Literary Paper of The Grapes of Wrath by Steinbeck -- Grapes Wrath ess

Literary Paper of The Grapes of Wrath by Steinbeck       Steinbeck wrote many marvelous books but a great classic is one titled TheGrapes of Wrath.  This is a story of a family called the Joads, and a tale of acourageous family who sought earnest and family unity.      In my paper I will examine the different ways the Joads tried to keepunited whether just within their immediate family or eventually with all theothers who shared the same struggles and sufferings.      Steinbecks dialogue and descriptions of the dusty roads, the mensquatting in the dirt drawing pictures while making major decisions, the way inwhich they traveled all puts you right into the middle of the family.  Onebecomes aware and wants to be a part of there unity and their long for security.Steinbecks use of the characters dialect is astoundingly splendid andunmistakenly realistic of the Joads culture.  Without this dialogue, it wouldn ot be as intense and vivid.      J. Homer Caskey, in Letters to the Editor says,     Steinbecks knowledge of the forces which hold     a family together and the forces which cause it     to disintegrate.  He understands that family     councils are an important part of the lives of     the Joads.       The major theme is the struggle and survival of the Joad family from thetime they lost their home, to the unity they felt and soon were a part of awhole community, one big family, and one big soul.  This theme... ...       James N. Vaughan, The Commonweal, (July 1939)          Vol. XXX, 10c No. 14                          BIBLIOGRAPHY           Steinbeck, Jo hn  The Grapes of Wrath,          New York, NY  1992           Caskey, Homer J. The Saturday Review, Letters to          the Editor,  Ohio University (May 1939)           Vaughan, James N. The Commonweal, (July 1939)      

Childhood Mortality in Nineteenth-Century England :: European Europe History

Childhood Mortality in Nineteenth-Century EnglandThe issue of childhood mortality is written into the works of Gaskell and Dickens with alarming regularity. In Mary Barton, Alice tells Mary and Margaret that to begin with Will was orphaned, his family had buried his six siblings. There is also the death of the Wilson twins, as well as Tom Bartons early death --an event which inspires his father conjuration to fight for labor rights because hes certain his son would have survived if hed had better food. In Oliver Twist, Dicks early death is typical of workhouse children who never recover from years of chronic malnutrition. And in Dombey and Son, Paul demonstrates that wealth does not guarantee longevity, as we watch him steadily weakened by some mysterious illness. Evidence is eachwhere that Gaskell, Dickens, and many of their contemporaries, utilize fiction to chronicle a sad fact of l9th century life Many children didnt live to become adults. At the Newell Historical Burial grou nd in Attleboro, the stone marking the graves of the Stanley family indicates that three children were either stillborn or died before their first birthdays. If there were any other children who survived childhood, they were probably daughters who were buried in their husbands family mends. A typical grave from the mid-19th century is a husbands stone flanked by two or even three wives each but the last having died in her 20s or 30s. Certainly many of these women died in childbirth, because their death dates match the birth dates on the childrens stones. Several children might be named after the father. In one family plot with eight children, three were named John because only the third one survived the first year. ApE time when the death of a toddler was as normal as this practice was quite common in both America and England. While all of Dombeys money couldnt save his son from dying, little Pauls diet, lifestyle, and medical attention gave him every advant period available. The relationship between poverty and childhood mortality is unmistakable. In Bostons Irish Catholic slums, Lemuel Shattuck found that between 1841 and 1845, 61% of the population died before the age of five. (Woodham-Smith, p. 252) Poor English children didnt fare any particularly in the manufacturing towns of London, Sheffield, Leocester, Manchester, and Liverpool. Statistics from the Sheffield General Infirmary between 1837 and 1842 reveal that of 11,944 deaths, half were children under age five

Drug Enforcement :: essays research papers fc

What we Prohibit We Cannot Control Restriction Before Education? in that respect is a definite problem regarding the laws that enforce drug use in the joined States today. Think about this question. Why are some of the most injurious, addictive, and take heed altering substances in the world--tobacco and alcohol--legal, while other drugs are illegal that potentially cause no harm and have very bittie abuse? The United States has declared 178 substances illegal. These substances are believed to be so dangerous that they are controlled at the highest level for medical use or forbidden outright, even for medical research. signally many of these substances are not physically harmful and have never caused a death. Every year, legal drug use results in about cardinal percent of all hospital admissions, with one hundred thirty six billion dollars in medical costs. It seems odd, then, to make such a big tubercle between legal and illegal drugs regarding the law.A startling fact, Congr essman Newt Gingrich, the Speaker of the House, proposed legislation that would impose the death penalty for people caught carrying as little as two ounces of marijuana. He excused his own past marijuana use by explaining that pot smoking was a sign that we were alive and in graduate school in that era. Prison sentences for being caught with a large amount of marijuana are ten years, mandatory minimum, with no parole allowed. A prison sentence for murder six point three years. That is the average served, with parole allowed. The average sentence for a first time, non-violent drug offender is longer than for rape, child molestation, bank robbery, or manslaughter.(Gahlinger 2) This is an appalling statistic. The government is enforcing harsher punishment on a marijuana smoker compared to a murderer The government is filling prisons with drug offenders that will not learn any topic while there. Most likely when their term in prison is over they will go back to the same thing that they were doing before they went in to the system. Billions of tax payer dollars are keeping these drug offenders behind bars when a drug treatment program could be assist them to correct current addictive behavior and how to curtail their thoughts and actions to a more positive lifestyle. While the government puts one drug offender away some other one is ready to step up to the plate and replace him or her. This is a never ending cycle. Why do we not speak of move abuse or a chain saw problem?

Honest Iago of Shakespeares Othello Essay -- Othello essays

Honest Iago of Othello To nearly of the world William Shakespeare is recognized as the greatest dramatist in history. His plays have been performed for centuries by various interpretations. Shakespeares vast knowledge, and writing style made his works interesting for both the intellectual, and the illiterate. One of these styles is the use of motifs, which is seen extensively in Othello. An important example that runs end-to-end Othello, is Iagos honesty. This motif gave existence to Shakespeares perfect villain. The most interesting character in the play Othello is the villain, Iago, commonly referred to as Honest Iago. Iago is smart, and well tuned to human behavior, and uses this knowledge to his advantage. He manipulates others to do things to help him reach his final goal revenge on Othello and Cassio. His greatest tool in doing so is his write up as an honest and fiducial person. Othello believes Iago is a person of exceeding honesty, and knows all qualitie s, with the learned spirit of human dealings. Act III, Scene iii. The other characters believe this as well, and Iago becomes a confidant for most of them. The reputation Iago has, is encouraged by the other characters as well as himself. After Cassio and Roderigo fight, Othello arrives and Iago is the first that he asks an explanation from Honest Iago, that looks dead with grieving, speak. Who began this? Act II, scene iii. Even after Iago would not answer, Montano tells Othello to ask Iago again Your officer, Iago, can inform you Act II, scene iii, knowing that Iago would speak the truth. Both Othello and Montano are intensifying Iagos integrity here. Othello... ...aintain it, and encourage its existence. In most stories, especially during Shakespeares time, the villain is openly deceitful, and evil. Moreover, they are usually unattractive, and automatically disliked by the other characters. Shakespeare, in his brilliance, made Iago to be a charming, witty pers on, who is a friend to all. This was something unknown to the audience of his time. Shakespeare used this as a way of expressing an idea that anyone could have ulterior motives with their actions, and not to trust people with ease. He turn to the difference between reputation and a persons true character, and how they are rarely the same. In doing so, he created the most perfect villain of all of his works. Work Cited Shakespeare, William. Othello. Ed. Kenneth Muir. The invigorated Penguin Shakespeare. London Penguin Books, 1996.

Free Essay on Whartons Ethan Frome: Symbols and Symbolism :: Ethan Frome Essays

Symbolism in Ethan Frome Ethan Frome, the classic novel written by Edith Wharton contains a great amount of symbolism. The symbolism allows the characters to express themselves more clearly to the reader. It brings incidents and personalities in concert in meaning. The storys symbolic events is what pulls characters together in time of need. Starkfield Massachusetts is a boring cold farm town. People become actually ill at that place from the terribly harsh winters. Winter greatly affects the actions and behaviors of the characters. No quote better describes the harsh winters of Starkfield, and the effect that it had on the townspeople, than the following When I had been there a little longer, and had seen this phase of crystal clearness followed buy long stretches of sunless cold when the storms of February had pitched their white tents ab break through the devoted village and the mistaken cavalry of March winds had charged down o their support I began to understand why Star kfield emerged from its six months siege like a starved station capitulating without quarter (7). A nonher truly symbolic point of the story is the Elm tree. The Elm tree symbolizes the end and the escape of two lives. Even though Mattie an Ethan were not killed by the sled crash, that was their purpose. The Elm tree also symbolizes strength and courage. After the crash, the Elm tree was still standing, while Ethan and Mattie were terribly inju ruddy. If Ethan was a stronger person he would not have crashed into the tree with Mattie. He would have had the strength to say no in the first place. Zeena who was once a hypochondriac, recovered, and now she takes care of Mattie and Ethan. It was a miracle, considering how sick she was-but she seemed to be raised right up just when the call came to her. (131) The incident with the red dish is the most symbolic event in the story. The red dish was a wedding present given to Zeena by one of her relatives. When the red dish broke, it symb olized the breaking of Ethans heart when he found out that Zeena wanted Mattie to leave. Zeena never used the dish, she kept it in the closet. One day when Zeena went to get her medicine, she discovered that dish was broken, and that someone attempted to glue it back together.

Free Essay on Whartons Ethan Frome: Symbols and Symbolism :: Ethan Frome Essays

Symbolism in Ethan Frome Ethan Frome, the classic novel written by Edith Wharton contains a great amount of symbolism. The symbolism allows the characters to express themselves more clearly to the reader. It brings incidents and personalities unneurotic in meaning. The storys symbolic events is what pulls characters together in time of need. Starkfield Massachusetts is a boring cold farm town. People become really ill there from the terribly harsh winters. Winter greatly affects the actions and behaviors of the characters. No quote better describes the harsh winters of Starkfield, and the effect that it had on the townspeople, than the following When I had been there a little longer, and had seen this phase of crystal clearness followed buy long stretches of sunless cold when the storms of February had pitched their white tents ab forbidden the devoted village and the idle cavalry of March winds had charged down o their support I began to understand why Starkfield emerged fr om its six months siege like a starved station capitulating without quarter (7). Another truly symbolic point of the story is the Elm tree. The Elm tree symbolizes the end and the escape of two lives. Even though Mattie an Ethan were not killed by the sled crash, that was their purpose. The Elm tree also symbolizes strength and courage. After the crash, the Elm tree was still standing, while Ethan and Mattie were terribly inju going. If Ethan was a stronger person he would not have crashed into the tree with Mattie. He would have had the strength to say no in the first place. Zeena who was once a hypochondriac, recovered, and now she takes care of Mattie and Ethan. It was a miracle, considering how sick she was-but she seemed to be raised right up just when the call came to her. (131) The incident with the red dish is the most symbolic event in the story. The red dish was a wedding present given to Zeena by one of her relatives. When the red dish broke, it symbolized the breakin g of Ethans heart when he found out that Zeena wanted Mattie to leave. Zeena never used the dish, she kept it in the closet. One day when Zeena went to get her medicine, she discovered that dish was broken, and that someone attempted to glue it back together.

Periodontics

Tissues of the periodontium (Chapter 2) Periodontium * The weaves that surround, support, and attach to the teeth Components of the periodontium 1. chewing gum 2. periodontic ligament 3. cement 4. Alveolar tusk hold up of the periodontium * To support the teeth and literal constructions The gum tree * The subgross component of the periodontium inside the mouth * Described as pink, pink-red, blue, purple, or pigmented * It arsehole have the appearance _or_ semblance much darker when melanin pigmentation is present * Factors that mask the color change of glue * Food * Medications The three types of gum 1. liberal gumwood 2. Attached gingiva 3.Alveolar mucosa Mucogingiv al junction * Appears as a line that marks the data link in the midst of the inclined gingiva and the alveolar consonant mucosa Alveolar mucosa * The moveable create from raw material loosely attached to the vestigial boe * It is attached but moveable * The muster up is inactive and shiny Attach ed gingiva * Extends coronally from the mucogingival junction * It is continuous with the oral exam epithelium and is traverseed with keratinized stratified squamous epithelium * It is firmly attached to the alveolar mug up un comparable the free or moldingal gingiva * It DOES eat supplement fibers, which is why on the lingual aspect of maxillary teeth the ttached gingiva will blend with the attached palatal mucosa Rete pegs * Ridges of epithelium that form the connection between the free or attached gingiva and the underlying junction tissue * If gingiva is furbish upthy, it appears stippled, which is due to the rete pegs * If gingiva is non healthy, it will appear flat and shiny, due to a lack of rete pegs Function of rete pegs 1. Add strength to the gingiva 2. Nourish the gingiva Free gingiva or free marginal gingiva * Surrounds the tooth and crests a cuff or collar of gingiva extending coronally closely 1. mm * Usually a groove called the free gingival groove demons trates the free marginal gingiva from the attached gingiva * Appears to be attached to the tooth but whitethornbe separated by an instrument like a periodontic probe Gingival sulcus or crevice * A crevice or groove around each individual tooth * Sulcular epithelium is the continuation of the oral epithelium coering the free gingiva * Healthy sulcus is 1 to 3 mm probe deepness Sulcular or gingival crevicular politic * Liquid in the gingival sulcus Components diffuse through the basement membrane and the junctional epithelium Components of crevicular fluid 1. Connective tissue 2. Epithelium 3. Inflammatory mobile phones 4. Serum 5. Microbial plant Functions of the crevicular fluid 1. Cleanses the sulcus 2. Antimicrobial action 3. Plasma proteins improve adhesion of the epithelium to the teeth 4. Antibody drill to defend the gingiva Junctional epithelium * Separates the periodontal ligament form the oral environment * Protects the attachment to the tooth to the surrounding ti ssues * Approximately 15-20 cells If the base of scoop is damaged, it takes 4-6 weeks to heal Interdental papilla (interdental gingiva/gingival papilla) * The gingiva that fill embrasure spaces, which is the interproximal space beneath a contact point of 2 teeth * Shape depends on the teeth it is between but we generally consider the papillae pyramidal or triangulate * In health, it should fill embrasure and the tip pointed, not blunt or fruitless * Other descriptions pointed, bulbous, blunted, take, or cratered Col Depression between the lingual and facial papillae in posterior teeth that conforms to the proximal contact atomic number 18a * Usually absent in anterior teeth be act of the lack of lingual facial width at most coronal portion * Often supersensitised to infection because of its non-keratinization keratinisation * The process w hereby keratinocytes migrate from the basal grade of the epithelium to the aerofoil and flatten out in the process * These flattened cell s unveil a superficial layer that is similar to skin where no cell nuclei atomic number 18 present * Least common form of epithelium in oral infernal region spoken epithelium * The oral cavity is primarily make of stratifies squamous epithelium cells * The major(ip)ity of cells are keratinocytes and melanocytes which produce melanin which gives the gingiva a pigmented appearance (dark brown) Parakeratinized * The epithelium appears keratinized but the cells of the superficial layers retain their nuclei * Lightly keratinized (dorsal ascend of spiel) Non-keratinized * No signs of keratinization (no keratin) are present (epithelial surface) Keratinized Non-keratinizedPalate (most) Sulcular epithelium Tongue Alveolar mucosa Attached gingiva Junctional epithelium Oral epithelium Cols of papillae Cheeks (least) buccal mucosa Components Gingival epithelium 1. Oral epithelium 2. Sulcular epithelium 3. Junctional epithelium chemical formula healthy gingiva Color Uniformly coral or wak ing pink varying with thickness and degree of keratinization may to a fault vary due to amount of melanin (pigment) sizing Fits snuggle around the tooth, not overdone when healthy Contour 1.Marginal gingiva flat/knife edged 2. Papilla 1. Pointed and pyramidal in normal contact 2. Blunted/absent if diastema is present Texture 1. Free gingiva smooth 2. Attached gingiva stippled of rete pegs Consistency Firm and resilient (bounces back quickly) haemorrhage No spontaneous shed blood upon probing Exudate (pus) None Probing depth Average is 1. 8mm (0-3mm is the normal range) Periodontal ligament * Fills the space between the cementum and bring up * Remember that teeth have a shock absorbing cushion space of 0. -1. 5 mm next to the cram and they are not rigidly fixed in their sockets * The attachment implement consists of 1. Alveolar bone 2. Periodontal ligament 3. Cementum * The fibrous connective tissue that surround and attaches the roots of the teeth to the alveolar bone * This connective tissue is made of fiver bundles (mainly collagen) and cells * The fiber bundles in the PDL are made of collagen arranged in bundles and spread throughout the PDL Function of the periodontal ligament 1.Maintains the relation of a tooth to hard/soft tissues 2. Supplies nutrients and removes waste via dividing line and lymph vessels 3. Protect the vessels and fondnesss from injury 4. Resists occlusal forces (shock absorbers) 5. Transmits occlusal forces to the bone Sharpeys fibers * The terminal clangour-like fibers of the principle fiber bundles in the periodontal ligament that are naval divisionially inserted into the outer portion of the cementum at 90 degrees and then attached to the alveolar bone at the other end Five dealer fiber groups of the periodontiumApical fibers * Run from the root apex to adjacent surrounding bone * Function to resist vertical forces Oblique fibers * Run from the root above the apical fibers obliquely toward the occlusal * Function to res ist vertical and unexpected strong forces Horizontal fibers * From the cementum in the middle of each root to adjacent alveolar bone * Function To resist intrusive forces Alveolar crest fibers * From the alveolar crest to the cementum just below the CEJ * Function to resist intrusive forces Interradicular fibers * Run from the cementum between the roots of multi-rooted teeth to the adjacent bone * Function to resist vertical and lateral sources Cementum * Outer most layer of the root of a tooth * Helps anchor the teeth * Made of a mineralized fibrous matrix (collagen and fibers) and cells (cementoblasts and cementocytes) * Attaches teeth to the alveolar bone b anchoring the periodontal ligament * No vascular or nerve connections * Cannot transmit pain, therefore not sensitive to scaling procedures * Renewable Cementoenamel junction * The junction point between enamel and cementum * non always smooth, thunder mug be due to alterations in cemented surface and the tissues involved Th ree scenarios occur at the CEJ 1.Cementum will overlap enamel (60%) 2. Cementum and enamel meet (30%) 3. Cementum and enamel fail to meet leaving a narrow zone of exposed dentin (10%) Alveolar process * Support scheme for teeth * Extensions of the bone from the body of the mandible and maxilla * Lines the sockets of the teeth and provides support for the sockets * The walls of the sockets are called the lamina dura * The process also provides attachments for the periodontal ligament Components of the alveolar process * Alveolar bone * summary bone * Trabecular and cancellous bone The alveolar process utilisations as a unit, as indicated by its gradual resorption when teeth are lostCurrent concepts of microbiology and periodontal unsoundness (chapter 4) Microorganism * Microscopic living organisms which imply bacterium, viruses, and fungi * Bacteria single-cell * Viruses very small and not capable of growth or reverberation without living hosts * Fungi plant-like organisms tha t occur as yeasts or molds Bacterial classifications 1. structural forms (shape) 2. Cell wall structure 3. oxygen environment 4. Metabolism 5. Motility Morphologic forms (shape) * Involved in establishment biofilm governance 1. Cocci spherical, most common form in boldness is streptococci 2. Rods or bacilli generally rectangular or rod like 3. Spirochetes spirals Cell wall structure Bacteriologic technique (gram staining) of using a double dye staining system to differentiate the structure of the cell walls * Two wall types 1. Gram positive stains purple (crystal violet dye applied first) 2. Gram negative stains red (safranin dye applied second) Oxygen environment Aerobe/Aerobic organism Requires oxygen to live and grow Anaerobe/Anaerobic organism Grows in complete or almost complete absence of oxygen Facultative anaerobic organism Can use oxygen when present but can use anaerobic fermentation when oxygen is absent deem anaerobe Cannot survive in an aerobic environment Aeroto lerant anaerobes Grow in both types of environment Capnophile Requires or prefers carbon dioxide for growth Metabolism The sum of total of chemical substance changes occurring in the body chemical process of transforming foods into abstruse tissue elements and or transforming complex body substances into simple ones, along with the production of heat and energy * anabolism The building up of tissue maintenance and repair of the body * Catabolism The breaking down of tissue into smaller move from energy production and excretory product Motility * Bacteria either are or arent motile * Flagella are long fine wavy filamentous structures used for motility * exsanguinousthorn have one or more than flagella * Flagella may be located at either end, both ends, or encircling cell Microbial season * Flora organisms together in a locale * Oral flora various bacteriuml and other microscopic organisms that inhabit the oral cavity common oral flora * Predominant microorganisms present in healthy state * Streptococcus mitis * Actinomyces species Streptococcus oralis (sanguis II) Dental cheek The cause * Dental memorial tablet is THE major etiologic operator in the initiation and progression of periodontal sickness * Epidemiologic studies have shown that poor oral hygiene amplifications the prevalence and severity of periodontal unhealthiness * Microorganisms other than bacterium can be ground in governance (ex. yeasts, protozoa, and viruses) * The difference between dental plaque and material alba is the strength/ fastening of the deposit * Material alba is loosely adherent, soft accumulations of bacterial/cellular debris and can be upstage by mechanistic action (ex. strong water) The interpretation of dental plaque (Not on test) An accumulation of bacteria on the surface of teeth or other solid oral structures and is not pronto removed administration formation 3 stages 1. Pellicle formation * The acquired pellicle forms on the tooth surface * It is acell ular * It is an organic and tenacious film composed of glycogen proteins from saliva * It will pop out to form within minutes after a tooth surface is entirely polished 2. Bacterial colonization * Bacteria from indigenous oral micro flora attach to the pellicle and form microbial colonies in layers as the bacteria grow and multiply * An intermicrobial substance is formed mainly from saliva and from polysaccharides produced by certain bacteria from sucrose or sugar in the regimen 3. Plaque Maturation As plaque ages, a change in the types of microorganisms occurs within plaque * Plaque that is up to 2 days old consists primarily of cocci * By 2-4 the filaments replace the cocci * By days 4-7, filamentous forms subjoin and rods and fusiform bacteria appear * By 7-14 vibrios and spirochetes and more gram negative and anaerobic microorganisms appear * Bacterial plaque, if not mechanically disturbed, produces a great proportion of those microorganisms associated with periodontal illn ess Dental plaque growth * After the first day of plaque growth, gram (+) streptococci decrease in number * During the next 3 weeks of imperturbable plaque formation, cocci stay put to decrease because of an increase in filamentous bacteria.These filaments actually invade and replace umteen of the streptococci that inhabit the deeper levers * As plaque increase in thickness, further changes occur in the environment * When plaque is allowed to grow undisturbed, it poses more anaerobic * The level of oxygen diminishes as a guide of O2 consumption by facultative organisms * This lowers 02 level and allows the growth of obligate anaerobes * A more mature plaque harbors increasing number of obligate anaerobic organisms such(prenominal)(prenominal) as spirochetes and gram (-) rods * At this point, no excess bacterial species join the plaque, although the volume of bacteria may continue to increase * Mature plaque has the say-so difference to invade the subgingival space and to caus e localized gingival disease varlet 74 (figure 4-9) The difference between above/subgingival plaque Characteristic Supragingival SubgingivalLocation * At or above (coronal to) the margin of the free gingiva * Apical to the margin of the free gingiva, between tooth and gingival bag epithelium Origin * Salivary glycoproteins form pellicle * MOs from saliva are selectively attached to the pellicle * Apical growth of bacteria from supragingival plaque Distribution * Starts on proximal surfaces * Heaviest on areas not cleaned daily by long-sufferings * Cervical 3rd * Lingual mandibular molar * Pits and fissures * Shallow pocket * Attached plaque covers compression * Unattached plaque extends to the periodontal attachment Adhesion * Firmly attached to acquired pellicle, other bacteria and tooth surfaces * Adheres to tooth surface potassium hydrogen tartrate Sources of nutrientsFor bacterial proliferation * Saliva * Ingested food * Tissue fluid (sulcus) * Exudates * Leukocytes Bacteri a * archaean plaque mostly gram + cocci * Older plaque increases in filaments (3-4 days) * more than complex flora increase rods (4-9 days) * Depends on pocket depth. Apical part dominated by spirochetes, cocci, and rods coronal part has more filaments. * Environment is conducive to growth of anaerobic population Significance * Etiology of * Gingivitis * Supragingival calculus * Dental dental caries * Etiology of * Gingivitis * Periodontal infections * Subgingival calculus Pathogens in plaque The virulence for pathogenicity of a microorganism is its ability to cause disease * For a microorganism to be virulent it must * Be established in close proximity to the periodontal tissue * Must be able to withstand the forces of saliva and gingival crevicular fluid that are capable of sweeping it away * Normally cellular defense systems are able to rid the microbe from the host * However, periodontal pathogens have real a concoction of strategies to evade or overcome these mechanisms * Example Actinobacillus Actinomycetemcomitans (AA) defends themselves against phagocytosis by 1. releasing inhibitors of directed migration (inhibits chemotaxis) 2.Produces anti-phagocytic surfaces that prevent the polymorphonuclear lymphocytes (PMNS) or neutrophils killing mechanisms * Has very slippery surface slippery surface makes it extremely operose to latch onto bacteria, therefore PMNs cannot properly engulf it and PMNs may be destroy releasing toxins that produce osteoclasts * AA is a major pathogen Plaque tissue destruction 1. Bacteria themselves do not need to be present within the tissue to be a major participant in the destructive process 2. Some bacterial products may promptly injure the hose cells and tissues 3. Others may interact with a variety of cells and activate the humeral and cellular immune reactions that secondarily affect the integrity of the periodontium Direct effect of plaque * P. gingivalis * Produces collagenase, the enzyme that degrades collagen * LPS or endotoxins ( which is a component of a gram (-) bacterial outer membrane) nduces incendiary reactions and dumbfounds osteoclasts Indirect effects of plaque * Toxins from p. gingivalis and other gram (-) organisms stimulate the immune answer, releasing prostaglandin E2, and interleukin 1B from macrophages and fibroblasts, which can induce bone resorption Gingivitis associated plaque * summation thickness and mass of plaque * Increase in gram negative motile rods and spirochetes which are normally aerobic (require o2) * Fuso-bacterium nucleatum * Various species of prevotella and treponema * Campylobater rectus Periodontitis associated plaque * Prophyromonas gingivalis * Prevotella intermedia * Bacteroides forsy gum olibanum * Treponema denticola * Peptostreptococcus micros Plaque biofilm summary Plaque is a biofilm meaning that it is an accumulation of microbes on the surface of teeth or other solid surfaces, not readily removed by rinsing * Plaque biofilm provides round protection for its resident microorganisms, increasing their survival * Therefore essential to physically remove plaque biofilms occasional to maintain gingival and periodontal health- keeps plaque immature * Bacteria that colonize in the first few hours do not possess pathogenicity as the bacteria that dominate plaque after 34 hours. (plaque virulence increase with age) The role of calculus and other extrinsic factors in periodontal disease (chapter 5) chalkstone * potassium hydrogen tartrate (tartar) is mineralized bacterial plaque, a hard tenacious mass thats forms on natural teeth, dentures, and other dental appliances generally by the deposit of calcium and inorganic phosphate salts * 90% of word time on calculus removal and 5 % on plaque control * Not all plaque calcifies.Generally it takes 24 hours to 2 weeks to begin mineralization * Plaque can be mineralized in 2 days and up to 90% in 2 weeks * Formation rates influenced by diet and composition of microbial flora * Ca lculus can visit drainage from a pocket by helping to trap bacteria and debris * improve is prevented and advancement of the disease is encouraged Role of calculus in periodontal disease- pathogenicity * Originally the focus was on calculus as a mechanical spikelet * Now the focus is on calculus as a rough surface for plaque growth and retention, and a reservoir for toxic microbial and tissue breakdown products because of its permeable surface * Spicules small pieces and usually subgingival * Granular similar to spicules but are a lot smaller * Veneer common in lower anteriors and the buccal of the upper molars. It is important to air dry onward checking if all is removedComparison of clinical characteristics of calculus supragingival vs. subgingival Characteristic Supragingival Subgingival Also known as * Supramarginal calculus or salivary calculus * Submarginal calculus or serumal calculus Source of minerals * Saliva * Crevicular fluid Formation dismays * Along inner surface of supragingival plaque * In attached subgingival plaque Attached to/by * Acquired pellicle directly to tooth surface * Penetration into cementum Intercrystalline bonding, mechanically locking into surface irregularities (caused by redness of Sharpeys fibers) war paint * Inorganic Material(70-90%) 1. Calcium phosphate(75. 9%)2. Calcium carbonate(3. %) * Traces of magnesium, sodium, potassium, fluoride, zinc, strontium * Similar to supra but increase in calcium, magnesium and fluoride (higher % in crevicular fluid) * Sodium content increases with pocket depth Factors that influence formation * Elevated salivary pH * Concentration of calcium in saliva * Concentration of salivary bacterial protein and lipid * low-spirited individual inhibitory factors * Higher total salivary lipid levels * Some medications(beta blockers, diuretics, thyroid supplements reduce the formation of supra everydayly found (individual teeth) * Coronal to margin of gingiva * Can be fine line progress ging ival margin * Cover large portion of clinical crown * Apical to gingival margin * Can extend to bottom of the pocket and follows contour of soft tissue attachment. * As tissue recedes, subgingival calculus can become supra Common Distribution Patterns * Lingual surface of mandibular anteriors (Whartons Duct) * Facial surface of max. molars (Stensons Duct) * Does not necessarily mean there are SUB deposits.Generally harmonious except when * Teeth are malpositioned * Functional irregularities * Oral hygiene inconsistent * Heaviest in interpoximal areas * Lightest on facial surfaces * Occurs with or without SUPRA deposits Shape * Determined by tooth anatomy, contour of gingival tissue, pressure from lips, tongue and cheeks * Generally bulky gross deposits may form calculus bridge between teeth or cover gingival margin or extend to incisal/occlusal edges * Generally flattened to conform with pressure from pocket wall * Ledge or ring like * Thin, smooth (veneers) * Spiny, spur-like * G ranular (grainy) * Spicules (irregular amounts) Consistency/Texture * Moderately hard * Porous (may come off in pieces that slow break off from adjoining calculus) * Newer deposits are softer * Harder and more dense than supra * Brittle/flint like * May feel a snap as calculus is dislodged * Newest deposits (bottom of pocket) are less hard Size and Quantity * Depends on * Efficacy of personal oral care * Diet * Function/use * Tobacco use * Related to same as supra plus * Pocket depth * duration Supragingival calculus * Porous and rough * Provides lattice on which plaque can grow * B peal the bacteria close to the tissue * Interferes with oral self-cleaning mechanism * Makes plaque removal more uncorrectable * Found on the clinical crowns of any tooth above the margin of the gingiva * Readily megascopic * Tightly adherent to the teeth * Yellowish-white in color, darkens with age * It is an organic matrix of plaque, microorganisms, glucans, lycol-proteins and lipids * Calcium is de posited in layers * 70-90% is inorganic mineral content Subgingival calculus * Associated with the progression of periodontal disease * Periodontal pockets almost always contain subgingival calculus * Provides a reservoir for bacteria and endotoxins that are related to the disease process * Can cause greater disease progression than plaque alone * Located below the gingival margin * Attached to cementum or dentin * Tenacious and blackened in color * Also dark green due to organic matrix products of the subgingival plaque * Color also comes from blood products * Commonly deposited in rings or ledges on root surfaces The mineral content is derived from crevicular fluid rather than from saliva as supra * Similar inorganic mineral content as supra * Can be found anywhere subgingivally * Attaches by means of attached pellicle or mechanical locking into undercuts and irregularities in tooth surfaces * Therefore more difficult to remove * Improper removal of calculus will leave a smooth o uter collar called burnished calculus Calculus removal * Calculus is more readily removed from some tooth surfaces than others * Ease of removal related to mode of attachment of the calculus to tooth surface * Can be attached to acquired pellicle, mechanical locking into undercuts or minute irregularities in tooth surface or direct contact between intercellular matric and tooth surfaceConditions that affect periodontal health 1. Malocclusion * Is not a cause of periodontal disease * Poorly aligned teeth will make it harder for daily plaque control, but malocclusion is not an imitator of pathology 2. lose teeth * Teeth harder to clean as they can tip in if one is missing 3. Bulky restorations * Poorly contoured restorations may cause plaque traps, increase gingival inflammation, may complicate plaque control and this does contribute to periodontal disease 4. Partial dentures * They should be cleaned daily * Calculus can stick on plastic teeth and stain on dentures * Poor fitting den tures can also irritate the gingiva tenor to remove dentures at night. Soak in water 5. Mouth breathing * This can lead to localized gingival inflammation * Usually on maxillary anterior facials * It is associated with an increase in plaque and gingivitis 6. Food impaction * A common local factor that contributes to the initiation and progression of periodontal disease * Food is an excellent breeding ground for bacteria * Forceful wedging of food may also tear epithelial attachment 7. Orthodontic appliances * Fixed appliances have increase plaque retention and are difficult for self-care * Minimal increase in periodontics but increase in gingivitis Tobacco use on periodontal disease It is a pretend factor for periodontal disease (can help cause it) * Smoking will constrict white blood cell supply and retard PMNs (type of leukocyte). PMNs have decrease ability to phagocytosis * It has been determined that smokers are 2. 5 times more likely to have periodontal disease * The vascula r reaction to inflammation is reduced in smokers THEREFORE Gums look normal and pink and there less haemorrhage and less response to fighting disease * Smokeless tobacco is associated with a specific type of gingivitis called gingivitis toxica it is associated with the destruction of gingiva and bone underling the area where the smokeless tobacco rests in the mouth Systemic factors in periodontal disease (chapter 16) Systemic factors * Systemic pertaining to or affecting the whole body Systemic factors may complicate or intensify the periodontal disease * Systemic problems in some tolerants may * Increase their susceptibility to infection * Interfere with wound better * Require modification of standard approaches to treatment * Complicate factors associated with patient cooperation * More significant responses to bacterial plaque and other local predisposing factors Blood disorders (Dyscrasias) * A blood dyscrasia is any disorder that affects cellular elements of the blood (red o r white blood cells) * Most common are anemia (need to know tablet or capsule form of iron taken), leukemia, abnormal bleeding * Most have an oral manifestation * In addition to changes to tissue there is * Increased bleeding Lowered resistance to infection due to the impaired function of defensive white blood cells-polymorphonuclear neutrophilic leukocytes (PMNs or neutrophils) Aplastic Anemia * Bone marrow has very reduced ability to produce most of the components of blood * May be due to icon to toxic chemicals or certain drugs * May have no known etiology, ie. Idiopathic aplastic anemia * Patients have * Rapidly progressing periodontal disease * rosy-cheekeduction in neutrophils agranulosis * A rare disease involving destruction of bone marrow * Caused by antipsychotic drugs or an autoimmune diseases such as Lupus (corticosteriods) * Sharp drop in WBCs bacterial invasion is rapid * Patients have * Ulcerations in mouth or pharynx Gingival bleeding * Increase in salivation * An flavour in the mouth Cyclic Neutropenia * Unknown etiology * Periodic reduction in neutrophils * Patients have * Flare-ups of periodontal disease during depletion of neutrophils Leukemia * Cell malignancies of bone marrow with a decrease in WBC and platelets * Etiology is unknown, although linked to certain viruses and ionizing radiation exposure * Abnormal WBC proliferate and suppress the normal WBC function (fighting infection) * Reduction in blood platelets means clotting ability is reduced * Clients with chronic leukemia have * Increase susceptibility to infections * Decrease healing ability natural gingival bleeding * Acute forms have sudden onset and lead to death if not treated in a few months * Oral manifestations involve painful ulcerations, spontaneous gingival bleeding, dry mouth, and secondary infections Endocrine dysfunctions * Periodontal disease is associated with endocrine changes or endogenous sex hormone changes * Puberty associated gingivitis melodramatic in crease in hormone levels causes gingival inflammation * Menstrual cycle associated gingivitis significant observable changes especially at ovulation * Menopause tissue can be fragile. May have osteoporosis with loss of alveolar bone Diabetes Mellitus Usually hyperglycemic due to defect in insulin (hormone) secretions or insulin action * Either a relative or absolute lack of insulin or in qualified function of insulin * Type I (juvenile diabetes) absolute insulin deficiency * Type II (adult diabetes) most common * Insulin secretion may be lower or higher than normal * Cannot use insulin effectively * Oral findings * Increased gingival inflammation * Periodontitis is more frequent and oft more sever * Increase in tooth mobility * Decrease in saliva flow * Fruity (acetone) breath due to glucose in sulcular fluid * Delayed healing and an increased chance for oral candidiasis (thrush) Pregnancy Increase in gingival inflammation * Tissues are red, swollen * Can lead to periodontitis wit h loss of alveolar bone * Inflammation due to plaque * Due to increase in estrogen and progesterone * These can cause dilation of gingival capillaries and thus increase permeability and increase in gingival crevicular fluid. This allows for more bacteria to enter and form plaque Nutritional deficiencies * Healthy tissues depend on adequate supply of nutritive material * Hard or fibrous foods provide stimulation necessary for the maintenance of the PDL and alveolar bone and also stimulate the gingival tissues Vitamins Function Oral manifestations (deficiencies)Vitamin A Growth and bone development XerostomiaHyperkeratosis of gingiva Vitamin K Synthesis of blood clotting factors Prolonged bleeding Vitamin D Promotes absorption of calcium and phosphorus Hypo-calcification of enamel, bone, dentin, and cementum Vitamin B Helps with growth and tissue regeneration and maintains integrity of the oral mucosa Poor wound healing, gingival inflammation, angular chelosis Vitamin C Collagen forma tion, promotes healing Blue to red gingiva, bleeding, loss of PDL support, poor wound healing Infectious diseases * Acquired immune deficiency (AIDS) * Caused by HHHIV (human immunodeficiency virus) * Transmitted by needle sharing, sexual activities, infected mothers to their newborns, transfer of blood, possibly saliva * HIV infects and eventually kills a wide range of cells but particularly CD4-positive helper T cells * Helper T cells are thymus derived lymphocytes that promote certain immunologic reactions * The depletion of these helper T cells can firmness of purpose in severe immune-suppression that makes the person susceptible to any life threatening fungal, bacterial, and viral infections * Oral manifestations * Hairy leukoplakia usually on lateral border of tongue * Those with AIDS usually have promptly progressive periodontitis Cardiovascular disease 1. Hypertension * Blood pressure communicates 160/95 mmHg (systolic/diastolic) * Normal is 120/80 mmHg * Avoid elective t reatment if uncontrolled * Typical medications are diuretics and vasodilators * Drugs often cause xerostomia 2. Cardiac arrhythmias * Irregular heartbeat * Often due to stress 3. Anticoagulant therapy * Blood thinners to reduce the risk of blood clots that can block circulation to vital organs * Consult with doctor prior to seeing Instrumentation can cause prolonged bleeding * Usual medications are a) Warfarin (Coumadin) (INR levels) b) Heparin c) Aspirin Psychological stress * Emotional stress is associated with an increased risk of developing periodontitis * Stress may induce secretion of Norepinephrine which may make the periodontal tissues more susceptible to damage from plaque Neurological disorders * Patients with nervous and neuromuscular diseases present with 3 basic problems 1. Physical inability to perform adequate oral hygiene procedures due to a decrease in motor skills 2. May have a mental or physical inability to cooperate with the clinician 3.May have changes in oral tissues that increase the risk from dental disease * Ex. phenytoin-influenced gingival enlargement gingival enlargement with administration of anticonvulsive drugs that are used to control seizures. Mechanism is not completely understood Oral Cancer * Most frequent type is squamous cell carcinoma, develops from epithelial cells * Strongly linked to tobacco and pipe smoking * Chronic use of snuff (smokeless tobacco) * Be suspicious of long standing un-healing sores (anything longer than 2-3 weeks) * Red or white lesions on the lips or in the mouth What you can do * A thorough head and neck examination should be a routine part of each patients dental visit.Clinicians should be particularly vigilant in checking those who use tobacco or excessive amounts of alcoholic beverage * EXAMINE your patients using the head and neck examination described here * TAKE A HISTORY of their alcohol and tobacco use * INFORM your patients of the connexion between tobacco use, alcohol use, and oral crab by person * FOLLOW-UP to make sure a definitive diagnosing is obtained on any possible signs/symptoms of oral crab louse The exam * This exam is abstracted from the standardized oral examination method recommended by the World Health Organization. The method is consistent with those followed by the Centers for malady Control and Prevention and the National Institutes of Health.It requires adequate lighting, a dental mouth mirror, two 22 gauze, and gloves it should take no longer than 5 minutes Oral cancer screening Incidence and survival * Oral or pharyngeal cancer will be diagnosed in an estimated 30,000 Americans this year, and will cause almost 8,000 deaths. On average, only half of those with the diseases will survive more than five years The importance of early detection * Early detection saves lives deaths from oral cancer could be dramatically reduced. The five-year survival rate for those with localized disease at diagnosis is 76% compared with only 19% for those whose ca ncer has spread to other parts of the body.Early detection of oral cancer is often possible. Tissue changes in the mouth that might signal the beginnings of cancer often can be seen and felt easily Warning signs 1. Lesions that might signal oral cancer * Two lesions that could be precursors to cancer a) Leukoplakia (white lesions) b) Erythroplakia (red lesions) * Although less common than leukoplakia, erythroplakia and lesions with erythroplakic components have a much greater potential for becoming cancerous * Any white or red lesion that does not resolve itself in two weeks should be reevaluated and considered for biopsy to obtain a definitive diagnosis 2. Other possible signs/symptoms of oral cancer A lump or thickening in the oral soft tissues * Soreness or a look that something is caught in the throat * Difficulty chewing or swallowing * Ear pain * Difficulty moving the jaw or tongue * Hoarseness * Numbness of the tongue or other areas of the mouth * Swelling of the jaw that ca uses dentures to fit poorly or become uncomfortable * If the above problems persist for more than two weeks, a thorough clinical examination and laboratory tests, as necessary, should be performed to obtain a definitive diagnosis * If a diagnosis cannot be obtained, referral to the appropriate specializer is indicated Risk factors 1. Tobacco /alcohol use * Increases the risk of oral cancer Using both tobacco and alcohol poses a much greater risk than either substance alone 2. Sunlight * Exposure to sunlight is a risk factor for lip cancer 3. Age * Oral cancer is typically a disease of older people usually because of their longer exposure to risk factors * Incidence of oral cancer rises steadily with age, reaching a bloom in persons aged 65-74 * For African americans incidence peaks about 10 years earlier 4. Gender * Oral cancer strikes twice as often as it does women Oral changes due to drugs 1. Xerostomia dry, smooth, shiny mucosa * Diuretics (Dyazide) * Histamines (Benadryl) * A ntidepressants (Tofranil) * Antihypertensive (Seroasil) 2.Glossitis/Stomatitis lesions o the tongue small multiple ulcers * Anticoagulants (Warfarin) 3. Lichenoid eruptions white striations red patched of ulcers * CNS drugs (Aldomet) * Diuretics (Lasix) 4. Oral candidiasis/thrush multiple with patches * Antibiotics (Vibramycin) 5. Hairy tongue elongations of filiform papillae * Antibiotics (Tetracycline) Dental hygienists role * Consult with other health care providers for clients with systemic factors * Hygienists may be in a position to recognize changes at an early stage * Cautions 1. Heart attack need to wait at least 6 months before treating 2. Pregnancy must finish 1st trimester 3.Cancer deep scaling could be open channel for infection to reach bone so treatment contraindicated during chemo and radiation 4. Medical histories * Antibiotics a) What? b) How long? c) How much? * Cancer a) How long ago? b) Advised against cleaning or pre-meds? * Kidney disease a) On dialysis? b) Ho w long has treatment been going on? c) Pre-med? * Blood thinners a) Advised against cleanings? b) What are they on? c) Dose? d) How long on meds? e) Date of last work up? The diseases of the gingiva (chapter 6) Gingivitis * Inflammation of the gingival tissue with no apical migration of the junctional epithelium beyond the cementoenamel junction (CEJ) * Manifests as Color change (red/pink-red) * Edema (swelling of tissues) * Exudates (pus) * Tendency to bleed readily * Major indicators of gingivitis are * Bleeding in response to gentle probing * Clear gingival fluid flow, or exudates, which appears to increase with the severity of the gingivitis * Gingivitis appears directly related to the amount of plaque on the tooth surface and the amount of time that the plaque is allowed to remain undisturbed- the plaque is considered nonspecific because it is not associated with any specific type of microorganisms Three stages of gingivitis 1. Stage I gingivitis (initial or sub-clinical) * No clinical signs yet Occurs in the first few days of contact between microbial plaque and gingival tissues * Is an acute inflammatory response characterized by dilation of the blood vessels * PMN (neutrophils) are the principal defense in acute inflammation- they phagocytoze (engulf) bacteria and their products * Small amounts of plasma leak into surrounding tissues causing hydrops * Exudate from early gingival inflammation is composed mostly of serum and it is referred to as gingival fluid flow- the fluid is clear, not yellow like pus, because few cells are present at this point * Lymphocytes will also appear at this stage (almost all are T-lymphocytes) * Collagen degradation will start to occur (collagen will start to break down) 2. Stage II gingivitis (early stage) * These lesions begin to form 4-7 days after plaque has accumulated in the gingival sulcus * Increase in T-lymphocytes- they are localized in the connective tissue under the epithelium of the gingival sulcus * Exudates increases and may appear white or yellow clinically tissues will appear slightly red and swollen * Collagen fibers in connective tissue is destroyed by the inflammation and is replaced by blood plasma and inflammatory cells * Collagen fibers that attach the underlying connective tissue to the junctional epithelium are also destroyed * Gingival stippling if present, will begin to disappear causing the gingiva to appear shiny * The junctional epithelium will slightly start to lengthen against the root surface * Bleeding will occur upon probing * This stage may continue for 21 days or longer * It is the earliest clinical evidence of gingivitis 3. Stage III (established stage) * Occurs between 15-21 days * T and B lymphocytes are found in equal amounts indicating that tissue destruction by the inflammatory reaction is taking place * More collagen destruction during this stage * Junctional epithelium also continues prolongation clinical probing depths will increase for 2 reasons a) Prob e can penetrate deeper due to collagen destruction b) Edema causes swelling of tissue and therefore may present as a deepening of the pocket * The increase of blood vessels and inflammatory cells in that area will cause visible plus formation * Capillary proliferation also causes the gingiva to appear red * Tissues may appear cyanotic (blue) in extreme cases of congested blood cells within the gingiva * The presence of many O2 depleted RBCs give the bluish color * This stage can persist for many months or years Summary of stages Stage Clinical signs Pathogenic eventsStage I (Initial) * None * Blood vessels * Polymorphonuclear (PMNs) leukocytes migrate into CT * Plasma leaks into CT * Gingival fluid exits pockets * T-lymphocytes predominate Stage II (Early) * Gingiva may redden * Stippling disappears * Exudates may appear * Bleeding usually occurs on probing * T-lymphocytes increase * Cells congregate under sulcular epithelium * Gingival fluid increases * Collagen is destroyed * Len gthened JE is disrupted * Fibroblasts destroyed Stage III (Established) * Gingiva is redden * Gingiva may appear blue-red * Probing depths increase * Pus forms * Tissue swells * Capillaries proliferate * T and B lymphocytes occur in equal numbers * Extensive collagen destruction * JE thickens and rete pegs extend into the CT * Plasma cells infiltrate * Edema increases Microbiology suss out * The mature plaque found in long-standing gingivitis has a large % of gram-bacteria (this change from gram (+) plaque associated with health, to predominantly gram (-) plaque, or pathogenic plaque is a characteristic of gingivitis) Types of gingivitis 1. Plaque associated gingivitis * Most common form of gingivitis in general population Directly related to presence of bacterial plaque on tooth surface * Clinically, gingivitis causes a redden gingival margin, with pocket formation as a result of gingival swelling and edema, hypertrophy, and deepened penetration of periodontal probes on clinical military rank * Surface of the gingiva may appear glazed or smooth, and stippling when present in health, usually disappears microscopically there is an increase in capillaries along the gingival margin, and the epithelium lining in the sulcus is ulcerated when periodontal probe is placed in the crevice 2. Necrotizing ulcerative gingivitis * A disease that occurs occasionally in vernal adults Is a periodontal disease that can occur with NO BONE LOSS and a bacterial component * Related to excess stress-common outbreaks at universities and colleges * truly painful * AKA trench mouth widespread among soldiers in WWI (stress or poor oral hygiene) * Sudden onset of burning mouth and inability to eat * affection most commonly begins in the interdental papillae after a few days, the tips of the papillae appear punched out and covered by a white necrotic pseudomembrane * Attached gingival tissues usually appear inflamed * Often a distinctive odor termed fetor oris that is unique to the d isease * There is a presence of two microorganisms a) cigar-shaped bacillus b) Spirochetes * May have a fever Antibiotics (penicillin and metronidazole) are useful in treatment, but only if the patient has systemic symptoms of fever and severe queasiness * Treatment is to completely debride the tissues of plaque and to begin a home regiment of plaque control * Careful debridement with curettes or ultrasonic scaler can be performed over a few appointments after appointment can rinse with a dilute solution of hydrogen peroxide and warm water * Untreated, this disease may lead to bone loss and become Necrotizing Ulcerative Periodontitis (NUP) or periodontitis 3. Endocrine-influenced gingival disease * Gingivitis is often influenced by steroid-type hormones produced by the endocrine glands. These include a) Puberty b) Pregnancy several changes in the gingiva have been associated 1. As hormone levels increase during 2nd trimester, gingival inflammation may * Increase, even with nigh p laque control The gingiva may be come dark red or hyperplastic and may bleed excessively * Changes may occur as the pregnancy progresses but most improves with good home care and removal of irritants- some not till after the baby is born 2. Some may also get a pregnancy tumor-tissue is highly inflamed, bleeds easily, and may cause teeth to become mobile * When female hormone levels are increased, there is an increase in some subgingival bacteria, such as bacteroids species, and gingival inflammation may be greater * Estrogen may also regulate cellular proliferation, keratinization, and vascular proliferation, and vascular fragility in the gingival tissues * The extent of hormone related changes is related to the level of plaque control- poor plaque control aggravates the condition 4. Drug-induced gingival enlargement Various medications can cause changes in gingival tissue * Anti-seizure meds most commonly associated with gingival overgrowth * Gingival tissue may become fibrotic and enlarged (enlargement may be caused by changes in the epithelial cells and the fibroblasts that create a more dense CT) * Overgrowth begins with interdental papillae which enlarge until they coalesce involving all of the attached gingiva * An increase in bacterial plaque causes an increase in gingival overgrowth in patients taking these medications-excellent plaque control is needed here * Patients may have heavy calculus and increased levels of inflammation because of plaque retention * Treatment requires good oral home care, regular debridement, root homework, and often surgical reduction of the enlargements * Some cardiac meds also cause overgrowth-include nifidine and verapamil used to control BP * Cylcosporine (immunosuppressant in transplant patients) also causes gingival overgrowth also used to treat MS can cause excessive accumulation of CT in many other tissues of the body Plaque induced gingivitis can be modified by crowded teeth, restorations, orthodontic appliances, et c Gingival disease can be modified by malnutrition vitamins A, B1, B2, B6, and C The Diseases of the supporting tissues of the periodontium (chapter 7) Periodontal disease * Broad term referring to any disease of the tissues surrounding teeth * 2 basic classifications 1. Gingivitis 2. Periodontitis Periodontitis an inflammatory disease of the periodontium characterized by the loss of connective tissue attachment, destruction of bone, and possible tooth mobility * Periodontal pockets a clinical manifestation of tissue destruction associated with bone loss (apical migration of sulcus) Periodontitis pathogenesis of periodontal pockets 1. Bacterial contend from plaque biofilm * In the early stages of periodontitis, the bacterial flora of the gingival pocket is similar to that of gingivitis * As the disease becomes more sever, the flora become more complex 2. Connective tissue loss * Associated with enzymes secreted by healthy and inflammatory cells (collagenase degradation) * Phagocyto sis of collagen by fibroblasts 3. Epithelial cells proliferate and migrate apically 4. Junctional epithelium detaches from root surfaces * As it becomes engorges with inflammatory cells 5.Gingiva swells and moves coronally from increased amount of cellular and serum elements 6. Epithelial lining of pocket loses integrity * Leukocytes and products of inflammatory response escape into pocket space and in opposite thrill the tissue is permeable to bacterial products * This process results in a periodontal pocket the patient cannot clean adequately. This the disease cycles as follows * Biofilm gingival inflammation pocket formation biofilm formation * Exposed cementum absorbs bacterial products and becomes soft and necrotic * Repair is minimal unless necrotic tissue is removed by root planning Periodontitis microbiology The continued presence of pathogenic plaque bacteria causing the inflammatory process to extend into the PDL, cementum, and alveolar bone leading to the loss of attac hment of the gingiva to the tooth and the loss of supporting bone * The predominant organisms are gram anaerobic rods * P. gingivalis seems to be the most important periodontal pathogen based on its numeric presence (highest in numbers) Periodontitis spread * Two mechanisms have been proposed for the initiation of the spread of infection 1. The bacteria and their products may break down the wall between the junctional and sulcular epithelium and cause detachment of the JE 2.The bacteria products may interfere with the normal growth and maintenance of the junctional and sulcular epithelium permitting it to break down * In either case, as inflammation progresses the sulcular epithelium increases in thickness and begins to infiltrate into the underlying connective tissue * Pockets deepen because of the breakdown of collagen fibers by enzymes such as collagenase, which is released by some of the plaque bacteria and the hosts inflammatory response * Because bone is an active tissue with continuous resorption and formation it is not possible to determine histologically on the dot when bone loss has occurred as a result of periodontitis * When bone resorption exceeds apposition, a net decrease in the amount of bone occurs Periodontal bone loss The loss of crestal alveolar bone through the inflammatory process * Osteoclast bone resorption is driven by plaque and most derived mediators such as bacterial enzymes, prostaglandins, interleukins, and tumor necrosis factor * When disease established, plasma cells and lymphocytes present * Plasma cells important in antigen-antibody reactions which activates events attracting additional inflammatory cells * These cells cause additional destruction of collagen fibers * Bacteria stimulate lymphocytes which release lymphokines * Lymphokines have many effects on inflammatory system including production of chemical factors that activate osteoclasts * Osteoclasts increase emaciated resorption Types of bone loss 1. Horizontal Occu rs when entire width of interdental bone is resorbed evenly 2.Vertical Defect produced when interdental bone adjacent to root surface is more rapidly resorbed, leaving angular uneven morphology Two types of periodontal pockets * Describes relationship of pocket to crestal bone 1. Suprabony base of pocket occurs above the crest of the alveolar bone 2. Infrabony pocket base is apical to crest of alveolar bone Clinical attachment loss * Total attachment loss from CEJ * Combines recession and probing depth (pocket depth) (only exists when recession is present) * Provides more complete assessment of loss of support than probing alone * Why? Crest of alveolar bone is not at CEJ but 1-2 mm apical to it * Page 131 figure 7-2 Furcation * When attachment lose occurs vertically and horizontally between toots of multi-rooted teeth Etiology As in gingivitis, plaque biofilm is the principle cause of all forms of periodontitis * Therefore, treatment directed at its elimination or reduction * The composition of the flora differ significantly from patient to patient and from pocket to pocket, as does patients susceptibility to it * This variability makes causes of periodontitis less obvious than plaque biofilm + gingivitis relationship * All conditions that retain biofilms or prevent its removal play significant roles as they do in gingivitis * In addition, deeper periodontal pockets house greater amounts of subgingival plaque that is impossible for the patient to remove * Most patients with periodontitis have high proportions of anaerobic gram ve bacteria Classification of periodontal disease * American academy of periodontology * Periodontitis can be * localise (? 30% of involved sites) * Generalized ( 30% of involved sites) The defining element for classifying periodontal disease is probing depth, the level of attachment loss from the CEJ indicates bone loss * Page 130 box 7-2 Chronic periodontitis * Most common form of periodontal disease * Bacterially induced inflammati on of the periodontium * True periodontal pockets result from apical migration of JE * A degree of false pocketing resulting from gingival edema or fibrosis is commonly present * Characterized by bone resorption that progresses slowly and predominantly in a horizontal direction * May have pre-clinical onset in adolescence and if not halted by therapy it appears to progress continually for life * Usually not clinically significant until 35 years of age may occur at any age * More common in males than females Severity of this disease is directly related to the accumulation of plaque and calculus on the surface of the teeth * Preventable (not associated with abnormalities in host defense) * Rate of periodontal destruction varies depending on disease activity and patients resistance * Can be localized or generalized * Progresses slowly until teeth are lost by weighing machine or extraction * Appears to occur in episodic bursts (can be quiet and then rapidly comes on) * Progresses in th e presence of dental plaque * Disease activity halts or stops when the host resistance controls the disease process through therapy or natural defenses * Classified as slight, moderate, or severe Aggressive periodontitis Applied to those periodontal diseases that progress rapidly with massive bone loss * Attachment loss 1mm/year is considered to be an aggressive type * Can be localized or generalized * Often associated with young people * Microbiology similar to chronic periodontitis Types of aggressive periodontitis * Early onset periodontitis (page 137-140) 1. prepubescent periodontitis * Rare may affect 1o or 2o with bone severe gingival inflammation, rapid bone loss, early tooth loss 2. Juvenile periodontitis * Localized juvenile periodontitis (usually 2o molars and incisors, minimal plaque and calculus, AA) * Generalized juvenile periodontitis (rarer, heavy calculus and plaque, p. gingivalis +E corrodens with AA) * Rapidly progressive periodontitis (page 140-142) * Refractory periodontitis (page 142) Unresponsive to thorough and varied periodontal treatments) Class VI periodontitis as a manifestation of systemic disease 1. Associated with hematologic disorders 2. Associated with genetic disorders 3. Not otherwise specified Class IV periodontitis as manifestation of systemic disease * Lesions associated with HIV * Oral candidiasis * Karposi sarcoma type of oral cancer usually seen on the palate * A malignant neoplasm associated with HIV infection and manifesting as brown or purplish tumors on the gingiva near the teeth or on the skin * Xerostomia * Unilateral/bilateral swelling of the salivary glands * Gingivitis * Spontaneous bleedingClass V necrotizing periodontal disease 1. NUG necrotizing ulcerative gingivitis 2. NUP necrotizing ulcerative periodontitis * Necrotic gingival tissue-pseudo membrane * Pain * Fetid breath odor * Punched out papillae * Gingival bleeding * Progression of NUG * Bone loss AND connective tissue attachment loss Class IV abscess of periodontium * Acute localized purulent infection * Usually untreated choric periodontitis * Pockets pathogenic bacteria becomes occluded (cannot escape) * Associated with rapid bone loss * Requires immediate attention * Untreated- seeks drainage route and becomes chronic * Episodes of localized swelling * Periocoronitis is associated with the 8s Treatment involves debridement and systemic antibiotics Class VII periodontitis associated with endodontics * Periodontal pocket can progress to join an endodontic lesion * Treatment endodontic therapy must be blameless before scaling Class VIII developmental or acquired deformities and conditions The role of abnormal occlusion and jaw dysfunction in periodontal treatment (chapter 10) Normal * Occlusal function- the dynamic state during talking, chewing, swallowing * Orthofunction the state if morphofunctional harmony in which the forces developed during function are within adaptive range means health and comfort with no pathological ch ange Abnormal Dysfunction is a state of morphofunctional disharmony in which forces developed during mastication cause pathogenic/pathologic changes in tissue Role of abnormal occlusion and jaw dysfunction * These changes can cause bone loss * Poor occlusion alone does not cause or create periodontitis, it only exacerbates it * Antiaxial forces directed along tooth and periodontium can cause resorption or a hypertrophic response * Some areas will break down, others show no injury Factors * Certain factors affect the response of teeth and periodontal structures to normal and abnormal functions * Size/shape of roots * Quality/quantity of alveolar bone * Presence of plaque * Missing teeth * Oral habits (parafunctional activity ie. contrition and clenching) Parafunctional activity 1. Bruxism Grinding or gnashing of teeth when not chewing or swallowing , usually during sleep * May lead to acute pulpitis, wear faucets, occlusal trauma, and muscle fatigue (summed up in periodontal injury, pain and jaw discomfort) 2. Clenching * Clamping and forcing the teeth together without grinding 3. Crepitation (crepitis) * A grinding noise in the TMJ from damage to the disc and articulating joint surfaces Traumatic occlusion * An occlusion that has caused injury to the teeth, muscles or TMJ * Primary traumatic occlusion is made when heavy occlusal forces exceed the adaptive range causing injury to tissues and bone * Secondary traumatic occlusion is made when normal forces exceed capability of a periodontium already affected by periodontal disease (ie. denture wear or lack) Assessing TMJ/occlusal dysfunction 1. Muscle palpation Normal muscles are equal in length and they should contract and relax without discomfort or pain * Myalgia is a pain in the muscle 2. Mandibular grounds * Normal opening/ culmination of the jaw should be smooth and symmetrical * On average a person should be able to open about 40 mm * Page 222 and 223 3. Assessing occlusion * There should be a firm well disturbed pattern of occlusal contacts * Observe the patient opening and closing * You should note on closing any deviation to the left or right * The posterior teeth should have even contact and maximum inter-cuspation * front teeth should have light to no contact 4. Radiographic evaluation These changes from excessive forces can be observed in periapical films * Widening of PDL (caused by resorption of bony support) * Increased density of surrounding bone (hypertrophic response) * Increased cementum at apices (hypertrophic response) 5. Subjective questionnaire * Screens for patient reported signs and symptoms * Several questions assessing pain, noises, comfort level, headaches, injury, arthritis, former treatment * Ex. questions page 221 Prevention is key * Attention to form and function of aspects of head and neck * Form morphology of teeth, bones, and TMJ * Function morphology including neuromuscular system * Masticatory system is complex but adaptive to function When adaptive capacity exceeded, dysfunction ranges from discomfort to debilitation Temporal Mandibular Disorder (TMD) * Group of musculoskeletal conditions that produce pain or dysfuction in the masticatory system * When it involves muscles and not joint, it is referred to as extracapsular * When it involves the TMJ, it is referred to as intracapsular Etiology * Multifactorial therefore difficult to diagnose and treat * Stress * History of other diseases arthritis and psychological problems * Car accident * Sports injury Microtrauma * Number of minor habits or events that cause damage to masticatory structures * Bruxism * Postural habits * Oral habits (pen, pin, nail down holding, nail biting, etc. Symptoms of temporal mandibular disorder (TMD) * Pain and tenderness in the muscles of mastication * Pain and tenderness in the TMJ * Painful clicking of the joint during function * limit of mandibular motion * You may also see muscle swelling and patient may complain of ringing in the ears * Arthr algia pain in a joint structure Consideration for treatment * Short appointments * Aids during treatment- bite blocks to help keep mouth open * Home care suggestions- small tooth brush heads * Post treatment care- no gum chewing, possible medication, soft diet, warm towel * Frequent recalls Clinical Assessment (chapter 8) Clinical assessment of periodontal disease Assessment represents the 1st phase of the dental hygiene process, provides the foundation for the subsequent diagnosis, planning, implementation, and evaluation of dental and dental hygiene care * Data collection a systemic process of collecting information from multiple sources to help evaluate the health status of the patient. An example of data collection is the medical history * backing this is the information gathered during the assessment and is a reference tool, an historical record also has a medical and legal function * mental test includes extraoral and intraoral, oral hygiene, periodontal and dentition assess ments * Evaluation At this point, the patients current progress (or lack thereof), is compared with baseline data and the stated goal.The evaluation is used to determine if the patient should be re-treated, referred, or placed on a maintenance program * Interpretation being able to decipher and understand your findings clinically or radiographically Examination of gingival tissues clinical markers * Periodontal screening and recording system (PSR) * Was introduced in 1993 * Is a periodontal disease detection system * To be used in the screening process * A specifically designed probe is used * Bleeding, overhangs, defective margins, supra/subgingival calculus are assessed while pocket depth is mensurable * A PSR code is given to each sextant * The code that best describes the most periodontally involved tooth in a sextant is assigned to that sextant PSR scale Code Description * diagonal area of the probe remains completely visible * No calculus or defective margins are detected * Gingival tissues are healthy, with no bleeding on probing 1 * Colored area of the probe remains completely visible in the deepest probing depth in the sextant * No calculus or defective margins are detected * There is bleeding on probing 2 * Colored area of the probe remains completely visible in the deepest probing depth in the sextant * Supra or sub gingival calculus is detected or defective margins are detected 3 * Colored area of the probe remains partly visible in the deeper probing depth in the sextant 4 * Color

Causes of increasing alimentation prices

The divertive utilization of strain alignments to bio sacks issue is considered a result of the arise food prices of our recent age. The resultant utilization of alimentations, more than so rice hulls in many countries is in high spiritsly preferred for use in biofuels production. Bio-extraction of ethanol from plants is considered as environmentally friendly as some analysts secernate it contributes to curbing the issue of global warming by reducing the concentrations of green house gases in the atmosphere. Because the waste product of rice becomes commercialized, it makes rice of any figure or species to be valuable and consequently makes its price sum up.(Saha et al, 2004) Unfair trade agreements imposed by rich nations that try to undermine poor nations making them unavailing to determine their policies of food production have also contributed to a high localized provision in rice. A good example can be cited by Shah (2008) where she reveals that the Doha World Trade Or ganization meeting intended to ascertain poor nations profitability in global trade did not materialize due to the veritable nations view that the undeveloped nations would not ensure the end part of their bargain in the talks.The technology of genetic modification has also fuelled the high prices in foods in comparison of total foods and genetically circumscribed mavens due to the cheap prices of the later in terms of competition. However, research by environmentalists has shown that the genetically modified (GM) foods have negative attributes to the ecological set up and consequently the human health system.The prevalence of the GM foods in the developed nations has seen implore of the higher priced organic foods increase in time due to the health resultants associated with the former. The increasing population has seen the choose of food increase causing its consequential higher production. sieve being a staple meal in Asia has seen its exports being restricted to ensure that people specifically in the Asian nations of India and Chain can live their people with enough food. China with a population of about 1.3 billion people is the highest populated nation in the world followed by India. The governments priority to feed the people comes first and consequently has seen the exportation control of outlandish produce to other nations causing a shortage of food in the global market which by laws of scotchs dictates increase in commodity prices when supply is low. The exorbitant costs of inorganic fertiliser and other farm inputs for agricultural practices have also contributed to the increasing food prices.This is because the costs of production argon also reflected in the end price of the agricultural produce, therefore if the price of oneness input increases, it will inevitable cause a rise in the end product as the farmer can not take up that cost for the benefit of the consumers since it will be tantamount to losses in business. In the UK, far mers are facing a 15% hike in fertilizer prices that is hurting the agricultural sector. This surge in prices is cited to have arisen from anti dumping taxes on nitrogenous fertilizers in the UK from some nations since 2000 that has seen a monopoly in the supply of fertilizer.(Walker, 2007) From the starting signal of 2003 when the Iranian invasion began, oil prices have been going up exponentially that indirectly instituted high price of food. This was and is being attributed to low production levels of crude oil, thus diminishing supply due to the increasing preference of biofuels. The link between the soaring food prices and the high energy prices is that food needs to be transported to one part of land to another more specifically in relation to our globalized world that increases distances of destination.The modes of transportation used are mostly powered by by-products of fogey fuels that are expensive as could be seen by the highest recorded price of over a hundred dollars per barrel at the beginning of 2008. (Shenk 2008) As a consequence, the cost of energy is passed down to the end user making the commodity price higher than usual. This is a global problem since the crude oil prices are the equivalent all over because of their sole control by the Oil Producing and Exporting Countries (OPEC) arrangements.The new problem of climate change is also predicted to cause notwithstanding increases in food prices. The variations in climate across nations that solely depend of agriculture for their growth is evaluate to fall drastically as unpredictable endure patterns take charge causing situations of extreme drought and floods in different places. These alterations in climate will reduce agricultural productivity and food shortage will become imminent across the affected nations. It is now being observed that Australia, one of the largest wheat producing countries is in its third year of drought.Its respect as the world producer of wheat is now in jeopar dy as its silos are becoming empty will the wheat prices are increasing. (Stancich, 2009) The problem of attacks from ramble pests and weeds is also associated in the ever increasing food prices. In Central as well as the Southern parts of the Vietnam nation, according to a recent study Zeigler (2009), rice crops have been attacked by the tungro crop virus originating from the brown plant hopper insect. And furthermore, its spread is being predicted into China together with Thailand and Columbia.Pricing of rice is obviously expected to increase as the supply would have been greatly diminished while demand keeps growing. The continuing undervaluation of the US dollar which is used as a bench mark for trading in many nations is also attributed to the increasing food prices. Globalized nations are feeling the pinch of the current economic crisis of the US and business has gone down meaning that many sectors of the economy are being hurt more specifically in the agricultural sector.Far mers in the developed nations have cope better with the high prices of this global recession compared to their counterparts in the developing nations where production has reduced. A low supply with a high demand implies that food prices would increase in the developing nations unlike in developed nations where it would remain relatively stable. In India -one of the major rice producers- the effect of the global monetary crunch in many sectors of the economy such as the agricultural industry has seen its 2008 GDP drop to 7% while further reduction is expected for 2009 at 5%. (World Bank Group, 2009 2)Sporadic economic growth in different nations all over the world has been identified as a contributor to the increase in commodity prices. As the economy of a nation increases so as the living standards of the citizens. This makes purchasing power go a notch higher due to demand for better goods and services. This causes incompatibilities between demand and supply arising that sees the increase in prices. This is exhibited in the case with China that has been marked by speedy economic development that has exacerbated this global crisis that is catalyzed by its enormous population.(Zu H. & Khan, 1997) Effects of alimentation price increases As an effect, the high food prices could be succeeded by civil unrest especially among the poor nations which can be exemplified by the riots emanating from exorbitantly high food prices in Burkina Faso as well as Cameroon where its was compounded by the expensive fuel costs. The country of Indonesia has also been characterized by such frustrations when there was recent scarcity in Soya beans. Rise in inflation is a notable effect of increased food prices more especially in developing nations.Most developing nations operate on deficits and a down turn from increased food prices puts strains on the governments functionality due to limited financial resources. This sees the issue of relief coming in from developed nations to help the affected. Increase in poverty becomes patent due to high food prices as people reduce their consumption so as to sustain themselves in future days. On an optimistic view, the soaring food prices have also the effect of causing governments to intervene by pushing for increased production of food in their countries to cushion the poor from hunger.(FAO, 2009) purpose Though there has been tremendous growth in food production all over the world, the predictions of the future are still pessimistic as demand continues growing high. This is in reference to the stagnated supply that can not reach counterpoise with the demand hence the future is determined by new sources of supply to cope with the vacuum in supply that would ensure price stability. Therefore, foreign alimentations such as bananas, mangoes, pineapples, and exotic fish among others will not fetch the same price as today due to these imbalances in supply and demand.To mitigate this, an in depth intervention through soci al protection for the short and vast period requirements in conjunction with initiatives on alimentations for the poor should be implemented. Research into new agricultural opportunities should be intensified so as to achieve equilibrium in supply and demand of alimentations. This will go far in guarantying steady prices of food in the global market. And resultantly, agricultural trade regulations that burr high-octane production in the developing nations should be renegotiated with rich nations that discourage them so that a healthy and productive world can be achieved.(OECD, 2007) References FAO, (2009). Bumper rice craw could bring down consumer prices. Planete Urgence. Retrieved on April 20th 2009. From http//www. infosdelaplanete. org/5123/bumper-rice-harvest-could-bring-down-consumer-prices. html? L=EN Hu Z. & Mohsin S. Khan (1997). Why Is China Growing So Fast? ECO noneIC ISSUES NO. 8 International Monitoring Fund (IMF). Washington D. C. Yan Z. (2008). China seeks a balanc e between food security and the urbanization. Retrieved on April 20th 2009. From http//www. china-embassy. org/eng/zt/t516240. htm Walker D. (2007).Fuel and fertilizer Situation. John Wiley and Sons, Inc Stancich R. (2009). Climate change and food prices. Climatechangecorp. Retrieved on April 20th 2009. From http//www. climatechangecorp. com/content. asp? ContentID=5252 OECD (Organization for Economic Co-operation and Development) (2007). Agricultural Policies in OECD Countries Monitoring and Evaluation. Paris OECD. Saha, B. C. , Iten, L. B. , Cotta, M. A. , Wu, Y. (2004). Fuel ethanol production from rice hull abstract. American Chemical Society. Paper No. BI0T 101. Retrieved on 20th April 2009. Fromhttp//www. ars. usda. gov/research/publications/Publications. htm? seq_no_115=156041 Shenk M. (2008) . Oil Climbs Above $126 to Record as Dollar Weakens Against Euro. EU News, Havensworks. com http//www. havenworks. com/world/eu/ World Bank Group, (2009). Impact of Global Financial Cri sis on South Asia. Retrieved on April 20th 2009. From http//74. 125. 47. 132/search? q=cachey57oApfcEXgJsiteresources. worldbank. org/SOUTHASIAEXT/Resources/223546-1171488994713/3455847-1232124140958/gfcsouthasiafeb172009. pdf+global+financial+crisis%2Bfood+prices&cd=2&hl=en&ct=clnk

A Woman of No Importance, Final Act Essay

Wilde uses many dramatic effects throughout the play to shock and amuse the audience and many of them preserve be seen in this final scene. The item that this conversation between Mrs Arbuthnot and Lord Illingworth takes place in Mrs Arbuthnots house, her personal space and territory puts her at an advantage and it shows that Lord Illingworth is surrendering his usual control everyplace his situations By Lord Illingworth referring to Mrs Arbuthnot as Rachel we be again made aware that we are listening to two people who guard a strong away relationship.She calls him George Harford while he uses her name far less often that in the persuasive Act 2. During this scene, Lord Illingworth speaks with awareness of the legal situation, he knows he can never make Gerald legitimate but he is ordaining to leave him property What more can a gentleman desire in this innovation? and Mrs Arbuthnots response of No function more, I am quite sure turns this in to a class confrontation. When Mr s Arbuthnot says I told you I was not interested, and I request you to go. this is a threat to conventional society and the audience would curb been shocked by this.She treats Lord Illingworth as he once treated her, in stringently financial terms and she tells him that Gerald no longer needs his money, You come too late. My son has no need of you. You are not necessary. She whence goes on to exempt to him that Gerald and Hester are in love and they dont need his money because Hester already has money of her own. Lord Illingworth asks where they will go and Mrs Arbuthnots reply We will not tell you, and if you find us we will not know you. You seem surprised.What welcome would you get from the girl whose lips you tried to soil, from the boy whose life you have shamed, from the mother who dishonor comes from you? is very melodramatic and it also relives the fact that Lord Illingworth tried to kiss Hester and this is when Gerald found out that he was his father, Lord Illingwor th you have insulted the purest thing on Gods earth. This leaves Lord Illingworth to admit that he wants Gerald, Rachel, I want my son. Wilde uses many props in this scene, the main one being the letter Gerald has written to Lord Illingworth imploring him to marry his mother.The audience know what is written in the letter before Lord Illingworth does and this adds drama and tension because the audience are delay for the big reveal and to see what happens. This letter also links back to the letter that Lord Illingworth sees in Act 2 and says What a curious handwrite It reminds me of the handwriting of a woman I used to know years ago. and his dismissal of it so simply. The stage direction of Mrs Arbuthnot watches him all the era is very distinguished because she wants to see his reaction.Ironically his proposal of marriage after reading Geralds letter uses similar language to Mrs Arbuthnots when explaining to Gerald why she would refuse him, for her marriage would be a sacrifi ce and for Lord Illingworth it would be a surrender. For Mrs Arbuthnot to say this at this point in the play would have been very uncommon for the time because the audience would be expecting a happy ending, for the fallen women to marry the father of her child or for it to end like a melodrama, in tragedy.For the first time, Mrs Arbuthnot is rejoicing against Lord Illingworth with the repetition of his own words when she says, Children begin by loving their parents. After a time they judge them. Rarely if ever do they exempt them. Lord Illingworth is clearly surprised at this response and then resorts to cruelty. His parting speech creates an exciting climax as the censorship of the time wouldnt leave alone anyone to say the word bastard on the stage.Wildes stage direction of Mrs Arbuthnots use of the glove Mrs Arbuthnot snatches up glove and strikes Lord Illingworth across the casing with it is a very good use of a prop because in the time this play was written a glove was a very virile item and being hit with one was a sign of violence and confrontation. The audience is allowed a shock, due to the word about to be spoken and then they get a relief as the taboo is maintained by Mrs Arbuthnot cutting Lord Illingworth off before he can finish his execration because she will not let him say the word because she doesnt want to hear him say this about her beloved son.The villain is punished and Mrs Arbuthnots respectability is ma intained. All of this is typical of a melodrama and we the audience now feel something has been accomplished. Wildes use of stage directions are very well placed and are very dramatic, especially the last few lines of this scene when Mrs Arbuthnot falls sobbing on the sofa and it reinforces that this play is a melodrama because people are not normally this dramatic in normal everyday life.Gerald and Hester now return to Mrs Arbuthnot and we have the image of a man and a woman in a tend which has been mentioned previously through out the play and is a sign of sex and fertility and in this scene it shows the audience the image of a new family emerging. Due to Hester having changed her views from believe that women who have children outside of the laws of marriage should be punished, A woman who has sinned should be punished, shouldnt she? And that the children should also carry this shame, Yes, it is right that the sins of the parents should be visited on the children.It is a sound law. It is Gods law. to her now saying I was wrong. Gods law is only love. Because she is in love with Gerald and has managed to listen and understand all of the things that Mrs Arbuthnot has had to face to bring up Gerald alone. At the end of the play when Gerald sees the glove lying on the floor Mrs Arbuthnot picks up and changes the title line of the play and once again mirrors Lord Illingworths statement about seeing the letter from Mrs Arbuthnot, Oh o one. No one in particular. A Man of no importance. Unmarried and defian t she enters into a chic and better world although the 19th century attitudes to marriage are still upheld in a way because even though she has won against Lord Illingworth and she has managed to remark Gerald and now has the love and respect of Hester the audience are still left with the image of them being exiled to America, where they have less strict views on illegitimacy and have more freedom.

Pacific Northwest Settling Establishments Essay

Contact at trading posts had originally introduced the Native Americans to Christianity. The British Protestants and French-Canadian trappers who were mostly of Catholic faith did this. The trappers were impressed by Native religion and didnt see any problem between Christianity and Native religion. Fur companies usually encouraged their men to get Native American wives and marry into the tribes to make guile relationships stronger.The Whitman established their mission with the Cayuse at Waiilatpu near Walla Walla. Spalding was assigned to convert the Nez Perce people and founded a mission at Lapwai, Idaho. This was one of the most successful missions.In 1838, two Catholic priests, Fathers Blanchet and Modesta Demers arrived at Fort Walla Walla to imagine the possibilities of beginning a Catholic mission in the area. According to historians the Roman Catholic missionaries were much much successful with the Native Americans.The Native Americans were convinced of the Missionaries tac tics and customs from a few different ways. One of the ways that was used was that they didnt promote in-migration into the area. Their customs in church were interesting to the Native Americans and helped to encourage practicing their beliefs as well as the fact that mission sites were extensive. To help convert they didnt punctuate changing the Native Americans culture, but instead promoted theirs to make the Natives want to change. Instead of requiring Native Americans to live on or close to the Missions, they traveled alongside with them. In some ways the Missionaries used reverse physiology to convince the Native Americans that their practices were better.The significance of having the missionaries approach and try to chance the Native Americans was very significant. If it werent significant, the Native Americans that were oppose Christianity wouldnt have acted so forcefully, and so many conflicts would not have arose. To all Native Americans, the significance was of great im pact whether thought to be controlling or negative. It was also of great significance to the coarse of history. If the Missionary Era never occurred, things might be a lot different as far-off as religion goes for the 21st century.

Haemon’s Speech Analysis

Haemons Speech Analysis Pride and stubbornness can be harmful things, and Haemon touches upon this at bottom his speech to Creon as he attempts to dissuade his father from taking Antigones life. Using rhetorical devices such as tone, ethical, emotional, logical appeal, and metaphor, Haemon manages to make an impact on Creons eventual decision as he speaks in Antigones defense.Starting at the beginning of his speech, Haemon ventures to convince Creon to change his mind about his harsh sentiment against Antigone, not by raising his voice or attempting to beat his earnest views into his father, but by using great tact and endeavoring to find a plebeian ground with Creon, possibly trying to understanding his fathers position on the matter at hand. First, Haemon alleges that reason is Gods crowning hold to man, and that his father is right to warn him against losing that reason.He even keenly asserts that he never wants to say that Creon has reasoned badly, continuing on to make diff erent mindful concessions. However, when this thoughtful mode of speaking doesnt take any immediate effect, Haemon starts to become more candid with his words, implying (although not directly) that Creons actions are inequitable and stubborn, taking care to adopt a point of view that is constructively criticizing as opposed to being completely insulting. He rationally cautions his father against the wit of him having all of the power, noting that if Creon continues upon that path he will eventually turn out an empty man.He states that even people like his father must be able to stop, listen, and learn from othersnot be completely fixed and unchangeable, because no man in the world is completely infallible. A few lines afterwards in the speech, in addition to his amiable tone, Haemon also begins to use some emotional appeal, acknowledging his love and respect for his father, affirming that nothing is closer to him than his fathers happiness, and that he values his fathers fortune a s much as his own.Haemon also logically recognizes his youthfulness and lack of wisdom as well, although he sharp uses what the people of Thebes have been muttering and whispering to support his argument, using aspects of ethical appeal to attest that Antigones innocence is what the people of his fathers urban center would want, realizing that while Creon would like first and foremost to be a good ruler, e also wishes to be well-liked by his people. Then coming to closing lines of his speech, Haemon begins to divagate in clever metaphors here and there, first comparing a stubborn tree being torn up and then a fast and never-slackened flat solid going head over heels and under the water to his father, indicating that this is the type of thing what will happen if Creon thinks that he alone can be right.And in the very end, Haemon leaves his father with some loaded words, advising that Creon listen to him, because while men should be right by instinct, they are all too apt(predica te) to be led astray, and that the smartest thing would be to learn from those who can are willing to teach them how to stay, or even make their own paths, in life.