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WELCOME TO 19th TRIPLE “O ” MEET

WELCOME TO 19th TRIPLE “O ” MEET. BORN: September 3, 1924. Born - March 27, 1845,. BORN- December 11,1843, . TRIPLE O PRESENTATION. DR. ASIF IQBAL 2 ND year MDS DEPARTMENT OF ORAL AND MAXILLOFACIAL PATHOLOGY. Macroscopic Pathology:. HARD TISSUES. SOFT TISSUES. OSTEOMYELITIS.

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WELCOME TO 19th TRIPLE “O ” MEET

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  1. WELCOME TO 19th TRIPLE “O” MEET BORN: September 3, 1924 • Born - March 27, 1845, • BORN- December 11,1843, 

  2. TRIPLE O PRESENTATION DR. ASIF IQBAL 2ND year MDS DEPARTMENT OF ORAL AND MAXILLOFACIAL PATHOLOGY.

  3. Macroscopic Pathology: HARD TISSUES SOFT TISSUES

  4. OSTEOMYELITIS The word “osteomyelitis” originates from the ancient Greek words • osteon (bone) and • muelinos (marrow) • Itis-Inflammation • By meaning osteomyelitis is an inflammation of the bone and bone marrow.

  5. Events Of Tubercular Osteomyelitis • Inflammation of bone and bone marrow • Ischemia • Necrosis • Resorption of bone • Sequestrum formation • Involucrum formation 7. Cause - Tuberculosis

  6. 1.INFLAMMATION • Components of inflammation • RBC’s • WBC’s • Blood vessels • Macrophage

  7. INFLAMMATION OF BONE AND BONE MARROW Bone marrow Bone

  8. INFLAMMATION OF BONE AND BONE MARROW INFLAMMATION BONE

  9. INFLAMMATORY CELLS UNDER HIGHER MAGNIFICATION INFLAMMATION

  10. 2.SEQUESTRUM • It is a devitalizedavascular segment of bone, surrounded by pus/infected granulation tissue • Its outer surface is usually jagged/irregular due to erosive process by proteolytic enzymes in granulation tissue.

  11. Sequestrum (dead bone) formation BONY TRABECULAE WITHOUT OSTEOCYTES AND OSTEOBLASTS INFLAMMATION INFLAMMATION 10x

  12. SEQUESTRUM(HIGHER MAGNIFICATION)TRABECULAE WITHOUT CELLS(OSTEOBLAST AND OSTEOCYTES) ABSENCE OF OSTEOBLASTS ABSENCE OF OSTEOCYTES

  13. SEQUESTRUM UNDERGOING RESORPTION (IRREGULAR MARGIN) IRREGULAR MARGIN OF BONY TRABUCULAE 40x

  14. TUBERCULOSIS Characterized by granuloma formation Accumulation of- • Activated macrophages(EPITHELOID CELLS) • Lymphocytes, • Giant cells (LANGHANS GAINT CELLS) • and Fibroblasts.

  15. Role of Granuloma in Tuberculosis • Prevents dissemination of the mycobacteria • GRANULOMA FORMATION • Provides a local environment for interaction of cells of the immune system.

  16. MYCOBACTERIUM TUBERCULOSIS

  17. MYCOBACTERIUM TUBERCULOSIS being killed by macrophage(Scanning electron microscopy) EPITHELIOID CELLS (MACROPHAGE) MYCOBACTERIUM TUBERCULOSIS

  18. Granuloma formation

  19. TUBERCULOSIS. GRANULOMA FORMATION GRANULOMA Ciliated pseudo stratified columnar epithelium 4x

  20. TUBERCULAR GRANULOMA (HIGHER MAGNIFICATION) GRANULOMA 10x

  21. TUBERCULAR GRANULOMA (HIGHER MAGNIFICATION) LYMPHOCYTES LANGHANS GIANT CELLS LANGHANS GIANT CELLS EPITHELIOID CELLS EPITHELIOID CELLS 40x

  22. LANGHANS GIANT CELL(Horse shoe shape arrangement of nuclei) LANGHANS GIANT CELLS EPITHELIOID CELLS

  23. TUBERCULAR GRANULOMA (HIGHER MAGNIFICATION) LANGHANS GIANT CELLS EPITHELIOID CELLS LYMPHOCYTES 40x

  24. NECROSIS NECROSIS

  25. INVOLUCRUM (New Bone Formation) It is derived from the word “volvere” i.e. to wrap. It is the result of reactive new bone formation by periosteal reaction, in an attempt to wall off the infection by forming a thick tense wall.

  26. NEW BONE FORMATION(INVOLUCRUM) New bone periosteum

  27. NEW BONE FORMATION(INVOLUCRUM) New bone periosteum

  28. PSEUDOSTRATIFIED EPITHELIUM(RESPIRATORY EPITHELIUM) PSEUDOSTRATIFIED EPITHELIUM

  29. (HIGHER MAGNIFICATION) PSEUDOSTRATIFIED EPITHELIUM

  30. DIAGNOSIS • Features are suggestive of tuberculousosteomyelitis.

  31. Total cases of osteomyelitis- 20. Total cases of Oral tuberculosis - 3. Out of these three cases:- • Lower anterior gingiva. • Lymph node. • Maxilla.

  32. HISTORY OF OSTEOMYELITIS

  33. WHY OSTEOMYELITIS IS GENERALLY SEEN IN MANDIBLE? • The mandible has a relatively poor blood supply, which deteriorates with age. • The cortical plates are thick. • The blood supply to mandible is primarily via the inferior alveolar artery and secondarily via the periosteum. Any compromise to this supply is a critical factor in development of OM in the mandible. REFERENCE: Chapotel S. Tuberculosemandibularie. Rev Odent 1930;51:444-445 Thomas KH. Oral Pathology. In: Kimpton H, editor. A textbook of oral pathology. 3rded. Philadelphia: WB Saunders Company; 1950:891-895.

  34. WHY MAXILLA IS AFFECTED IN TUBERCULOUS OSTEOMYELITIS? • Maxilla is more vascular than Mandible. • Therefore haematogenous spread is generally to the maxilla. Reference : Gupta KB, Manchanda M, Yadav SPS, Mittal A. Tubercular osteomyelitis of mandible. Indian J Tuberc. 2005;52:147–50

  35. CONCLUSION Our case is unique :- • SITE-MAXILLA • ETIOLOGY-TUBERCULOSIS • YOUNGER AGE

  36. REFERENCE • Gupta KB, Manchanda M, Yadav SPS, Mittal A. Tubercular osteomyelitis of mandible. Indian J Tuberc. 2005;52:147–50 • Chapotel S. Tuberculosemandibularie. Rev Odent 1930;51:444-445 • Thomas KH. Oral Pathology. In: Kimpton H, editor. A textbook of oral pathology. 3rded. Philadelphia: WB Saunders Company; 1950:891-895.

  37. SOME FAMOUS PERSONALITY WHO DIED OF TUBERCULOSIS BECAUSE OF UNAVAILABILITY OF TREATMENT AT THEIR TIME

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