Diseases of pulp & periapical tissues (1)


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Diseases of pulp & periapical tissues (1)

  1. 1. Diseases Of Pulp &Periapical Tissues By SMIJAL
  2. 2. DiseasesOfDentalPulp
  3. 3. Etiology: FACTORS PHYSICAL INJURY CHEMICAL INJURY MICROBIAL FACTORSAcute Injury Bacterial invasion by: •M edicaments or•Injury on tooth materials applied to•Cavity preparation without •Dental caries dentin diffuses water spray through dentinal •Fractured tooth where•Vigorous polishing tubules. exposed pulp•Root planning in P therapy DL • Anachoretic infection•Restoration – improper due to presence of insulation bacteria in circulating blood stream.Chronic Injury•Attrition -abrasive food & bruxism•Abrasion -abnormal tooth brushing
  4. 4. Classification Of Pulpitis1. Acute & Chronic2. Based on extend - Partial pulpitis (confined a portion of pulp) - Subtotal pulpitis3. i. If inflammatory process confined within a portion: - Focal /Partial pulpitis ii. If most of pulp diseased:-Total /Generalized pulpitis4. Another classification of acute & chronic based on presence or absence of direct communication between pulp & oral environment: - Open pulpitis (pulpitis aperta) communicated exist. - Closed pulpitis (pulpitis clausa) no communication exist.
  5. 5. Focal Reversible Pulpitis ( Pulp Hyperemia) Mild, transient, localized inflammatory response.CLINICAL FEATURES: Tooth is sensitive to thermal changes, especially cold. P - short duration, disappears on withdrawal of thermal ain irritant. Affected tooth responds to stimulation of electric pulp tester at lower level of current indicating low pain threshold. Teeth usually show deep caries, metallic restoration with defective margins.
  6. 6. HISTOLOGICAL FEATURES: Dilation of pulp blood vessels. Edema fluid collection due to damage of vessel wall & allowing extravasations of R C or diapedesis of W C. B B Slowing of blood flow & hemoconcentration due to transudation can cause thrombosis. Reparative or reactionary dentin in adjacent dentinal wall.TREATMENT & PR OGNOSIS: 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.
  7. 7. Dentin Dilation of blood vesselsInflammatory cell infiltrate
  8. 8. Acute Pulpitis Irreversible condition characterized by acute, intense inflammatory response in pulp.CLINICAL FEATURES: Teeth extremely sensitive to thermal changes. H or cold stimuli cause increase in pain intensity & ot persists. Pain - poorly localized since pulp of individual tooth is not represented in sensory cortex. Intrapulpal abscess formation cause severe pain lancinating or throbbing type. (10 – 15mins) Intensity of pain can increase when patient lies down.
  9. 9. Acute pulpitis withIntrapulpal abscess
  10. 10. P ulp vitality test indicats increased sensitivity at lowlevel of current.Pulpal pain is due to: - pressure built up due to lack of exudateescape. - pain producing substances from inflammation.Pain subsides when drainage is established or whenpulp undergoes complete necrosis.T tooth is not tendered to percussion unless the hepulpal inflammation has spread beyond the root apexinto the periapical region.
  11. 11. HISTOLOGIC 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)
  12. 12. TREATMENT & PROGNOSIS: Drainage of exudate from pulp chamber. Pulpotomy & placing calcium hydroxide over entrance of root canal. Root canal treatment. Extraction of tooth.
  13. 13. Chronic Pulpitis Persistent inflammatory reaction in pulp with little or non constitutional symptoms.CLINICAL FEATURES: P ain 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. W open carious lesion & with exposure of pulp ide cause relatively little pain. M anipulation with small instruments often elicits bleeding but with little pain.
  14. 14. HISTOLOGIC FEATURES: Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective tissue reaction. Capillaries are prominent; fibroblastic activity & collagen fibers in bundles. W hen 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, which is called Pyogenic M emberane
  15. 15. TREATMENT & PROGNOSIS: Root canal therapy Extraction of tooth.
  16. 16. Chronic Hyperplastic Pulpitis (pulp polyp) Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass.CLINICAL FEATURES: 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. M commonly affected are deciduous molar & Ist ost permanent molars. Pulp is relatively insensitive because few nerves in hyperplastic tissue.
  17. 17. 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 pulpitis. - So careful examination is made to determine whether connection is with pulp or gingiva.HISTOLOGIC FEATURES: H yperplastic tissue is basically granulation tissue, consisting delicate CT fibers & young blood capillaries. Inflammatory infiltrates – lymphocytes, plasma cells &
  18. 18. Stratified sq. epithelium covering polyp Granulation tissue Carious toothPulpal tissue
  19. 19. Stratified squamous type epithelial lining resembles oral mucosa with well formed rete pegs. 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. W hen pulp polyp is present for a long time, persistent rubbing of buccal mucosa may help in grafting of epith. cells.TREATMENT & PROGNOSIS: Extraction of tooth or pulp extripation.
  20. 20. Gangrenous Necrosis of PulpUntreated pulpitis results complete necrosis ofpulp.As this is associated with bacterial infection – pulpgangrene.It is associated with foul odor when pulp is opened forendodontic treatment.In sickle cell anemia, blockage of pulp vessels bedefective RB results pulp necrosis. CNon vital pulp maintain general histology being nonpurulent.T may be due to trauma or infarct. his
  21. 21. Necrosis of pulp
  22. 22. REVERSIBLE PULPITIS IRREVERSIBLE PULPITIS• M – moderate inflammatory • Sharp, severe, radiating pain ild condition. of long duration & varying intensity.• Nature of pain is mild & diffuse. • Pain continues even after the stimulus is removed.• B rief duration & can be produce cold stimuli that elicits the pain • Pain may exacerbate with mostly, although hot, sweet or bending over or lying down. sour food may also initiate the • It may progress to more severe pain. pain that is gnawing or• Once stimulus is removed, pain throbbing. is usually subsides. • Increased by stimulus, like• T ooth responds to electric pulp heat & at times relieved by tester at lower currents. cold although the cold may intensify the pain.• Reversible pulpitis if allowed to progress can led to • W hen infection extends into irreversible pulpitis. PDL - apical periodontitis.
  23. 23. DiseasesOfPeriapical Tissues
  24. 24. Pulpitis Acute chronic Apical peiodontitis Acute chronic Periapical abscess Periapical granulomaAcute chronic Periodontal cyst Osteomyelitis Acute chronic Focal Diffuse Periosteitis Cellulitis Abscess
  25. 25. Apical PeriodontitisInflammation of P around apical portion of root. DLCause: spread of infection following pulp necrosis,occlusal trauma, inadvertent endodontic procedures etc.Types: 1.Acute Apical Periodontitis 2.Chronic Apical Periodontitis
  26. 26. Acute Apical PeriodontitisCLINICAL FEATURES:• Thermal changes does not induce pain.• Slight extrusion of tooth from socket.• Cause tenderness on mastication due to inflammatory edema collected in P . DL• Due to external pressure, forcing of edema fluid against already sensitized nerve endings results in severe pain.RADIOGRAPHIC FEATURES:• Appear normal except for widening of PDL space.
  27. 27. HISTOLOGIC FEATURES:• P shows signs of inflammation -vascular dilation DL -infiltration of P Ns M• Inflammation is transient, if caused by acute trauma.• If irritant not removed, progress into surrounding bone resorption.• Abscess formation may occur if it is associated with bacterial infection Acute periapical abscess / Alveolar abscess.TREATMENT & PROGNOSIS:• Selective grinding if inflammation due to occlusal
  28. 28. Chronic Apical Periodontitis (Periapical Granuloma) M common sequelae of pulpitis or apical periodontitis. ost If acute (exudative) left untreated chronic (proliferative). Periapical granuloma is localized mass of chronic granulation tissue formed in response to infection. B term is not accurate since it doesn’t shows true ut granulomatous inflammation microscopically .CLINICAL FEATURES: Tooth involved is non vital /slightly tender on percussion. Percussion may produce dull sound instead metallic due to granulation tissue at apex.
  29. 29. M pain on chewing on solid food. ild Tooth may be slightly elongated in socket. Sensitivity is due to hyperemia, edema & inflammation of P . DL In many cases, asymptomatic. Fully developed granuloma seldom presents more severe clinical symptoms. No perforation of bone & oral mucosa forming fistulous tract unless undergoes acute exacerbation.RADIOGRAPHIC FEATURES: Thickening of P at root apex. DL As concomoitent bone resorption & proliferation of granulation tissue appears to be radiolucent area.
  30. 30. T radiopaque line or zone of sclerotic bone sometimes hin seen outlining lesion. Long standing lesion may show varying degrees of root resorption.HISTOLOGIC FEATURES: Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous immature blood capillaries with bone resorption. Capillaries lined with swollen endothelial cells. Its is relatively homogenous lesion composed of macrophages, lymphocytes & plasma cells. Lymphocytes produces IgG, IgA, IgM & IgE modulators of disease activity.
  31. 31. Plasma cells containing Russels body are found extracellularly. T lymphocytes produce cytotoxic lymphokines, collagenase & other enzymes & destructive lymphokines. Collection of cholesterol clefts, with multinuclear gaint cells. Epithelial rests of Malassez may proliferate in response to chronic inflammation & may undergo cystification.Bacteriologic Features: Strep. viridans, strep. Hemolyticus, non hemolytic strep, staph. aureus, staph. Albus, E coli & pnemococci are isolated from lesion.TREATMENT & PROGNOSIS: Extraction & RCT with /without apicoetomy.
  32. 32. Periapical Granuloma Root Apex Granulation Tissue
  33. 33. Residual Cyst T ype of inflammatory odont. cyst in edentulous alveolar ridge. Occur due to extraction of tooth, leaving periapical pathology untreated or incomplete removal of periapical granuloma / cyst.RADIOGRAPHIC FEATURES: Round / ovoid radiolucency in alveolar ridge. Lumen may show radiopacity - dystrophic calcificationTREATMENT & PROGNOSIS: Cyst should curetted & lining should be subjected to histopathological examination.
  34. 34. Periapical Abscess (Dento-Alveolar abscess, Alveolar Abscess) Developed from acute periodontitis /periapical granuloma. Acute exacerbation of chronic lesion Phoenix Abscess Cause due to – pulp infection, traumatic injury pulp necrosis, irritation of periapical tissues ( endo procedures).CLINICAL FEATURES: Features of acute inflammation. Tenderness of tooth, which relives after pressure application.
  35. 35. Periapical abscess
  36. 36. Extension to bone marrow spaces produce osteomyelitis, but clinically considered as Dento-Alveolar abscess – swelling of tissues. Chronic abscess generally presents no features, since it is mild, well circumscribed area of suppuration which spread from local area.RADIOGRAPHIC FEATURES: Slight thickening of P space. DL Radiolucent area at apex of root.HISTOLOGIC FEATURES: Area of suppuration composed of P N leukocytes, M lymphocytes, cellular debris, necrotic materials & bacterial colonies. Dilation of blood vessels in P & bone marrow space. DL
  37. 37. Inflammatory infiltrate, cellular debris, necrotic materials etc..Periapical abscess
  38. 38. Marrow space show inflammatory infiltrates. Tissue around area show suppuration containing serous exudate.TREATMENT & PROGNOSIS: Drainage of abscess by opening pulp chamber or extraction. RCT. If untreated, causes osteomyelitis, cellulites & bacteremia & formation of fistulous tract opening to oral mucosa. Cavernous sinus thrombosis has been reported.
  39. 39. Osteomyelitis Inflammation of bone & marrow contents. Secondary changes due to inflammation of soft tissue content of bone.Predisposing F actors: - trauma, accidents, gunshot wounds, radiation damage, P aget’s disease & osteoporosis. - systemic conditions like malnutrition, acute leukemia, uncontrolled DM sickle cell anemia & chronic alcoholism. , Types: 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis: i. Chronic Focal Sclerosing Osteomyelitis ii. Chronic Diffuse Sclerosing Osteomyelitis
  40. 40. Acute osteomyelitis Chronic Serious sequelae of Osteomyelitis periapical infection, results  Develops from in spread into medullary untreated, acute osteo. spaces with necrosis of Or arise from dental bone. infection without CLINICAL FEATURES preceeding acute stage. Acute & subacute osteo.  Clinical features are similar involve either to acute, except: maxilla/mandible.  Signs & symptoms – milder, Some osteo. refered as with less pain. neonatal maxillitis in infants & young children - hematogenous origin.
  41. 41.  Infants – seriously ill & may  Leucocytes slightly greater not survive disease. than normal. Adults - severe pain, trismus  Teeth may not be loose & & parasthesia of lips in sore, so mastication is mand. & elevated possible even though jaw temperature with regional may not be perfectly lymphadenopathy. comfortable. W C count elevated. B  Acute exacerbation may Teeth involved is loose, occur periodically. eating difficult.  Temperature still elevated, P exudate from gingival us but mild. margins.  Suppuration may perforate Until periostitis, no swelling bone & overlying skin or or no reddening on skin mucosa to form fistulous /mucosa. tract & empty on surface.
  42. 42. RADIOGRAPHIC FEATURES Evidence until disease for 1-  Single /multiple 2weeks. radiolucencies. L of continuity of lamina  Irregular margins. oss dura.  R oot resorption. Trabeculae - fuzzy, indistinct  Lamina dura less apparent, & radiolucent. blends with surrounding Saucer shaped irregular granular sclerotic bone. margins. Moth eaten appearance.
  43. 43. Acute Osteomyelitis: Osteomyelitis Ill defined area of radiolucency of right body of mandible.Chronic Osteomyelitis: OsteomyelitisIll defined area of radiolucencyof right body of mandible onextracton site.
  44. 44. HISTOLOGIC FEATURES Inflam. Exudate in medullary  Chronic inflam. Reaction in spaces. bone - exudate & pus Inflam. Cells – neutrophillic accumulation in medullary P nuclear leucocytes, M spaces. occasional lymphocytes &  Lymphocytes, plasma cells & plasma cells. macrophages. Destroyed osteoblasts lining  Osteoblastic & osteoclastic bony trabeculae. activity occur parallely with Depending duration of irregular bony trabeculae process – trabeculae loss formation with reversal viability & undergo slow lines. resorption.  L ater stages - Sequestrum may develop
  45. 45. Acute Osteomyelitis Nonvital bone shows absence of osteocytes in lacunae. Peripheral resorption, bacterial colonisation & inflam. Response.Chronic OsteomyelitisChronic inflamation &reactive fibrous CTfilling intertrabecularspaces.
  46. 46. TREATMENT & PROGNOSIS: Drainage, debridement & antimicrobial therapy. W hen intensity of disease attenuated – sequestrum seperates from living bone & gradually exfoliates through mucosa. If large – surgical removal. Acute SO may preceed to develop periosteitis, soft tissue abscess / cellulitis.
  47. 47. Chr.Focal Sclerosing O Chr.Diffuse Sclerosing O A reaction to mild bacterial  Due to diffuse periodontal infection entering bone disease. through carious tooth in persons ’ving higher degree of tissue resistance & tissue reactivity. CLINICAL FEATURES Commonly in children &  Common in older, with young adults & rarely old edentulous mandibular jaw. age.  On exacerbation: vague Common tooth: mand Ist pain, unpleasant taste & molar. mild suppuration many times with fistula formation No other signs & symptoms opening to mucosa & drains. other than mild pain.
  48. 48. RADIOGRAPHIC FEATURES W circumscribes radiopaque  Cotton wool appearance. ell mass of sclerotic bone  Sometimes bilateral. extending below apex on roots.  Bilateral involvement in both maxilla & mandible. Root outline nearly visible with intact lamina dura.  Border between sclerosis & normal bone is indistinct. P space widened & is DL important to distinguish  Pattern may actually mimic cementoblastoma. Paget’s disease or cemento osseus dysplasia. Lesion border: abutting normal bone, may smooth & distinct or appear to blend into surrounding bone in contrast to focal cemento osseus dysplasia. Radiopacity stands out
  49. 49. Focal sclerosing osteomyelitisDiffuse sclerosing osteomyelitis
  50. 50. HISTOLOGIC FEATURES Dense mass of bony  Dense irregular trabeculae, trabeculae with little some borderd by active layer interstitial marrow tissue. of osteoblasts. Osteocytic lacunae is empty.  Mosaic pattern, indicates Trabeculae show reversal & periodic resorption & repair. resting lines giving P agetoid  Soft tissue in between appearance. trabeculae – fibrous & show If interstitial soft tissue proliferating fibroblast, present – fibrotic & inflitrate capillaries with lymphocytes & plasma cells. of few lymphocytes . Osteoblastic activity ‘ve  P N leucocytes present, if M completely subsided. lesion is in acute phase.  Sometimes, inflam component is completely burned out, leaving sclerotic bone & fibrosis.
  51. 51. Focal sclerosing osteomyelitisDiffuse sclerosing osteomyelitis
  52. 52. TREATMENT & PROGNOSIS Endodontic treatment  Surgical removal Extraction  If tooth is present, must Surgical removal of sclerotic extracted. lesion is not indicated unless  Sometimes sclerosed bone will symptomatic. remain after resolution & remodelling.
  53. 53. Apical Periodontal Cyst(Radicular Cyst, Periapical Cyst, Root End Cyst)Common odontogenic cyst encountered.True cyst, since consits of pathological cavity lined byepithelium &fluid filled.Epithelium may be derived from: -respiratory epith (communicating with maxillary sinus) -oral epith fibrous tract -oral epith proliferating apically from PDL pocket
  54. 54. Etiopathogenisis Caries, trauma, periodontal disease Pulp death Apical bone inflammation Granuloma formation Stimulation, then proliferation of epithelial cell rests of Malassez Cystification
  55. 55. CLINICAL FEATURES:• Most cases are Assymptomatic• Age: commonly 20-60 yrs, decidous teeth.• Common tooth maxillary anteriors.• Non vital tooth/deep caries/restoration which is painfull on percussion.• In some cases, cyst may undergo acute exacerbation & develop abscess that may proceed to cellulitis/ fistula.RADIOGRAPHIC FEATURES:• Radolucency – round/ ovoid with a narrow opaque margin which is continuous with lamina dura.• In long standing cyst bone resorption of affected teeth & occasional resorption of adj. teeth may be seen.
  56. 56. HISTOPATHOLOGY• Lined by non keratinized stratified sq epith.• Newly formed cyst - Epith lining thickness is uneven, due to hyperplasia• In established cyst – lining thickness is even.• Presence of Mucous secreting goblest cells in cyst lining.• Transmigration of inflam. Infiltrate through epithelium.• Supporting CT – focally/diffusely infiltrated with a mixed inflam. Cell population.• Foci of dystrophic calcification, cholestrol clefts & multinucleated foreign body gaint cell seen on cyst wall.• Rushton bodies are found in cyst lining or CT.• Russels bodies (plasma cell surrounded by immunoglobulin) seen.
  57. 57. Cyst lumen consist of watery, straw colored, blood tinged fluid to semi fluid materials, with low conc. Of protien.TREATMENT & PROGNOSIS: Extraction & curettage of apical zone. RCT with apicoectomy. Surgery If left untreated – slowly increase in size & undergo bone resorption but seldom there is a remarkable compensating expansion of cortical plates.
  58. 58. Apical periodontal cyst
  59. 59. Sclerotic Cemental MassesBenign fibro-osseous jaw lesions of unknown etiology, occurring predominantly in middle-aged black females; lesions present as large painless radiopaque masses usually involving several quadrants of the jawCLINICAL FEATURES: Just same as in Diffuse sclerosing osteomyelitis – present with multiple symmetric lesion, pain, drainage & localized expansion.RADIOGRAPHIC FEATURES:• Same as in DSO - Lesions appear as multiple sclerotic masses, located in two or more quadrants, usually in the tooth-bearing regions.HISTOLOGIC FEATURES:Differences:• Cemental masses instead of sclerotic bone Cementum – large solid masses with smooth, lobulated margins, with globular accretion pattern.
  60. 60. Florid Osseus Dysplasia Another disease similar to DSO & Sclerotic cemental masses; described by Melrose & his associates. characterized by lesions in upper/ lower jaw that occur when normal bone is replaced with a mix of CT and abnormal bone. It affect middle age Black and Asian women . Cause – obstruction of normal interstitial fluid by fibro osseus proliferation.RADIOGRAPHIC FEATURES: FOD appears as well-defined mixed (radiolucent-radiopaque) or totally radiopaque & has a radiolucent periphery & surrounding sclerosing border similar to Periapical Cemental Dysplasia. “cotton wool” appearance or large amorphous regions of calcifications.TREATMENT: Usually no treatment necessary.
  61. 61. Chronic Osteomyelitis with Proliferative Periosteitis( Garre’s Chronic nonsuppurative sclerosing osteitis, periosteitis ossificans) A distinctive type of osteomyelitis with focal gross thickening of periosteum, & peripheral reactive bone formation resulting from mild infection or irritation. It is essentially a periosteal osteosclerosis analogous to chronic focal endosteal sclerosis & diffuse sclerosing osteomyelitis.CLINICAL FEATURES: young age <25yrs, mostly involve anterior of tibia. Greater opportunity for infection enter maxilla & mandible, due to peculiar anatomic arrangement of teeth.
  62. 62. Cases in jaws; occurs in mandible bicuspid & molar region - children & young adults. Maxilla is seldom affected, reason not clear. Toothache or jaw pain & bony hard swelling on outer surface of jaw – usually for several weeks duration. Due to overlying soft tissue infection/cellulitis that involves periosteum cause reactive periosteitis.RADIOGRAPHIC FEATURES: Reveals a carious tooth opp: to hard bony mass. Occlusal radiograph: focal overgrowth of bone on outer surface of cortex, which described as duplication of cortical layer. M ass is smooth & well calcified & may show thin but definite cortical layer.
  63. 63. CT scan of new proliferative periosteitis with onion skinFirm swelling laminations.on lateral &inferior borderof rightmandible
  64. 64. HISTOLOGIC FEATURES:• Supracortical but subperiosteal mass is composed of much reactive new bone & ostoeid, with osteoblast bordering many trabeculae.• Trabeculae orient perpendicular to cortex, with trabeculae arranged in parellel to each other or reticular form.• CT between bony trabeculae is rather fibrous & show diffuse or patchy sprinkling of lymphocytes & plasma cells.• Periosteal reaction – infection from caries perforating cortical plate & become attenuated, stimulating periosteum rather than producing usual suppurative periosteitis.TREATMENT & PROGNOSIS OGNOSIS:• Endodontic treatment or extraction, with no surgical intervention for periosteal lesion except for biopsy.
  65. 65. Periosteal bone formation / neoperiosteosis may occur invariety of other conditions & care must be taken to excludethem from diagonosis.Include infantile cortical hyperosteosis (Caffey’s disease),hypervitaminosis A, syphilis, leukemia, E wing’s sarcoma,metastatic neuroblastoma & even a fracture callus.