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Inflammation by Dr. Amit T. Suryawanshi, Oral Surgeon, Pune

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Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.

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Inflammation by Dr. Amit T. Suryawanshi, Oral Surgeon, Pune

  1. 1. Inflammation Dr. Amit T. Suryawanshi Oral and Maxillofacial Surgeon Pune, India Contact details : Email ID - amitsuryawanshi999@gmail.com Mobile No - 9405622455
  2. 2. Contents • Introduction. • Definition. • Historical background. • Cardinal signs of inflammation. • Types of inflammation. • Pathophysiology of inflammation. • Inflammatory cells & mediators. • Clinical perspectives. • Conclusion. • References.
  3. 3. Introduction • Survival of all living organisms requires that they should eliminate foreign invaders , such as infectious pathogens & damaged tissues . These functions are mediated by complex host immune response called as an Inflammation.
  4. 4. Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Hence without inflammation, wounds and infections would never heal.
  5. 5. Inflammation • Definition – The word inflammation is derived from Latin word inflammare, which means “to set on fire.”
  6. 6. Inflammation Inflammation is defined as “a protective response intended to eliminate the original cause of cell injury , necrotic tissues and tissues resulting from original insult . ” Terms ending with suffix “ itis” denote inflammation .
  7. 7. Historical Background 1. Word inflammation – Latin word inflammare ( meaning – to set on fire ) 2. Celsus – A roman physician and medical writer (30 BC to 45 AD ) gave 4 cardinal signs of inflammation saying “ Rubor et tumor cum calore et dolore.” (meaning - Redness and swelling come with heat and pain )
  8. 8. 3. Virchow added 5th Cardinal sign of inflammation in 1871 i.e. functio laesa (loss of function) 4. Cohnheim gave First description of diapedesis in 1873. 5. Lewis described Inflammation as the ‘‘triple response’’ to injury in 1927
  9. 9. Cardinal signs of inflammation & Its Physiological rationale Cardinal Signs Physiological rationale 1. Rubor ( Redness) Increased Blood flow 2. Tumor (Swelling ) Exudation of fluid 3. Calor (Heat) Increased Blood flow , Exudation of fluid, Release of inflammatory mediators 4. Dolor ( Pain ) Stretching of pain receptors and nerves by inflammatory exudates , chemical mediators 5. Functio laesa (Loss of function) Pain, Disruption of tissue structure, Fibroplasia and metaplasia
  10. 10. Types of inflammation 1. Acute inflammation – It is the rapid response to the injury or microbes or other foreign substances that is designed to deliver leukocytes & plasma proteins to the site of injury . Causes – 1. Infections – Bacterial , viral , fungal or parasitic 2. Trauma –Blunt or Penetrating 3. Tissue necrosis- 4. Foreign bodies – sutures 5. Immune reactions
  11. 11. • Outcomes of acute inflammation- 1. Resolution 2. Progression to chronic inflammion. 3. Scarring or fibrosis
  12. 12. 2. Chronic inflammation – It is inflammation of prolonged duration in which active inflammation, tissue injury & healing proceed simultaneously . Causes – 1. Persistent infection 2. Immune mediated inflammatory diseases 3. Prolonged exposure to potentially toxic agents
  13. 13. • Outcomes of Chronic inflammation- 1. Resolution 2. Scarring or fibrosis
  14. 14. Pathophysiology of inflammation
  15. 15. Normal Inflammed (Vasodilation in capillary bed) Arteriole Venule Capillary bed
  16. 16. Leukocyte Transmigration , Chemotaxis & Phagocytosis
  17. 17. Resolution of Inflammation
  18. 18. Pathophysiology of inflammation
  19. 19. Inflammatory cells 1. Blood leukocytes – Neutrophils , Macrophages, Lymphocytes. 2. Plasma cells 3. Connective tissue cells – Fibroblasts, Mast cells. 4. Cells of vascular walls .
  20. 20. Inflammatory mediators • Definition – Chemical substances that trigger certain processes in an inflammatory reaction. Cell derived Plasma derived Histamine Kinin system mediators Serotonin C- reactive protein Neutrophilic proteases Complement system mediators Interleukins( IL-1 . TNF- α ) Chemokines Arachidonic acid (PG, LT) PAF
  21. 21. • Plasma proteins & extracellular matrix also play an important role in process of inflammation.
  22. 22. Differences between Acute & Chronic Inflammation Acute inflammation Chronic inflammation Definition It is the rapid response to the injury or microbes or other foreign substances that is designed to deliver leukocytes & plasma proteins to the site of injury . It is inflammation of prolonged duration in which active inflammation, tissue injury & healing proceed simultaneously . Onset Rapid Insidious Duration Short ( Few minutes to days ) Long (Days to years )
  23. 23. Acute inflammation Chronic inflammation Specificity Non- specific Specific, where immune response is activated Cells involved Neutrophils Lymphocytes , plasma cells , macrophages , fibroblasts Vascular changes Active vasodilation , Increased vascular permeabilty New vessels formation (Neoangiogenesis ) Fluid exudation & edema Present Absent Cardinal signs Present Absent
  24. 24. Acute inflammation Chronic inflammation Tissue necrosis Absent Ongoing Systemic manifestations High grade fever Low grade fever, weight loss , anemia
  25. 25. Clinical Perspectives
  26. 26. Inflammatory diseases Acute inflammatory diseases- Chronic inflammatory diseases - 1. Acute suppurative osteomyelitis 1. Chronic suppurative osteomyelitis 2. Chronic focal sclerosing osteomyelitis 3. Chronic diffuse sclerosing osteomyelitis. 4. Garre’s osteomyelitis
  27. 27. Acute inflammatory diseases- Chronic inflammatory diseases - Acute Pericoronitis Chronic Pericoronitis Acute Sialadentitis Chronic Sialadentitis Acute Maxillary sinusitis Chronic Maxillary sinusitis Acute Stomatitis Chronic Stomatitis Infectious arthritis _ _ Rheumatoid arthritis
  28. 28. Rheumatoid arthritis It is a debilitating systemic disease of unknown origin , characterized by progressive involvement of the TM joint ,(particularly bilateral involvement) • Etiology – 1. Unknown 2. The is evidence that it may be a hypersensitive reaction to bacterial toxins specifically of streptococci.
  29. 29. Clinical features – General – 1. Slight fever, Weight loss, Fatigue Extraoral – 1. Swelling over joint region , Stiffness , pain on movement . 2. Clicking is uncommon. 3. Over period of years there may be ankylosis but its not inevitable.
  30. 30. • Radiographic appearance -
  31. 31. Infectious Arthritis • Incidence- very rare. • Etiology – Infection – Gonococci, Streptococci, staphylococci, pneumococci & tubercle bacillus .
  32. 32. • Etiopathogenesis – 1. Spread can be hematogenous , Lymphatic or by direct extension of foci of infection . 2. Most commonly , it spreads directly from foci of infection. - Adjacent cellulitis - Osteomyelitis Which may follow - Dental infection. - Infection of parotid gland, ear.
  33. 33. • Clinical features – 1. Severe pain in joint , tender on palpation in joint region. 2. Trismus. 3. Results in ankylosis , most commonly fibrous ankylosis .
  34. 34. Osteomyelitis • Definition – It is defined as an inflammation of marrow spaces of bone with tendency of involvement of cortical plates and periosteum. • Etiology – 1. Dental infection Predisposing factors – 1. Fractures 2. Gunshot wounds 3. Radiation damage 4. Paget's disease 5. osteopetrosis
  35. 35. • Systemic factors – 1. Malnutrition 2. Acute leukemia 3. Uncontrolled diabetes mellitus 4. Sickle cell anemia 5. Chronic alcoholism
  36. 36. Types of osteomyelitis – 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis 3. Chronic focal sclerosing osteomyelitis 4. Chronic diffuse sclerosing osteomyelitis. 5. Garre’s osteomyelitis
  37. 37. Acute suppurative osteomyelitis • Definition- • “Acute suppurative osteomyelitis of jaw is a sequela of periapical infection that often results in a diffuse spread of infection throughout the medullary spaces, with subsequent necrosis of bone .” • Etiology – Dental infection
  38. 38. • Clinical features – 1. Severe pain , trismus , paresthesia of lip 2. Elevation of temprature 3. Regional lymphadenopathy 4. Pus may exude through gingival pocket 5. In maxilla , infection spread is local, while in mandible its diffuse .
  39. 39. Radiographic appearance -
  40. 40. Chronic Suppurative Osteomyelitis • Chronic suppurative osteomyelitis may develop in inadequately treated acute osteomyelitis or may arise from dental infection without preceding acute stage. • Etiology – 1. Followed by acute osteomyelitis 2. Dental infection
  41. 41. • Clinical features – 1. Mild pain , trismus , paresthesia of lip 2. Elevation of temprature 3. Regional lymphadenopathy 4. In acute exacerbation ,the suppuration may perforate the bone , mucosa and overlying skin to form a fistulous tract.
  42. 42. Cutaneous fistula Intraoral fistula with draining abscess
  43. 43. Radiographic appearance -
  44. 44. Chronic Focal Sclerosing Osteomyelitis • It is an unusual reaction to the mild bacterial infection entering the bone through a carious tooth in persons who have a high degree of tissue resistance and reactivity . • Here , tissue reacts to the infection by proliferation of cells rather than destruction.
  45. 45. • Etiology – Mild dental infection • Clinical features – 1. No signs and symptoms except for mild pain due to infected pulp.
  46. 46. • Radiograph –
  47. 47. Chronic Diffuse Sclerosing Osteomyelitis • It is analogous to the focal form of disease , representing proliferative reaction of the bone diffusely to the low- grade infection. • Etiology – 1. Generalized periodontal disease. 2. Multiple teeth infection (mild)
  48. 48. • Clinical features – 1. No clinical indications of its presence. 2. Occasionally , there is acute exacerbation of the chronic infection results in vague pain , unpleasant taste , mild suppuration & formation of fistula over the mucosal surface.
  49. 49. • Radiograph-
  50. 50. Garre’s Osteomyelitis • It is also called as chronic ,non-suppurative osteomyelitis with proliferative periostitis . • This is distinctive osteomyelitis in which there is focal gross thickening of the periosteum with peripheral reactive bone formation resulting from mild irritation or infection. • Etiology – Dental infection
  51. 51. • Clinical features- 1. Toothache or pain in the jaw 2. Bony hard swelling on the outer surface of the jaw.
  52. 52. • Radiographic appearance-
  53. 53. Pericoronitis • Definition – • “Pericoronitis is an inflammation of the gingiva that covers the chewing surface of the molars which have not fully erupted in the oral cavity. Most commonly , it occurs with third molar which is impacted or erupting .”
  54. 54. Clinical features – 1. Pain 2. Swelling and erythema over the gingiva covering the tooth . 3. Trismus 4. Halitosis 5. Bad taste 6. Submandibular lymphadenopathy.
  55. 55. Sialadenitis • It is an inflammatory disease of the major salivary glands characterized by swelling of the glands believed to be the result of infection. • Etiology – 1. Bacterial or viral infection 2. Mostly occurs in debilitated patients suffering from dehydration , suppression of salivary secretion or sialolithiasis or after a surgery
  56. 56. Clinical features – • Oral or facial pain, especially while eating • Erythema over the side of the face or upper neck (Parotitis) • Swelling (particularly in preauricular region, below the jaw, or on the floor of the mouth) • Trismus • Fever • Xerostomia • Bad taste • Pus may drain into the mouth.
  57. 57. Extraoral Parotitis Sialadenitis of Submandibular gland
  58. 58. Maxillary Sinusitis • Inflammation of mucosa of Maxillary sinus is Maxillary sinusitis . • Etiology – 1. Infection 2. Trauma 3. Allergy 4. Infected odontogenic cyst 5. Oroantral communication or fistula 6. Displaced tooth or root
  59. 59. Signs - Extraoral- 1. Tenderness over cheek . Intraoral- 1. Percussion of maxillary molars show tenderness. 2. Existence of oroantral fistula with or without polypoid mass extruding from socket . 3. Fetor oris on blowing the nose.
  60. 60. Symptoms 1. Nasal blocking following rhinitis 2. Postnasal discharge with constant irritation requiring clearing of throat. 3. Heavy feeling of head. 4. Constant throbbing pain in upper part of cheek or entire side of face which is exacerbated by bending down. 5. Chills , fever ,difficulty in breathing .
  61. 61. Stomatitis • Stomatitis is an inflammation of the mucous lining of any of the structures in the oral cavity. Etiology – • Poor oral hygiene • Dietary protein deficiency • Infections • Iron deficiency anemia • Ill fitting dentures • Mouth burns from hot food or drinks • Medications • Allergic reactions • Radiation therapy
  62. 62. Clinical features • Pain • Mouth ulcers • Burning sensation • Paresthesia • Bad taste • Excessive salivation
  63. 63. Clinical features Denture stomatitis Oral ulcers
  64. 64. Necrotizing fasciitis • “It is defined as a rapidly progressing infection located in the deep fascia with secondary necrosis of subcutaneous tissue , usually sparing the muscles and accompanied by high fever ” Etiology – • Infection- Streptococcus pyogenes Predisposing factors – • Diabetes mellitus , malignancy , drug addiction
  65. 65. Clinical features- • High fever . • Erythmatous cellulitis with ill-defined margins • Severe pain but affected area is anesthetized. • Progression of disease is rapid with change in skin colour from red blue to green in 36 hours • By 4th to 5th day , it leads to cutanous gangrene. • Skin bullae may devlope • There is no lymphadenopathy.
  66. 66. Acute Necrotizing Ulcerative Gingivits • It is an endogenous oral infection that is characterized by necrosis of gingiva. • Etiology – • Infection – Fusiform bacilli , spirochetes • Predisposing factors – 1. Local factors- • Poor oral hygiene • Preexisting gingivitis • Smoking • Emotional stress
  67. 67. • Systemic factors – • Nutritional deficiency – Vit.- B2 , C • Debilitating diseases – I. Leukemia II. Aids III. Syphilis
  68. 68. Clinical features – 1. Onset is sudden with Pain , profuse salivation, & metallic taste. 2. Spontaneous gingival bleeding. 3. Loss of sense of taste. 4. Fetid odor 5. Typical “ Punched out ” crater like ulceration mostly on interdental papilla ,gingiva becomes brown in colour.
  69. 69. Conclusion • It is necessary for the oral surgeons to have knowledge about inflammation to diagnose inflammatory diseases and inflammatory lesions and to treat them in Surgical or conservative approach .
  70. 70. References Books- • Robbin’s Basic Pathology 8th edition • Shafer‘s Textbook Of Oral Pathology 6th edition • Atlas of Pathology Articles- • Tufts OpenCourseWare © 2008 Tufts University • BJSM article
  71. 71. Thank you

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