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2010-09-21 00:54:50


oral1050 part 2
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  1. What is acute inflammation?
    • is the early response of a tissue to an injury
    • it is non-specific and follows the same pattern each time
    • short duration
    • if the cause is removed quickly, repair will take place, if not then it will evolve into a chronic inflammation
    • consists of changes in blood flow in the area of the injury, increased permeability of local blood vessels and the escape of fluid from the blood into the vessels
  2. What are the five signs of inflammation? And what are some signs that its spread systematically?
    • redness = erythema
    • heat
    • swelling = oedema
    • pain
    • loss of normal function

    • fever
    • increase in the number of white blood cells (leucocytosis
    • swelling and tenderness of lymph nodes (lymphadenopathy)
  3. Describe the process of acute inflammtion:
    • 1. injury occurs
    • 2. brief local constriction of arterioles and pre-cappilary sphincters. Decrease in blood flow in the cappillaries of the microcirculation
    • 3. subsquent dialation of the vessels occurs in the local microcirculation - increase in local blood flow
    • 4. blood vessels dilate untill acute phase finished (state of engorgement = hyperaemia)
    • 5.permeability of the walls change making it easier for fluid from the blood to exude from the vessels into surrounding tissues = swelling = oedema
    • 6. as plasma fluid being lost = blood flow slows down thus allowing white blood cells to move nearer to the vessel walls then normal = process called margination (the white blood cells involved are neutrophils or polymorphs which are multinucleated with granular cytoplasm
    • 7. white blood cells start to leave the blood vessels through the altered junctions between endothelial cells and move towards sites of specific injury --> are attached by materials that have been released from damaged cells = movement = chemotaxis
    • 8. neutrophils binds to micro-organisms or dead cell products and phagocytose
    • 9. once eaten neutrophils attach with materials contained in the lysosomes - destroy and kill themselves = potent enzymes released = collection of dead neutrophils = pus
    • 10. monocytes then arrive through the circulation process of adherence to the endothelium and migration into the tissues once into tissues called macrophages = phagocytose microorganisms and debris
  4. What are the outcomes of Acute Inflammation?
    • - resolution = bruising = no damage has occured to the connective tissue framework and no cells are nonrecoverable
    • - repair = scar = healing by scar formation
    • - abscess formation = pus in a confined space. Pus that has accumulated in a cavity formed by the tissue on the basis of an infectious process or other foreign materials ALWAYS A MUST TO DRAIN
    • - progression to chronic inflammation = only when the source of the infection has not been removed
  5. What is chronic inflammation?
    • chronic inflammation is a tissue response to injury only when the acute inflammatory repsonse cannot remove the cause of the injury
    • - histologically, neutrophils become less common and lymphocytes and monocytes are seen. Macrophages are also present
  6. What is granulomatous inflammation? What is a granuloma?
    is a distinctive chronic inflammatory response to something that inflammatory cells find indigestible. A granuloma ia a tumor like mass of inflammatory tissue = is an attempt to wall off the material
  7. What is hypertrophy and hyperplasia?
    • trophy = increase in the size of a tissue due to increase in the size of the cells
    • plasia = tissue size increased due to increase in the number of cells within the tissues
  8. Define regeneration and repair:
    • Regeneration : restoration of a tissue to a state indistinguishable from the original state before the injury - not always possible
    • Repair: begins with proliferation of cells to lay down new connective tissue fibres (fibroblasts) and cells to create new blood vessels (angioblasts) within that time = can occur in two ways = PRIMARY AND SECONDARY INTENTION
  9. What is primary intention and list the stages?
    a type of repair that aims at minimising the scar = desired outcome in surgical incisions

    • Stages:
    • - within minutes = primary blood clot forms
    • - within 24 hours = acute inflammation occurring and polymorphs (wbc) have now infiltrated the blood clot and is mopping up dead/bacteria cells. Early regeneration taking place in the epithelial cells around the edges
    • - within 2 days = mononuclear cells are coming to the wound - turn into macrophages and outnumber the polymorphs = continue to eat
    • - within 5 days = entire volume of wound = granulation tissue = blood clot material being removed by digestion from tissue enzymes released by the phagocytes = collagen is laid down by fibroblasts - contributing to the strenth of the repair
    • - within 1 week = fibrin scab sloughs off = initial repair
    • - 2weeks = fibroblasts have multiplied and collagen is very common = remodelling earlier fibres and aiding in wound strength
    • - 4 weeks = skin is fully restored but hairs and glands are not replaced. = collagen fibres have begun to contract in the connective tissue layer = shrinking the wound = blood supply decreasing = wound will never be as strong as it use to be
  10. What is secondary intention and list the steps:
    • occurs when wound edges cannot be opposed well or when significant amounts of tissue are absent.
    • more likely to get inflammation and infection
    • initially a much larger blood clot forms = resulting in larger fibrin meshwork in the wound forming a scar
    • when teeth are extracted = heal by secondary intention
    • * when granulation occurs = epithelium grows under the meshwork

    • - Early = blood clot forms immediately - blood vessels close off due to smooth muscle contriction and the clotting process. Vessels in the remaining peridontal tissue become engorged with blood and chomotactic factors factors are released to attract neutrophils to the area. Clot matures= has a fibrinous layer over the top to protect it. This mature and contracts causing gingival tissues around the socket to collapse in = gingival area is hyperaemic and oedematous
    • - first week = fibroblasts and blood vessels (from pd ligaement) proliferate and move to the clot = early granulation occurs with phagocytes being sure to remove dead cells and fibrin so fibroblasts can come in. On surface = re-epithelisation of the wound is occurring and are dividing on surface of the blood clot. Around crest of gingival bone = remodelling starting to begin therefore osteoclasts are resorbing sharp edges on bone remaining
    • *patients are asked not to rinse or drink for 4 hours after so blood clot isnt lost.
    • - second week = blood clot replaced by granulation tissue = fibrinous remnants of clot look whittish-brown and new blood vessels and fibroblasts have begun to infiltrate the clot. Bone has been remodelled by osteoclastic activity and osteoblasts are laying down new bone. On the surface significant re epithelisation is under way
    • -third week = extraction socket is completely replaces with granulation tissue. Around the socket wall small trabecular of ostieod or uncalcified bone are visable (microscopically). Osteoclasts are remodelling the original cribiform plate of teh socket wall - becomes less dense
    • - fourth week = process where bone is being deposited in the granulation tissue = initially bone is poorly calcified therefore new bone radiographically evident only after 2 months.

    Final product is a bony contour lower than height of alveolar bone around adjacent teeth!

    Dry socket is when the blood clot is lost. Antibiotics are not used as not a bacterial infection.