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IN THE NAME OF GOD
GINGIVITIS PERIODONTITIS
Changes in gingiva from normal to pathologic pocket are associated with different proportions of bacterial cells in dental plaque Healthy - coccoid cells and straigt rods Disease - spirochetes and motile rods
POCKET FORMATION Bacteria causes inflammatory change in connective tissue wall of the gingival sulcus. Degeneration of surrounding connective tissue, including gingival fibers Destruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edema Immediately apical to this is a zone of partial destruction and then an area of normal attachment
POCKET FORMATION Bacteria causes inflammatory change in connective tissue wall of the gingival sulcus. Degeneration of surrounding connective tissue, including gingival fibers Destruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edema Immediately apical to this is a zone of partial destruction and then an area of normal attachment
Bone  Loss Extension  Of  Gingival  Inflamation    In  to The  Supporting  Periodontal  Tissue
Rate  Of  Lone Loss Loe  :             A: 0.2 mm  Facial  Surface              B: 0.3mm  Proximal  Surface                    If  Disease  Untreated
LOE  et al: 1.Approximately  8% Had  Rapid  Progression   characterized  By  Alveolar  Loss Of  Attachment  Of  0.1 to 1mm 2.A proximately 81 % had moderate  progression with a yearly loss  of  attachment of  0.05 to 0.5 3. 11% had minimal or no progression  of  destructive  disease  (0.05 to 0.09 mm yealy)
Period  of  destruction Destruction occurs  in an episodic Intermitant  fashion  with  period  of   inactivity
Four  theories  for  the onset  of  destructive  period
Burst  of  desturctive  activity  are Associated  with  subgingival  ulceration  And  an acut   inflammatory  reaction , Resulting in  rapid  loss  of  alveolar  Bone
* Burst  of  destruction  activity      Coincide with the  conversion  of  a Predominance  tlymphocyte   lesion  to  One  with  a predominance  of  b Iymphocyte  plasma  cell infiltrate
Period  of  exacerbation are  associated    With  an Increased  of  the  loss– unattached       Motile   gram– negative , unaerobic  pocket  flora And  period of  remission  coincidewith  the  Formation  of  adense  unattached  non motile  Gram  positive  flora with  a tendency  to  Mineralized  .
[object Object],[object Object]
Exostoses Palatal Exostoses  40% Mandibulartorous
Trauma  From  Occlusion
Buttressing  Bone formation CentralPeripheral (Lipping )
Food  Impaction
Patterns Of  Bone Destruction
Horizontal  Bone  LossVertcal Bone Loss
The  Most  Common  Pattern  Of Bone loss      Bone is   Reduced  In  Height
Bone  Deformities (Ossous  Defects ) Radiographs  Care  Full  Probing  Surgical  Exposure
Vertical or  angular  defect Number  Of  Osseous  Wall  One   Wall   Defect  Two   Wall  Defect Three Wall  Defect
One  wall  defect (hemi septum)
Two  wall  defect
Three wall  defect (Intra bony  defect ) Mesial of  second and  third  maxillary and Mandibular  molars
Combind  defect
Osseous  craters 1/3  Of  all defect  2/3  Of  all mandibular  defect  Twice in  posterior  as  anterior  segment
Reasons  for  high  frequency  of  craters A . The inter dental area  collects  plaque  and is difficult  to  clean  B . The normal flat  or  even  concave faciolingualshape  of  the  inter  dental  septum  in lower  molars  may  favor  crater  formation   C . Vascular paterns  from  the  gingiva to  the  center  of  the  crest  may  provide  a pathway  for  inflammation
Bulbuas  bone  contours Exostoses Buttresing  bone  formation   More common in maxilla  than  in  the  mandibule
Reversed architecture Loss of  inter dental septum  without  Loss  of  lingual  and  buccal  plates  More  common in maxilla
Ledges Plateau—like bone margin caused  by     Resorption of  thickend bony plates
Furcation  involvement Horizontal  defect ( I , II , III , IIII ) Vertical  defect ( A , B , C  ) Tarnow
Bone Loss
Bone Loss
Bone Loss
Bone Loss

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Bone Loss

  • 1.
  • 2. IN THE NAME OF GOD
  • 4. Changes in gingiva from normal to pathologic pocket are associated with different proportions of bacterial cells in dental plaque Healthy - coccoid cells and straigt rods Disease - spirochetes and motile rods
  • 5. POCKET FORMATION Bacteria causes inflammatory change in connective tissue wall of the gingival sulcus. Degeneration of surrounding connective tissue, including gingival fibers Destruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edema Immediately apical to this is a zone of partial destruction and then an area of normal attachment
  • 6. POCKET FORMATION Bacteria causes inflammatory change in connective tissue wall of the gingival sulcus. Degeneration of surrounding connective tissue, including gingival fibers Destruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edema Immediately apical to this is a zone of partial destruction and then an area of normal attachment
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12. Bone Loss Extension Of Gingival Inflamation In to The Supporting Periodontal Tissue
  • 13. Rate Of Lone Loss Loe : A: 0.2 mm Facial Surface B: 0.3mm Proximal Surface If Disease Untreated
  • 14. LOE et al: 1.Approximately 8% Had Rapid Progression characterized By Alveolar Loss Of Attachment Of 0.1 to 1mm 2.A proximately 81 % had moderate progression with a yearly loss of attachment of 0.05 to 0.5 3. 11% had minimal or no progression of destructive disease (0.05 to 0.09 mm yealy)
  • 15. Period of destruction Destruction occurs in an episodic Intermitant fashion with period of inactivity
  • 16. Four theories for the onset of destructive period
  • 17. Burst of desturctive activity are Associated with subgingival ulceration And an acut inflammatory reaction , Resulting in rapid loss of alveolar Bone
  • 18. * Burst of destruction activity Coincide with the conversion of a Predominance tlymphocyte lesion to One with a predominance of b Iymphocyte plasma cell infiltrate
  • 19. Period of exacerbation are associated With an Increased of the loss– unattached Motile gram– negative , unaerobic pocket flora And period of remission coincidewith the Formation of adense unattached non motile Gram positive flora with a tendency to Mineralized .
  • 20.
  • 21. Exostoses Palatal Exostoses 40% Mandibulartorous
  • 22.
  • 23. Trauma From Occlusion
  • 24. Buttressing Bone formation CentralPeripheral (Lipping )
  • 26. Patterns Of Bone Destruction
  • 27. Horizontal Bone LossVertcal Bone Loss
  • 28. The Most Common Pattern Of Bone loss Bone is Reduced In Height
  • 29. Bone Deformities (Ossous Defects ) Radiographs Care Full Probing Surgical Exposure
  • 30. Vertical or angular defect Number Of Osseous Wall One Wall Defect Two Wall Defect Three Wall Defect
  • 31. One wall defect (hemi septum)
  • 32. Two wall defect
  • 33. Three wall defect (Intra bony defect ) Mesial of second and third maxillary and Mandibular molars
  • 35. Osseous craters 1/3 Of all defect 2/3 Of all mandibular defect Twice in posterior as anterior segment
  • 36. Reasons for high frequency of craters A . The inter dental area collects plaque and is difficult to clean B . The normal flat or even concave faciolingualshape of the inter dental septum in lower molars may favor crater formation C . Vascular paterns from the gingiva to the center of the crest may provide a pathway for inflammation
  • 37. Bulbuas bone contours Exostoses Buttresing bone formation More common in maxilla than in the mandibule
  • 38. Reversed architecture Loss of inter dental septum without Loss of lingual and buccal plates More common in maxilla
  • 39. Ledges Plateau—like bone margin caused by Resorption of thickend bony plates
  • 40. Furcation involvement Horizontal defect ( I , II , III , IIII ) Vertical defect ( A , B , C ) Tarnow