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MAKALAH MODUL 1

MAKALAH MODUL 1

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Published by: Oky Laksa Indra Kencana on Nov 24, 2010
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Sections

  • 1.1 Background
  • 1.2.1 To find the real factor that causing the mobile tooth
  • 1.2.2 To discover the truth value of the public assumption that says ³if one
  • 1.3 Problem
  • 1.4 Hypothesis
  • 1.5 Benefits
  • 2.1.1. Structure
  • 2.1.2 Commercial
  • 2.2 Cardioascular System
  • 2.3.1 The Impact Of Diabetes
  • 2.3.2 What causes diabetes?
  • 2.3.3 The different types of diabetes
  • 2.3.4 Diabetes Symptoms
  • 2.3.5 How is diabetes diagnosed?
  • 2.3.6 The oral glucose tolerance test
  • 2.3.7 Why is blood sugar checked at home?
  • 2.3.8 Hemoglobin A1c (A1c)
  • 2.3.9 The Chronic Complications Of Diabetes
  • 2.4.Hyperglycemia
  • 2.5. Angiopathy
  • 2.6.1 Passive immunity
  • 2.6.2. Active immunity
  • 2.7.1 Molecular Structure
  • 2.7.2 Fibriliar Structure
  • 2.7.4 Types and associated disorders
  • 2.7.5 Use of Collagen
  • 2.8. Strepptococcus Mutans
  • 2.9. Plaque
  • 2.10. Calculus
  • 2.11.1 Abscess
  • 2.11.2 Pulp
  • 2.11.3 Gingiva
  • 4.1 Local factor and systemic factor of mobile tooth
  • 4.2.1 Periodontitis
  • 4.3.1 Diabetes Mellitus
  • 4.4 Mechanism of periodontitis in diabetes mellitus
  • 4.5 Solutions to minimize the oral effect of Diabetes Mellitus
  • 5.1 Conclusion
  • 5.2 Suggestion
  • 7. Guyton A.1996. Fisiologi Kedokteran .Eke -9. Penerjemah : Setiawan I
  • 8. Jones JH, Mason DK. 1980. Oral Manifestation of Sistemic Disease. Ed. 8
  • 10. Cohen DW.1990. Diabetes Mellitus and Periodontal Disease. J Periodontal 41
  • 11. Marwati E.1992. Infeksi Jaringan Lunak mulut pada Penderita Diabetes
  • 12. Suzuki, John B. 1988. Dental Clinics of North America Vol.32, No.2
  • 13. Mulawarmanti, Dian, 2006. DENTA Jurnal Kedokteran Gigi FKG-UHT
  • 14. Widyastuti, Ratih, 2009. Jurnal Ilmiah Teknologi Kedokteran Gigi FKG
  • 15. Herring, Marvin E., Shah, Shiwan K. 2006. JAOA Clinical Practice Vol.106
  • 19. Kidd, Edwina, Fejerskov, Ole. 2008. Dental Caries The Disease And its
  • 20. http://journal.unair.ac.id/detail_jurnal.php?id=874&med=2&bid=3 [dental
  • 21. http://journal.unair.ac.id/detail_jurnal.php?id=855&med=2&bid=3 [dental
  • 22. Md Ayu Lely S., Indirawati T., 2003. Pengaruh Glukosa Darah yang
  • 23. www.emc.maricopa.edu/faculty/farabee/biobk/biobookcircsys.html
  • 24. www.medicinenet.com/diabetes_mellitus/article.htm
  • 27. Dethlefsen L, McFall-Ngai M, Relman DA: An ecological and evolutionary
  • 32. Zumft WG: Cell biology and molecular basis of denitrification
  • 34. Lundberg JO, Weitzberg E, Gladwin MT: The nitrate-nitrite-nitric oxide
  • 36. Baumann B, Snozzi M, Zehnder AJB, vanderMeer JR: Dynamics of
  • 37. Goretski J, Zafiriou OC, Hollocher TC: Steady-State Nitric-Oxide
  • 38. Conrad R: Soil Microbial Processes and the Cycling of Atmospheric Trace
  • 41. Horn MA, Schramm A, Drake HL: The earthworm gut: An ideal habitat for
  • 45. Bayindir YZ, Polat MF, Seven N: Nitric oxide concentrations in saliva and
  • 48. Selwitz RH, Ismail AI, Pitts NB: Dental caries
  • 49. Pihlstrom BL, Michalowicz BS, Johnson NW: Periodontal diseases
  • 50. www.wikipedia.org

CHAPTER 1 INTRODUCTION

1.1 Background Indonesian society is a multiple community. On Indonesian society has developed a variety of assumptions about the various things that continue to develop from time to time, this assumptions of course assuming its truth value is questionable, it is still very difficult to distinguish between reality or just a myth. The presumption of this community extends about various things, without exception dental health problems. At this time there is a perception in the community around us that if one tooth on the pull, it will cause the other teeth rocking and eventually will join revoked as well. This assumption leads people reluctant to have their teeth taken by dentist, this may in fact may exacerbate their own oral health.In other side, according to the science of dentistry there are two factor that can cause mobile tooth. They are local factor and systemic factor. It is interesting to examine the truth of this assumption, to align public views on this issue and to find out factors causing tooth rocking actual factor, and explain to the public the process of mobile tooth.

1.2 Objective 1.2.1 To find the real factor that causing the mobile tooth.. 1.2.2 To discover the truth value of the public assumption that says ³if one tooth on the pull, it will cause the other teeth rocking and eventually will join revoked as well.´

1.3 Problem 1.3.1 What is cause of mobile tooth? 1.3.2 Is the people assumption that if one tooth on the pull, it will cause the other teeth rocking and eventually will join revoked as well right?
1

1.4 Hypothesis People assumption that if one tooth on the pull, it will cause the other teeth rocking and eventually will join revoked as well is wrong.

1.5 Benefits 1.5.1 To be able to know the real factor that cause mobile tooth. 1.5.2 To inform the truth value of the public assumption about mobile tooth.

2

CHAPTER 2 GLOSSARY 2.1.Glucose Glucose (C6H12O6), a simple sugar (monosaccharide), is an important carbohydrate in biology. Cells use it as a source of energy and a metabolic intermediate. Glucose is one of the main products of photosynthesis and starts cellular respiration. Starch and cellulose are polymers derived from the dehydration of glucose. The name "glucose" comes from the Greek word glukus ( meaning "sweet." The suffix "-ose" denotes a sugar. Glucose can adopt several different structures, but all of these structures can be divided into two families of mirror-images (stereoisomers). Only one set of these isomers exists in nature, those derived from the "right-handed form" of glucose, denoted D-glucose. D-glucose is often referred to as dextrose, especially in the food industry. The term dextrose is derived from dextrorotatory glucose.[2] Solutions of dextrose rotate polarized light to the right (in Latin: dexter = "right" ). This article deals with D-glucose. The mirror-image of the molecule, L-glucose, is discussed separately. 2.1.1. Structure Although it is called a "simple sugar" (meaning that it is a monosaccharide), glucose is a complicated molecule because it adopts several different structures. These structures are usually discussed in the context of the acyclic isomer, which exists in only minor amounts in solution. Glucose is derived from hexanal, a chain of six carbon atoms terminating with an aldehyde group. The other five carbon atoms each bear alcohol groups. Glucose is called an aldohexose. In solution, glucose mainly exists as the six-membered ring containing a hemiacetal group, which arises from the reaction of the hydroxy group at
3

),

This cyclic form of glucose is called a glucopyranose. corn husk and sago are all used in various parts of the world.1. An inaccurate but superficially attractive from is observing whether the C-1 hydroxyl alternative method of distinguishing is below or above the plane of the ring. The ring closing process can give rise to two isomers. Many crops can be used as the source of starch. The asymmetric center at C-1. this may fail if the glucose ring is drawn upside down or in an alternative chair conformation. is called the anomeric carbon atom. wheat. the designation means that the hydroxyl group attached to C-1 is positioned trans to the -CH2OH group at C-5. an approximately 1:1 mixture of glucose and fructose. cornstarch (from maize) is used almost exclusively.2 Commercial Glucose is produced commercially via the enzymatic hydrolysis of starch. the site of the hemiacetal. 2. 4 .C-5 and the aldehyde at C-1. of which two isomers exist. In the United States. to a final stable ratio of : 36:64. The and forms interconvert over a timescale of hours in aqueous solution. Containing five carbon atoms and one oxygen atom. Most commercial glucose occurs as a component of invert sugar. which are labeled -glucose and -glucose. cassava. cellulose could be hydrolysed to glucose. this ring is a derivative of pyran. called anomers. rice. Maize. but this process is not yet commercially practical. These anomers differ in terms of the relative positioning of the hydroxyl group linked to C-1. The ratio would be : 11:89 if it were not for the influence of the anomeric effect. while means that it is cis. In principle. in a process called mutarotation. When D-glucose is drawn as a Haworth projection or in the standard chain conformation.

is where the blood enters the heart. Passing through a valve. the atrium (pl. Arteries have three layers of thick walls. A diagram of arterial structure is shown in Figure 3. The pulmonary artery is the only artery that carries oxygen-poor blood. the ventricle. Figure 3. Arterial walls are able to expand and contract.whfreeman. by Sinauer Associates (www. Life: The Science of Biology.com) and WH Freeman (www. The upper chamber of the heart. another layer of connective tissue is quite elastic. 4th Edition. Structure of an artery.. The pulmonary artery carries deoxygenated blood to the lungs. Contraction of the ventricle forces blood from the heart through an artery.2. carbon dioxide 5 .sinauer. used with permission.com). The aorta is the main artery leaving the heart. atria). Image from Purves et al. Arteries are blood vessels that carry blood away from heart.2 Cardioascular System The vertebrate cardiovascular system includes a heart. Smooth muscle fibers contract. gas exchange occurs. and a series of blood vessels. In the lungs. The heart muscle is composed of cardiac muscle cells. which is a muscular pump that contracts to propel blood out to the body through arteries. blood enters the lower chamber. allowing the arteries to carry blood under high pressure.

Small arterioles branch into collections of capillaries known as capillary beds. 6 . shown in Figures 4 and 5.830). Capillary with Red Blood Cell (TEM x32. as shown in Figure 6. Arterioles are small arteries that connect larger arteries with capillaries. and hormones are exchanged across the thin walls of capillaries. Nutrients. Figure 4. the wall is only one cell layer thick.com. oxygen diffuses in. allowing materials to flow in and out of capillaries as well as the passage of white blood cells. wastes.diffuses out. Structure and blood flow through a vein. used with permission. Control of blood flow into capillary beds is done by nerve-controlled sphincters. Some capillaries have small pores between the cells of the capillary wall. are thin-walled blood vessels in which gas exchange occurs. an exampe of one is shown in Figure 4. Changes in blood pressure also occur in the various vessels of the circulatory system. although blushing is one manifestation of blood flow into capillaries. Capillaries. Capillaries are microscopic in size. The above illustration is from Figure 5.DennisKunkel. In the capillary. This image is copyright Dennis Kunkel at www. Capillaries are concentrated into capillary beds.

and hormones and the removal of carbon dioxide. and the area of the arteries. The circulatory system functions in the delivery of oxygen. used with permission. as shown in Figure 7. 4th Edition. and veins of the circulatory system. Capillary structure.. by Sinauer Associates (www.. Image from Purves et al. 7 . Capillaries are the points of exchange between the blood and surrounding tissues.com) and WH Freeman (www.com).sinauer. by Sinauer Associates (www.whfreeman. Figure 7.whfreeman.sinauer. Materials cross in and out of the capillaries by passing through or between the cells that line the capillary. velocity. and relationships of capillaries to arteries and veins. 4th Edition. Changes in blood pressure.Figure 6. Life: The Science of Biology. capillaries.com) and WH Freeman (www.com). nutrient molecules. Life: The Science of Biology. Image from Purves et al. used with permission. ammonia and other metabolic wastes.

whfreeman. Veins carry blood from capillaries to the heart. ions. Plasma is about 60 % of a volume of blood. 4th Edition. as shown in Figure 8. used with permission. The veins have valves that prevent back-flow of blood. and gases.The extensive network of capillaries in the human body is estimated at between 50. blood in veins is oxygen-poor. Mammalian blood consists of a liquid (plasma) and a number of cellular and cell fragment components as shown in Figure 21. cells and fragments are 40%. Venules are smaller veins that gather blood from capillary beds into veins. Plasma has 90% water and 10% dissolved materials including proteins. Pressure in veins is low. Life: The Science of Biology.4.000 and 60. hormones. It acts as a buffer. These channels can open and close by the action of muscles that control blood flow through the channels.000 miles long. Figure 8. glucose. so veins depend on nearby muscular contractions to move blood along.sinauer. maintaining pH near 7.com).com) and WH Freeman (www. Thoroughfare channels allow blood to bypass a capillary bed. With the exception of the pulmonary veins. Capillary beds and their feeder vessels. by Sinauer Associates (www. Blood Plasma is the liquid component of the blood. Plasma contains 8 .. Image from Purves et al. Blood leaving the capillary beds flows into a progressively larger series of venules that in turn join to form veins. The pulmonary veins carry oxygenated blood from lungs back to the heart.

responsible for the color of feces. are flattened. Humans have a total of 25 trillion red blood cells (about 1/3 of all the cells in the body). Macrophages release white blood cell growth factors. Antigen-antibody complexes are phagocytized by a macrophage. The liver degrades the heme units and secretes them as pigment in the bile. T-cells attack cells containing viruses. and have 200 million hemoglobin molecules per cell. as is shown by Figures 17 and 18. They are made from stem cells in bone marrow. Neutrophils enter the tissue fluid by squeezing through capillary walls and phagocytozing foreign substances. doubly concave cells about 7 µm in diameter that carry oxygen associated in the cell's hemoglobin. They are small. Platelets survive for 10 days before being removed by the liver and spleen. skull.nutrients. are larger than erythrocytes. White blood cells (leukocytes) are less than 1% of the blood's volume. salts. 4 to 6 million cells per cubic millimeter of blood. Red blood cells. Each second two million red blood cells are produced to replace those thus taken out of circulation. There are 150. White blood cells can squeeze through pores in the capillaries and fight infectious diseases in interstitial areas Platelets result from cell fragmentation and are involved with clotting. have a nucleus. also known as leukocytes. wastes. ribs. They carry chemicals essential to blood clotting. Proteins in the blood aid in transport of large molecules such as cholesterol. important components of the immune system. Iron from hemoglobin is recovered and reused by red marrow. White blood cells. Platelets are cell fragments that bud off megakaryocytes in bone marrow. proteins. Red blood cells are continuously manufactured in red marrow of long bones. B-cells produce antibodies. They function in the cellular immune response. after which they are destroyed in liver and spleen. Mature erythrocytes lack a nucleus. There are five types of leukocytes. causing a population increase for white blood cells. and vertebrae.000 to 9 . and lack hemoglobin. etc. Lymphocytes fight infection. Life-span of an erythrocyte is only 120 days. also known as erythrocytes.

It has also led to HIV transmission due to the use of transfusions and use of contaminated blood products. Platelets stick and adhere to tears in blood vessels. Providing correct proteins (clotting factors) has been a common method of treating hemophiliacs. or both. they also release clotting factors. A hemophiliac's blood cannot clot.3. 10 .000 platelets in each milliliter of blood.300. or action. that result from defects in insulin secretion. 2. Diabetes Mellitus Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels.

Diabetes is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis). insulin is released from the pancreas to normalize the glucose level. 2. the body can. 2. usually secondary to a destructive process affecting the insulin producing beta cells in the pancreas." This is the primary problem in type 2 diabetes. and nerve damage. production of defective insulin (which is uncommon). When the blood glucose elevates (for example. Diabetes is a chronic medical condition. In type 2 diabetes. there also is a steady decline of beta cells that adds to the process of elevated blood sugars. an estimated additional 12 million people in the United States have diabetes and don't even know it. The absolute lack of insulin. and results in a condition known as "insulin resistance.3. is the main disorder in type 1 diabetes. In addition. if someone is resistant to insulin. kidney failure. These types of damage are the result of damage to small vessels. the absence or insufficient production of insulin causes hyperglycemia. Normally.2 What causes diabetes? Insufficient production of insulin (either absolutely or relative to the body's needs).3. leading to strokes. it lasts a lifetime.1 The Impact Of Diabetes Over time. blood glucose levels are tightly controlled by insulin." and excessive muscle loss in the ancient world. or the inability of cells to use insulin properly and efficiently leads to hyperglycemia and diabetes. Essentially. meaning that although it can be controlled. In patients with diabetes. Insulin lowers the blood glucose level. Diabetes affects approximately 17 million people (about 8% of the population) in the United States. and other large blood vessel diseases. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine. diabetes can lead to blindness. commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with "sweet urine. coronary heart disease. to 11 . This latter condition affects mostly the cells of muscle and fat tissues.Diabetes mellitus. a hormoneproduced by the pancreas. referred to as microvascular disease. after eating food). hence the term sweet urine. This is referred to as macrovascular disease.

some degree. However. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. in patients with diabetes. if production decreases and insulin cannot be released as vigorously. glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. After time. such a regulatory system helps to keep blood glucose levels in a tightly controlled range. After a meal. the insulin release from the pancreas is turned down. Without insulin. In normal individuals.) In addition to helping glucose enter the cells. insulin is also important in tightly regulating the level of glucose in the blood. relatively insufficient for the body's needs. The abundant. unutilized glucose is wastefully excreted in the urine. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. As outlined above. 12 . the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. increase production of insulin and overcome the level of resistance. Insulin Hormon Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. the insulin is either absent. or not used properly by the body. and is carried by the bloodstream to all the cells in the body where it is utilized. the blood glucose level rises. the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. In response to the increased glucose level. hyperglycemia develops. In certain types of diabetes. Carbohydrates are broken down in thesmall intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream. Glucose is a simple sugar found in food. When the blood glucose levels are lowered. (The pancreas is a deep-seated organ in the abdomen located behind the stomach. All of these factors cause elevated levels of blood glucose (hyperglycemia).

In persons with type 1 diabetes.3. The patient with type 1 diabetes must rely on insulin medication for survival. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is. though the details are not fully understood. anti-insulin antibodies and anti13 .2. which are responsible for insulin production. In type 1 diabetes. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies. called type 1 and type 2. such as type 1 diabetes. genetically inherited. the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. and is rendered incapable of making insulin. the beta cells of the pancreas. are attacked by the misdirected immune system.3 The different types of diabetes There are two major types of diabetes. in part. In autoimmune diseases. the pancreas undergoes an autoimmune attack by the body itself. or juvenile onset diabetes mellitus. Type 1 diabetes was also called insulin dependent diabetes mellitus (IDDM). Antibodies are proteins in the blood that are part of the body's immune system. Exposure to certain viral infections (mumpsand Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Abnormal antibodies have been found in the majority of patients with type 1 diabetes.

the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels.) Finally. These antibodies can be measured in the majority of patients. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy. the release of insulin by the pancreas may also be defective and suboptimal. but do so relatively inadequately for their body's needs. the American Diabetes Association does not recommend general screening of the population for type 1 diabetes. 14 . such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. In addition to the problems with an increase in insulin resistance. particularly in the face of insulin resistance as discussed above. there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. and may help determine which individuals are at risk for developing type 1 diabetes. Of all the patients with diabetes. Type 2 diabetes was also referred to as non-insulin dependent diabetes mellitus (NIDDM). At present. however. In fact. usually before 30 years of age. patients can still produce insulin. LADA is a slow. lean individuals. In many cases this actually means the pancreas produces larger than normal quantities of insulin.glutamic decarboxylase antibodies. Type 1 diabetes tends to occur in young. though screening of high risk individuals. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). older patients do present with this form of diabetes on occasion. only approximately 10% of the patients have type 1 diabetes and the remaining 90% have type 2 diabetes. In type 2 diabetes. or adult onset diabetes mellitus (AODM). The control of gluconeogenesis becomes compromised. progressive form of type 1 diabetes.

However. Gestational diabetes usually resolves once the baby is born. type 2 diabetes is now more common than type 1 diabetes in childhood. we are seeing an alarming number patients with type 2 diabetes who are barely in their teen years. and this holds true in children as well as adults. higher body weight. for the first time in the history of humans. Most of these cases are a direct result of poor eating habits.While it is said that type 2 diabetes occurs mostly in individuals over 30 years old and the incidence increases with age. diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy(gestational diabetes . Regarding age. Diabetes can occur temporarily during pregnancy. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. and in certain Native American communities 20% to 50%. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight. While there is a strong genetic component to developing this form of diabetes. especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Finally. 25%50% of women with gestational diabetes will eventually develop type 2 diabetes later in life. Patients with gestational diabetes are usually asked to undergo an oral glucose tolerance test about six weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy. in Hispanics 15%. the prevalence in African Americans and Asian Americans is estimated to be 10%. The prevalence of diabetes in persons 65 to 74 years of age is nearly 20%.see below). or if any evidence 15 .the most significant of which is obesity. there are other risk factors . data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. Blood sugar elevation during pregnancy is called gestational diabetes. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes. Compared with a 6% prevalence in Caucasians. In fact. Type 2 diabetes is also more common in certain ethnic groups. and lack of exercise.

Diabetes can also result from other hormonal disturbances. Dehydration causes increased thirst and water consumption. or "unmask" latent diabetes. "Secondary" diabetes refers to elevated blood sugar levels from another medical condition. In Cushing's syndrome. In acromegaly. such as chronic pancreatitis(inflammation of the pancreas by toxins like excessive alcohol). In addition. which promotes blood sugar elevation. leading to hyperglycemia. y The inability of insulin to perform normally has effects on protein. or surgical removal of the pancreas.4 Diabetes Symptoms y The early symptoms of untreated diabetes are related to elevated blood sugar levels. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease. one that encourages storage of fat and protein. a pituitary gland tumor at the base of the brain causes excessive production of growth hormone. y A relative or absolute insulin deficiency eventually leads to weight loss despite an increase in appetite.3. Insulin is an anabolic hormone. trauma. and loss of glucose in the urine. 16 . 2.(such as impaired glucose tolerance) is present that may be a clue to the patient's future risk for developing diabetes. fat and carbohydrate metabolism. certain medications may worsen diabetes control. This is seen most commonly when steroid medications (such as prednisone) are taken and also with medications used in the treatment of HIV infection (AIDS). that is. such as excessive growth hormone production (acromegaly) and Cushing's syndrome. the adrenal glands produce an excess of cortisol. High amounts of glucose in the urine can cause increased urine output and lead to dehydration.

y Fluctuations in blood glucose levels can lead to blurred vision.3.6 The oral glucose tolerance test Though not routinely used anymore. y Normal fasting plasma glucose levels are less than 100 milligrams per deciliter (mg/dl). and is addressed elsewhere. but in the range of 100126mg/dl. 2. and vaginal areas. Patients with diabetes are prone to developing infections of the bladder. It is easy to perform and convenient. This can also be done accurately in a doctor's office using a glucose meter. y Fasting plasma glucose levels of more than 126 mg/dl on two or more tests on different days indicate diabetes. y A random blood glucose test can also be used to diagnose diabetes. a single sample of blood is drawn and sent to the laboratory for analysis. nausea and vomiting. A blood glucose level of 200 mg/dl or higher indicates diabetes.3. skin. While patients with IFG do not have the diagnosis of diabetes. 2. Extremely elevated glucose levels can lead to lethargy and coma. After the person has fasted overnight (at least 8 hours). It is still commonly used 17 .y y Some untreated diabetes patients also complain of fatigue. When fasting blood glucose stays above 100mg/dl.5 How is diabetes diagnosed? The fasting blood glucose (sugar) test is the preferred way to diagnose diabetes. this condition carries with it its own risks and concerns. this is known as impaired fasting glucose (IFG). the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes.

1%-5% of people whose test results show impaired glucose tolerance actually eventually develop 18 . and y y the person should not be taking medicines that could affect the blood glucose. but are at high risk for progressing to diabetes. With an oral glucose tolerance test. as an inpatient in a hospital). such as polycystic ovary syndrome. For the test to give reliable results: y y the person must be in good health (not have any other illnesses.for diagnosing gestational diabetes and in conditions of pre-diabetes. Each year. Blood samples are taken at specific intervals to measure the blood glucose. Some physicians simply get a baseline blood sample followed by a sample two hours after drinking the glucose solution. y The morning of the test. the glucose levels rise and then fall quickly. the person fasts overnight (at least eight but not more than 16 hours). In a person without diabetes. Usually. After this test. The classic oral glucose tolerance test measures blood glucose levels five times over a period of three hours. People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT). not even a cold). for example. the person receives 75 grams of glucose (100 grams for pregnant women). the person should be normally active (not lying down. For three days before the test. the glucose is in a sweet-tasting liquid that the person drinks. glucose levels rise higher than normal and fail to come back down as fast. the fasting plasma glucose is tested. In someone with diabetes. Then first. the person should not smoke or drink coffee. People with impaired glucose tolerance do not have diabetes. the person should have eaten a diet high in carbohydrates (200-300 grams per day). There are several methods employed by obstetricians to do this test. but the one described here is standard.

and all values between 0 and 2 hours are less than 200 mg/dl. but is its own clinical disease entity that requires treatment and monitoring. most physicians are now understanding that impaired glucose tolerance is nor simply a precursor of diabetes. 19 .diabetes. In addition. y Gestational diabetes: A woman has gestational diabetes when she has any two of the following: a 100g OGTT. or a 3-hour glucose level of more than 140 mg/dl. y Impaired glucose tolerance: A person is said to have impaired glucose tolerance when the fasting plasma glucose is less than 126 mg/dl and the 2-hour glucose level is between 140 and 199 mg/dl. Evaluating the results of the oral glucose tolerance test Glucose tolerance tests may lead to one of the following diagnoses: y Normal response: A person is said to have a normal response when the 2-hour glucose level is less than 140 mg/dl. Weight loss andexercise may help people with impaired glucose tolerance return their glucose levels to normal. a 1hour glucose level of more than 180 mg/dl. In the medical community. a fasting plasma glucose of more than 95 mg/dl. some physicians advocate the use of medications. to help prevent/delay the onset of overt diabetes. a 2-hour glucose level of more than 155 mg/dl. Recent studies have shown that impaired glucose tolerance itself may be a risk factorfor the development of heart disease. y Diabetes: A person has diabetes when two diagnostic tests done on different days show that the blood glucose level is high. such as metformin (Glucophage).

Medtronic and Navigator). not only the current glucose reading. This device has a visual screen that allows the wearer to see. Each meter has its own advantages and disadvantages (some use less blood. but also the graphic trends. Sure Step and Freestyle. at this time the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives. some have a larger digital readout. The test results are then used to help patients make adjustments in medications. the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. it can only give a calculated suggestion as to whether the wearer should give insulin. etc). Attached to this is a transmitter that sends the data to a pager-like device. This cannula allows for frequent sampling of blood glucose levels.7 Why is blood sugar checked at home? Home blood sugar (glucose) testing is an important part of controlling blood sugar. and if so. and physical activities. for example. which reads the value. 20 . Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. In some devices.2. some take a shorter time to give you results. There are many meters on the market. and at bedtime. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Accu-Check Advantage. The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. All of these devices need to be correlated to fingersticks for a few hours before they can function independently. Blood glucose levels are usually tested before and after meals. diets. at least three continuous glucose sensors are approved in the United States (Dexcom. There are some interesting developments in blood glucose monitoring. One Touch Ultra. how much). Currently. The devices can then provide readings for 35 days. However.3. The Medtronic version is specifically designed to interface with their insulin pumps. The blood sugar level is typically determined by pricking a fingertip with alancing device and applying the blood to a glucose meter.

it gives us an idea of how much sugar is around for the preceding three months.5%). and when it's around for a long time. 2.8 Hemoglobin A1c (A1c) To explain what an hemoglobin A1c is. sugar sticks too. When sugar sticks to these cells. if they change their diet and so on. and to the development of an artifical pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly . While there are no guidelines to use A1c as a screening tool.9 %. In poorly controlled diabetes. 21 . and in well controlled patients it's less than 7. and they are a great tool for education as well. if they decide to embark on a new exercise regimen. The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months). It is also important to remember that these devices can be used intermittently with fingersticks.0% or above. This kind of system takes us one step closer to closing the loop. If they become ill.Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process. it's harder to get it off. think in simple terms. In most labs. it gives a physician a good idea that someone is diabetic if the value is elevated.the ultimate goal. it is used as a standard tool to determine blood sugar control in patients known to have diabetes. providing more information on how they are responding to new lifestyle changes or stressors. The red blood cells that circulate in the body live for about three months before they die off.3. Sugar sticks. Right now. and the value does not bounce as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows. the normal range is 4%-5. a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well.0% (optimal is <6. they can use the sensor to supplement their fingerstick regimen. its 8. In the body. particularly to proteins. For example.

2. with significant anemia.5% should be the goal. For example. and thus the A1c is altered. studies have shown that there is about a 10% decrease in relative risk formicrovascular disease for every 1% reduction in A1c. Data also suggests that the risk of macrovascular disease decreases by about 24% for every 1% reduction in A1c values. the red blood cell count is low. though there are not yet at goal.µ A1c(%) 6 7 8 9 10 11 12 Mean blood sugar (mg/dl) 135 170 205 240 275 310 345 The American Diabetes Association currently recommends an A1c goal of less than 7. 22 . This may also be the case in sickle cell disease and other hemoglobinopathies. The closer to normal the A1c.7 and drops to 8. if a patient starts off with an A1c of 10. they have managed to decrease their risk of microvascular complications by about 20%. It should be mentioned here that there are a number of conditions in which an A1c value may not be accurate. So.0%. the lower the absolute risk for microvascular complications. Of interest. Other Groups such as the American Association of Clinical Endocrinologists feel that an A1c of <6.

2. acidosis. Diabetic ketoacidosis can be caused by infections. In addition. Insulin is vital to patients with type 1 diabetes . Severely elevated blood sugar levels due to an actual lack of insulin or a relative deficiency of insulin. Antibiotics are given for infections. and even death. coma. infection. Without prompt medical treatment. Without insulin. missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. which in turn leads to excessive loss of fluid and electrolytes in the urine. abnormal blood sugar levels. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid. and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. a condition called diabetic ketoacidosis (DKA). and insulin. severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). Dehydration can be very severe. and abdominal pain. and dehydration can be reversed rapidly. In patients with type 2 diabetes. With treatment. results in the process of ketosis and the release of ketones into the blood. and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. or trauma all which may increase insulin requirements. ketoneproduction. A hyperosmolar coma usually occurs in elderly patients 23 . stress. This dysregulation. stress. This condition can lead to coma (hyperosmolar coma). This leads to increased urine glucose. Abnormally low blood sugar levels due to too much insulin or other glucoselowering medications. Accompanied by dehydration. usually in a hospital intensive care unit.1. patients with diabetic ketoacidosis can rapidly go intoshock. and patients can recover remarkably well.they cannot live with out a source of exogenous insulin. vomiting. electrolytes. patients with type 1 diabetes develop severely elevated blood sugar levels. Symptoms of diabetic ketoacidosis include nausea. Ketones turn the blood acidic.

the brain is suffering from a lack of sugar. irreversible brain death. Like diabetic ketoacidosis. Untreated. it is called an insulin reaction. These include glucose containing drinks. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. the equivalent of half a glass of juice). In patients with diabetes. confusion. in the worse case scenario. a hyperosmolar coma is a medical emergency. At this point. severely low blood sugar levels can lead to coma.with type 2 diabetes. low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion. to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. low blood sugar can lead to central nervous system symptoms such as dizziness. Since in general. seizures. Blood glucose is essential for the proper functioning of brain cells. The complication and death rates from hyperosmolar coma is thus higher than in DKA. Sometimes. but usually it occurs when blood sugars are less than 65 mg/dl. Even cake frosting applied inside the 24 . When low blood sugar levels occur because of too much insulin. Therefore. or glucose tablets in doses of 15-20 grams at a time (for example. concomitant medical conditions are more likely to exist. and this usually occurs somewhere around levels of <40 mg/dl. and. The treatment of low blood sugar consists of administering a quickly absorbed glucose source. soft drinks (not sugar-free). patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications. The actual level of blood sugar at which these symptoms occur varies with each person. Hypoglycemia means abnormally low blood sugar (glucose). and these patients may actually be sicker overall. weakness. Unlike patients with type 1 diabetes. type 2 diabetes occurs in an older population. such as orange juice. and tremors.

Spontaneous bleeding from the new and brittle blood vessels can lead to retinalscarring and retinal detachment. a medic alert bracelet should be worn by all patients with diabetes. strokes. Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels. kidneys and nerves (microvascular disease). thus impairing vision. since obviously the patients will not be able to do it themselves in an emergency situation. 2. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms). Eye Complications The major eye complication of diabetes is called diabetic retinopathy.9 The Chronic Complications Of Diabetes These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease.cheeks can work in a pinch if patient cooperation is difficult. Families and friends of those with diabetes need to be taught how to administer glucagon. such as those involving the eyes. and new but brittle blood vessels (neovascularization). leading to coronary heart disease (angina orheart attack). If the individual becomes unconscious.glucagon can be given by intramuscular injection. and pain in the lower extremities because of lack of blood supply (claudication). Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Approximately 50% of patients with diabetes will develop some degree of diabetic 25 . Glucagon causes the release of glucose from the liver (for example.3. and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Another lifesaving device that should be mentioned is very simple. it promotes gluconeogenesis). To treat diabetic retinopathy a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels.

Initially. and 80% of diabetics have retinopathy after 15 years of the disease. Later on. In essence. This allows for a more accurate assessment of what kind of glasses prescription is required.retinopathy after 10 years of diabetes. and by aggressively treating high blood sugar levels. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. the kidneys lose their ability to cleanse and filter blood. blurry vision is very common in poorly controlled diabetes. the blood flow to the nerves is limited. Cataracts and glaucoma are also more common among diabetics. diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Nerve damage Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. It is also important to note that since the lens of the eye lets water through. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. leaving the nerves without blood flow. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in diabetic patients. Kidney damage Kidney damage from diabetes is called diabetic nephropathy. if blood sugar concentrations vary a lot. The progression of nephropathy in patients can be significantly slowed by controllinghigh blood pressure. kidney transplantation can be considered. The onset of kidney disease and its progression is extremely variable. The accumulation of toxic waste products in the blood leads to the need for dialysis. In patients who do not want to undergo chronic dialysis. the lens of the eye will shrink and swell with fluid accordingly. and they get damaged or die as a result (a term 26 . As a result.

Because of poor blood circulation. burning. causingnausea. and other infected parts. When the nerve disease causes a complete loss of sensation in the feet.known as ischemia). ulcers. Shoes or other protection should be worn as much as possible. Erectile dysfunction can also be caused by poor blood flow to the penis from diabetic blood vessel disease. Gabapentin (Neurontin). The pain of diabetic nerve damage may respond to traditional treatments with gabapentin (Neurontin). patients may not be aware of injuries to the feet. minor foot injuries can lead to serious infection. diabetic foot injuries may not heal. Sometimes. While many of these medications are not FDA indicated specifically for the treatment of diabetes related nerve pain. they are used by physicians commonly. Diabetic neuropathy can also affect nerves to the stomach and intestines. carbamazepine (Tegretol). though unfortunately blood glucose control and the course of neuropathy do 27 . phenytoin (Dilantin). desipramine (Norpraminine). and aching of the feet and lower extremities. phenytoin (Dilantin). and fail to properly protect them. weight loss. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. diarrhea. Symptoms of diabetic nerve damage include numbness. feet. or with topically-applied capsaicin (an extract of pepper). and even gangrene. Amitriptyline (Elavil) and desipramine (Norpraminine) are medications that are traditionally used for depression. and carbamazepine (Tegretol) are medications that are traditionally used in the treatment of seizure disorders. The pain of diabetic nerve damage may also improve with better blood sugar control. necessitating surgical amputation of toes. amitriptyline (Elavil). Diabetic nerve damage can affect the nerves that are important for penile erection. impotence). due to ineffective contraction of the stomach muscles). and other symptoms of gastroparesis (delayed emptying of food contents from the stomach into the intestines. causing erectile dysfunction (ED.

is so widely used in organisms. This reaction (glycation) reduces or destroys the function of many enzymes. disaccharides and monosaccharides.not always go hand in hand. relative to other hexose sugars. Pregabalin (Lyrica) which has an indication for diabetic neuropathic pain and duloxetine (Cymbalta) are newer agents used in the treatment of diabetic neuropathy. many of the 28 . -Glucose is stored in mainly the liver and muscles as glycogen. Scientists can speculate on the reasons why glucose. -It is distributed and utilized in tissues as free glucose. Function Glucose metabolism and various forms of it in the process. Newer medications for nerve pain have recently come to market in the US. -Glucose-containing compounds and isomeric forms are digested and taken up by the body in the intestines. Nevertheless. One reason might be that glucose has a lower tendency. including starch. to react non-specifically with the amino groups of proteins. and not another monosaccharide such as fructose (Fru). The low rate of glycation is due to glucose's preference for the less reactive cyclic isomer. glycogen.

in the United States and other countries (e. Japan..long-term complications of diabetes (e. or Millimoles per litre (mmol/l). 2. meaning sweet. Glucose levels are measured in either: Milligrams per decilitre (mg/dl). -glyc-. and -emia. some journals now use mmol/l as the primary unit but quote mg/dl in parentheses. renal failure. France. but symptoms may not start to become noticeable until even higher values such as 15-20 mmol/l (270-360 mg/dl). or high blood sugar is a condition in which an excessive amount of glucose circulates in the blood plasma. However. Comparatively: 72 mg/dl = 4 mmol/l 90 mg/dl = 5 mmol/l 108 mg/dl = 6 mmol/l 126 mg/dl = 7 mmol/l 144 mg/dl = 8 mmol/l 29 . Colombia).g. blindness. enzyme-regulated addition of glucose to proteins by glycosylation is often essential to their function..Hyperglycemia The origin of the term is Greek: hyper-. meaning "of the blood" Hyperglycemia. and peripheral neuropathy) are probably due to the glycation of proteins or lipids. hyperglycaemia. meaning excessive. chronic levels exceeding 7 mmol/l (125 mg/dl) can produce organ damage. In contrast. This is generally a glucose level higher than 10 mmol/l (180 mg/dl). which can be acquired by dividing (mg/dl) by factor of 18.4. Scientific journals are moving towards using mmol/l.g. Egypt.

Chronic hyperglycemia can be measured via the HbA1c test. with mmol/l levels from 8 to 15. leading to the complications of diabetes. including kidney damage. The definition of acute hyperglycemia varies by study. In fasting adults. Temporary hyperglycemia is often benign and asymptomatic. whereas a consistent range below 70 mg/dl or 4 mmol/l is considered hypoglycemic. In general. 30 . neurological damage. Blood glucose levels can rise well above normal for significant periods without producing any permanent effects or symptoms.180 mg/dl = 10 mmol/l 270 mg/dl = 15 mmol/l 288 mg/dl = 16 mmol/l 360 mg/dl = 20 mmol/l 396 mg/dl = 22 mmol/l 594 mg/dl = 33 mmol/l Glucose levels vary before and after meals. the normal range for most people (fasting adults) is about 80 to 110 mg/dl or 4 to 6 mmol/l. the definition of "normal" varies among medical professionals. A subject with a consistent range above 126 mg/dl or 7 mmol/l is generally held to have hyperglycemia. However. cardiovascular damage. and at various times of day. blood plasma glucose should not exceed 126 mg/dl or 7 mmol/l. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply. damage to the retina etc. chronic hyperglycemia at levels more than slightly above normal can produce a very wide variety of serious complications over a period of years.

scrapes. Blurred vision 5. Dry or itchy skin 10.In diabetes mellitus (by far the most common cause of chronic hyperglycemia). Stupor 31 . Weight loss 7. with the first three comprising the classic hyperglycemic triad: 1. Polyphagia . 6. Dry mouth 9.frequent hunger. It is most often seen in persons who have uncontrolled insulin-dependent diabetes.frequent urination. especially pronounced hunger 2. Fatigue (sleepiness). groin rash.) 8. etc. Polydipsia . Tingling in feet or heels 11. Polyuria . Recurrent infections such as vaginal yeast infections. Cardiac arrhythmia 14. Impotence (male) 12. especially excessive thirst 3. treatment aims at maintaining blood glucose at a level as close to normal as possible. especially excessive urination 4. Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). or external ear infections (swimmer's ear) 13. in order to avoid these serious long-term complications.frequent thirst. Poor wound healing (cuts. The following symptoms may be associated with acute or chronic hyperglycemia.

depending on the type and state of the disease. Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus. hyperglycemia is the result. Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver). 32 . hyperglycemia is usually caused by low insulin levels (Diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (Diabetes mellitus type 2). but it makes the prescription of oral hypoglycemic medication difficult to manage. Intermittent hyperglycemia may be present in prediabetic states. With normal glucose levels. When the mechanisms fail in a way that allows glucose to rise to abnormal levels. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder. the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20-30 minutes. This hunger is not usually as pronounced as in Type I diabetes. especially the juvenile onset form. and in fact chronic hyperglycemia is the defining characteristic of the disease. and so glucose levels must be precisely maintained by the body's internal control mechanisms.Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. which in turn makes it difficult or impossible to remove excess glucose from the blood. The resulting drop in blood sugar level to below the normal range prompts a hunger response. producing osmotic diuresis. In diabetes mellitus. Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys (glycosuria). This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat.

amongst other things . such as a fasting plasma glucose. The amount of increase varies from person to person and from inflammatory response to response. When the body is stressed. protease inhibitors. pentamidine. epinephrine.[7] and some antipsychotic agents. random plasma glucose. however.Drugs Certain medications increase the risk of hyperglycemia. endogenous catecholamines are released that .Physical trauma. produces hypoglycemia. can also hyperglycemia. Physiological stress Hyperglycemia occurs naturally during times of infection and inflammation. thiazide diuretics.serve to raise the blood glucose levels. cause significant 33 . Human and animal studies suggest that this is not benign. Further testing. chronic use. no patient with first-time hyperglycemia should be diagnosed immediately with diabetes if that patient is concomitantly ill with something else. As such. surgery and many forms of severe stress can temporarily increase glucose levels. and that stressinduced hyperglycemia is associated with a high risk of mortality after both stroke and myocardial infarction. Some of the newer. must be performed.[9] Plasma glucose >120 mg/dl in the absence of diabetes is a clinical sign of sepsis. Critical illness A high proportion of patients suffering an acute stress such as stroke or myocardial infarction may develop hyperglycemia. even in the absence of a diagnosis of diabetes. or two-hour postprandial plasma glucose level. L-asparaginase. double action anti-depressants like Zyprexa. and Cymbalta.[8] The acute administration of stimulants such as amphetamine typically produces hyperglycemia. niacin. including beta blockers. corticosteroids.

Acute and severe hyperglycemia can be treated by direct administration of insulin in most cases.Treatment Treatment of hyperglycemia requires elimination of the underlying cause. the walls of the smaller blood vessels become so thick and weak that they bleed. In macroangiopathy. treatment of diabetes when diabetes is the cause. and slow the flow of blood through the body. fat and blood clots build up in the large blood vessels. develop microangiopathy and may cause blindness (so-called proliferative diabetic retinopathy). and capillaries). The best known and most prevalent angiopathy is the diabetic angiopathy. The decrease of blood flow through stenosis or clot formation impair the flow of oxygen to cells and biological tissues (called ischemia) and lead to their death (necrosis and gangrene. tissues which are very sensitive to oxygen levels. Thus. In microangiopathy. leak protein. a complication that may occur in chronic diabetes. stick to the vessel walls. and to kidney cells.. which in turn may require amputation). and block the flow of blood. Damage to nerve cells may cause peripheral neuropathy. Angiopathy Angiopathy is the generic term for a disease of the blood vessels (arteries. 34 .1 Classification There are two types of angiopathy: macroangiopathy and microangiopathy. 2.g. 2. such as the retina.5. under medical supervision. e.5. veins. diabetic nephropathy (Kimmelstiel-Wilson syndrome).

in spite of low insulin). 5.see diabetic nephropathy . leading to apoptosis. there is leaking of albumin and other proteins into fluid compartments. Pathophysiology Hyperglycemia resulting from diabetes mellitus does not result in a net increase in intracellular glucose in most cells. In diabetic retinopathy the end-result is often blindness due to irreversible retinal damage. It also the most common cause of amputation in the US. subsequently. chronic dysregulated blood glucose in this condition causes a marked toxicity toward those classes of vascular endothelium which passively assimilate glucose (i. as insulin is required for glucose uptake. pericyte death may result in reduced capillary integrity. The glomeruli of the kidneys are especially sensitive . However. a. While not exclusive. such as ischemic heart disease.Macroangiopathy.2 Diabetic Angiopathy Diabetic angiopathy is a form of angiopathy associated with diabetes mellitus. on the other hand. usually toes and feet.e. whose pathophysiologies are largely identical. may cause other complications. and almost always as a result of 35 . 2. stroke and peripheral vascular disease which contributes to the diabetic foot ulcers and the risk of amputation. notably the pericytes of various microvasculatures. b. Pericytes express enzymes which convert glucose into osmologically-active metabolites. often as a result of gangrene. Prognosis and Complications Diabetes mellitus is the most common cause of adult kidney failure worldwide. Over time. the term is generally an umbrella for the two most common forms: Diabetic retinopathy and Diabetic nephropathy.where protein leakage caused by late-stage angiopathy results in diagnostic proteinuria and eventually renal failure.

also associated with diabetes mellitus. Adaptive immunity is often sub-divided into two major types depending on how the immunity was introduced. Naturally acquired immunity occurs through contact with a disease causing agent. Other components of the immune system adapt themselves to each new disease encountered and are able to generate pathogen-specific immunity. or other unwanted biological invasion. Both naturally and artificially acquired immunity can be further subdivided depending on whether immunity is induced in the host or passively transferred from a immune host. The non-specific components act either as barriers or as eliminators of wide range of pathogens irrespective of antigenic specificity. It is often found on the shin. and is short lived -. Prognosis is generally poor for all forms of Diabetic angiopathy.usually lasting only a few months -whereas active immunity is induced in the host itself by antigen. There is also Neuropathy. and lasts much longer. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. Immunity involves both specific and non-specific components. as symptomatology is tied to the advancement of the underlying pathology i.e. disease. "Diabetic dermopathy" is a manifestation of diabetic angiopathy. type 1 and 2. 36 . sometimes life-long. 2. Passive immunity is acquired through transfer of antibodies or activated T-cells from an immune host.peripheral vascular disease. the early-stage patient displays either non-specific symptoms or none at all.6. when the contact was not deliberate. The diagram below summarizes these divisions of immunity. whereas artificially acquired immunity develops only through deliberate actions such as vaccination. Immunity Immunity is a biological term that describes a state of having sufficient biological defenses to avoid infection.

cell mediated immunity is active when the organisms¶ own T-cells are stimulated and passive when T cells come from another organism. when high levels of human (or horse) antibodies specific for a pathogen or toxin are transferred to nonimmune individuals. in the form of readymade antibodies.[8] a. Naturally acquired passive immunity Maternal passive immunity is a type of naturally acquired passive immunity.[9] IgG is the only antibody isotype that can pass through the placenta. Similarly. 2. and refers to antibody-mediated immunity conveyed to a fetus by its mother during pregnancy. or to reduce the symptoms of ongoing or immunosuppressive diseases. but the body does not develop memory.A further subdivision of adaptive immunity is characterized by the cells involved.[7] Passive immunity provides immediate protection.[9] Passive immunity is also provided through the transfer of IgA antibodies found in breast milk that are transferred to the 37 . whereas the protection provided by cell mediated immunity involves T-lymphocytes alone. This occurs around the third month of gestation. Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response. humoral immunity is the aspect of immunity that is mediated by secreted antibodies. Humoral immunity is active when the organism generates its own antibodies. therefore the patient is at risk of being infected by the same pathogen later. when maternal antibodies are transferred to the fetus through the placenta. Maternal antibodies (MatAb) are passed through the placenta to the fetus by an FcRn receptor on placental cells. and can also be induced artificially. Passive immunity can occur naturally. from one individual to another.1 Passive immunity Passive immunity is the transfer of active immunity.6. and passive when antibodies are transferred between individuals.

[7] Immunity derived from passive immunization lasts for only a short period of time. as human or animal blood plasma. Passive transfer is used prophylactically in the case of immunodeficiency diseases. such as hypogammaglobulinemia.[7] It has. and to treat poisoning. until the newborn can synthesize its own antibodies. In unmatched donors this type of transfer carries severe risks of graft versus host disease. and serum sickness. which can be administered in several forms. and prior to the advent of antibiotics. been used to treat certain diseases including some types of cancer and immunodeficiency.[10] c. Passive transfer of cell-mediated immunity Passive or "adoptive transfer" of cell-mediated immunity. and there is also a potential risk for hypersensitivity reactions. even after sulfonamide antibiotics were introduced.[8] b.gut of the infant. Artificially acquired passive immunity Artificially acquired passive immunity is a short-term immunization induced by the transfer of antibodies. as pooled human immunoglobulin for intravenous (IVIG) or intramuscular (IG) use. however.[8] The artificial induction of passive immunity has been used for over a century to treat infectious disease. protecting against bacterial infections. Immunoglobulin therapy continued to be a first line therapy in the treatment of severe respiratory diseases until the 1930¶s. This type of transfer differs from a bone marrow 38 . which are often difficult to find. is conferred by the transfer of "sensitized" or activated T-cells from one individual into another. It is rarely used in humans because it requires histocompatible (matched) donors. and in the form of monoclonal antibodies (MAb).[10] It is also used in the treatment of several types of acute infection. was often the only specific treatment for certain infections. especially from gamma globulin of non-human origin.

reinfection at later time points leads to a rapid increase in antibody production and effector T cell activity. This type of immunity is both active and adaptive because the body's immune system prepares itself for future challenges. and are able to mount a strong response if the pathogen is detected again. in which (undifferentiated) hematopoietic stem cells are transferred. These later infections can be mild or even inapparent.cells develop.transplant. Active immunity often involves both the cell-mediated and humoral aspects of immunity as well as input from the innate immune system. 2.6. Due to the formation of immunological memory. Throughout the lifetime of an animal these memory cells will ³remember´ each specific pathogen encountered. memory B-cells and T. Due to the formation of immunological memory.2. The time course of an immune response. These later infections can be mild or even inapparent. The innate system is present from birth and protects an individual from 39 . When B cells and T cells are activated by a pathogen. Active immunity Picture 2. The time course of an immune response. reinfection at later time points leads to a rapid increase in antibody production and effector T cell activity.

attenuated vaccines are composed of micro-organisms that have been cultivated under conditions which disable their ability to induce disease. whereas adaptive immunity arises only after an infection or immunization and hence is "acquired" during life. bubonic plague. These responses are more durable and do not generally require booster shots. measles. and develops a primary immune response. Artificially acquired active immunity Artificially acquired active immunity can be induced by a vaccine. b. There are four types of traditional vaccines: y Inactivated vaccines are composed of micro-organisms that have been killed with chemicals and/or heat and are no longer infectious.[7] The term vaccination was coined by Edward Jenner and adapted by Louis Pasteur for his pioneering work in vaccination. a substance that contains antigen. cholera. used prior 40 . Most vaccines of this type are likely to require booster shots. Many disorders of immune system function can affect the formation of active immunity such as immunodeficiency (both acquired and congenital forms) and immunosuppression. and mumps. Examples are vaccines against flu. The method Pasteur used entailed treating the infectious agents for those diseases so they lost the ability to cause serious disease. y Live. which Pasteur's work built upon. and hepatitis A. rubella. Pasteur adopted the name vaccine as a generic term in honor of Jenner's discovery.pathogens regardless of experiences. Naturally acquired active immunity Naturally acquired active immunity occurs when a person is exposed to a live pathogen. A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.[7] This type of immunity is ³natural´ because it is not induced by deliberate exposure. which leads to immunological memory. Examples include yellow fever. a. y Toxoids are inactivated toxic compounds from micro-organisms in cases where these (rather than the micro-organism itself) cause illness.

ligament and skin. In muscle tissue it serves as a major component of endomysium. especially in the flesh and connective tissues of mammals. y Subunit -vaccines are composed of small fragments of disease causing organisms. In nature. the gut. bone.[3] Gelatin. Collagen.to an encounter with the toxin of the micro-organism. It is approximately 300 nm long and 1. tendinous muscles.7. and accounts for 6% of the weight of strong. is mostly found in fibrous tissues such as tendon.[1] It is the main component of connective tissue. and is also abundant in cornea.7. and is the most abundant protein in mammals. and intervertebral disc.[2] making up about 25% to 35% of the wholebody protein content. Collagen constitutes 1% to 2% of muscle tissue. which is used in food and industry. each possessing the conformation of a left-handed helix (its name is 41 .5 nm in diameter. 2. blood vessels. A characteristic example is the subunit vaccine against Hepatitis B virus. is collagen that has been irreversibly hydrolyzed.1 Molecular Structure The tropocollagen or "collagen molecule" is a subunit of larger collagen aggregates such as fibrils. 2. Collagen Collagen is a group of naturally occurring proteins. Most vaccines are given by hypodermic injection as they are not absorbed reliably through the gut. Live attenuated Polio and some Typhoid and Cholera vaccines are given orally in order to produce immunity based in the bowel. cartilage. Examples of toxoidbased vaccines include tetanus and diphtheria. made up of three polypeptide strands (called alpha chains). in the form of elongated fibrils. it is found exclusively in animals.

With type I collagen and possibly all fibrillar collagens if not all collagens. each triple-helix associates into a right-handed super-super-coil that is referred to as the collagen microfibril. Each microfibril is interdigitated with its neighboring microfibrils to a degree that might suggest that they are individually unstable although within collagen fibrils they are so well ordered as to be crystalline. The relatively high content of proline and hydroxyproline rings. With glycine accounting for the 1/3 of the sequence. tissue regulation and infrastructure. inert methyl group. many sections of its non-proline rich regions have cell or matrix association / regulation roles. a right-handed structure). cell adhesion. and alanine (Ala). A distinctive feature of collagen is the regular arrangement of amino acids in each of the three chains of these collagen subunits. Chemically-reactive side groups are not needed in structural proteins as they are in enzymes and transport proteins. where X may be any of various other amino acid residues. Proline or hydroxyproline constitute about 1/6 of the total sequence. accounts 42 .with 10% serine. such as silk fibroin. however collagen is not quite just a structural protein. a triple helix or "super helix". this means that approximately half of the collagen sequence is not glycine. a fact often missed due to the distraction of the unusual GX1X2 character of collagen alpha-peptides. Due to its key role in the determination of cell phenotype.not to be confused with the commonly occurring alpha helix. with their geometrically constrained carboxyl and (secondary) amino groups. whose side group is a small. Such high glycine and regular repetitions are never found in globular proteins save for very short sections of their sequence. proline. along with the rich abundance of glycine. About 75-80% of silk is (approximately) -GlyAla-Gly-Ala. These three left-handed helices are twisted together into a righthanded coiled coil. proline or hydroxyproline. The sequence often follows the pattern Gly-Pro-X or Gly-X-Hyp. a cooperative quaternary structure stabilized by numerous hydrogen bonds. This kind of regular repetition and high glycine content is found in only a few other fibrous proteins. and elastin is rich in glycine.

These two amino acids help stabilize the triple helix²Hyp even more so than Pro. In collagen. it plays a unique role in fibrous structural proteins. For the same reason. Therefore in each D-period repeat of the microfibril.for the tendency of the individual polypeptide strands to form left-handed helices spontaneously.2 Fibriliar Structure The tropocollagen subunits spontaneously self-assemble. There is some covalent crosslinking within the triple helices. Larger fibrillar bundles are formed with the aid of several different classes of proteins (including different collagen types).7. Each D-period contains 4 and a fraction collagen molecules. and a variable amount of covalent crosslinking between tropocollagen helices forming well organized aggregates (such as fibrils). there is a part containing five molecules in cross-section²called the ³overlap´ and a part containing only 4 molecules. the rings of the Pro and Hyp must point outward. glycoproteins and proteoglycans to form the 43 . Gly is required at every third position because the assembly of the triple helix puts this residue at the interior (axis) of the helix. This is because 300 nm divided by 67 nm does not give an integer (the length of the collagen molecule divided by the stagger distance D). in both the gap and overlap regions. where there is no space for a larger side group than glycine¶s single hydrogen atom. without any intrachain hydrogen bonding. Because glycine is the smallest amino acid with no side chain. The triple-helices are also arranged in a hexagonal or quasi-hexagonal array in cross-section. whose body temperatures are lower than most warm-blooded animals. the molecules are staggered from each other by about 67 nm (a unit that is referred to as µD¶ and changes depending upon the hydration state of the aggregate).[22][23] In the fibrillar collagens. into even larger arrays in the extracellular spaces of tissues. with regularly staggered ends. 2. a lower concentration of them is required in animals such as fish. called the "gap".

Type I collagen gives bone its tensile strength. 2. however. hard. y Collagen One: skin. Collagen fibrils are semicrystalline aggregates of collagen molecules.different types of mature tissues from alternate combinations of the same key players.7. ligature. which is (approximately) hydroxyapatite. 29 types of collagen have been identified and described. is of type I.4 Types and associated disorders Collagen occurs in many places throughout the body.[23] Collagen's insolubility was a barrier to the study of monomeric collagen until it was found that tropocollagen from young animals can be extracted because it is not yet fully crosslinked. So far. III. and changed in development and disease. bone (main component of bone) y Collagen Two: cartilage (main component of cartilage) 44 . However. Forty nm gaps between the ends of the tropocollagen subunits (approximately equal to the gap region) probably serve as nucleation sites for the deposition of long. staggered array. Collagen fibers are bundles of fibrils. advances in microscopy techniques electron microscopy (EM) and atomic force microscopy (AFM)) and X-ray diffraction have enabled researchers to obtain increasingly detailed images of collagen structure in situ. and how tissues are constructed in growth and repair. organs. Collagen fibrils/aggregates are arranged in different combinations and concentrations in various tissues to provide varying tissue properties. In bone. Over 90% of the collagen in the body. and IV. II. fine crystals of the mineral component. tendon. vascular. entire collagen triple helices lie in a parallel. It is in this way that certain kinds of cartilage turn into bone. These later advances are particularly important to better understanding the way in which collagen structure affects cell-cell and cell-matrix communication. Ca10(PO4)6(OH)2 with some phosphate.

which is used in many foods. This process describes the formation of gelatin. ligaments. hair and placenta Collagen-related diseases most commonly arise from genetic defects or nutritional deficiencies that affect the biosynthesis.y Collagen Three: reticulate (main component of reticular fibers). commonly found alongside type I.7. Besides food. and photography 45 . assembly. the three tropocollagen strands separate partially or completely into globular domains. it can be advantageously used for its satiating power a. It strengthens blood vessels and plays a role in tissue development. Tough bundles of collagen called collagen fibers are a major component of the extracellular matrix that supports most tissues and gives cells structure from the outside. It is also used in cosmetic surgery and burns surgery. secretion. It is present in the cornea and lens of the eye in crystalline form. Industrial uses If collagen is sufficiently denatured. e. by heating. e. containing a different secondary structure to the normal collagen polyproline II (PPII). Collagen has great tensile strength. fibrous structural proteins whose functions are quite different from those of globular proteins such as enzymes. but collagen is also found inside certain cells. postranslational modification. or other processes involved in normal collagen production. Hydrolyzed collagen can play an important role in weight management.g. y y Collagen Four: forms bases of cell basement membrane Collagen Five: cells surfaces. it is responsible for skin strength and elasticity.5 Use of Collagen Collagen is one of the long. and its degradation leads to wrinkles that accompany ageing. random coils. including flavored gelatin desserts.[30][31] Along with soft keratin. 2.g. bone and skin. as a protein. cosmetic. cartilage. tendons. and is the main component of fascia. gelatin has been used in pharmaceutical.

Collagen adhesive was used by Egyptians about 4. not that they are partially structured). mainstream scientific research has not shown strong evidence to support these claims.[34] 46 .000 years old. The oldest glue in the world. which are permanent. the word collagen means "glue producer" and refers to the early process of boiling the skin and sinews of horses and other animals to obtain glue. However. carbon-dated as more than 8. and to hold utensils together. synthetic plastic adhesives. including leather.000 years ago. softening again upon reheating. Manufacturers of collagen-based dietary supplements claim that their products can improve skin and fingernail quality as well as joint health.) rather than just a protein deficiency. Animal sinews and skins.500 years ago. and Native Americans used it in bows about 1. kolla. was found to be collagen²used as a protective lining on rope baskets and embroidered fabrics. arthritis etc.[32] From a nutritional point of view. dry skin. which may have to be reopened for repairs²an application incompatible with tough. also in crisscross decorations on human skulls. collagen and gelatin are a poor-quality sole source of protein since they do not contain all the essential amino acids in the proportions that the human body requires²they are not 'complete proteins' (as defined by food science.industries. have been used to make useful articles for millennia. From the Greek for glue. but survived due to the dry conditions. and so they are still used in making musical instruments such as fine violins and guitars.[33] Collagen normally converts to gelatin. Animal glues are thermoplastic.[citation needed] Individuals with problems in these areas are more likely to be suffering from some other underlying condition (such as normal aging. Gelatin-resorcinol-formaldehyde glue (and with formaldehyde replaced by less-toxic pentanedial and ethanedial) has been used to repair experimental incisions in rabbit lungs.

Medical uses The cardiac valve rings. and even human. sources and are 47 . when used cosmetically.b. These collagens may be derived from bovine. hyaluronic acid or polyacrylamide gel are readily available. 3. Some points of interest are: 1. Most manufacturers use donor animals from either "closed herds". Calcium deposition within collagen occurs as a natural consequence of aging. Individual valvular leaflets are arguably held in shape by collagen under great extremes of pressure. the central body and the cardiac skeleton of the heart summarily represent a unique and moving collagen anchor to the fluid mechanics of the heart. equine or porcine. Collagen has been widely used in cosmetic surgery. 4. or from countries which have never had a reported case of BSE such as Australia. These fixed points in an otherwise moving display of blood and muscle enable current cardiac imaging technology to arrive at ratios essentially stating blood in cardiac input and blood out cardiac output. porcine (pig) tissue is also widely used for producing collagen sheet for a variety of surgical purposes. this can be virtually eliminated by simple and inconspicuous patch testing prior to cosmetic use. there is a chance of allergic reactions causing prolonged redness. and 2. as a healing aid for burn patients for reconstruction of bone and a wide variety of dental. Collagens are widely employed in the construction of artificial skin substitutes used in the management of severe burns. most medical collagen is derived from young beef cattle (bovine) from certified BSE (Bovine spongiform encephalopathy) free animals. Specified imaging such as calcium scoring illustrates the utility of this methodology. however. orthopedic and surgical purposes. especially in an aging patient subject to pathology of the collagen underpinning. alternatives using the patient's own fat. Brazil and New Zealand.

except through the effect of individual amino acid supplementation.sometimes used in combination with silicones.3. growth factors and other substances. mutans.mutans are gram positive. studying cell behavior and cellular interactions with the extracellular environment. Suppliers such as Trevigen manufacture rat and bovine Collagen I and mouse Collagen IV. Although it cannot be absorbed through the skin.107 CFU/ml (colony forming units). mutans to the acquired pellicle. derived from donor cadavers. mutans are more aciduric than other streptococci and be cultured in a media at a pH as low as 4.8. mutans have specific receptor sites known as adhesins on its cell surface that attach to acquired enamel pellicle through adhesion promoting proteins found in saliva that help to facilitate the adhesion of S. placentas and aborted fetuses. glycosaminoglycans. S. fibroblasts. Although expensive. mutans range from undetectable to 106 . there is no reason for orally ingested collagen to affect connective tissue in the body. Human salivary concentrations of S.[36] Collagen is also frequently used in scientific research applications for cell culture.[35] Because proteins are broken down into amino acids before absorption. 48 . Strepptococcus Mutans Clark in 1924 isolated this particular streptococcus and named it as S. may minimize the possibility of immune reactions. It synthesizes insoluble polysaccharide from sucrose that is regarded as an important characteristic contributing to the caries inducing properties of S. Recently an alternative to animal-derived collagen has become available. collagen is now being used as a main ingredient for some cosmetic makeup. non-motile. catalase-negative cocci. mutans due to its varying morphological nature. this human collagen. Collagen is also sold commercially as a joint mobility supplement. S. S. 2. These can colonize on tooth surfaces and dentures.

fusobacterium. mutans have an efficient rapid metabolism of sugars to lactic and other organic acids. ‡ S. ‡ S. S. ‡ The samples can be isolated from tooth surfaces before the development of caries. Plaque Dental plaque can be defined as a diverse community of micro-organisms found on the tooth surface as a biofilm. mutans produces intracellular polysaccharide which acts as a food reservoir during low concentration of dietary carbohydrates. eubacterium and gram negative bacteria like neisseria. Human serotypes are limited to three namely c. mutans. The complex and diverse oral microflora consists of a wide range of species of bacteria. mutans have the ability to transport sugars rapidly in competition with other plaque bacteria even at low pH. 2. porphyromonas. mycoplasmas and yeasts. spirochaetes that are found in the oral 49 . mutans have the ability to initiate and maintain microbial growth. staphylococcus. mutans are acidogenic and aciduric in nature. lactobacillus. These can be cultured in blood agar and can be seen as alpha hemolytic cocci in chains. prevotella. viruses. e and f. ‡ S.Currently seven distinct species of human and animal mutans streptococcus and eight serotypes (a-h) are recognized based on the antigenic specificity of cell wall carbohydrates. actinomyces. veillonella. Listed below are properties related to cariogenicity of S. metabolism and acid production in sites with a low pH. ‡ The samples produce water soluble and insoluble extracellular polysaccharide from sucrose which helps in the colonization of tooth surfaces by consolidating microbial attachment.9. Various groups of gram positive bacteria such as streptococcus. ‡ S. ‡ The samples can attain the critical pH for enamel demineralization more rapidly than other common plaque bacteria. embedded in an extracellular matrix of polymers of host and microbial origin.

they have different effect on the gingiva. dye probes for specific compounds combined with 50 . 1973). protein breakdown product such as hydrogen sulphide. such as incubation with isotopically-labelled substrates. rapid bacterial growth and remodeling phase. and protein breakdown product. endotoxins. This organized mass of bacteria is glued to the tooth surface near and under the gingival margin. The substances that leak through seem to be the endotoxins and protein breakdown products. As it extend into the sulcus. or (iii) metagenomic analysis of a certain body region. (ii) quantification of micro-organisms that are thought to mediate a certain process. The most important products of microcosm are enzymes. Since these products differ. Established methods of microbial ecology that allow the direct measurement of metabolic conversions in natural microbial samples from humans under different experimental conditions. it is easy to understand the effect it has on the gingival tissues. 1970. The formation of plaque can be divided into three stages namely initial colonization. When we consider plaque as a small world of microorganisms. indole and skatole are most irritating and are capable of setting up the type of inflammatory reaction we seen gingivitis and periodontitis (Frostell. Recent studies have shown that the possibility exists that the endotoxins are capable of establishing an inflammatory reaction within the gingiva on an immunologic or allergic basis (Ranney and Zander. 1969) The human body is naturally colonised by a diverse array of micro-organisms whose metabolic activity is important for human physiology and health. they act on the sulcular lining to loosen the epithelial cells. Horton.cavity including the dental plaque. The mucopolysaccharide substance between the cells tends to break down and ³leakage´ occurs from the crevice into the underlying connective tissue. many of products of microcosm are in intimate contact with the sulcural epithelial lining. a microcosm. There is evidence that as the enzymes are produced by bacteria. Bacterial plaque seem to be most consistent one factor in the etiology of gingivitis and periodontitis. On the other hand. Most studies that assess the functional potentials and controls of these complex communities rely on: (i) the characterisation of individual isolates or enrichments.

because dietary NO3. Denitrification is performed by facultative anaerobic micro-organisms and is coupled to the oxidation of reduced organic carbon or reduced inorganic compounds.in saliva.in addition to NO3. even though NO3.can be converted by oral micro-organisms to NO2-.co-occur in significant concentrations with micro-organisms in various body regions. the human-associated microbial biofilm community of dental plaque and bacteria that cover other oral surfaces are exposed to NO3-. Experiments with rat tongues as well as tooth and other surfaces in the human mouth have shown that salivary NO3. denitrification (the respiratory reduction of nitrate (NO3-) or nitrite (NO2-) via nitric oxide (NO) to nitrous oxide (N2O) or dinitrogen (N2) is believed to be insignificant in humanassociated microbial communities.> NO2. Thus. including fermentation. Detection of NO in air incubated in the human mouth has led to the hypothesis that bacterially-derived salivary NO2. The underlying processes have 51 . Surprisingly. Notably. qnorB or cnorB for NO reductases. The reductive sequence (NO3.> NO > N2O > N2) of denitrification is mediated by periplasmic and membranebound enzymes specific for each step. and nosZ for N2O reductase. nitrogen cycling biofilms and ingested bacteria within different invertebrates guts. sulfate reduction. such as the human oral cavity. However. are rarely reported. nirS and nirK for NO2. hydrogen sulfide or hydrogen.microscopy or electrochemical microsensors. investigations of plaque metabolism have focused on aerobic respiration and acid fermentation of carbohydrates. different microbial pathways. human saliva contains NO3.reductase.concentrations in the millimolar range. The most important genes for the detection of denitrification in complex microbial samples are narG for NO3.is concentrated in salivary glands after it is absorbed from the intestine into the blood. explaining the presence of NO2. methanogenesis and acetogenesis. such as soils.is chemically reduced to NO in acidic microenvironments in the oral cavity.reductases. Denitrifying bacteria release NO or N2O as intermediates during metabolic activity in pure culture and in complex microbial communities. However.and NO2 . such as ferrous iron. have been proposed to occur in humans.

NO. including a recently developed NO microsensor. periodontal diseases might be especially affected by nitrogen metabolism of dental plaque. which induce production of high. Bacterial lipopolysaccharides stimulate production of proinflammatory cytokines.is absorbed into plasma. cytotoxic NO concentrations by certain immune system cells. at low concentrations.in human saliva a stable oxidation product of NO synthase-derived NO that is produced by gingival cells to regulate the gum immune and vascular systems. driving the biological conversion of salivary NO3. oral nitrogen metabolism is important for human physiology. acting as an antimicrobial agent against pathogenic bacteria and stimulating gastric blood flow. Moreover. It is still unclear whether microbial nitrogen metabolism in human dental plaque is significant in comparison to other oral surfaces. The formation of NO2 . but not well understood role in periodontal diseases. to demonstrate in situ NO formation during denitrification in dental 52 . Therefore. NO2. Furthermore. where it serves as a NO source for the regulation of vasodilatation under hypoxic conditions.to NO in the acidic stomach. is an important signalling molecule that coordinates functions of immune system cells that are involved in inflammatory processes. we hypothesise that dental plaque represents a habitat for microbial denitrification in humans.as a denitrification intermediate by oral micro-organisms leads to chemical conversion of NO2. In the present study. Due to the possible formation of NO. and to the final product N2. We use direct microbial ecology methods. high NO levels during inflammation induce expression of matrix metalloproteinases in neutrophiles.never been directly demonstrated because NO could not be measured in dental biofilms over relevant spatial scales. plaque nitrogen metabolism might be important to dental health. other investigators considered NO2. Besides its potential importance to dental health. NO plays a complex.to the denitrification intermediates NO and N2O. affecting almost every human being. which mediate soft tissue degradation. if NO is generated as a side product at the gum-plaque interface. As an inflammatory disorder of gum tissue surrounding the teeth. Dental plaque causes periodontal diseases and dental caries.

plaque and to show that NO is formed at concentrations that are significant for signalling to host tissue. 53 . exposing the root surfaces and increasing sensitivity to heat and cold. a sticky. Periodontitis and all periodontal diseases are bacterial infections that destroy the attachment fibers and supporting bone that hold the teeth in the mouth. More significant. Inflammation or infection of the gums is called gingivitis. 2. however. Teeth may even loosen because of bone destruction. microorganisms are always present in human supragingival and subgingival calculus. colorless film that constantly forms on teeth.11.concentrations and to the presence of plaque. we aim to show the in vivo significance of plaque denitrification for the formation of denitrification intermediates by correlating the oral accumulation of N2O in humans to salivary NO3-/NO2. are the bacteria that form part of the matrix and surround the calcified surface. Left untreated. While it has been shown that bacteria are not essential to calculus formation (Baer ad Newton. including the gingiva. Because of the hard. 2. gingivitis can turn into periodontitis. calculus irritates the gingival tissues by physical irritations. As that happens. Calculus Calculus is closely related to bacterial plaque in as much as the plaque is the matrix in which the calcium and phosphorus salt are deposited. The main cause of periodontal disease is a bacterial plaque. If allowed to progress.10. periodontal ligament and alveolar bone. Calculus is interesting in that it is both a mechanical and a bacterial irritant. In addition. The irritation an etiologic agent in periodontal disease. the gums may recede. these diseases can lead to tooth loss. the invasion and destruction of the underlying bone that anchors the teeth in place. Peridontitis Periodontitis could be defined as a disorder of supporting structures of teeth. crusty surface. 1960).

and periodontitis are most commonly used. the more damage they can do. Unfortunately. usually within 24 hours.These conditions can arise for a variety of reasons. Initially. brushing and flossing can't eliminate tartar ² only a professional cleaning can remove it. Although you remove plaque every time you brush your teeth. spongy gums. A severe deficiency of vitamin C can lead to scurvy and result in bleeding. But as the terms periodontal disease. a white substance that makes plaque more difficult to remove and that acts as a reservoir for bacteria. it re-forms quickly. the mildest form of periodontal disease. In time. Periodontitis begins with plaque. But ongoing inflammation eventually causes pockets to develop between your gums and teeth that fill with plaque. the part of your gum around the base of your teeth. sticky film forms on your teeth when starches and sugars in food interact with bacteria normally found in your mouth. This invisible. This is gingivitis. The longer plaque and tartar remain on your teeth. the pockets become deeper and more bacteria accumulate. and eventual tooth loss. The warning signs of gum disease include : 54 . If too much bone is destroyed. And at least one periodontal disease . tartar and bacteria. eventually advancing under your gum tissue.is thought to have a strong genetic basis. Plaque that stays on your teeth longer than two or three days can harden under your gumline into tartar (calculus). gingivitis. they refer to disease that is caused by the build up of dental plaque. they may simply irritate and inflame the gingiva. These deep infections cause a loss of tissue and bone.the uncommon but highly destructive juvenile periodontitis . you may lose one or more teeth.

Some infections also develop when pulp is left behind during a root canal. Most people notice a swelling in the gum at the site of the infection. debridement and curettage. it leaves room for bacteria to proliferate in various parts of the mouth. Some people also notice that their teeth become more sensitive to hot and cold foods as the infection evolves. Dental sores are usually caused by an infection that gets started within a tooth. the chamber containing the dental pulp is called the pulp chamber. 2. If a tract develops. swollen or tender gums gums that have pulled away from the teeth persistent bad breath pus between the teeth and gums loose or separating teeth a change in the way your teeth fit together when you bite a change in the fit of partial dentures 2. food particles can get into the tooth and act as a hosting ground for bacteria. facial tissue. which develops from the connective tissue of the dental papilla. Wound abscesses do not generally need to be treated with antibiotics. and throat. but they will require surgical intervention.y y y y y y y y bleeding gums during tooth brushing red. No matter how you look at it. they can also develop in the jaw bones.2 Pulp The dental pulp is the soft tissue of the tooth. when teeth are not cleaned and taken care of properly. The pulp contains blood 55 . pain and irritation as the abscess becomes larger. For example. The vast majority of dental infections are caused by poor dental hygiene.11.1 Abscess A dental abscess or sore is a bacterial infection that develops in the mouth. pus may start to drain from it. if you have a cracked or chipped tooth. While most dental abscesses develop in the gums.11. Within the crown.

holding them in place and protecting the jaw and teeth roots from infections. 2. the gingiva also create a seal which prevents bacteria. The base of this tissue is firmly anchored to the bone. This connective tissue has a strong fibrous underlayer. Within the root is the radicular pulp. The gingiva are very tough. Gingivitis can lead to complications 56 . the condition is known as gingivitis. covered in a layer of mucous membranes. and caring for them is critical to maintaining oral health. while the upper portion is free. where it could cause trauma or infection. plaque. When a patient's gingiva become chronically inflamed. The coronal pulp is within the crown. the gingiva are a very important part of the oral anatomy. Patients may find that their gums are very tender after brushing their teeth.11. and other foreign material from entering the roots of the teeth. along with swelling and bleeding.vessels and nerves that enter through the apical foramen. In addition to anchoring the teeth. Known informally as the gums. or that the gums bleed freely after oral care or eating. Classic symptoms of gingivitis can include changes in the color of the gingiva. allowing the gingiva to run between the teeth to help stabilize them and keep them in place.3 Gingiva Gingiva is tough connective tissue which lines the base of the teeth. designed to resist trauma from chewing and hard foods which enter the mouth.

Other gingival diseases can include gingival cancer. Sometimes gum recession is caused by gingivitis. Over time. the gingiva can recede. or occur on its own. 57 . in which the gums grow grossly enlarged.which include serious infections. Receding gums are a cause for concern because they can expose a patient to the risk of infections and destabilize the teeth. but it can also be associated with other oral problems. and gingival hyperplasia. in which the cells in the gums become malignant. and it is an issue which needs to be addressed.

58 .

hidroksipatit and others. Therefore. Human eat food that contain carbohydrate. its existence in the mouth is according from environment balance. It is common case is the shift of adjacent tooth and antagonist teeth towards the empty room that revocation. Principle. one liter of salivary flow in the mouth. salivary and plaque so that there is no mineral disappear from tooth tissues.2 Local factor 4. Every day. The stability of enamel is affected by pH and salivary composition. Usually. there is a stability between environment and tooth. Enamel at long time will be dissolved by salivary against is not solid with calcium and phosphate.1 Local factor and systemic factor of mobile tooth Sometimes when there are mobile teeth. There is two kinds of carbohydrate. It can be dissolves in water.1 Periodontitis Periodontal tissues can change because of environment influence.CHAPTER 4 DISCUSSION 4. but without tooth replacement.2. Slowly teeth will adapt to form a new composition. that is polysaccharide. the incomplete teeth in a jaw is usually not used to chew. and disaccharide. how to chew will be changed. then it¶s extracted. In addition. the result will occur caries that cause periodontitis. Polysaccharide will be changed 59 . some people are reluctant to make dentures. Enamel is consist of mineral like Ca10(PO4)6-(OH)2. because they consider the manufacture of false teeth to fill the room used the revocation is not important. monosaccharide. 4.

Monosaccharide and disaccharide will be ferment by dental plaque and the effect is the condition of the mouth will be in acid. saliva derived glycoprotein deposits start to cover the tooth surface with what is referred to as "pellicle". such as Porphyromonas gingivalis. While the dental plaque formation continues Gram-negative species become dominant over the Gram-positive species. and oral spirochetes (Treponema species). and Actinomyces viscosus becoming what is known as dental plaque. new Gram-negative species may be found. PH become 5.to monosaccharide and disaccharide. Some minutes after brushing your teeth. Bacteria cells interact with pellicle components enabling plaque to firmly adhere to the tooth surface. Campylobacter rectus. also because buffer capacity of salivary is not fulfill. The formation of pellicle is the first step in dental plaque formation. The result of decreasing is enamel under plaque become demineralization because builder material of enamel dissolve. One week after the first plaque accumulation. Substances produced by the already accumulated bacteria enrich the plaque environment making it favourable for the growth of other species of bacteria. Prevotella intermedia. The pellicle is then colonized by Gram-positive bacteria such as Streptococcus sanguis. Streptococcus mutants. Actinobacillus actinomycetemcomitans. The overgrowth of Gram-negative anaerobic bacteria is considered as pathogenic plaque As the result of acid formation by bacteria in plaque. and Capnocytophaga. Actually Dental plaque formation starts almost immediately after tooth brushing. Eikenella corrodens. These new species include also Gram-negative bacteria such as Fusobacterium nucleatum.5 at the limit surface of enamel and plaque. After 1 to 3 days following the initiation of plaque formation: the first bacteria colonies start to multiply and expand and new bacteria species start to colonize the tooth plaque. 60 .

Along with increasing PH. The effect is there is no prop tissues and the tooth become loose. Calculus usually found in proximal part of the teeth. ligament tissues will be damaged. At the middle phase. During a day. then pore in enamel will be expanding. This makes the attachment of the subgingiva calculus more tenacious and difficult to remove. because calcium and phosphate is dissolved from enamel. liquid will be disappear and also enamel translucent character. The sediment is called Calculus. Because more calculus enter and cling into ligament tissues. there will be formed sediment of calcium and phosphate from enamel. keep enamel translucent character. will be develop white spot. More acid release happened in the mouth. because liquid in small pore. new white spot is seen as clinical after dried by air sprayer. Gingival will be drop off. white spot can be seen without help. A more irregular subgingival cemental surface allows deposits to form into the cemental irregularities. tea. It also tends to be darker or black in color. 61 . and calculus will enter around ligament tissues. The shape of white spot is fit with the shape of plaque. Calculus cumulation causes gingival open widely. both types occur together. This is called caries.etc) and appear dark brown or black. tobacco. All calculus can however absorb extrinsic stains (coffee. Furthermore. So in the part that is not clean. Supra-gingival calculus is adherent to the teeth and Subgingival calculus forms on root surfaces below the gingival margin and can extend deep into periodontal pockets. Because the way of drainage. more calculus cumulation on sideline of teeth.At early phase. PH will be decrease under crisis value 5.5 and at last PH become neutral. there will be acid release. Every time plaque is supplied by sugar. Often. A. Calculus Calculus is classified by location into supra-gingival and sub-gingival calculus.

they produce lactic acid. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. Periodontitis involves loss of bone. In dentin from the deepest layer to the enamel. alveolar bone. In the pulp. and cementum. Abscess causes gingival diseases named periodontitis. Pulp will be infected. Periodontitis is an inflammation of the gingival unit (gingival and alveolar mucosa) and extends to the periodontal ligament. If caries is not treated. the zone of destruction. The translucent zone represents the advancing front of the carious process and is where the initial demineralization begins. caries will spread until the pulp.B. and the zone of bacterial penetration. As the bacteria consume the sugar and use it for their own energy. Abscess or fistula (the road from the pus) can form in soft connective tissue. 62 . Caries Enamel is a highly mineralized acellular tissue. The effects of this process include the demineralization of crystals in the enamel. and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. caused by acids. over time until the bacteria physically penetrate the dentin. the distinct areas affected by caries are the translucent zone. there is tooth nerve and blood tube.

3. Gingivitis is an inflammatory process affecting the soft tissues surrounding the teeth. polyphagia. As the periodontal disease progresses.1 Diabetes Mellitus Diabetes mellitus is a metabolic disorder with characteristic hyperglycemia. In a state of uncontrolled hyperglycemia is characterized by polyuria.3 Systemic factor 4.Periodontitis causes inflammantion in gingival and make ligament periodontal tissues apart from alveolar bone. In diabetes mellitus can occur a number of complications caused by high blood glucose levels (hyperglycemia). the tooth will eventually be lost. Bacterial toxins and the body's enzymes fighting the infection start to break down the bone and connective tissue that hold teeth in place. with the consequent increase in the amount of glycated IgG. The glycosylation state of hyperglycemia and experience will reduce 63 . the pockets deepen and more gingival tissue and alveolar bone are destroyed. Ultimately all the supporting structures of the tooth may be lost. This divorce make a small space known as periodontal pocket. if periodontitis is left untreated. polydipsia. Some protein bodies in diabetes mellitus with hyperglycemia will have glycosylation. But the inflammatory does¶t extend into the alveolar bone. The tooth gradually loosens and. periodontal ligament. Diabetes mellitus as known as diabetes is a disease caused by lack of insulin in the body resulting in ganngguan Primary glucose metabolism disorder characterized by increased levels of glucose in the blood exceeds the normal value. Periodontitis can be the conversion of gingivitis. The primary factor of gingivitis is bacterial plaque. or cementum like periodontitis does. because disruption of insulin production from pancreatic beta cells. insulin dysfunction or disruption of insulin receptor on the target organ. 4.

and alveolar bone resorbsi kedlaman pocket. 3. polyphagia. Criteria of DM Diagnostic Classic symptoms : polyuria. Gigngiva tissue resistance and diabetes mellitus peridontal tissue decreased. In diabetes mellitus frequent disruption of immune defenses that resulted in the nature of leukocyte decreased phagocytosis. No. periodontal. It was reported that there is a correlation between blood glucose levels with the prevalence of severity of gingival inflammation. due to a change in the composition of collagen. so that people with diabetes mellitus susceptible to infection. loss.the affinity of IgG antibodies against the antigen.1 mmol/l) 2. Diabetic neuropathy factors caused a decline in autonomic reflexes and no ability to vasoconstriction of blood vessels and capillary. polydipsia.1 mmol/l) 2 hours after 75 gram glucose load 64 . The elasticity of blood vessel walls disappear and thickening of proliferation. Blood glucose levels when fasting • 126 mg/dl (7. decreased antibody formation so that the immune will be decreased. the regulation of diabetes mellitus and oral hygiene. If chronic complications occurred in patients with diabetes mellitus will occur quality of blood vessels disorder known as Angiopathy diabetic. hyalinization causes the blood vessels become stiff and easily broken. there arose a leak.0 mmol/l) Blood glucose levels • 200 mg/dl (11. weight 1.grains that result in decreased blood of the local network defense since the release of grain grain blood such as leukocyte and decreasing supply of nutrients and oxygen to the tissues that hamper healing. The leak resulted in the release of proteins and grains . increased blood glucose levels for a while • 200mg/dl (11.

4.4

Mechanism of periodontitis in diabetes mellitus

Diabetics have an oral bacterial flora similar to that found in nondiabetics, but their response to infection is not same. Diabetics have been shown to have markers of systemic inflammation, and it has been postulated that this inflammatory state can lead to increased destruction of the chronically infected periodontium. These markers include elevated C-reactive protein, fibrinogen and decreased albumin. Not only do diabetics have increased levels of systemic pro-inflammatory mediators, the local environment of the periodontium is also affected by higher levels of inflammation. An example of local inflammation occurs when monocytes increase production of inflammatory cytokines in response to insult; this increase in inflammatory mediators remains even after removal of the offending stimulus. Diabetics, therefore, have increased systemic and local inflammation, which contributes to increased destruction of the periodontium. Furthermore, diabetics have an altered response to wound healing and an abnormal immune response. Fibroblast function is impaired because of the high levels of glucose, and collagen availability is decreased by higher levels of the proteins that degrade collagen, that is, matrix metalloproteinases. The decreased fibroblast function and collagen availability alter the healing response in diabetics. The immune response, which is considered a characteristic trait of diabetes, includes abnormal chemotaxis; adherence and phagocytosis of neutrophils. This provides an altered environment in which oral bacteria can thrive; therefore, systemic and local inflammation, altered wound healing and an abnormal immune response contribute to destruction of the periodontium in diabetic individuals. Disruption of insulin secretion or insulin resistance causes disruption of the insulin receptor resulting in hyperglycemia. hyperglycemia causes fat and protein glycosylation will experience in non-systematic, forming Schiff bases, which then form amadori products. amadori degradation products generate reactive carbonyl

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compounds that react with free amino group which then form the AGE that is irreversible, unstable, reactive, and can cause vascular dysfunction. AGE is a toxic compound that can trigger mutagenesis of bacteria. AGE was formed over the case of DM. The main chemical compounds found in AGEs in the human body are pentosidine and carboxy methyl lysine. AGEs will be captured by the AGE receptor (RAGEs) in endothelial and will form a reactive free radical compounds. Accumulation of AGEs affect cell migration and phagocytosis activity polimorphonuclear (PMN) and macrophages against microbes / pathogens. Maturation and gradual changes in subgingival microflora and when accompanied by a pocket depth of ulcer showed the changes of chronic systemic disease, characterized by secretion of IL-1ß and TNF- , insulin resistance that affect glucose metabolism. Interaction between macrophage phagocyte cells with AGEs induced expression of cytokines and induce oxidative stress. Simultaneously, periodontal infection can induce persistent insulin resistance, followed by hyperglycemia, glikolosasi nonsimatik the irreversible, accumulation of AGE-binding proteins, which then accompanied by destruction and degradation of connective tissue proliferation. Molecular mechanisms of periodontitis in patients with diabetes mellitus is based on changes in host response and collagen metabolism. The main factors that affect host response to the development of complications of diabetes mellitus is a long exposure to hyperglycemia network that will generate AGEs. AGEs bind to receptors AGEs (RAGEs) on endothelial cells, monocytes, macrophages and fibroblasts. Furthermore, AGEs change the collagen tissue to increase a formation of crosslinking and the formation of reactive oxygen intermediates (ROI) such as the formation of free radicals. Fibers of collagen that has changed accumulate in the tissues and being thick in basalis membrane. And will occur the oxygen diffusion disorder, leukocyte migration, immune factor diffusion that will cause periodontitis

66

In addition, hyperglicemia will increase the collagenase synthesis. The increse of collagenase activity in Diabetes Mellitus patient occur the defect of collagen tissue, then will break the periodontal tissue component in diabetic patient. The common oral manifestations of diabetes include the following: gingivitis; periodontal disease; multiple periodontal abscesses, xerostomia and salivary gland dysfunction; recurring bacterial, viral and fungal (Candida) infections; dental caries; periapical abscesses; loss of teeth; delayed wound healing; burning mouth syndrome; taste impairment; and oral lichen planus.

4.5

Solutions to minimize the oral effect of Diabetes Mellitus

When it is discovered that a patient with advanced dental disease also has diabetes, extractions should not be performed, unless absolutely necessary, until the systemic condition is brought under control. Acute abscesses, however, require immediate drainage. Admittedly, complete regulation may not be possible while dental infection is still present, but the glycemia can be reduce. With the amelioration of the diabetic status there may be dramatic improvement in the acute periodontal condition. The teeth may become firmer, gingival inflammation may subside, suppurative exudates from the gingival crevices may decrease, and soreness and sensitivity may lessen. At this stage dental evaluation may be carried out and necessary treatment instituted. Teeth in a hopeless condition may now be extracted and residual fluctuating, uncontrollable sugar levels to a more manageable state. Thus, the treatment of periodontal disease may facilitate the practical regulation of diabetes. Under good medical control and with enlightened dental care, the diabetic patient shows no greater tendency to postdental surgical complications than his nondiabetic counterpart. Dental treatment is in most instances a stressful event, and,

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Control the glycemia regularly (min. Check your gingival or periodontal. The rational administration of sedatives and analgesics preoperatively The steps of treatment for diabetic patient : 1. Scaling : Scaling is a type of cleaning that removes plaque and calculus from the teeth at and slightly below the gumline. then clean the plaque and calculus every 3-6 month Treatment of plaque and calculus A. B. Those patients receiving intermediate and long-acting insulin in the morning before breakfast may be treated safely in the early afternoon also. every 3 month) because the good condition of glycemia will be improve periodontal disease 2. Dental appointment should be in the morning.therefore. Root Planing : Root planing smoothes root surfaces. generally about an hour and a half after breakfast and the administration of the morning insulin. Every effort should be made to allay apprehension and minimize pain. certain precautions in the handling of the diabetic dental patient are judicious and advisable. so the supportive tissues can better reattach to the tooth surface 68 .

and calculus both above and below the gingival D. Periodontal Debridement: This includes the removal of plaque. An adjunctive option to scaling and root planing may be provided in either pill form or applied directly to the infected area (gum pocket) in the form of antibiotic powder. including debridements of calculus and removal of plaque. Prophy / Prophylaxis: A preventive procedure to remove local irritants to the gingiva. E. Periodontal disease is a bacterial disease and the key to controlling or eliminating it is the effective reduction or elimination of the harmful bacteria.C. An antibacterial mouth rinse also may be prescribed to help control the harmful effects of and reduce bacterial plaque. Scaling and root planing can be done utilizing a non-surgical (closed) approach or a surgical (open) approach y A non surgical approach is when access to the root surfaces is via the sulci or periodontal pockets. y A surgical approach is when full thickness tissue flaps are reflected to expose the root surfaces and gain direct access to them y The efficacy of subgingival plaque and calculus removal utilizing a non surgical approach is limited. Pockets up to 5mm may be 69 .

3. then become abscesses. Gingival is easy to inflame. Why we do not use permanent false tooth such as µbridge¶? Because it makes another teeth also mobiling How about dental implant? Diabetic patient has serious problem with his periodontal. Substitute the missing tooth Sometimes we meet diabetic patient that loss his tooth by itself. So we need removable dentures for substitute it. brush your teeth in the right way twice a day 4. but deeper pockets often will require an open or sugical approach. Use good toothbrush.adequately debrided using a closed approach. Implant only makes it worse 70 .

and also safe for the diabetic patient¶s periodontal PERIODONTIA Diabetes Mellitus (DM) is a predisposing factor to onset of infection. In the mouth. It do not makes another teeth mobiling. In Diabetic patient. Chronic periodontal infection causes systemic inflammation which will increase insulin resistance and hyperglycemia. DM can increase the number of bacteria that cause abnormalities in the periodontal tissues and if it continues to cause tooth becomes wobbly.So removable dentures is the best way to substitute the missing tooth. the risk of getting infected with periodontal tissue even 2-4 times greater than non-diabetic patients. 71 .

by 72 . extraction should be followed by a tampon for 30 minutes. After paraesthesia. hiperaemi mucosa. should regularly control the blood glucose level of at least three months b. c. Recommends brushing with a toothpaste contain triclosan/ copolymer of at least two times a day and HbA1c test at least three monts. This disease is due to high blood sugar levels exceed 600 mg which resulted in easy shock patients. Patients with diabetes mellitus have a higher risk of tooth extraction. One of the acute complications of diabetes mellitus is non ketotik hiperosmoler coma. palate and tongue felt dry/ burning. It is suggested that the lower the degree of shakiness teeth in patients with diabetes mellitus.Insulin resistance inhibits optimal glycemic control and increase the risk of heart disease. This is done so that bleeding can be resolved. before surgery should be performed insulin therapy. a. by inhibiting the inflammatory response against gram-negative bacterial infections such as those found in periodontal disease. In people with type 1 diabetes. xerostomia. there is little difference between patients with DM type 1 and type 2. Blood clots in people with diabetes mellitus. ORAL SURGERY Tooth extraction in patients with disorders of systemic disease requires serious consideration of some aspects of action and reaction. either IDDM or NIIDM slightly disturbed. Diabetes may be the main cause gingival lesions. The addition of insulin to prevent shock At surgery. b. loss of tongue papilla and vascular problems early. For patients wit IDDM. a. It means the patient¶s cloting time does not like the non-diabetic.

b. for example in the use of orthodontia device (wire) can causes gingivitis.giving injections of insulin therapy. In addition. Serious chronic illness and reduce physiological adaptable. 73 . patients usually reluctant to return to control because no confidence against the typical bad breath. a. because with the use of wire. the provision of local anesthesia. In DM patients there is a tendency mobile tooth. will generate too much pressure on the teeth. by giving injections of insulin because of insulin are not sufficient. patients with DM should be avoided from vasoconstrictor substances because they contain adrenaline that can increase glucose in the blood. PROSTHODONTIA Systemic diseases such as diabetes mellitus can inhibit prostodontia maintance. Need to avoid major changes in the conditions of the oral cavity or artificial tooth shape drastically. ORTHODONTIA Patients with DM on orthodonsia treatment. This can inhibit the development of growth occurring observation. xerostomia is a symptom of diabetes mellitus can also inhibit Orthodontic retention by inhibiting the adhesion between the base of removable dentures with oral mucosa with oral mucosa and salivary fluid power cohesion. need not be given an injection of insulin. In patients with diabetes mellitus. While in type 2 diabetes. so teeth become mobile that will untimately lead to tooth loss. Avoided printed materials using because these materials adsorbs plaster moist oral cavity. In addition. This is one of the contra-indication teeth spread.

we must control our tooth condition in dentist 3. local factor and systemic factor. 5. Use false tooth for diabetes¶s suffer ( not allow use implant ) 74 . Every 6 month.1 Conclusion The cause of mobile tooth divided into two factors. Control the glycemia regularly (min. 5. Second. If blood glucose level isn¶t controlled influence mobile tooth. So from our disccusion. systemic factor caused by diabetes mellitus. First. Increase oral hygine with tooth brushing frequently (Use good toothbrush. local factor caused by streptococcus mutans which is appear plaque around our tooth and make our mouth become very acid. At last.2 Suggestion To avoid the factors of mobile tooth we should : 1. we conclude that people¶s opinion is wrong. brush your teeth in the right way twice a day ) 2. Check your gingival or periodontal. every 3 month) because the good condition of glycemia will be improve periodontal disease 4.CHAPTER 5 SUMMARY 5. in our tooth occur periodentitis and periodental abses which is make mobile tooth. then clean the plaque and calculus every 3-6 month .

Suzuki.1990.32. London W.Ltd: pp 309 -41.B. Cohen DW. W. Edisi ke-3 Jakarta. 13.15-6. 5. Donoseputro M. 461-65.654-65.65-66. Kumpulan makalah Basic Mol Biology course on Mitochondrial. 8.B2. Hlm. Penerjemah : Setiawan I. Majalah Ilmu Kedokteran Gigi FKG USAKTI . Carranza FA .REFERENCES 1.August. Ed. No.2003. 9. Tjokroprawiro A 1996. Infeksi Jaringan Lunak mulut pada Penderita Diabetes Mellitus . Brian L.EGC . Fisiologi Kedokteran . Ltd. 1980.485.19 ± 1 Fisiologi Kedokteran.Penerjemah: WF.32837. Edisi ke-3 Jakarta.1221-34. Philadelphia.1-9. Buku Ajar Ilmu Penyakit Dalam .Eke -9.Penerbit Buku Kedokteran .PT. Ganong Periodontal . Dental Clinics of North America Vol. 1988. Jakarta. 391. Diagnosis. Saunders Co. B1. et al . Diabetes Mellitus and Periodontal Disease. hlm.1 Agustus 2006. 841 ± 5.Mealey and Thomas W. 2006 : Clinical Periodontology . Guyton A. Jones JH. 2006 : 8 . Diabetes Mellitus dan Macam ± macam Diit Diabetes Mellitus B. Mason DK.B3 . terapi. 8. 10th.Oates : Diabetes Mellitus and Periodontal Disease : J 2. 75 . Marwati E.1992. J Periodontal 41 : hlm 709.606-7.2. 2006. 10.76-81.No 11 hlm.Gramedia Pustaka Utama : hlm 8. Mekanisme Molekuler Periodontitis pada Diabetes Mellitus. Oral Manifestation of Sistemic Disease. Airlangga University Press: hlm.1-7 6.EGC Penerbit Buku Kedokteran :hlm 183-6. John B. Saunders Co. 4. Gaya Baru: hlm. Tjokroprawiro A 2000 Diabetes mellitus klasifikasi. Dian. 7. 12. 3. Jakarta.1 No. Edisi ke-17 .B. Widjajakusuma D.349-50. 11. DENTA Jurnal Kedokteran Gigi FKG-UHT Vol.1996.Edisi ke -10 Surabaya. Mulawarmanti. Tjokroprawiro A 1998. pp 331 -13.1995.

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Doel JJ. 50. Smith L. Allaker RP: Evaluation of bacterial nitrate reduction in the human oral cavity. Doglio P. Bayindir YZ. Johnston P. Palmer RJ: Communication among oral bacteria. Benjamin N: Chemical Generation of Nitric-Oxide in the Mouth from the Enterosalivary Circulation of Dietary Nitrate. Pera P. Culo F: Nitric oxide synthesis is decreased in periodontitis. Johnson NW: Periodontal diseases. 46. Bucca C: Oral nitric oxide during plaque deposition. Egland PG. Ismail AI. Polat MF. 49. Rogers M. Kolenbrander PE. 45. Pihlstrom BL. Foster JS. Green S.org 78 .42. Ivic-Kardum M. Aurer A. Andersen RN. Lombardo S. 44. Michalowicz BS. Selwitz RH. Brogan R. Duncan C. Rolla G. Leifert C. Aleksic J. Colagrande P. 47. Dougall H. Aurer J. Carossa S. Pitts NB: Dental caries.wikipedia. www. Brussino L. Benjamin N. Golden M. 43. Blehert DS. 48. Seven N: Nitric oxide concentrations in saliva and dental plaque in relation to caries experience and oral hygiene. Hector MP.

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