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Diseases of pulp

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Diseases of the pulp
Diseases of the pulp
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Diseases of pulp

  1. 1. Diseases of The Pulp Prepared by, VISHAL KURIAN
  2. 2.  Pulpitis is the inflammation of the pulp tissue  Usually caused by caries penetrating the dentin  Most common manifestations are tooth ache &increased sensitivity to hot & cold  Pulp inflamed > pressure build ups on pulp cavity > pressure on nerves & surrounding tissues > pain
  3. 3. Causes of Pulpal Inflammation  (1) Mechanical Cause  traumatic accident  iatrogenic damage for dental procedure  attrition  abrasion  (2) Thermal Cause  uninsulated metallic restoration  during cavity preparation  polishing
  4. 4.  (3) Chemical Cause  arise from erosion  or inappropriate use of acidic dental material  (4) Bacterial Cause  can damage pulp through toxins secreted by bacteria from caries
  5. 5. Classification 1) Based on Severity of Inflammation (1) Reversible -Symptomatic ( acute) - Asymptomatic ( Chronic) (2) Irreversible a) Acute - abnormally responsive to cold -abnormally responsible to hot b)Chronic - Asymptomatic with pulp exposure - Hyperplastic - Internal resorption (3) Pulp Degeneration - Calcific (4) Pulp Necrosis
  6. 6. (2) According to Involvement  Acc. To involvement: 1. Focal / subtotal /partial pulpitis (inf. Is confined to a portion of pulp) 2. Total / generalized pulpitis ( most part of the pulp is involved)  Acc. To severity : 1.Acute 2.Chronic  Acc. To presence or absence of direct communication b/w pulp & oral evironment: 1.Pulpitis asperta (open) 2.Pulpitis clousa (closed)
  7. 7. Reversible pulpitis  Pathogenesis:  Stimuli of short duration eg. Cutting dentin  mild to moderate inflammatory condition of pulp  caused by noxious stimuli  pulp is capable of returning to un-inflammed state  following removal of stimuli  Causes:  agent capable of injuring pulp like:- • trauma • disturbed occlusal relationship • thermal shock
  8. 8. Clinical Features  sharp pain lasting for a moment  often brought on by cold than hot food or beverages and by cold air  does not continue when the cause has been removed  tooth responds to electric pulp testing at lower current
  9. 9.  Ranges from hyperemia to mild to moderate inflammation of the affected area.  Reperative dentine  Dilated blood vessels  Edema  Presence of immunologic response Histopathological features:
  10. 10. Management  prevention  periodic care  early insertion of filling if a cavity has developed  removal of noxious stimuli
  11. 11. Focal reversible pulpitis  earliest form  also known as pulp hyperemia  excessive accumulation of  blood within pulp tissue  leads to vascular congestion
  12. 12. Clinical Features  sensitive to thermal changes  particularly to cold  application of ice or cold fluids to tooth result in pain  disappears upon removal of thermal irritant or restoration of normal temperature  responds to electrical test stimulant at lower level of current  indicates lower pain threshold than that of adjacent normal teeth  teeth show: • deep carious lesion • large metallic restoration • restoration with defective margins
  13. 13.  Management  removal of irritants before the pulp is severely damaged  Carious lesion should be excised & restored or defective filling is replaced.  If primary cause is not corrected, extensive pulpitis may result in death of pulp.
  14. 14. Histopathologic features: Dilation of pulp blood vessels. Edema fluid collection due to damage of vessel wall & allowing extravasations of RBC or diapedesis of WBC. Slowing of blood flow & hemoconcentration due to transudation can cause thrombosis. Reparative or reactionary dentin in adjacent dentinal wall
  15. 15. Acute pulpitis  extensive acute inflammation of pulp  frequent sequel of focal reversible pulpitis Usually occurs in a tooth with a large carious lesion /restoration Commonly a defective restoration around whivh there has been recurrent caries
  16. 16.  Causes  tooth with large carious lesion  defective restoration where there has been recurrent caries  pulp exposure due to faulty cavity preparation
  17. 17.  Clinical Features  severe pain is elicited by thermal changes  pain persists even after thermal stimulus disappears or been removed  may be continuous  intensity may be increased when patient lies down  application of heat may may cause acute exacerbation of pain  tooth reacts to electric pulp vitality tester at a lower level of current than adjacent normal teeth
  18. 18. HISTOLOGICAL FEATURES Edema in pulp with vasodilation. Infiltration of polymorphonuclear leukocytes along vascular channels & migrate through endothelium lined structures. Destruction of odontoblasts at pulp dentin border. Rise in pressure due to inflammatory exudate local collapse of venous part of circulation Tissue hypoxia & anoxia Destruction of pulp & abscess formation. Abscess consists pus, leukocytes & bacteria. Numerous abscess formation cause pulp liquefaction & necrosis. (acute suppurative pulpitis)
  19. 19. TREATMENT & PROGNOSIS: Drainage of exudates from pulp chamber. Pulpotomy & placing calcium hydroxide over entrance of root canal. Root canal treatment. Extraction of tooth.
  20. 20. CHRONIC PULPITIS  may develop with or without episodes of acute pulpitis  More frequewntly occurs as chronic type from the onset.  CLINICAL FEATURES: Pain is not prominent, mild, dull ache which is intermittent. Reaction to thermal changes is reduced because of degeneration of nerves. Response to pulp vitality tester is reduced. Wide open carious lesion & with exposure of pulp cause relatively little pain. Manipulation with small instruments often elicits bleeding but with little pain.
  21. 21. HISTOLOGIC FEATURES: Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective tissue reaction. Capillaries are prominent; fibroblastic activity & collagen fibers in bundles. When granulation tissue formation occurs in wide open exposed pulp surface – ulcerative pulpitis. (with bacterial stains & micro org. in carious lesion) If pulpal reaction vacillates between an acute & chronic phase causes pulp abscess formation, which is surrounded by fibrous CT wall.
  22. 22. TREATMENT & PROGNOSIS: Root canal therapy Extraction of tooth.
  23. 23. Chronic Hyperplastic pulpitis  also called as pulp polyp or pulpitis aperta  Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass.  a form chronic pulpitis  Occurs either as a chroniv lesion from onset or as a chronic stage of a previously ACUTE PULPITIS
  24. 24. Children & young adults with high degree of tissue resistance & reactivity & responds to proliferative lesions. Pulp - pinkish red globule of tissue protruding from chamber & extend beyond caries. Most commonly affected are deciduous molar & Ist permanent molars. Pulp is relatively insensitive because few nerves in hyperplastic tissue. Clinical feaures:
  25. 25. Lesion bleeds profusely upon provocation. Due to excellent blood supply high tissue resistance & reactivity in young persons leads to unusual proliferative property of pulp. Some cases, gingival tissue adjacent, may proliferate into carious lesion & superficially resemble hyperplastic pulpitisa
  26. 26. HISTOLOGIC FEATURES: Hyperplastic tissue is basically granulation tissue, consisting delicate CT fibers & young blood capillaries. Inflammatory infiltrates – lymphocytes, plasma cells & polymorphs. Stratified squamous type epithelial lining resembles oral mucosa with well formed rete pegs.
  27. 27.  TREATMENT & PROGNOSIS: Extraction of tooth or RCT. Grafted epithelial cells are believed to be desquamated epith. Cells, which carried by saliva. Origin of these cells is unknown. They are degenerated superficial squames, which ’ve lost dividing capacity. When pulp polyp is present for a long time, persistent rubbing of buccal mucosa may help in grafting of epith. cells
  28. 28. Necrosis  death of pulp  may be partial or total depending on whether part or the entire pulp is involved
  29. 29.  Causes  sequeala of inflammation  can also occur following trauma • pulp is destroyed before an inflammatory reaction
  30. 30.  Types  (1) Coagulation Necrosis • tissue is converted into tissue mass consisting chiefly of coagulated  proteins  fats  water  (2) Liquefaction Necrosis • results when proteolytic enzymes convert the tissue into softened mass liquid or amorphous debris
  31. 31.  Clinical Features  no painful symptoms  discoloration of tooth • 1st indication that the • pulp is dead  history of pain lasting from a few minutes to a few hours followed by complete + sudden cessation of pain
  32. 32.  Management  preparation + obturation of root canals

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