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Darshan Dental College, Loyra, Udaipur

Role of Nutrition & hormones in orthodontics.

Guided by Dr. Prabhuraj k. Dr.Sabarinath P Dr.Tarulata S. Dr.Deepti Rajdan Dr.Jigar Doshi Dr.Amit Kumar Presented By Kunal Rathore

Introduction Definition of nutrition according to Council of food and nutrition of the American Medical Association asThe science of food, the nutrients and other substances therein ,their action ,interaction and balance in relation to health and diseases and the processes by which the organism ingest, digest, absorbs, transports, utilizes and excretes food substances Nutrients There are six major classes of nutrients: carbohydrates, dietary fiber, fats, minerals, protein, vitamins, and water. These nutrient classes can be categorized as either macronutrients (needed in relatively large amounts) or micronutrients (needed in smaller quantities). The macronutrients include carbohydrates, fats, protein, and water. The micronutrients are minerals and vitamins. The macronutrients (excluding water) provide structural material (amino acids from which proteins are built, and lipids from which cell membranes and some signaling molecules are built), and energy. Some of the structural material can be used to generate energy internally, and in either case it is measured in joules or kilocalories (often called "Calories" and written with a capital C to distinguish them from little 'c' calories). Carbohydrates and proteins provide 17 kJ approximately (4 kcal) of energy per gram, while fats provide 37 kJ (9 kcal) per gram., though the net energy from either depends on such factors as absorption and digestive effort, which vary substantially from instance to instance. Vitamins, minerals, fiber, and water provide energy, but are required for other reasons. A third class of dietary material, fiber (i.e., non-digestible material such as cellulose), is also required, for both mechanical and biochemical reasons. Molecules of carbohydrates and fats consist of carbon, hydrogen, and oxygen atoms. Carbohydrates range from simple monosaccharides (glucose, fructose, galactose) to complex polysaccharides (starch and fiber). Fats are triglycerides, made of assorted fatty acid monomers bound to a glycerol backbone. Some fatty acids, but not all, are essential because they cannot be synthesized in the body. Protein molecules contain nitrogen and often sulfur in addition to carbon, oxygen, and hydrogen. The fundamental components of protein are nitrogen-containing amino acids, some of which are essential. Some of the amino acids are convertible (with the expenditure of energy) to glucose in a process known as gluconeogenesis. By breaking down existing protein, some glucose can be produced internally; the remaining amino acids are discarded, primarily as urea in urine.. This occurs normally only during prolonged starvation..

Other micronutrients include antioxidants and phytochemicals, which are said to influence (or protect) some body systems. Their necessity is not as well established as it is for vitamins and minerals. Most foods contain a mix of some or all of the nutrient classes, together with other substances, such as toxins of various sorts. Some nutrients can be stored internally (e.g., the fat soluble vitamins), while others are required more or less continuously. Poor health can be caused by a lack of required nutrients or, in extreme cases, too much of a required nutrient. For example, both salt and water (both absolutely required) will cause illness or even death in excessive amounts. Carbohydrate Carbohydrates include sugars, starches and fiber. They constitute a large part of foods such as rice, noodles, bread, and other grain-based products. Carbohydrates may be classified chemically as monosaccharides, disaccharides, or polysaccharides depending on the number of monomer (saccharide or sugar) units they contain. Monosaccharides, disaccharides, and polysaccharides contain one, two, and three or more sugar units, respectively. Polysaccharides are often referred to as complex carbohydrates because they consist of long, sometimes branched chains of single sugar units. Mono- and disaccharides are called simple carbohydrates. Dietary advice frequently but erroneously suggests that complex carbohydrates are superior to simple because they take longer to digest and absorb. Simple carbohydrates, on the other hand, are said to cause a spike in blood glucose levels rapidly after ingestion. These claims are false. In fact, many digestible polysaccharides are processed as rapidly as simple sugars in the human body. On the other hand some simple carbohydrates (fructose, for example) are processed in a different way and do not spike blood sugar. Thus the distinction between "complex" and "simple" does not predict the nutritional value or impact of carbohydrates. A better way of determining what effect particular foods may have on blood sugar and ultimately on health in general is the glycemic index. Carbohydrates are not essential nutrients but are typically an important part of the human diet. While it would not be accurate to categorize all carbohydrates as "bad" nutritionally, some carbohydrate sources may well have deleterious effects on health, especially when consumed in large quantities. Highly processed carbohydrates (sugars and starches) as well as fructose consumed in large quantities have been implicated in negative health outcomes. Insufficient carbohydrate consumption can result in the production of ketones in the body. Ketones are formed when the body does not have sufficient glucose to fully metabolize fats. Dietary fiber Dietary fibre is a carbohydrate (or a polysaccharide) that is incompletely absorbed in humans and in some animals. Fiber supplies 1.5 to 2.5 calories per gram, less than the 4 calories per gram provided by non-fibre carbohydrates. Dietary fibre from plants consists mainly of cellulose, a large carbohydrate polymer that is indigestible because humans do not have the required enzymes to disassemble it. There are two subcategories: soluble and insoluble fibre. Whole grains, fruits (especially plums, prunes, and

figs), and vegetables are good sources of dietary fibre. There are many health benefits of a high-fibre diet. Dietary fiber helps reduce the chance of gastrointestinal problems such as constipation and diarrhea by increasing the weight and size of stool and softening it. Insoluble fibre, found in wholewheat flour, nuts and vegetables, especially stimulates peristalsis -- the rhythmic muscular contractions of the intestines which move digesta along the digestive tract. Soluble fibre, found in oats, peas, beans, and many fruits, dissolves in water in the intestinal tract to produce a gel which slows the movement of food through the intestines. This may help lower blood glucose levels because it can slow the absorption of sugar. Additionally, fibre, perhaps especially that from whole grains[vague], is thought to possibly help lessen insulin spikes, and therefore reduce the risk of type 2 diabetes. The link between increased fibre consumption and a decreased risk of colorectal cancer is still uncertain. The Role Of Carbohydrates In The Body Five subheadings follow in this lesson subdivision, but there is actually only one basic role of carbohydrates in the human diet: to supply energy. It should always be kept in mind that carbohydrates or calories alone cannot adequately supply our energy needs, for we must have our carbohydrates in combination with other needs, such as proteins, water, vitamins, minerals, fats, etc. This means that a diet of refined sugar, refined rice, flour products and other "food fragments," though it supplies calories, cannot satisfactorily comprise the bulk of anyone's diet. A person on such a diet would suffer many problems, for the organism is not capable of living long or well on bare carbohydrates alone. They must be obtained in combination with the other essential food factors to be truly useful in the overall energy production and nutrition of the organism.

Carbohydrates Supply Energy

The body uses carbohydrates directly from the monosaccharide glucose. Glucose is in the blood and extracellular fluids (lymph) and can be made from glycogen. Glycogen is stored in the liver and muscles and in smaller amounts in the other organs and tissues of the body. Energy is derived from glucose by the splitting of the glucose molecules into smaller compounds and oxidizing these to form water, which frees quite a large amount of energy.

When carbohydrates needed for the functioning of the central nervous system, the muscles and the other body systems and functions are insufficient in the diet (as during a fast or on a weight-loss diet), stored adipose tissue (fat) is broken down into glucose to make up the caloric deficit. Some amino acids, instead of being used to make proteins, are deaminated and used as carbohydrates to supply energy. The formation of glucose from amino acids is called gluconeogenesis. This phenomenon enables one to maintain normal blood sugar levels during a fast.

Practically the entire fat store of the body can be used up without detriment to health. Because of this fact, and the fact that the body can also create carbohydrates from amino acids, fasting is a very safe practice from the standpoint of maintenance of normal blood sugar levels, of normal neurological functioning and of meeting all the body's various energy needs.

Carbohydrates Provide Fuel for the Central Nervous System

Nerve cells are very dependent upon glucose for their functioning. According to physiology texts, the glycogen in nervous tissues remains constant and is not mobilized for conversion to glucose. When insufficient carbohydrates are consumed to meet the energy needs of the central nervous system, besides the occurrence of gluconeogenesis, another phenomenon occurs during a fast of three weeks or more: The cells of the central nervous system adapt their metabolic apparatus to use ketone bodies in place of glucose. (Ketone bodies are substances synthesized by the liver as a step in the metabolism of fats.) The nerve cells obtain their needed functional energy from these metabolites. This explains why patients with blood sugar problems (diabetes or hypoglycemia) do not suffer ill effects during a fast. In fact, they benefit by fasting.

Carbohydrates Provide Fuel for the Muscular System Carbohydrates provide the major fuel for muscular exercise. Fats and proteins can be used only indirectlyby first being converted into carbohydrates. For this reason, a proper diet should consist primarily of carbohydratesnot primarily of proteins and fats as are commonly consumed in conventional nonvegetarian (and some lacto- and lacto-ovo vegetarian) diets.

The muscles use the glycogen present in the muscle cells and glucose in the bloodstream. However, glycogen from the muscles is more efficiently used than glucose because the breakdown of glycogen for use does not require energy input at the time, whereas a certain amount of energy is used to bring the blood sugar into the metabolic system of the muscles. (It does require energy to build up the glycogen supply in the first place, but this happens during periods of rest when plenty of energy is available.) If a diet high in carbohydrates is not consumed, tremendous muscular exertion over long periods and/or extreme and prolonged stress (as being stranded for weeks in Antarctica) can result in accelerated breakdown of body protein and stored body fat. The protein breakdown is evidenced by an increased excretion of nitrogen in the urine, and the fat breakdown is evidenced by a rise in the level of ketone bodies in the urine and in the blood. The blood sugar level is simultaneously lower.

The body works much more efficiently from carbohydrate intake than from broken-down body protein and fats because protein and fat molecules, when used as fuel, yield less than their total caloric value in the form the muscles can use. The remaining portion is used for the conversion of these molecules into suitable fuel. This conversion takes place in the liver and adipose tissue, which supply the body's organs with fuel via the bloodstream. The fact that the body can and will use body fats and proteins when the supply and stores of blood sugar and glycogen are not great enough to meet the demand for energy exemplifies two facts: 1) The organism is provident. It has many back-up arrangements for survival in emergency situations when sufficient carbohydrates are not available. 2) An appropriate balance between supplying body needs (such as rest and carbohydrates) and expending energy (muscular, nervous or other) should be strived for to attain optimum health and well-being. It has been found that people who are accustomed to doing prolonged or strenuous work have larger stores of glycogen (and of phosphate esters) in their muscles than those not accustomed to much physical activity. It is, therefore, beneficial to do regular vigorous exercise to increase our storage of muscle glycogen. We will then be prepared to expend energy for longer and more strenuous exercise whether it be in an emergency or in pursuing pleasure. Carbohydrates Supposedly Spare Proteins Physiology textbooks refer to this so-called role or function of carbohydrate in the body as "its proteinsparing action." However, it is incorrect to attribute action (other than chemical action) to carbohydrates or other inanimate substances. Besides, "sparing protein" is not a function or role of carbohydrates at all. Carbohydrates simply furnish our fuel or energy needsand nothing more.

What is being said in the textbooks is that proteins consumed will be used for tissue building and maintenance rather than being used as an emergency source of energy as long as the carbohydrate intake is sufficient. This is true, but it is only another way of saying that carbohydrates are the primary and most efficient source of energy or fuel and that it is best not to try to meet our fuel needs from proteins. It is stating the true fact that carbohydrates, not proteins, supply our primary nutrient needs.

"Sparing proteins" is not a separate and distinct function or role of carbohydrates any more than preventing scurvy is a separate and distinct function of vitamin C in the body. Vitamin C supplies body needs, but its role is not prevention of scurvy or of anything else. Viewing nutrients as preventative agents of diseases is another way of saying that diseases are normal, that they are an inevitable part of life that will and must occur unless prevented by the proper nutrients. That is a backwards way of viewing healthit's the disease approach, or the medical approach. Just as good things happen to us if we think positive thoughts and visualize success, harmony, etc., good health will exist as long as we live

healthfullyand that includes consuming the correct amounts of the foods to which we were biologically adapted in nature to eat.

In short, the so-called "protein-sparing action" of carbohydrates is not only not an action, but sparing proteins is not a distinct role of carbohydrates separate from their energy-providing role. Carbohydrates Supposedly Supply "Dietary Fiber" "Dietary fiber" is a fairly new term coined to describe the cellulose inside plant cells. Cellulose is known to be indigestible by humans, though it is digested and used for energy by herbivores. The claims made about "the beneficial role of dietary fiber in preventing diseases" are so popular and so widely made that they are practically accepted as fact. However, cellulose, though in fact a carbohydrate because it is utilized as such by herbivores, does not serve the role of a carbohydrate in human physiology. Because it cannot be digested and utilized by humans, it cannot provide us with energyand providing energy is the only role of carbohydrates in human nutrition.

The above statements may come as a surprise to most readersbut read on and we'll clarify further.

It has been observed that certain so-called primitive tribes in Africa and elsewhere who consume diets high in fiber are less likely to develop certain colon diseases and metabolic disorders than their kinsmen who live in urban areas and eat low-fiber foods similar to those consumed in so-called developed countries. Based on the high correlation between low-fiber diets and human gastrointestinal diseases, many hospitals and clinics have changed their dietary management of diverticulosis. They are experiencing good results with a diet containing more instead of less cellulose. We do not deny that high-fiber diets are more wholesome as a rule than low-fiber diets, nor do we deny the fact that people who consume diets closer to nature and therefore higher in fiber (cellulose) have fewer gastrointestinal diseases and a lower rate of bowel cancer. What we argue against is the thinking that the fiber itself is primarily responsible for the prevention of these diseases and disorders. Since cellulose is indigestible, it cannot be utilized by the body as a nutrient. It is simply passed through with the other wastes. Its presence or absence in the feces is insignificant. What is significant is how much and what kinds of toxins are there (and elsewhere). The ingestion of too many toxins from all sources, as well as the retention of toxic wastes produced within the body, results in diseases. The presence or absence of indigestible plant fibers does not prevent or cause diseases. Processed, highly-refined, so-called foods (they do contain carbohydrates) do not deserve the label foods because they are not whole foods. Parts of processed foods are missingthey were removed intentionally in the refining process. (Fiber [cellulose] is one of those missing parts.) This makes them

incomplete or fragmented foods. Eating fragmented foods results in problems in the body. Therefore, they should not be eaten. Refined sugar and products containing refined sugar, as well as refined flour products, are the most salient examples of processed food fragments that produce toxic effects in the body. Being devoid of vitamins and minerals in their natural form (the only form they can be used in), these products are like drugs within the body. In addition, calcium and other minerals, as well as B vitamins, must be utilized by the body to metabolize refined products. Because the refined products are devoid of nutrients except carbohydrates, calcium is taken from the bones. Most "civilized" diets contain cooked foods, foods not normal to humans, refined and processed foods and drugs and medications. Refined sugar, flours, white rice and processed cereals are some of the worst culprits, but there are many, many more sources of toxins in the diet. Also, incompatible food combinations result in the production of toxins in the stomach and elsewhere in the digestive tract, and these toxins also contribute to gastrointestinal disturbances and diseases. Much more could be said about the sources of toxins within the body that result in disease, but this has been discussed in previous lessons and will also be further discussed in future lessons. For now, it is sufficient for us to explain that low-fiber diets not only lack the natural cellulose which should be left intact in the whole food, but they also contain or give rise to a host of toxins that result in disease conditions. It is not the lack of fiber itself that causes diverticulosis and other gastrointestinal problems but the overall unwholesomeness of the foods ingested in so-called civilized society. (Of course, you should understand that what is eaten is only part of the picture and that how it's eaten, how much is eaten, the amount of exercise, sleep, fresh air, etc., indulged are also important factors in human nutrition.) Deficiency of carbohydratesAlmost nothing is known of the effect of carbohydrate deficient diet on the oral cavity. There is a group of disease, which represents a primary genetically determined disturbance of the mucopolysaccharide metabolism. Rare disorder and is characterized by the following features-

Hurler syndrome-Head appears large with prominent forehead and puffy eyelids -Nasal congestion with noisy breathing -Shortening and broadening of the mandible with wide intergonial - Increased arch length from ramus to ramus - Dentition-small and misshaped teeth. distance

-Soft tissue gingival hyperplasia. Fat A molecule of dietary fat typically consists of several fatty acids (containing long chains of carbon and hydrogen atoms), bonded to a glycerol. They are typically found as triglycerides (three fatty acids attached to one glycerol backbone). Fats may be classified as saturated or unsaturated depending on the detailed structure of the fatty acids involved. Saturated fats have all of the carbon atoms in their fatty acid chains bonded to hydrogen atoms, whereas unsaturated fats have some of these carbon atoms double-bonded, so their molecules have relatively fewer hydrogen atoms than a saturated fatty acid of the same length. Unsaturated fats may be further classified as monounsaturated (one doublebond) or polyunsaturated (many double-bonds). Furthermore, depending on the location of the doublebond in the fatty acid chain, unsaturated fatty acids are classified as omega-3 or omega-6 fatty acids. Trans fats are a type of unsaturated fat with trans-isomer bonds; these are rare in nature and in foods from natural sources; they are typically created in an industrial process called (partial) hydrogenation. There are nine kilocalories in each gram of fat. Saturated fats (typically from animal sources) have been a staple in many world cultures for millennia. The American Heart Association recommends limiting intake of all fats in the diet, but particularly advises keeping saturated and trans fat intake below the level of unsaturated fat (e.g., vegetable oil) intake. Saturated and some trans fats are typically solid at room temperature (such as butter or lard), while unsaturated fats are typically liquids (such as olive oil or flaxseed oil). Trans fats are very rare in nature, and have been shown to be highly detrimental to human health, but have properties useful in the food processing industry, such as rancidity resistance. Essential fatty acids Most fatty acids are non-essential, meaning the body can produce them as needed, generally from other fatty acids and always by expending energy to do so. However, in humans, at least two fatty acids are essential and must be included in the diet. An appropriate balance of essential fatty acidsomega-3 and omega-6 fatty acidsseems also important for health, although definitive experimental demonstration has been elusive. Both of these "omega" long-chain polyunsaturated fatty acids are substrates for a class of eicosanoids known as prostaglandins, which have roles throughout the human body.. They are hormones, in some respects. The omega-3 eicosapentaenoic acid (EPA), which can be made in the human body from the omega-3 essential fatty acid alpha-linolenic acid (LNA), or taken in through marine food sources, serves as a building block for series 3 prostaglandins (e.g. weakly inflammatory PGE3). The omega-6 dihomo-gamma-linolenic acid (DGLA) serves as a building block for series 1 prostaglandins (e.g. anti-inflammatory PGE1), whereas arachidonic acid (AA) serves as a building block for series 2 prostaglandins (e.g. pro-inflammatory PGE 2).. Both DGLA and AA can be made from the omega-6 linoleic acid (LA) in the human body, or can be taken in directly through food.. An appropriately balanced intake of omega-3 and omega-6 partly determines the relative production of different prostaglandins, which is one reason why a balance between omega-3 and omega-6 is believed important for cardiovascular health. In industrialized societies, people typically consume large amounts

of processed vegetable oils, which have reduced amounts of the essential fatty acids along with too much of omega-6 fatty acids relative to omega-3 fatty acids. The conversion rate of omega-6 DGLA to AA largely determines the production of the prostaglandins PGE1 and PGE2. Omega-3 EPA prevents AA from being released from membranes, thereby skewing prostaglandin balance away from pro-inflammatory PGE2 (made from AA) toward anti-inflammatory PGE1 (made from DGLA). Moreover, the conversion (desaturation) of DGLA to AA is controlled by the enzyme delta-5-desaturase, which in turn is controlled by hormones such as insulin (up-regulation) and glucagon (down-regulation).. The amount and type of carbohydrates consumed, along with some types of amino acid, can influence processes involving insulin, glucagon, and other hormones; therefore the ratio of omega-3 versus omega-6 has wide effects on general health, and specific effects on immune function and inflammation, and mitosis (i.e. cell division). Importance of fats in living organisms Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement. Fats play a vital role in maintaining healthy skin and hair, insulating body organs against shock, maintaining body temperature, and promoting healthy cell function. Fats also serve as energy stores for the body, containing about 37.8 kilojoules (9 Calories) per gram of fat. They are broken down in the body to release glycerol and free fatty acids. The glycerol can be converted to glucose by the liver and thus used as a source of energy. Fat also serves as a useful buffer towards a host of diseases. When a particular substance, whether chemical or bioticreaches unsafe levels in the bloodstream, the body can effectively diluteor at least maintain equilibrium ofthe offending substances by storing it in new fat tissue. This helps to protect vital organs, until such time as the offending substances can be metabolized and/or removed from the body by such means as excretion, urination, accidental or intentional bloodletting, sebum excretion, and hair growth. While it is nearly impossible to remove fat completely from the diet, it would also be unhealthy to do so. Some fatty acids are essential nutrients, meaning that they can't be produced in the body from other compounds and need to be consumed in small amounts. All other fats required by the body are nonessential and can be produced in the body from other compounds.

Protein Proteins are the basis of many animal body structures (e.g. muscles, skin, and hair). They also form the enzymes that control chemical reactions throughout the body. Each molecule is composed of amino acids, which are characterized by inclusion of nitrogen and sometimes sulphur (these components are responsible for the distinctive smell of burning protein, such as the keratin in hair). The body requires

amino acids to produce new proteins (protein retention) and to replace damaged proteins (maintenance). As there is no protein or amino acid storage provision, amino acids must be present in the diet. Excess amino acids are discarded, typically in the urine. For all animals, some amino acids are essential (an animal cannot produce them internally) and some are non-essential (the animal can produce them from other nitrogen-containing compounds). Twenty-one proteinogenic amino acids are found in the human body, along with non-proteinogenic amino acids (e.g. gamma-aminobutyric acid). Ten of the proteinogenic amino acids are essential and, therefore, must be included in the diet. A diet that contains adequate amounts of amino acids (especially those that are essential) is particularly important in some situations: during early development and maturation, pregnancy, lactation, or injury (a burn, for instance).. A complete protein source contains all the essential amino acids; an incomplete protein source lacks one or more of the essential amino acids. Sources of dietary protein include meats, tofu and other soy-products, eggs, legumes, and dairy products such as milk and cheese. Excess amino acids from protein can be converted into glucose and used for fuel through a process called gluconeogenesis. The amino acids remaining after such conversion are discarded. Functions of Proteins in the Body Proteins play a major role in ensuring your health well being. There are innumerable functions of proteins in the body. Well, the primary functions of proteins include building and repairing of body tissues, regulation of body processes and formation of enzymes and hormones. Read further to explore information about protein role in health

Proteins aid in the formation of antibodies that enable the body to fight infection. Proteins serve as a major energy supplier. There are distinctive kinds of proteins, each performing a unique function in the body. Proteins form a major part of your body, next to water. The composition of proteins in the body is like that muscle contains about 1/3 protein, bone about 1/5 part and skin consists of 1/10 portion. The rest part of proteins is in the other body tissues and fluids. Even blood contains loads of proteins. In fact the hemoglobin molecule is nothing but proteins. Our body requires proteins for the purpose of maintenance and healthy growth. The need for consuming proteins is especially more for infants, young children, pregnant women and recovering patients. There is a constant breakdown of proteins in the body and this explains the reason why we need to consume proteins on a regular daily basis. It becomes of prime importance to ensure that you have your daily-recommended protein intake, so as to improve your health fitness. Dietary minerals Dietary minerals are the chemical elements required by living organisms, other than the four elements carbon, hydrogen, nitrogen, and oxygen that are present in nearly all organic molecules. The term "mineral" is archaic, since the intent is to describe simply the less common elements in the diet. Some

are heavier than the four just mentioned, including several metals, which often occur as ions in the body. Some dietitians recommend that these be supplied from foods in which they occur naturally, or at least as complex compounds,. or sometimes even from natural inorganic sources (such as calcium carbonate from ground oyster shells). Some minerals are absorbed much more readily in the ionic forms found in such sources. On the other hand, minerals are often artificially added to the diet as supplements; the most famous is likely iodine in iodized salt which prevents goiter. Macrominerals Many elements are essential in relative quantity; they are usually called "bulk minerals". Some are structural, but many play a role as electrolytes.Elements with recommended dietary allowance (RDA) greater than 200 mg/day are, in alphabetical order (with informal or folk-medicine perspectives in parentheses): Calcium, a common electrolyte, but also needed structurally (for muscle and digestive system health, bone strength, some forms neutralize acidity, may help clear toxins, provides signaling ions for nerve and membrane functions) Chlorine as chloride ions; very common electrolyte; see sodium, below Magnesium, required for processing ATP and related reactions (builds bone, causes strong peristalsis, increases flexibility, increases alkalinity) Phosphorus, required component of bones; essential for energy processing[18] Potassium, a very common electrolyte (heart and nerve health) Sodium (also see salt), a very common electrolyte; not generally found in dietary supplements, despite being needed in large quantities, because the ion is very common in food: typically as sodium chloride, or common salt. Excessive sodium consumption can deplete calcium and magnesium,[verification needed] which has been shown can lead to high blood pressure and osteoporosis (Note: Some sources suggest high blood pressure is due to high water retention per osmosis). Sulfur, for three essential amino acids and therefore many proteins (skin, hair, nails, liver, and pancreas). Sulfur is not consumed alone, but in the form of sulfur-containing amino acids Trace minerals Many elements are required in trace amounts, usually because they play a catalytic role in enzymes.[19] Some trace mineral elements (RDA < 200 mg/day) are, in alphabetical order: Cobalt required for biosynthesis of vitamin B12 family of coenzymes. Animals cannot biosynthesize B12, and must obtain this cobalt-containing vitamin in the diet Copper required component of many redox enzymes, including cytochrome c oxidase Chromium required for sugar metabolism

Fluoride required for maintenance of bone structure Iodine used by the thyroid gland to produce thyroid hormone (thyroxine and triiodothyronine), may also be used by other important organs such as the thymus, salivary glands, breast, and stomach (see Extrathyroidal iodine and Iodine and cancer risk; for this reason iodine may be needed in larger quantities than others in this list Iron required for many enzymes, and for hemoglobin and some other proteins Manganese (processing of oxygen) Molybdenum required for xanthine oxidase and related oxidases Nickel present in urease Selenium required for peroxidase (antioxidant proteins) Vanadium (There is no established RDA for vanadium. No specific biochemical function has been identified for it in humans, although vanadium is required for some lower organisms.) Zinc required for several enzymes such as carboxypeptidase, liver alcohol dehydrogenase, and carbonic anhydrase

Table 71-2 Deficiencies and Toxicities of Metals




Tolerable Upper (Dietary) Intake Level


No biologic determined

function Developmental defects, male 20 mg/d (extrapolated sterility, testicular atrophy from animal data) mass, Renal insufficiency (milk-alkalai 2500 mg/d (milksyndrome), nephrolithiasis, alkalai) impaired iron absorption Nausea, vomiting, diarrhea, 10 mg/d (liver hepatic failure, tremor, mental toxicity) deterioration, hemolytic anemia, renal dysfunction


Reduced bone osteoporosis


Anemia, growth retardation, defective keratinization and pigmentation of hair, hypothermia, degenerative

changes in osteopenia, deterioration Chromium


elastin, mental

Impaired glucose tolerance

Occupational: renal failure, ND dermatitis, pulmonary cancer Dental and skeletal fluorosis, 10 mg/d osteosclerosis (fluorosis) Thyroid dysfunction, acne-like T4, eruptions 1100 g/d (thyroid dysfunction)

Fluoride Dental caries Iodine Thyroid enlargement, cretinism



abnormalities, Gastrointestinal effects 45 mg/d of (nausea, vomiting, diarrhea, elemental iron kilonychia, pica, anemia, constipation), iron overload (GI side effects) work performance, impaired with organ damage, acute cognitive development, systemic toxicity premature labor, maternal mortality perinatal


Impaired growth and skeletal General: Neurotoxicity, 11 mg/d development, reproduction, Parkinson-like symptoms (neurotoxicity) lipid and carbohydrate Occupational: Encephalitis-like metabolism; upper body rash syndrome, Parkinson-like syndrome, psychosis, pneumoconiosis neurologic Reproductive abnormalities and fetal 2 mg/d extrapolated from animal data

Molybdenum Severe abnormalities


Cardiomyopathy, heart failure, General: Alopecia, nausea, vomiting, abnormal nails, 400 striated muscle degeneration emotional lability, peripheral (hair, neuropathy, lassitude, garlic changes) odor to breath, dermatitis Occupational: Lung and nasal carcinomas, liver necrosis,

g/d nail

pulmonary inflammation Phosphorous Rickets (osteomalacia), Hyperphosphatemia proximal muscle weakness, rhabdomyolysis, paresthesia, ataxia, seizure, confusion, heart failure, hemolysis, acidosis 4000 mg/d

Zinc Growth retardation, taste and smell, alopecia, dermatitis, diarrhea, immune dysfunction, failure to thrive, gonadal atrophy, congenital malformations Note: ND, not determined; GI, gastrointestinal.

General: Reduced copper 40 mg/d absorption, gastritis, sweating, (impaired copper fever, nausea, vomiting metabolism) Occupational: Respiratory distress, pulmonary fibrosis

Vitamins As with the minerals discussed above, some vitamins are recognized as essential nutrients, necessary in the diet for good health. Vitamin D is the exception: it can be synthesized in the skin, in the presence of UVB radiation. Certain vitamin-like compounds that are recommended in the diet, such as carnitine, are thought useful for survival and health, but these are not "essential" dietary nutrients because the human body has some capacity to produce them from other compounds. Moreover, thousands of different phytochemicals have recently been discovered in food (particularly in fresh vegetables), which may have desirable properties including antioxidant activity (see below); however, experimental demonstration has been suggestive but inconclusive. Other essential nutrients that are not classified as vitamins include essential amino acids (see above), choline, essential fatty acids (see above), and the minerals discussed in the preceding section. Vitamin deficiencies may result in disease conditions, including goitre, scurvy, osteoporosis, impaired immune system, disorders of cell metabolism, certain forms of cancer, symptoms of premature aging, and poor psychological health (including eating disorders), among many others.[20] Excess levels of some vitamins are also dangerous to health (notably vitamin A), and for at least one vitamin, B6, toxicity begins at levels not far above the required amount. Deficient or excess levels of minerals can also have serious health consequences.

Vitamin A. The principal form of vitamin A is retinol; the aldehyde (retinal) and the acid (retinoic acid) are also active forms of vitamin A. Retinol can be derived directly from animal sources or through conversion from carotene (found abundantly in carrots) in the small intestine. Vitamin A is important in the production and regeneration of rhodopsin of the retina and in the normal growth of the skin. Vitamin Adeficient individuals develop night blindness and skin lesions. Vitamin D. Vitamin D is a group of fat-soluble compounds collectively known as the calciferols. Vitamin D3 (also called cholecalciferol or activated dehydrocholesterol) in the human body is derived from two main sources: the skin, which contains a rich source of 7-dehydrocholesterol that is rapidly converted to cholecalciferol when exposed to UV light, and dietary vitamin D3. Vitamin D is essential for normal development and growth and the formation of bones and teeth. Vitamin D deficiency can result in rickets, a disorder of normal bone ossification manifested by distorted bone movements during muscular action.

ROLE OF VITAMIN D3 ON BONE : Active vitamin D, is a steroid hormone, which like other steroid hormones has its receptors within the cytosol of cells. The D3 receptors are found ubiquitously in all tissues. The receptor-D3 complex is transferred to the nuclear DNA for specific gene transcription (Heddad, 1987). 1,25(OH)2D3 reacts specifically on bone, although it targets other organs involved with mineral metabolism such as kidneys, parathyroids, and small intestines (Reichel et al., 1989). Cholecalciferol from skin is hydroxylated in the 25 position in the liver and in the 1 position in the kidney. 1,25(OH)2D3 with endocrine or paracrine function, has an effect on all cells of bone either directly or indirectly. It is a potent stimulator of resorptive activity, by increasing the number of osteoclasts. It increases the size of the ruffled border, an increase in nucleii indicating coalescence of monocytes and an increase of osteoclastic lysosomal enzymes. 1'25 (OH)2D3 increases calcitonin receptors on multinucleated giant cells in bone marrow cultures (Takahashi,1 988), but not in mature osteoclasts in vivo which could indicate that osteoclast precursor cells are activated but not the mature osteoclasts( Merke et al., 1986; Narbeitz et al., l9g3). Indirectly, 1'25(OH)2D3 might activate osteoclasts by prodding osteoblasts and immune system cells to secrete osteoclast activating substrates( McSheehya nd Chambers,1 987). It plays a roll, as well, to inhibit T-cell gamma interferon which in turn is a potent inhibitor of osteoclast stimulatory activity. The resultant effect of all this activity is for 1,25(OH)2D3to increase osteoclast activity and bone resorption. This then, causes a net increase of Ca++ ions into the circulation and a potential increase of bone formation. Concomitantly,1 ,25(OH)2D3 increases the ability of intestinal resorptive cells to absorb Ca++ (Reichel et al., 1989).This favors osteogenesis by increasing plasma Ca++ ions and the concentration gradient pathway of Ca++ into the extracellular bone compartment. Contrarily, 1,25(OH)2D3 deficiency leads to decreased bone formation with an increase in non-mineralized osteoid. Osteoblasts , osteoblast-like cells, osteoprogenitor cells, and bone lining cells all have 1,25(OH)2D3 receptors indicating a predelective site on osteoblasts and implying a direct effect on bone production by bone producing cells. Vitamin E. The major dietary vitamin E is _-tocopherol. Vegetable oils are rich in vitamin E. Vitamin E is a potent antioxidant and therefore prevents lipid peroxidation. Tocopherol deficiency is associated with increased red cell susceptibility to lipid peroxidation, which may explain why the red cells are more fragile in vitamin Edeficient individuals than in healthy individuals. Vitamin K. Vitamin K can be derived from green vegetables in the diet or the gut flora. Vitamin K is essential for the synthesis of various clotting factors by the liver. Vitamin K deficiency is associated with bleeding disorders. The Water-Soluble Vitamins Are C, B1, B2, B6, B12, Niacin, Biotin, and Folic Acid Vitamin C. The major source of vitamin C (ascorbic acid) is green vegetables and fruits. It plays an important role in many oxidative processes by acting as a coenzyme or cofactor. Vitamin C deficiency is associated with scurvy, a disorder characterized by weakness, fatigue, anemia, and bleeding gums. Vitamin B1. Vitamin B1 (thiamine) plays an important role in carbohydrate metabolism. Thiamine deficiency results in beriberi, characterized by anorexia and disorders of the nervous system and heart.

Vitamin B2. Vitamin B2 (riboflavin) is a component of the two groups of flavoproteinsflavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). Riboflavin plays an important role in metabolism. Riboflavin deficiency is associated with anorexia, impaired growth, impaired use of food, and nervous disorders. Niacin. Niacin plays an important role as a component of the coenzymes NAD(H) and NADP(H), which participate in a wide variety of oxidation-reduction reactions involving H_ transfer. Niacin has been used to treat hypercholesterolemia, for the prevention of coronary artery disease. It decreases plasma total cholesterol and LDL cholesterol, yet increases plasma HDL cholesterol. Niacin deficiency is characterized by many clinical symptoms, including anorexia, indigestion, muscle weakness, and skin eruptions. Severe deficiency leads to pellagra, a disease characterized by dermatitis, dementia, and diarrhea. Vitamin B6 . Vitamin B6 (pyridoxine) is involved in amino acid and carbohydrate metabolism. A deficiency of this vitamin is often associated with anemia and CNS disorders. Biotin. Biotin acts as a coenzyme for carboxylase, transcarboxylase, and decarboxylase enzymes, which play an important role in the metabolism of lipids, glucose, and amino acids. Biotin is so common in food that deficiency is rarely observed. Folic Acid. Folic acid is usually found in the diet as polyglutamyl conjugates (pteroylpolyglutamates). It is required for the formation of nucleic acids, the maturation of red blood cells, and growth. Folic acid deficiency causes a fall in plasma and red cell folic acid content and, in its most severe form, the development of megaloblastic anemia, dermatological lesions, and poor growth. Vitamin B12. The discovery of vitamin B12 (cobalamin) followed from the observation that patients with pernicious anemia who ate large quantities of raw liver recovered from the disease. Subsequent analysis of liver components isolated the cobalt-containing vitamin, which plays an important role in the production of red blood cells. A glycoprotein secreted by the parietal cells in the stomach called the intrinsic factor binds strongly with vitamin B12 to form a complex that is then absorbed. Vitamin B12 is transported in the portal blood bound to the protein transcobalamin. Individuals who lack the intrinsic factor fail to absorb vitamin B12 and develop pernicious anemia.

Water It is not fully clear how much water intake is needed by healthy people, although some assert that 67 glasses of water daily is the minimum to maintain proper hydration.The notion that a person should consume eight glasses of water per day cannot be traced to a credible scientific source. The effect of, greater or lesser, water intake on weight loss and on constipation is also still unclear. The original water intake recommendation in 1945 by the Food and Nutrition Board of the National Research Council read: "An ordinary standard for diverse persons is 1 milliliter for each calorie of food. Most of this quantity is contained in prepared foods." The latest dietary reference intake report by the United States National

Research Council recommended, generally, (including food sources): 2.7 liters of water total for women and 3.7 liters for men. Specifically, pregnant and breastfeeding women need additional fluids to stay hydrated. The Institute of Medicinewhich recommends that, on average, women consume 2.2 litres and men 3.0 litres of water dailyadvises pregnant women consume 2.4 litres (approx. 9 cups) and breastfeeding women consume 3 litres (approx. 12.5 cups) because an especially large amount of fluid is lost during nursing.[26] For those who have healthy kidneys, it is somewhat difficult to drink too much water,but (especially in warm humid weather and while exercising) it is dangerous to drink too little. While overhydration is much less common than dehydration, it is also possible to drink far more water than necessary which can result in water intoxication, a serious and potentially fatal condition.In particular, large amounts of de-ionized water are dangerous. Normally, about 20 percent of water intake comes in food, while the rest comes from drinking water and assorted beverages. Water is excreted from the body in multiple forms; including urine and feces, sweating, and water vapor in the exhaled breath. To help understand importance of water in the body, the International Bottled Water Association (IBWA at lists 13 things water does in the body: 1. Brain is 75% water. Moderate dehydration can cause headaches and dizziness,2. Water is required for expiration,3. Regulates body temperature,4. Carries nutrients and oxygen to all cells in the body,5. Blood is 92% water,6. Moistens oxygen for breathing.,7. Protects and cushions vital organs.,8. Helps to convert food into energy.,9. Helps body absorb nutrients.,10. Removes waste.,11. Bones are 22% water.,12. Muscles are 75% water.,13. Cushions joints Antioxidants As cellular metabolism/energy production requires oxygen, potentially damaging (e.g. mutation causing) compounds known as free radicals can form. Most of these are oxidizers (i.e. acceptors of electrons) and some react very strongly. For the continued normal cellular maintenance, growth, and division, these free radicals must be sufficiently neutralized by antioxidant compounds. Some are produced by the human body with adequate precursors (glutathione, Vitamin C), and those the body cannot produce may only be obtained in the diet via direct sources (Vitamin C in humans, Vitamin A, Vitamin K) or produced by the body from other compounds (beta-carotene is converted to Vitamin A by the body,[29] and Vitamin D is synthesized from cholesterol by sunlight). Phytochemicals (below) and their subgroup, polyphenols, make up the majority of antioxidants; about 4,000 are known.. Different antioxidants are now known to function in a cooperative network. For example, Vitamin C can reactivate free radicalcontaining glutathione or Vitamin E by accepting the free radical itself. Some antioxidants are more effective than others at neutralizing different free radicals. Some cannot neutralize certain free radicals. Some cannot be present in certain areas of free radical development (Vitamin A is fat-soluble and protects fat areas, Vitamin C is water soluble and protects those areas). When interacting with a free radical, some antioxidants produce a different free radical compound that is less dangerous or more

dangerous than the previous compound. Having a variety of antioxidants allows any byproducts to be safely dealt with by more efficient antioxidants in neutralizing a free radical's butterfly effect. Although initial studies suggested that antioxidant supplements might promote health, later large clinical trials did not detect any benefit and suggested instead that excess supplementation may be harmful. Phytochemicals A growing area of interest is the effect upon human health of trace chemicals, collectively called phytochemicals. These nutrients are typically found in edible plants, especially colorful fruits and vegetables, but also other organisms including seafood, algae, and fungi. The effects of phytochemicals increasingly survive rigorous testing by prominent health organizations. One of the principal classes of phytochemicals are polyphenol antioxidants, chemicals that are known to provide certain health benefits to the cardiovascular system and immune system. These chemicals are known to down-regulate the formation of reactive oxygen species, key chemicals in cardiovascular disease. Perhaps the most rigorously tested phytochemical is zeaxanthin, a yellow-pigmented carotenoid present in many yellow and orange fruits and vegetables. Repeated studies have shown a strong correlation between ingestion of zeaxanthin and the prevention and treatment of age-related macular degeneration (AMD). Less rigorous studies have proposed a correlation between zeaxanthin intake and cataracts. A second carotenoid, lutein, has also been shown to lower the risk of contracting AMD. Both compounds have been observed to collect in the retina when ingested orally, and they serve to protect the rods and cones against the destructive effects of light.. Another carotenoid, beta-cryptoxanthin, appears to protect against chronic joint inflammatory diseases, such as arthritis.. While the association between serum blood levels of beta-cryptoxanthin and substantially decreased joint disease has been established, neither a convincing mechanism for such protection nor a cause-and-effect have been rigorously studied. Similarly, a red phytochemical, lycopene, has substantial credible evidence of negative association with development of prostate cancer. As indicated above, some of the correlations between the ingestion of certain phytochemicals and the prevention of disease are, in some cases, enormous in magnitude. Yet, even when the evidence is obtained, translating it to practical dietary advice can be difficult and counter-intuitive. Lutein, for example, occurs in many yellow and orange fruits and vegetables and protects the eyes against various diseases. However, it does not protect the eye nearly as well as zeaxanthin, and the presence of lutein in the retina will prevent zeaxanthin uptake. Additionally, evidence has shown that the lutein present in egg yolk is more readily absorbed than the lutein from vegetable sources, possibly because of fat solubility.[35] At the most basic level, the question "should you eat eggs?" is complex to the point of dismay, including misperceptions about the health effects of cholesterol in egg yolk, and its saturated fat content.

As another example, lycopene is prevalent in tomatoes (and actually is the chemical that gives tomatoes their red color). It is more highly concentrated, however, in processed tomato products such as commercial pasta sauce, or tomato soup, than in fresh "healthy" tomatoes. Yet, such sauces tend to have high amounts of salt, sugar, other substances a person may wish or even need to avoid. Intestinal bacterial flora It is now also known that animal intestines contain a large population of gut flora. In humans, these include species such as Bacteroides, L. acidophilus, and E. coli, among many others. They are essential to digestion, and are also affected by the food we eat. Bacteria in the gut perform many important functions for humans, including breaking down and aiding in the absorption of otherwise indigestible food; stimulating cell growth; repressing the growth of harmful bacteria, training the immune system to respond only to pathogens; producing vitamin B12, and defending against some infectious diseases.

Eur J Clin Nutr. 1994 Feb;48 Suppl 1:S161-76; discussion S177. Adequacy of dietary mineral supply for human bone growth and mineralisation. Prentice A, Bates CJ. MRC Dunn Nutrition Unit, Cambridge, UK. Abstract The evidence on the relationship between dietary mineral supply and bone development in children has been extensively reviewed. Data from children and primates suggest that overt deficiencies of Ca, P and Zn are likely to produce rickets and growth retardation, while the effects of Mg deficiency on human bone are unknown. The manifestations of marginal deficiencies are little understood. The biological needs for Ca, P, Mg and Zn in childhood have been calculated based on mineral deposition rates, using published values for the mineral content of the human body, and on obligatory endogenous losses. As a rough guide, the estimated biological requirements for the Ca, P, Mg and Zn can be taken as 200, 100, 4 and 1 mg/d respectively. A comparison of measured daily intakes of children in developing countries with biological requirements was made. This revealed that P and Mg intakes were many times higher than estimated needs. Ca intakes at all ages were found to be close to the biological requirement for children in many Third World societies, before any allowance for possible poor absorption. Zn intakes approach estimated needs in breast-fed infants, particularly during weaning, but are 4-5 times higher in older children. Poor absorption from phytate-rich diets could affect Zn supply. Supplementation studies indicate that raising Zn intakes can increase height gains in certain vulnerable groups, such as infant and adolescent boys. In conclusion, the evidence suggests that inadequate dietary intakes of Ca and Zn may contribute to linear growth retardation in children of developing countries but more research is needed. NUTRIENT RDA DEFICIENCY DOSEASE SOURCE


440 gms

Underweight, underheight, Wheat, rice potato, etc., weight loss, lethargy, anaemia As above, fatty liver, Milk, eggs, fish meat, kwashiorkor, marasmus. beans, nuts Deficiency of fat soluble vit. Butter, A,D,E and K. veg.oils, fats margarine


70 gms


50 gms


5000 I.U.

Night blindness Carrots, leafy vegetables, xerophathalmia, egg yolk, milk. keratomalacia, susceptibility to infections. Rickets, osteomalacia. Egg yolk, sun light

Vit.D. Vit.E.

400-800 I.U. 25-30 mgs

Muscular dystrophy, hepatic Lettuce, soya, corn meat, necrosis liver and fish Hemorrhages. Spinach, bacteria. intestinal


70-140 mgs


75 mgs

Scurvy, scorbutic gums, Citrous fruits, hemorrhages, anaemia. vegetables, liver. Impaired wound healing. Beriberi, polyneuropathy, Yeast, palpitations, leg weakness. nuts. Same as above cereals,


Vit.B1 (Thiamine)

1.2 mg


Vit.B2 (ribofllllavin) Vit.B6 (Pyridoxine)

1.4 mg 2.2 mg

Same as above

Anorexia, seborrheic eczema Liver, groundnuts cereals, polyneuropathy, convulsions pulses, Pellagra, Dermatitis, dementia Liver, meat, fish cereals. diarrhea, angular stomatitis cheilosis, gloss it is, anorexia. Fatigue, headache, weakness Widely distributed. peculiar gait, reduced resistance to infections. Anemia, retardation of growth Yeast liver kideney. weakness, infertility.


16 mg

Penthothenic acid

4-7 mg


400 ug

Vit.B12 (Cyanocobalamin)

1 ug

Pernicious anaemia, kgloss it is Liver meat, eggs, milk. mucosal atrophy.

BALANCED DIET A balanced diet is defined as one which contains a variety of foods in such quantities and proportions that the need for energy, amino acids, vitamins, minerals, fats, carbohydrates and other nutrients is adequately met for maintaining health, vitality and general well being and also makes small provision for extra nutrients to withstand short duration of leanness. In constructing a balanced diet the dietary goals recommended by the WHO should be borne in mind: 1. Protien should account for appox. 15-20% of daily energy intake 2. Dietary fats should be limited to approx. 20-30% of total daily intake 3. Saturated fats should be avoided 4. Excessive consumption of refined carbohydrates should be avoided 5. Carbohydrates rich in natural fibre should be taken. However diet should be adapted to the special needs of growth, pregnancy, lactation, physical activity and medical disorders. Nutrition in Orthodontics

NUTRITION IN GROWTH AND DEVELOPMENT Nutrition plays a vital role in the growth and development of an individual. Development is a process which commences at conception and continues through birth until death. The perceptible visible evidences of developmental changes is Growth. Guilford in 1874 was amongst the first to advocate dietary deficiencies as an underlying cause of dentofacial irregularities. Important relationship exists between diet and development which can be seen during the nutrition of the foetus; placenta is the provider of the essential nutrient substrates and fetal tissue synthesizes its own proteins and nucleic acids. Therefore interferences with substrate availability results in decreased protein metabolic activity. Miller suggested that critical periods exist during the development of an organ and that stress imposed by the nutritional imbalance during critical periods can result in irreversible changes. Critical periods are defined as that time in the development of an organ system which is marked by the rapid synthesis and accretion of protein. The critical period roughly equates with the intense hyperplastic

growth phase. If imbalance occurs during hyperplastic phase then it causes irreversible damage to the tissues. If it occurs during hypertrophic phase then the growth may stop temporarily but will catch up later when adequate amounts of missing nutrients become available. Dietary deficiencies of essential nutrients during the critical periods of growth have caused retardation of growth and morphologic alterations of the orofacial area in both humans and animals. It has been shown in animal studies that certain hormones like the pituitary hormone are sensitive to nutritional deficiencies. Animals fed on diets deficient in folic acid , riboflavin and zinc , have borne offsprings with increased risk of cleft lip and palate. Even short periods of malnutrition (7-12 months) have resulted in an increase in open bites, a reduction in dimension of dental arches with inadequate space for teeth, insufficient dental eruption, the absence of natural diastema between the front deciduous teeth and shorter roots and interosseous rotation of the permanent teeth. Malnutrtion has also been associated with shorter mandibles in the antero posterior dimension, marked reduction in the ascending ramus, condylar region and the setting of the premolars; dentoalveolar inclination in the incisor region and reduction in the mesio-distal dimension of the third molars. Radiologic, histologic and histo chemical studies have demonstrated such abnormalities in osseous tissues as the reduction of the cortex and enlargement of the medulary spaces and a weakening of the osteoblastic and osteoclastic activity. Effect on bones: Kuftinec concluded bone develops in a manner similar to other soft tissues. First the soft tissue matrix is laid down followed by the formation of the hard tissue components. In animal studies, a high rate of bone growth can readily be demonstrated around the time of weaning when the animal changes from a relatively low protein to a high protein diet which is during the hyperplastic growth phase. Therefore it is the critical period in the development of bone. It is important to point out that growing bone is different to mature bone in its response to the environment. Any nutritional deficiency occurring during the active growth can be disastrous. Vitamin A defieciency which frequently accompanies protein calorie malnutrition may result in inadequate bone growth patterns with concomitant malalignment and malocclusion of the teeth. An excess of vitamin A during the critical growth period markedly inhibits the neural crest cell development and upsets the normal balance between bone formation and resorption. Increased Vitamin A also causes softening of the skull due to decrease in the calcium deposition. Calcium, Vitamin D and phosphorus are essential for the formation of bones and teeth. Deficiencies of these nutrients cause retarded jaw , teeth and condyle development. Deficiency of Vitamin D causes rickets, maxillary dysplasia, succeptibility to muscular traction. Facial sutures close with difficulty leading to openbite, transverse hypodimension and misshapen palate. Cleft lip and palate

Worlds most common birth defect is the cleft lip and cleft palate (1 in 900 births). A variety of nutrient deprivation or excess as well as terratogenic agents can produce a very high incidence of this congenital anomaly as palatal tissues are very succeptible to environmental changes. During palatal development a number of macromolecules increase during the critical ctages of palatal fusion like glycoproteins, enzymes, actin and mucopolysaccharides. If these are not supplied in the required amounts due to nutritional deficiency then will lead to the anomaly. Studies suggest that an excess of vitamin A during this phase may lead to cleft palate formation. INFLUENCE OF FOOD CONSISTENCY ON OROFACIAL DEVELOPMENT Mouth is affected by a complex system of forces generated by muscular and respiratory functioning. Much of this force generates as a result of masticatory activities that are dependant on the physical consistency of the food that is eaten. Soon after birth, the new born learns that food results from the action of sucking, followed by a feeling of well being. As a result of the sucking and pressing actions, that are associated with breast feeding, the baby develops the earliest important functional influences on both the thrust and physiologic growth of the mandible. In edentulous infants the centric occlusion and the control of lateral and protrusive movements are permitted and exercised by the interplay of the coronoid apophysis and the zygomatic arches. Breast nursing also aids greatly in developing the muscles of the lips, cheeks, tongue, pharynx and palate. These muscles are later used in speech and as a result we see comparatively fewer speech problems in such children. In animals , a soft diet doesnt provide adequate stimulus for the proper mastication, resulting in narrower maxillary arches. Similar observations have been made in humans leading to arch collapse syndrome. Waugh, Klatsky and Fisher documented a direct relation between reduction in chewing power and demand made on supporting structures leading to underdeveloped muscles of mastication and incidence of malocclusion. Singh and Chawla (1994) conducted a study on the contribution of diet in malocclusion in north Indian population. They stated that occasional or no consumption of coarse and fibrous food had a positive influence on the incidence of class II div 1 and skeletal type of malocclusions. The diets of rural populations, which usually contain an abundance of raw vegetables offer adequate muscular stimulation and hence orthodontic problems. It thus appears that these changes to softer food caused unfavorable changes in muscle tone and a tendency for skeletal and dental problems to develop. Effect of Nutrition on Teeth : Nutrition is most important during the period of time when teeth are undergoing matrix formation and calcification. It was futher shown that these processes could be influenced by maternal, infant and childhood diet.

Under such circumstances the physical and chemical properties of the enamel could be altered in the direction of increased dental caries succeptibility. Since the formation of primary and permanent teeth begins in uterine life and continues until the twelfth year( except the thid molars), it is the responsibility of the dentist to advice regarding dental health in young children and pregnant mothers. Food stuffs rich in calcium, phosphorus, Vitamin A,C and D should be recommended. The formative period of teeth can be divided into 3 segments; matrix formation, matrix calcification and pre eruptive maturation. Nutritional disturbances during matrix formation may manifest themselves in imperfect enamel formation. The enamel matrix being an epithelial tissue , is influenced by the deficiency of vitamin A. deficiency of this vitamin results in atrophy of ameloblasts. The enamel that forms subsequently is hypoplastic and theoretically at least favours the accumulation of carbohydrates and microorganisms. It is also well known that vitamin C is essential for the dentin and that initial dentin amrix formation must take place before enamel matrix formation can proceed. Consequently severe Vitamin c deficiency has had the secondary effect of producing enamel hypoplasia. Now provided that enamel matrix formation has proceeded normally , a variety of situations may intervene to alter the enamel matrix calcification. For example, enamel hypoplasia can be produced by dietary deficiency of calcium and phosphorus. Another vitamin essential for enamel calcification is vitamin D. With adequate quantities of vitamin D the texture of forming enamel surface approaches perfection, but in deficiency hypoplastic changes are observed. Studies have also shown that Magnesium deficiencies lead to the development of Bruxism habit in individuals. DIET: Diet affects teeth in 2 distinct ways. One is the local effect and depends on the intra oral chemical or physical action on the external surfaces of the teeth of the . the other is the systemic nutritional factor , which is important during the period of tooth development. Effects of carbohydrates , proteins and fats on Dental Caries: Carbohydrates: They have been demonstrated to be important etiologic agents in dental caries. Immediately following the bathing of the teeth with carbohydrates there is a drop in pH of the plaque, the return of the tooth plaque to its original base line pH is rather slow, about an hour. This drop in pH is indicative of acid production and most investigators conclude that bacterially produced acids are a major factor in the production of incipient carious lesions. Carbohydrates associated with formation of dental caries must: Be present in the diet in meaningful quantities Be cleared slowly or ingested frequently


Be readily fermented by cariogenic bacteria

Although it is well known that carnivorous animals rarely develop tooth decay and that persons ingesting high protein diet have no particular succeptibility to dental caries. It is too early to assess the importance of this finding in terms of dental caries etiology. However, it does point out to the possibility that under certain conditions modifications of the constituents dietary proteins may affect caries initiation. Fats: Dietary fats have a limited influence on dental caries. Experiments with animal suggest that the inhibition mechanism is a local one, very possibly associated with an oil film on the tooth surface. Thus altering the surface properties of the enamel and possible interference with the metabolism of oral microorganisms. Demineralisation: A common concern in orthodontics is the potential development of decalcification, caries and periodontal problems. These problems can be associated with bonds or bands when combined with an improper diet involving unregulated sugar consumption and inadequate oral hygiene. The relationship between dental caries and the ingestion of fermentable carbohydrates has known for a long time. Many foods contain substances called buffers that neutralize any acids formed for eg. Calcium from milk or protein from meat can neutralize or absorb acids. Feathrstone and Glatz in 1985 showed that measurable demineralization occurred in 4 weeks time, especially gingival to bands or brackets. Plaque accumulation has been shown to occur on brackets and some of the resins used to bond them. Brackets and some of the resins used to bond them. Bracket configuration, presence of wires, elastics, springs and other attachments interfere with the patients ability to keep some portion of the teeth and brackets clean. Clinical observation indicate that one of the most common sites for demineralization appear to lie at the junction between the bonding resin and the enamel, commonly gingival to the bracket base. ACTION OF FLOURIDE IN LIMITING TOOTH DECAY Fluoride in the concentration of 1ppm in drinking water is known to inhibit dental caries, primarily by altering the physical and chemical properties of the tooth. It is recognized that fluoride incorporated into the tooth at the time of calcification show a definite resistance to tooth decay, mechanism being the conversion of hydroxylappatite crystals of enamel to fluorapatite. When dilute solution of fluoride is brought in contact with fully calcified enamel a union of fluoride and enamel results. When teeth are subjected to topical fluoride , fluorine displaces the hydroxyl ions

from the hydroxyapatite crystal and forms fluorapatite which has reduced acid solubility. Also topical fluoride application decreases the permeability of the enamel. But care should be taken against excess fluoride consumed in the diet as it can cause cause systemic manifestations like osteoflurosis and if consumed during the tooth development , it can lead to dental fluorosis characterized by brownish and corroded appearance of teeth. Signs and Symptoms 1. increased density of various bones particularly pelvis and vertebrae. 2. increased calcification of ligaments, tendons and muscle insertions resulting in vague pains of hands and feet. 3. in its severest form it can lead to joint stiffening virtually immobilizing the patient. ROOT RESORPTION Root resorption is a common iatrogenic problem associated with orthodontic treatment. Resorption can be external- as a reaction to periodontal tissue, or internal- as a reaction to pulp. Many investigators have evaluated the effects of dietary factors on root resorption. Marshall as early as 1930 concluded that animals on deficient diets showed greater degree of resorption than do those on adequate diets, using the same appliance and the resorbed areas are greater in extent and are repaired more slowly in animals with deficient diets. This was supported by the study of Beck in 1931 on dogs, the animals with calcium and vitamin deficient diets were more succeptible to root resorption. Enstrom et al in 1988 investigated the effect of orthodontic force on periodontal tissues in normal and hypocalcaemic rats. Their observations gave the information that the increase in the occurrence and severity of root resorption in moderate hypocalcaemia was related to an increase in alveolar bone turnover. Glodie and King in 1984 conducted a study to investigate the tooth movement cycle and the area of root surface resorption in rats stressed with lactaion and diets deficient in calcium. Their results showed greater magnitude of tooth movementand overall root resoption was less in the animals which were stressed with diet . this manifestation was attributed to increased bone metabolism and decreased bone density. NUTRITIONAL INFLUENCE ON PERIODONTIUM Majority of the research findings on the effects of nutrition on oral and periodontal tissues point to the following: 1. There are nutritional deficiencies that produce changes in the oral cavity, these changes include alterations of the lips, oral mucosa, bone as well as the periodontal tissues. 2. There are no nutritional deficiencies that by themselves cause gingivitis or periodontal pocket.

There are however, nutritional deficiencies that can aggravate the injurious effects of the local irritants on the periodontium. Physical character of diet: Soft diet leads to plaque and calculus formation whereas hard and fibrous food provide surface cleansing action and stimulation which leads to decreased plaque and gingivitis. Chewing of fibrous food s doesnt increase gingival keratinisaton as believed, but it produces a type of oral muscular activity or physiotherapy that can have a beneficial stimulatory effect on strengthening the periodontal ligament and increasing the density of the alveolar bone. Effect of vitamin deficiency on periodontium. 1. Vitamin A deficiency leads to keratinizing metaplasia of the epithelium, increased susceptibility to infection and disturbances in bone growth, shape and texture. Animal experiments suggest that vit A deficiency may predispose to periodontal disease. 2. Vitamin B deficiency leads to gingivitis, glossitis and glossodynia, angular chelitis and inflammation of the oral mucosa.Folic acid deficient animals present necrosis of the gingival, periodontal ligament and alveolar bone without inflammation. The absence of inflammation ia the result of deficiency induced granulocytopenia. 3. Vitamin C its deficiency leads to Scurvy. It has been suggested that a role in periodontal disease by one of the following mechanisms: ascorbic acid may play

a) Low levels of ascorbic acid influence the metabolism of collagen within the periodontium, thereby affecting the ability of the tissue to regenerate and repair itself. b) Vit C deficiency interferes with bone formation and remodeling of the periodontal bone c) Its deficiency may aggravate the gingival response to plaque and worsen the edema, enlargement and bleeding Mc Canlies et al studied the effect of Vit C on the mobility of pig incisors under orthodontic forces and observed increased osteoclastic activity and large resorption lacunae in pigs with decreased or no Vit C in diet. 4. Vitamin D - It is essential for the absorption of calcium, for the maintenance of Ca and PO4 balance and for the formation of teeth and bones. Its deficiency is characterized by the osteoporosis of alveolar bone and cemental resorption. Effect Of Orthodontic treatment On nutrient Intake As studied earlier, Diet can affect the periodontal health, oral microbial composition, wound healing, protein synthesis growth and I.Q. But when a person is undergoing orthodontic treatment, his or her

dietary requirements and habits change which sjould be kept in mind before commencing the treatment. The diet of adolescent patients becomes more important because moving teeth creates an increased nutrient demand. The physical and physiological and emotional stresses caused by orthodontic treatment sets in motion hormonal reactions that increase nutrient mobilization and utilization. This raises the nutritional requirement of the patient.maintenance of diet is especially important to mprevent infection, promote growth and development and allowing the healing of periodontal tissues during treatment. Giordan (1997) studied the effect of orthodontic treatment on nutritional intake of the patient and concluded that there was a significant decrease in the fiber content of diet and higher fat and low carbohydrate soft food consumption. Strause and Saltzmann also concluded that there was a decrease in the Mn and Cu intakes during orthodontic treatment, which may lead to decreased bone remodeling. NUTRITIONAL CONSIDERATION IN ORTHODONTIC TOOTH MOVEMENT Tooth movement involves biologic responses to orthodontic forces, which may influenced by ascorbic acid. 17-72% of orthodontic patients are deficient in Vitamin C. lack of Vitamin C interferes with collagen synthesis thus affecting both periodontal ligament and the formation of osteoid. Animal studies have shown that vitamin C deficiency causes enlarged endosteal spaces with osteoclasts, uneven periosteal surfaces with osteoclastic activity. Vitamin C deficiency also affects the stability of orthodontic correction (ie); it affects retention. This has been confirmed from experiments on guinea pig incisors, where the vitamin C deficient group experienced more relapse. NUTRITIONAL CONSIDERATIONS IN SURGICAL PATIENTS: The mouth is the portal for entry of food into the body thus maxillofacial surgery of these structures may result in impaired food intake both prior to and after surgery. We must ensure adequate nutritional support in such patients. Patients require both an energy source and a protein source. Carbohydrates, proteins and fatty acids are sources of energy. Glucose is the energy source foe vital organs like brain. However hyperglycemia is not desirable. Fatty acids produce produce more energy and certain essential fatty acids must be supplied by the diet. Protein is not an energy source but its primary purpose is for cellular proliferation and protein synthesis. Protein is also important for imparting strength to the fracture repair. If it is absent then the wound healing is delayed. Vitamin A helps in epithelialization, collagen synthesis & cross linking and fibroblast differentiation. Vitamin C deficiency leads to impaired wound healing and collagen synthesis. Vitamin D and Calcium help in the healing of the hard tissues. Vitamin E acts as an antioxidant and thus reduces the damage

from the free oxygen radicals. Large doses of Vitamin E also inhibit healing. Vitamin K helps in activation of various clotting factors and thus is essential for blood clot formation during healing. Nutritional intake is dependant on several variables and one of them is Taste. Zinc and protein deficiency impairs taste bud regeneration, thus impairing the taste sensation of the patient which in turn affects the dietary intake of the patient.

Endocrinology The activities of various organs in our body are controlled by two systems namely, nervous system and endocrine system. These two control systems are interrelated. Most of the functions of nervous system are executed by hormonal substances. And, most of the endocrine functions are controlled by nervous system. The endocrine system constitutes endocrine glands which are situated in different parts of the body. The functions of these glands are mediated by chemical substances which are called chemical messengers, chemical mediators or first messengers or hormones The endocrine glands are also called ductless glands because the hormones secreted by them are directly released into blood. The hormones are transported by blood to the target organs or tissues in differenct parts of the body, where the actions are executed.

CHEMISTRY OF HORMONES Hormones are classified into three types, depending upon their chemical nature( Tabte6. 5-1). i. Steroid hormones, ii. Protein hormones and iii. Derivatives of the amino acid, called tyrosine. STEROID HORMONES Steroid hormones are the hormones derived from cholesterol or its derivatives. Steroid hormones are the corticosteroids and sex hormones. PROTEIN HORMONES The protein hormones are large or small peptides. Proteins hormones are the hormones secreted by pituitary gland parathyroid glands, pancreas and placenta. DERIVATIVES OF THE AMINO ACID TYROSINE

There are two types of hormones, which are the derivatives of the amino acid called tyrosine. Thyroid hormones and adrenal medullary hormones are derived from tyrosine. HORMONAL ACTION INTRODUCTION Any hormone that causes changes in the target cells does not act directly on the cellular structure. First the hormone combines with receptors present in the target cells to form a receptor-hormone complex. This receptor hormone complex induces various changes or reactions in the cells. HORMONE RECEPTORS The receptors of the hormones are large proteins present in the target cells of the hormones. Each cell has thousands of receptors. The important characteristic feature of the receptors is that, each receptor is highly specific for one single hormone i.e. each receptor can combine with only one hormone. Thus, any hormone can act on a target cell, only if the target cell has the receptor for that particular hormone. Situation of the Hormone Receptors The receptors are situated in cell membrane, cytoplasm or nucleus of the cells as follows: 1. Cell membrane: Receptors of catecholamines(adrenaline and noradrenaline) and those of protein hormones(hormones of pituitary gland, parathyroid gland and pancreas) are situated in the cell membrane. 2. Cytoplasm: Receptor of steroid hormones is situated in cytoplasm of target cells. 3. Nucleus: Receptor of thyroid hormones is situated in the nucleus of the cell.


Definition: A hormone is a chemical substance that is secreted into the internal body fluids by one cell or a group of cells and has a physiological control effect on other cells of the body

Hormones may be local hormones or general hormones: Local hormones are the ones, which have specific local effects on the adjoining tissues. Examples of local hormones are acetylcholine released at the parasympathetic and skeletal nerve endings Most of the general hormones are secreted by specific endocrine glands. These hormones are transported in the blood to all parts of the body and cause many different reactions. A few of the general hormones affect all or almost all cells of the body. Examples are growth hormone, which causes growth in almost all cells of the body. Others affect only specific tissues called target tissues because only these tissues have the specific target cell receptors that will bind the hormones to initiate their actions. For instance, adrenocorticotropin from the anterior pituitary specifically stimulates the adrenal cortex, causing it to release adrenocortical hormones.

Overview of the Important Endocrine Glands and their Hormones:

Anterior Pituitary Hormones: 1. 2. 3. 4. 5. 6. Growth Hormone Adrenocorticotropin Thyroid-stimulating hormone Follicle-stimulating hormone Leutenizing hormone Prolactin

Posterior Pituitary Hormones: 1. Antidiuretic hormone



Adrenal Cortex: 1. 2. Cortisol Aldosterone

Thyroid Hormone: 1. 2. Thyroxine and triidothyronine Calcitonin

Islets Of Langerhans In The Pancreas: 1. 2. Insulin Glucagon

Ovaries: 1. 2. Estrogen Progesterone

Testes: Testosterone Parathyroid Gland: Parathormone

The Pituitary Hormones:

The pituitary gland, also called the hypophysis or master endocrine gland, is a small gland that lies in the sella turcica, a bony cavity at the base of the brain. It is connected to the hypothalamus by the pituitary stalk. The pituitary gland is divisible into two parts: adenohypophysis or anterior pituitary and neurohypophysis or posterior pituitary. The pituitary gland secretes six important hormones that have just been reviewed.

Control of Pituitary Secretions by the Hypothalamus: Almost all secretions from the pituitary gland are controlled by hormonal or nervous signals originating from the hypothalamus.

Secretion from the posterior pituitary is controlled by nerve signals that originate in the hypothalamus and terminate in the posterior pituitary. In contrast, hormones called hypothalamic releasing and inhibitory hormones, which are secreted within the hypothalamus and then conducted to the pituitary through the hypothalamic-hypophyseal portal vessels, control secretion of the anterior pituitary. The hypothalamus, in turn, receives these signals from all possible sources in the nervous system. For example, when a person is exposed to pain, a portion of the pain signal is transmitted to the hypothalamus. All the major anterior pituitary hormones besides Growth Hormone exert their principal effects by stimulating target glands. The functions of each of these hormones are discussed with the respective target glands.

Growth Hormone: Growth hormone, also called somatotrophic hormone or somatotropin does not function through a target gland. It causes growth of almost all tissues of the body that are capable of growing by causing both increase in the size and number of cells and specific differentiation of certain types of cells such as bone cells and muscle cells.

Although growth hormone causes increased growth in almost tissues of the body, its most obvious effect is to increase growth of the skeletal frame. This results from: 1) increased deposition of protein by the chondrocytic and osteogenic cells 2) increased rate of reproduction of these cells 3) the specific effect of converting chondrocytes into osteogenic cells Growth hormone causes an increase in the length of the long bones where the epiphyses at the ends of the bones are separated from the shafts. However, once the epiphyses have united with the shafts, growth hormone has no further ability to lengthen the bones. In intramembranous bone growth, growth hormone strongly stimulates the osteoblasts. These bones can continue to enlarge throughout life under the influence of growth hormone. For instance, the jawbones can be stimulated to grow even after adolescence, causing forward protrusion of the lower jaw.

In animal experiments, it is seen that when experimental animals are treated with growth hormone, new bony trabeculae are formed in a more vertical orientation causing a closing of the Stutzmann Angle. It us also seen that when blood level of STH (or testosterone) increases, supplementary lengthening of the mandible is greater than the maxilla. Metabolic Effects of Growth Hormone: Apart from causing growth, GH has many metabolic effects as well, including 1) increased rate of protein synthesis in all cells of the body 2) increased mobilization of fatty acids from adipose tissue, increased free fatty acids in the blood, increased use of the fatty acids for energy 3) decreased rate of glucose utilization throughout the body Regulation of Secretion: The secretion of growth hormone varies depending on a number of factors: 1. Age: The level of growth hormone reaches a peak during adolescence after which it decreases slowly with aging, finally falling to about 25 percent of the adolescent level in very old age. 2. Rate: The rate of growth hormone secretion varies in relation to the persons state of nutrition or stress such as during (i) starvation especially during severe protein deficiency (ii) hypoglycemia or low concentration of fatty acids in the blood (iii) strenuous exercise (iv) excitement (v) trauma. It characteristically increases during the first two hours of deep sleep The Somatomedins: Although growth hormone is generally regarded as the principal hormone regulating skeletal growth, evidence has accumulated that growth hormone does not itself stimulate linear growth, but rather induces the formation of a secondary growth-promoting factor. Although originally designated sulfation factor (because it stimulates the incorporation of radioactive sulfate into glycosaminoglycans of cartilage), this term has now been replaced by the more generic name somatomedin. The prefix

somato connotes the hormonal relationship to somatotropin, whereas the suffix medin indicates that somatomedin is an intermediary in growth hormone action. Discovery of Somatomedins: The discovery of somatomedins is attributed to the pioneering work of Salmon and Daughaday. These researchers drew on the experience of earlier workers who had shown that radioactive sulfate (35SO 4) preferentially accumulated by cartilage in-vivo, and that this accumulation is reduced following hypophysectomy and restored by the administration of growth hormone. Salmon and Daughaday incubated small costal cartilage segments obtained from hypophysectomized rats with 35SO 4 in a nutrient medium containing the test sera. They showed that normal serum stimulated 35SO 4 uptake by cartilage in vitro whereas serum from hypophysectomized rats or hypopituitary children failed to do so. When growth hormone was administered to a hypopituitary dwarf, his serum regained its ability to stimulate 35SO 4 uptake in vitro. Their most provocative observation, however, was that when serum from hypopituitary children was enriched by direct addition of growth hormone in vitro, it had no stimulatory effect on sulfate uptake. Since growth hormone was itself inactive in this assay, it became apparent that the sulfation factor activity of plasma, although induced in vivo by growth hormone administration, was not growth hormone itself. Origin of Somatomedins: So far the mechanism by which growth hormone stimulates somatomedin production remains unclear. Liver, however, appears to be one site of production. Following administration of growth hormone labeled with iodine 125, almost none is concentrated in the skeleton, whereas very high concentrations are found in the liver, kidney and adrenal cortex. Since the somatomedin molecule appears to be about one third as large as growth hormone, it might be reasonable to suspect that it arises from degradation of growth hormone itself. According to this hypothesis, growth hormone would serve as a prohormone in a matter analogous to the release of insulin from proinsulin. Another possibility is that proinsulin might serve as a prohormone for somatomedin as well as for insulin itself. Evidence has been advanced that somatomedin is not only insulin-like in its biological actions but that highly specific cellular receptors in tissues are incapable of distinguishing between insulin and somatomedin. At least four somatomedins have been identified denoted by the suffixes A, B, C, D. Actions of Somatomedins: Studies were undertaken to determine which of the metabolic effects ascribed to growth hormone are due to growth hormone itself and which require mediation of somatomedin. Although growth hormone itself stimulates protein synthesis in liver and muscle in vitro, these effects are weak and require unphysiologically high doses. All known growth hormone actions on cartilage are attributable to

somatomedin rather than a direct effect of growth hormone. For most of the extra-skeletal effects of growth hormone, it remains to be determined which are due to a direct action of growth hormone and which require induction of somatomedins. Abnormalities of Growth Hormone Secretion: 1. Dwarfism: Most cases of dwarfism result from generalized deficiency of anterior pituitary secretion during childhood. In general, the features of the body develop in proportion to one another, but the rate of development is greatly decreased. The panhypopituitary dwarf does not pass through puberty and never secretes a sufficient quantity of gonadotropic hormones to develop adult sexual functions. In some dwarfs, the deficiency is of growth hormone alone; these individuals do mature sexually. 2. Gigantism: Gigantism results from acidophilic tumors of the anterior pituitary during adolescence. As a result, large quantities of growth hormone are produced. All body tissues grow rapidly, including the bones. If the condition occurs before adolescence, the person becomes a giant as tall as 8 feet. The giant ordinarily has hyperglycemia and full-blown diabetes may also occur. 3. Acromegaly: If an acidophilic tumor occurs after adolescence- that is, after the epiphyses of the long bones have fused with the shafts- the person cannot grow taller, but the soft tissues can continue to grow and the bones can grow in thickness. This condition is known as acromegaly. Enlargement is especially marked in the bones of the hands and feet and in the membranous bones including the cranium, nose, bosses on the forehead, supraorbital ridges, lower jawbone and portions of the vertebrae because their growth does not cease at adolescence. Consequently, the lower jaw protrudes forward, the forehead slants forward, the nose increases to as much as twice its normal size, the fingers become extremely thickened and the hands develop a size twice the normal. Antidiuretic Hormone (ADH, Vasopressin): ADH is secreted by the posterior pituitary gland. Vasopressin( VP) is an octapeptide hormone formed in neuronal cells of the hypothalamus and stored in the posterior lobe of the pituitary. Physiological Functions of ADH: Extremely minute quantities of ADH when injected into a person can cause antidiuresis, that is, decreased excretion of water by the kidneys. In the absence of ADH, the collecting tubules and ducts are almost impermeable to water, which allows extreme loss of water into the urine. In the presence of ADH, the permeability of the collecting tubules and ducts greatly increases and allows most of the water to be reabsorbed, thereby conserving water in the body. EFFECTS ON BONE It has a stimulatory effect on proliferation of stromal cells. In vitro, VP significantly increases the numbers of bone colonies, indicating proliferation of osteogenic stem cells. VP has no effect on osteoprogenitor cells limiting the differentiation of osteoblasts and consequently having little effect on bone growth (Yashar and Bernard, 1996).

Regulation of ADH Production: Osmotic concentration of the extracellular fluid regulates ADH production. Increased concentration of the extracellular fluid stimulates ADH production and vice versa. Vasoconstrictor Effects of ADH: Higher concentrations of ADH have a potent effect of constricting arterioles everywhere in the body and therefore increasing the arterial blood pressure. For this reason, ADH is also called vasopressin. One of the stimuli for causing intense ADH secretion is decreased blood volume. This occurs especially strongly when the blood volume decreases 15 to 25 percent.

The Thyroid Hormones: The thyroid gland is located immediately below the larynx on either side and anterior to the trachea. It secretes two important hormones: thyroxine and triidothyronine that have a profound effect of increasing the metabolic rate of the body. Most of the hormone secreted by the thyroid gland is thyroxine. However, almost all of the thyroxine is eventually converted into thriidothyronine, the more potent form. Functions of Thyroid Hormones: 1) Increased transcription of genes: Thyroid hormones cause nuclear transcription of large numbers of genes. Therefore, in all cells of the body the number of enzymes, structural proteins and transport proteins increases. The net result is increase in the functional activity of all the cells of the body. 2) Effect on growth: Thyroid hormone has both general and specific effects on growth. In human beings, the effect of thyroid hormone on growth is manifest mainly in growing children. In hypothyroid children, the rate of growth is greatly retarded. In hyperthyroid children, the rate of skeletal growth is greatly accelerated causing the child to become considerably taller at an earlier age. However, the bones also mature more rapidly and the epiphyses close at an early age so that the eventual height of the child may actually be shortened. The specific effect of thyroid hormone on growth pertains to its requirement to promote growth and development of the brain at an early age. 3) Effects on specific bodily mechanisms:

i. On Carbohydrate Metabolism: Thyroid hormone stimulates all aspects of carbohydrate metabolism including rapid uptake of glucose by the cells, enhanced glycolysis, gluconeogenesis and even increased insulin secretion with all its secondary effects. ii. On Fat Metabolism: Increased thyroid hormone depletes the fat stores of the body, decreases the quantity of cholesterol and increases the free fatty acids in the plasma by causing mobilization of lipids from the fat tissue. It also greatly accelerates the oxidation of free fatty acids by the cells.

iii. On Basal Metabolic Rate: Because thyroid hormone increases metabolism in all cells of the body, excess quantities of this hormone can increase the BMR 60 to 100% above normal. iv. On Cardiovascular System: Increased BMR increases blood flow, which increases the cardiac output and heart rate. v. On Skeletal System: These hormones produced by thyroid clear cells (parafollicular cells) in a general way increase cellular metabolism and in particular increase bone growth and development (E rnsta ndF roesch,l 9g7). Osteoprogenitor cells proliferate and differentiate into osteoblasts by the stimulation of thyroid hormone receptors on their plasma membranes (Krieger et al., 1988). Thyroid hormone therapy and hyperthyroidism often leads to bone resorption (Mosekilde and Melsen, 1978), sometimes acting in concert with 1,25(OH)2D3 and PTH (Cross et al., 1989). While there are contradictory effects, the vector of bone resorption and bone apposition is in the direction of bone apposition.

Regulation of Thyroid Secretion: The secretion of thyroid hormones is under feedback control from the hypothalamus and the anterior pituitary and is affected by the circulating levels of T3 and T4 in the plasma. When the level of T3 and T4 falls in the plasma, it sends a negative feedback signal to the hypothalamus and the anterior pituitary gland. This causes increased secretion of thyrotropin releasing hormone from the hypothalamus and thyroid stimulating hormone from the anterior pituitary both of which eventually result in increased secretion of T3 and T4 from the thyroid gland. This restores the normal plasma levels of these hormones following which the feedback signal ceases.

Disorders of Thyroid Secretion: 1. Hyperthyroidism (Graves Disease, Thyrotoxicosis): The symptoms of hyperthyroidism include a high state of excitability, intolerance to heat, increased sweating, mild to extreme weight loss, muscle weakness, nervousness and other psychic disorders, extreme fatigue but inability to sleep. Exophthalmos: Most people with hyperthyroidism develop some degree of exophthalmos or protrusion of the eyeballs. The cause of exophthalmos is edematous swelling of the retro-orbital tissues and degenerative changes in the extraocular muscles. In some patients, the condition becomes severe enough that the eyeball protrusion stretches the optic nerve enough to damage vision. More often the eyes are damaged because the eyelids do not close completely over the protruding eyeballs. As a result, the eyes become dry and irritated and often infected, resulting in ulceration of the cornea. 2. Hypothyroidism: Hypothyroidism results in myxedema in adults and cretinism in children.

Myxedema: Myxedema develops in adults with almost total lack of thyroid function. These patients show fatigue and extreme somnolence with sleeping up to 12 to 14 hours a day, muscular sluggishness, decreased cardiac output and weight gain. There is swelling of the face with bagginess under the eyes. Cretinism: Cretinism is caused by extreme hypothyroidism in fetal life, infancy and childhood. Apart from the features of hypothyroidism seen in the adult, this condition is characterized especially by failure of growth and mental retardation. The Adrenocortical Hormones: The two adrenal glands lie at the superior poles of the two kidneys. Each gland is composed of two distinct parts- the outer adrenal cortex and the inner adrenal medulla. The adrenal medulla secretes the hormones epinephrine and norepinephrine in response to sympathetic stimulation. The adrenal cortex secretes hormones called corticosteroids. These hormones are of two major types- mineralocorticoids and glucocorticoids. In addition, small amounts of sex hormones called androgenic hormones are also secreted by the adrenal cortex. The mineralocorticoids are so called because they affect the electrolytes of the extracellular fluidssodium and potassium in particular. The glucocorticoids have gained their name because they have an important effect in increasing the blood glucose concentration. Aldosterone is the principal mineralocorticoid and cortisol is the principal glucocorticoid. Functions of Mineralocorticoids- Aldosterone Total loss of adrenocortical secretion causes death of a person unless the person receives extensive salt therapy. Aldosterone causes reabsorption of sodium and loss of potassium in the collecting tubules. Without mineralocorticocoids, the potassium ion concentration of the extracellular fluid rises, the sodium and chloride concentrations decrease, the total extracellular fluid volume and blood volume become greatly reduced. The person develops diminished cardiac output, which proceeds to a shock-like state followed by death. Regulation of Aldosterone Secretion: Four factors are known to play essential roles in aldosterone secretion. In the probable order of their importance, they are as follows: 1. Increased potassium ion concentration in the extracellular fluid greatly increases aldosterone secretion 2. Increased activity of the rennin-angiotensin system also greatly increases aldosterone secretion

3. Increased sodium ion concentration in the extracellular fluid very slightly decreases aldosterone secretion 4. ACTH from the anterior pituitary is necessary for aldosterone secretion but has little effect in controlling the rate of secretion.

Functions of Glucocorticoids: Cortisol


On Carbohydrate Metabolism:

i. Stimulation of Gluconeogenesis: By far the best-known metabolic effect of cortisol is gluconeogenesis, that is, synthesis of carbohydrates from non-carbohydrate sources such as proteins, fats etc. by the liver ii. Decreased Glucose Utilization by the Cells: Cortisol causes a moderate decrease in glucose utilization by cells everywhere in the body .Both the increased rate of gluconeogenesis and the reduction in the rate of glucose utilization causes the blood glucose concentrations to rise. This condition is called adrenal diabetes. 2. On Protein Metabolism: Cortisol causes reduction of the protein stores in essentially all body cells except those of the liver. This is caused by both decreased protein synthesis and increased catabolism of protein already in the cells. Cortisol also depresses the formation of RNA and subsequent protein synthesis. At the same time, cortisol also increases the liver and plasma proteins 3. On Fat Metabolism: Cortisol promotes mobilization of fatty acids from adipose tissue. This increases the concentraton of free fatty acids in the plasma, which also increases their utilization for energy. 4. In Stress and Inflammation: Almost any type of stress, physical or neurogenic, causes increased adrenocortical secretion of cortisol. The different types of stress that increase cortisol release are trauma of almost any type, infection, intense heat or cold, surgery etc. Glucocorticoids inhibit arachadonic acid formation and therefore PG. PROSTAGLANDINS Most cells in the body and osteoblasts in bone secrete prostaglandins( PG). pGE, as a product of arachadonic acid from cell membrane phospholipids, is the predominant prostaglandin in bone.Several cytokines and hormones induce PGE secretion in bone which in turn effects cytokine activity, stimulating osteoclast activation( Schelling et al.' 1980) and loss of osteoblastic junctional complexes( Shene t al., 1986).Oppositely, pG can stimulate bone formation. While osteoclasts are normally increased in bone and bone marrow cultures with PGE2 it also can sometimes initially inhibit the activity of osteoclasts in tissue culture (yonaga et al-, 1919; Ibbotson et al., 1984).PGs stimulate osteoprogenitor cells to proliferate and differentiate so that osteogenesi is increased(c hyun and Raisz,l 9g4; Jeee t al., l9g5; ueda et al., l9g0). 5. FUNCTION OF GLUCOCORTICOIDS ON SKELETAL SYSTEM: Glucocorticoids affect bone mass by, first of all, decreasing intestinal Ca++ absorption. This causes a decrease in plasma Ca++ which through

negative feedback stimulates the parathyroid gland to secrete PTH. Oversecretion could lead to secondary hyperparathyroidism (Gennari, tSdS; peJt et al., l9g4). Extensive use of glucocorticoids invariably causes massive loss of trabecular bone (Bressote t al;.,1 979) sometimes through action on osteoblast receptors which inhibit osteogenesis . Glucocorticoids block the synthesis of various osteogenic proteins which, in effect, reduces bone formation as well (peck et al., 1967). Glucocorticoid receptors on osteoblasts ,when activated, inhibit Type I procollagen formation and activated receptors on osteoprogenitor cells inhibit mitosis. The predominant effect of glucocorticoids is to inhibit IGF-I synthesis in osteoblasts which inhibits mitosis, which leads to a decrease of bone formation and therefore leads to a decrease in bone mass.

Vitamin D, Parathyroid Hormone and Calcitonin: Vitamin D and its role in Calcium and Phosphate Absorption: Vitamin D has a potent role in increasing calcium absorption from the intestinal tract. However, Vitamin D itself is not the active substance that actually causes these effects. Instead the Vitamin D must first be converted through a succession of reactions in the liver and the kidneys to the final active product, 1,25-dihydroxycholecalciferol also called calcitriol. Parathyroid Hormone: Parathyroid hormone is secreted by the four parathyroid glands, which are located immediately behind the thyroid gland. Parathyroid hormone causes rapid increase in blood calcium and drop in phosphate levels. The rise in calcium is caused by: 1. Increased calcium and phosphate absorption from the bone 2. Decreased renal excretion of calcium Decline in phosphate concentration is caused by excessive renal phosphate excretion. Effect of Parathyroid Hormone on Intestinal Absorption of Calcium and Phosphate: Parathyroid hormone greatly enhances both calcium and phosphate absorption from the intestines by increasing the formation in the kidneys of calcitriol from Vitamin D. Control of Parathyroid Secretion: Even the slightest decrease in calcium ion concentration in the extracellular fluid causes the parathyroid glands to increase their rate of secretion within minutes. If the decreased calcium ion concentration persists, as in rickets, the glands will hypertrophy. On the other hand, any condition that increases the calcium ion concentration above normal causes decreased activity and reduced size of the parathyroid glands. Such conditions include: (1) excess quantities of calcium in the diet (2) increased Vitamin D in the diet (3) bone absorption caused by other factors

ROLE OF PARATHYROID ON SKELETAL SYSTEM AND BONE: A polypeptide, PTH, is produced by the principal cells of the parathyroid glands. The hormone is secreted when lowered levels of calcium circulate through the vascular system of the gland. This feedback system also inhibits secretion when calcium levels rise. Multinucleated osteoclasts although without receptors to PTH, ultimately respond to PTH stimulation by activating dormant osteoclasts or by developing new osteoclasts from the fusion of mitotic monoblastic precursors( Rouleaue t al., 1988;B aron et al., 1986;Burger et al., 1986). In osteoclasts PTH stimulates cell adhesion molecules, increases motility, size, ruffled borders subadjacent acidity, and lysosomal enzyme production( Barone t al., 1989).This activation takes several hours. Physiologically, activated osteoclasts resorb bone, releasing calcium from the calcified matrix into the vascular circulation. PTH binds to cell membrane receptors in osteoprogenitor cells, osteoblasts and osteocytes( Rouleaue t al., 1988).The affect is to generally increase metabolism, to cause osteoblasts to become osteolytic, exposing bone surfaces and releasing osteoclast activating factors such as prostaglandins(H oltrop et al., 1974;M iller, 1978).PTH can have contradictory effects on osteoblastic activity (Tam et al., 1982):its immediate effect is to inhibit secretory activity (Hock et 'at., 1989b).I n the long term PTH can cause differentiation of osteoprogenitor cells into osteoblasts (Skjodt et al., 1992). Parathyroid hormone-related peptide (PTH-RP), a long chain peptide, is produced by many tissues and malignancies associated with hypercalcemia such as hyperparathyroid adenomas( Goltzman et al., 1989;B roaduse t al., 1988).PTH-RP and PTH have common receptor sites in bone (Nissensone t al., 1988). Both stimulate bone resorption although PTH-RP does not stimulate the differentiation of osteoblasts from osteoprogenitor cells and is not involved with the coupling effect in bone. It is secreted by osteoblasts probably having paracrine functions like other cytokines( Hock et al., 1989a).

Hypoparathyroidism and Hyperparathyroidism: Hypoparathyroidism: Hypoparathyroidism causes hypocalcemia, which results in tetany. Whem the extracellular fluid calcium ion concentration falls below normal, the nervous system becomes progressively more excitablebecause this causes this causes increased neuronal membrane permeability of to sodium, allowing easy initiation of action potentials and causing them to discharge spontaneously to elicit tetanic muscle contractions. Tetany in the hands, which usually develops before tetany develops in other parts of the body, is called carpopedal spasm. Tetany ordinarily occurs when the calcium ion concentration falls from its normal level of 9-11 mg/dl to about 6 mg/dl. Hyperparathyroidism: Hyperfunctioning of the parathyroid glands results in hypercalcemia. When the level of calcium in the body fluids rises above, the nervous system is depressed and the reflex activities of the central nervous system can become sluggish. Other features include constipation and lack of appetite. Symptoms of hypercalcemia begin to appear when the blood level of calcium rises above 12 mg/dl and become marked above 15 mg/dl. Calcitonin:

Calcitonin is secreted by the thyroid gland. This hormone also plays an important role in calcium metabolism. It is antagonistic in its action to parathormone and decreases the blood calcium levels by the following two mechanisms: 1. 2. It decreases the absorptive activity of the osteoclasts It also decreases the formation of new osteoclasts

ROLE OF CALCITONIN IN SKELETAL SYSTEM This 32-amino acid peptide is primarily secreted by parafollicular cells in the thyroid gland and to a Iesser extent by neurons (Heersche et al., 1974). Calcitonin is secreted by calcitonin producing cells when vascular Ca++ levels are high (Deftos and Roos, 1989). It reacts with target cells by binding to cell membrane receptors. The first cellular messenger is cAMP. Primarily, it binds to osteoclast receptors. The osteoclasts respond by reducing the size and shape of their ruffled borders with attending inhibition of cell adhesion (Chambers et al., 1984). This allows the osteoclast to become motile, immediately reducing the numbers of osteoclasts on the bone surfaces (Chambers et al., 1982). The resultant effect is significantly to reduce bone resorption for about 20-24 hours (Wener et al., 1972).After this time, however, there may be a rebound effect which increases the numbers of osteoclasts to, or above baseline( Klaushofere t al., 1989).I n part, this may follow calcitonin-mediated monocyte deactivation (Nong et al., 1989). Calcitonin has its major influence on osteoclast inhibition although there are some reports which emphasize its facilitory action on osteoblasts (F arleye t al., 1988,1 989a,b ).

Insulin and Glucagon: Insulin is secreted by the cells of the Islets of Langerhans. The hormone is associated with energy abundance, that is, when there is great abundance of energy giving foods in the diet, especially excess amounts of carbohydrates and proteins, insulin is secreted in great quantity. Effects of Insulin: 1. On Carbohydrate Metabolism:

i. Muscle: The resting muscle membrane is only slightly permeable to glucose. However, when the muscle is stimulated by insulin, the membrane permeability greatly increases. Insulin also stimulates the synthesis of muscle glycogen. ii. Liver: One of the most important effects of insulin is to cause most of the glucose absorbed after a meal to be immediately stored as glycogen. Then, between meals, when the blood glucose level begins to fall, insulin secretion decreases rapidly and the liver glycogen is split back to glucose. When the

quantity of glucose entering the liver cells is more than can be stored as glycogen, insulin promotes the conversion of all this excess glucose into fatty acids. Insulin also inhibits gluconeogenesis. iii. Brain: Secretion of insulin has little or no effect on uptake of glucose by the brain as even in the absence of insulin brain tissue can take up glucose, unlike other cells of the body. 2. On Fat Metabolism: Insulin is a fat sparer. First insulin increases the utilization of glucose by most of the bodys tissues, which automatically decreases the utilization of fat. Insulin also promotes fatty acid synthesis, all of which lead to fat storage in adipose tissue. 3. On Protein Metabolism: Insulin promotes protein formation and prevents the degradation of proteins. 4. On Growth: Insulin has a synergistic effect on growth along with growth hormone since it is required for the synthesis of proteins. It has been seen that in depancreatized and hypophysectomized rats, the administration of either growth hormone or insulin one at a time causes almost no growth. Yet a combination of these two hormones causes dramatic growth. Control of Insulin Secretion: Formerly, it was believed that insulin secretion is controlled almost entirely by blood glucose concentration. However, it is now known that there are other factors that play an important role as well. Amino acids administered in the absence of a rise in blood glucose concentration cause only a small increase in insulin secretion. However, when administered at the time of raised blood glucose levels, the glucose-induced secretion of insulin may be twice as much in the presence of excess amino acids. Thus, amino acids strongly potentiate the glucose stimulus for insulin secretion. Gastrointestinal hormones like gastrin, secretin which are secreted after a meal cause an anticipatory increase in insulin secretion in preparation for the glucose and amino acids to be absorbed from the meal.

Glucagon: Glucagon, a hormone secreted by the -cells of the Islets of Langerhans when the blood glucose concentration falls, has several functions that are diametrically opposite to those of insulin. Effects on Glucose Metabolism: The major effects of glucagon on glucose metabolism are: (1) breakdown of liver glycogen (glycogenolysis) (2) increased gluconeogenesis in the liver. Both these effects greatly enhance the availability of glucose to other parts of the body. Other Effects:

Glucagon activates adipose cell lipase making increased quantities of fatty acids available to the energy systems of the body. It also inhibits the storage of triglycerides in the liver, which prevents the liver from removing fatty acids from the blood; this also makes fatty acids available to other tissues of the body. Regulation of Glucagon Secretion: Increased blood glucose concentration inhibits glucagon secretion. The blood glucose concentration is the most potent factor that controls glucagon secretion. The effect of blood glucose concentration on glucagon secretion is exactly opposite to that of insulin secretion. Excitatory Effect of Amino Acids: High concentrations of amino acids, as occur in the blood after a protein meal, stimulate the secretion of glucagon. This is the same effect that amino acids have on insulin secretion. Thus, in this instance, the glucagon and insulin responses are not opposite. Excitatory Effect of Exercise: In exhaustive exercise, the blood concentration of glucagon increases fourfold to fivefold. What causes this is not understood because the blood glucose concentration does not necessarily fall. A beneficial effect of glucagon is that it prevents a fall in blood glucose. . SEX HORMONES Estrogens, progestins, and androgens all have osteo-stimulatory actions. It is well known that loss of estrogen in post-menopausal women leads to bone loss and osteoporosis( Raisz et al., l9g3). One mechanism of estrogen action is to increase the osteogenic activity of 1,25(OH)2D3 and calcitonin (Cieema et al.' 1989).Estrogen therapy therefore tends to decrease the onslaught of osteoporosis( Raisz, 19gg; Bjomsson et al.' 1989).But research to find estrogen receptors on osteoblasts has been ambiguous and the effects on various osteogenic substrates is variable( Chen and Feldman,1 978; Colstone t at., tOSl;. Estrogens may have indirect effects on osteoclast activity by reducing its resorptive function (Arnett et al., 1989).Like estrogens, androgens have a stimulatory effect on osteoblasts (E inhorn et al., l9g9). Testosterone: Apart from its effects in causing growth of the secondary sexual characters, testosterone has some other functions as well: Effect on Bone Formation and Muscle Development: One of the most important male characteristics is the development of increasing musculature after puberty, about 50 percent more than the females, which is a function of testosterone. Because of the great effect that testosterone has on the body musculature, it is widely used by athletes to improve their muscular performance. Testosterone is also used in old age as a youth hormone to improve muscle strength and vigor. Effect on Bone Growth and Calcium Retention: Testosterone increases the total quantity of bone matrix and causes calcium retention. The increase in bone matrix is believed to result from the general protein anabolic functions of testosterone. Because of the ability of testosterone to increase the size and strength of bones, it is often used in old aged men to treat osteoporosis.

Estrogen: Apart from its effect in causing growth of the female secondary sexual characters, estrogens serve other functions such as: Effect of Estrogens on the Skeleton: Estrogens cause increased osteoblastic activity. Therefore, at puberty, the female growth rate becomes rapid for several years. However, estrogens also cause early uniting of the epiphysis with the shafts of the long bones. This effect is much stronger in the female than in the male. As a result, growth of the female usually ceases several years earlier than growth of the male.

Osteoporosis of the Bones Caused by Estrogen Deficiency in Old Age: After menopause, the ovaries secrete almost no estrogens. This estrogen deficiency leads to (1) diminished osteoblastic activity (2) decreased bone matrix (3) decreased deposition of bone calcium and phosphate. In severe cases, this can lead to osteoporosis. Because this can greatly weaken the bones and lead to bone fracture, a large share of post-menopausal women are treated prophylactically with estrogen substitutes.

Prostaglandins and tooth movement J. R. Sandy and M. Harris Eur J Orthod (1984) 6 (3): 175-182. Abstract The effect of flurbiprofen, a prostaglandin cycloxygenase inhibitor, on tooth movement was studied using New Zealand white rabbits. Under general anaesthesia, springs were ligated between the lower first molars and incisors resulting in approximation of these teeth. Experimental animals were matched to a control animal of the same sex and weight. Experimental animals were administered daily flurbiprofen (10 mg/Kg) via a catheter passed orally into the stomach. Control animals received the vehicle only. A pair of animals (experimental and matched control) was sacrificed after 3 and 10 days, and the remaining animals after 14 days. The movement of incisors and molars was measured directly, and movement between the first and second molars measured from radiographs. Osteoclast activity in the area of crestal bone adjacent and mesial to the first molar was examined histologically.

Direct and radiographic measurements showed movement within the experimental and control groups, but no significant difference between them. However, the radiographic measurements showed a trend towards decreased tooth movement in the experimental animals.

This observation, together with a significant decrease in the number of osteoclasts in the bone adjacent to the induced tooth movement in the experimental animals, suggests non-steroidal anti-inflammatory drugs can partially inhibit orthodontic tooth movement. The most likely mechanism is the inhibition of prostaglandin synthesis with a resultant inhibition of osteoclast activity and bone resorption. However these findings suggest other undefined mechanisms remain unaffected.

American Journal of Orthodontics Volume 80, Issue 3, September 1981, Pages 256-262 Original article The effect of altered bone metabolism on orthodontic tooth movement*1 Ronald J. Midgett Ph.D., Robert Shaye D.D.S., and James F. Fruge, Jr. D.D.S. From the Louisiana State University School of Dentistry, New Orleans, La., USA Abstract The purpose of this study was to determine how bone remodeling changes induced by nutritional hyperparathyroidism affect tooth movement through alveolar bone. Twelve beagle dogs, approximately 1 year old, were randomly divided into two groups of six. The controls were fed a standard dog diet (calcium 0.54 percent, phosphorus 0.42 percent). The experimental diet was identical to that fed the controls except for a decrease in the calcium (0.12 percent) to phosphorus (1.20 percent) ratio. At the tenth week of diet administration, following extraction of the lower third premolars, the second and fourth premolars were moved toward each other with a reciprocal elastic force of 100 Gm. Twelve weeks later the animals were killed and the mandibles were prepared for laboratory evaluation, which included Paragon 1301 staining of undecalcified sections, scanning electron microscopy, and a bone ash analysis. Radioimmunoassays during the experiment showed that the test animals had significantly elevated levels of parathyroid hormone, indicating a probable state of hyperparathyroidism. The clinical data revealed more rapid tooth movement in the experimental animals. Laboratory data indicated that the hyperparathyroid animals had significantly decreased bone density, as well as bone remodeling changes consistent with high PTH levels. These findings suggest that, in addition to applied force, tooth movement is dependent upon the state of calcium metabolism in alveolar bone.

CALCIUM METABOLISM OR CALCIUM HOMEOSTASIS The Homeostatic Pathways for Calcium and Phosphorus Differ Quantitatively

Both calcium and phosphate are obtained from the diet. The ultimate fate of each substance is determined primarily by the gastrointestinal (GI) tract, the kidneys, and the bones. Calcium Handling by the GI Tract, Kidneys, and Bones. Dietary intakes may vary widely, but an average diet contains approximately 1,000 mg/day of calcium. Intakes up to twice that amount are usually well tolerated, but excessive calcium intake can result in soft tissue calcification or kidney stones. Only about one third of ingested calcium is actually absorbed from the GI tract; the remainder is excreted in the feces. The efficiency of calcium uptake from the GI tract varies with the individuals physiological status. The percentage uptake of calcium may be increased in young growing children and pregnant or nursing women; often it is reduced in older adults. Approximately 150 mg/day of calcium actually enter the GI tract from the body. This component of the calcium flux partly results from sloughing of mucosal cells that line the GI tract and also from calcium that accompanies various secretions into the GI tract. This component of calcium metabolism is relatively constant, so the primary determinant of net calcium uptake from the GI tract is calcium absorption. Intestinal absorption is important in regulating calcium homeostasis. Bone in an average individual contains approximately 1,000 g of calcium. Bone mineral is constantly resorbed and deposited in the remodeling process. As much as 500 mg/day of calcium may flow in and out of the bones. Since bone calcium serves as a reservoir, both bone resorption and bone formation are important in regulating plasma calcium concentration. In overall calcium balance, the net uptake of calcium from the GI tract presents a daily load of calcium that will eventually require elimination. The primary route of elimination is via the urine, and therefore, the kidneys play an important role in regulating calcium homeostasis. The 150 mg/day of calcium excreted in the urine represent only about 1% of the calcium initially filtered by the kidneys; the remaining 99% is reabsorbed and returned to the blood. Therefore, small changes in the amount of calcium reabsorbed by the kidneys can have a dramatic impact on calcium homeostasis.