Acute radiation syndrome /certified fixed orthodontic courses by Indian dental academy


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  • Acute radiation syndrome /certified fixed orthodontic courses by Indian dental academy

    1. 1.
    2. 2.        Introduction Radiation biology Radiation Chemistry Effects of Radiation Relevance of Radiation Exposure in orthodontics Radiation Protection Bibliography
    3. 3. Introduction  X-rays are a form of electromagnetic radiation  Ability to ionize matterwhich is the initiating event in radiation induced biologic changes
    4. 4.  IS THE STUDY OF THE EFFECTS OF IONIZING RADIATION ON THE LIVING SYSTEM.  Deterministic Severity of response  proportional to dose severity Stochastic probability of a response occur and not hat is dose dependent
    5. 5.     Free radical production RH + Photon R + H+ + e These free radicals are unstable ,short lived and highly reactive. Fate of the free radical _ 1) Dissociation R X + Y 2) Cross linking R + S RS
    6. 6. thus there is formation of structurally and functionally biologic molecules differing from original molecule.there by inducing biological change.
    7. 7.  Radiation acts on living system either DIRECT INDIRECT Direct ionization of biologic absorbed by H2O macromolecules with IONIZED formation of unstable free radicals. free and change the macro molecule photon H2O Resultant radical interact
    8. 8.  Most radiosensitive cells are are 1)undergoing mitoses 2)having a high mitotic rate 3)are most primitive in differentiation
    9. 9. Cells are usually divided into five categories of radiosenstivity 1)vegetative inter mitotic cells  2)differentiating inter mitotic cells 3)multipotential connective tissue cells 4)reverting post mitotic cells 5)fixed post mitotic cells
    10. 10. )vegetative intermitotic cells—most radiosensitive Eg:precursor cell–spermatogenicerythoblastic ,basal cells of the oral mucous membrane. 2)differentiating intermitotic cells –Eg: intermediate cells of hemapoietic ,replicating cells of the inner enamel epithelium
    11. 11. Multi potential connective tissue cells – ---Eg intermediate radio sensitivity --- : endothelial cells,fibroblasts  Reverting post mitotic cells ---radio resistant ---Eg: acinar and ductal cells of salivary gland and pancreas,parenchymal cells of liver ,kidney and thyroid  Fixed post mitotic cells---most radioresistant ---Eg:neurons ,striated muscle cells ,squamous cells close to the surface of oral mucous membrane and erythocytes 
    12. 12. Relative Radio sensitivity of Various Organs High Intermediate Low Lymphoid Fine vasculature Optic lens Bone marrow Growing cartilage Mature Growing bone eryhtocytes Intestines Salivary glands Muscle Mucous Lungs cells membrane Kidney Neurons Liver
    13. 13.
    14. 14. Radiation effects may be spoken In terms :the short term effects which bring about …mitosis linked cell death the long term effects that bring about….fibro atrophic cell death
    15. 15.    Primarily determined by the sensitivity of the parenchymal cells of the respective tissue Raidly proliferatingcell loss mitosis linked reduction in the number of mature cells . In tissues that undergo little proliferation the radiation induced hypoplasia is not evident
    16. 16.    Determined by the extent of damage to the fine vasculature of the tissue Endothelial cells---multi potential connective tissue cells---intermediate radio sensitivity.. Thus over a period of time ---capillaries ,degenerate and undergo necrosis. Permeability increased
    17. 17.    progressive fibrotic processes begins around the capillaries This fibrotic scar tissue will eventually cause obliteration of blood vessels---depriving the cells of nutrition ,oxygen and elimination of waste Eventually leading to loss of cell function ,decreased resistance to infection and death of all cell types…with the net result of PROGESSIVE FIBROATROPHY
    18. 18.
    19. 19.
    20. 20. • Oral mucous membrane * Short term effects –related to the radiosensitive vegetative intermitotic cells of the basal layer of the mucous membrane. * Initially —redness and inflammation— mucositis *as therapy continues – formation of whitish yellow pseudomembrane—desquamated epithelial layer *2 months after therapy—rapid healing--• mucosa becomes atrophic,thin relatively avascular.
    21. 21. *are radiosensitive—extensive degeneration *loss of taste acuity during second or third week of radiotherapy *recovery usually takes between 60-120 days
    22. 22.       The parenchymal component of salivary glands is radiosensitive Short-term effects –inflammatory response Long-term effect progressive fibrosis,adiposis,loss of fine vasculature with parenchymal degeneration---accounting for xerostomia. Marked reduction of salivary flow is seen in the 1st two weeks Xerostomia ,decreased ph of saliva (6.5to 5.5)--this is low enough to cause decalcification Buffering capacity falls by 44%
    23. 23.    Flora thus becomes more acidogenic in saliva and plaque ---this along with thick viscous ,acidic saliva---renders patient susceptible to radiation caries. Oral micro flora changes –strept.mutants,lactobacillus and candidasis Recovery—6 to 12 months If not –unlikely that there will be significant recovery
    24. 24.
    25. 25. Rampant form of decay  Irradiation of the teeth does not influence the decay but the changes induced in the salivary glands and saliva are responsible for this decay  There are three types of radiation caries -----superficial lesions—B,O,Li,P surfaces -----primarily involving cementum and dentin in the cervical region -----dark pigmentation of the entire crown 
    26. 26.  Reducing ----daily application for 5 minutes of a viscous topical 1% neutral NaF gel -------- avoidance of dietary sucrose
    27. 27. Teeth
    28. 28.       Severity of damage is dose dependent If irradiation precedes calcification –tooth bud destroyed After calcification has begun—inhibition of cellular differentiation –malformations and arresting growth Adult teeth are relatively radioresistant Pulpal tissue –reverting and fixed postmitotic cells—may show long –term fibroatrophy No discrenible effect on the crystalline structure of enamel ,dentin or cementum
    29. 29.      Primary damage—results from damage to the vasculature of the periosteum and cortical bone Also the radiation tends to destroy osteoblasts and to a lesser extent osteoclasts Bone marrow fatty bone marrow and fibrous connective tissue marrow  hypo vascular,hypoxic and hypo cellular Degree of mineralization reduced brittle
    30. 30.
    31. 31.    Decreased vascularity -renders bone susceptible to infections Source of these infections may be from radiation –induced breakdown of the oral mucous membrane ,mechanical damage tooth extraction ,denture sore,PD lesion or radiation caries... Mandible > maxilla
    32. 32. Relevance of Radiation in Orthodontia
    33. 33. • • • Most commonly taken radiographs in Orhtodontia are :-lateral cephalogram panoramic radiograph hand- wrist x-rays Exposure of critical organs which are:active bone marrow thyroid gland salivary glands optic lens
    34. 34.  Exposure is of low doses …example for the formation of cataract 2Sv(200 rem)but in opg dose exposed to in the form of scattered radiation is only 80 microSv  Also studies by Danforth and Gibbs Thyroid160-370 microGys Pitutary 70-490 microGys Salivary glands 393 microGys     As these doses are well below the maximum permissible dose the harmful effects still remain uncertain  Harmful effects manifest as increased probability of a normally occurring disease  Bear in mind ALARA principle
    35. 35.  Harmful effects manifest as increased probability of a normally occurring disease  Bear in mind ALARA principle
    36. 36. Two categories :-ouupationally exposed  Non occupationally exposed Whole body Isolated areas of body Occ.exp. 0.05Svyear 0.75Svyear  Non occ. 0.005Svyear Exp. 0.075Svyear
    37. 37.  Two aspects:Patient Protection Protection of Personnel
    38. 38. Patient protection 1) 2) 3) 4) 5) 6) Intensifying screens Focal spot to film distance Collimation Filtration Lead aprons and collars Good radiographic techniques
    39. 39.  Barrier/position and distance rule  Operator never hold film  Personnel should wear film badges Regular checks of x-ray equipment for spills 
    40. 40. IS A COLLECTION OF SIGNS AND SYMPTOMS EXPERIENCED BY PERSONS AFTER ACUTE WHOLE BODY EXPOSURE TO RADIATION 1)Prodromal Period 2)Hematopoietic Syndrome 3)Gastrointestinal Syndrome 4)Cardiovascular Syndrome 
    45. 45. 7 to 15 Gy causes extensive damage to the rapidly proliferating epithelial cells of the intestinal villi with resultant –denudation of mucosal surface ,loss of plasma and electrolytes these changes are responsible for diarrhea,dehydration,and weight losses well as invasion of endogenous intestinal bacteria producing septicemia.
    46. 46.  These damages along with the hematopoietic damage together contribute to the signs and symptoms of GASTROINTESTINAL SYNDROME
    47. 47. Exposure to a dose in the range of 50Gy will cause death in a few minutes to 2 days There is collapse of the cardiovascular system and autopsies reveal necrosis of the cardiac muscle . Damage to the nervous system manifests as patient showing intermittent stupor ,incoordination,disorientation and convulsions
    48. 48.
    49. 49.  Introduction  Mechanisms of Cross Infection  Important Pathogens in Infection Control  Control of Cross-Infection  Sterilization in Orthodontics
    50. 50. Introduction  Pathways for CrossContamination Patient to dental team Dental team to patient    Patient to patient Dental office to community Modes of disease spread :-Direct contact Indirect contcat Droplet infection
    51. 51.  Mechanism or site of entry into body:through breaks in skinmucous membrane through inhalation
    52. 52.
    53. 53.  There are several important disease in infection control but the ones of most significance in the dental office are:- Hepatitis B virus HIV Herpes Simplex Virus
    54. 54. Infectious agent Disease or condition Route of transmission Incubation period Communicable period Hepatitis A virus ‘Infectious hepatitis’ Type A Hepatitis Feco-oral, Food , water, shellfish 2 to 6 wks (av. 28 to 30 days) Hepatitis B Virus ‘Serum hepatitis’ Type B Hepatitis Blood, saliva, body fluids,sexual contact, perinatal 2 to 6 months ( av. 60 to 90 days ) 2 to 3 wks before onset (jaundice) through 8 days after Before, during & after clinical signs 2 to 10 weeks Carrier state: indefinite All phases 2 to 6 months Like HBV 15 to 64 days Not known. Maybe like HAV 3 months to 5 years From asymptomatic through onset of opportunistic infections Delta Hepatitis Virus ( HDV ) Delta Hepatitis Non-A, Non-B Hepatitis Virus Non-A, non-B hepatitis Coinfection with HBV, Blood, Sexual contacts, Perinatal Similar to HBV Epidemic non-A non-B Feco-oral Human Immunodeficienc y Virus ( HIV ) Contaminated water Acqired Blood & blood Immunodeficiency products Syndrome ( AIDS ) ( infected i.v needles ), sexual contact, perinatal, 2 years for transfusion case )
    55. 55. Herpes Simplex Virus Acute Herpetic gingivostomatitis Saliva, direct contact ( lip, hand ) Type I ( HSV -1 ) Herpetic labialis Type II (HSV-2 ) Ocular herpetic infections Indirect contact (on objects, limited survival) Herpetic Whitlow Varicella-zoster virus (VZV) 2 to 12 days Acute stomatitis: 7wks after recovery Sexual contact Asymptomatic infection: with viral shedding Chickenpox Direct contact Shingles 2 to 3 weeks Reactivation period: with viral 5 days prior to shedding onset of rash until crusting of vesicles 4 to 6 weeks Prolonged Pharyngeal excretion 1yr after infection Months to years Indirect contact Airborne droplet Epstein- Barr Virus ( EBV ) Infectious mononucleosis Direct contact Cytomegalovirus ( CMV ) Neonatal CMV infection Perinatal Inexact Direct contact(most body secretions) 3 to 8wks after transfusion CMV disease Labialis: one day before onset until lesions are crusted Saliva Blood transfusion
    56. 56. Treponema pallidum Syphilis Direct contact 10 days to 10 weeks Transplacental Variable and indefinite Maybe 2 to 4 years Neisseria gonorrhoea Gonorrhea Direct contact Group A streptococci (Beta-hemolytic) Streptococcal sore throat Respiratory droplets Streptococcus pyogenes Scarlet fever 2 to 9 days Direct contact Impetigo Indirect contact (short survival of organism) During incubation Continued for monthsand years if untreated 1 to 3 days 10to 21 days, untreated Many nasal oropharyngeal carriers Erysipelas Staphylococcus aureus Abscesses Saliva 4 to 10 days Staphylococcus epidermidis Boils (furuncles) Exudates Impetigo Nasal discharge Variable and indefinite Bacterial pneumonia While lesions drain and carrier state persists
    57. 57. Influenza viruses Influenza Nasal discharge Measles Virus (Morbilivirus) Rubeola (measles) Respiratory droplets Direct contact Rubella virus (Togavirus) Saliva Rubella (German measles) Airborne droplets Nasopharyngeal secretions 24 to 72 hrs 3 days from clinical onset 8 to 13 days to fever, 14 days to rash Few days before fever to 4 days after rash appears 16 to 23 days From 1wk to at least 4 days after rash appears Dirrect contact Congenital Rubella Syndrome Mumps virus (Paramyxovirus ) Infectious parotitis Polio virus types 1,2,3 Poliomyelitis Airborne droplets Maternal infection, first trimester Direct contact (saliva) 2 to 3 wks (average 18 days) Airborne droplets Direct contact (saliva), Droplet, 7 to 14 days Feco-oral Mycobacteriu m Tuberculosis Tuberculosis Droplet nuclei Sputum Upto 6 months Infants shed virus for months after birth From 1 to 7 days before sympoms until 9 days after swelling Probably most infectious 7 to 10 days before and after onset of symptoms Long, repeated exposure usually
    58. 58.
    59. 59.    An infection-control program comprises two distinct areas: exposure control and hazard communication. Exposure control covers sterilization and disinfection, waste management, and employee including personal protective equipment and bodily-fluid-exposure protocols. Hazard communication requirements include a periodic checklist for OSHA compliance, drills for hazard communication plans (chemical spills, emergency first aid, and fire or tornado evacuation), secondary labeling of hazardous chemicals, Material Safety Data Sheets, x-ray updates, and properly displayed state and federal posters.
    60. 60.    Sterilization it is the process of destroying all forms of microbial life Disinfection it is defined as the removal of or inactivation of microbes.thus it implies only some and not all pathogenic organisms can be eliminated by this method. Anti-septicsthese are substances that prevent the growth or action of microbes by either destroying them or inhibiting their actions
    61. 61.    Sanitizersreduce the microbial population to safe levels as judged by public health requirements.they are usually chemical agents that kill close to 99.9%of the organisms. Germicideskill the growing forms but not necessarily the resistant spores. Bacterio static agents agents which have the ability to inhibit he growth of bacteria.
    62. 62.   Is a process intended to kill all microorganisms whether vegetative or pathogenic . It is the highest level of microbial killing that can be achieved
    63. 63.  The protocol for sterilization of instruments is usually 1)holdingpresoaking 2)pre cleaning 3)sterilization process 4)aseptic storage and handling of instruments
    64. 64.     If instrument not to be cleaned immediately soak in holding solution prevents salivablood from drying up. Holding solution usually is a germicidal Discard solution at least once a day Avoid prolonged soakingcorrosion
    65. 65. Reduces amount of microbes present ,but more importantly removes blood saliva and other materials that may insulate microbes from the sterilizing agent.  May be achieved by ultrasonic manual 
    66. 66. A) Physical agents B) Sunlight C) Dry heat:flaming incineration hot air D) Moist heat :  boiling steam under pressure E) Filtration:membranes asbestos pads
    67. 67. F) Ultraviolet light G)Radiation H)Micro-wave I)Lasers
    68. 68.  In dentistry the procedures used are:- 1)Heat sterilization 2)Gaseous sterilization 3) Liquid chemicals sterilization
    69. 69. a) Moist heat:-steam pressure autoclave b) Unsaturated chemical vapour:- chemiclave c) Dry heat:- conventional dry heat ovens :- short cycle high temperature dry heat ovens
    70. 70.    Sterilizes by bringing about oxidation as well as denaturing proteins It is the latent heat and not the pressure built inside by steam within the closed chamber that is responsible for killing of the microbes Two cyclesStandard..20 –30 250°f Flash cycles..3-10 273°f
    71. 71.  Advantages time efficient,good penetration  Disadvantages 1)may lead to corrosion of susceptible instruments. 2)items sensitive to elevated temperatures get damaged
    72. 72.    Chemical solution heated in a closed solution-chemical vapor kills the microbes 0.23%formaldehyde,72.38%ethanol along with acetone,ketone and water 20 min at 270°f
    73. 73.   Advantages 1)eliminates or reduces the corrosion of susceptible instruments. 2)dry instruments available at end of cycle Disadvantages 1)items sensitive to elevated temp.will get damaged 2)pre drying of inst.a must
    74. 74.
    75. 75. Conventional dry heat ovens *heat chambers wherein heated air is circulated by gravity convection  *320f for 30 min *place packs at least 1 cm apart to allow for the hot air to circulate between wrapped instruments
    76. 76.
    77. 77. Short –cycle high temperature dry heat ovens  Are force draft ovens  370°f to 375°f for 6 to 12 mins Advantages :-1)instruments sensitive to corrosion may be safely sterilized 2)effective rapid cycles are possible 3)items dry at end of cycle
    78. 78. Disadvantage Instruments sensitive to elevated temp. will get damaged Ethylene oxide sterilization  for complex, delicate , heat sensitive inst. aeration of about 24hours must pror to use of instruments especially porous and plastic ones
    79. 79.
    80. 80.     Even though seen to be used commonly it does not kill spores and does not bring about sterilization of instruments Heat reaches and kills the blood borne pathogens 100° for 10 min. Thus more than sterilization it is a process of high level disinfections
    81. 81.
    82. 82.
    83. 83.   Chemical agents are used for controlling of microbes on body surfaces and on inanimate objects are grouped under disinfectants These includeantiseptics sanitizing degerming disinfecting agents
    84. 84.      1)destroy all forms of microorganisms within a practical period of time 2)non-toxic,non-allergic,non-irritating 3)non-corrosive,non-discolouring ,nondegrading 4)good wettability and penetrabilityfor effective contact even in the presence of blood and exudate 5)readily soluble in available solvents
    85. 85. Spaulding in 1972 A. High level disinfectants Eg:-ethylene oxide gas,immersion glutheraldehyde solutions  B. Intermediate level disinfectants Eg:-formaldehyde ,chlorine compounds,alochol,iodophors ad phenolic compounds
    86. 86. C.Low level disinf. Narrowest anti-microbial activity Eg:- quaternary ammonium comps
    87. 87.  A) Alcohols  B) Aldehydes  C) Halogens  D) Surfactants  E) Quanternary ammonium compounds  F) Phenols and Phenolic compound
    88. 88. Alcohols bactericidal and fungicidal but not sporicidal MOA :- denature proteins solvent action on lipids Ethyl and isopropyl alcohols…most commonly used optimum conc. 70% range 60-95% If conc.falls below 45%antmicrobial activity is slow and uncertain A.
    89. 89. Alkalating agents Formaldehyde Gaseous state …used as a fumigant MOA :- protoplasmic poison denaturing proteins  Disadvantage:-pungent odour ,irritating t skin ,poor penetrating and slow acting 
    90. 90. Gluteraldehyde :less pungent volatile and irritating with better disinfectant properties broad spectrum of activity2%sol.bactericidal,tub erculocidal and virucidal in 10 mins and sporicidal in 10 hours gluteraldehyde+iodine comp. +bleach recommended for use against Hb virus where sterilization not feasible 
    91. 91.    They also have a low surface tension and can thus penetrate blood and exudate thus reaching instruments surfaces Also used for disinfection of impressions Cidex , sporicidin, glutorex
    92. 92.
    93. 93.  Iodine  Iodophors  Chlorine
    94. 94. Chlorine Sanitizing agent Elemental chlorine used for water purification may also be used as a surface disinfectant conc. 2.5% gloves must be worn corrosive to metals 
    95. 95. Iodine :- used for wound and skin antisepsis Tinctures of iodine are usually used in 1,5and 7% conc. Which destroy 90%of bacteria in 90,60 and 15 sec. respectively • Iodophors:- composed of complexes of iodine and surface active organic carrier molecules from which iodine gradually released . 
    96. 96. Soaps :- degerm the skin by mecanical removal of microbes bacterostatic and bacteriocidial
    97. 97.  Phenols :-  As disinfectants and antiseptics  MOA:-denaturing of proteins or damage to cell membrane  Bacteroicidal and bacteriostatic…but poor viricidal properties
    98. 98.
    99. 99.  These include :-  Gloves  Mouth masks  Protective eyewear  Hand washing  Immunization
    100. 100.  The need for gloving  The practices of gloving not only provides protection to dentist but also to the patient
    101. 101.  For eg:Dentist treats dentist contracts herpes…herpes whitlox patient with herpes simplex to patients treated in future
    102. 102.     Disposable gloves Do not wash gloves with detergents in an attempt to reuse While leaving chairside remove gloves While working chair side try and put to use the practice of double gloving
    103. 103.  Protection from microbes Eg:HSV, Hepatitis B  Protection against physical damage    Protection from impact damage Protection from splashes of chemicals
    104. 104.  Preferable to use goggles over glasses as former not only provides protection from front splash and impacts but also from side impacts and splashes
    105. 105. Two types of micro flora  resident flora transient flora
    106. 106.  Resident flora:colonize and become resident can never be completely eliminated less imp. In causing disease
    107. 107.  Transient flora:acquired whilst dealing with contaminated objectssurfaces do not colonize or survive for long periods on the hand usually pathogenic can be removed by following a good hand washing protocol
    108. 108.    Hand washing products containing low levels of microbial agents used in a 10 –30 sec.hand wash routine minimizes the no.of transient flora and aids in reducing the no.of resident flora too. Chlorhexidine digluconate ,povidine iodine,parachlorometaxylonol Washing of hands before and after gloving very imp.
    109. 109.
    110. 110.    Protect mucous membrane of mouth and nose from contact with aerosolssprayssplashes of oral fluids from patients…also in turn protect patient Composed of material that filters out 95%99.9%of 2-3 micrometer size particles that directly contact it They should be form-fitting over the bridge of the nose to reduce fogging of eyewear
    111. 111.   Dispose mask once it gets moist resistance to airflow through the mask increasesmore unfiltered air is allowed to pass by the edge of the mask Use disposable maskschanging between patients
    112. 112.  Hepatitis The HBV is an infectious agent associated with acute and chronic hepatitis . Major cause of necrotizing vasclitis,cirrhosis , and primary hepatocellular carcinoma. Found primarily in blood and blood products …may also be present in other body fluids… saliva , semen,tears,urine
    113. 113.      Transmitted parenterally,sexual contact,mother to fetus HBV relatively environmentally stable… potential for indirect transmission via contact with contaminated inst. Best protection is by immunization Two vaccines Recombivax HB and EngerixB Regime :-1.0ml doses given at 0, 1, and 6 mths
    114. 114.   Following vaccination protective levels of antibodies are believed to persist for seven years Need for booster dose is being debated
    115. 115.  autoclave or chemiclave .  The only major obstacle of pliers sterilization is related to their corrosion suceptibility.
    116. 116.  corrosion resistance of orthodontic grade steel is directly proportional to its chromium content and inversely proportional to its carbon content . disruption of chromium oxide layer renders them suceptible to corrosion.  Instruments made of carbon or 400 series steel are more susceptible than those made of 300 series steel.
    117. 117.    first be cleaned thoroughly and rinsed with distilled water . do not allow contaminants to dry Tap water to be avoided– use only distilled water
    118. 118. *   Chrome-plated instruments should be autoclaved separately from stainless steel ones. Detergents with chloride bases should not be used , Purple or black staining is caused by exposure to ammonia.
    119. 119.    Contaminated archwires are sterilized in divided plastic containers Cut to appropriate length and kept overnight in gluteraldehyde solution Thereafter stored in binsuntil ready to be used
    120. 120. Recycling of archwires  the relative high costs of archwires has lead to one trying out the practice pf reclcycling of arch wires  Both cold and heat sterilization have been tried  Heating cycle should not exceed 235 C for a total of 20 minsto keep impact on wires properties to the minimum.
    121. 121. Studies on Recycling of Orthodontic Arch wires
    122. 122.  Effect of sterilization on mechanical properties and surface topography of 0.017” x 0.025” NiTinol and Titanal wires Three methods:dry heat at 180 c for 60 min formaldehyde alcohol vapour ,132c for 30 min steam autoclave ,121 c for 20 min at 15-20 psi 
    123. 123.         Tests conducted:Three point bending—elastic moduli Surface topography –laser scattering Tensile properties—instron utm Results:No significant change in tensile properties with any sterilization procedure No change in elastic moduli No apparent effect on surface topography
    124. 124. Effects of cold disinfectabnts on mechanical properties and surface topography of 0.017” x 0.025” NiTinol and Titanal wires  Three disinfectants tested:2%acidic phetaraldehyde for 10 hours  Cholorine dioxide for 6 hours  Iodophor for 10 hours ..mixture at the ratio of 1/256 with water. 
    125. 125.   Tests :Bending ,tensile,laser spectroscopy Results :No change in elastic moduli No change in surface topography No change in tensile properties 
    126. 126. Counter tops:-wipe counter tops with effective disinfectants.  Impressions:easily contaminated with blood and saliva microorganisms easily transferred from contaminated impressions to casts where they can remain viable for upto 7 days…thus providing a path for cross contamination from the clinic to the laboratory personnel 
    127. 127.    Impressions after being removed from the mouth should be rinsed under running water …this enables the removal of adhering microorganisms They are then placed into plastic bags with appropriate disinfectants for approximately 15 mins…followed by their removal and rinsing of the disinfectant…they are now ready to be poured If the impression is sensitive to immersion an alternate would be to spray the impression with the appropriate disinfectant and wrap it with a paper towel moistened with the same disinfectant for 15 mins.
    128. 128.    White and Pharoah: Oral Radiology:Principles and Interpretations Robert langleins,Olaf e.langland,McDavid:Panoramic Radiogaph Casebow, M.P.:patient doses from Orthopantomograph x-ray exposures,Br. J. Radiol.,46:230,1973
    129. 129.    Chris H. Miller and Charles J. Palenik:Infection Control and management of Hazardous Materials for the Dental Team Mayshew,Kusy:Recycling of orthodontic wires:Am. J. Ortho 1988 Buckthal,Kusy: Am. J. Ortho.1998
    130. 130. Leader in continuing dental education