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inflammation/ dental implant courses


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inflammation/ dental implant courses

  1. 1. INFLAMMATION INDIAN DENTAL ACADEMY Leader in continuing Dental Education
  4. 4. Introduction War is the metaphor for inflammation. Both are necessary evils .
  5. 5. The word inflammation is derived from the state of being inflammed. To inflamme means to “ set afire” which conjurs up the color red , a sense of heat and often pain The word is derived from the latin word enflammare
  6. 6. HISTORICAL HIGHLIGHTS W Cornelius Celsus (ancient Rome) described rubor (redness), calor (heat -- this applies only to the skin), dolor (pain), and tumor (which then simply meant "swelling") as the "cardinal signs of inflammation WJohn Hunter (the great early surgeon, * 1793, * first characterized inflammation as a nonspecific body response. WRudolf Virchow added functio laesa (loss of function) as the fifth cardinal sign of inflammation, and his student, Julius Cohnheim, provided the basic studies of the pathologic microanatomy of inflammation. W Elie Metchnikoff (* 1892) was the first to observe and study phagocytosis. (* This is the same Metchnikoff who popularized yogurt as a "health and longevity food". He died at age 70.)
  7. 7. • Paul Ehrlich developed the idea of humoral immunity early in the 20th century. (This is the same Ehrlich who developed the "magic bullet" for syphilis, and most of the stains we still use.) • Thomas Lewis demonstrated that inflammation is brought about by chemical mediators, most of which act locally. Someone may still ask you about the "triple response of Lewis" to a superficial scratch: (1) an immediate red scratch mark; (2) a red flare around the scratch mark; (3) a red swollen area ("wheal") around the flare. (Try it!) Dr. Lewis found that he could eliminate the flare, but not the others, by cutting the autonomic nerve supply (i.e., preventing the "axon reflex"). This experiment led to the discovery of histamine.
  8. 8. DEFINITION AND CAUSES DEFINITION. Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is body defence reaction in order to eliminate or limit the spread of injurious agent. AGENTS CAUSING INFLAMMATION. Physical agents like heat, cold,radiation,mechanical trauma. Chemical agents like organic and inorganic poisons. Infective agents like bacteria,virus,parasites. Immunological agents like cell mediated and antigen-antibody reactions.
  9. 9. FOUR CARDINAL SIGNS RUBOR(redness) TUMOR(swelling) CALOR(heat) DOLOR(pain) The fifth sign functio laesa (loss of funtion)was later added by Virchow Signs of inflammation were first described in the Egyptian papyrus in 3000BC
  10. 10. ACUTE INFLAMMATION Acute inflammation is the immediate and early response to injury,is of relatively short duration,lasting from a few minitues up to a few days,and is characterized by fluid and plasma protien exudation and by a predominantly neutrophilic leucocyte accumulation. It has three major components a) Alteration in vascular caliber b)Structural changes in microvasculature c)Emigration of the leucocytes These changes account for five classical signs of acute inflammation. 1-Heat(calor) 2-Redness(rubor) 3-Swelling(tumor) 4-Pain(dolor) 5-Loss of function(functio laesa)
  11. 11. CAUSES OF ACUTE INFLAMMATION 1. MICROBIAL INFECTION a. Viruses- by death of individual cells or by intercellular multiplication b. Bacteria- endotoxins or exotoxins 2. HYPERSENSITIVITY REACTIONS Parasitic infections 3. PHYSICAL AGENTS Trauma, Radiation, Heat, Cold 4. IRRITANTS and CORRESIVE CHEMICALS Acids and Alkalies
  12. 12. VASCULAR CHANGES CHANGES IN VASCULAR FLOW AND CALIBER • Transient vasoconstriction(seconds) • Vasodilation involving arteriole first • Local increase in blood flow redness and warmth(erythema) Increased permeability resulting in exudation of protien rich fluid into the extravascular tissues Red blood cells become concentrated increasing the viscosity and slowing the circulation(process called STASIS) Leucocytes (neutrophils) accumulate along the vascular endothelial surface(process called MARGINATION)
  13. 13. After adhering to endothelial cells the leucocytes squeeze between them and miagrate through the vascular wall into interstitial tissue(process called emigration)
  14. 14. INCREASED VASCULAR PERMEABILITY • In earliest phase,vasodilation and increased blood flow increase intra vascular hydrostatic pressure. • This results in filtration of fluid from the capillaries called Transudate. • Soon eclipsed by increased vascular permeability ,and flow of protien rich fluid and cells called Exudate into the interstitium • This reduces the intravascular osmotic pressure,while increasing the osmotic pressure of the interstitial fluid. • Net result is out flow of water and ions into the extravascular tissues ,accumulation is called Edema. How does the normally non penetratable endothelial layer become leaky during acute inflammation ?
  15. 15. FIVE MECHANISM ARE KNOWN Endothelial cell contraction - Immediate transient response(15-30 min) - Capillaries and arterioles are unaffected Junctional retraction - -reversible mechanism -occurs 4-6 hr after initial stimulus -persists for 24 hr or more -structural reorganization of cytoskeleton -induced by cytokine mediator(TNF&IL-1)
  16. 16. Direct endothelial injury -vascular leakage by causing endothelial cell necrosis and detachment - seen in severe injuries eg burns or infection - reaction is called immediate sustained response - venules,capillaries,arterioles,can all be affected -direct injury may also induce a delayed prolonged leakage,begins after a delay of 2-12hr.lasts for several hours or even days and involves venules and capillaries eg mild to moderate thermal injury.Bacterial toxins,uv or x-irradiation -Attributed to apoptosis,and actions of cytokines.
  17. 17. Leukocyte dependent endothelial injury -due to leukocyte accumulation during inflammatory response -leukocyte may be activated,releasing toxic oxygen species and proteolytic enzymes which cause endothelial injury or detachment -injury restricted to sites where leukocytes can adhere to the endothelium(venules,and pulmonary capillaries)
  18. 18. Increase transcytosis -via an vesiculovacuolar pathway -augments venular permeability,following exposure to certain mediators (vascular endothelial growth factor VEGF)
  19. 19. LEUKOCYTE CELLULAR EVENTS Extravasation of leukocytes from vascular lumen to extravascular space is divided into Margination and rolling Adhesion and transmiagration between endothelial cells Miagration in interstial tissue toward a chemotactic stimulus
  20. 20. MARGINATION AND ROLLING • In normal blood flow red and white blood cells travel along the central axis • As vascular permeability increases fluid exits the vascular lumen and blood flow slows • As a result leukocytes settle out of central column, marginating to vessel periphery • Subsequently they tumble on the endothelium, transiently sticking along the way, a process called rolling. ADHESION AND TRANSMIAGRATION • Leukocytes firmly adhere to the endothelial surface before crawling between the cells and basement membrane into extravascular space(diapedesis) • It occurs predominantly in venules of systemic vasculature and capillaries of lungs • Neutrophils predominate for the first 6-24 hr followed by monocyte in subsequent 24-48hr
  21. 21. Neutrophils are short lived,undergoing apoptosis within 24-48hr after exiting the blood stream Monocyte survive longer and persists for long periods as tissue macrophages CHEMOTAXIS AND ACTIVATION After extravasation leukocyte emigrate toward the site of injury along a chemical gradient in a process called chemotaxis Both endogenous and exogenous substances can act as chemotactic agent for leukocyte including: -soluble bacterial products,paricularly peptides with N-formyl methionine termini -components of complement system,particularly C5a -products of lipoxygenase pathway of arachidonic acid (AA)metabolism, leukotrieneB4 (LTB4) -cytokines
  22. 22. Chemotactic agents binds to spesific receptor on the leukocyte cell surface and induce an intracellular cascade of phospholipid metabolites,eventually culminating in increased intracellular calcium The increased cytosolic calcium triggers the assembly of cytoskeletal contractile elements necessary for movement Leukocytes move by extending pseudopods that anchor themselves to the extracellular matrix and then pull the remainder of the cell after. Besides stimulating locomotion ,chemotactic factors also induce other leukocyte responses,generically referred to as leukocyte activation. If agents producing the chemotactic factor can be ingested by the leukocyte (ie phagocytosed)digestion and destruction of the phagocytosed material may yield breakdown products that have chemotactic properties Neutrophils themselves can be stimulated to release chemotactic factors that attract macrophages
  23. 23. PHAGOCYTOSIS AND DEGRANULATION PHAGOCYTOSIS CONSISTS OF THREE STEPS: • Recognition and attachement of the particle to the ingesting leukocyte -It is facilitated by coating microorganism with serum proteins generically called Opsonins , which in turn bind to specific receptor on the leukocyte -Most important opsonins are the immunoglobulins(IgG)molecule (specifically the Fc portion of the molecule),and the C3b fragment of complement(and its stable C3bi form) -In many cases the binding of IgG is responsible for triggering the activation of the complement cascade that results in deposition of C3b fragment on targeted particles. -Microbial surface can directly induce complement activation by IgG Independent alternative pathway • Engulfment with subsequent formation of a phagocytic vacuole -Binding of opsonized particle triggers engulfment -Psedopods are extended around the object to be engulfed,eventually forming a phagocytic vacuole.
  24. 24. • KILLING OR DEGRANULATION OF THE INGESTED MATERIAL -The membrane of the phagocytic vacuole then fuses with the membrane of a lysosomal granule, resulting in discharge of the granules content into the phagolysosome and degranulation of leukocytes. -Bacterial and other microbial killing is accomplished largely by reactive oxygen species. -Phagocytosis stimulates an oxidative burst ;characterized by a sudden increase in oxygen consumption. -Generation of oxygen metabolites is due to rapid activation of a leukocyte NADPH oxidase,which oxidizes NADPH(reduced nicotinamide adenine dinucleotide phosphate)and in the process reduces oxygen to superoxide ion .
  25. 25. -Superoxide is then converted mostly by spontaneous dimutation into hydrogen peroxide -Quantity of hydrogen peroxide produced are insufficient to effectively kill most bacteria. -Lysosomes of neutrophils (azurophilic granules) contain the enzyme myeloperoxidase(MPO)and in the presence of halide converts hydrogen peroxide to hypocholorous radical which is a powerful oxidant and antimicrobial agent that kills bacteria by halogenation or by protein or lipid peroxidation - Even in absence of oxidative burst other constituent of leukocyte granules are capable of killing bacteria and other infectious agent,these include 1)BPI(bactericidal permeability increasing protein) 2)lysosomes 3)lactoferrin and defensins(group of peptides)
  27. 27. CHEMICAL MEDIATORS OF INFLAMMATION MOST LIKELY MEDIATORS IN INFLAMMATION • VASODILATION -Prostaglandins(PGI2,TXA2) -Nitric oxide • INCREASED VASCULAR PERMEABILITY -Vasoactive amines -C3a and C5a -Bradykinin -Leukotriens C4,D4,E4 -Platelet factor Chemotaxis, leukocyte activation -C5a -Leukotriens B4 -Bacterial products -Chemokines(IL8)
  28. 28. FEVER -IL1,IL6,TNF alpha PAIN -Prostaglandins -Bradykinin TISSUE DAMAGE -Neutrophils and macrophages lysosomal enzyme -oxygen metabolite -Nitric oxide
  29. 29. CHRONIC INFLAMMATION Chronic inflammation is characterized by 1)Inflitration with mononuclear (chronic inflammatory cell)including macrophages,lymphocytes and plasma cells. 2)Tissue destruction induced by inflammatory cells 3)Repair involving new vessel proliferation(angiogenesis) and fibrosis. Chronic inflammation may follow acute inflammation Chronic inflammation arise in following settings: 1)Persistent infections eg Treponema pallidum(syphilis),mycobacterium (tubercle bacilli), certain fungi 2)Prolonged exposure to potentially toxic agents eg non-degradable exogenous material (inhaled particulate silica)silicosis in lungs,endogenous agents such as elevated plasma lipid components(atherosclerosis).
  30. 30. 3)Autoimmune diseases Individual develops an immune response to self antigens and tissues ,eg Rheumatoid artheritis CHRONIC INFLAMMATORY CELLS • Macrophages ,which are diffusely scattered in connective tissue,or clustered in organs such as the liver(kupffer cells),spleen and lymph nodes,CNS,lungs(alveolar macrophages) • Monocytes emigrate at the site of injury within the first 24 to 48 hr,when they reach extravascular tissue they undergo transformation into larger phagocytic cells called macrophages • Macrophages secrete a wide variety of biologically active products -Acid and neutral proteases -complement component and coagulation factors -reactive oxygen species and NO -Eicosanoids -cytokines.IL1,TNF,growth factors
  31. 31. At the site of acute inflammation where the irritant is cleared and process is resolved macrophages eventually die or wander off, into lymphatics. In case of chronic inflammation macrophage accumulation persists. Other type of cells are -lymphocytes (T&B) -plasma cells -eosinophils Plasma cells are the terminally differentiated end products of B-cell activation,produce antibodies directed against antigen. Eosinophils found in inflammatory sites around parasitic infections,as part of immune reaction,mediated by immunoglobulin E(IgE) associated with allergies. Eosinophil-specific granules contain major basic protiens(MBP), a highly charged cationic protein that is toxic to parasites but also cause epithelial cell lysis.
  32. 32. GRANULOMATOUS INFLAMMATION • A Distinctive pattern of chronic inflammation characterized by aggregation of activated macrophages that have acquired an enlarged,squamous cell like (called epitheliod ) appearance • Tuberculosis is archetypal granulomatous disease.
  33. 33. RESOLUTION Resolution involves the return of injured tissue to normal structure and function. Most important cell in resolution is macrophage,it has the responsibility of: -Phagocytosing -Digesting dead tissue,dead inflammatory cell,red blood cell and fibrin in the exudate. Resolution can only occur if destruction has not been extensive and parenchymal cells are capable of resolution . More highly specialized the tissue ,the less the capacity for regeneration. Cells involved in healing are : -Neutrophils,release of lysosomal enzyme may contribute to digestion of debris.
  34. 34. -Macrophages, primary role is debridement, other is to secrete growth factors that stimulate proliferation of fibroblasts and new blood vessels. -Fibroblast, synthesize and secrete collagen, proteoglycans, fibronectin in the healing wound. After these molecules are released from the cell they aggregate to form collagen fibrils. As fibers are formed ,the tensile strength of the wound increases. -Platelets, platelets participate in clot formation and provide mitogens(substances that stimulate cell division) and chemoattractants for fibroblast. • Alternative to resolution is fibrous repair.
  35. 35. SYSTEMIC EFFECTS OF INFLAMMATION • Fever is the most prominent manifestation. it depends on the humoral signals from the body. It is coordinated by the hypothalamus and involves a wide range of endocrine, autonomic and behavioral responses. The components of the so called acute phase reaction include the cytokines(IL-I,IL-6) and TNF. • Acute phase reaction include,slow-wave sleep,anorexia,hypotension etc. • IL-6, stimulates hepatic synthesis of plasma proteins notably fibrinogen, which cause erythrocyte to agglutinate. • IL-1 and TNF, act on the thermoregulatory center of the hypothalamus via local prostaglandin E production to induce fever( hence the efficacy of asprin and NSAIDs in reducing fever). • Leukocytosis (increased white blood cell count,15000 or 20000 cells/ micro liter ) • Parasitic infections induce eosinophilia.
  36. 36. GINGIVAL INFLAMMATION The sequence of events in the development of gingivitis is analyzed in three different stages 1-Stage one gingivitis:The initial lesion First manifestation of gingival inflammation are vascular changes,dilation of capillaries and increased blood flow.Clinically this response to bacterial plaque is not apparent. 2-Stage two gingivitis :the early lesion After 4-7 days clinical signs of erythema may appear,prominent cells are lymphocytes,bleeding on probing may also be evident 3-Stage three gingivitis:the established lesion In chronic gingivitis(stage III) the blood vessels become engorged and congested ,venous return is impaired,and the blood flow becomes sluggish,results in localized gingival anoxemia,which superimposes a some what bluish hue on the reddened gingiva.
  37. 37. • STAGE FOURTH GINGIVITIS:THE ADVANCED LESION Extension of the lesion into alveolar bone characterizes a fourth stage that has been named the advenced lesion or phase of periodontal breakdown. CLINICAL FEATURES OF GINGIVITIS • Gingival bleeding-from gingival sulcus on gentle probing • Color changes –in chronic gingivitis red or bluish red color(normal is coral pink),in acute gingivitis change may be marginal,diffuse,or patch like • Changes in consistency-(normally firm and resilient) both destructive(edematous) and reparative(fibrotic)changes coexist and consistency is determined by their relative predominance. • Change in surface texture-loss of stippling,in chronic inflammation surface is either smooth and shiny or firm or nodular. • Gingival recession • Changes in contour
  38. 38. Clinical features of gingivitis
  39. 39. PERIODONTITIS Periodontitis results from extension of the inflammatory process initiated in the gingiva to the supporting structures of the tooth It can be classified as: -Slowly progressive periodontitis(adult periodontitis) -Rapidly progressive periodontitis: 1-Adult onset(age >20 yr) 2-Pubertal and adolescent onset(age 11-19 yr) 3-Prepubertal onset(age<11 yr) -Nectrosing ulcerative periodontitis -Refractory periodontitis
  40. 40. Clinical features are: -Gingival inflammation -Loss of stippling -Blunted or rolled gingival margins -Flattened or cratered papillae -Bone loss -Infrabony pockets
  41. 41. Clinical features of periodontitis
  42. 42. Prosthodontic considerations • Post-extraction,and after preprosthetic surgical procedures tissue need to be given rest to heal,inflammaed mucosa can be detected clinically,no specific protocol exist,but at least a min of 15 days rest is given.(time required for a wound to heal by secondary intention) • Sequeale caused by wearing removable prosthesis
  43. 43. • In the interface between a prosthesis and the oral mucosa,microbial plaque may have important negative or harmful effects. • A prosthesis may promote infection of the underlying mucosa,caries and periodontal disease adjacent to overdenture abutments ,periimlant gingivitis and chemical degradation or corrosion of prosthetic materials.
  44. 44. Direct sequelae caused by wearing dentures Denture stomatitis-(denture sore mouth or inflammatory papillary hyperplasia or chronic atrophic candidosis) In randomized population the prevalence of denture stomatitis is 50% among complete denture wearer. Classification Type I –a localized simple inflammation or pinpoint hyperemia
  45. 45. Type II- An erythematous or generalized simple type seen as more diffuse erythema involving a part or the entire denture covered mucosa. Type III-Granular type (inflammatory papillary hyperplasia), commonly in central part of the hard palate and alveolar ridges.
  46. 46. Inflammed basal seat,tissue rest massage,and prescription of trearment liner should be advocated
  47. 47. Strains of genus candida ,in particular Candida albicans, may cause denture stomatitis. Still this condition Is not a spesific disease entity because other causal factors exist such as bacterial infection,mechanical irritation,or allergy. Etiology- TypeI most often is trauma induced, typeIIand typeIII most often are caused by microbial plaque accumulation(bacteria and yeast) on the fitting denture surface and the underlying mucosa. Association of candida with angular chelitis or glossitis indicates a spread of the infection from the denture covered mucosa to the angles of the mouth or the tounge. Predisposing factors are presence of denture in the oral cavity,wearing denture day and night,infection disappear if dentures are not worn. Other important factors that can modulate host-parasite relationship and increase the suseptibility to candida–associated denture stomatitis may be ageing ,malnutrition, immunosuppresion, raditation therapy,diabetes mellitus ,antibacterial antibiotics.
  48. 48. Management and preventive measures Efficient plaque control/correction of denture wearing habits, patients should be instructed to remove the denture during night,after meals and scrub them with soap before reinserting them. Mucosa should be kept clesn and massaged with soft toothbrush Old and ill fitting dentures should be replaced or corrected,rough areas should be smoothed or relined with soft tissue conditioner. Anti-fungal drugs used in patients where clinical diagnosis has been confirmed by mycological examination, burning sensation, infection has spread to pharynx or, patient with debilitating diseases. Local therapy with nystatin, amphotericinB, miconazole, clotrimazole, preferred to systemic therapy with ketaconazole or fluconazole because of resistance of candida species.
  49. 49. • For the reduction in the risk of relapse following precautions should be taken -treatment with anti fungal for four weeks -when lozenges are used denture should be taken out during sucking - Maintain denture hygiene, wear denture as seldom as possible,keep them dry in disinfectant solution of 0.2% to 2.0% chlorhexidine during nights.
  50. 50. Fixed partial denture Periodontal factors- The goals of periodontal therapy for the prosthodontic patient are: -Resolve inflammation -Convert periodontal pocket depths to clinically normal sulcular depths -Establish physiologic gingival architecture -Provide adequate zone of attached gingiva -Adequate oral hygiene Margin placement- the gingiva are healthiest when margins are placed well above(ie 1-2mm)the gingival crest. Biologic width- to avoid encroaching on the biologic width ,the tooth preparation must terminate at least 2mm coronal to alveolar crest. Severing the natural dentogingival attachment will produce chronic gingival inflammation, pocket formation, and osseous defects.
  51. 51. Elective crown lengthening with controlled ostectomy and apically positioned flap is more desirable.
  52. 52. Periodontal injury caused by occlusal forces is called trauma from occlusion. Occlusal traumatism does not affect the gingiva ,however in presence of inflammation it alters the path of inflammation into the periodontal ligament space and lead to infraosseous pockets. This does not affect the marginal gingiva , but affects the bone ,this is called the zone of codestruction: trauma from occlusion in presence of inflammation. A classic example is poorly constructed RPD that causes gingival irritation with concomitant twisting force to the abutment tooth.
  53. 53. PERIODONTITIS vs PERIIMPLANTITIS THE SAME DISEASE ? THE SAME TREATMENT ? The soft and hard tissues surrounding an osseointegrated implant show some similarities Difference lies in collagen fiber being nonattached and parallel to implant surface. A periodontitis like process,periimplantitis can affect dental implants and can result in loss of implant. Bacterial plaque is the primary etiological factor in loss of both teeth and implant. Clinical findings include marked gingival inflammation,deep pocket, and progressive bone loss. Indications for implant removal -Severe peri implant bone loss(>50% of implant length) -Bone loss involving implant vents or holes -Rapid ,severe bone destruction(within one year of loading) -Non surgical and surgical therapy ineffective
  54. 54. Initial phase of treatment of peri-implantitis -Occlusal therapy- analysis of the fit of prosthesis ,occlusal evaluation,change in prosthesis design. -Anti-infective therapy- removal of plaque ,polishing of all accessible surface with pumice, subgingival irrigation of peri-implant pockets with 0.12% chlorhexidine,systemic anti microbial therapy for 10 consecutive days. Surgical techniques for treatment of peri-implantitis. Indications for resective therapy are -moderate to advanced bone loss -one and two wall bone defect -implant position in nonaesthetic area Apically displaced flap techinique and osseous resective therapy are used to correct horizontal bone loss and moderate vertical bone defects and to reduce overall pocket depth.
  55. 55. Surface polishing :Implantoplasty- surfaces with threads or roughened topography (eg hydroxyapatite)should be altered with high speed diamond burs and polishers to produce a smooth continous surface. It is performed before osseous resective therapy. Peri-implant regenerative therapy -Guided tissue regeneration and bone graft technique have been suggested. Maintenance every three months
  56. 56. Moderate to severe peri-implantitis with soft tissue Removal of implants 6 months before surgery And one week of antibiotic therapy Hyperplasia and deep pockets
  57. 57. Elevated flap showing bone loss around implants Membranes placed over the peri-implant bone defect
  58. 58. Removal of membranes after 4 months Post-operative evaluation 1 1/2 yr later,
  59. 59. NON STEROIDAL ANTI-INFLAMMATORY ANALGESICS Classification: 1. Analgesic and anti-inflammatory. 2. Analgesic but poor antiinflammatory. 1. Analgesic and antiinflammatory: a. Salicylates- e.g. Aspirin, salicylamide. b. Pyrazolone derivatives – e.g. Phenylbutazone, oxyphenbutazone. c. Indole derivatives – e.g. Etodolac, indomethacin. d. Propionic acid derivatives – e.g. Ibuprofen, naproxen, ketoprofen, fenoprofen. e. Anthranitic acid derivatives – e.g. Mephenamic acid, enfenamic acid. f. Aryl-acetic acid derivatives – e.g. diclofenac. g. Oxicam derivatives – e.g. piroxicam. h. Pyrrolo-pyrrole derivatives – e.g. ketorolac.
  60. 60. Analgesic but poor antiinflammatory: a. Para aminophenol derivatives – e.g. Paracetamol (Acetaminophen). b. Pyrazolone derivatives – E.g. Metamizol, Propiphenazone. c. Benzoxazocine derivatives – E.g. Nefopam. Mechanism of Action:  NSAID’s are peripherally acting because their analgesic and anti inflammatory effects are, to a large extent, produced through a peripheral mechanism.  They block the cyclooxygenase pathway by inhibiting cycloxygenase, an enzyme involved in the biosynthesis of arachidonic acid into prostaglandins, which are involved in the pain mechanism.  There are 2 isoforms of cyclooxygenase COX-1 and COX-2 and although all NSAID’s inhibit both forms, the two isoforms differ slightly in their sensitivity to NSAID inhibition.
  61. 61.  This difference becomes therapeutically important because COX-2 appears to be more involved with synthesis of prostaglandins at sites of inflammation, whereas COX-1 is more involved at sites where adverse effects of NSAID’s are expressed.  Aspirin is the classic and prototypical drug and along with NSAID’s is more effective for the intermittent, sharp pain caused by inflammation which is characteristic of dental pain.
  62. 62. • Glucocorticiods: are powerful anti-inflammatory agents • They may act by down regulating the expression of specific target genes including COX-2 genes encoding cytokines( IL-1 and TNF) • They also upregulate genes that encode potent anti-inflammatory proteins such as lipocortin • Lipocortin 1 inhibits the release of AA from membrane phospholipids
  63. 63. CONCLUSION • WAR AND INFLAMMATION Both are more-or-less stereotyped responses to outside threats. There are specialized troops (white cells), including suicide-commandos (neutrophils), long-term siege armies (granulomas), and many others. There are supply routes (vessels), communications and intelligence (mediators), and a huge array of lethal weapons (inflammatory enzymes). In war as in inflammation, there will be damage to both the enemy and to friendly forces, and there will very likely be severe damage to the battlefield itself. Despite idealistic rhetoric about "the laws of war", when the fighting starts, there is really only one law for the soldiers: "Kill your enemy." Like it or not, if you want peace, you must be prepared to fight under certain conditions. Like it or not, if you want to be healthy, your body must be able to mount an inflammatory response. Force will always rule our world. Our best hope is that this will be the force of good laws. And the best for which we can hope from the inflammatory response is that, for most of our lives, it will do us more good than harm. • Probably your own death will be caused by your last inflammatory response.
  64. 64. REFERENCES • Kumar, Cotran, Robbins, Basic Pathology, sixth edition • Trowbridge,Emling, Inflammation A Review of The Process third edition • Govan,McFarlane, Pathology Illustrated fourth edition • Harsh Mohan, Textbook of Pathology, second edition • Carranza,Newman, Clinical Periodontology , eighth edition • Zarb,Bolender, Prosthodontic treatment for edentulous patients twelfth edition • William F.P.Malone, Tylman’s theory and practice of fixed prosthodontics, eigth edition • Carl E Mish, Implant Dentistry, second edition
  65. 65. THANK YOU