Inflammation by Dr. Amit Suryawanshi .Oral & Maxillofacial Surgeon, Pune , India
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Description: 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 & your replies are welcomed!
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Inflammation by Dr. Amit Suryawanshi .Oral & Maxillofacial Surgeon, Pune , India
- 1. Inflammation Dr. Amit T. Suryawanshi Oral and Maxillofacial Surgeon Pune, India Contact details : Email ID - amitsuryawanshi999@gmail.com Mobile No - 9405622455
- 2. Contents • Introduction. • Definition. • Historical background. • Cardinal signs of inflammation. • Types of inflammation. • Pathophysiology of inflammation. • Inflammatory cells & mediators. • Clinical perspectives. • Conclusion. • References.
- 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. 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. Inflammation • Definition – The word inflammation is derived from Latin word inflammare, which means “to set on fire.”
- 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. 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. 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. 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. 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. • Outcomes of acute inflammation- 1. Resolution 2. Progression to chronic inflammion. 3. Scarring or fibrosis
- 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. • Outcomes of Chronic inflammation- 1. Resolution 2. Scarring or fibrosis
- 15. Normal Inflammed (Vasodilation in capillary bed) Arteriole Venule Capillary bed
- 16. Leukocyte Transmigration , Chemotaxis & Phagocytosis
- 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. 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. • Plasma proteins & extracellular matrix also play an important role in process of inflammation.
- 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. 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. Acute inflammation Chronic inflammation Tissue necrosis Absent Ongoing Systemic manifestations High grade fever Low grade fever, weight loss , anemia
- 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. 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. 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. 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.
- 31. Infectious Arthritis • Incidence- very rare. • Etiology – Infection – Gonococci, Streptococci, staphylococci, pneumococci & tubercle bacillus .
- 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. • Clinical features – 1. Severe pain in joint , tender on palpation in joint region. 2. Trismus. 3. Results in ankylosis , most commonly fibrous ankylosis .
- 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. • Systemic factors – 1. Malnutrition 2. Acute leukemia 3. Uncontrolled diabetes mellitus 4. Sickle cell anemia 5. Chronic alcoholism
- 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. 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. • 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 .
- 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. • 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. Cutaneous fistula Intraoral fistula with draining abscess
- 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. • Etiology – Mild dental infection • Clinical features – 1. No signs and symptoms except for mild pain due to infected pulp.
- 46. • Radiograph –
- 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. • 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. • Radiograph-
- 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. • Clinical features- 1. Toothache or pain in the jaw 2. Bony hard swelling on the outer surface of the jaw.
- 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. 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. 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. 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. Extraoral Parotitis Sialadenitis of Submandibular gland
- 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. 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. 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. 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. Clinical features • Pain • Mouth ulcers • Burning sensation • Paresthesia • Bad taste • Excessive salivation
- 63. Clinical features Denture stomatitis Oral ulcers
- 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. 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.
- 67. 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
- 68. • Systemic factors – • Nutritional deficiency – Vit.- B2 , C • Debilitating diseases – I. Leukemia II. Aids III. Syphilis
- 69. 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.
- 70. 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 .
- 71. 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
- 72. Thank you
Editor's Notes
- LEWIS triple response - Inflammation is characterized by vascular events ,mediated by local chemicals and by axons .
- Metaplasia- Normal transformation of tissue from one type to another, as in the ossification of cartilage to form bone.
- When there is an inflammation . There is vasodilation .resulting in increased blood flow .this vascular expansion is cause of the erythema .as microvasculature becomes more permeable , protein rich fluid moves into extravascular tissue .this causes RBCs to be more concentrated , thereby increasing blood viscosity ..slowing the circulation called as stasis.as stasis develops leukocytes begin to accumulate along the endothelial surface….
- Activating substances released by bacterial and dead tissues go and adhere to the vessel walls which facillitates adhesion and activation of leukocytes …………4 steps of leukocytic recruitment 1.Margination 2. rolling . 3. adhesion .4.transmigration or diapedesis 5. margination ininterstitial tissue towars chemotactic nucleus . C3a c5a chemokines are inflam mediators which dilates and increases permeability of vessel weall while lipopolysacharides , IL- 1 , TNf alpha facilitates adhesion and activation of leukocytes …
- When inflammation subsides Phagocytes or macrophages clear leukocytes and dead tissues . Fluid and proteins are removed by lymphatic drainage as well as macrophages … Macrophages also release growth factors to new blood vessels and fibroblas to carry on fibrosis and sccaring .
- Kinin system mediators- activaed by necrosis.
- Prevalence – begins in early adult life , more common in women … women to men ration is 2:1
- Distribution of joint movement is polyarticular, frequantly bilaterally symmetrical ,stiffness is more in morning and diminishes throughout day … Tmj is involved in approximatly 20 % of cases of Rheumatoid arthritis . Rheumatoid arthritis in children is called as still’s disease . Class II div . 1 malocc. Reduced height of ramus and shortnd body due to failure of growth centre.
- OPG showing degerated and stunted condyle giving Sharpened pencil appearance. Treatment-oF Rheum arth No specific treatment . But remarkable benefits may be achieved from the administration of ACTH or cortisone Once limitation of motion is occurred , surgical intervention in the form of condylectomy should be done .but there is great tendency for ankylosis.
- Treatment of infectious arthri– 1. Administration of antibiotics .penicillines 500 mg 2. In advanced cases , Condylectomy or meniscectomy .
- Garre’s osteo= chronic osteomyelitis with proliferative periostitis
- Most common bacteria are staphylococcus aureus and albus
- Treatment Removal of foci of infection Debridement , drainage Surgical removal of sequestrum Antimicrobial therapy
- OPG at initial presentation …Osteolysis of the bone, derived from apical pathology, is noted in the incisor and canine region on both sides as well as in the molar region on the right Side.. Which is an indication of acute suppurative osteomyelitis . ..
- Treatment Removal of foci of infection Debridement , drainage Surgical removal of sequestrum Antimicrobial therapy
- Extraoral photograph showing Cutaneous fistula over the right inferior border of mandible 2-3 cm anteriorly to the angle of mandible . Intraoral photograph showing a clinically extensive secondary chronic osteomyelitis of the anterior region of mandible with multiple fistula and abscess formations.
- a An OPG of a patient with chronic osteomyelitis Showing osteolysis in the mandibular body region In periapical region of the right first molar with a sequestra is noted at the base of the right mandibular corpus with adjacent periosteal reaction.
- Treatment – Extraction of offending tooth or endodontic treatment . Surgical removal of sclerotic lesions is not indicated unless symptomatic
- Intraoral peripaical radiograph showing periapical infection of roots 1st mandibular molar and sclerosis of surrounding bone .. Treatment – Extraction of offending tooth or endodontic treatment . Surgical removal of sclerotic lesions is not indicated unless symptomatic
- Treatment – Remove foci of chronic infection. Acute episodes are treated with antibiotics If tooth is present in the region then extraction should be done surgically , to remove sclerosed bone along with the tooth.
- Panoramic radiograph showing multiple radioopaque lesions in the periapical region og mandibular teeth giving Cotton wool appearance Treatment – Remove foci of chronic infection. Acute episodes are treated with antibiotics If tooth is present in the region then extraction should be done surgically , to remove sclerosed bone along with the tooth.
- This sweeling indicates that its of several weeks duration . Treatment Extraction or Endodontic treatment of carious tooth with no surgical intervention for periosteal lesion except for biopsy .
- This is occlusal view of mandible in which there is focal gross thickening of the periosteum with peripheral reactive bone formation …. Treatment Extraction or Endodontic treatment of carious tooth with no surgical intervention for periosteal lesion except for biopsy .
- bad taste =Parageusia is bcoz of pus . Treatment --Warm saline rinses , antibiotics and analgesics .operculectomy , Surgical removal of impacted tooth .
- Mumps is common infection and often causes parotitis
- The gland may be painful, most often if there is an infection caused by bacteria.. Staphyloccs aureus and mycobacterium t. Treatment – In some cases, no treatment is needed. If there is pus or a fever, or if the infection is caused by bacteria, antibiotics may be prescribed. If there is an abscess, surgery to drain it or aspiration may be done. Practice good oral hygiene. Brushing your teeth and flossing thoroughly at least twice per day may help with healing and prevent an infection from spreading. If you are a smoker, stop smoking to help with recovery. Warm salt water rinses (1/2 teaspoon of salt in 1 cup of water) may be soothing and keep the mouth moist. Drink lots of water with lemon drops to increase the flow of saliva and reduce swelling. Massaging the gland with heat may help.
- Inflammation of most or all of the paranasal air sinuses is known as Pansinusitis. Infection – periapical abcess , common cold , URTI Trauma – fracture of antral floor or walls
- Cheek swelling in severe infection
- Postnasal discharge may lead to pharyngitis. Management – Conservative - steam, saline nasal rinses, topical decongestants, oral decongestants, mucolytic agents, antihistamines and intranasal corticosteroids. Functional endoscopic sinus surgery (FESS)
- Infections – herpetic stomatitis
- Treatment – Treatment of the underlying cause Oral hygiene measures Diluted bicarbonate of soda mouthwash Topical local anesthetics Anesthetic mouthwash
- Treatment – Treatment of the underlying cause Oral hygiene measures Diluted bicarbonate of soda mouthwash Topical local anesthetics Anesthetic mouthwash Treatment of mouth ulcers – mouth ulcers includes avoiding spicy, hot or acidic foods,…. Treatment of oral thrush includes a topical antifungal medication or an oral anti-fungal pill and good oral hygiene. Treatment of cold sores caused by herpes simplex includes antiviral medication and the use of ice packs. Canker sores often need no treatment, although a pain relieving gel or lozenges may be recommended until the canker sore has healed. Vitamins B 12 and zinc are given if deficiency is there to treat ulcers ……
- Affected area is anestherised due to cutanous nerve destruction cutanous gangrene is due to thrombosis of nutrient vessels.
- Management –drugs active against anaerbic bacteria Metronidazole continuous wound care should be taken Irrigation and debridement with H2O2 , followed by gauze soaked in charcoal lime & boric acid solution should be applied. Hyperbaric oxygen therapy Split skin graft .
- It is also called as a trench mouth .because there was a sudden outbreak of this diseasein world war1 & 2 . Where troops in trenches used to have this infection ……or Vincent’s infection .and when it spreads to the soft palate it is called as Vincent’s angina where pain , interdental ulcerations and gingival bleeding are considered to be the diagnostic triad.
- Etiopathology– Tissue destruction is caused by endogenous organisms that act either directly on the tissue or indirectly by triggering an inflammatory reaction.
- Management – Involved area is isolated with cotton rolls and dried . Then topical anesthetic is applied after 2-3 mins ,areas are gently swabbed with cotton pellt to remove pseudomembrane. Then area is cleansed with warm water. Patient is asked to rinse mouth after every 2 hrs with warm swater and 3% H2O2 . Chlorhexiden 0.12% are also effective . Patients with severe anug and lymphadenopathy are treated with penicillins or erythromycin 500mg 6 hrly. Or metro 400mg 8 hrly .for 7 days...after disease is diminished gingival curretage and root planing is done. Copious fluid and nutrient supplements are advised.