dentinsterilizing : 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
- 15. 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
- 16. Pulpal pathosis Severity& duration of illness Host capacity Reversible pulpitis Irreversible pulpitis Total necrosis
- 17. Inflammatory process Irritationof dental pulp – mediators: Histamine, Bradykinin, Arachidonic acid metabolites Lysosomal granule products: Elastase, Cathepsin G, Lactoferrin Protease inhibitors: Antitrypsin, CGRP, Substance P
- 18. Inflammatory process Mastcells: Histamine, Leukotrienes, PAF Released: Physical injury to mast cells or bridging of IgE Bradykinin, Substance P, Neurokinin A Plasma/ Tissue kallikreins Kininogens Kinins
- 19. Inflammatory process iCGRPrelease : PGE2 Pulpal nerve fibers: SP, CGRP- protective Mild- moderate injuries: iCGRP Severe: iCGRP Cellular damage Arachidonic acid
- 20. Immunologic Responses Bacteria& by products: Antigen Immunocompetent cells – Normal pulp Ig levels in inflamed pulps Arthus reaction Delayed hypersensitivity reactions Necrotic foci & pulpal necrosis
- 21. Healthy pulp Pulp: vital; free of inflammation Prosthetic reasons First hours after traumatic pulp exposure
- 22. Pulpitis Vital &inflamed No info on: Degree of inflammation Reversible/ irreversible Two clinical diagnoses for inflamed pulp Symptomatic pulpitis Asymptomatic pulpitis
- 23. 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
- 24. Lesion Progression Moderateto 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
- 25. Accumulation of inflammatorycells within the pulp horn Beer. Pocket Atlas of Endodontics
- 26. Neutrophilic granulocytes inPredentin layer & Dentin tubules Beer. Pocket Atlas of Endodontics
- 27. Lesion Progression capillarypressure & permeability Exudation tissue pressure: passive compression & complete collapse of venules Increased pressure Inablity to expand Lack of collateral circulation Pulpal necrosis
- 28.
- 29. PULPITIS Acute/ Chronic:Clinical differentiation Partial/ Total Infected/ Sterile: smear or culture Acute: Precipitous short course Violently painful Chronic: Practically symptomless Slightly painful Longer duration Exposed pulp: caries/ trauma Hyperplastic pulpitis Ulcerative pulpitis
- 30.
- 31. CONTENTS Introduction Differentclassifications Normal pulp Reversible pulpitis Irreversible pulpitis Chronic hyperplastic pulpitis Necrotic pulp Pulp degeneration Previously treated pulp Previously initiated therapy
- 32. 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%
- 33. 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
- 34. Grossman 1. Inflammatory diseasesof the dental pulp a. Reversible pulpitis (i) Symptomatic (acute) (ii) Asymptomatic (chronic) b. Irreversible pulpitis (i) Acute - Abnormally responsive to cold - Abnormally responsive to heat
- 35. Grossman (ii) Chronic - Asymptomaticwith pulp exposure - Hyperplastic pulpitis - Internal resorption 2. Pulp degeneration a. Calcific (radiographic diagnosis) b. Others (histopathologic diagnosis) 3.Necrosis
- 36. Baume Symptomless vitalpulp: 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
- 37. 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
- 38. William T.Johnson Normal Reversible pulpitis Irreversible pulpitis
- 39. American Board of Endodontics(ABE)- 2007 Normal pulp Reversible pulpitis Irreversible pulpitis Symtomatic Asymptomatic Pulp necrosis Previously treated Previously initiated therapy
- 40. Reit, Petersson &Molven Pulpa sana Pulpitis Necrosis pulpae Periodontitis apicalis chronica/ acuta
- 41. Walton & Torabinejad Normal Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis
- 42. Torabinejad & Shabahang Normal pulp Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis Previously treated pulp
- 43. Tronstad Healthy pulp Asymptomatic pulpitis Symptomatic pulpitis Necrotic pulp
- 44. Ingle & Beveridge Incipient acute pulpalgia Moderate & advanced acute pulpalgia Chronic pulpalgia Hyperplastic pulposis Necrosis
- 45. Castelucci Healthy pulp Hyperemia Pulpitis Necrosis
- 46. Beer & Baumann Asymptomatic pulp pathology Reversible pulpitis Irreversible pulpitis Pulpal necrosis
- 47. Abbott a.Clinically normal pulp b.Reversiblepulpitis Types: Acute, Chronic c. Irreversible pulpitis Types: Acute Chronic, Necrobiosis d. Pulp necrosis Types: Necrosis without infection, Necrosis with infection
- 48. Abbott e. Pulpless Canals Types:Pulpless and no signs of infection Pulpless and infected f. Degenerative Changes Types: Atrophy, Pulp canal obliteration(calcification)- Partial, Total Hyperplasia Internal resorption- Inflammatory, Replacement
- 49. Abbott g. Previous RootCanal Treatment Types : Satisfactory – No signs of infection - Infected Technically inadequate - No signs of infection - Infected h. Endodontic- Periodontal Lesions
- 50. Abbott h. Endodontic- PeriodontalLesions Classification 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
- 51. Application of theInternational 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
- 52. Application of theInternational 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 dentine Excludes: pulpal calcifications (K04.2) pulpal stones (K04.2 Gutmann et al. JOE — Volume 35, Number 12, December 2009
- 53. Application of theInternational 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 sinus Includes: 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
- 54. K04.7 Periapicalabscess without sinus Dental abscess } Dentoalveolar abscess } without sinus Periodontal abscess of pulpal origin } K04.8 Radicular cyst Includes: cyst apical periodontal periapical K04.80 Apical and lateral K04.81 Residual K04.82 Inflammatory paradental Excludes: developmental lateral periodontal cyst (K09.04) K04.89 Radicular cyst, unspecified K04.9 Other and unspecified diseases of pulp and periapical tissues Gutmann et al. JOE — Volume 35, Number 12, December 2009
- 55. Normal pulp Aclinical 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
- 56. No painfulresponse: palpation & percussion Radiographs: clearly delineated canal- tapers to apex, intact lamina dura, no calcification/ resorption.
- 57. Reversible Pulpitis Mildto 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
- 58. Reversible Pulpitis Clinicalcondition 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
- 59. Reversible Pulpitis -Causes Incipient caries Cervical erosion Occlusal attrition Thermal shock: Operative procedures Deep periodontal curettage Enamel fracture
- 60. Causes Trauma: Occlusal/ Blow Fresh amalgam filling: contact with cast restoration Circulatory disturbances Local vascular congestion
- 61. Reversible Pulpitis- Histopathology Reparativedentin Disruption of odontoblast layer Dilated blood vessels Extravasation of oedema fluid Immunologically competent chronic inflammatory cells & occasional acute cells
- 62. 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
- 63. Diagnosis Patient’s symptoms Momentarysharp 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
- 64. Treatment Prevention Early restoration Desensitization – marked gingival recession Cavity varnish/ cement base Care in cavity preparation & polishing Sedative dressing- ZOE dressing Vitality tests
- 65. Treatment & Prognosis Sealing & insulating exposed dentin/ vital pulp Continuous / increased irritation- moderate to severe inflammation Irreversible pulpitis Pulpal necrosis Favorable: irritant removed early enough Persistence: irreversible pulpitis
- 66. 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
- 67. 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
- 68. 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
- 69. Areas ofmicroabscesses: 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
- 70. Symptomatic Irreversible Pulpitis Aclinical 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.
- 71. Symptomatic Irreversible Pulpitis Prolongedpainful response to cold: relieved by heat Prolonged painful response to heat : relieved by cold. Painful response to both Moderate/ severe Sharp/ dull
- 72. Localized/ referred Continuous/ intermittent Later: ‘boring, gnawing, throbbing’ Triggered by change in posture Cavity with no outlet: intense pain Kept awake at night
- 73. Asymptomatic Irreversible Pulpitis Aclinical 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
- 74. Diagnosis Grayish scumlike layer: exposed pulp Odor of decomposition Probing painful & hemorrhage : deeper areas of pulp Drop of pus: gaining access
- 75. Diagnosis Radiographs Little use Helps identification of suspect teeth Advanced stages: thickening of PDL Mobility, percussion & palpation: Negative
- 76. Diagnosis Thermal tests Early:Persistent pain after removal of stimulus Late: normal response, feeble EPT: marked variation from normal
- 77. Differential diagnosis Reversible Paindisappears 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
- 78. Differential diagnosis Irreversible Earlysymptomatic: 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
- 79. Differential diagnosis Pain ofnon-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
- 80. Treatment & Prognosis Pulpectomy Pulpotomy: emergency procedure Surgical removal: not restorable Favorable prognosis: Proper endodontic therapy & post endodontic restoration
- 82. 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
- 83. Causes & Symptoms Slow progressive carious exposure Large open cavity Young resistant pulp Chronic low grade stimulus Symptomless: discomfort during mastication
- 84. Chronic Hyperplastic Pulpitis- Histopathology Surface covering: Stratified squamous epithelium (deciduous) Gingiva/ mucosa/ tongue Young vascular connective tissue+ PMNs+ lymphocytes+ plasma cells Nerve fibers
- 85. Diagnosis Fleshy, reddishpulpal 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
- 86. 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
- 87. 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
- 89. Necrotic pulp Clinicalcondition 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
- 90. Necrotic pulp Nonvital/ 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
- 91. 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
- 92. Necrotic pulp Intermediate products- unpleasant odor Indole Skatole Putrecine Cadaverine End products H2S NH3 Fatty substances Indican Protamines Water CO2
- 93. Necrotic pulp Histopathology Necroticpulp tissue Cellular debris Microorganisms Normal/ slight evidence of inflammation: peripaically Cause Bacteria Trauma Chemical irritation
- 94. Necrotic pulp- Symptoms No painful symptoms if otherwise normal Discoloration: first symptom Dull/ Opaque: lack of normal translucency Grayish/ Brownish discoloration By chance discovery
- 95. 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
- 96. Diagnosis Non responsiveto vitality testing Presence of various degrees of inflammatory response- teeth with multiple canals: confusion Minimal response-EPT: conduction through moisture
- 97. Diagnosis Spread ofinflammatory reactions to periradicular tissues: sensitive to percussion & palpation Radiographs: large cavity/ filling , open approach to RC, thickening of PDL
- 98. Treatment & Prognosis RCT Surgical removal Favorable: proper endodontic therapy
- 100. Pulp Degeneration Seldomrecognized 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
- 101. Calcific Degeneration/Hard tissue changes Pulp calcification Resorption
- 102. Pulp Calcification Extensive- pulpstones/ diffuse Trauma Caries Periodontal disease Other irritants Sources: Thrombi in vessels & collagen sheaths around vessel walls
- 103. Pulp stones Pulpchamber generally Laminated structure: Skin of an onion Source: True/ False Position: canal wall- Free - Attached/ Adherent - Embedded/ Interstitial
- 104. Pulp Calcification Calcific 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
- 105. Pulp Calcification Increasedpain 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
- 106. 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
- 107. Internal resorption- Histopathology Osteoclasticactivity Lacunae- filled by osteoid tissue Granulation tissue MNGCs/ Dentinoclasts Chronic inflammation Metaplasia of pulp: Bone/ Cementum
- 108. 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
- 109. Treatment & Prognosis Routine endodontic therapy Obturation: Plasticized GP method Root perforation: MTA repair Prognosis: Best before perforation Guarded: perforation Surgical repair
- 110. Atrophic Degenration Histopathologicaldiagnosis Older people Fewer stellate cells, increased intracellular fluid Less sensitive pulp tissue ‘Reticular atrophy’- delay of fixative agent reaching pulp: artifact
- 111. Fibrous degeneration Cellularelements 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
- 112. Pulp artifacts Unsatisfactory fixation: Fatty degeneration of pulp Vacoulization Tumor metastasis Rare Terminal stages Direct local extension from jaw
- 113. 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
- 114. PREVIOUSLY TREATED PULP Symptomatic/ asymptomatic Completion of partial RCT Retreatment of failed RCT Endodontic surgery Extraction
- 115. 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
- 116. Dental pulp inSystemic diseases Systemic viral infections Genetic & developmental disorders Endocrine disorders Cancer
- 117. Genetic disorders Hypophosphatemicrickets Taurodontism Dens invaginatus Dentinogenesis imperfecta amelogenesis imperfecta Gaucher’s disease
- 118. Systemic viral infections Glicket al HIV: dental pulp & periradicular tissues- reinforcing universal precautions HSV-I &II: pain, pulpal necrosis & internal resorption Gregory et al- 1975 Solomon et al- 1986 Sigurdsson & Jacoway- 1995
- 119. 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
- 120. Diabetes mellitus Presenceof 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
- 121. Diabetes mellitus Limiteddental 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
- 122. New investigation EphA7genetic expression: marked in inflamed human dental pulp Pathogenesis, diagnosis & therapy of tumors: lymphoma & GIT Dong Y et al. JOE — Volume 39, Number 2, February 2013
- 123. 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
- 124. 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
- 125. 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
- 126. 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