rationaleofendodontictreatment-191120103352.pdf
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The document discusses focal infection caused by microorganisms from infected dental sites. It describes the inflammatory response and pulp tissue changes, including degenerative changes like fibrosis, resorption and calcification. It outlines the classic "FISH" zones of reaction to dental infection: the zone of infection, contamination, irritation, and stimulation. It also presents Kronfeld's mountain pass theory, which likens the tissue reaction zones to a mobilized army defending the periapex from bacterial invaders entering through infected root canals.
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1)HIGHLY SEDATIVE-DIPHENHYDRAMINE,DIMENHYDRINATE,PROMETHAZINE,HYDROXYZINE 2)MODERATELY SEDATIVE- PHENARIMINE,CYPROHEPTADINE, MECLIZINE,CINNARIZINE
3)MILD SEDATIVE-CHLORPHENIRAMINE,DEXCHLORPHENIRAMINE
TRIPROLIDINE,CLEMASTINE
SECOND GENERATION ANTIHISTAMINICS-FEXOFENADINE,
LORATADINE,DESLORATADINE,CETIRIZINE,LEVOCETIRIZINE,
AZELASTINE,MIZOLASTINE,EBASTINE,RUPATADINE. Mechanism of action of 2nd generation antihistaminics-
These drugs competitively antagonize actions of
histamine at the H1 receptors.
Pharmacological actions-
Antagonism of histamine-The H1 antagonists effectively block histamine induced bronchoconstriction, contraction of intestinal and other smooth muscle and triple response especially wheal, flare and itch. Constriction of larger blood vessel by histamine is also antagonized.
2) Antiallergic actions-Many manifestations of immediate hypersensitivity (type I reactions)are suppressed. Urticaria, itching and angioedema are well controlled.3) CNS action-The older antihistamines produce variable degree of CNS depression.But in case of 2nd gen antihistaminics there is less CNS depressant property as these cross BBB to significantly lesser extent.
4) Anticholinergic action- many H1 blockers
in addition antagonize muscarinic actions of ACh. BUT IN 2ND gen histaminics there is Higher H1 selectivitiy : no anticholinergic side effects
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Receptor Discordance in Breast Carcinoma During the Course of Life
Definition:
Receptor discordance refers to changes in the status of hormone receptors (estrogen receptor ERα, progesterone receptor PgR, and HER2) in breast cancer tumors over time or between primary and metastatic sites.
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Monitoring:
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- 2. Complete debridement of root canal system followed by 3D obturation.
- 3. FOCAL INFECTION • It is localized or generalized infection caused by dissemination of microorganism or toxic products from a focus of infection.
- 4. Mechanism of focal Infection • Metastasis of microorganism from infected focus • Carrying toxins or toxic by- product through blood stream and lymphatic channels to site of reaction.
- 5. Portal For Entry of Micro Organism • Dental caries • Open dentinal tubules • Accessory and lateral canals • Defective restoration
- 6. Inflammation • Local response of living tissue to injury. • Signs of inflammation: • Rubor (redness) • Tumor(swelling) • Color • Dolor (pain) • Function lasea (loss of function)
- 7. Types of Inflammation Acute: polymorph nuclear lymphocytes Chronic: lymphocytes, macrophages, plasma cells.
- 8. Pulp Tissue Changes Following Inflammation • Degenerative changes: • Fibrous • Resorptive • Calcific
- 9. • Suppuration is another form of degeneration which is due to injury to polymorphonuclear cells. • It causes release of proteolytic enzymes with resulting liquefaction of dead tissues thus leading to formation of pus or suppuration.
- 10. • Proliferative changes: • Produced by irritants • Strong enough to produce degeneration or destruction • Principal cells : • Fibroblast (cellular fibrous tissue)
- 11. Formation of abscess (dead neutrophils + cellular debris) Breakdown of tissue Release proteolytic enzymes Result in death of neutrophil Release lactic acid Phagocytose the bacteria and cellular debris Attract at site of injury (24hrs) Inflammatory cells: Neutrophils:
- 12. Formation of abscess Breakdown of tissue Release proteolytic enzymes Result in death of eosinophil Release lactic acid Phagocytose the bacteria and cellular debris Attract at site of injury (24hrs) Inflammatory cells: Eosinophils:
- 13. Fuse to other macrophages to produce Multi nucleated giant cells (eg:osteoclast) Act scavenger of dead cells, tissues, foreign bodies Development of chronic inflammation Remain at site of inflammation for approx. 2 months Monocytes reach site of inflammation and change into macrophages Inflammatory cells: Macrophages:
- 14. Inflammatory cells: Lymphocytes: T lymphocytes B-lymphocytes T helper cells- present in acute phase of lesion T suppressor- predominate in later stage prevent rapid expansion of lesion. On getting signals from antigen and T helper cells they transform into plasma cells and secrete antibodies.
- 15. ENDODONTIC IMPLICATION • “FISH” established foci of infection and found 4 well defined zones of reaction 1. Zone of infection 2. Zone of contamination 3. Zone of irritation 4. Zone of stimulation
- 16. ZONE OF INFECTION • Polymorphnuclear leukocytes • Present in the center • Micro-organism along with necrotic cells present • Destructive components are released from phagocytes.
- 17. ZONE OF CONTAMINATION • Round cell infiltration • Cellular destruction (bacteria & toxins discharged from central zone). • Bone destruction • Lymphocytes present
- 18. ZONE OF IRRITATION • Toxins in this area more diluted • Collagen fibers digested by phagocytic cells, macrophages. • Osteoclast leads to bone destruction • Histologically it represent preparation for repair.
- 19. ZONE OF STIMULATION • Characterized by fibroblast, osteoblast. • Built as a wall of defense around zone of irritation • Act as a scaffolding on which osteoblast built new bone. •
- 21. KRONFELD’S MOUNTAIN PASS THEORY • Applied Fish concept so as to explain the tissue reaction in and around granulomatous area. • Zone A: • Bacteria in infected root canal with invaders entrenched behind high and in accessible mountains and foramina serving mountain passes.
- 22. • Zone B: • Proliferative changes of granuloma represents a mobilized army defending the periapex (plains) from bacteria (invaders). • Few bacteria (invaders) enter the periapex (plains) through the mountain pass they destroy leukocytes (defenders). • This mass attack result in major battle analogous to acute inflammation.
- 23. • Zone C: • Complete elimination of invaders from mountain entrenchment will eliminate the need for defense forces in the plains . • Once this is accomplished the defending army of leukocytes withdraws the local destruction and the environment returns to its normal pattern.
- 24. SUMMARY • Focal infection • Pulp Tissue Changes Following Inflammation • FISH” zones 1. Zone of infection 2. Zone of contamination 3. Zone of irritation 4. Zone of stimulation • Kronfeld’s mountain pass theory