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  1. 1. DISEASES OF THE PULP Prepared by: Dr. Rea Corpuz
  2. 2. Pulp formative organ of tooth builds primary dentin during development of tooth secondary dentin after tooth eruption reparative dentin in response to stimulation as long as odontoblast remain vital
  3. 3. Pulpitis most common cause of dental pain loss of teeth in younger persons usual cause is caries penetrating the dentin
  4. 4. Pulpitis UNTREATED Death of pulp Spread of Infection throughapical foramina into periapical tissuesCauses Periapical Periodontitis
  5. 5. Causes of PulpalInflammation (1) Mechanical Cause (2) Thermal Cause (3) Chemical Cause (4) Bacterial Cause
  6. 6. Causes of PulpalInflammation (1) Mechanical Cause  traumatic accident  iatrogenic damage for dental procedure  atrrition  abrasion
  7. 7. Causes of PulpalInflammation (2) Thermal Cause  uninsulated metallic restoration  during cavity preparation  polishing
  8. 8. Causes of PulpalInflammation (3) Chemical Cause  arise from erosion  or inappropriate use of acidic dental material
  9. 9. Causes of PulpalInflammation (4) Bacterial Cause  can damage pulp through toxins secreted by bacteria from caries
  10. 10. Classification (1) Based on Severity of Inflammation (2) According to Involvement
  11. 11. (1) Based on Severity of Inflammation (1) Reversible Pulpitis (2) Irreversible Pulpitis (3) Pulp Degeneration (4) Pulp Necrosis
  12. 12. (1) Based on Severity of Inflammation (1) Reversible Pulpitis  Symptomatic (acute)  Aysptomatic (chronic) (2) Irreversible Pulpitis  Acute • Abnormally responsive to cold • Abnormally responsive to heat
  13. 13. (1) Based on Severity of Inflammation (2) Irreversible Pulpitis  Chronic • Asymptomatic with pulp exposure • Hyperplastic • Internal resorption
  14. 14. (1) Based on Severity of Inflammation (3) Pulp Degeneration  Calcific (4) Pulp Necrosis
  15. 15. (2) According to Involvement (1) According to Involvement (2) According to Severity (3) According to presence or absence of direct communication between dental pulp + oral environment
  16. 16. (2) According to Involvement (1) According to Involvement  Focal or Subtotal or Partial Pulpitis  Total or Generalized Pulpitis
  17. 17. (2) According to Involvement (2) According to Severity  Acute  Chronic
  18. 18. (2) According to Involvement (3) According to presence or absence of direct communication between dental pulp + oral environment  Pulpitis Aperts (open pulpitis)  Pulpitis Clausa (closed pulpitis)
  19. 19. Reversible Pulpitis mild to moderate inflammatory condition of pulp caused by noxious stimuli pulp is capable of returning to un-inflammed state following removal of stimuli
  20. 20. Reversible Pulpitis Causes  agent capable of injuring pulp like: • trauma • disturbed occlusal relationship • thermal shock
  21. 21. Reversible Pulpitis Clinical Features  sharp pain lasting for a moment  often brought on by cold than hot food or beverages and by cold air
  22. 22. Reversible Pulpitis Clinical Features  does not continue when the cause has been removed  tooth responds to electric pulp testing at lower current
  23. 23. Reversible Pulpitis Management  prevention  periodic care  early insertion of filling if a cavity has developed  removal of noxious stimuli
  24. 24. Focal ReversiblePulpitisearliest form also known as pulp hyperemia excessive accumulation of blood within pulp tissue leads to vascular congestion
  25. 25. Focal ReversiblePulpitis Clinical Features  sensitive to thermal changes  particularly to cold  application of ice or cold fluids to tooth result in pain
  26. 26. Focal ReversiblePulpitis Clinical Features  disappears upon removal of thermal irritant or restoration of normal temperature  responds to electrical test stimulant at lower level of current
  27. 27. Focal ReversiblePulpitis Clinical Features  indicates lower pain threshold than that of adjacent normal teeth
  28. 28. Focal ReversiblePulpitis Clinical Features  teeth show: • deep carious lesion • large metallic restoration • restoration with defective margins
  29. 29. Focal ReversiblePulpitis Management  removal of irritants before the pulp is severely damaged
  30. 30. Irreversible Pulpitis persistent inflammatory condition of pulp may be symptomatic or asymptomatic caused by noxious stimulus
  31. 31. Irreversible Pulpitis Causes  bacteria involvement of pulp through caries  chemical  thermal  mechanical injury
  32. 32. Irreversible Pulpitis Clinical Features Early Stage  paroxysm of pain caused by: • sudden temperature changes like cold, sweet, acid foodstuffs
  33. 33. Irreversible Pulpitis Clinical Features Early Stage  pain often continues when cause has been removed  may come and go spontaneously
  34. 34. Irreversible Pulpitis Clinical Features Early Stage  pain • sharp • piercing • shooting • generally severe
  35. 35. Irreversible Pulpitis Clinical Features Early Stage  pain • bending over exacerbates pain which • lying down is due to change in • change of position intrapulpal pressure
  36. 36. Irreversible Pulpitis Clinical Features Late Stage  pain • more severe as if tooth is under • throbbing constant pressure
  37. 37. Irreversible Pulpitis Clinical Features Late Stage  pain • patient is often awake at night due to pain • increased by heat and sometimes relieved by cold, although continued application of cold may intensify pain
  38. 38. Irreversible Pulpitis Management  complete removal of pulp or pulpectomy  placement of intracanal medicament  to act as disinfectant or obtundent • cresatin • eugenol • formocresol
  39. 39. Clinical Difference Reversible Pulpitis Irreversible Pulpitis  pain is generally traceable  more severe to a stimulus  lasts longer  cold water  pain may come  air without any apparent stimulus
  40. 40. Acute Pulpitis extensive acute inflammation of pulp frequent sequel of focal reversible pulpitis
  41. 41. Acute Pulpitis Causes  tooth with large carious lesion  defective restoration where there has been recurrent caries  pulp exposure due to faulty cavity preparation
  42. 42. Acute Pulpitis Clinical Features  severe pain is elicited by thermal changes  pain persists even after thermal stimulus disappears or been removed
  43. 43. Acute Pulpitis Clinical Features  may be continuous  intensity may be increased when patient lies down  application of heat may may cause acute exacerbation of pain
  44. 44. Acute Pulpitis Clinical Features  tooth reacts to electric pulp vitality tester at a lower level of current than adjacent normal teeth
  45. 45. Acute Pulpitis Clinical Features  pressure increases because of lack of escape of inflammatory exudate  rapid spread of inflammation through pulp with pain + necrosis
  46. 46. Acute Pulpitis Management  early stages of pulpotomy (removal of coronal pulp)  placing material that favors calcification such as: • calcium hydroxide over entrance of root canals
  47. 47. Acute Pulpitis Management  root canal filing with inert material like gutta percha should be done
  48. 48. Chronic Pulpitis may develop with or without episodes of acute pulpitis many pulps under large carious cavities die painlessly 1st indication is then development of periapical periodontitis, either with pain or seen by chance in radiograph
  49. 49. Chronic Pulpitis Clinical Features  dull aching type  more often intermittent than continuous
  50. 50. Chronic Pulpitis Management  root canal therapy  followed by crown restoration
  51. 51. Chronic HyperplasticPulpitis also called as pulp polyp or pulpitis aperta essentially an excessive exuberant proliferation of chronically inflammed dental pulp tissue
  52. 52. Chronic HyperplasticPulpitis pulpal inflammation due to an extensive carious exposure of a young pulp development of granulation tissue covered at times by epithelium resulting from long standing low grade infection
  53. 53. Chronic HyperplasticPulpitis Causes  slow progressive exposure of pulp  bacterial infection
  54. 54. Chronic HyperplasticPulpitis Clinical Features  most commonly involved are deciduous molars + 1st permanent molar • excellent blood supply • large root opening
  55. 55. Chronic HyperplasticPulpitis Clinical Features  asymptomatic  seen only in teeth of children + young adults
  56. 56. Chronic HyperplasticPulpitis Clinical Features  polypoid tissue appears • fleshy • reddish pulpal mass filling most of pulp chamber or cavity • or even extend beyond confines of tooth
  57. 57. Chronic HyperplasticPulpitis Clinical Features  polypoid tissue appears • sometimes, if mass is large enough • interferes with closure of mouth
  58. 58. Chronic HyperplasticPulpitis Clinical Features  polypoid tissue appears • may cause discomfort during mastication • due to pressure of food bolus
  59. 59. Chronic HyperplasticPulpitis Clinical Features  polypoid tissue appears • tissue easily bleeds because of rich network of blood vessels • tooth may respond or not at all to thermal test
  60. 60. Chronic HyperplasticPulpitis Management  elimination of polypoid tissue  followed by extirpation of pulp  hyperplastic tissue bleeeding can be controlled by pressure  extraction of tooth can also be done
  61. 61. Necrosis death of pulp may be partial or total depending on whether part or the entire pulp is involved
  62. 62. Necrosis Causes  sequeala of inflammation  can also occur following trauma • pulp is destroyed before an inflammatory reaction
  63. 63. Necrosis Types  (1) Coagulation Necrosis  (2) Liquefaction Necrosis
  64. 64. Necrosis Types  (1) Coagulation Necrosis • soluble portion of tissue is precipitated • or converted into a solid material
  65. 65. Necrosis Types  (1) Coagulation Necrosis • tissue is converted into tissue mass consisting chiefly of coagulated  proteins  fats  water
  66. 66. Necrosis Types  (2) Liquefaction Necrosis • results when proteolytic enzymes convert the tissue into softened mass liquid or amorphous debris
  67. 67. Necrosis Clinical Features  no painful symptoms  discoloration of tooth • 1st indication that the pulp is dead
  68. 68. Necrosis Clinical Features  history of pain lasting from a few minutes to a few hours followed by complete + sudden cessation of pain
  69. 69. Necrosis Management  preparation + obturation of root canals
  70. 70. References: Books  Cawson, R.A: Cawson’s Essentials of Oral Oral Pathology and Oral Medicine, 8th Edition • (page 60)  Ghom, Ali & Mhaske, Shubhangi: Textbook of Oral Pathology • (pages 420-425)