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Pulp and periapical disease
- 1. Pulpal & periapical diseases BY DIAA ELDIN TEACHING ASSISTANT, NUB ENDODONTIC DEPARTMENT
- 2. Introduction Structure & function of the dentin pulp complex Inflammation & histopathology of inflammation Pathways of the pulp & etiology of pulpal pathosis
- 3. Structure & function of dentin pulp complex Dental pulp complex Dentin structure &Permeability Dental pulp : (histology ,function & special environment)
- 5. Dentin structure & permeability A) dentin structure component D.T : (number ,diameter) B) factors affecting dentin permeability -number of D.T -thickness -exposed dentin -smear layer
- 6. Dental pulp A) histology : 1- cellular structures a) fibroblast
- 7. b) odontoblast Arises from ??? Where ??? Shape function c) Immunocompetent cells d) Reserve cells
- 8. 2) extracellular matrix 3) pulp microvasculature & lymph 4) nerves of the pulp : (sensory & sympathetic) C fibersA delta fibers 0.4-1.2 UM2-5 UMdiameter 0.5-2 M/S12-30 M/Sspeed NOYESmyelinated Throbbing,achingSharp,pricklingpain highlowthreshold painPain,temperature,touchresponse
- 9. b) Functions of the dental pulp 1) formative 2) nutritive 3) defensive 4) nervous
- 10. 4) nervous Dentin innervation Hydrodynamic theory Dentinoblastic transduction Predentin – inner dentinal zone Subdentinoblastic, dentinoblastic Chemical – electrical - mechanical
- 12. Pulpal & periapical inflammation Definition Is there difference ?? Objectives of inflammatory
- 13. Histopathology of inflammation 1) preinflammatory 2) inflammatory b) proliferative a) exudative early late
- 14. 1) Exudative phase a) Early exudative phase [ Blood ] • SERUM -COMPLEMENT-FIBRINOGEN-KININOGEN • PNLS – MONOCYTES [ Damaged tissues ] • BRADYKININ - LYSYLBRADYKININ - ARACHIDONIC ACIDS • HISTIOCYTES - RESERVE CELLS [ Suppuration ] (neutrophils)
- 15. b) Late exudative phase • SENSITISED LYMPHOCYTES : { B - CELLS PRODUCING ANTIBODIES } OPSONINS - AGGLUTENINS - PRECIPTINS - ANTITOXINS { T - HELPER - T - SUPRESSIVE - T - KILLER CELLS - - CELLS PRODUCING LYMPHOKINS -OAF - MAF -MIF }
- 16. 2- - Proliferative phase
- 17. Significances pf pulp anatomy in inflammation compliance temperature Collateral circulation repaire
- 18. Etiological factors of pulp diseases 1) living irritants Open cavity haematogenous periodontal Adjacent teeth
- 21. 2) non-living irritants a) mechanical irritation 2) odontoiatrogenic1) accidental
- 22. b) Thermal irritation odontoiatrogenic
- 23. Electrical irritation Aeronautical irritation
- 24. Chemical irritation odontoiatrogenic idiopathic
- 25. PULPAL PATHOSIS PULPAL INFLAMMATION PULPAL NECROSIS PULPAL IRRITATION PERIAPICAL PATHOSIS
- 26. PROGRESSION OF PULPAL PATHOSIS Bacteria +Byproducts in deep layers of Dentin Pulp is affected by bacterial byproducts before actual bacterial invasion (via exposed D.T.) Local cellular invasion When actual exposure occurs, pulp is locally infiltrated with PMNs Followed by liquefaction necrosis at site of exposure Eventually necrosis spreads all across pulp then if not treated to periapical tissues
- 27. CLASSIFCATION OF DISEASES OF THE PULP Grossman’s Clinical Classification Pulpitis Reversible Irreversible Acute Chronic Pulp Degeneration Pulp Necrosis
- 28. Inflammatory diseases of the pulp according to Severity & duration: i) Acute ii) Chronic iii)Subacute Presence or absence of symptoms: i)Symptomatic ii)Asymptomatic Ability to heal: i)Reverible ii) Non reversible
- 29. 1-Inflammatory diseases of the pulp (Pulpitis) A- HYPERALGESIA- HYPERSENSITIVITY- REVERSIBLE PULPITIS- HYPERSENSITIVE DENTIN-HYPEREMIA- HYPERACTVE PULPALGIA B – IRREVERSBLE PULPITIS a) SYMPTOMATIC PULPITIS :PAINFUL PULPITIS: ACUTE PULPITIS b) ASYMPTOMATIC PULPITIS: NON PAINFUL PULPITIS: CHRONIC PULPITIS- i. CHRONIC ULCERATIVE PULPITIS ii. CHRONIC HYPERPLASTIC PULPITIS iii. CLOSED FORM OF CHRONIC PULPITIS
- 30. A- HYPERSENSITIVITY- REVERSIBLE PULPITIS- HYPERSENSITIVE DENTIN-HYPEREMIA- HYPERACTVE PULPALGIA Definition: A clinical diagnosis based on subjective and objective findings indicating that the inflammation should resolve and the pulp return to normal Etiology: Histopathology: Range from hyperaemia to mild to moderate inflammatory changes limited to the are a of involved D.T., V.D.→ ↑I.P.P. → Oedema → W.B.C.s infiltration →followed by odontoblast differentiation and reparative dentin formation
- 31. B – IRREVERSBLE PULPITIS SYMPTOMATIC IRREVERSBLE PULPITIS :PAINFUL PULPITIS: ACUTE PULPITIS Definition: A clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing. (lingering thermal pain, spontaneous pain, referred pain) Etiology: Histopathology:
- 32. B – IRREVERSBLE PULPITIS b) ASYMPTOMATIC PULPITIS: NON PAINFUL PULPITIS: CHRONIC PULPITIS- Definition: A clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing. (no clinical symptoms) i. CHRONIC ULCERATIVE PULPITIS ii. CHRONIC HYPERPLASTIC PULPITIS iii. CLOSED FORM OF CHRONIC PULPITIS • Etiology:
- 33. CHRONIC PULPITIS Examination & diagnosis: Non painful - mild discomfort Spontaneous pain Heat elicits pain Exacerbation with lowered body immunity Delayed reaction to EPT X - ray may be -ve , internal resorption or condensing osteitis
- 34. CHRONIC ULCERATIVE PULPITIS Chronic inflammation with abscess formation at the exposure site, and the abscess is surrounded by granulomatous tissues Examination & diagnosis: Painful with food impaction All signs of chronic pulpitis
- 35. CHRONIC HYPERPLASTIC PULPITIS Seen in young permanent cariously exposed teeth It is an attempt of healing and repair by walling off the irritation Proliferative reaction of the pulpal granulation tissue with formation of a polyp May become epithelialized from desquamated epithelial cells
- 36. PULP NECROSIS Definition: A clinical diagnostic category in dicating death of the pulp. The pulp is usually nonresponsive to pulp testing. 2 types are present. LIQUEFACTIVE NECROSIS (WITH GOOD BLOOD SUPPLY.) COAGULATIVE NECROSIS (WITH DIMINISHED BLOOD SUPPLY.)
- 37. Examination & diagnosis: If not treated ►►►Periapical leson of endodontic origin Usually non painful untill the periapex is envolved. Radiographic findings are -ve unless there is a concomitant periapical disease. -Ve with EPT except (some times) in liquefactive necrosis &multi rooted teeth.
- 38. RETROGRESSIVE PULP CHANGES (Pulp Degeneration) 1 - ATROPHY AND FIBROSIS Definition: waisting away or decrease in sze of the pulp, with age. MAY BE CONSIDERED AS AGE CHANGES. Histopathology: Mature collagen incrase / unit area and the cells deminish in no. And size. Excessive secondary dentin deposition deminishes the size of the pulp chamber & canal lumen. Decrease in blood supply.
- 39. 2- CALCIFICATIONS DYSTROPHIC CALCIFICATION IN DEAD OR DEGENERATING TISSUES.( LOCAL ALKALINITY). DENTICLES According to location: FREE EMBEDED ATTACHED According tostructure: True False
- 40. INTERNAL RESORPTION ETIOLOGY: Unknown , often histore of trauma Or chronic pulpitis. Or pulpotomy Examination & diagnosis The pulp is vital . Delayed response to EPT In the pulp chamber it forms the pink spot. In the canal it may perforate causing a lateral lesion. At the cervical level it may be mixed with external cervical resorption. Radiographically,in int. Resorption disrupts the canal while in ext .Resorption the canal contour is unaltered.
- 42. SYMPTOMATIC (ACUTE) APICAL PERIODONTITIS SYMPTOMATIC (ACUTE) APICAL PERIODONTITIS Definition: Inflammation of the apical periodontium producing clinical symptoms including a painful response to biting and/or percussion . It might or not be associated with apical radiolucent area. • Etiology: • ) Histopathology: (as explained before)Inflammatory reaction in apical periodontal ligament ? Dilation ob B.V.? Exudation and accumulation of PMNs ?Distension of P.L. and extrusion of tooth ----with continuous irritation ---?loss of alveolar bone • Examination & diagnosis: • : Treatment : R.C.T---- – TOOTH REDUCTION OUT OF OCCLUSION
- 43. ACUTE APICAL ABSCESS : Definition: An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset , spontaneous pain , tenderness to tooth pressure, pus formation and swelling of associated tissues • Etiology: • Histopathology: Inflammatory reaction in apical periodontal ligament ? Dilation ob B.V.? Exudation and accumulation of PMNs ?Distension of P.L. and extrusion of tooth ----with continuous irritation ---?loss of alveolar bone---- localized area of liquefactive necrosis containing PMNs , debris , cell remnants and purulent exudate
- 44. Examination & diagnosis: Tooth severely painful & tender • Localized vestibular swelling or facial cellulitis• Pain starts severe and decrease after swelling • Patient may become febrile with lympf nodes affection • Tooth becomes loose • -Ve EPT findings except in liquefactive necrosis & multiple canals • Radiograph: HAZY APICAL RAREFACTION
- 45. RECRUDECENT ABSCESS (PHOENIX ABSCESS) Definition: ACUTE EXACERBATION OF A PRE- EXISTING CHRONIC PERIAPICAL PATHOSIS RECRUDECENT ABSCESS • Clinically often undistinguishable from AAA • DIAGNOSIS IS BASED ON PATIENT HISTORY, CLINICAL PICTURE AND RADIOGRAPHIC FINDINGS REVEALING THE PREVIOUS CHRONIC PERIAPICAL PATHOSIS
- 46. CHRONIC APICAL PERIODONTITIS Definition::Inflammation of the apical periodontiumof pulpalorigin, that does not produce clinical symptoms and radiographicallyappears as apical R.L. area Inflammation of the apical periodontiumof pulpalorigin, that does not produce clinical symptoms and radiographicallyappears as apical R.L. area – asymptomatic or slight discomfort – little or no pain on percussion • X-ray: – apical radiolucency or Condensing osteitis: radiopaque
- 47. PULPOPERIAPICAL OSTEOSCLEROSIS • Productive response of periapical bone to a low-grade long standing pulpal irritation • Increase in density of bone due to osteoblastic hyperactivity • Seen in young permenant teeth with carious exposures & chronically inflammed pulps
- 48. CHRONIC APICAL ABSCESS (SUPPURATIVE APICAL PERIODONTITIS) Nonpainful low grade long standing chronic inflammatory reaction to pulpal irritants • It represents a balance between body resistance and the periapical pathosis • Formation of pus that drainsthrough a sinus tract • Ill defined periapical radiolucency • The tooth may be slightly mobile
- 49. PERIAPICAL GRAMULOMA • Examination & diagnosis: • Non painful• -Ve EPT findings • Well defined periradicular radiolucency• Histopathology: • periapical granulomatous tissue • Encapsulated with a fibrous capsule • May show epithelial strands • May transform into a phoenix abcess if infected or manipulated
- 50. PERIAPICAL CYST Definition::Inflammatory cyst due to extension of infection from pulp into surrounding periapical tissues • Histopathology: • Central fluid-filled epithelium-lined cavity surrounded by granulation tissue and a fibrous capsule • Forms on heals of a periapical granuloma • Examination & diagnosis: • Well defined apical radiolucency • Non painful untill infected (phoenix abscess) • Slowly growing destroying bone and moving teeth