1 / 69

PERIAPICAL DISEASE

kaethe
Download Presentation

PERIAPICAL DISEASE

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Classification of inflammatory processes of MFA. Periodontitis: etiology, pathogenesis, classification, clinical course, complications, prophylaxis. Odontogenic granuloma of the face: clinic, treatment. Detained and halfdetained teeth. Etiology, clinic, diagnostics, treatment, complications. Pericoronaritis. Odontogenic jaw periostitis: etiology, clinic, diagnostics, treatment, complications, prophylaxis.

  2. PERIAPICAL DISEASE Classified as: • Acute Apical Periodonitis • Acute Apical Abscess • Chronic Apical Periodontitis (Diffuse, Suppurative Apical Periodontitis with sinus tract, Apical cyst) • Condensing Osteitis

  3. Definition • The fundamental lesion of chronic periapical inflammation is known as ´´chronic apicalperiodontitis´´ • While this designation is the preferred one, most dentists know it by the term ´´dental granuloma´´ • The lesion is not a granuloma at all because it is not composed of granulomatous chronic inflammation.

  4. Classification • 1) Diffuse type: - small, recurrent amount of tissue damage - cellular infilltration with lymphocytes, plasma cells, phagocytic mononuclear cells, fibroblasts which produce granulation tissues for repair of damaged area GRANULOMA: formation of large nodule of granulation tissue that is slowly increase in size Resorption of hard tissue, granulation tissue around apex (outlined by capsule of fibrous tissue)

  5. 2)Chronic suppurative periodontitis -central cavity which is accompanied with fistula and stroma - its known as chronic apical abscess ( chronic alveolar abscess) • 3) Apical cyst - true cyst: pathologic cavity which contain fluid or semi-fluid substance that is lined by epithelium and surrounded by connective tissue capsule

  6. Case 1,fig.1a 21-years old woman-non successful endodontic treatment tooth N.22,apical clear radiolucency confirming an established lesion bigger than 3mm,it shows features of lamina dura disruption and bone structural changes Case 1,fig.1b Measurement of the tooth canal length

  7. Case 1,fig.1c Final endodontic treatment Foredent and gutapercha Case 1,fig.1d 5 months after the endodontic treatment without any surgical procedure,intraoral x-ray shows chronic apical periodontitis, partial restitution of the periapical region

  8. Case 2,fig.2a Orthopantogram image,unsuccessful endodontic treatment d.N.22, Cystis radicularis D.N.22

  9. Case 2,fig.2c 3months after the therapy-Cystectomio sec.PARTSCH II. et resectio apicis dentis N.22 Retrograde root canal endodontic therapy with amalgam Egalisatio,suturae Case 2,fig.2b Intraoral image D.22-Cystis radicularis processus alveolaris maxillae reg.frontalis purulenta

  10. Fig.B Granuloma periapicalis and infection transmission paths

  11. Chronic apical periodontitis. Extensive tissue destruction in the periapical region of a mandibular first molar occurred as a result of pulpal necrosis. Lack of symptoms together with presence of a radiographic lesion is diagnostic.

  12. Periapical radiolucencies associated with mandibular incisors. These teeth were vital, and a diagnosis of cemental dysplasia was made.

  13. Periodontitis chronica circumscripta d.14 Periodontitis chronica circumscripta d.41

  14. PULPITIS PATHWAYS

  15. PATHOGENESIS OF PULPAL INFLAMMATION

  16. SPREAD TO ADJACENT STRUCTURES

  17. SPREAD TO ADJACENT STRUCTURES

  18. SPREAD TO ADJACENT STRUCTURES

  19. CLINICAL FEATURES • HYPERSENSITIVE TOOTH UPON BITING OR PERCUSSION • NEGATIVE RESULTS IN BOTH ELECTRIC OR THERMAL STIMULI • BEING ACUTE IN NATURE, ON RADIOGRAPH THERE IS MILD THICKENING OF THE APICAL PERIODONTAL LIGAMENT SPACE. • IN CASES OF RECURRING CHRONIC EVENTS, PERIAPICAL CHANGES (LUCENCIES) MAYBE SEEN (PERIAPICAL GRANULOMA)

  20. PERIAPICAL GRANULOMA • IN CASES OF LOW GRADE BUT CHRONIC INFLAMMATION AT THE APEX OF A NON VITAL TOOTH GRANULOMA IS USED ON AGAINST THE TERM ABSCESS WHICH IS OF ACUTE IN NATURE.

  21. PULP ABSCESS

  22. TREATMENT • DRAINAGE ESTABLISHMENT WITHIN THE TOOTH ITSELF OR ON THE SURROUNDING SOFT TISSUES • ANTIBIOTIC THERAPY • SKILLED AND THOUGHTFUL MANAGEMENT MUST BE EMPLOYED SINCE ANY DELAY MAY CAUSE ANY LETHAL CONSEQUENCE.

  23. COMPLICATIONS • PUS MAY DRAIN ON NATURALLY OCCURING DRAINS TERMED AS FISTULAS OR SINUS TRACTS WHICH MAY BE SEEN ON SKIN OR ON THE PALATE • IF THERE IS NO DRAIN MADE CELLULITIS ENSUES AFTER THE PUS BUILDUP. IT IS AN ACUTE INFLAMMATORY SPREAD ON THE NEARBY SOFT TISSUES • ENZYMES ARE PRODUCED BY HIGHLY VIRULENT MICROORGANISMS PRESENT

  24. COMPLICATIONS • BILATERAL SUBMANDIBULAR AND SUBLINGUAL SPACES ARE KNOWN AS “LUDWIG'S ANGINA” • FATALITIES USUALLY RESULTS FROM BACTEREMIA FROM INFECTION SPREADING INTO THE MAJOR BLOOD VESSELS OR THROUGH A RETROGRADE SPREAD OF INFECTION INTO THE FACIAL EMISSARY VEINS INTO THE CAVERNOUS SINUS, CAVERNOUS SINUS THROMBOSIS

  25. CAVERNOUS SINUS

  26. Severe Ludwig's Angina

  27. IMPACTED TEETH • An impacted tooth is one that is partially erupted or unerupted and will not eventually assume a normal arch relationship withother teeth and tissues.

  28. Causes of Impacted Teeth • Role of civilization • Local causes of Impaction • Systemic causes of impaction

  29. Local causes of Impaction • Lack of space in the dental arch for eruption; • The density of the overlying or surrounding bone; • Long continued chronic inflammation with resultant increase in the density of the overlying mucous membrane; • Premature loss of the primary teeth; • Acquired diseases, such as necrosis due to infection or abscesses, and inflammatory changes in the bone due to exanthematous diseases in children;

  30. Lack of space in the dental arch for eruption

  31. Impacted teeth occur in the following order • Mandibular third molars • Maxillary third molars • Maxillary cuspids • Mandibular bicuspids • Mandibular cuspids • Maxillary bicuspids • Maxillary central incisors • Maxillary lateral incisors • Maxillary or mandibular first molars are rarely impacted

  32. Impacted teeth

  33. Classification of impacted mandibular third molars • A. Relation of the tooth to the ramus of the mandible and the second molar; • B. Relative depth of the third molar in bone; • C. The position of the long axis of the impacted mandibular third molar in relation to the long axis of the second molar : vertical, horizontal, inverted, mesioangular, distoangular, buccoangular, linguangular.

  34. Classification of impacted mandibular third molars

  35. Radiographic visualization of impacted teeth

  36. The removal of impacted mandibular third molars

  37. Scheme of Periconitis

  38. Scheme of Periostitis ( upper jaw )

  39. Scheme of Periostitis ( lower jaw )

  40. Acute Periostitis left upper jaw

  41. Acute Periostitis left lover jaw

  42. Acute Periostitis of hard pallate

  43. Surgical treatment of periostitis

  44. Treatment of abscess of hard pallatine

  45. Class1 • the space between the anterior part of the ascending ramus and the distal surface of the 2nd molar is sufficient to accommodate the mesiodistal diameter of the crown of the third molar.

  46. Class2 • the space between the anterior part of the ascending ramus and distal surface of the 2nd molar is less than the mesiodistal diameter of the crown of the third molar (part of the tooth located within the ramus)

More Related